CONNECT

Questions & Answers

I get two to three hundred emails every week asking for advice and although I try and answer them all it’s a daunting task and at times I get several months behind in my emails. At present I have over 500 emails in my inbox asking questions and asking for help that I do intend to answer so if you’re one of the ones that emailed me rest assured you will eventually get an answer.

 

In the hopes of stemming the tide of emails I’m introducing a Question and Answer section that will highlight some of the more common questions sent to me, as well as some of the ones that while not as common, will be of interest to many of you. I’ve removed all identifying information from both the question and my answer to protect their privacy.




1. 

I am a competitive drugfree powerlifter. My sole intent is to go from the 308 weight class down to the 242s, gradually. I have a high fat content in my blood so as it is, and wish to clean it up asap. My only concern with this diet is that it may increase the fat content in my blood, instead of decrease it.

2. 

I have tried so many other products for my cellulite problem and lower body fat. I have spent enough money on fat reducing creams and cellulite reducers  to supply an army. I am skeptical already, but I am willing to let lipoflush do its job, as long as I am using the product to its full potential. What is the best time to take it? I want to make sure that it does not affect my sleep patterns.

 

3. 

This may be a strange request but I crack my knuckles all the time, more of a habit than anything else except at times it does kind of unstuck a joint that feels better after I crack it. My question is will my knuckle cracking affect my grip so that it may affect my deadlift? Also will it cause arthritis later on? One more thing, what happens when you crack your knuckles? I’ve heard that it’s just some gas in the joint that gets moved around?

 

4. 

A Canadian friend has recommended a Canadian product for post workout recovery and also some other products from the same company. To me, I don't see anything there that is not covered in your products that I take. In fact the recovery product seems anemic compared to the Max-PTN that you have me on.Can you see any new magic or mystery here?

 

5. 

I just purchased online the Growth Hormone and Testo Boost products. I am a national level competitve powerlifter here in the U.S. who is drug-free and my next competition is 7 weeks away. I wanted to ask the Dr. what is the "best" protocol for me to use in taking the GH and Testo Boost products. What is the best time of day? Should I consume on an empty stomach or with food? Should I cycle for a particular period of time? And any other valuable info I could receive from the Doctor. Please ask him if he would reply to this e-mail. I would appreciate it.

 

6. 

I wanted to ask of your advice regarding homeopathic testosterone and growth hormone creams that are applied to the skin. How effective are they? Do they work better because they bypass the liver? What is your professional advice? I am just curious to know.

 

7. 

I use Resolve prior to working out and it's been a big help in energizing my training and in upping my weights. I use 5 tabs most days about a half hour before training, and on my heavy days I use 8 to 10 tabs. I noticed that Resolve contains a lot of ingredients, including NAC. I was reading that NAC can replace Milk Thistle in terms of liver cleansing, something that I'm interested in since liver problems run in my family. Any thoughts and is there enough in Resolve to do that? Also how much Beta Ecdysone is there in your Resolve propriatory blend?

 

8. 

Mike at the powerlifting magazine suggested I contact you. I hope I take no liberties in doing so? I’m 46 and began powerlifting 6 yrs ago. Over that time I progressed steadily from 185lbs to 250lbs bodyweight (never drugs and on a vegetarian diet) and progressed to handle weights of over 600lbs on the deadlift and squat and over 400 on the bench, all using just knee wraps and belt. Recently I developed a minute bone chip in my elbow and was x-rayed. The radiologist concluded I had degenerative joint disease from ‘wear and tear’ based solely on the presence of numerous osteophytes. He found zero loss in joint space. I have slightly less than normal ROM but I have ALWAYS had this even from a young man. My arms work smoothly with no crepitus whatsoever. I was blood tested for any other conditions and found negative.

Depressed at what the DJD diagnosis meant for my training, I wanted a more expert opinion, and saw an elbow surgeon who ran CT scans. The surgeon diagnosed that I did NOT have DJD but merely 'bilateral periarticular osteophytosis' as a result of “Wolff’s Law’ reaction to the heavy weights. These spurs cause clicking sometimes and can cause pain but according to the surgeon the CT indicates that my cartilage was found ‘intract’. The surgeon was the only doctor who knew of this apparent non-arthritic weight-lifting-associated 'condition'. I would like to ask your expert view on just how common my condition is among people who handle heavy weights and why do most doctors not have a clue about it?

 

9. 

First may I say how enormously grateful and indeed highly impressed I am that you have so generously taken the time to respond to my query. Your level of generosity is unheard of here in the UK  as is your level of knowledge and experience - we would never get such kind consideration in our NHS system. I am TRULY indebted to you for your thoughts so far.

My gym life is so important to me that I genuinely do not know how I would cope if I ever had to give it up (which was exactly what the radiologist told me to do!), after he asked "why anyone ever wants to lift weights I do not know?" I was furious about that 'instruction' and I have to say that two years on, my elbows feel fine despite continuing with the weights!

Second, the information you offered is extremely helpful. I am an ex-medical student myself (specialising in zoonosis and epidemiology) and we were constantly 'taught' that arthritis/osteoarthritis is a condition diagnosable ONLY where cartilage is lost. To learn that that is incorrect is not entirely surprising (I was warned at med school that "in 10 years 50% of what you've learned will be found wrong"!).

It is confusing though, if arthritis is something that in elbows can occur with cartilage intact - and the abstracts you kindly included certainly say that - then this seems to turn the usual definition of arthritis 'on its head'. From my understanding, arthritis in general is something that follows the 'pathology' of 1. cartilage damage, 2. roughened areas and osteopthytes aggravating joint capsule/ligaments, 3. inflammatory responses damaging soft and hard tissues and so on in a downward spiral. But if cartilage (I guess the most 'important' anatomical feature of a joint) remains intact in an elbow, then is the 'true' condition not more periarticular, like a 'degenerative capsulitis'? Am I talking total nonsense? Probably!

Certainly, in my own case I could not imagine smoother elbow operation. And from my x-rays/CT scan, the osteopthytes seem to be located exactly where the 'clicking' and rare discomfort occurs. For example, there is a fairly large, I should guess 4mm or so 'claw-like' osteophyte on each radial head that seems to be positioned precisely under the annular ligament of radius, and when I rotate my forearm it makes a painless clicking sound. Certain weight-lifting moves cause pain, but only certain ones. Biceps curls with a straight bar are painful and it feels like it centers on that radial annular ligament/osteophyte zone. Pushing moves never hurt, even if I do close-grip bench with 440lbs.

Your thoughts about genotype and polymorphism sound so sensible! You got me thinking, and I recall that my father's elbows always cracked/clicked whenever he would get out of a chair, even when he was in his 30's. The 'clicking' he produces was not synovial gas bubbles or whatever as occurs in hands, I know those well! He never had pain or any complaints. I appreciate this elbow clicking happens to many people now and again, but it would fit that he may have passed a 'genetic osteophyte development trait' to me too!

Once again, please know of my enormous thanks for your thoughts. I owe you!

I shall order some of your Metabolic diet on Monday and I shall indeed report back on how I get on with.

Thanks Mauro, you've been great!
 

10. 

Hi Doc,

Things are going good wgt wise. Still staying @230. Which is fine. I saw you had an article on supplementation in PL USA this month. Seems different than what you have on the directions for GHBoost and Testoboost. I been taking GHboost in the morning and LipoFlush first thing in the morning along w 2 Testoboost. After breakfast I take Inside Out and Metabolic and MVM. Same after lunch. I was taking the Resolve before wkout too.

Just ordered the PowerDrink and ThermoCell. I don't want to get to crazy w the supps but I want to get a little more boost for the wkout. Seems lately I been lethargic. I swithched to training 3 days instead of 2. SAt Squat\DL, Monday Bench\accesories Thursday Bench\accessory.

Can you give me a breakdown of how I should be using the supplements. I'm thinking I need to increase the TestoBoost and GHBoost. Also it seems like the supps are kicking in later on after the wkout. I did take 3 GhBoost tonight before wkout and 3 after wkout along w 3 testoboost. Seems like it has my metabolism rolling now after lifting over an hour ago.

Kinda floundering here. I want to get the most out of my wkouts w the supplementation I'm on. Thanks. If you can help that would be great!

 

11. 

First off it is an honor to be talking to you. Your research has been very helpful to me in helping to achieve my dreams of becoming a professional football player. But let me save you time and ask my question. I have seen countless of "sample" workout programs for football players and all are quite conflicting. One has me doing ten to fifteen reps a set while the other is preaching one reps to five reps. I am a lineman and I need power and strength but also need to be quite quick. In your intellectual opinion, what type of program should I be following?

 

12. 

I've heard you on radio shows and have read about the metabolic diet as well, and i appreciate you sharing your knowledge which has been very valuable to people like myself. I just wanted to seek your opinion on something.

Q- How do anabolic steroids and growth hormone affect the chances of mutating your genes? And can it lead to genetic diorders in your offspring?

I was having discussion about steroids with a friend who is a Biotechnology and genetics major at university and she thinks that... Androgens and GH can cause mutations to both the X and Y chromosomes in men, which can reduce chances of conceiving a child or lead to abnormalities ie. down syndrome in the off springs if such mutated genes are passed on.

 

13. 

First of all, I want you to know that I love your supplements. I started taking them last year and I am in the best shape of my life, lifting personal bests. I currently take 4 LipoFlush and 4 ThermoCell and 2 GH in the am before working out. I just started with your Creatine as well. I then take 5 Regulate before going to work.

I then take the Lipo and Thermo in the afternoon.

At night, I take 3 GH, 4 Testo with a serving of Myosin.

I also use the MRP when I have to miss a meal.

I keep carbs below the 50 grams per day.

My question is with the GH and Testo. Can I up the dose? If so, what do you recommend?
 

14. 

Hi Dr. Di Pasquale, my dad has been using your Testoboost as you suggested and things are going well for him. I was considering using your supplements for myself, for competitive powerlifting, combined with the anabolic solution for powerlifters. However my concern is that over time my body will become less responsive to the supplements (even basic supplements like creatine) and as a result the gains from them will not be at the same level. I realize that taking a lot of effective supplements now will increase the amount of muscle I'm building in the short term, but if the effectiveness decreases over time I would be better off to wait before using them to maximize my performance and muscle size in the long term, and allow me to be bigger and stronger in the end. Is there any evidence that would support such a concern? If not, then i might as well start using the supplements now so I can receive faster growth and results now and have it continue on later.

(I wasn't sure I properly explained my concern so I included the folowing example with weight/muscle gain)
For example; if there were 2 identical powerlifters both weighing 220 lbs. one decided to take creatine while the other did not. Obviously the one taking creatine (PL A) would make more progress in the short-term than the one not taking creatine (PL B). Let's say that in the same amount of time PL A got to 240 lbs. (using creatine), while PL B got to 230 lbs. (without creatine), and now they have both hit a plateau. Since PL A has already been using creatine his body has adapted to the supplementation and therefore the creatine doesn't help him to progress past this point, while PL B adds in creatine to his regimen and quickly blasts through his plateau and reaches 250 lbs., 10lbs. more than bodybuilder A who took creatine from the beginning.


Is this example plausible? (I realize that PL A could have then added in another supplement to break through his plateau, but I left out such things to simplify this example)
If I remember correctly, creatine is made from 3 amino acids and so the likelihood of your body adapting to it would likely be the same as that of protein. Also, in my example i used creatine as an example, but my concern is not only with creatine but with all supplements in general, but i guess a few specific examples would be Testoboost, GHboost, Metabolic, Resolve.

My plan would be to first start using the Anabolic Solution for Powerlifters, and then add in the basics such as Amino, and Power Drink. Once the basics are covered I would then build on these things by using Creatine Advantage, and possibly GHboost and Testboost, and possibly others. But all this depends on my training phase and budget. What do you think of this plan? Any help would be great? Thanks a lot and God bless.

 

15. 

I am a USAPL (and hopefully IPF in the future) lifter and would like to begin supplementation more effectively. I usally take creatine & glutamine along with my non-liftlting supplements (glucosamine, multivitamin, baby aspirin and omega 3). What supplements would be best for me to increase strength? I am 46 years old, 180 pounds and ~12% body fat. I just thought that Dr MD would know what works best for us drug free lifters. I also plan on ordering his book " The Anabolic Solition" but wanted to know what supplements to buy so I can get started earlier. Also, if you can suggest the times (& dosages) to use the supplements that would also be appreciated.

 

16. 

I started lifting as a pathetically scrawny 5'10" 120 lb 15yr old. I lifted heavy, ate well, and grew leaps and bounds (from a natural lifter's standpoint).  Recently, I returned to running, (something I originally did on the track team in middle school) I lost about 10 pounds of fat and I'm a highly defined 5'10 1/2" 175 lbs at age 33. I couldn't be more pleased with my V-taper and shape, though I have a problem which has plagued me from day one. I'm a terrible bench presser.  I've tried many programs and methods, and my raw max is 270 lbs in training (perfect form) and 260 lbs in competetion (I've only been to one meet which was last year.) For reps, I can put up 200 lbs for 13.

As an individual with a science background and degree in biology, I've analyzed myself deeply with respect to lifting. I have very long upper arms. I can curl with the big guys -- 150 lbs perfectly strict.  But the bench continues to plague me.  I'm 33 yrs old now and my bench has been slow to progress over the last 18 yrs.  My goal is to add 30 lbs and bench 300 lbs raw. I find gaining body weight is not particularly helpful and I've tried wide grip, close grip, etc.  I noticed that my squat increased substantially when placing the bar lower on my back -- apparently improved leverage.  Doctor, I'd greatly appreciate any advice or help that you can offer.  I do not use drugs, nor do I use supplements and prefer to avoid doing so.

Thanks for your GREAT column in Powerlifting USA.  I read it religiously.

 

17. 

I am getting ready to start dropping weight for next season. The goal is to hit 285 before dropping into my weight class as needed. I am about 320 right now but would like to drop my weight so that I keep most of my muscle mass and drop the excess body fat.

I've been on the mass phase of the Anabolic Solution for PL and it's helped me pack on the weight. I may have stayed on it a bit too long as I'm heavier than I wanted to get. I am about to start the cutting phase of the anabolic solution for powerlifters or would you suggest the radical diet instead.

I was also wondering about your new thermal product. I use lipoflush and ghboost when I diet would it be better to use the new product as well and why?

 

18. 

I have been using Testoboost on and off the past five years. At first I used it during and after doing a cycle of steroids and it worked well for me both ways. Now I'm off steroids after being on and off since the 1990s and don't intend or want to use again. I also stopped taking the Testoboost when I stopped the steroids since I wanted to get back to normal. My problem is that my testosterone levels are now too low even though I've been off for four months.

I'm not sure what the problem is but would you recommend Testoboost to help me increase my testosterone level? If so is there anything else you would recommend to get me back to normal? I’m kinda desperate as I don’t want to go back to using again if I can help it.

Thank you very much for your time and your great product.

 

19. 

I know you're a busy man, but I'd appreciate a quick word of advice.  I'm in my third week of the Anabolic Solution Diet for Bodybuilders and I'm doing great.  I feel energized even at very low levels of daily carbs.  In a couple of weeks I'm doing a long mountain bike ride of around 40 miles in one day.  So far, the only cardio activity I've done on the diet has been cross-country skiing for about an hour and a half.  It was during the initial assessment phase and I was fine during the ski, but did feel pretty drained afterwards.

So my question is, how should I eat around this long bike ride?  It will be on a Saturday, so it will be during a carb-up day.  Should I just carb-up like normal or will feeding my body carbs during this day convince my body to use carbs instead of fat for energy?

Thank you so much for your hard work and your time.

 

20. 

I think I’ve always been a mesomorph as I had more muscle than most guys my age without doing any exercise or even working. I got hooked on bodybuilding after looking at some muscle mags a friend let me borrow and I couldn’t believe the progress I’ve made in just over a year. Every one thinks I’m on steroids but I don’t even take any vitamins.

 

I started training in earnest last year and put on a lot of weight, most of it muscle. Since I concentrated more on my upper body than my lower I put on a lot of mass on my chest, shoulders and arms and got a lot stronger to the point that I’m considering doing some powerlifting as well as continuing on with my bodybuilding..

 

I’m not complaining except for the stretch marks. They’re all over the place especially in my pec-delt area and to a lesser extent my upper arms, biceps more than triceps. I’ve tried creams, lotions, vitamins but nothing helps so I’ve backed off on my training, which I really didn’t want to do.

 

Any advice on preventing them from getting worse when I get back into training again, which I’d like to do as soon as possible, and any advice on how to make the ones I’ve got less gross would really be appreciated.

 

21. 

Just to start off with let me tell you that I read your column in PL USA religiously and it’s the first thing I read in every issue.

 

Last week I read your information on nutritional supplements in your Elite Performance Newsletter and I agree with your take on the ridiculousness of the nutritional supplement ads that use heavy steroid users as models for their supplements. It’s a joke and a con job when they try to make you believe that they got their results from using the supplement line that’s being hyped as the reason for their massive physiques and strength, when instead it’s their use of 1,000 mg to 5,000 mg a day of steroids and countless other hormones and drugs that made them that way. I also understand your take on trying to maximize your natural potential by using targeted nutritional supplements and that their use will improve your body composition and performance but won’t come close to providing the results from massive use of hormones and other drugs.

 

Lately, however, there seems to be this big nitric oxide craze. Everything I’ve read on nitric oxide seems to point to the effectiveness of these supplements in doing just about everything such as allowing you to exercise longer and harder, put on more muscle, have more endurance and so on.

 

Also many of the products that are being heavily hyped in the magazines and on the internet are based on large amounts of arginine and other amino acids, and more recently on nitrates and nitrites, to dramatically up the levels of nitric oxide in the body. The people I’ve talked to that use these nitric oxide enhancer products say they work as they use them before training and feel it gives them more of a pump and better workouts. What’s your take on these nitric oxide enhancers that seem to have become the number one selling supplement for many of the big supplement companies?

22. 

Do you recommend a grand glycogen depletion workout on friday before carb up to increase the glycogen loading phase of the diet, a workout involving whole body and lots of volume?

 

23. 

What are the differences in the Anabolic Solution for bodybuilders vs powerlifters? As wrestlers we have some concerns from both areas. We need strength and even a certain amount of mass for our particular style of wrestling (Russian Sambo). We are also concerned with dropping fat to meet weight class requirements and to increase speed and agility. Is there enough of a significant difference between the two where we would need to reference both versions? Or would one serve our needs better than the other?

 

24. 

You recommend 30grams of carbs a day on weekdays,is it important to reach ketosis before carb up as recommended by dan duchaine in bodyopous,or do you not recommend reaching that state?

 

25. 

You say that you should eat no more than 30 grams of carbs for the first 12 days and then following week days. However I see in some of your sample diets in the Metabolic Diet and on line at your site www.MauroMD.com that you have a carb value of up 50 carbs a day in the 4000 and 4500 strict versions. Is this a mistake or did you mean to divert from the 30 gram limit?

 

26. 

You say that you should eat no more than 30 grams of carbs for the first 12 days and then following week days. However I see in some of your sample diets in the Metabolic Diet and on line at your site www.MauroMD.com that you have a carb value of up 50 carbs a day in the 4000 and 4500 strict versions. Is this a mistake or did you mean to divert from the 30 gram limit?

 

27. 

I am getting most of my protein through fish and lean meats and protein powders, Iam getting at least 25% of my fats from good fats but the rest is from dairy fats such as double cream and cheese I know these are very high in sat fats but are not heated or processed in any way. I am taking lots of flax seed oil and GLA and EPA etc, is my health at risk?

 

28. 

I have been reading some of your diets on line and they are quite different to what I am doing. Should i be following the diets you have on line to get results?

 

29. 

I'm mostly interested in losing weight and looking good but I'm not interested in doing any more exercise than what I get from doing my job and working at home. Can I still use the Metabolic Diet to lose weight?

 

30. 

I’ve just finished reading the Anabolic Solution. One question though, since I’ve a lot of fat to lose. How long may I stay on the cutting phase before I start seeing diminishing returns?

 

31. 

I just started the diet and notice some low carb foods will say they have 0 sugar carb, however, they have several other carb types (i.e. alcohol carbs). I noticed on your website that you say fiber carbs do not count. Are there any other carbs that do not count?

 

32. 

I had a couple of questions regarding your stance on the metabolic shift to fat burning and ketosis. In many of the resources I've been able to gain access to, they have indicated that one of the most important metabolic adaptations which spares nitrogen/protein losses during carbohydrate restriction is the adaptation of the CNS/brain to metabolizing ketones for fuel, thereby decreasing the drive for gluconeogenesis. This apparently coincided with the adaptation of skeletal muscle shifting a strong metabolic preference to fatty acids instead of ketones and/or glycolysis. Preventing ketogenic adaptations appeared to maintain nitrogen losses on starvation/ketogenic diets. I noticed that your Metabolic Diet places little emphasis on ketosis and that the protein/fat ratio in the metabolic diet would likely keep someone out of the significantly ketogenic state. Do you feel that the CNS adaptations to ketosis are not significantly important to decreased catabolism/protein sparing effects of low carb/high fat diets or that the metabolic shift of skeletal muscle is independent from the adaptations of the CNS and are more a result of primary fuel availability? Or is it that the increased protein intake is able to overcome gluconeogenic drive for catabolism of muscle mass?

 

33. 

Would you say the home scales that give you your fat percentage are more accurate than the calipers?

 

34. 

I am following the Anabolic Solution. When do I take the Creatine Advantage in relation to my weight workouts and also my off-days (or cardio-only days) and also in relation to meals?

 

35. 

If I'm following the metabolic diet, is it OK to still supplement with CLA since I heard that it helps to lose body fat and weight?

 

36. 

I have both the Metabolic Diet and Anabolic Solution book for Powerlifting books and have been following the shifting of the macronutrients between weekdays and weekends. Right now I’m starting to cut back and entering the cutting phase to minimize body fat and keep muscle so I’m more effective at my bodyweight class. Although I’ve read both books and looked on line, I’m still a bit confused: Just how much protein should I be eating in the various phases, not so much in the mass phase but more so in the cutting phase when I cut back on calories? As I drop the calories in order to lose weight, mostly in body fat, should I cut back on the protein and keep fat intake high or the other way around?

 

37. 

I am 32 years old and probably won't ever compete in a bodybuilding competition, but you never know. But I do want to gain as much lean muscle mass as possible. I am very serious about meeting this goal and am looking for direction. I am looking at The Metabolic Diet book and The Anabolic Solution for Bodybuilders book. Which book do you think will better help me?

 

38. 

I started the Metabolic Diet last week and I'm having problems with constipation. What can I do to regulate my bowels?

 

39. 

Hi I've been reading some of your articles in PL USA. I thought you might be able to shed some light on a question i have. I need to determine whether its is beneficial to consume protein whilst drinking alcohol and if so why? For example, would drinking a protein enriched beer be beneficial? I have found heaps of material explaining why it's bad to consume alcohol and the effects drinking has on protein synthesis etc. But nothing regarding this topic. Any information you could give me would be awesome Thanks for your time.

 

40. 

I had a couple of questions regarding your stance on the metabolic shift to fat burning and ketosis. In many of the resources I've been able to gain access to, they have indicated that one of the most important metabolic adaptations which spares nitrogen/protein losses during carbohydrate restriction is the adaptation of the CNS/brain to metabolizing ketones for fuel, thereby decreasing the drive for gluconeogenesis. This apparently coincided with the adaptation of skeletal muscle shifting a strong metabolic preference to fatty acids instead of ketones and/or glycolysis. Preventing ketogenic adaptations appeared to maintain nitrogen losses on starvation/ketogenic diets. I noticed that your Metabolic Diet places little emphasis on ketosis and that the protein/fat ratio in the metabolic diet would likely keep someone out of the significantly ketogenic state. Do you feel that the CNS adaptations to ketosis are not significantly important to decreased catabolism/protein sparing effects of low carb/high fat diets or that the metabolic shift of skeletal muscle is independent from the adaptations of the CNS and are more a result of primary fuel availability? Or is it that the increased protein intake is able to overcome gluconeogenic drive for catabolism of muscle mass?

 

41. 

I have tried so many other products for my cellulite problem and lower body fat. I have spent enough money on fat reducing creams and cellulite reducers to supply an army. I am skeptical already, but I am willing to let lipoflush do its job, as long as I am using the product to its full potential. What is the best time to take it? I want to make sure that it does not affect my sleep patters. Also what diet plan do you suggest. I have about 60 pounds I need to lose?

 

42. 

I’m a 42 yr old powerlifter - for my own recreation, at least for now. I need help choosing which of you books will help me lose 50 lbs of unwanted fat, while maintaining muscle, strength, and energy levels.

 

43. 

I was wondering which book I should get the anabolic solution for bodybuilders or the metabolic diet. My main hobby is bodybuilding for the last couple years but I haven't given my diet very much thought until recently. I have always carried around about 20 extra pounds so I wasn't sure which book would be best for me. I also wanted to start my assessment phase but I was confused on the amount of fats. Being a bodybuilder I consume about 210 grams of protein daily and was wondering how many grams of fats I need. The website suggests 40-60% of fats but I don't know if that’s 40-60% of daily calories or 40-60% of daily gram intake.

 

44. 

Can you recommend some supplements that helps to efficiently increase and transfer oxygen to the muscles during an intense workout?

In Jui Jitsu we roll for 5 minute rounds, sometime 3 rounds back to back and I am gassing out after about 7 mins...breathing really hard. I know part of it is controlling the breathing, and I'm working on that, but I want to know if there is something else I can do to help with this. I know you're busy, but when you have time, let me know your thoughts.

 

45. 

Can diabetics take advantage of the Metabolic Diet? I asked my doctor and he didn’t know enough about your diets to say one way or the other. At this point I’m on a high carb, low fat diet but I don’t think it’s the best diet for me since I’m having problems keeping my sugar under control, and I’m holding a lot of body fat. Although I try and do some form of exercise most days of the week what's the best exercise program to follow with the diet?

 

46. 

I just have a question. First thing is that i have just read two of your book ( the metabolic diet and the anabolic diet for powerlifters) , they are really fantastic. I just want to know about coconut oil. Is it allowed on the diet since it is a fat and is it healthy or not? Can i use it raw or for frying instead of other oils like canola ?

 

47. 

Is it better to have a cold or hot shower after training and whichever one is best, how long should I shower to get whatever benefits there ar?. If this sounds like I am confused it's because I am. I've been told that a hot shower is better because it relaxes you, that a cold shower is better as it keeps injuries down and will help you recover better, and that you should take a hot shower for a few minutes, then immediately a cold shower for a few minutes and then hot and then cold and so on for up half an hour. Then there's the whole bit about cold water immersion rather than a cold shower. Personally I'd just like to have a warm shower to clean off after training but if doing it a specific way is better for my performance then I'll try it out.

48. 

My name is Frank and I've ordered products from you over the last few years. However, I've run into some problems that just aren't going away even though I've seen other people, including doctors and specialists. These problems are ongoing and making me desperate to find help for them since I can't train and feel tired most of the time. I'd like to contact Dr. Di Pasquale regarding a private consultation with him. First of all does he do one on one consultations, and secondly I would like to know how much he would charge me. 

49. 

I've been on your Anabolic Diet for Powerlifters and have never felt better. I don't mean this in the sense that my lifts have gone up or that I'm leaner but more muscular, even though both of those are true. What I mean is that I feel better, not depressed anymore although I wouldn't really call it depression as it was more like a sadness that I'd wake up with in the morning and would stay with me for the day, sometimes better sometimes worse. The tighter I am with the diet, the better I feel.

 

What I go back to a low fat, high carb diet, even though I don't eat junk carbs, I go back to feeling not all that good. So I just switch back to your diet and things are better. I know that this is not all in my head although at times in the past I've been tempted to see a psychiatrist. I hesitated because I did go to counseling when I went to university but it really didn't help. Anyways just wanted to let you know what I've been going through and how your diet affects me. Do you have any explanation as to why diet affects me so much, and is it the same for others?
50. 

Dr Di: What do you know about this company’s supplement lineup? I have a good friend who swears by these, he is diabetic also and thinks these products are the best in the world. I am sure you know the real answer and I think he should be taking your products.

51. 

Hi Dr Dipasquale, hope your well!

Following on from Carl's announcement on Super Human Radio (SHR) that your taking questions through your e-mail for the SHR show, I would like to ask the following in the hopes that you can clear up a massive source of confusion and frustration I've been feeling regarding post workout (pwo) nutrition:

I've read your article pwo carbs may be counterproductive and listened to several podcasts where you elucidate the same, no problem there and makes a lot of sense and something I've stuck to religiously since starting the Anabolic Diet for powerlifters - Oct'08 - abstain from carbs and keep protein/amino acids and fat high pwo! I’ve seen and heard the Anabolic Diet (the updated version in your Anabolic Solution for Powerlifters) and pwo nutrition etc discussed on several forums and shows and they mainly discuss the role of insulin and they go on to say that it's high insulin levels that should be avoided pwo as well as carbs.

 

Now, the AS booksuggests Power Drink during the workout and Amino immediately pwo. I thought that the whey and amino acids in Power Drink have the ability to spike Insulin pretty darn good and rapid, I'm not sure whether it's of the same magnitude as carbs but I think it might be pretty significant. Therefore, is it glycogen supercompensation in muscle cells and it's detrimental effects on insulin sensitivity (IS) that should be avoided pwo or is it high insulin levels in general that should be avoided; as a result of what I have heard I now see this as carbs=increase in insulin=decrease in IS=bad & Whey/Aminos=increase in insulin=would you get the same decrease in IS as a result just as you would with carbs?

 

I'm slightly worried that I may be short changing the anabolic effects even thoughI'm using your supplements and trying to get better results from training by taking them as you suggest during and after training which provides me with the essential amino acids, and especially the BCAA and Glutamine. But I am worried that I’m stimulating too much insulin and that it will stop me from maintaining prolonged increases in protein synthesis even though I’m sticking to your regimen – and as per your regimen I’m following up an hour later with your MRP LoCarb, which I mix with some raw eggs and a few tablespoons of flax seed and olive oil in order to give me some added protein and fat.

 

Also, you mention several times on podcasts and in some articles off your MetabolicDiet.com site, that whey is not a good source of protein due to it's rapid oxidation/gluconeogenesis rate and suggest if you were to take in powder to take a casein product yet your Power Drink contain whey, mostly as a pure whey isolate. Also your MRP contains both whey and casein, rather than just casein alone, and you've mentioned in one of your books that the absorption rates of different proteins are not affected when taken together. At which point does it become deleterious to use whey, it can't be all bad as it's formulated into your products or should Whey now be avoided indefinately?

Thank you for your time, take care and I look forward to looking over your new master site and also looking forward to when it goes live.

52. I’m a drug tested athlete who has been using your LipoFlush for a few years now. It’s a great product as it not only keeps my body fat levels down without me having to lose muscle mass but also gives me loads of energy for training and has improved my performance. However, recently I was told by my coach that LipoFlush contains a substance that is banned by WADA/IOC and will cause a positive drug test. That substance is citrus aurantium. I was at a loss at how to respond as I’ve been tested several times while on LipoFlush and never tested positive. On the other hand even though I’ve never tested positive I need some assurance that I won’t test positive in future drug tests.


1. 

I am a competitive drugfree powerlifter. My sole intent is to go from the 308 weight class down to the 242s, gradually. I have a high fat content in my blood so as it is, and wish to clean it up asap. My only concern with this diet is that it may increase the fat content in my blood, instead of decrease it.

 

Since you’re attempting to lose a significant amount of weight, the best way for you to do that is to follow the principles behind my Radical Diet (basically a variant of my Metabolic Diet), increasing the calories that I recommend for quick weight loss so that the loss of weight (mostly fat) is more gradual. I’ve done numerous follow ups on people, including powerlifters, that followed the diet and I’ve yet to find one that didn’t improve their lipid profile.

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2. 

I have tried so many other products for my cellulite problem and lower body fat. I have spent enough money on fat reducing creams and cellulite reducers  to supply an army. I am skeptical already, but I am willing to let lipoflush do its job, as long as I am using the product to its full potential. What is the best time to take it? I want to make sure that it does not affect my sleep patterns.

 

 

LipoFlush can be used in the AM and mid day and should not disturb your sleep. You can take it anytime but if pills tend to upset your stomach, you can use it just before meals. A lot of people also use the LipoFlush 15 minutes or so prior to exercising, as long as the you are not exercising in the evening.

LipoFlush is a stand alone product and effective product for weight and fat loss. 

Consistently using LipoFlush twice a day should do the trick for you. I would take it as I have outlined above. You can start off with 2 tabs twice a day and up that to 4 tablets twice a day.

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3. 

This may be a strange request but I crack my knuckles all the time, more of a habit than anything else except at times it does kind of unstuck a joint that feels better after I crack it. My question is will my knuckle cracking affect my grip so that it may affect my deadlift? Also will it cause arthritis later on? One more thing, what happens when you crack your knuckles? I’ve heard that it’s just some gas in the joint that gets moved around?

 

 

First of all let me say that I crack my knuckles once or twice a week and have done so for decades. In my case nothing bad has come of it - no arthritis, no effect on my grip strength. In talking to lifters and other athletes over the years who also cracked their knuckles I haven’t heard that they suffered any problems.

 

Besides my personal experience and observation a recent study published just last month looked at the effects of knuckle cracking and hand osteoarthritis. I’ve copied the citation and abstract below. You can also get the full text of this paper at http://www.jabfm.org/cgi/content/full/24/2/169, and the PDF version of the paper at http://www.jabfm.org/cgi/reprint/24/2/169.

 

 

The first few paragraphs of the full paper states:

 

Knuckle cracking (KC) is a behavior that involves manipulation of the finger joints that results in an audible crack, and it is often done habitually. Prevalence estimates vary between 25% and 54%, depending on the population studied. The behavior can become habitual because of immediate joint tension release and increased joint range of motion.

 

During an attempt to crack a knuckle, the joint is manipulated by axial distraction, hyperflexion, hyperextension, or lateral deviation. This lengthens part or all of the joint space and greatly decreases intra-articular pressure, causing gases that have dissolved in the synovial fluid to form microscopic bubbles, which coalesce. When the joint space reaches its maximum distraction (up to 3 times its resting joint space distance), joint fluid rushes into the areas of negative pressure. The larger bubbles suddenly collapse into numerous microscopic bubbles, leading to the characteristic cracking sound. The maneuver leaves the joint space wider than it had been and synovial fluid more widely distributed. The stretching of joint ligaments required to produce the widened joint space also leaves the joint with greater range of motion. It typically takes at least 15 minutes for the joint to be able to be cracked again because of the time required for the microscopic bubbles to fully dissolve into solution and for the joint space to retract back to its resting position.

 

The paper then addresses the urban legend that KC leads to arthritis of the hand joints.The authors conclude that KC does not seem to be a factor in osteoarthritis of the hands.

 

 

So the bottom line from this study is that a history of habitual knuckle cracking, including the total duration and cumulative exposure to knuckle cracking, is not associated with an increased risk of hand osteoarthritis. And from my own and others experience it also doesn’t seem to affect grip strength.

 

There is however, one caveat here. I wouldn’t recommend forced cracking of the knuckles in an injured hand as this may increase inflammation and delay healing. So if it hurts to crack the knuckles, then don’t until the inflammation dies down and the injury is healed.

 

---------------------------------------

 

J Am Board Fam Med. 2011 Mar-Apr;24(2):169-74.

Knuckle cracking and hand osteoarthritis. Deweber K, Olszewski M, Ortolano R.

Source: Department of Family Medicine, Uniformed Services University of the Health Sciences, Bethesda, MD 20814, USA. kdeweber@usuhs.mil

Abstract: BACKGROUND: Previous studies have not shown a correlation between knuckle cracking (KC) and hand osteoarthritis (OA). However, one study showed an inverse correlation between KC and metacarpophalangeal joint OA.

METHODS: We conducted a retrospective case-control study among persons aged 50 to 89 years who received a radiograph of the right hand during the last 5 years. Patients had radiographically proven hand OA, and controls did not. Participants indicated frequency, duration, and details of their KC behavior and known risk factors for hand OA.

RESULTS: The prevalence of KC among 215 respondents (135 patients, 80 controls) was 20%. When examined in aggregate, the prevalence of OA in any joint was similar among those who crack knuckles (18.1%) and those who do not (21.5%; P = .548). When examined by joint type, KC was not a risk for OA in that joint. Total past duration (in years) and volume (daily frequency × years) of KC of each joint type also was not significantly correlated with OA at the respective joint.

CONCLUSIONS: A history of habitual KC-including the total duration and total cumulative exposure-does not seem to be a risk factor for hand OA.

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4. 

A Canadian friend has recommended a Canadian product for post workout recovery and also some other products from the same company. To me, I don't see anything there that is not covered in your products that I take. In fact the recovery product seems anemic compared to the Max-PTN that you have me on.Can you see any new magic or mystery here?

 

 

I don’t like to put down other companies products. But in fairness to you, I have to say that yes there's no magic or mystery in the formulations.

In fact, because they're Canadian products, which have strict government limitations on what can be used and how much in Canadian made supplements (see some examples urls below that will give you some examples of some ingredients that can't be used in Canadian supplements), they're vastly inferior to what I offer in my products. Also Health Canada mandates that Canadian products have to classify the ingredients in them as medicinal – strange choice of words for nutritional supplement ingredients.

http://webprod.hc-sc.gc.ca/nhpid-bdipsn/ingredReq.do?id=5188?=eng

http://webprod.hc-sc.gc.ca/nhpid-bdipsn/ingredReq.do?id=4882?=eng

http://webprod.hc-sc.gc.ca/nhpid-bdipsn/ingredReq.do?id=4901?=eng

http://webprod.hc-sc.gc.ca/nhpid-bdipsn/ingredReq.do?id=4896?=eng

http://webprod.hc-sc.gc.ca/nhpid-bdipsn/ingredReq.do?id=5774?=eng

http://webprod.hc-sc.gc.ca/nhpid-bdipsn/ingredReq.do?id=4639?=eng

As such, comparing Max-PTN with this recovery product is like comparing children’s chewable vitamins to my MVM. Max-PTN is a combo of three supplements meant to be used after training in order to maximize the anabolic and fat burning effects of exercise, and to facilitate recover, for many hours after training. BTW if you look up the Max-PTN updated info on my new site www.MauroMD.com, you’ll find the second half of the information is an article that you’ll find useful, titled Post Exercise Nutrition for Maximizing the Anabolic Effects of Exercise. In this article I outline what you should do after training in order to increase protein synthesis and keep you in an anabolic and fat burning state for at least 24 hours after training.

My views on post training nutrition have caused considerable controversy since my views on the ideal post training nutrition protocol are very different from the general consensus of using carbohydrates alone or a combination of carbohydrates and protein after training. However, lifters and other athletes who have tried it find it works much better for them as far as body composition and performance than what the carbs or protein carbs combination that they were using.

Getting back to Canadian supplements, the bottom line is that they generally suck, which is why I manufacture all of my products in the US where I can use the ingredients I want in the quantities I find most effective. This is also the reason why many nutritional supplement stores in Canada usually carry US products “under the counter” to sell to people who know the difference and want more effective supplements.

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5. 

I just purchased online the Growth Hormone and Testo Boost products. I am a national level competitve powerlifter here in the U.S. who is drug-free and my next competition is 7 weeks away. I wanted to ask the Dr. what is the "best" protocol for me to use in taking the GH and Testo Boost products. What is the best time of day? Should I consume on an empty stomach or with food? Should I cycle for a particular period of time? And any other valuable info I could receive from the Doctor. Please ask him if he would reply to this e-mail. I would appreciate it.

 

 

GHboost and TestoBoost work synergistically together to enhance the anabolic effects on skeletal muscle and energy metabolism. In fact, a paper published last month states that both growth hormone and testosterone support each other’s anabolic effects and that neither works as well without the other. Something I’ve been saying for almost 4 decades. I’ll be doing an article based on this paper and expounding on the more complex synergism between GHboost and TestoBoost. The paper is: Birzniece V, Meinhardt UJ, Umpleby MA, Handelsman DJ, Ho KK. Interaction between Testosterone and Growth Hormone on Whole-Body Protein Anabolism Occurs in the Liver. J Clin Endocrinol Metab. 2011 Apr;96(4):1060-7.

 

 

Other papers have also shown the synergism. For example: Gibney J, Wolthers T, Johannsson G, Umpleby AM, Ho KK. Growth hormone and testosterone interact positively to enhance protein and energy metabolism in hypopituitary men. Am J Physiol Endocrinol Metab. 2005 Aug;289(2):E266-71.

 

The best things about GHboost and TestoBoost is that they naturally increase GH and Testosterone, as well as increasing IGF-1 levels, insulin sensitivity, and have a host of other beneficial effects. Look up the PDF files in my store on both as they’ll give you loads of evidence based information. A recent paper has shown that increasing endogenous levels of GH and Testosterone is the way to go for getting the most out of your training. I’ve copied the citation and abstract from PubMed below.

 

Keeping this in mind I would use both before and after training both to enhance the beneficial effects of your training on strength and to enhance recovery after training.

 

Start with 2 TestoBoost and 3 GHboost both before and after training. On days you don’t train take 4 TestoBoost and 5 GHboost about a half hour before bed with a protein drink (have a look at NitAbol in my store) or a protein snack without carbs. Taking both on non training days improves recovery as well as extending the anabolic effects between training sessions.

 

 

I always suggest that athletes cycle their supplements, using more as they get closer to major competitions and not use them when they’re taking time off or just training light such as after a competition or if they’re training relatively light. In fact since both GHboost and TestoBoost naturally maximize endogenous levels of growth hormone and testosterone, they can be cycled just like drug using athletes cycle their exogenous hormones. The big difference of course is that both my products increase endogenous levels and don’t suppress the hypothalamic-pituitary-testicular axis, and don’t have the adverse effects of the drugs. Going off both for periods of time also doesn’t result in states of hormone deficiency as do the drugs. And lastly, for drug tested athletes, both have absolutely no chance of causing a positive drug test.

 

You can take them on an empty stomach or with food. I suggest that you don’t take them with carbs as I mentioned above.

 

 

FYI I’ve attached some info that will be on my new master site – which will hopefully be up by the end of May this year. It’s in draft mode right now but if you wish you can have a look at what’s up if you go to www.MauroMD.com.

 

 

I’m working on the final draft of the new info for TestoBoost version IV, which will be out about the same time as my site goes live. It’s an improvement over the already potent version III. When you reorder ask for the version IV as it will be ready before it’s put into the store. I’ve attached the latest finished draft of the new TestoBoost ver IV. Let me know if you have any other questions and also how you do with the supplements.

 

Eur J Appl Physiol. 2011 Feb 16. [Epub ahead of print]
Physiological elevation of endogenous hormones results in superior strength training adaptation.

Rønnestad BR, Nygaard H, Raastad T.

Source: Lillehammer University College, PB. 952, 2604, Lillehammer, Norway, bent.ronnestad@hil.no.

Abstract:: The purpose of this study was to determine the influence of transiently elevated endogenous hormone concentrations during exercise on strength training adaptations. Nine subjects performed four unilateral strength training session per week on the elbow flexors for 11 weeks. During two of the weekly sessions, leg exercises were performed to acutely increase the systemic anabolic hormone concentration immediately before the exercises for one of the elbow flexors (L + A). On the two other weekly training sessions, the contralateral elbow flexors were trained without prior leg exercises (A). By randomizing one arm of the subjects to serve as a control and the other as experimental, both conditions have the same nutritional and genetic environment. Serum testosterone and growth hormone was significantly increased during the L - A training session, while no hormonal changes occurred in the A session. Both A and L + A increased 1RM in biceps curl, peak power in elbow flexors at 30 and 60% of 1RM, and muscle volume of the elbow flexors (p < 0.05). However, only L + A achieved increase in CSA at the part of the arm flexors with largest cross sectional area (p < 0.001), while no changes occurred in A. L + A had superior relative improvement in 1RM biceps curl and favorable muscle adaptations in elbow flexors compared to A (p < 0.05). In conclusion, performing leg exercises prior to arm exercises, and thereby increasing the levels of serum testosterone and growth hormone, induced superior strength training adaptations compared to arm training without acute elevation of hormones.
 

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6. 

I wanted to ask of your advice regarding homeopathic testosterone and growth hormone creams that are applied to the skin. How effective are they? Do they work better because they bypass the liver? What is your professional advice? I am just curious to know.

 

 

The homeopathic creams are totally useless, beyond a placebo effect if you believe in them.Over the years I’ve kept an open mind about homeopathy but after experimenting with homeopathic preparations including the so called hormonal creams and finding no statistically relevant results, I am extremely skeptical.

 

As well as my personal trials, if you look at the literature, as I have over the last several decades, homeopathic remedies have never been shown in any valid and rigorous research to be any more effective than placebo.

 

 

Bottom line in my opinion is that homeopathy offers absolutely no objective benefits, although subjectively, depending on what results you expect from their use, you may get some benefits but the benefits are not from the homeopathic preparations but rather from your own expectations and thus mindset.

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7. 

I use Resolve prior to working out and it's been a big help in energizing my training and in upping my weights. I use 5 tabs most days about a half hour before training, and on my heavy days I use 8 to 10 tabs. I noticed that Resolve contains a lot of ingredients, including NAC. I was reading that NAC can replace Milk Thistle in terms of liver cleansing, something that I'm interested in since liver problems run in my family. Any thoughts and is there enough in Resolve to do that? Also how much Beta Ecdysone is there in your Resolve propriatory blend?

 

 

First of all let me tell you that there's 200 mg of beta ecdysone (used for its anabolic effects) and 100 mg of NAC (N-acetylcysteine - used for its antioxidant and other effects) in 5 tabs of Resolve. You can read more about the ingredients in Resolve, and what they do if you look at the PDF file on Resolve at www.MDPlusStore.com.

To answer your basic question, I think that both NAC and milk thistle are hepatoprotectant (see abstract below) and it's quite likely that they would complement each other as far as their liver protectant effects. I think, however, that milk thistle is the more active of the two in that regard and has more research to back up its beneficial hepatic effects whereas there's not as much to back up NAC's effects outside of NAC's protective effects on acetaminophen induced liver damage. I use both NAC and milk thistle in MVM, Antiox and ReNew. I use NAC in a few more of my products as against milk thistle as NAC, being a thiol, has superior antioxidant effects, plus other effects that are beneficial for athletes (see abstract below).

As far as how much of each ingredient I use in my formulations, that requires I keep in mind the function of the formulation, as well as the number of products that may contain various ingredients.

Since many athletes including top level powerlifters, bodybuilders and elite Olympic and professional athletes use several of my products together I keep in mind not only the amount of an ingredient in an individual product but the amount in my whole line when I formulate them. As such, I'm careful to not over do any one ingredient to as to negate any possible adverse effects. For example, take vitamin D. If someone used all of my products with vitamin D in it the total wouldn't be more than 2,000 IU per day. This includes the new MVM, which contains 800 IU, and the new version IV TestoBoost - due out by the end of February or early March, which will contain 400 IU.

I also use ingredients that act additively and/or synergistically to provide certain desired effects. This makes my targeted multi-ingredient products more effective than other nutritional supplement products on the market, but at the same time safer since I don't have to use any potentially harmful dosages of any one ingredient to get the desired effects.

So, as far as the dosage of NAC, 100 mg is a good dose as far as anti-oxidant effects, especially when used together with other antioxidants, but more would be better if you're looking for significant hepatoprotective effects against oxidative stress. And that's available to athletes who use several of my supplements, as many do in complex regimens to improve body composition and performance. For example, a number of my supplements contain NAC at the 100 mg level, including Antiox, ReNew, Joint Support, and InsideOut. MVM contains 50 mg of both NAC and milk thistle.

 

--------------------------------

Phytother Res. 2010 Oct;24(10):1423-32.

Milk thistle in liver diseases: past, present, future. Abenavoli L, Capasso R, Milic N, Capasso F.

Department of Experimental and Clinical Medicine, University Magna Graecia, Catanzaro, Italy. l.abenavoli@unicz.it

Abstract Silybum marianum or milk thistle (MT) is the most well-researched plant in the treatment of liver disease. The active complex of MT is a lipophilic extract from the seeds of the plant and is composed of three isomer flavonolignans (silybin, silydianin, and silychristin) collectively known as silymarin. Silybin is a component with the greatest degree of biological activity and makes up 50% to 70% of silymarin. Silymarin is found in the entire plant but it is concentrated in the fruit and seeds. Silymarin acts as an antioxidant by reducing free radical production and lipid peroxidation, has antifibrotic activity and may act as a toxin blockade agent by inhibiting binding of toxins to the hepatocyte cell membrane receptors. In animals, silymarin reduces liver injury caused by acetaminophen, carbon tetrachloride, radiation, iron overload, phenylhydrazine, alcohol, cold ischaemia and Amanita phalloides. Silymarin has been used to treat alcoholic liver disease, acute and chronic viral hepatitis and toxin-induced liver diseases.

-------------------------

J Vet Pharmacol Ther. 2010 Feb;33(1):95-9.

Evaluation of prophylactic and therapeutic effects of silymarin and N-acetylcysteine in acetaminophen-induced hepatotoxicity in cats. Avizeh R, Najafzadeh H, Razijalali M, Shirali S.

Department of Clinical Sciences, Faculty of Veterinary Medicine, Shahid Chamran University, Ahvaz, Iran.

Abstract Cats most commonly receive toxic amounts of acetaminophen (APAP) because owners medicate them without consulting a veterinarian. The aim of this study was to compare the hepatoprotective action of silymarin and N-acetylcysteine (NAC) against APAP poisoning. Twenty healthy cats were randomly allotted to five equal groups. Animals in group A were given APAP (single dose 150 mg/kg, p.o.); groups B and C consisted of cats that received NAC (100 mg/kg, p.o.) or silymarin (30 mg/kg, p.o.) concurrent with APAP administration respectively; groups D and E were treated like groups B and C, respectively, but 4 h after APAP administration. The serum concentrations of alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP), lactate dehydrogenase (LDH), methemoglobin, and total and direct bilirubin were measured before APAP administration and 4, 24, and 72 h later. A single oral administration of APAP significantly elevated serum concentrations of ALT, AST, ALP, LDH, methemoglobin, and total and direct bilirubin. In both the groups receiving APAP plus NAC or silymarin, levels of serum enzyme activities, methemoglobin, and total and direct bilirubin remained within the normal values. It was concluded that silymarin as well as NAC can protect liver tissue against oxidative stress in cats with an APAP intoxication.

--------------------

Respir Physiol Neurobiol. 2009 Jan 1;165(1):67-72. Epub 2008 Oct 17.

Effects of N-acetylcysteine on respiratory muscle fatigue during heavy exercise. Kelly MK, Wicker RJ, Barstow TJ, Harms CA.

Department of Kinesiology, Kansas State University, 1A Natatorium, Manhattan, KS 66506, United States.

Abstract Respiratory muscle fatigue (RMF) occurs during heavy exercise in humans. N-acetylcysteine (NAC) infusion has been shown to reduce RMF, suggesting that oxidative stress is a contributing factor. The purpose of the present study was to determine the effect of an acute oral dose of NAC on RMF during heavy exercise. Subjects (n=8) were given either placebo (PLA) or NAC (1,800 mg) 45 min prior to a 30 min constant load (85V(O)(2peak)), discontinuous exercise test. Maximum respiratory pressures (inspiratory, PI(max); expiratory, PE(max)) and venous blood samples were made prior to and following each 5 min of exercise. There was no difference (p>0.05) in PI(max) between NAC (127.9+/-34.1 cm H(2)O) or PLA (134.1+/-28.1cm H(2)O) at rest. During exercise, PI(max) was significantly lower with PLA ( approximately 14%) compared to NAC at 25 and 30 min suggesting less RMF with NAC. There were no differences (p>0.05) between groups in PE(max), V(O)(2), V(E), or heart rate at rest or throughout exercise. These results suggest that an acute dose of NAC reduces RMF during heavy exercise.

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8. 

Mike at the powerlifting magazine suggested I contact you. I hope I take no liberties in doing so? I’m 46 and began powerlifting 6 yrs ago. Over that time I progressed steadily from 185lbs to 250lbs bodyweight (never drugs and on a vegetarian diet) and progressed to handle weights of over 600lbs on the deadlift and squat and over 400 on the bench, all using just knee wraps and belt. Recently I developed a minute bone chip in my elbow and was x-rayed. The radiologist concluded I had degenerative joint disease from ‘wear and tear’ based solely on the presence of numerous osteophytes. He found zero loss in joint space. I have slightly less than normal ROM but I have ALWAYS had this even from a young man. My arms work smoothly with no crepitus whatsoever. I was blood tested for any other conditions and found negative.

Depressed at what the DJD diagnosis meant for my training, I wanted a more expert opinion, and saw an elbow surgeon who ran CT scans. The surgeon diagnosed that I did NOT have DJD but merely 'bilateral periarticular osteophytosis' as a result of “Wolff’s Law’ reaction to the heavy weights. These spurs cause clicking sometimes and can cause pain but according to the surgeon the CT indicates that my cartilage was found ‘intract’. The surgeon was the only doctor who knew of this apparent non-arthritic weight-lifting-associated 'condition'. I would like to ask your expert view on just how common my condition is among people who handle heavy weights and why do most doctors not have a clue about it?

 

 

Your case is unusual as most people with the changes you describe have associated pain and stiffness. Primary osteoarthritis of the elbow usually presents with osteophytes but an intact joint space and cartilage. So by this criteria you would seem to have primary arthritis of the elbow, but what’s perplexing is the lack of pain and stiffness. Regardless, the osteophytes that have formed can occur with the use of weights or any heavy manual labor. As far as Wolf’s Law, it merely states that bone will adapt to whatever load it’s subjected to – have a look at http://en.wikipedia.org/wiki/Wolff's_law. It doesn’t explain why you’ve formed osteophytes around your elbow joint when most people don’t. It’s quite likely that you have a genotype with a polymorphism that makes you susceptible to osteophyte formation around joints that have been mechanically stressed, such as from lifting.

I’ve seen a dozen or so cases of primary arthritis of the elbow over the last several decades as it’s not all that common.  With the lack of the usual symptoms it would be hard for most doctors to diagnose. It would have been an easier diagnosis if you had presented with the typical features - one of an arthritic process with osteophyte formation, little or no change in the joint space and cartilage, and some capsular contraction that limits ROM to variable degrees depending on the pathology present.

In the cases I’ve seen, more severe than what you’re describing, most several went on to surgery to remove the osteophytes and release any significant contractions. This was done mostly by arthroscopic surgery. In all cases the ones operated on in this way went back to benching once they healed, progressing very slowly from light to heavier weights. Unfortunately I haven’t kept track of them so don’t know how they did over the long term.

FYI I’ve copied five abstracts of papers that you may find useful.

In your case, since your elbows function pretty normally except for clicking and occasional pain, it might be worth while to try a nutritional supplement like my Joint Support for several months to see if halts the osteophyte formation and even results in some regression.

Let me know how things go.

----------------------------------------------------------------

J Am Acad Orthop Surg. 2008 Feb;16(2):77-87.
Primary osteoarthritis of the elbow: current treatment options.
Cheung EV, Adams R, Morrey BF.

Department of Orthopaedic Surgery and Sports Medicine, Stanford Hospital and Clinics, Stanford , CA 94305-5335 , USA .

Abstract: In the elbow, as in other joints, primary osteoarthritis is characterized by pain, stiffness, mechanical symptoms, and weakness. But primary osteoarthritis of the elbow is unique in that there is relative preservation of articular cartilage and maintenance of joint space, with hypertrophic osteophyte formation and capsular contracture. Medical treatment and physical therapy may be initiated in the early stages of the disease process. Surgical treatment options include arthroscopic osteocapsular débridement, open ulnohumeral arthroplasty, distraction interposition arthroplasty, and total elbow arthroplasty. The potential for instability and loosening following total elbow arthroplasty in the setting of primary osteoarthritis limits the clinical application of this procedure. This patient population is generally younger than that recommended for total elbow arthroplasty, and their higher functional demands have limited the long-term success of this treatment option. The improvement in arthroscopic débridement techniques is perhaps the greatest advancement in the treatment of osteoarthritis of the elbow in recent years.

----------------------

J Hand Surg Am. 2009 Apr;34(4):761-8.
Elbow arthritis: current concepts.
Kokkalis ZT, Schmidt CC, Sotereanos DG.

Department of Orthopaedic Surgery, Allegheny General Hospital , Pittsburgh , PA 15212 , USA .

Abstract: The purpose of this article is to provide an update and analyze current management, treatment options, and outcomes of elbow arthritis. This article focuses on studies that have been published in the past 5 years. Nonoperative management may provide symptomatic relief in the early stages of the disease process for most patients. Surgical treatment is guided by disease etiology and severity, patient age, and functional demands. Arthroscopic or open synovectomy, debridement arthroplasty, and interposition arthroplasty are generally recommended for the young and active patient population, whereas for low-demand and elderly patients with end-stage painful arthritis, total elbow arthroplasty is considered a more suitable surgical option. Advances in arthroscopic techniques and implant design have led to substantial improvements in treatment of elbow arthritis.

----------------------

J Hand Surg Am. 2008 May-Jun;33(5):746-59.
Surgical options for the arthritic elbow.
Gallo RA, Payatakes A, Sotereanos DG.

Shoulder and Sports Medicine Service, Hospital for Special Surgery, New York , NY 10021 , USA . august_gallo@yahoo.com

Abstract: Elbow arthritis is a debilitating condition manifesting as a painful, stiff elbow. Surgical treatment is based on disease etiology, severity of degeneration, and patient age. Rheumatoid elbows with mild to moderate disease benefit from arthroscopic debridement and synovectomy, whereas capsular release and ulnohumeral arthroplasty can relieve painful elbows with early posttraumatic arthritis and osteoarthritis. Age and functional requirements are treatment determinants for moderate to severe arthritis. Rheumatoid, low-demand, and elderly patients are candidates for total elbow replacement; posttraumatic and osteoarthritic elbows in younger patients with considerable functional demands are treated with interpositional arthroplasty. Total elbow allografts and elbow arthrodeses are considered only in salvage situations.

-----------------------

J Bone Joint Surg Am. 2006 Feb;88(2):421-30.
Management of elbow osteoarthritis.
Gramstad GD, Galatz LM.

Department of Orthopaedic Surgery, Washington University School of Medicine, Campus Box 8233, 660 South Euclid Avenue, St. Louis, MO 63110-1093, USA.

Abstract: Primary osteoarthritis of the elbow is characterized by painful stiffness, mechanical symptoms, and the presence of hypertrophic osteophytes. Preservation of the joint space is common and may account for the good results that are usually achieved with nonoperative treatment and nonprosthetic arthroplasty. Elbow osteoarthritis typically affects middle-aged men who engage in strenuous manual activity. Open or arthroscopic capsular release and removal of impinging osteophytes are the primary surgical treatment options. The relative sparing of joint cartilage makes elbow osteoarthritis unique in this regard and amenable to this treatment. Arthroplasty is rarely indicated for primary osteoarthritis of the elbow and should be reserved for elderly individuals with low demands for whom other treatment options have failed.

---------------------

Bull NYU Hosp Jt Dis. 2007;65(1):61-71.
Elbow arthritis.
Soojian MG, Kwon YW.

NYU Hospital for Joint Diseases, Department of Orthopaedic Surgery, New York , New York 10003 , USA .

Abstract: Patients with elbow arthritis typically present with complaints of pain and stiffness. Rheumatoid arthritis is the most common cause of elbow arthritis, followed by posttraumatic arthritis and primary osteoarthritis. Nonoperative management consisting of oral analgesics, intra-articular steroid injections, physical therapy, and splinting may provide symptomatic relief in the majority of patients. If these modalities fail, operative treatment is guided by the severity of disease as well as several patient-related factors such as age, activity level, and expectations. Total elbow arthroplasty can provide satisfactory results in the majority of patients with significant degeneration of the elbow. However, due to issues regarding prosthesis longevity, this procedure is generally avoided in young active patients. Other operative treatment options for such patients include arthroscopic or open synovectomy, debridement arthroplasty, and interpositional arthroplasty. As all of these operations may provide a satisfactory outcome for the appropriate patient, a thorough preoperative evaluation is essential in choosing the suitable surgical procedure for each individual patient.
 

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9. 

First may I say how enormously grateful and indeed highly impressed I am that you have so generously taken the time to respond to my query. Your level of generosity is unheard of here in the UK  as is your level of knowledge and experience - we would never get such kind consideration in our NHS system. I am TRULY indebted to you for your thoughts so far.

My gym life is so important to me that I genuinely do not know how I would cope if I ever had to give it up (which was exactly what the radiologist told me to do!), after he asked "why anyone ever wants to lift weights I do not know?" I was furious about that 'instruction' and I have to say that two years on, my elbows feel fine despite continuing with the weights!

Second, the information you offered is extremely helpful. I am an ex-medical student myself (specialising in zoonosis and epidemiology) and we were constantly 'taught' that arthritis/osteoarthritis is a condition diagnosable ONLY where cartilage is lost. To learn that that is incorrect is not entirely surprising (I was warned at med school that "in 10 years 50% of what you've learned will be found wrong"!).

It is confusing though, if arthritis is something that in elbows can occur with cartilage intact - and the abstracts you kindly included certainly say that - then this seems to turn the usual definition of arthritis 'on its head'. From my understanding, arthritis in general is something that follows the 'pathology' of 1. cartilage damage, 2. roughened areas and osteopthytes aggravating joint capsule/ligaments, 3. inflammatory responses damaging soft and hard tissues and so on in a downward spiral. But if cartilage (I guess the most 'important' anatomical feature of a joint) remains intact in an elbow, then is the 'true' condition not more periarticular, like a 'degenerative capsulitis'? Am I talking total nonsense? Probably!

Certainly, in my own case I could not imagine smoother elbow operation. And from my x-rays/CT scan, the osteopthytes seem to be located exactly where the 'clicking' and rare discomfort occurs. For example, there is a fairly large, I should guess 4mm or so 'claw-like' osteophyte on each radial head that seems to be positioned precisely under the annular ligament of radius, and when I rotate my forearm it makes a painless clicking sound. Certain weight-lifting moves cause pain, but only certain ones. Biceps curls with a straight bar are painful and it feels like it centers on that radial annular ligament/osteophyte zone. Pushing moves never hurt, even if I do close-grip bench with 440lbs.

Your thoughts about genotype and polymorphism sound so sensible! You got me thinking, and I recall that my father's elbows always cracked/clicked whenever he would get out of a chair, even when he was in his 30's. The 'clicking' he produces was not synovial gas bubbles or whatever as occurs in hands, I know those well! He never had pain or any complaints. I appreciate this elbow clicking happens to many people now and again, but it would fit that he may have passed a 'genetic osteophyte development trait' to me too!

Once again, please know of my enormous thanks for your thoughts. I owe you!

I shall order some of your Metabolic diet on Monday and I shall indeed report back on how I get on with.

Thanks Mauro, you've been great!
 

 

Unfortunately conditions that aren’t really arthritis are often lumped in under a broad arthritis umbrella. In your case you obviously don’t have the symptoms or pathology seen in true arthritic conditions such as osteo, rheumatoid, gouty, septic, etc. forms of arthritis. In fact you could indeed call your problem a periarticular one rather than arthritic. And it may be that your condition may not progress to any significant disease, or at the very most require some surgery to remove any osteophytes that may be limiting motion or causing significant pain.
 

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10. 

Hi Doc,

Things are going good wgt wise. Still staying @230. Which is fine. I saw you had an article on supplementation in PL USA this month. Seems different than what you have on the directions for GHBoost and Testoboost. I been taking GHboost in the morning and LipoFlush first thing in the morning along w 2 Testoboost. After breakfast I take Inside Out and Metabolic and MVM. Same after lunch. I was taking the Resolve before wkout too.

Just ordered the PowerDrink and ThermoCell. I don't want to get to crazy w the supps but I want to get a little more boost for the wkout. Seems lately I been lethargic. I swithched to training 3 days instead of 2. SAt Squat\DL, Monday Bench\accesories Thursday Bench\accessory.

Can you give me a breakdown of how I should be using the supplements. I'm thinking I need to increase the TestoBoost and GHBoost. Also it seems like the supps are kicking in later on after the wkout. I did take 3 GhBoost tonight before wkout and 3 after wkout along w 3 testoboost. Seems like it has my metabolism rolling now after lifting over an hour ago.

Kinda floundering here. I want to get the most out of my wkouts w the supplementation I'm on. Thanks. If you can help that would be great!

 

 

There are a number of ways to use my supplements, some more flexible than others. I'll be outlining some of these in various places on my site, mostly in my Q&A and under the info on individual supplements in the store. For detailed info make a point at looking at the detailed information on each of my products in the store.

Resolve for example is mostly used prior to training and has special effects when used that way. There are people using Resolve as a picker upper at different times of the day for various reasons, for example for an energy pick me up, or

As far as GHboost it can be used before bed, and before and after training. The amount you take is dependent on what you need and how they affect you. For example, some athletes use GHboost before and after training and before bed on days they don't train.

Just to let you know that in testing I found that one dose of 5 tabs taken nightly had the similar effects of IGF-1 levels as 3-4 IU of GH taken daily. Two doses, taken before training and before bed raised that to around 5-6 IU per day. I didn't measure the effects of GHboost at higher doses but I would assume that taking an extra dose would raise the effects by another 20 to 30 percent, although since there's a point of diminishing returns with higher doses, it may only increase the effects by say 10%.

Regardless of the effects of GHboost in raising GH and IGF-1, GHboost used with Amino after training is very effective in prolonging the anabolic response after exercise, and even more so if used after training along with food/supplements low in carbs thus producing an synergism between GH, IGF-1, hyperaminoacidemia, and insulin, secondary to prolonged post exercise insulin sensitivity - see the second issue of my Elite Performance Newsletter - pages 155 to 163.

Also the use of TestoBoost (see https://www.mdplusstore.com/pdfs/testoboost.pdf) acts synergistically with GHboost and the above effects I described, to increase the anabolic response. For more info on this have a look at the third issue of my Elite Performance Newsletter, pages 50-54.

As far as the supps kicking in later, that's not a bad thing as it seems that in you the sups have a prolonged action. In your case it might be worth while to take the pretraining sups an hour or so before training to not only prime your metabolism prior to working out but prolonging the effects through and after your training session.

Supplement regimens can vary dramatically depending on the individual. I've written a suggested regimen for you below that should get things moving.

Try this regimen out and let me know after a few weeks how you're doing and we'll make changes if necessary, perhaps cutting back on some, increasing others, etc. However, don't hesitate to write at any time if you have any questions, especially after reading some more on the sups, or want to know more about the supplements and how to take them.

Also keep in mind that there will be more info on an almost daily basis on why, how and when to use the sups on my site so periodically have a look at my blogs, Q&A, and in the store. Also I'll be posting new information on a regular basis through my newsletter. To get the newsletter simply sign up at www.MauroMD.com.

---------------------------

In the AM in and around breakfast

2 MVM 2 EFA+ 2 LipoFlush 2 InsideOut


With lunch

2 MVM 2 EFA+ 2 InsideOut 2 LipoFlush


An hour or so before training

3 GHboost 3 TestoBoost 3 Resolve 3 ThermoCell


During Training

1-2 scoops of Power Drink in water


After training

4 GHboost 3 TestoBoost 12 Amino


With supper

4 Metabolic


On days you don't train take 5 GHboost and 4 TestoBoost before bed.

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11. 

First off it is an honor to be talking to you. Your research has been very helpful to me in helping to achieve my dreams of becoming a professional football player. But let me save you time and ask my question. I have seen countless of "sample" workout programs for football players and all are quite conflicting. One has me doing ten to fifteen reps a set while the other is preaching one reps to five reps. I am a lineman and I need power and strength but also need to be quite quick. In your intellectual opinion, what type of program should I be following?

 

 

Go for the strength in your weight training (low reps and heavy weights) and the quickness when training on the field. Trying to obtain sports related skills by altering weight training routines, increasing reps, using weights to mimic sport actions, etc., just doesn’t work.

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12. 

I've heard you on radio shows and have read about the metabolic diet as well, and i appreciate you sharing your knowledge which has been very valuable to people like myself. I just wanted to seek your opinion on something.

Q- How do anabolic steroids and growth hormone affect the chances of mutating your genes? And can it lead to genetic diorders in your offspring?

I was having discussion about steroids with a friend who is a Biotechnology and genetics major at university and she thinks that... Androgens and GH can cause mutations to both the X and Y chromosomes in men, which can reduce chances of conceiving a child or lead to abnormalities ie. down syndrome in the off springs if such mutated genes are passed on.

 

 

There’s no doubt that the issues surrounding the heritability of epigenetic changes are complex and we have a lot to learn – see abstract below and link to that full paper.

However, as I delve more into the issues involved I’ve come to the following conclusion, which of course is not fixed in stone and will change if valid information to the contrary becomes available. In general is seems that most epigenetic marks are erased at meiosis so it is likely relatively rare for them to be passed on in a hereditary way - although the situation is different in plants where it can happen fairly easily in plants, perhaps because gametes are not set aside early as they are in many animals but arise from somatic tissue at appropriate meristems. Even then, if epigenetic changes are passed on to following generations it seems that the effects usually vanish 3 or 4 generations after the environmental stimulus has passed.

The bottom line is that while the environment results in epigenetic changes in an individual to produce specific phenotypes, it’s not likely that these phenotypes are transmitted although the potential for epigenetic changes to the same environmental stimuli likely persists to some degree depending on the mix of genes from the parents that determines the genotype of the offspring.

I’ll be presenting my rationale and possible consequences in an upcoming newsletter.

As far as the transgenerational transfer of epigenetic changes brought about by the use/misuse of androgens and GH, and other drugs and hormones, I doubt that this occurs but again my opinions are not written in stone. Abuse of androgenic-anabolic steroids can definitely reduce the chance of conceiving but this is due to their detrimental effects on the hypothalamic-pituitary-testicular axis.

------------------------------------------

J Exp Biol. 2010 Jan 1;213(1):3-16. Epigenetics and transgenerational transfer: a physiological perspective. Ho DH, Burggren WW.

Department of Biological Sciences, University of North Texas, 1155 Union Circle #305220, Denton, TX 76203-5017, USA. daoho@my.unt.edu

Abstract: Epigenetics, the transgenerational transfer of phenotypic characters without modification of gene sequence, is a burgeoning area of study in many disciplines of biology. However, the potential impact of this phenomenon on the physiology of animals is not yet broadly appreciated, in part because the phenomenon of epigenetics is not typically part of the design of physiological investigations. Still enigmatic and somewhat ill defined is the relationship between the overarching concept of epigenetics and interesting transgenerational phenomena (e.g. 'maternal/parental effects') that alter the physiological phenotype of subsequent generations. The lingering effect on subsequent generations of an initial environmental disturbance in parent animals can be profound, with genes continuing to be variously silenced or expressed without an associated change in gene sequence for many generations. Known epigenetic mechanisms involved in this phenomenon include chromatin remodeling (DNA methylation and histone modification), RNA-mediated modifications (non-coding RNA and microRNA), as well as other less well studied mechanisms such as self-sustaining loops and structural inheritance. In this review we: (1) discuss how the concepts of epigenetics and maternal effects both overlap with, and are distinct from, each other; (2) analyze examples of existing animal physiological studies based on these concepts; and (3) offer a construct by which to integrate these concepts into the design of future investigations in animal physiology.

Free full text is available at http://jeb.biologists.org/cgi/reprint/213/1/3.
 

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13. 

First of all, I want you to know that I love your supplements. I started taking them last year and I am in the best shape of my life, lifting personal bests. I currently take 4 LipoFlush and 4 ThermoCell and 2 GH in the am before working out. I just started with your Creatine as well. I then take 5 Regulate before going to work.

I then take the Lipo and Thermo in the afternoon.

At night, I take 3 GH, 4 Testo with a serving of Myosin.

I also use the MRP when I have to miss a meal.

I keep carbs below the 50 grams per day.

My question is with the GH and Testo. Can I up the dose? If so, what do you recommend?
 

 

You can up the dose and many athletes do especially when they're training the hardest. The best times are before and after training and before bed.

 

As an example I've copied the regimen followed by an elite powerlifter for a few months prior to competing as he maximizes his strength and body composition.

 

I'm not by any means suggesting you follow his extreme supplementation but by looking at his regimen you can see when and how much GHboost and TestoBoost he is using and use that as a guide for increasing your intake of both at appropriate training intensities.

 

BTW, although the regimen below involves taking a lot of supplements, I did the same or more when I was competing, sometimes taking over 250 tabs a day, although what I took then wasn’t nearly as sophisticated or effective as what I’ve made available today in my store at www.MDPlusStore.com.

 

Hope this helps.

 

------------------------------

 

1. In the morning with breakfast.

Tablets can be spread out and used right before and during breakfast.

 

MVM – 3 tabs

 

EFA+ - 3 capsules

 

Antiox – 3 tabs

 

LipoFlush – 2 tabs

 

TestoBoost – 4 tabs

 

GHboost – 5 tabs

 

Amino – 12 tabs

 

2. Before, During and After Training

 

Before – take ½ hour to ¼ hour before – can be spread out over 15 minutes or so

 

Resolve – 2 tabs

 

ThermoCell 35 – 2 tabs

 

LipoFlush – 2 tabs

 

GHboost – 5 tabs

 

TestoBoost – 4 tabs

 

InControl – 2 tabs

 

Creatine Advantage – 1 scoop

 

Amino – 12 tabs

 

During

 

Power Drink – 1-2 scoop diluted out with 20-30 ounces of water.

 

Right after

 

Amino – 12 tabs with water

 

TestoBoost – 4 tabs

 

GHboost – 5 tabs

 

Joint Support – 3 tabs

 

ReNew – 2 tabs

 

Creatine Advantage – 1 scoop

 

Between one and two hours after

 

MRP LoCarb mixed with water

 

4. With Supper

 

MVM – 3 tabs

 

EFA+ - 3 capsules

 

Antiox – 3 tabs

 

Joint Support – 3 tabs

 

ReNew – 4 tabs

 

5. A few hours After Supper

 

Amino – 10 tabs

 

GHboost – 5 tabs

 

5. Before Bed

 

GHboost – 5 tabs

 

TestoBoost – 4 tabs

 

2 Scoops of Myosin Protein mixed with water (blender is best), either flavor

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14. 

Hi Dr. Di Pasquale, my dad has been using your Testoboost as you suggested and things are going well for him. I was considering using your supplements for myself, for competitive powerlifting, combined with the anabolic solution for powerlifters. However my concern is that over time my body will become less responsive to the supplements (even basic supplements like creatine) and as a result the gains from them will not be at the same level. I realize that taking a lot of effective supplements now will increase the amount of muscle I'm building in the short term, but if the effectiveness decreases over time I would be better off to wait before using them to maximize my performance and muscle size in the long term, and allow me to be bigger and stronger in the end. Is there any evidence that would support such a concern? If not, then i might as well start using the supplements now so I can receive faster growth and results now and have it continue on later.

(I wasn't sure I properly explained my concern so I included the folowing example with weight/muscle gain)
For example; if there were 2 identical powerlifters both weighing 220 lbs. one decided to take creatine while the other did not. Obviously the one taking creatine (PL A) would make more progress in the short-term than the one not taking creatine (PL B). Let's say that in the same amount of time PL A got to 240 lbs. (using creatine), while PL B got to 230 lbs. (without creatine), and now they have both hit a plateau. Since PL A has already been using creatine his body has adapted to the supplementation and therefore the creatine doesn't help him to progress past this point, while PL B adds in creatine to his regimen and quickly blasts through his plateau and reaches 250 lbs., 10lbs. more than bodybuilder A who took creatine from the beginning.


Is this example plausible? (I realize that PL A could have then added in another supplement to break through his plateau, but I left out such things to simplify this example)
If I remember correctly, creatine is made from 3 amino acids and so the likelihood of your body adapting to it would likely be the same as that of protein. Also, in my example i used creatine as an example, but my concern is not only with creatine but with all supplements in general, but i guess a few specific examples would be Testoboost, GHboost, Metabolic, Resolve.

My plan would be to first start using the Anabolic Solution for Powerlifters, and then add in the basics such as Amino, and Power Drink. Once the basics are covered I would then build on these things by using Creatine Advantage, and possibly GHboost and Testboost, and possibly others. But all this depends on my training phase and budget. What do you think of this plan? Any help would be great? Thanks a lot and God bless.

 

 

It’s a good idea to just follow the diet at first and build up a base. Once you’ve done that you can include a few basic supplements and then more as needed.

Even when you start using a number of supplements you don’t need to take them all the time. I recommend that people cycle most of my supplements according to their training and lifestyle. It's my belief that the body adjusts to most things over time as it tries to reach a homeostatic state. Cycling supplements prevents this from happening and thus in the long term is more effective than taking them all the time.  

How you cycle them depends on your circumstances and goals. If you periodize your training I would suggest that you increase the number and their dosages during the time you're training the hardest and take less when you're not and none when you're training the least. The only exception to this is if you’re using the supplement to normalize certain hormonal and metabolic parameters. In these cases the supplements can be effectively used continuously for much longer periods of time.

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15. 

I am a USAPL (and hopefully IPF in the future) lifter and would like to begin supplementation more effectively. I usally take creatine & glutamine along with my non-liftlting supplements (glucosamine, multivitamin, baby aspirin and omega 3). What supplements would be best for me to increase strength? I am 46 years old, 180 pounds and ~12% body fat. I just thought that Dr MD would know what works best for us drug free lifters. I also plan on ordering his book " The Anabolic Solition" but wanted to know what supplements to buy so I can get started earlier. Also, if you can suggest the times (& dosages) to use the supplements that would also be appreciated.

 

 

There are a number of supplements that can be used to maximize body composition and strength. As an example, I’ve copied a sample regimen that is currently being used with great success by an IPF top lifter in the 198 lb class. This regimen is obviously not written in stone and one can begin with much less and then ramp up the use of supplements depending on the phase of training and pre-competition.

 

 

My Anabolic Solution for Powerlifters book will guide you through the use of both the diet and supplements. BTW all of the supplements listed below are 100% safe to use for drug tested athletes.

 

 

 

 

------------------------------------------------------------------

 

Sample PL Supplement Regimen

 

Supplements are used at 4 main times during the day:

 

1. ASAP after waking with breakfast or with an MRP LoCarb shake.

 

MVM – 2 tabs

EFA+ - 2 caps

Antiox – 2 tabs

TestoBoost – 2 tabs

 

2. Before, during, immediately after training and an hour or so after training.

 

Before Training

 

LipoFlush – 2 tabs

ThermoCell 35 – 2 tabs

GHboost – 3 tabs

 

During

 

Power Drink – consume at least two scoops during training from beginning to end – can be diluted out to taste.

 

Immediately After

 

Amino – 10 tabs

Creatine Advantage – 1 scoop

GHboost – 3 tabs

TestoBoost – 3 tabs

 

 

3. With Supper

 

MVM – 2 tablets

EFA+ - 2 caps

Antiox – 2 tabs

 

 

4. Just before going to bed

 

TestoBoost – 4 tablets

GHboost – 4 tablets

Myosin Protein – 2 scoops or more with water

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16. 

I started lifting as a pathetically scrawny 5'10" 120 lb 15yr old. I lifted heavy, ate well, and grew leaps and bounds (from a natural lifter's standpoint).  Recently, I returned to running, (something I originally did on the track team in middle school) I lost about 10 pounds of fat and I'm a highly defined 5'10 1/2" 175 lbs at age 33. I couldn't be more pleased with my V-taper and shape, though I have a problem which has plagued me from day one. I'm a terrible bench presser.  I've tried many programs and methods, and my raw max is 270 lbs in training (perfect form) and 260 lbs in competetion (I've only been to one meet which was last year.) For reps, I can put up 200 lbs for 13.

As an individual with a science background and degree in biology, I've analyzed myself deeply with respect to lifting. I have very long upper arms. I can curl with the big guys -- 150 lbs perfectly strict.  But the bench continues to plague me.  I'm 33 yrs old now and my bench has been slow to progress over the last 18 yrs.  My goal is to add 30 lbs and bench 300 lbs raw. I find gaining body weight is not particularly helpful and I've tried wide grip, close grip, etc.  I noticed that my squat increased substantially when placing the bar lower on my back -- apparently improved leverage.  Doctor, I'd greatly appreciate any advice or help that you can offer.  I do not use drugs, nor do I use supplements and prefer to avoid doing so.

Thanks for your GREAT column in Powerlifting USA.  I read it religiously.

 

 

My bench press was and continues to be the worst of my three lifts. While I squatted and deadlifted over 700 lbs as a middleweight, my best competition bench was 424 lbs. While that’s not a bad bench when you consider it was done raw as I never used a bench shirt, it still wasn’t up to par with the other two lifts, which were both done with only the use of knee wraps and a belt – no squat suit, deadlift suit, special shorts, or even tennis balls under the knees.

Even though my leverages were less than optimal, mainly because of my relatively long arms (great for the deadlift but bad for the bench) I painstakingly built my bench up over 150 lbs over about an eight year period, finding out what worked and what didn’t, until I became a decent bencher. In the end it was the assistance exercises, along with lots of flat benches, that allowed me to keep making steady, although somewhat slow, progress. The assistance exercise that helped me the most was the incline bench press, done at about a 30 degree angle with a shoulder width grip. In fact in my workout area I had a bench set to that incline that was only used for that exercise. I also found dips, with added weight between my legs, and heavy bent over barbell rows useful. I worked up to 200 lb weighted dips, 375 lbs for 3 reps in the incline bench, and 475 lbs for 5 reps in the bent over rows (using wrist straps).

When I was trying to get my bench up I trained best on a 10 day cycle benching every 5 days. I did heavy flat benches doing a total of 8 sets after warming up in declining sets working up to one rep max one day, and 5 days later I did incline bench presses 5 sets of 5, weighted dips 4 sets of 8, and bent over rows to a max 5 reps, then 5 days later I did the flat bench to max again and so on. I did this for 2 months or so then changed to a more conventional routine in order to maintain my strength levels. After about a month or so I went back to the 10 day cycle.

While I followed this routine fairly closely, it wasn’t written in stone as I would make changes according to my competition schedule, injuries, etc. Sometimes I would toss in some other assistance exercises such as partial benches using boards on my chest, and various loading and unloading techniques with a workout partner. However, I never got the results from the other assistance exercises as I did with the inclines, dips, and bent over barbell rows. The point is that while the routine I followed may help you, you should experiment with other assistance exercises to find out which ones work best for you.

I know that you’re against using supplements but I did find them useful when I was on the 10 day cycles as they allowed me to work out harder and recuperate faster. In between I cut back on supplement use. At the very least, I would dramatically increase your protein intake when you’re training the hardest.

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17. 

I am getting ready to start dropping weight for next season. The goal is to hit 285 before dropping into my weight class as needed. I am about 320 right now but would like to drop my weight so that I keep most of my muscle mass and drop the excess body fat.

I've been on the mass phase of the Anabolic Solution for PL and it's helped me pack on the weight. I may have stayed on it a bit too long as I'm heavier than I wanted to get. I am about to start the cutting phase of the anabolic solution for powerlifters or would you suggest the radical diet instead.

I was also wondering about your new thermal product. I use lipoflush and ghboost when I diet would it be better to use the new product as well and why?

 

 

I think I'd try the Radical Diet at first to get the initial 20 lbs off or so and then depending on how you do go on to the Cutting Phase of the Anabolic Solution for PL. That's the progression I use for anyone wanting to lose any significant amount of weight over a relatively short period of time.

The new ThermoCell 35 can be used alone but for best results it's meant to be used with LipoFlush for maximum effects. In your case the new Paradigm Combo, plus TestoBoost, along with the Radical Diet would give you the best results as far as losing body fat and maintaining muscle mass. Have a look at the info on the Paradigm Combo in my store - just follow the links to find what level of information you need.

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18. 

I have been using Testoboost on and off the past five years. At first I used it during and after doing a cycle of steroids and it worked well for me both ways. Now I'm off steroids after being on and off since the 1990s and don't intend or want to use again. I also stopped taking the Testoboost when I stopped the steroids since I wanted to get back to normal. My problem is that my testosterone levels are now too low even though I've been off for four months.

I'm not sure what the problem is but would you recommend Testoboost to help me increase my testosterone level? If so is there anything else you would recommend to get me back to normal? I’m kinda desperate as I don’t want to go back to using again if I can help it.

Thank you very much for your time and your great product.

 

 

I formulated both TestoBoost (see https://www.mdplusstore.com/pdfs/testoboost.pdf) andGHboost (see https://www.mdplusstore.com/pdfs/GHboost.pdf) to help maximize functioning of the hypothalamic-pituitary-testicular axis (HPTA) as a natural and healthy alternative to the use of anabolic agents including steroids, growth hormone and IGF-1.

 

However, even though I didn't formulate TestoBoost to be used while on steroids and as post cycle therapy, it's being used for that purpose by many athletes who swear by it.

 

One of the major problems of using steroids is that it can seriously affect a person's ability to make his own testosterone. That's because the control mechanisms for testosterone production in the body are dampened down by steroid use. Since the body is being provided with testosterone, the main components involved in the internal production of testosterone are no longer needed.

 

As such, the factory, represented by the brain-testicular axis or more correctly the hypothalamic-pituitary-testicular axis (HPTA), basically shuts down.

 

In some cases, such as high dosages and long term use, and also if a person is particularly affected by the steroids used, even if the use is moderate and for short periods, the HPTA just doesn't ever get back to normal. These people then suffer with what is known as hypogonadotropic hypogonadism (HH)- the axis no longer works like it should and accepts low levels of testosterone as normal. This is essentially a down regulation of the HPTA at multiple levels.

 

Why the system doesn't return to normal isn't known but it might be because the machinery itself has been dormant too long and even though it's still able to function, it's now become dysfunctional. It's even possible that in some cases the machinery, including the testicles, have been irreparably damaged and thus can only function at a level that’s lower than it could before steroid use.

 

Regardless of the causes there are various ways to treat this problem although there's no guarantee of success. Current methods include the use of compounds that decrease estrogen effects in the body (such as clomiphene and anastrozole), human chorionic gonadotropin that stimulate the testicles to produce testosterone, menotropins, and gonadotropin releasing hormone agonists (I've copied the abstract of a recent study below that used a single dose of triptorelin to normalize the HPTA in a long term steroid user - this case the treatment worked but that's not necessarily the case with many others).

 

My suggestion is to see your doctor about your HH and get his or her input. If you need more info on the various treatments, let me know and I'll send it to you so you can show your doctor.

 

However, regardless of what therapy your doctor recommends, including waiting it out a bit longer to see it things get back to normal on their own, I also recommend that you go on both TestoBoost and GHboost for several months as treatment, and hopefully with his or her blessing.

 

As I mentioned I formulated both as an alternative to drug use. As such, in those not using drugs TestoBoost works to help optimize physiological levels of testosterone while GHboost works on growth hormone and IGF-1.

 

Both also have beneficial effects on the testosterone and growth hormone machinery even with the use of exogenous testosterone and growth hormone by stimulating the endogenous system to some degree and thus both provide some of the intermediate compounds that normally wouldn't be produced, and by preventing the complete shutdown of the machinery. And both for the same reasons are both useful for post cycle therapy.

 

As an adjunct to treating HH I've found that it’s necessary to optimize the level of both as the growth hormone axis is also involved in normalizing the HPTA. Growth hormone is involved in the secretion of sex steroids in complex ways. As such, treatment of hypogonadotropic hypogonadism secondary to various factors including the use of anabolic steroids, should involve the growth hormone axis, including IGF-1 And other insulin like factors.

 

For example, IGF-1 can stimulate the expression of GnRH gene in the hypothalamus, may influence the growth, maturation and differentiation of GnRH neurons, accelerates LH and FSH secretion and can regulate the proliferation and differentiation of adult Leydig cells, and control the biosynthesis of testicular hormones (Liu XP, Wang Y, Qin DN. Effects of insulin-like growth factor-1 on the regulation of hypothalamus-hypophysis-testis axis. Zhonghua Nan Ke Xue. 2007 Feb;13(2):171-4 - see abstract below.).

 

Both TestoBoost and GHboost are complex formulations that do a lot for all athletes as well as helping people with androgen and growth hormone problems, including helping with replacement therapy. You should read what I’ve written on TestoBoost and GHboost at www.mdplusstore.com – click on the PDF link of both supplements for the full info pieces – both of which are around 40 pages long. The direct link to the GHboost PDF file is https://www.mdplusstore.com/pdfs/GHboost.pdf and the one for TestoBoost is https://www.mdplusstore.com/pdfs/testoboost.pdf - you might want to print them out and bring them to your doctor.

 

I’ve also copied below the abstracts of a some papers that you will find useful. 

 

Best of luck and let me know how things go.

 

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Fertil Steril.2010 Apr 21. [Epub ahead of print]

Anabolic steroids purchased on the Internet as a cause of prolonged hypogonadotropic hypogonadism.

Pirola I, Cappelli C, Delbarba A, Scalvini T, Agosti B, Assanelli D, Bonetti A, Castellano M.

Internal Medicine and Endocrinology Unit, Department of Medical and Surgical Sciences, University of Brescia, Brescia, Italy.

OBJECTIVE: To report a case of hypogonadotropic hypogonadism due to the chronic abuse of anabolic steroids purchased over the Internet. DESIGN: Case report. SETTING: Endocrinology unit of the University of Brescia. PATIENT(S): A 34-year-old man. INTERVENTION(S): A single dose (100 mug) of triptorelin (triptorelin test). MAIN OUTCOME MEASURE(S): Clinical symptoms, androgen normalization, levels of serum testosterone, follicle-stimulating hormone, and luteinizing hormone. RESULT(S): Within 1 month, the patient's serum testosterone was in the normal range, and he reported a return to normal energy and libido. CONCLUSION(S): The World Anti-Doping Code has proved to be a very powerful and effective tool in the harmonization of antidoping efforts worldwide, but it is insufficient to combat this illegal phenomenon. To tackle the serious side effects caused by doping we believe that it is necessary to increase monitoring and adopt severe sanctions, particularly with regard to Internet sites

 

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Zhonghua Nan Ke Xue.2007 Feb;13(2):171-4.

[Effects of insulin-like growth factor-1 on the regulation of hypothalamus-hypophysis-testis axis]

Liu XP, Wang Y, Qin DN.

Department of Physiology, Shantou University Medical College, Shantou, Guangdong 515041, China. xiaoxiaoliu1982@163.com

It has been demonstrated that insulin-like growth factor-1 (IGF-1) stimulates the proliferation and division of cells, facilitates the individual growth and development and regulates the material metabolism. Furthermore, it regulates male reproductive development and testicular endocrine functions. IGF-1 can stimulate the expression of GnRH gene in the hypothalamus of prepubertal male mice. However, it has no effect on or even inhibits GnRH gene expression in adult mice. IGF-1 may influence the growth, maturation and differentiation of GnRH neurons. It also accelerates LH and FSH secretion in hypophysis. IGF-1, produced locally in the testis and combined with its specific receptor, can regulate the proliferation and differentiation of adult Leydig cells, cause Sertoli cells to play different functions and control the biosynthesis of testicular hormones.

 

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J Clin Endocrinol Metab.2010 Jun 30. [Epub ahead of print]

The Long-Term Clinical Follow-Up and Natural History of Men with Adult-Onset Idiopathic Hypogonadotropic Hypogonadism.

Dwyer AA, Hayes FJ, Plummer L, Pitteloud N, Crowley WF Jr.

Harvard Reproductive Endocrine Sciences Center and the Reproductive Endocrine Unit of the Department of Medicine (A.A.D., F.J.H., L.P., N.P., W.F.C.), Massachusetts General Hospital, Boston, Massachusetts 02114.

Context and Objective: Adult-onset idiopathic hypogonadotropic hypogonadism (AHH) is a rare disorder characterized by an isolated failure of gonadotropin secretion occurring after an otherwise normal sexual maturation in men. This study aims to examine the etiology and long-term natural history of this disorder. Design and Setting: Long-term follow up, including detailed clinical, biochemical, and genetic examinations, were performed and compared with those at diagnosis. Patients: Patients included 10 men with AHH [serum testosterone (T) <125 ng/dl]. Interventions: Overnight neuroendocrine studies, semen fluid analyses, and genetic screening were performed (KAL1, FGFR1, PROK2, PROKR2, NELF, TAC3, TACR3, and GNRH1) over a decade of longitudinal follow up. Results: Follow-up evaluations were conducted 10.6 +/- 5.9 yr after initial studies and revealed that the clinical characteristics and seminal fluid analyses of AHH men (body mass index, 28.8 +/- 4.1 vs. 27.0 +/- 4.3 kg/m(2); testicular volume, 18 +/- 6 vs. 19 +/- 6 ml) do not change over a decade with no spontaneous reversals. Several men exhibited some variability in their endogenous GnRH-induced LH secretory patterns, including emergence of endogenous pulsatility in three individuals. However, all remained hypogonadal (T . Conclusions: 1) AHH in men appears to be a long-lasting condition. 2) Although minor changes in the abnormal pattern of endogenous GnRH-induced LH secretion occurred in some AHH patients, all remained frankly hypogonadal.

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19. 

I know you're a busy man, but I'd appreciate a quick word of advice.  I'm in my third week of the Anabolic Solution Diet for Bodybuilders and I'm doing great.  I feel energized even at very low levels of daily carbs.  In a couple of weeks I'm doing a long mountain bike ride of around 40 miles in one day.  So far, the only cardio activity I've done on the diet has been cross-country skiing for about an hour and a half.  It was during the initial assessment phase and I was fine during the ski, but did feel pretty drained afterwards.

So my question is, how should I eat around this long bike ride?  It will be on a Saturday, so it will be during a carb-up day.  Should I just carb-up like normal or will feeding my body carbs during this day convince my body to use carbs instead of fat for energy?

Thank you so much for your hard work and your time.

 

 

It takes a few months to be fully fat adapted even though changes take place in less than a week during the induction phase. As such, your body is still somewhat dependent on carbs as an immediate source of energy although that will change as you stay on the diet. When you’re fully fat adapted you’ll function at a higher VO2Max on fatty acids rather than carbs as the body will find ways to deliver more oxygen to the working muscles and thus improve aerobic energy production as against anaerobic.

Also because my phase shift diets are not just low carb diets in that there is a higher carb phase, you’ll be able to utilize both the glycogen stored in muscle when it’s really needed, as well as the intramuscular fat droplets that abut to the mitochondria and thus deliver immediate energy via the release of fatty acids. Theoretically, and practically for those that stay on the diet, you get the best of both worlds as far as energy production, decreased fatigue, and increased stamina and strength.

There is some information on all of this in my articles and in the store under the supplements. However, I’ll be explaining all of this in more detail in upcoming articles and likely touch on various aspects in upcoming blogs.  

As far as your bike ride, I would just stick to your routine and see how it goes. At this point you’ll likely use up a varying proportion of your body fat (which is the intention of my phase shift diets so as to improve body composition and performance), stored glycogen and dietary carbs for fuel during the 40 mile trek.

I’d be interested to know how the ride goes and how you perform and feel during and after the ride.

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20. 

I think I’ve always been a mesomorph as I had more muscle than most guys my age without doing any exercise or even working. I got hooked on bodybuilding after looking at some muscle mags a friend let me borrow and I couldn’t believe the progress I’ve made in just over a year. Every one thinks I’m on steroids but I don’t even take any vitamins.

 

I started training in earnest last year and put on a lot of weight, most of it muscle. Since I concentrated more on my upper body than my lower I put on a lot of mass on my chest, shoulders and arms and got a lot stronger to the point that I’m considering doing some powerlifting as well as continuing on with my bodybuilding..

 

I’m not complaining except for the stretch marks. They’re all over the place especially in my pec-delt area and to a lesser extent my upper arms, biceps more than triceps. I’ve tried creams, lotions, vitamins but nothing helps so I’ve backed off on my training, which I really didn’t want to do.

 

Any advice on preventing them from getting worse when I get back into training again, which I’d like to do as soon as possible, and any advice on how to make the ones I’ve got less gross would really be appreciated.

 

 

I get a lot of emails about stretch marks, not only from bodybuilders and power athletes but also from those who put on a lot of weight and want to lose the weight as well as the stretch marks. Also get emails from women who got stretch marks from being pregnant or want to prevent them during the pregnancy.

 

Stretch marks are tears in the skin that happen when it just can’t stretch as fast as it needs to. The skin has some ability to stretch over time if it needs to without tearing. But if the process overwhelms the stretching capacity of the skin then it tears and produces stretch marks. Some people develop stretch marks easier than others but everyone has limits on how fast skin can stretch without tearing.

 

Stretch marks initially are red to purplish in color and eventually fade and blend in somewhat with the rest of the skin. The process usually takes several weeks to months before the stretch marks lose most of the red/pinkish color.

 

You can read more about stretch marks in the InsideOut nutritional supplement product info on my site www.MauroMD.com. Also in the article on stretch marks on my site – use the search function for articles to find it.

 

In this article you can find my suggestions on how to deal with stretch marks including the use of InsideOut, a nutritional supplement I formulated to deal with skin problems including stretch marks.

 

What I’d like to also help you with is how you can still train while at the same time preventing the stretch marks from getting worse.

 

The key in your case is to switch from a bodybuilding routine to a powerlifting one. The reason behind my suggestion is that bodybuilding routines are best for maximizing hypertrophy while powerlifting routines are best for maximizing strength while allowing a more modest amount of hypertrophy, a rate that your skin should be able to accommodate without further tearing.

 

First of all let me tell you what I experienced in my long powerlifting career.

 

I found that by keeping to a more anaerobic routine, lots of sets, low reps, lots of time between sets, and heavy weights, I could get stronger without adding a lot of muscle mass. This allowed me to improve my lifts year after year while staying in the same weight class. I did gain some muscle but made up for it by losing body fat until my body fat levels were in the low single digits.

 

On the other hand when I decided I wanted to move up one or two weight classes I introduced some workouts with lighter weights, more reps, and less rest between sets. I found that I gained more muscle mass but not a proportional amount of strength. For example although I moved up two to three weight classes, and looked more massive with fat levels in the higher single digits, my lifts didn’t go up like I thought they would. I had a lot more muscle but was only moderately stronger.

 

The reason behind this phenomenon is that strength training increases muscle size mainly by increasing the number of myofibrils in the muscle cells, which are the actual contractile elements made up of actin and myosin that are responsible for the strength in muscle. It’s the increase of these myofibrils that result in a degree of muscular hypertrophy that is mainly strength related.

 

Doing powerlifting movements will develop these fibers and increase strength but they won’t produce large muscles, or at least not to the extent seen in elite bodybuilders. As such, this type of training is ideal for you right now as you’ll be able to train hard just differently than you have been. And you’ll get your shot at powerlifting and maybe even competing if that’s what you find you want to do.

 

Bodybuilding workouts on the other hand results in more hypertrophy because besides increasing the number of myofibrils in the muscle cells it also increases the sarcoplasm, the content inside the muscle cells that includes everything except the myofibrils. This fluid portion of the sarcoplasm is increased much more in aerobic type exercises than in the more anaerobic exercises used by those who train mainly for strength. This combination of myofibril and sarcoplasmic increase in size makes for a higher muscle mass, which is further increased by the increase in capillary density seen in the more aerobic bodybuilding routines. Although the muscle mass is significantly increased the muscle is no stronger because of the increase in sarcoplasmic volume.

 

For more information on this topic see pages 49 and 50 of Science and practice of strength training By Vladimir M. Zatsiorsky, William J. Kraemer, published by Human Kinetics, 2006.

 

Most of the powerlifters that have bodybuilding type physiques incorporate significant amounts of bodybuilding movements into their powerlifting routines, periodized mostly into the first few stages of their training.

 

The bottom line for you is that you can still train hard and satisfy that iron bug while at the same time getting stronger by training the way powerlifters train. This won’t worsen your stretch marks. Once the stretch marks fade you can if you want, include more of the bodybuilding routines over a longer period of time so that the skin will be able to accommodate the longer term increased muscle hypertrophy.

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21. 

Just to start off with let me tell you that I read your column in PL USA religiously and it’s the first thing I read in every issue.

 

Last week I read your information on nutritional supplements in your Elite Performance Newsletter and I agree with your take on the ridiculousness of the nutritional supplement ads that use heavy steroid users as models for their supplements. It’s a joke and a con job when they try to make you believe that they got their results from using the supplement line that’s being hyped as the reason for their massive physiques and strength, when instead it’s their use of 1,000 mg to 5,000 mg a day of steroids and countless other hormones and drugs that made them that way. I also understand your take on trying to maximize your natural potential by using targeted nutritional supplements and that their use will improve your body composition and performance but won’t come close to providing the results from massive use of hormones and other drugs.

 

Lately, however, there seems to be this big nitric oxide craze. Everything I’ve read on nitric oxide seems to point to the effectiveness of these supplements in doing just about everything such as allowing you to exercise longer and harder, put on more muscle, have more endurance and so on.

 

Also many of the products that are being heavily hyped in the magazines and on the internet are based on large amounts of arginine and other amino acids, and more recently on nitrates and nitrites, to dramatically up the levels of nitric oxide in the body. The people I’ve talked to that use these nitric oxide enhancer products say they work as they use them before training and feel it gives them more of a pump and better workouts. What’s your take on these nitric oxide enhancers that seem to have become the number one selling supplement for many of the big supplement companies?

 

There’s loads of literature on the beneficial effects of nitric oxide (NO or NOx) on increasing blood flow to muscles and other parts of the body secondary to the dilating effect of nitric oxide on blood vessels. And there’s also lots of studies showing that the use of large amounts of L-arginine increases nitric oxide levels, and also that the intake of nitrites and nitrates also significantly increases nitric oxide levels, even more than large amounts of L-arginine since the mechanisms of nitric oxide production between them are different and likely additive.

 

But while upping levels of nitric oxide will give you a better pump while you’re working out, and may even allow you to experience less fatigue, there’s a very dark side to these supplements, at least for anyone that is looking to increase muscle hypertrophy, enhance body composition, and improve athletic performance.

 

First of all let me say that I’m not against the use of arginine in nutritional supplements as it has several useful effects. If used in lower doses studies have shown that it may increase nitric oxide but only to physiological levels, which is beneficial, and it also has beneficial effects on protein synthesis, the immune system, increasing growth hormone levels, increasing insulin sensitivity, and serving as substrates for other amino acids, creatine, and polyamines.

 

And it’s been shown that in higher doses, and especially if combined with nitrate/nitrite, it increases NO formation dramatically and facilitates vasodilation, improves sexual functioning, and helps keep you cool during exercise.

 

But now here comes the dark side. While physiological elevations of NO are beneficial and have no adverse effects, excessive production of NO, whether through the exogenous use of one or more of arginine, and nitrates/nitrites can result in a lowering of endogenous testosterone production since nitric oxide inhibits Leydig cell steroidogenesis. (see citations and abstracts below).

 

So while dramatically increasing nitric oxide in the body has some benefits, and provides more of a pump when training giving the impression that it's a potent ergogenic aid, its detrimental effects on testosterone makes the use of nitric oxide supplements containing one or more of large amounts of L-arginine, L-arginine precursors, nitrates and nitrites counter productive for muscle hypertrophy, body composition and athletic performance.

 

It’s because of the counter productive effects of increasing nitric oxide levels in the body that TestoBoost, my testosterone boosting supplement, only contains 100 mg of arginine. And ditto for all of the other supplements in my supplement line, including Resolve, my pre-workout primer, that contain L-arginine (none contain nitrites or nitrates) also contain levels that don’t appreciably affect NO.

 

It’s also worthwhile mentioning that D-aspartate works opposite to NO as far as its effects on testosterone production. And again that’s why my TestoBoost version IV (the new version of TestoBoost that was released in May of 2011 – see the detailed info on my new site www.MauroMD.com) has virtually no effects on NO production but contains high levels of D-aspartate to help maximize your endogenous testosterone production.

 

FYI, I’ve included several citations and abstracts from the medical and scientific literature on nitric oxide and d-aspartate. I think it’s important to provide this information as well as my own thoughts and comments so you can better evaluate all the claims being made by companies hyping all the many benefits of their nitric oxide enhancers and also see some of the literature on the beneficial effects of D-aspartate on testosterone production.

 

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Mol Cell Endocrinol. 2002 Aug 30;194(1-2):39-50.

 

Nitric oxide potently inhibits the rate-limiting enzymatic step in steroidogenesis. Drewett JG, Adams-Hays RL, Ho BY, Hegge DJ. Department of Pharmacology, Physiology and Therapeutics, University of North Dakota School of Medicine and Health Sciences, 501 North Columbia Road, 58203, Grand Forks, ND 58203, USA. james.drewett@uc.edu Abstract This study tested the hypothesis that nitric oxide (NO) inhibits the rate-limiting catalytic step in steroidogenesis, cytochrome P450 cholesterol side-chain cleaving enzyme (CYP11A1), independent of soluble guanylyl cyclase (GC-S) stimulation. To assess CYP11A1 activity, pregnenolone levels were quantified in murine adrenocortical Y1 cells in the presence of the 3beta-hydroxy-Delta(5)-steroid dehydrogenase inhibitor, 2alpha-cyano-17beta-hydroxy-4,4',17alpha-trimethylandrost-5-ene-3-one. The NO donor, (Z)-1-[2-(2-aminoethyl-N-(2-ammonioethyl)amino]diazen-1-ium-1,2-diolate(deta nonoate), inhibited vasoactive intestinal peptide-, forskolin- and 22alpha-hydroxycholesterol (22HC)-facilitated pregnenolonogenesis in the absence of GC-S activation and in the presence of a GC-S inhibitor, 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one (ODQ). CYP11A1 was also heterologously expressed in monkey COS7 cells. Deta nonoate inhibited 22HC-facilitated activity of the over-expressed enzyme in the absence of GC-S activation and in the presence of ODQ. The NO-independent, GC-S agonist, 1-benzyl-3-(5'-hydroxymethyl-2'-furyl)indazole did not inhibit steroidogenesis. The IC(50) for effects of free NO on CYP11A1 was potent and in the 0.4-2 microM range. These results support the hypothesis that NO inhibits the rate-limiting enzyme in steroidogenesis independent of GC-S activation.

 

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Biol Reprod. 2010 Sep;83(3):434-42. Epub 2010 May 12.

 

Testosterone-induced modulation of nitric oxide-cGMP signaling pathway and androgenesis in the rat Leydig cells. Andric SA, Janjic MM, Stojkov NJ, Kostic TS. Reproductive Endocrinology and Signaling Group, Department of Biology and Ecology, Faculty of Sciences, University of Novi Sad, Novi Sad, Serbia. Abstract Testosterone, acting as a systemic and local factor, is one of the major regulatory molecules that initiate and maintain testicular function. In the present study, different experimental approaches were used to evaluate the role of testosterone in regulation of the nitric oxide (NO)-cGMP pathway in Leydig cells derived from normal and hypogonadotropic male rats treated with testosterone for 24 h and 2 wk. Real-time quantitative PCR and Western blot analysis revealed increased inducible NO synthase (NOS2) expression followed by increased NO secretion from Leydig cells ex vivo after continuous treatment with testosterone for 2 wk in vivo. The cGMP-specific phosphodiesterases Pde5, Pde6, and Pde9 were up-regulated, whereas PRKG1 protein was decreased after a 2-wk testosterone treatment. Induction of Nos2 and Pde5 in Leydig cells was blocked by androgen receptor antagonist. In experimental hypogonadotropic hypogonadism, expression of NOS2 was significantly reduced, and treatment with testosterone increased NOS2 expression above control levels. PDE5 protein level was unchanged in hypogonadal rats, whereas treatment of hypogonadal rats with testosterone significantly increased it. In contrast, hypogonadism and testosterone replacement reduced PRKG1 protein in Leydig cells. In vitro treatment with testosterone caused gradually increased Nos2 gene expression followed by increased nitrite and cGMP production by purified Leydig cells. In summary, testosterone up-regulated NO signaling via increased NOS2 expression and contributed to down-regulation of cGMP signaling in Leydig cells. Thus, testosterone-induced modulation of NO-cGMP signaling may serve as a potent autocrine regulator of testicular steroidogenesis.

 

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Med Hypotheses. 2000 Oct;55(4):310-3.

 

Is steroid deficiency the cause of tolerance in nitrate therapy? Panesar NS. Department of Chemical Pathology, the Chinese University of Hong Kong, Shatin, New Territories, Hong Kong. nspanesar@cuhk.edu.hk Abstract The award of the Nobel Prize in Physiology and Medicine for 1998 bears witness to the 'explosive' field of nitric oxide (NO), and who would have thought the explosive nitroglycerin owed its therapeutic effectiveness to this little molecule? NO is also involved in causing penile erection, which has brought sildenafil to the aid of patients with erectile dysfunction. However, emerging evidence in animals and in vitro studies indicates that NO also inhibits steroidogenesis, which may have repercussions in humans. The decrease in androgen secretion may impact on secondary sexual characteristics, including penile size. The tolerance to the nitrate therapy in angina, characterized by volume expansion and not due to sodium retention, may also be related to steroid hormone deficiency. Decreased cortisol secretion may impair water excretion, resulting in volume expansion. Impaired aldosterone secretion would cause hyponatraemia with resultant raised renin. I hypothesize that continuous therapy with nitrates and sildenafil will result in diminished levels of steroid hormones with predicted sequelae.

 

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Toxicol Appl Pharmacol. 2000 Dec 15;169(3):222-30.

 

Decreased steroid hormone synthesis from inorganic nitrite and nitrate: studies in vitro and in vivo. Panesar NS, Chan KW. Department of Chemical Pathology, The Chinese University of Hong Kong, Shatin, New Territories, SAR China. nspanesar@cuhk.edu.hk Abstract Nitrites and nitrates are consumed nonchalantly in diet. Organic nitrates are also used as vasodilators in angina pectoris, but the therapy is associated with tolerance whose mechanism remains elusive. Previously, we found inorganic nitrate inhibited steroidogenesis in vitro. Because adrenocorticoids regulate water and electrolyte metabolism, tolerance may ensue from steroid deficiency. We have studied the effects of nitrite and nitrate on in vitro synthesis and in vivo blood levels of steroid hormones. In vitro, nitrite was more potent than nitrate in inhibiting human chorionic gonadotropin (hCG)-stimulated androgen synthesis by Mouse Leydig Tumor cells. At concentrations above 42 mM, nitrite completely inhibited androgen synthesis, and, unlike nitrate, the inhibition was irreversible by increasing hCG concentration. The cAMP production remained intact but reduced with both ions. The nitric oxide (NO) scavenger, 2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxy-3-oxide (c-PTIO) significantly increased hCG- or cAMP-stimulated androgen synthesis in all buffers, suggesting that NO is a chemical species directly involved in the nitrite/nitrate-induced inhibition. This is further supported by c-PTIO countering the inhibitory action of methylene blue on androgen synthesis. Rats given distilled water containing 50 mg/L NaNO(2) or NaNO(3) for 4 weeks drank significantly less daily. At the end, their blood corticosterone and testosterone levels were significantly decreased. The adrenocortical histology showed bigger lipid droplets, which are pathogonomic of impaired steroidogenesis. Nitrite and nitrate are metabolized to NO, which binds heme in cytochrome P450 enzymes, thereby inhibiting steroidogenesis. Therapeutic nitrates likewise may decrease adrenal (and gonadal) steroidogenesis. Cortisol deficiency would impair water excretion causing volume expansion, and aldosterone deficiency would cause sodium loss and raised renin. Paradoxically, volume expansion without sodium retention and raised renin has all been reported in tolerance.

 

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Theriogenology. 2007 Jan 15;67(2):249-54. Epub 2006 Sep 22.

 

D-Aspartic acid and nitric oxide as regulators of androgen production in boar testis. Lamanna C, Assisi L, Vittoria A, Botte V, Di Fiore MM. Department of Life Sciences, Second University of Naples, via Vivaldi 43, 81100 Caserta, Italy. Abstract D-Aspartic acid (D-Asp) and nitric oxide (NO) are two biologically active molecules playing important functions as neurotransmitters and neuromodulators of nerve impulse and as regulators of hormone production by endocrine organs. We studied the occurrence of D-Asp and NO as well as their effects on testosterone synthesis in the testis of boar. This model was chosen for our investigations because it contains more Leydig cells than other mammals. Indirect immunofluorescence applied to cryostat sections was used to evaluate the co-localization of D-Asp and of the enzyme nitric oxide synthase (NOS) in the same Leydig cells. D-Asp and NOS often co-existed in the same Leydig cells and were found, separately, in many other testicular cytotypes. D-Asp level was dosed by an enzymatic method performed on boar testis extracts and was 40+/-3.6 nmol/g of fresh tissue. NO measurement was carried out using a biochemical method by NOS activity determination and expressed as quantity of nitrites produced: it was 155.25+/-21.9 nmol/mg of tissue. The effects of the two molecules on steroid hormone production were evaluated by incubating testis homogenates, respectively with or without D-Asp and/or the NO-donor L-arginine (L-Arg). After incubation, the testosterone presence was measured by immunoenzymatic assay (EIA). These in vitro experiments showed that the addition of D-Asp to incubated testicular homogenates significantly increased testosterone concentration, whereas the addition of L-Arg decreased the hormone production. Moreover, the inclusion of L-Arg to an incubation medium of testicular homogenates with added D-Asp, completely inhibited the stimulating effects of this enantiomer. Our results suggest an autocrine action of both D-Asp and NO on the steroidogenetic activity of the Leydig cell.

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22. 

Do you recommend a grand glycogen depletion workout on friday before carb up to increase the glycogen loading phase of the diet, a workout involving whole body and lots of volume?

 

 

All that business about depletion diets on Friday to maximize glycogen supercompensation on Saturday and Sunday can actually be counter productive. First of all anytime you're in starvation mode, which is what happens on Friday if you succeed in depleting liver and muscle glycogen, you lose muscle, albeit perhaps less once you're fat adapted but you're still in an undesirable catabolic state. If you're in starvation mode on the Friday, a depletion workout will increase muscle catabolism even further. The idea behind my diets is to cycle to diet so that the overall effect is an increase in protein synthesis and a decrease in protein catabolism, while at the same time maximizing the oxidation of body fat and decreasing lipogenesis. Bottom line, in my view, is that it's not necessary to go into ketosis, at least as far as having significant ketonuria, in order to get the changes in body fat and body composition that accrue from using cyclic low carb/moderate to high carb diets such as the Anabolic and Metabolic Diets.

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23. 

What are the differences in the Anabolic Solution for bodybuilders vs powerlifters? As wrestlers we have some concerns from both areas. We need strength and even a certain amount of mass for our particular style of wrestling (Russian Sambo). We are also concerned with dropping fat to meet weight class requirements and to increase speed and agility. Is there enough of a significant difference between the two where we would need to reference both versions? Or would one serve our needs better than the other?

 

 

The differences in the two Anabolic Solution books are due to the differences in the two sports. In bodybuilding the emphasis is on maximizing muscle mass, minimizing body fat, and on appearance. In powerlifting the emphasis is on maximum strength at certain bodyweights, which also means maximum functional muscle at any one bodyweight. Having been both a competitive wrestler and powerlifter, I would suggest that you buy the Anabolic Solution for Powerlifting as it will suit your purposes better, especially in dropping bodyweight while at the same time maximizing strength, muscle mass and performance. For more information see the FAQ on stretch marks as it contains information on how the way you train affects muscle hypertrophy and strength.

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24. 

You recommend 30grams of carbs a day on weekdays,is it important to reach ketosis before carb up as recommended by dan duchaine in bodyopous,or do you not recommend reaching that state?

 

 

Reaching ketosis, at least as far as being able to measure it using a ketostix, believe it or not, doesn't relate in the least to how well you do on the diet. Keep in mind that the depth of ketosis is NOT indicative of the degree of fat oxidation or lipolysis. I don't even suggest you check your urine. The important thing is to fine tune the diet until you get the results you want. Once you've adapted to the diet, you'll use up most of the ketones you produce as a source of energy and as such shouldn't show much ketones in the body during the weekdays.

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25. 

You say that you should eat no more than 30 grams of carbs for the first 12 days and then following week days. However I see in some of your sample diets in the Metabolic Diet and on line at your site www.MauroMD.com that you have a carb value of up 50 carbs a day in the 4000 and 4500 strict versions. Is this a mistake or did you mean to divert from the 30 gram limit?

 

 

As far as the 30 gram carb limit, it's not written in stone. As you increase your caloric intake, especially at the high end, you can increase the carb intake without causing any problems as far as adapting to the diet. Again, the diet plans at the end of my book are only examples and each person has to find the best carb levels that suits their metabolism. For some, the 30 carb limit, even when taking in 4500 calories, may work best. For others, depending on their abilities to oxidize fat as their main fuel, 100 grams of carbs or even more, may work best. The troubleshooting guide that I included in the Metabolic Diet is geared to helping you find that level of carbs that works best for your metabolism, at least as far as maximizing muscle mass and minimizing body fat.

Keep in mind that I usually recommend that you increase your calories in the high carb phase more than the low carb phase of the Metabolic Diet. This information was more evident in my Anabolic Diet (a 100 page how to book for bodybuilders), which has grown into the Anabolic Solution (which combines an updated Anabolic Diet with the use of targeted nutritional supplements to get maximum body composition results). For example, one bodybuilder who has been on the diet for over 5 years does it this way. In his bulk up phase he usually takes in about 3500 calories during the weekdays and then may take as much as 12,000 calories a day on the weekends (no kidding). He gains the weight he wants and then starts cutting back drastically on the weekend calories (if he got up to 12,000 calories a day on the weekends then he begins his definition phase with a cut of 2,000 calories per week for the first three week, 1000 calories per week for the next two weeks and then about 200 calories per week) and about 100 calories a day per week on the weekday calories. Keep in mind that his cutting phase lasts about 16 weeks. Depending on how his fat/weight is doing he may make minor modifications on this plan.

To give you an idea of how this worked for him he weighed 217 lbs at 6% bodyfat the last major contest he was in prior to starting my diet (he had been competing for almost ten years). After two years of following my diet he weighed 254 lbs at 5% bodyfat and won his division of the Mr. Universe. Mind you his diet wasn't very good prior to going on my diet so I can't take all the credit. It's quite possible that he would have made some progress just by improving his diet along conventional means. On the other hand you don't see those changes in a seasoned pro unless something drastic happens. Also keep in mind that there were no other changes except for the diet and targeted nutritional supplements - I made him some custom supplements for the nutritional supplement regimen that I wanted him to follow. He had to take a lot of pills from various sources since he didn't have the luxury of using my present line of targeted multi-ingredient nutritional supplements..

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26. 

You say that you should eat no more than 30 grams of carbs for the first 12 days and then following week days. However I see in some of your sample diets in the Metabolic Diet and on line at your site www.MauroMD.com that you have a carb value of up 50 carbs a day in the 4000 and 4500 strict versions. Is this a mistake or did you mean to divert from the 30 gram limit?

 

 

As far as the 30 gram carb limit, it's not written in stone. As you increase your caloric intake, especially at the high end, you can increase the carb intake without causing any problems as far as adapting to the diet. Again, the diet plans at the end of my book are only examples and each person has to find the best carb levels that suits their metabolism. For some, the 30 carb limit, even when taking in 4500 calories, may work best. For others, depending on their abilities to oxidize fat as their main fuel, 100 grams of carbs or even more, may work best. The troubleshooting guide that I included in the Metabolic Diet is geared to helping you find that level of carbs that works best for your metabolism, at least as far as maximizing muscle mass and minimizing body fat.

Keep in mind that I usually recommend that you increase your calories in the high carb phase more than the low carb phase of the Metabolic Diet. This information was more evident in my Anabolic Diet (a 100 page how to book for bodybuilders), which has grown into the Anabolic Solution (which combines an updated Anabolic Diet with the use of targeted nutritional supplements to get maximum body composition results). For example, one bodybuilder who has been on the diet for over 5 years does it this way. In his bulk up phase he usually takes in about 3500 calories during the weekdays and then may take as much as 12,000 calories a day on the weekends (no kidding). He gains the weight he wants and then starts cutting back drastically on the weekend calories (if he got up to 12,000 calories a day on the weekends then he begins his definition phase with a cut of 2,000 calories per week for the first three week, 1000 calories per week for the next two weeks and then about 200 calories per week) and about 100 calories a day per week on the weekday calories. Keep in mind that his cutting phase lasts about 16 weeks. Depending on how his fat/weight is doing he may make minor modifications on this plan.

To give you an idea of how this worked for him he weighed 217 lbs at 6% bodyfat the last major contest he was in prior to starting my diet (he had been competing for almost ten years). After two years of following my diet he weighed 254 lbs at 5% bodyfat and won his division of the Mr. Universe. Mind you his diet wasn't very good prior to going on my diet so I can't take all the credit. It's quite possible that he would have made some progress just by improving his diet along conventional means. On the other hand you don't see those changes in a seasoned pro unless something drastic happens. Also keep in mind that there were no other changes except for the diet and targeted nutritional supplements - I made him some custom supplements for the nutritional supplement regimen that I wanted him to follow. He had to take a lot of pills from various sources since he didn't have the luxury of using my present line of targeted multi-ingredient nutritional supplements..

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27. 

I am getting most of my protein through fish and lean meats and protein powders, Iam getting at least 25% of my fats from good fats but the rest is from dairy fats such as double cream and cheese I know these are very high in sat fats but are not heated or processed in any way. I am taking lots of flax seed oil and GLA and EPA etc, is my health at risk?

 

 

I've found that most people on the Metabolic Diet don't run into any significant adverse changes to their serum cholesterols, especially if they take in a reasonable amount of good fats such as the omega three and omega six EFAs (flax - ALA and LA, fish oils - EPA and DHA, GLA, etc.) and the monosaturates like the oleic acid from olive oil. If you're at all worried have your serum cholesterol levels done and even compare them to what they were before you went on the diet.

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28. 

I have been reading some of your diets on line and they are quite different to what I am doing. Should i be following the diets you have on line to get results?

 

 

Obviously you have looked at the sample diets that I have on line at MauroMD.com. However, you have to keep in mind that they're just sample diets so people can get an idea of how to plan their own diet. So even though they're different from what you're doing keep in mind that as long as you keep the carbs down, you can eat almost anything in whatever quantity that's fits into the number of calories you set for yourself. For example if you're a bodybuilder or power athlete trying to maximize muscle mass and minimize body fat, your macronutrient intake as far as protein and fats will vary but the carbs will always be low in the low carb phase of the diet.


The adequacy of the diet should be measured against the results you're getting. The whole idea of the diet is to experiment and find just the right combination and calories that works for you, whether you're in a mass, strength, cutting or even precontest phase. If you're getting results then you're doing it right and all you need to do is tweak it one way or the other to keep making progress in the various training phases.

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29. 

I'm mostly interested in losing weight and looking good but I'm not interested in doing any more exercise than what I get from doing my job and working at home. Can I still use the Metabolic Diet to lose weight?

 

 

I get this question a lot, from both men and women. Mostly I simply answer with a yes, the Metabolic Diet can be used on it's own even if you don't do any bodybuilding or endurance exercise. However, my phase shift diets, which include the Metabolic Diet, the Anabolic Diet, the Radical Diet and the Anabolic Solution, all work better better if you exercise. However, I think it's time I answered the question in more detail.

 

Obviously nutrition is as important for women as it is for men. Since women and men are physiologically different there are some differences. For example, women need fewer calories than men because of their smaller size and muscle mass. Also testosterone in men helps them to lose body fat faster since it increases their metabolic rate. The decreased number of calories needed by women also means that they're more prone to weight gain.

 

The best approach to losing weight is by reducing calorie intake and increasing utilization of energy with exercise, so that you go into a calorie deficit and have to use up some of our tissue to make up the difference from calorie intake and calories needed to maintain the status quo. By following my phase shift diets, and for you the Metablic Diet is ideal, you will burn more body fat rather than muscle. That is the purpose of the Metabolic Diet when used for weight loss is to go into calorie deficit and lose weight by mostly burning up and thus losing body fat. Keeping muscle and losing fat even if you lose the same amount of weight will make you look fitter and result in a "tighter body."

 

Exercise, while not absolutely required to lose weight/body fat, it will help by increasing that calorie deficit and thus allowing you to reach your goals faster. It's also important to realize that the more muscle you have and/or keep, the easier it is to keep the weight off. That’s because the more muscle you have the more calories you burn. skeletal muscle is a key thermogenic (calories lost as heat) tissue and can account for a significant amount of daily calories (which is provided by using body fat as fuel), the amount of calories you expend, and the amount of fat oxidized, is proportional to muscle mass. Thus by maintaining your muscle mass it's easier to lose weight and body fat and easier to maintain the weight and fat loss.

 

Lean muscle has the highest resting metabolic (calorie burning) rate of any tissue. The more muscle you have, the more calories you burn, day and night! Muscle burns calories even at rest, while fat tissue is virtually dead weight. Loss of calorie-gobbling lean muscle tissue makes it easier to regain lost fat weight on fewer maintenance calories after your diet is over, contributing to the familiar "yo-yo, syndrome.

 

Overall the Metabolic Diet is ideal for the woman looking to lose fat, tone up and look good. Most women don't want to get big muscles and the Metabolic Diet won't do that even if you weight train, unless you're on a hard-core bodybuilding program. However, on the Metabolic Diet you'll keep more of the muscle you now have, and at the same time you'll lose more body fat.

 

Exercise, especially weight training, accentuates the anticatabolic/anabolic (but not to the point of leading to excess muscles, unless of course, as mentioned before, that's your goal) and fat burning effects of the Metabolic Diet by increasing calorie output, decreasing muscle breakdown, and increasing both the breakdown of body fat and fat burning. This is important since there is some evidence that exercise in those accustomed to a high carb diet, while increasing fat breakdown, decreases fat burning, with the result that much of the fat broken down reforms, with no net loss of body fat.

 

The bottom line is that by maintaining your muscle mass, with or without exercise (although exercise will help) you will:

· Lose more body fat
· Experience less plateaus
· Look fit and toned
· Have a much easier time maintaining your weight and fat loss for the long term.

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30. 

I’ve just finished reading the Anabolic Solution. One question though, since I’ve a lot of fat to lose. How long may I stay on the cutting phase before I start seeing diminishing returns?

 

 

You can stay on the cutting phase almost indefinitely. That’s because if the cutting phase is done gradually and methodically so as to minimize the loss of lean body mass, there’s no end to the amount of fat you’ll lose if you stick at it. If it's done properly you can pretty well go down to whatever body fat level you aim for.

On the other hand, unless you're a competitive bodybuilder, it's not necessary to go down to extremely low levels of body fat as it's inevitable that you'll lose more muscle mass than if you go back to a controlled mass phase before you hit that ultra low body fat level. Doing it this way (in moderation) in successive cycles (so that you add mass in each cycle and then lose the fat) will ensure that you'll gradually pile on the muscle with each mass/strength/cutting cycle and still hit pretty low body fat levels. If you go through several of these moderate cycles and you want to compete, you'll hit those low body fat levels at a much higher muscle mass than if you'd been extreme with each cycle.

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31. 

I just started the diet and notice some low carb foods will say they have 0 sugar carb, however, they have several other carb types (i.e. alcohol carbs). I noticed on your website that you say fiber carbs do not count. Are there any other carbs that do not count?

 

 

While your question seems simple to answer, it in fact can be quite complicated. In fact when you look at the issues in detail you discover that runs the gamut of explaining why a carb may not be a carb, that a non carb may be a carb and everything in between.


I believe that anything that disrupts fatty acid breakdown and oxidation is detrimental to the diet, at least in the initial stages where you are trying to determine the lowest level of carbs that works best for your metabolism. As such, some foods or ingredients, while not technically carbs, should be factored in as if they were carbs. This includes alcohol, glycerin or glycerol, lactate and pyruvate. Some foods or ingredients, while technically carbs, don't act as regular carbs on the metabolism. For example inulin and oligofructose, storage carbs that are found in some plants, have just under 1/3 the effect of regular carbs on metabolism and as such can be taken into account at that level - for example 3 grams of inulin would be equivalent to one gram of carbs. The reason for this is that inulin and oligofructose have a ß(2 1) bonds linking the fructose molecules. These bonds render them nondigestible by human intestinal enzymes. Thus, inulin and oligofructose pass through the mouth, stomach and small intestine without being metabolized. As such, almost all of the inulin or oligofructose ingested enters the colon where it is totally fermented by the colonic microflora. The energy derived from fermentation is largely a result of the production of mostly short-chain fatty acids and some lactate, which are metabolized and contribute 1.5 kcal/g of useful energy for both oligofructose and inulin. However, because most of these products are likely mostly absorbed into the portal vein and therefore enter the body proper, and because I consider lactate and short chain fatty acids as equivalent to carbs, this 1.5 calories per gram, out of a possible 4 calories per gram., has to be factored into your carb intake.


Insoluble fiber, even though technically a carb, is not absorbed and as such doesn't impact on your systemic macronutrient mix. So insoluble fiber shouldn't be counted in either the carb or calorie columns. Soluble fiber is another story and is somewhat of a gray area in the carb/calorie equation. Pectin, for example, undergoes vigorous fermentation in the cecum and produces high levels of short-chain fatty acids. So while fiber, both soluble and insoluble are good for you and good for the diet, you can't
overdo it. Regulate, a fiber formulation that works optimally for those on my Metabolic Diet, is a mixture of insoluble and soluble fibers, which at 10 caps a day provides a negligible carb equivalent of one gram. For the same effectiveness you'd have to take 5 carb grams worth of other fiber preparations, such as Metamucil.

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32. 

I had a couple of questions regarding your stance on the metabolic shift to fat burning and ketosis. In many of the resources I've been able to gain access to, they have indicated that one of the most important metabolic adaptations which spares nitrogen/protein losses during carbohydrate restriction is the adaptation of the CNS/brain to metabolizing ketones for fuel, thereby decreasing the drive for gluconeogenesis. This apparently coincided with the adaptation of skeletal muscle shifting a strong metabolic preference to fatty acids instead of ketones and/or glycolysis. Preventing ketogenic adaptations appeared to maintain nitrogen losses on starvation/ketogenic diets. I noticed that your Metabolic Diet places little emphasis on ketosis and that the protein/fat ratio in the metabolic diet would likely keep someone out of the significantly ketogenic state. Do you feel that the CNS adaptations to ketosis are not significantly important to decreased catabolism/protein sparing effects of low carb/high fat diets or that the metabolic shift of skeletal muscle is independent from the adaptations of the CNS and are more a result of primary fuel availability? Or is it that the increased protein intake is able to overcome gluconeogenic drive for catabolism of muscle mass?

 

 

As you've gathered from my books, for various reasons I'm not a fan of excessive ketosis (at least to the point of obsessing over ketonuria). First of all I believe that staying in ketosis may have long-term adverse effects (such as dehydration of various tissues and possible deterioration of cartilage and connective tissues, especially those that are weight bearing such as the vertebral disks). Secondly being constantly in ketosis is catabolic and counter productive for keeping or enhancing muscle mass. And thirdly I don't believe that achieving ketosis to the point of showing significant ketonuria is necessary for any of the beneficial effects of the Metabolic Diet on body composition. There are several reasons for my views and I'll try and outline them below. Keep in mind, however, that one of the more important ones is that the lack of the insulin-mediated anabolic effect. Insulin has been shown to both increase protein synthesis and decrease protein catabolism. In the Metabolic Diet, the anabolic effect of insulin (both direct and indirect - for example insulin in concert with GH leads to increases in muscle IGF-1 and subsequently to muscle hypertrophy) are harnessed while at the same time its lipogenic and anti-lipolytic effects are controlled. Purely ketogenic diets have other drawbacks as well. First of all staying in ketosis can lower metabolic rate and thyroid hormone levels and activity (specifically T3 levels). This can make it more difficult to increase protein synthesis and muscle hypertrophy. Also, as mentioned above, chronic ketogenic diets dehydrate the body and can have adverse effects on joint tissues, including spinal discs, and may result in increased injuries.

Those that argue that it's vital to show significant ketonuria, and that without it the protein sparing effect of the ketogenic diet is lost, are confusing the issues involved in switching the metabolism from a carb burning to a fat burning one. The point is that by titrating the Metabolic Diet to the lowest carb level that works for you, you're maximizing the fat loss, minimizing muscle catabolism, and more importantly using a macronutrient mix that is in tune to your genotypic and phenotypic makeup.

The bottom line is that you shouldn't worry about ketosis and ketone levels in the urine and instead concentrate on the progress you make and on making sure that you're at the lowest but most efficient dietary carb level for you (as per the troubleshooting chart and guide in the Metabolic Diet). The Metabolic Diet is geared to increasing the utilization of fat as a primary energy source, decrease protein catabolism and increase protein synthesis in a healthy way. The emphasis in the Metabolic Diet is on lowering dietary carb intake to a level that's optimal for you and that will maximize fat mobilization and oxidation, not ketonuria. As such, I don't recommend tracking urinary ketones because I think that the process is unnecessary.

As you know the Metabolic Diet is a cycling diet, not a strictly ketogenic diet. Unlike cycling ketogenic diets (CKDs) it's more dynamic in that it can be used to find the optimal level of carbs that matches any individuals metabolism and that will result in maximum results as far as altering body composition. This effect on body composition is helped by the weekly phase shift that results from the changes in macronutrient composition and the subsequent metabolic and hormonal environment.

Needless to say if you follow the strict part of the Metabolic Diet you will have significant degree of ketosis and variable levels of ketonuria. As you know ketones are formed all the time to some extent in everyone, just much more so as the dietary carb levels drop and fat intake increases. The amount of ketones that end up in the urine is a function of several factors including the amount formed secondary to carb availability, and insulin and glucagons levels, the extent to which they are able to be metabolized and used efficiently (a function of a person's genetic ability to oxidize fat and ketones efficiently and of time), and the efficiency of the gluconeogenic process and availability of gluconeogenic substrates thus decreasing the need for ketone formation.

Reaching ketosis, at least as far as being able to measure it using a ketostix, believe it or not, doesn't relate in the least to how well you do on the diet. Keep in mind that the depth of ketosis is NOT indicative of the degree of fat oxidation or lipolysis. I don't even suggest you check your urine for ketones never mind fussing over the degree of ketonuria. Again, the important thing is to fine tune the diet until you get the results you want. Once you've adapted to the diet, you'll use up most of the ketones you produce and as such shouldn't show much ketones in the body during the weekdays.

You have to understand that ketosis and ketonuria can be two different things. Anyone on a lower carb diet will burn more fatty acids, and subsequent to the breakdown of long chain fatty acids by the liver, produce more ketones and as such be in ketosis (defined as a blood concentration of ketones above .2 mmol/dl), but will not necessarily show ketones in the urine - ketosis may or may not result in ketonuria, the presence of ketone bodies in the urine. And it's the level of ketone bodies in the urine that people measure to determine if they're in ketosis and the degree of ketosis. In many people, especially those that are fat adapted and efficient in the use of ketones as an energy source, there may not be much spillage of ketones into the urine. For example, the Eskimo living on the traditional high fat, almost no carb diet, rarely shows any significant amount of ketonuria.

Also keep in mind that it's ketones and fatty acids that are burned as fuel initially when carb availability is low. Many tissues can oxidize fatty acids directly to get the energy they need. Some tissues, such as the brain and the nervous system can only use glucose (from dietary carbs and other substrates through gluconeogenesis or other processes - see below) and ketones as energy substrates. After adapting to a low carb, higher fat diet, ketosis becomes a minor pathway for energy metabolism in most tissues in the body, with muscle and other tissues (except for the brain, etc.) using free fatty acids as the main energy substrate.

The bottom line is that I tell people that they shouldn't worry about ketosis and ketone levels in the urine and instead concentrate on the progress they make and on making sure that they're at the best dietary carb level for them (as per the troubleshooting chart and guide in the Metabolic Diet).

And while I'm at it I must tell you that I'm not a proponent of depletion diets to maximize glycogen resynthesis. Firs of all depletion diets on Friday to maximize glycogen supercompensation on Saturday and Sunday can actually be counter productive. Anytime you're in starvation mode, you lose muscle, albeit perhaps less once you're fat adapted but you're still in an undesirable catabolic state. If you're in starvation mode on the Friday, a depletion workout will increase muscle catabolism even further. The catabolism is not worth the small increase in glycogen that occurs following a depletion diet. The idea behind my diets is to cycle to diet so that the overall effect is an increase in protein synthesis and a decrease in protein catabolism, while at the same time maximizing the oxidation of body fat and decreasing lipogenesis. Bottom line, in my view, is that it's not necessary to go into ketosis, at least as far as having significant ketonuria, in order to get the changes in body fat and body composition that accrue from using cyclic low carb/moderate to high carb diets such as the Anabolic and Metabolic Diets.

On the other hand, I agree with you to some extent about the importance of ketone production and utilization on low carb diets. The production of ketones does offer an alternative fuel supply to those tissues, like the brain which are unable to utilize free fatty acids directly as fuel but can utilize the smaller carbon groups (like ketones) aerobically via the TCA cycle.

But it's a misconception that the brain only uses glucose and ketones for fuel. In fact lactate has, over the last few years or so, been shown to be the preferred substrate for neurons whether provided endogenously, via the circulation or through the metabolic coupling that occurs between astrocytes and neurons (Magistretti PJ, Pellerin L. [Functional brain imaging: role metabolic coupling between astrocytes and neurons]. Rev Med Suisse Romande 2000 Sep;120(9):739-42.)

The lactate so preferred by neurons can be produced endogenously within the neuron and/or astrocyte from glucose by either glycolysis or gluconeogenesis via direct gluconeogenic precursors forming glucose first and then going through the glycolytic pathway, or intermediates between glucose and pyruvate (such as glycerol which I feel is overlooked for its importance to glucose and lactate production considering that it makes up approximately ten percent of fat by weight) that fit in somewhere between glucose and pyruvate, or synthesized via the tricarboxylic acid (TCA) cycle secondary to an increase in anapleurotic flux via the various reactions of amino acids, odd chain fatty acids, TCA intermediates, and removal of oxaloacetate or malate to form pyruvate and then lactate. The above schemata is grossly simp lified but it will do for this discussion.

That aside, the brain and nervous system, although arguably the reason behind ketone production at time of low glucose availability, is not a significant player as far as the body's metabolic shift from using carbs to using fatty acids as the primary fuel, and to harnessing the cyclical nature of the Metabolic Diet to achieve the beneficial changes in body composition. This all occurs secondary to the body's adaptation to the different macronutrient composition of the diet, which as you know is the route the body takes most of the time (for example the lipid content of cellular membranes will reflect the lipid content of the diet). Studies have also shown that the phase shift that occurs every week for anywhere between 12 and 36 hours (although as per my book the shift can be very flexible depending on the individual person's metabolism and reaction to the diet) does not adversely affect the established fat burning mode and as such does not reverse the enzymatic changes that have been induced as a result of the prior lower carb, higher fat phase.

This was shown again in a study published in December of 2000 (Louise M. Burke1, Damien J. Angus2, Gregory R. Cox1, Nicola K Effect of fat adaptation and carbohydrate restoration on metabolism and performance during prolonged cycling. J Appl Physiol 2000; 89(6):2413-2421.) in which the authors concluded that "5 days of exposure to a high-fat, low-CHO diet caused clear changes in fuel substrate utilization during submaximal exercise. At least some of these changes were independent of CHO availability because enhanced capacity for fat oxidation persisted despite restoration of muscle glycogen stores." Actually this study, while not as sophisticated as it might have been as far as its protocol, is an interesting read.

You ask about the necessity of ketones for protein sparing and the data that backs this up. First of all it's obvious that supplying the amino acid and other substrates that lead to an increased anapleurotic flux for gluconeogenesis and lactogenesis can be a catabolic process if the amino acids needed are rounded up endogenously. Supplying the amino acids via a high protein diet obviates most of the muscle catabolism. As such, in my mind protein sparing is thus mostly a function of increased protein intake and not dependant on ketone formation.

I think that it's important to realize that the studies are conflicting with some showing that ketones are protein sparing and others showing that they are not protein sparing. As well, most of the studies that show ketosis as being necessary for protein sparing are starvation or fasting diets (the Metabolic Diet being neither) and/or use ketone salts (which are not the same as an increase in endogenous ketones) as infusions. Looking at all the available literature and data it's my opinion that ketones are not protein sparing per se and as such excessive ketosis is counter productive and in the chronic state, catabolic in nature.

There is also one more big difference between the Metabolic Diet and the other ketogenic and CKD diets. You'll notice that I don't have people who start the diet worry about calories. I stress the metabolic transition phase first and once fat acclimatized, I have them vary their calories. The point being two fold. First of all the tiredness that some people feel when they first start a ketogenic type of diet is not all from the lack of carbs but to some extent is simply due to a lack of calories. Going on a starvation diet at the same time as a ketogenic diet is counter productive. In my Metabolic Diet I stress the metabolic shift before I stress calories.

Even more importantly is that once a person has made the shift and most tissues in the body are using free fatty acids, and the gluconeogenic (and lactogenic) processes are more efficient, then cutting back on calories on the Metabolic Diet also spares muscle protein and allows the gradual loss ofbody fat while maintaining or at time even increasing muscle mass.

Hopefully I've answered some of your questions although I'm sure others will pop up as you read my reply. Please don't hesitate to write again if you have further questions or comments.

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33. 

Would you say the home scales that give you your fat percentage are more accurate than the calipers?

 

 

Actually a good fat caliper is more accurate. The home scales are not very accurate since they are so affected by fluctuations in body fluid content. However, because they're so easy to use, changes in the readings can steer you in the right direction and in the long run they can at least tell you if you're losing or gaining body fat.
If you're going to use these scales then use them at the same time of day and under the same conditions. For example if you're going to weight yourself in the morning then do so after emptying your bladder and before eating or drinking anything. Also it might be worthwhile to get a caliper reading once in while so you can compare them to the scales. This way you'll be able to relate the readings from the scales to the percent body fat readings from the calipers and keep things real.

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34. 

I am following the Anabolic Solution. When do I take the Creatine Advantage in relation to my weight workouts and also my off-days (or cardio-only days) and also in relation to meals?

 

 

You can use Creatine Advantage at a number of times and circumstances. If you're loading up by using two doses a day, you can take one dose before and one dose after your weight and cardio workout days, and twice a day on an empty stomach on other days. If you're down to one dose a day as a maintenance dose there are reasonable grounds for either taking it either before or after training, or some do, half before and half after training.

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35. 

If I'm following the metabolic diet, is it OK to still supplement with CLA since I heard that it helps to lose body fat and weight?

 

 

It certainly is. In fact, because of its cardioprotective effects (by way of its antioxidant properties and by decreasing serum levels of triglycerides and LDL) and its positive effects on insulin sensitivity, nutrient partitioning and on energy and fat metabolism, I put conjugated linoleic acid (CLA) in several of my MD+ line of supplements, including LipoFlush, ThermoCell 35, EFA+, ReNew, and MRPLoCarb.

 

Conjugated Linoleic Acid (CLA), while not an essential fatty acid, has significant effects on body composition. It's a mixture of isomers of linoleic acid, which is found preferentially in dairy products, meat, and in cheese, milks and yogurt that have undergone heat treatment.

CLA has been shown to have properties above and beyond those of linoleic acid. It has shown potential as a powerful anticarcinogen , and exhibits potent antioxidant activity. Studies have suggested that CLA may be cytotoxic to human cancer cells in vivo.  

CLA has a wide range of biological effects.  It has potent antioxidant activity and has shown potential as an anticarcinogen. CLA has been shown to have significant anti-inflammatory properties and to inhibit inflammatory mediators such as PGE2, IL-6, and TNF-alpha, , and also acts as a COX-2 inhibitor. ,

Studies in animals and humans indicate that CLA supplementation decreases body fat and increases lean muscle mass. The increase in lean muscle mass is most pronounced in individuals who are exercising regularly.

CLA appears to reduce the ability of fat cells to take up fats from the bloodstream; it also inhibits the formation of new fat cells. CLA also helps cells burn fat at a higher rate, while fueling and preserving muscle, leading to a reduction in fat and an increase in lean muscle mass.

Numerous physiological effects in relation to body-weight control have been attributed to CLA in animals. In different animal models, CLA has been shown to reduce body fat and to increase lean body mass. , , But CLA has marked effects in humans as well and has been found to decrease body fat mass and support muscle mass in overweight humans.  , , ,

For example, a study published in the International Journal of Obesity found that those who were given CLA for a four week period had significant decreases in abdominal fat.  

As well, a recent study concluded that long term CLA supplementation not only helps to decrease body fat but also helps to maintain weight loss in the long term. A recent long term study found that a mixture of the two CLA isomers significantly lowered body fat mass in overweight humans at both 1 and 2 years.  It likely does this by affecting various enzymes involved in lipid formation and to a lesser extent enhancing fat breakdown. , ,

As well, CLA seems to have significant effects on weight regain, as it reduces fat uptake into adipocytes by decreasing the formation of fat and but not affecting fat breakdown. It likely does this by affecting various enzymes involved in lipid formation rather than enhancing fat breakdown, known as lipolysis. , , ,

Thus there is an overall increase in fat breakdown since the two processes are usually in dynamic equilibrium with as much fat being produced as is broken down. Decreasing fat formation changes the dynamics to one of overall increased fat breakdown and subsequently a decrease in overall body fat.

Of equal importance, for those wishing to maximize lean body mass, is the possible anti-catabolic effects of CLA. ,

The most recent study in a series of studies of the effects of CLA confirmed and expanded on the findings of the previous studies: CLA reduces body fat mass in specific regions of the body, especially the abdominal area in both men and women, and maintains or increases lean body mass.  

Adding to CLA's effects on body composition, another recent study found that CLA supplementation even increased fat oxidation and energy expenditure during sleep.  

The CLA in my products is a mixture of the cis 9, trans 11, trans 10, and cis 12 isomers. I did that because while there are studies hinting that body composition changes and increases in insulin sensitivity are due to the t10 and c12 isomers, while the c9 and t11 isomers also have significant effects on thermogenesis and FFA oxidation.

 

References:

 

Ip C, Singh M, Thompson HJ, Scimeca JA. Conjugated linoleic acid suppresses mammary carcinogenesis and proliferative activity of the mammary gland in the rat. Cancer Research 1994;54(5):1212-5.

Ip C, Scimeca JA, Thompson HJ. Conjugated linoleic acid. A powerful anticarcinogen from animal fat sources. [Review] Cancer 1994;74(3 Suppl):1050-4.

Pariza MW, Ha YL, Benjamin H, et al. Formation and action of anticarcinogenic fatty acids. Advances in Experimental Medicine & Biology 1991;289:269-72.

Shultz TD, Chew BP, Seaman WR, Luedecke LO. Inhibitory effect of conjugated dienoic derivatives of linoleic acid and beta-carotene on the in vitro growth of human cancer cells. Cancer Letters 1992;63(2):125-33.

Bhattacharya A, Banu J, Rahman M, Causey J, Fernandes G. Biological effects of conjugated linoleic acids in health and disease. J Nutr Biochem. 2006;17(12):789-810.

Zulet MA, Marti A, Parra MD, Martinez JA. Inflammation and conjugated linoleic acid: mechanisms of action and implications for human health. J Physiol Biochem. 2005;61(3):483-94.

Luongo D, Bergamo P, Rossi M. Effects of conjugated linoleic acid on growth and cytokine expression in Jurkat T cells. Immunol Lett 2003;90:195– 201.

Eder K, Schleser S, Becker K, Korting R. Conjugated linoleic acids lower the release of eicosanoids and nitric oxide from human aortic endothelial cells. J Nutr 2003;133:4083– 9.

Yu Y, Correll PH, Vanden Heuvel JP. Conjugated linoleic acid decreases production of pro-inflammatory products in macrophages: evidence for a PPAR gamma-dependent mechanism. Biochim Biophys Acta. 2002 15;1581(3):89-99.

Cheng WL, Lii CK, Chen HW, Lin TH, Liu KL. Contribution of conjugated linoleic acid to the suppression of inflammatory responses through the regulation of the NF-kappaB pathway. J Agric Food Chem. 2004 14;52(1):71-8.

DeLany JP, Blohm F, Truett AA, Scimeca JA, West D.B. Conjugated linoleic acid rapidly reduces body fat content in mice without affecting energy intake, Am J. Physiol 1999;276:R1172–R1179.

Belury MA. Dietary conjugated linoleic acid in health: physiological effects and mechanisms of action. Annu Rev Nutr 2002;22:505–531.

Parra P, Serra F, Palou A. Moderate doses of conjugated linoleic acid isomers mix contribute to lowering body fat content maintaining insulin sensitivity and a noninflammatory pattern in adipose tissue in mice. J Nutr Biochem. 2009 Feb 4. [Epub ahead of print]

Gaullier JM, Halse J, Hoye K, Kristiansen K, Fagertun H, Vik H, Gudmundsen O. Conjugated linoleic acid supplementation for 1 y reduces body fat mass in healthy overweight humans. Am J Clin Nutr. 2004;79(6):1118-25.

Eyjolfson V, Spriet LL, Dyck DJ. Conjugated linoleic acid improves insulin sensitivity in young, sedentary humans. Med Sci Sports Exerc. 2004;36(5):814-20.

Steck SE, Chalecki AM, Miller P, et al. Conjugated Linoleic Acid Supplementation for Twelve Weeks Increases Lean Body Mass in Obese Humans. J. Nutr. 2007 137 (5).

Blankson H, Stakkestad JA, Fagertun H, Thom E, Wadstein J, Gudmundsen O. Conjugated linoleic acid reduces body fat mass in overweight and obese humans. J Nutr 2000;130:2943-2948.

Riserus U, Berglund L, Vessby B. Conjugated linoleic acid (CLA) reduced abdominal adipose tissue in obese middle-aged men with signs of the metabolic syndrome: a randomised controlled trial. Int J Obes Relat Metab Disord. 2001;25(8):1129-35.

Gaullier JM, Halse J, Høye K, et al. Conjugated linoleic acid supplementation for 1 y reduces body fat mass in healthy overweight humans. Am J Clin Nutr 2004;79:1118–1125.

Gaullier JM, Halse J, Hoye K, Kristiansen K, Fagertun H, Vik H, Gudmundsen O. Supplementation with conjugated linoleic acid for 24 months is well tolerated by and reduces body fat mass in healthy, overweight humans. J Nutr. 2005;135(4):778-84.

Park Y, Albright KJ, Storkson JM, et al. Changes in body composition in mice during feeding and withdrawal of conjugated linoleic acid, Lipids 1999;34(3):243-248.

Pariza MW, Park Y, Cook ME. The biologically active isomers of conjugated linoleic acid, Prog Lipid Res 2001;40(4):283-298.

Choi Y, Kim YC, Han YB, et al. The trans-10,cis-12 isomer of conjugated linoleic acid downregulates stearoyl-CoA desaturase 1 gene expression in 3T3-L1 adipocytes, J Nutr 2000;130 (8):1920-1924.

Park Y, Albright KJ, Storkson JM, et al. Changes in body composition in mice during feeding and withdrawal of conjugated linoleic acid, Lipids 1999;34(3):243-248.

Pariza MW, Park Y, Cook ME. The biologically active isomers of conjugated linoleic acid, Prog Lipid Res 2001;40(4):283-298.

Choi Y, Kim YC, Han YB, et al. The trans-10,cis-12 isomer of conjugated linoleic acid downregulates stearoyl-CoA desaturase 1 gene expression in 3T3-L1 adipocytes, J Nutr 2000;130 (8):1920-1924.

Tarnopolsky MA, Safdar A. The potential benefits of creatine and conjugated linoleic acid as adjuncts to resistance training in older adults. Appl Physiol Nutr Metab. 2008 Feb;33(1):213-27.

Cook ME, Miller CC, Park Y, Pariza M. Immune modulation by altered nutrient metabolism: nutritional control of immune-induced growth depression. Poultry Science 1993;72(7):1301-5.

Miller CC, Park Y, Pariza MW, Cook ME. Feeding conjugated linoleic acid to animals partially overcomes catabolic responses due to endotoxin injection. Biochem Biophysic Res Comm 1994;198(3):1107-12.

Gaullier JM, Halse J, Hoivik HO, Hoye K, Syvertsen C, Nurminiemi M, Hassfeld C, Einerhand A, O'Shea M, Gudmundsen O. Six months supplementation with conjugated linoleic acid induces regional-specific fat mass decreases in overweight and obese. Br J Nutr. 2007;97(3):550-60.

Close RN, Schoeller DA, Watras AC, Nora EH. Conjugated linoleic acid supplementation alters the 6-mo change in fat oxidation during sleep. Am J Clin Nutr. 2007 Sep;86(3):797-804.

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36. 

I have both the Metabolic Diet and Anabolic Solution book for Powerlifting books and have been following the shifting of the macronutrients between weekdays and weekends. Right now I’m starting to cut back and entering the cutting phase to minimize body fat and keep muscle so I’m more effective at my bodyweight class. Although I’ve read both books and looked on line, I’m still a bit confused: Just how much protein should I be eating in the various phases, not so much in the mass phase but more so in the cutting phase when I cut back on calories? As I drop the calories in order to lose weight, mostly in body fat, should I cut back on the protein and keep fat intake high or the other way around?

 

 

Some of the information you're looking for is in the Metabolic Diet and Anabolic Solution for Powerlifters book you have, and some in the articles on my main site www.MauroMD.com. In the books I don't go into details on exactly how much protein you need to take in at every stage of the diets although I do give percentages of the macronutrients. My reasoning is that since by following the Metabolic Diet and the nutritional supplement plan as outlined in both books, you won't have to worry about protein intake as it will be more than adequate.

 

Since you’re trying to cut back on body fat I’ll assume that your competition is several weeks away and you’re trying to get closer to your weight class limit, shedding the remaining pounds the few days before the competition. As such, you’re likely training heavier and harder.

 

It's my feeling that intense muscular activity increases protein catabolism (breakdown) and protein use as an energy source. The less protein available, the less muscle you're going to be able to build. A high protein diet protects the protein in the muscle and the protein that may be turned into muscle by, among other things, providing another energy source for use during exercise.

 

The body will burn the dietary protein instead of the protein inside the muscle cells if your diet remains high in protein. In fact, studies have shown that the anabolic effects of intense training are increased by a high protein diet. When intensity of effort is at its maximum and stimulates an adaptive, muscle producing response, protein needs accelerate to provide for that increased muscle mass. As a side note it's also well known that a high protein diet is necessary for anabolic steroids to have full effect.

 

It's my belief that once a certain threshold of work intensity is crossed, dietary protein becomes essential in maximizing the anabolic effects of exercise. Exercise performed under that threshold, however, may have little anabolic effect and may not require increased protein. As a result, while serious athletes, as in your case, can benefit from increased protein other athletes who don't undergo similar, rigorous training may not.

 

On the average I recommend a minimum of 1 gram of high quality protein per pound of bodyweight every day for any person involved in competitive or recreational sports who want to maximize lean body mass However for those athletes heavily involved in strength events such as the Olympic field and sprint events, those in football or hockey, or weightlifters, powerlifters and bodybuilders, I recommend between 1.2 to 1.6 grams of high quality protein per pound of total bodyweight.

 

That means that if you weigh 200 lbs and want to put on a maximum amount of muscle mass, then you'll have to take in as much as 320 grams of protein daily. There are several competitive weightlifters, powerlifters and bodybuilders that I know that take in 2 to 3 grams of high quality protein per pound of bodyweight, and some that take even more.

 

If you're trying to lose weight and/or body fat as you are now, it's important to keep your dietary protein levels high. That's because the body oxidizes more protein to use for energy on a calorie deficient diet than it would in a diet that has adequate calories. The larger the body muscle mass, the more transamination of amino acids and subsequent formation of mostly either glucose or ketones occurs to fulfill energy needs. Thus for those wishing to lose weight but maintain or even increase lean body mass in specific skeletal muscles, I recommend at least 1.5 grams of high quality protein per pound of bodyweight.

 

If you’re following my phase shift diets, as you are, then the reduction in calories needed to lose weight should be at the expense of mainly the fats (since carbs are already low. The reason behind this is that you’re already fat adapted and fat is your primary fuel source. So if you don’t supply as much in the diet, your body will use body fat instead, which is what you want to maximize your body composition.

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37. 

I am 32 years old and probably won't ever compete in a bodybuilding competition, but you never know. But I do want to gain as much lean muscle mass as possible. I am very serious about meeting this goal and am looking for direction. I am looking at The Metabolic Diet book and The Anabolic Solution for Bodybuilders book. Which book do you think will better help me?

 

 

I'd recommend the Anabolic Solution for Bodybuilders as it's specifically geared for bodybuilders. The Metabolic Diet on the other hand, while it contains more information, including dozens of sample meals at the various calorie levels, is geared more for the person who wants to lean out while at the same time maintaining or even gaining some muscle, but not to the level of maximizing muscle mass. On the other hand a lot of bodybuilders, whether recreational or competitive, buy both books since the Metabolic Diet book has more information on phase shift dieting, and has lots of other information. Just to giv e you an idea the Metabolic Diet book weighs in at over 500 pages while the Anabolic Solution for Bodybuilders is around 240 pages.

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38. 

I started the Metabolic Diet last week and I'm having problems with constipation. What can I do to regulate my bowels?

 

 

There are several reasons why people get constipated on the Metabolic Diet, and it has to do with the lower carbohydrates. First of all high carb diets increase body water and always involve relatively high fiber intake. The most obvious solutions, therefore, is to make sure you drink plenty of water, maybe even doubling up on your normal water intake, and take in lots of fiber. Water by itself can help relieve constipation. When the body gets too little water, it syphons what it needs from internal sources. The colon is the primary source. The result? Constipation. When a person drinks enough water, normal bowel function returns. Increasing the water intake part is fairly easy. You just make sure you have water on hand at all times and when you have a glass, have two instead. Or simply have a glass or bottle of water at your side so that you remember to drink more.

 

But there's more to the story when you're on the Metabolic Diet. Because of the low carb intake and the high intake of high protein/fat foods, fiber intake is lowered while you're on the low carb part of the Metabolic Diet. When you take in less fiber than you're used to, and the bowels are affected resulting in constipation. While the water part is easy, the fiber part needs more of an explanation.

 

There are two basic fiber types that we should be taking - soluble and insoluble fiber. Having a mix of both works best for regulating the bowels. Many of the high fiber vegetables, such as brocolli, brussels sprouts, cabbage and cauliflower, and to some degree almost all other low carb vegetables, have a mixture of both soluble and insoluble fiber.

 

SOLUBLE FIBER: Not only does it help regulate the bowels but it's been shown to have beneficial effects against heart disease and diabetes. Unlike its insoluble sibling, soluble fiber absorbs water. It's also metabolized somewhat, broken down into various byproducts such as short chain fatty acids. By binding to certain fats and bile acids in the gut, soluble fiber helps reduce cholesterol levels. In cases where carbs are taken with the fiber, it slows the absorption of the carbs and decreases the insulin response. Some research also suggests that soluble fiber may contribute to the prevention of gallstones.

 

Some of the byproducts of soluble fiber's metabolism nourish the digestive tract's friendly flora, preventing the overgrowth of bad bacteria. In the past few years there’s been some research that connects the gut flora with various aspects of health and disease. In other words there appears to be a symbiotic relationship between the intestinal microbiota and the human host, which has effects on health, obesity, cancer, etc.. FYI I’ve copied some abstracts from recent papers from PubMed at the bottom of this email.

 

The downside of soluble fiber is twofold: Some of its metabolic byproducts are gases that may cause a significant degree of flatulence. Additionally, the absorption of water is a double-edged sword: Although theoretically making the stool bigger, softer, and easier to pass, it could have the opposite effect. If you don't drink extra liquids, you could get a case of constipation.

 

The best sources for those following a low-carb diet are psyllium seed husks, flax meal, oat bran, guar gum, and apple pectin. Other good sources are oranges, rice bran, legumes, locust bean gum and barley. (FYI, peanuts and soybeans are legumes. About half of the carbs from each are from fiber).

 

INSOLUBLE FIBER: Passing through the digestive tract relatively unchanged, insoluble fiber absorbs some potentially harmful toxins. This trait, along with a speedier transit time, apparently may decrease the risks of colon and breast cancer. A high intake also reduces problems associated with hemorroids and diverticular diseases.

 

While insoluble fiber produces little (if any) flatulence and won't threaten to dehydrate your intestines, it does not share the soluble form's ability to help stabilize blood sugar, and its cholesterol-lowering effect is only minimal. And it's important to remember that in general, because the insoluble fiber passes through undigested and there is minimal absorption, carbs that are insoluble fiber don't count when tallying up your daily carb intake. Soluble fiber is another matter and requires more of an explanation, which you’ll find if you search for soluble fiber in the FAQ and article sections on my site.

 

The best source of whole food fiber for those following a low-carb diet is wheat bran. Other sources include corn bran, brown rice, nuts, strawberries, pure cellulose, asparagus, celery, root vegetables, and lignin. While getting more fiber from food is important, and along with taking in more water may solve the constipation problem, it's often a good idea to take some fiber supplementation to supplement the fiber from food sources.

 

Because of the potential of bowel dysfunction, at least at first, while on my phase shift diets, I formulated Regulate, the ideal fiber supplement and probiotic for anyone who’s on my phase shift diets and either wants to prevent or treat bowel problems, as well as helping to induce a beneficial bacterial flora in the bowels. For more information on Regulate and how best to use it (along with more water) have a look at the PDF file that’s available in my store at www.MauroMD.com.

 

There is one more topic I'd like to cover in regards to the Metabolic Diet and constipation, and that's the use of L-carnitine, which is an ingredient in several of my supplements including LipoFlush, Metabolic, MRP-LoCarb, Resolve, and EFA+.

 

L-carnitine, a compound biosynthesized from the amino acids lysine and methionine, is essential for fatty acid transport and burning of fat for energy. As well, it's essential for proper muscle function and some studies have shown that carnitine supplementation improves exercise performance. It also has anti-inflammatory and immunomodulating effects. Because of all these beneficial effects L-carnitine is a vital supplement ingredient that should be an integral part of anyone on my phase shift diets including the Metabolic, Anabolic, and Radical Diets.

The interesting thing, however, as far as our discussion about constipation, is that L-carnitine can operate as a mild laxative, definitely a useful side effect of for anyone on my phase shift diets.

 

The bottom line is that if you're having constipation problems while on the Metabolic Diet you should drink more water, eat more high fiber vegetables and take a fiber supplement (such as Regulate that I formulated specifically for my phase shift diets) that has a blend of soluble and insoluble fibers.

 

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Pharmacol Ther. 2011 May;130(2):202-12. Epub 2011 Feb 2.

The gut microbiome as therapeutic target.

Cani PD, Delzenne NM.

Abstract

Obesity, type-2 diabetes and low-grade inflammation are becoming worldwide epidemics. In this regard, the literature provides a novel concept that we call "MicrObesity" (Microbes and Obesity), which is devoted to deciphering the specific role of dysbiosis and its impact on host metabolism and energy storage. In the present review, we discuss novel findings that may partly explain how the microbial community participates in the development of the fat mass development, insulin resistance and low-grade inflammation that characterise obesity. In recent years, numerous mechanisms have been proposed and several proteins identified. Amongst the key players involved in the control of fat mass development, Fasting induced adipose factor, AMP-activated protein kinase, G-protein coupled receptor 41 and G-protein coupled receptor 43 have been linked to gut microbiota. In addition, the discovery that low-grade inflammation might be directly linked to the gut microbiota through metabolic endotoxaemia (elevated plasma lipopolysaccharide levels) has led to the identification of novel mechanisms involved in the control of the gut barrier. Amongst these, the impacts of glucagon-like peptide-2, the endocannabinoid system and specific bacteria (e.g., Bifidobacterium spp.) have been investigated. Moreover, the advent of probiotic and prebiotic treatments appears to be a promising "pharmaco-nutritional" approach to reversing the host metabolic alterations linked to the dysbiosis observed in obesity. Although novel powerful molecular system biology approaches have offered great insight into this "small world within", more studies are needed to unravel how specific changes in the gut microbial community might affect or counteract the development of obesity and related disorders.

 

--------------------------------

 

Nat Rev Microbiol. 2011 Apr;9(4):279-90.

Unravelling the effects of the environment and host genotype on the gut microbiome.

Spor A, Koren O, Ley R.

Source

Department of Microbiology, Cornell University, Ithaca, New York 14853, USA.

Abstract

To what extent do host genetics control the composition of the gut microbiome? Studies comparing the gut microbiota in human twins and across inbred mouse lines have yielded inconsistent answers to this question. However, candidate gene approaches, in which one gene is deleted or added to a model host organism, show that a single host gene can have a tremendous effect on the diversity and population structure of the gut microbiota. Now, quantitative genetics is emerging as a highly promising approach that can be used to better understand the overall architecture of host genetic influence on the microbiota, and to discover additional host genes controlling microbial diversity in the gut. In this Review, we describe how host genetics and the environment shape the microbiota, and how these three factors may interact in the context of chronic disease.

 

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Genome Med. 2011 Mar 4;3(3):14. [Epub ahead of print]

Gut microbiome-host interactions in health and disease.

Kinross JM, Darzi AW, Nicholson JK.

Source

Section of Bimolecular Medicine, Department of Surgery and Cancer, Faculty of Medicine, Imperial College London, The Sir Alexander Fleming Building, South Kensington, London SW7 2AZ, UK. j.nicholson@imperial.ac.uk.

Abstract

ABSTRACT: The gut microbiome is the term given to describe the vast collection of symbiotic microorganisms in the human gastrointestinal system and their collective interacting genomes. Recent studies have suggested that the gut microbiome performs numerous important biochemical functions for the host, and disorders of the microbiome are associated with many and diverse human disease processes. Systems biology approaches based on next generation 'omics' technologies are now able to describe the gut microbiome at a detailed genetic and functional (transcriptomic, proteomic and metabolic) level, providing new insights into the importance of the gut microbiome in human health, and they are able to map microbiome variability between species, individuals and populations. This has established the importance of the gut microbiome in the disease pathogenesis for numerous systemic disease states, such as obesity and cardiovascular disease, and in intestinal conditions, such as inflammatory bowel disease. Thus, understanding microbiome activity is essential to the development of future personalized strategies of healthcare, as well as potentially providing new targets for drug development. Here, we review recent metagenomic and metabonomic approaches that have enabled advances in understanding gut microbiome activity in relation to human health, and gut microbial modulation for the treatment of disease. We also describe possible avenues of research in this rapidly growing field with respect to future personalized healthcare strategies.

 

------------------------------------------------

 

Annu Rev Med. 2011 Feb 18;62:361-80.

Interactions between gut microbiota and host metabolism predisposing to obesity and diabetes.

Musso G, Gambino R, Cassader M.

Source

Gradenigo Hospital, Department of Internal Medicine, University of Turin, Turin, Italy. giovanni_musso@yahoo.it

Abstract

Novel, culture-independent, molecular and metagenomic techniques have provided new insight into the complex interactions between the mammalian host and gut microbial species. It is increasingly evident that gut microbes may shape the host metabolic and immune network activity and ultimately influence the development of obesity and diabetes. We discuss the evidence connecting gut microflora to obesity and to type 1 and type 2 diabetes, and we present recent insights into potential mechanisms underlying this relationship: increased nutrient absorption from the diet, prolonged intestinal transit time, altered bile acid entero-hepatic cycle, increased cellular uptake of circulating triglycerides, enhanced de novo lipogenesis, reduced free fatty acid oxidation, altered tissue composition of biologically active polyunsaturated fatty acid, chronic low-grade inflammation triggered by the endotoxin toll-like receptor 4 axis, and altered intestinal barrier function.

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39. 

Hi I've been reading some of your articles in PL USA. I thought you might be able to shed some light on a question i have. I need to determine whether its is beneficial to consume protein whilst drinking alcohol and if so why? For example, would drinking a protein enriched beer be beneficial? I have found heaps of material explaining why it's bad to consume alcohol and the effects drinking has on protein synthesis etc. But nothing regarding this topic. Any information you could give me would be awesome Thanks for your time.

 

 

Interesting question.

 

You're right about the studies showing the detrimental effects of acute and chronic alcohol consumption on protein synthesis. Studies have also shown that alcohol consumption doesn't seem to increase protein catabolism so that the changes in muscle protein is due to the decrease in synthesis and not from an increase in protein degradation.

 

Some unpublished recent studies have also shown that maximal strength decreases by about a third for anywhere from one to three days after a bout of acute alcohol intake, the more intake the longer the decrease in strength lasts. Acute alcohol use within a day of training may also make you more prone to injuries.

 

Studies have shown that leucine has a beneficial effect in countering alcohol's effect on protein synthesis in heart muscle but is equivocal on the same effect in skeletal muscle.

 

It also appears that much of the effect of alcohol may be because of its effects on lowering levels of IGF-1, as well as effects on decreasing activity of mammalian target of rapamycin (mTOR) and two mTOR substrates [the 4E-binding protein (BP)1 and the ribosomal S6K1] that are involved in increasing protein synthesis.

 

It's known that amino acids, and especially BCAA have regulatory effects on protein synthesis partly by way of the two above mechanisms. As such, it's quite possible that a blend of amino acids, heavy on the BCAA, and increasing levels of IGF-1 and insulin (both known to accelerate protein synthesis), may just prevent the detrimental effects of acute alcohol intake on protein synthesis.

 

Unfortunately there are no studies as yet that prove a reduction in alcohol's effects on protein synthesis via the above mechanisms. However, in my experience the combo likely does.

 

If you're looking at supplements that may be beneficial I'd consider using GHboost and Amino prior to drinking. Amino is a multi-faceted amino acid mixture plus other nutrients that support protein synthesis, while GHboost has beneficial effects on insulin sensitivity and increases GH and IGF-1 levels. For detailed info on these look at the PDF files on Amino, GHboost, and Max-PTN in my store at www.mdplusstore.com.

 

FYI I've copied the abstracts of 2 papers that will provide you with some peripheral information on the topic.

 

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J Nutr. 2010 May;140(5):932-8. Epub 2010 Mar 17.

 

Alcohol-induced IGF-I resistance is ameliorated in mice deficient for mitochondrial branched-chain aminotransferase.

 

Lang CH, Lynch CJ, Vary TC.

 

Abstract

 

Acute alcohol intoxication decreases skeletal muscle protein synthesis by impairing mammalian target of rapamycin (mTOR). In 2 studies, we determined whether inhibition of branched-chain amino acid (BCAA) catabolism ameliorates the inhibitory effect of alcohol on muscle protein synthesis by raising the plasma BCAA concentrations and/or by improving the anabolic response to insulin-like growth factor (IGF)-I. In the first study, 4 groups of mice were used: wild-type (WT) and mitochondrial branched-chain aminotransferase (BCATm) knockout (KO) mice orally administered saline or alcohol (5 g/kg, 1 h). Protein synthesis was greater in KO mice compared with WT controls and was associated with greater phosphorylation of eukaryotic initiation factor (eIF)-4E binding protein-1 (4EBP1), eIF4E-eIF4G binding, and 4EBP1-regulatory associated protein of mTOR (raptor) binding, but not mTOR-raptor binding. Alcohol decreased protein synthesis in WT mice, a change associated with less 4EBP1 phosphorylation, eIF4E-eIF4G binding, and raptor-4EBP1 binding, but greater mTOR-raptor complex formation. Comparable alcohol effects on protein synthesis and signal transduction were detected in BCATm KO mice. The second study used the same 4 groups, but all mice were injected with IGF-I (25 microg/mouse, 30 min). Alcohol impaired the ability of IGF-I to increase muscle protein synthesis, 4EBP1 and 70-kilodalton ribosomal protein S6 kinase-1 phosphorylation, eIF4E-eIF4G binding, and 4EBP1-raptor binding in WT mice. However, in alcohol-treated BCATm KO mice, this IGF-I resistance was not manifested. These data suggest that whereas the sustained elevation in plasma BCAA is not sufficient to ameliorate the catabolic effect of acute alcohol intoxication on muscle protein synthesis, it does improve the anabolic effect of IGF-I.

 

------------------------

 

J Nutr. 2009 Aug;139(8):1439-44. Epub 2009 Jun 23.

 

Oral leucine enhances myocardial protein synthesis in rats acutely administered ethanol.

 

Vary T.

 

Abstract

 

Acute alcohol ingestion induces an inhibition of myocardial protein synthesis by impairing mRNA translation initiation. Elevating plasma leucine (Leu) concentrations via oral gavage stimulates mRNA translation initiation in several tissues, although the effect in heart has not been well defined. The experiments described herein were designed to test the effects of a gavage solution containing Leu on protein synthesis and potential mechanisms important in accelerating mRNA translation initiation in cardiac muscle of rats given ethanol acutely to mimic "binge" dinking. Gavage with Leu stimulated protein synthesis and enhanced the assembly of the active eukaryotic initiation factor (eIF)4G.eIF4E complex. Increased assembly of the active eIF4G.eIF4E complex was associated with a 130% rise in phosphorylation of eIF4G(Ser(1108)) and a decreased assembly ( approximately 30%) of inactive eIF4E-binding protein1 (4EBP1).eIF4E complex in rats-administered ethanol. The reduced assembly of the 4EBP1.eIF4E complex was associated with an increase in phosphorylation of 4EBP1 in the hyperphosphorylated gamma-form following Leu gavage. Phosphorylation of mammalian target of rapamycin on Ser(2448), an upstream regulator of phosphorylation of 4EBP1, was elevated following Leu gavage. Neither the phosphorylation of 70-kDa ribosomal protein S6 kinase on Thr(389) nor eIF4E phosphorylation was increased following Leu gavage under any condition. Leu gavage accelerates myocardial protein synthesis following acute ethanol intoxication by enhancing eIF4G.eIF4E complex assembly through increased phosphorylation of eIF4G and decreased association of 4EBP1 with eIF4E.

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40. 

I had a couple of questions regarding your stance on the metabolic shift to fat burning and ketosis. In many of the resources I've been able to gain access to, they have indicated that one of the most important metabolic adaptations which spares nitrogen/protein losses during carbohydrate restriction is the adaptation of the CNS/brain to metabolizing ketones for fuel, thereby decreasing the drive for gluconeogenesis. This apparently coincided with the adaptation of skeletal muscle shifting a strong metabolic preference to fatty acids instead of ketones and/or glycolysis. Preventing ketogenic adaptations appeared to maintain nitrogen losses on starvation/ketogenic diets. I noticed that your Metabolic Diet places little emphasis on ketosis and that the protein/fat ratio in the metabolic diet would likely keep someone out of the significantly ketogenic state. Do you feel that the CNS adaptations to ketosis are not significantly important to decreased catabolism/protein sparing effects of low carb/high fat diets or that the metabolic shift of skeletal muscle is independent from the adaptations of the CNS and are more a result of primary fuel availability? Or is it that the increased protein intake is able to overcome gluconeogenic drive for catabolism of muscle mass?

 

 

As you've gathered from my books, for various reasons I'm not a fan of excessive ketosis (at least to the point of obsessing over ketonuria). First of all I believe that staying in ketosis may have long-term adverse effects (such as dehydration of various tissues and possible deterioration of cartilage and connective tissues, especially those that are weight bearing such as the vertebral disks). Secondly being constantly in ketosis is catabolic and counter productive for keeping or enhancing muscle mass. And thirdly I don't believe that achieving ketosis to the point of showing significant ketonuria is necessary for any of the beneficial effects of the Metabolic Diet on body composition. There are several reasons for my views and I'll try and outline them below. Keep in mind, however, that one of the more important ones is that the lack of the insulin-mediated anabolic effect. Insulin has been shown to both increase protein synthesis and decrease protein catabolism. In the Metabolic Diet, the anabolic effect of insulin (both direct and indirect - for example insulin in concert with GH leads to increases in muscle IGF-1 and subsequently to muscle hypertrophy) are harnessed while at the same time its lipogenic and anti-lipolytic effects are controlled. Purely ketogenic diets have other drawbacks as well. First of all staying in ketosis can lower metabolic rate and thyroid hormone levels and activity (specifically T3 levels). This can make it more difficult to increase protein synthesis and muscle hypertrophy. Also, as mentioned above, chronic ketogenic diets dehydrate the body and can have adverse effects on joint tissues, including spinal discs, and may result in increased injuries.

Those that argue that it's vital to show significant ketonuria, and that without it the protein sparing effect of the ketogenic diet is lost, are confusing the issues involved in switching the metabolism from a carb burning to a fat burning one. The point is that by titrating the Metabolic Diet to the lowest carb level that works for you, you're maximizing the fat loss, minimizing muscle catabolism, and more importantly using a macronutrient mix that is in tune to your genotypic and phenotypic makeup.

The bottom line is that you shouldn't worry about ketosis and ketone levels in the urine and instead concentrate on the progress you make and on making sure that you're at the lowest but most efficient dietary carb level for you (as per the troubleshooting chart and guide in the Metabolic Diet). The Metabolic Diet is geared to increasing the utilization of fat as a primary energy source, decrease protein catabolism and increase protein synthesis in a healthy way. The emphasis in the Metabolic Diet is on lowering dietary carb intake to a level that's optimal for you and that will maximize fat mobilization and oxidation, not ketonuria. As such, I don't recommend tracking urinary ketones because I think that the process is unnecessary.

As you know the Metabolic Diet is a phase shift diet in which you cycle the macronutrients. As such, it's not a strictly ketogenic diet. Unlike cycling ketogenic diets (CKDs) it's more dynamic in that it can be used to find the optimal level of carbs that matches any individuals metabolism and that will result in maximum results as far as altering body composition. This effect on body composition is helped by the weekly phase shift that results from the changes in macronutrient composition and the subsequent metabolic and hormonal environment.

Needless to say if you follow the strict part of the Metabolic Diet you will have significant degree of ketosis and variable levels of ketonuria. As you know ketones are formed all the time to some extent in everyone, just much more so as the dietary carb levels drop and fat intake increases. The amount of ketones that end up in the urine is a function of several factors including the amount formed secondary to carb availability, and insulin and glucagons levels, the extent to which they are able to be metabolized and used efficiently (a function of a person's genetic ability to oxidize fat and ketones efficiently and of time), and the efficiency of the gluconeogenic process and availability of gluconeogenic substrates thus decreasing the need for ketone formation.

Reaching ketosis, at least as far as being able to measure it using a ketostix, believe it or not, doesn't relate in the least to how well you do on the diet. Keep in mind that the depth of ketosis is NOT indicative of the degree of fat oxidation or lipolysis. I don't even suggest you check your urine for ketones never mind fussing over the degree of ketonuria. Again, the important thing is to fine tune the diet until you get the results you want. Once you've adapted to the diet, you'll use up most of the ketones you produce and as such shouldn't show much ketones in the body during the weekdays.

You have to understand that ketosis and ketonuria can be two different things. Anyone on a lower carb diet will burn more fatty acids, and subsequent to the breakdown of long chain fatty acids by the liver, produce more ketones and as such be in ketosis (defined as a blood concentration of ketones above .2 mmol/dl), but will not necessarily show ketones in the urine - ketosis may or may not result in ketonuria, the presence of ketone bodies in the urine. And it's the level of ketone bodies in the urine that people measure to determine if they're in ketosis and the degree of ketosis. In many people, especially those that are fat adapted and efficient in the use of ketones as an energy source, there may not be much spillage of ketones into the urine. For example, the Eskimo living on the traditional high fat, almost no carb diet, rarely shows any significant amount of ketonuria.

Also keep in mind that it's ketones and fatty acids that are burned as fuel initially when carb availability is low. Many tissues can oxidize fatty acids directly to get the energy they need. Some tissues, such as the brain and the nervous system can only use glucose (from dietary carbs and other substrates through gluconeogenesis or other processes - see below) and ketones as energy substrates. After adapting to a low carb, higher fat diet, ketosis becomes a minor pathway for energy metabolism in most tissues in the body, with muscle and other tissues (except for the brain, etc.) using free fatty acids as the main energy substrate.

The bottom line is that I tell people that they shouldn't worry about ketosis and ketone levels in the urine and instead concentrate on the progress they make and on making sure that they're at the best dietary carb level for them (as per the troubleshooting chart and guide in the Metabolic Diet).

And while I'm at it I must tell you that I'm not a proponent of depletion diets to maximize glycogen resynthesis. Firs of all depletion diets on Friday to maximize glycogen supercompensation on Saturday and Sunday can actually be counter productive. Anytime you're in starvation mode, you lose muscle, albeit perhaps less once you're fat adapted but you're still in an undesirable catabolic state. If you're in starvation mode on the Friday, a depletion workout will increase muscle catabolism even further. The catabolism is not worth the small increase in glycogen that occurs following a depletion diet. The idea behind my diets is to cycle to diet so that the overall effect is an increase in protein synthesis and a decrease in protein catabolism, while at the same time maximizing the oxidation of body fat and decreasing lipogenesis. Bottom line, in my view, is that it's not necessary to go into ketosis, at least as far as having significant ketonuria, in order to get the changes in body fat and body composition that accrue from using cyclic low carb/moderate to high carb diets such as the Anabolic and Metabolic Diets.

On the other hand, I agree with you to some extent about the importance of ketone production and utilization on low carb diets. The production of ketones does offer an alternative fuel supply to those tissues, like the brain which are unable to utilize free fatty acids directly as fuel but can utilize the smaller carbon groups (like ketones) aerobically via the TCA cycle.

But it's a misconception that the brain only uses glucose and ketones for fuel. In fact lactate has been shown to be the preferred substrate for neurons whether provided endogenously, via the circulation or through the metabolic coupling that occurs between astrocytes and neurons (Magistretti PJ, Pellerin L. [Functional brain imaging: role metabolic coupling between astrocytes and neurons]. Rev Med Suisse Romande 2000 Sep;120(9):739-42.)

The lactate so preferred by neurons can be produced endogenously within the neuron and/or astrocyte from glucose by either glycolysis or gluconeogenesis via direct gluconeogenic precursors forming glucose first and then going through the glycolytic pathway, or intermediates between glucose and pyruvate (such as glycerol which I feel is overlooked for its importance to glucose and lactate production considering that it makes up approximately ten percent of fat by weight) that fit in somewhere between glucose and pyruvate, or synthesized via the tricarboxylic acid (TCA) cycle secondary to an increase in anapleurotic flux via the various reactions of amino acids, odd chain fatty acids, TCA intermediates, and removal of oxaloacetate or malate to form pyruvate and then lactate. The above schemata is grossly simp lified but it will do for this discussion.

That aside, the brain and nervous system, although arguably the reason behind ketone production at time of low glucose availability, is not a significant player as far as the body's metabolic shift from using carbs to using fatty acids as the primary fuel, and to harnessing the cyclical nature of the Metabolic Diet to achieve the beneficial changes in body composition. This all occurs secondary to the body's adaptation to the different macronutrient composition of the diet, which as you know is the route the body takes most of the time (for example the lipid content of cellular membranes will reflect the lipid content of the diet). Studies have also shown that the phase shift that occurs every week for anywhere between 12 and 36 hours (although as per my book the shift can be very flexible depending on the individual person's metabolism and reaction to the diet) does not adversely affect the established fat burning mode and as such does not reverse the enzymatic changes that have been induced as a result of the prior lower carb, higher fat phase.

This was shown again in a study published in December of 2000 (Louise M. Burke1, Damien J. Angus2, Gregory R. Cox1, Nicola K Effect of fat adaptation and carbohydrate restoration on metabolism and performance during prolonged cycling. J Appl Physiol 2000; 89(6):2413-2421.) in which the authors concluded that "5 days of exposure to a high-fat, low-CHO diet caused clear changes in fuel substrate utilization during submaximal exercise. At least some of these changes were independent of CHO availability because enhanced capacity for fat oxidation persisted despite restoration of muscle glycogen stores." Actually this study, while not as sophisticated as it might have been as far as its protocol, is an interesting read.

You ask about the necessity of ketones for protein sparing and the data that backs this up. First of all it's obvious that supplying the amino acid and other substrates that lead to an increased anapleurotic flux for gluconeogenesis and lactogenesis can be a catabolic process if the amino acids needed are rounded up endogenously. Supplying the amino acids via a high protein diet obviates most of the muscle catabolism. As such, in my mind protein sparing is thus mostly a function of increased protein intake and not dependant on ketone formation.

I think that it's important to realize that the studies are conflicting with some showing that ketones are protein sparing and others showing that they are not protein sparing. As well, most of the studies that show ketosis as being necessary for protein sparing are starvation or fasting diets (the Metabolic Diet being neither) and/or use ketone salts (which are not the same as an increase in endogenous ketones) as infusions. Looking at all the available literature and data it's my opinion that ketones are not protein sparing per se and as such excessive ketosis is counter productive and in the chronic state, catabolic in nature.

There is also one more big difference between the Metabolic Diet and the other ketogenic and CKD diets. You'll notice that I don't have people who start the diet worry about calories. I stress the metabolic transition phase first and once fat acclimatized, I have them vary their calories. The point being two fold. First of all the tiredness that some people feel when they first start a ketogenic type of diet is not all from the lack of carbs but to some extent is simply due to a lack of calories. Going on a starvation diet at the same time as a ketogenic diet is counter productive. In my Metabolic Diet I stress the metabolic shift before I stress calories.

Even more importantly is that once a person has made the shift and most tissues in the body are using free fatty acids, and the gluconeogenic (and lactogenic) processes are more efficient, then cutting back on calories on the Metabolic Diet also spares muscle protein and allows the gradual loss ofbody fat while maintaining or at time even increasing muscle mass.

Hopefully I've answered some of your questions although I'm sure others will pop up as you read my reply. Please don't hesitate to write again if you have further questions or comments.

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41. 

I have tried so many other products for my cellulite problem and lower body fat. I have spent enough money on fat reducing creams and cellulite reducers to supply an army. I am skeptical already, but I am willing to let lipoflush do its job, as long as I am using the product to its full potential. What is the best time to take it? I want to make sure that it does not affect my sleep patters. Also what diet plan do you suggest. I have about 60 pounds I need to lose?

 

 

LipoFlush can be used in the AM and mid day and should not disturb your sleep. You can take it anytime but if pills tend to upset your stomach, you can use it just before meals. A lot of people also use the LipoFlush 15 minutes or so prior to exercising, as long as the you are not exercising in the evening.  Consistently using LipoFlush twice a day should do the trick for you. I would take it as I have outlined above. You can start off with 2 tabs twice a day and up that to 4 tablets twice a day.

 

As far as the best diet, I suggest you start with my Radical Diet as you’ll lose weight the fastest without compromising your health or energy. I formulated LipoFlush so it could be used as stand alone product for weight and fat loss but it works the best if combined with my phase shift diets, in your case the Radical Diet, but also my Metabolic and Anabolic Diets, as well as my Anabolic Solution Diet/supplement programs, one meant for bodybuilders and the other for power athletes in powerlifting or for that matter any sport as the diet, supplement combination improves body composition and athletic performance.

 

I'm mentioning the other diets in case you're into training and after losing your weight want to further improve your body composition, fitness, and athletic peformance. If that's ever the case one of the other diets could be the next phase of your transformation.

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42. 

I’m a 42 yr old powerlifter - for my own recreation, at least for now. I need help choosing which of you books will help me lose 50 lbs of unwanted fat, while maintaining muscle, strength, and energy levels.

 

 

The best book for you is the Anabolic Solution for Powerlifting. You'll need to read the whole book first and then make the changes you need to make for your circumstances, especially for dropping that 50 lbs in body fat. For example, in chapter seven you would go right into the Cutting Phase (starts on page 150) and cycle between the Strength and Cutting Phases until you get to your desired body composition - level of lean body mass and body fat.

 

The book will explain everything to you as far as the diet and nutritional supplements to use so that you maintain energy levels and make steady progress, including strength gains and favorable changes in your body composition.

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43. 

I was wondering which book I should get the anabolic solution for bodybuilders or the metabolic diet. My main hobby is bodybuilding for the last couple years but I haven't given my diet very much thought until recently. I have always carried around about 20 extra pounds so I wasn't sure which book would be best for me. I also wanted to start my assessment phase but I was confused on the amount of fats. Being a bodybuilder I consume about 210 grams of protein daily and was wondering how many grams of fats I need. The website suggests 40-60% of fats but I don't know if that’s 40-60% of daily calories or 40-60% of daily gram intake.

 

 

Your best bet is the Anabolic Solution for Bodybuilders. The Anabolic Solution series of books (there are two now with more planned) build on the dietary foundation of the Metabolic diet and provides specific nutrition, training and supplement programs for specific sports, such as bodybuilding. The Anabolic Solution books do not have the extensive appendices of nutritional information and meal plans that the Metabolic Diet book has, however that information is available through my website, www.MauroMD.com.

 

The Anabolic Solution for Bodybuilders will explain the diet in detail. As far as the percentages of macronutrients, it refers to calories and not grams. For example if you limit your carb intake to 30 grams per day, it will usually make up anywhere from 4 to 10 percent of your calorie intake (daily calorie intake say between 1200 to 3000 calories). Of course in the bulking phase, if say you're taking 4500 calories per day, the 30 gram limit accounts for less than 3 percent of your calorie intake.

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44. 

Can you recommend some supplements that helps to efficiently increase and transfer oxygen to the muscles during an intense workout?

In Jui Jitsu we roll for 5 minute rounds, sometime 3 rounds back to back and I am gassing out after about 7 mins...breathing really hard. I know part of it is controlling the breathing, and I'm working on that, but I want to know if there is something else I can do to help with this. I know you're busy, but when you have time, let me know your thoughts.

 

 

Unfortunately there isn't just one supplement on its own that will do the trick. However, a combination of supplements will definitely help. That's because there are a number of mechanisms involved in decreasing fatigue - both physiological and psychological. And this applies to all athletes, both power and endurance as fatigue affects us all.

The mental aspect of decreasing fatigue is important and some of the supplements work on that end. Others work mostly on increasing oxygen delivery to the muscle mitochondria and thus maximizing ATP production and minimizing metabolic changes, such as lactic acidosis, that can lead to premature fatigue.

Decreasing fatigue and increasing oxygen carrying capacity involves a number of interdependent processes. As mentioned it involves both mind and body and the two are interdependent and work synergistically to decrease perceived exertion and increase power and endurance, resulting in markedly increased performance.

On the physical end a number of processes are involved (I've actually broken it down to 4 main ones) and each can be improved upon to increase exercise performance. The degree of improvement seen with improving each of these processes will depend on the individual athlete's circumstances.

For example, increasing breathing performance by strengthening the intrinsic and extrinsic chest and abdominal musculature may prove useful. Fatigue in these muscles can impact oxygen availability and delivery and increase perceived exertion. With increased strength and endurance in these muscles, the amount of air inhaled and exhaled per minute over both the short and long term can be increased (ventilatory capacity and rate can be increased and ventilatory muscle fatigue lessened) and this may enhance performance. These muscles can be strengthened in a number of ways including a device called PowerBreathe.

For more info on PowerBreathe see the product links and Medline abstracts at the end of this email.

The other processes involve but are not limited to the following:

"    oxygen concentration in the inhaled air (breathing a higher oxygen mixture)

"    ventilatory rate - how much air containing oxygen is moved in and out of the lungs per period of time and more important volume per minute of air that reaches the alveoli.

"    diffusion capacity between the oxygen and carbon dioxide in the lungs (alveoli) and the lung capillaries (this involves several processes including the shunting of blood away from poorly oxygenated parts of the lungs to the more richly oxygenated parts as well as the presence of factors such as inflammation that affect the diffusion of oxygen through the tissues separating the oxygen in the lung from the red blood cells in the capillaries)

"    the amount of oxygen delivered to working muscles via the circulation, which relates among others to cardiac and arterial efficiency and endurance (these tire as well), and oxygen carrying capacity (red blood cell mass in the body)

"    the extraction percentage between oxygen in the arterial and venous blood (the oxygen saturation differential), which is dependant on several factors including increasing blood flow through the muscles and more efficient extraction of oxygen from the capillaries

"    the diffusion of oxygen into the cellular space and more specifically the mitochondria

"    mitochondrial efficiency in utilizing the available oxygen, including adequate anaplerotic processes to keep the Krebs Cycle well stocked, the availability of various nutrients and micronutrients to facilitate ATP production.

There's a lot more to the story and many more variables, (such as delivery of oxygen to other tissues such as the brain - see 2 abstracts below, liver, kidneys, etc.) to consider but I've been long winded enough (bad pun). I'll be covering all of this in much more detail in the next two or three issues of my Elite Performance Newsletter , which is available for download from my site MauroMD.com. There's no charge for the newsletter. Maybe you can help me spread the word about EPN by sending the link to anyone you think might be interested.

The bottom line is that there's a lot you can do to decrease fatigue and that includes using specific supplements that will impact on all of the processes involved. The supplements will be even more effective by allowing increased training intensity and thus an increased training response, and they also work well when using other methods that affect one or more of the processes mentioned. On the supplement end I would suggest that you use a fairly simple combo of supplements that includes MVM, EFA+, GHboost, TestoBoost, and Resolve (go to www.MDPlusStore.com for more info on these and other MD+ supplements). If you wish I can set up a supplement regimen for you that includes this group of supplements, making changes as needed as we follow your progress.

BTW I have a lot of elite athletes, including fighters (boxers, wrestlers, MMA, etc.), on these same supplements, and in some cases several more, and they definitely help to decrease fatigue, enhance their oxygen carrying capacity and utility, and their power and endurance.

Hope this helps.

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"    http://www.powerbreathe.com/about-us/about-us-benefits.html

"    http://www.powerbreathe-usa.com.
 

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45. 

Can diabetics take advantage of the Metabolic Diet? I asked my doctor and he didn’t know enough about your diets to say one way or the other. At this point I’m on a high carb, low fat diet but I don’t think it’s the best diet for me since I’m having problems keeping my sugar under control, and I’m holding a lot of body fat. Although I try and do some form of exercise most days of the week what's the best exercise program to follow with the diet?

 

 

Diabetics have been and still are almost universally put on a high complex carbohydrate, low fat diet. Why? Because it's generally felt that this type of diet was necessary for controlling the diabetes and that it reduced the cardiovascular risk factors especially in overweight type 2 (non insulin using) diabetics.

 

In the past few years several studies have pointed out the low carb diet is less than ideal and that a diet higher in fat and protein and lower in carbs is the best diet for diabetics. For example, in a recent study the use of a monosaturated fatty acid enriched low calorie diet resulted in a lessening of cardiovascular risk factors compared to diabetics who were put on a low calorie, low fat diet.

 

For more information on the current status of low carbing for health and for those with metabolic diseases such as diabetes have a look at the paper by Hite et al published in June of 2011. FYI I’ve copied the citation and abstract from PubMed below.

 

But to answer your question, I’ve always recommended that both insulin dependent (type 1) and non-insulin dependent (type 2) diabetics take advantage of The Metabolic Diet to manage their glucose levels, improve their health, and lose weight and body fat as needed.

 

Type 2 diabetes, by far the most common, affects more than 90% of the almost fifteen million North Americans afflicted with diabetes. It goes hand in hand with obesity and is associated with insufficient insulin output and some degree of insulin resistance. Often weight loss and a proper diet is all that's needed to keep it under control. The Metabolic Diet, since it both decreases body weight and increases insulin sensitivity, is an excellent diet and lifestyle management plan for type 2 diabetics, and it's also useful for the smaller number of insulin dependent or type 2 diabetics.

 

The effect of The Metabolic Diet on insulin requirements in type 1 diabetics and on the use of medications in type 2 diabetics is variable. Although many diabetics find that their insulin or medication requirements may be lower, it may not be depending on the type of diet that was followed before embarking on The Metabolic Diet.

 

If the diabetic followed the usual dietary guidelines recommended for diabetics, that is a diet that is high in carbohydrates (45 to 50 percent of calories), low in fat (< 30 percent of calories), and low in cholesterol (< 300 mg) , then medication or insulin levels may go down during the low carb phase of the diet. If the diabetic disregarded the dietary guidelines and ate a diet higher in protein and fat and lower in carbohydrates, then the medication needed may not change appreciably.

 

Exercise is also important and you’re on the right track when you try and do something every day, whether it’s walking, jogging, cycling, resistance training or whatever. Not only can regular physical activity help transport glucose into muscle cells without the presence of insulin, but we also see an increase in insulin sensitivity secondary to exercise. The overall effect of exercise is to decrease the need for insulin and diabetic drugs needed to control the diabetes.

 

The exercise programs recommended on my site are useful for managing and decreasing the need for medication in both types of diabetics. I recommend a  combination of aerobic exercise and resistance training as both are important for your health, fitness, and increasing strength, which has specific benefits for everyone of all ages.

 

However, diabetics should be ready to adjust their meals, their insulin intake, or both to prevent hypoglycemia during, immediately after, or even six to 12 hours after exercise. In fact when you follow my phase shift diets, and/or use any of my supplement line it’s important to carefully watch what’s happening and to make adjustments in whatever medications you’re using for your diabetes.

 

Many diabetics have asked me just why they even need insulin or medications that imitate the action of insulin or stimulate insulin secretion if they hardly consume any carbs. The answer is that although the low carb portion of the diet allows the burning of fat for energy, there is still a need for insulin.

 

First of all the body will produce a certain amount of glucose from gluconeogenesis (see above) and the body needs insulin to properly use this glucose. Even more important, however, is that some stages of fatty acid oxidation require insulin. Although the initial steps of fatty acid oxidation do not require insulin, the final steps do especially the oxidization of ketone substrates into carbon dioxide and water.

 

Without insulin ketoacidosis would occur. This occurs because when there is a lack of dietary glucose, the body increases the use of fats for energy. It oxidizes fat to ketones without insulin but can't go any further unless insulin is present. If insulin is absent or reduced, the ketones build up and cause ketoacidosis, a potentially dangerous and sometimes fatal condition.

 

Most diabetics who have gone on the diet find that their blood glucose levels may go up if they overdo the carbs on the weekends. Weekdays are not usually a problem.

 

If a problem surfaces on weekends, then lower glycemic carbs should be used as the main source of carbs. Because different carbohydrates are digested at different rates and have different effects on glucose levels, glycemic indices have been developed for use in helping a diabetic in maintaining control of their blood sugar. Several studies have shown that low glycemic index foods produce low blood glucose and insulin responses and improve blood glucose control in Type 1 and Type 2 diabetic patients.

 

Both type 1 (insulin dependant) and type 2 (non insulin dependant) diabetics should monitor themselves very closely whenever they change diets or their exercise level. So it goes without saying that they should do so in the initial stages of The Metabolic Diet. With the availability of self-monitoring, I often recommend that diabetics check their glucose levels at various stages of the diet until they become familiar with the effects of the diet and exercise on their systems.

 

As well, serum cholesterol (total, HDL, and LDL) should also be checked while on this diet. If you're a diabetic and you're using the diet to lose body fat and firm up, you should find that these values should improve compared to your normal values. That is total and LDL levels should go down and HDL levels should go up.

 

I've had several diabetic patients on my diet and found that as they lost weight and became fitter, the amount of insulin or oral agents that they used dropped significantly. Some type 2 diabetics who were on oral agents were able to control their diabetes with diet and exercise alone.

 

Good luck while on the diet and let me know how you do. If you have any other questions don’t hesitate to email me.

 

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Nutr Clin Pract. 2011 Jun;26(3):300-8.

Low-carbohydrate diet review: shifting the paradigm.

Hite AH, Berkowitz VG, Berkowitz K.

Source

Valerie Goldstein-Berkowitz, 7 West 51st Street, New York, NY 10019; Valerie@centerforbalancedhealth.com.

Abstract

What does a clinician need to know about low-carbohydrate (LC) diets? This review examines and compares the safety and the effectiveness of a LC approach as an alternative to a low-fat (LF), high-carbohydrate diet, the current standard for weight loss and/or chronic disease prevention. In short-term and long-term comparison studies, ad libitum and isocaloric therapeutic diets with varying degrees of carbohydrate restriction perform as well as or better than comparable LF diets with regard to weight loss, lipid levels, glucose and insulin response, blood pressure, and other important cardiovascular risk markers in both normal subjects and those with metabolic and other health-related disorders. The metabolic, hormonal, and appetite signaling effects of carbohydrate reduction suggest an underlying scientific basis for considering it as an alternative approach to LF, high-carbohydrate recommendations in addressing overweight/obesity and chronic disease in America. It is time to embrace LC diets as a viable option to aid in reversing diabetes mellitus, risk factors for heart disease, and the epidemic of obesity.

 

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46. 

I just have a question. First thing is that i have just read two of your book ( the metabolic diet and the anabolic diet for powerlifters) , they are really fantastic. I just want to know about coconut oil. Is it allowed on the diet since it is a fat and is it healthy or not? Can i use it raw or for frying instead of other oils like canola ?

 

 

Coconut oil is mostly made up of 10 carbon chain saturated fatty acids, or what’s referred to as medium chain triglycerides. In its natural (extra virgin) state it can be a healthy oil to use for almost any purpose including using it raw or frying with it. It’s even useful for putting on your skin as a lotion. There is some evidence that coconut oil has antioxidant effects, and may have cardiovascular and anti-aging benefits.

 

I know that medium chain triglycerides (MCTs), are often used by athletes to enhance body composition as they do have a protein sparing effect, but this is mostly evident in those who are a higher carb diet. However, and this is a big one for those who follow my phase shift diets, coconut oil shouldn’t be used in the low carb phase of the diet..

 

The problem with short chain medium chain triglycerides is that they're used by the body preferentially over the long chain triglycerides (which make up body fat) because they bypass the metabolic processes that are set up to allow the body to burn its own subcutaneous and visceral fat and thus decreasing both the lipolytic effect of the diet and the transfer of fatty acids into the mitochondria where it undergoes beta oxidation.

 

MCTs are preferentially (and this is the important word for becoming fat adapted instead of being carb adapted) used as fuel for the body so that like carbs they can short change your metabolism away from burning the fatty acids that make up body fat. For example MCTs don’t require L-carnitine to shuffle them into the mitochondria so they’re more easily used up to produce energy for the body.

 

The long chain triglycerides found in most foods allowed in my Anabolic, Metabolic, Anabolic Solutions, and Radical Diets, and which make up our body fat, have other advantages over MCTs. First of all the LCTs have greater protein sparing effects than MCTs. MCTs, unlike LCTs, have little inhibitory effect on the activity of enzymes involved in lipogenesis (increased formation of body fat). As well, several studies have shown that LCTs increase lipolysis or the breakdown of body fat. Overall LCTs in contrast to MCTs, should result in decreased body fat levels, if used properly.

 

Thus if you're looking to maximize body composition using my phase shift diets, the use of short and medium chain fatty acids during the low carb phase can be counterproductive. 

 

Bottom line is that if you’re on one of my phase shift diets MCTs act like carbs and should be avoided on the low carb phase of the diet. Otherwise, I think coconut oil is a healthy alternative to most processed oils, and although I consider olive oil a healthier oil, olive oil shouldn’t be used for frying as cooking makes it susceptible to oxidative damage, something which is also true to a lesser extent of many of the other oils used for cooking, but not coconut oil.

 

For more information on MCTs, fiber, and disguised carbohydrates that can affect your metabolism in a way that is counter productive see the article Understanding Food Labels (about two thirds of the way down) on my site www.MauroMD.com.

 

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47. 

Is it better to have a cold or hot shower after training and whichever one is best, how long should I shower to get whatever benefits there ar?. If this sounds like I am confused it's because I am. I've been told that a hot shower is better because it relaxes you, that a cold shower is better as it keeps injuries down and will help you recover better, and that you should take a hot shower for a few minutes, then immediately a cold shower for a few minutes and then hot and then cold and so on for up half an hour. Then there's the whole bit about cold water immersion rather than a cold shower. Personally I'd just like to have a warm shower to clean off after training but if doing it a specific way is better for my performance then I'll try it out.

 

You're right about the confusion. I ran into that same dilemma when I was an active elite athlete in powerlifting. Unfortunately, at that time I never really resolved the issue as some of my training was done in a garage set up for powerlifting and after working out I just got out of my gear, put my clothes back on and headed home. When there were shower facilities, I'd just shower for a few minutes or so just long enough to get the sweat off and clean up.

 

In the past few decades I've tried cold water immersion as well as cold and hot alternating showers, and frankly I didn't find it did me any good as far as my powerlifting or with injuries. But then I wasn't a fan of the cold water and actually thought that warm showers did me more good in relaxing me after a hard training session.
 
Having said that I believe that cold/cool water immersion and contrast water therapy, alternating cold and hot similar to what you described can do some good under some scenarios. And certainly a lot of elite athletes are climbing on the bandwagon of either cold showers or cold water immersions, and contrast water therapy, even though both practices have been around for several decades.

As well, there is some research that does show clear benefits of post exercise water therapy mostly in situations where short term recovery is important, for example in tournament situations, or in competitions where the athlete must perform repeated bouts of exercise within one or two days. In these situations, enhancing recovery by water therapy (and by other means which we'll cover in an upcoming article) may well improve repeat performances.
 
The bottom line is to try some of the various water therapies and figure out if they work for you.
 
I'm in the process of writing a series of article on recovery techniques with one of these articles focusing on post exercise water therapy. When these articles are ready for publication I'll update this Q&A with links to them.
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48. 

My name is Frank and I've ordered products from you over the last few years. However, I've run into some problems that just aren't going away even though I've seen other people, including doctors and specialists. These problems are ongoing and making me desperate to find help for them since I can't train and feel tired most of the time. I'd like to contact Dr. Di Pasquale regarding a private consultation with him. First of all does he do one on one consultations, and secondly I would like to know how much he would charge me. 

 

Frank, this is Bonnie, Dr. Di Pasquale's right hand man so to speak. Yes he does do one on one consultations and his charges vary. It'd be best if you emailed me at Bonnie@MetabolicDiet.com and then I can get back to you. You can also call or fax me your request.

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49. 

I've been on your Anabolic Diet for Powerlifters and have never felt better. I don't mean this in the sense that my lifts have gone up or that I'm leaner but more muscular, even though both of those are true. What I mean is that I feel better, not depressed anymore although I wouldn't really call it depression as it was more like a sadness that I'd wake up with in the morning and would stay with me for the day, sometimes better sometimes worse. The tighter I am with the diet, the better I feel.

 

What I go back to a low fat, high carb diet, even though I don't eat junk carbs, I go back to feeling not all that good. So I just switch back to your diet and things are better. I know that this is not all in my head although at times in the past I've been tempted to see a psychiatrist. I hesitated because I did go to counseling when I went to university but it really didn't help. Anyways just wanted to let you know what I've been going through and how your diet affects me. Do you have any explanation as to why diet affects me so much, and is it the same for others?
 

I’ve heard this same story from a lot of people over the past four decades. I also feel better on my phase shift diets but never really looked into that aspect of it in any detail.

 

I knew that the essential fatty acids had important effects on the brain, and that there is a connection between the gut and the brain so that feeding had specific effects on the brain and vice-versa. In other words it’s not just as most people believe that the brain influences everything including the gastrointestinal system. The GI system also has dramatic effects on the brain and other systems in the body.

 

Lately, there’s been some research on the effects of dietary fat on gut-brain communications and a study published online July 25 in the Journal of Clinical Investigation was more definitive in explaining the effects of fatty acids on mood.

 

This paper (I’ve copied the abstract of this and other relevant papers below) found that fatty acids really are comfort foods in that they blunt the behavioral and nerve cell responses to sad emotion. The authors found that MRI images of the brain showed that fatty-acid intake lessened the neural responses to sad emotions in regions of the brain.

 

More research in this area still needs to be done but my guess is that certain people are more affected by fat intake than others but that everyone has some beneficial effects on mood from dietary fat.

 

My advice is to stay on the diet since it makes you feel better, and also as you mentioned you’re also getting some performance and body composition results. My only other suggestion is that you take my EFA+ supplement (look at the info on EFA+ in my master site, www.MauroMD.com,  in the articles and Q&A section, and in the store) as it should work with the diet to enhance your mood and performance.

 

 

------------------------------------------

 

J Clin Invest. 2011 Jul 25. pii: 46380. [Epub ahead of print]

Fatty acid-induced gut-brain signaling attenuates neural and behavioral effects of sad emotion in humans.

Van Oudenhove L, McKie S, Lassman D, Uddin B, Paine P, Coen S, Gregory L, Tack J, Aziz Q.

Abstract

Although a relationship between emotional state and feeding behavior is known to exist, the interactions between signaling initiated by stimuli in the gut and exteroceptively generated emotions remain incompletely understood. Here, we investigated the interaction between nutrient-induced gut-brain signaling and sad emotion induced by musical and visual cues at the behavioral and neural level in healthy nonobese subjects undergoing functional magnetic resonance imaging. Subjects received an intragastric infusion of fatty acid solution or saline during neutral or sad emotion induction and rated sensations of hunger, fullness, and mood. We found an interaction between fatty acid infusion and emotion induction both in the behavioral readouts (hunger, mood) and at the level of neural activity in multiple pre-hypothesized regions of interest. Specifically, the behavioral and neural responses to sad emotion induction were attenuated by fatty acid infusion. These findings increase our understanding of the interplay among emotions, hunger, food intake, and meal-induced sensations in health, which may have important implications for a wide range of disorders, including obesity, eating disorders, and depression.

 

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Nutr Clin Pract. 2011 Aug;26(4):409-25.

Essential Fatty acids and psychiatric disorders.

Perica MM, Delas I.

Source

Ivančica Delaš, Department of Chemistry and Biochemistry, School of Medicine, University of Zagreb, Šalata 3, HR-10 000 Zagreb, Croatia; ivancica.delas@mef.hr.

Abstract

Psychiatric disorders are a significant source of disability worldwide. Increasing evidence indicates that disturbances of fatty acids and phospholipid metabolism can play a part in a wide range of psychiatric, neurological, and developmental disorders in adults. Essential fatty acids, ω-3 and ω-6 polyunsaturated fatty acids, play a central role in the normal development and functioning of the brain and central nervous system. The aim of this article is to discuss the overall insight into roles of essential fatty acids in the development of mental disorders (depression, schizophrenia, bipolar disorder) and, in light of the fact that disturbances of fatty acid metabolism can play a part in the above-mentioned disorders, to investigate the current knowledge of lipid abnormalities in posttraumatic stress disorder. The information in this review was obtained after extensive MEDLINE searching of each topic area through relevant published studies from the past 20 years. References from the obtained studies were also used. This review summarizes the knowledge in terms of essential fatty acids intake and metabolism, as well as evidence pointing to potential mechanisms of essential fatty acids in normal brain functioning and development of neuropsychiatric disorders. The literature shows that ω-3 fatty acids provide numerous health benefits and that changes in their concentration in organisms are connected to a variety of psychiatric symptoms and disorders, including stress, anxiety, cognitive impairment, mood disorders, and schizophrenia. Further studies are necessary to confirm ω-3 fatty acids' supplementation as a potential rational treatment in psychiatric disorders.

 

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Nat Rev Neurosci. 2011 Jul 13;12(8):453-66. doi: 10.1038/nrn3071.

Gut feelings: the emerging biology of gut-brain communication.

Mayer EA.

Source

Center for Neurobiology of Stress, Division of Digestive Diseases, Departments of Medicine, Physiology and Psychiatry, David Geffen School of Medicine at University of California, Los Angeles, CHS 47-122 10833 Le Conte Avenue, Los Angeles, California 90095-7378, USA. emayer@ucla.edu.

Abstract

The concept that the gut and the brain are closely connected, and that this interaction plays an important part not only in gastrointestinal function but also in certain feeling states and in intuitive decision making, is deeply rooted in our language. Recent neurobiological insights into this gut-brain crosstalk have revealed a complex, bidirectional communication system that not only ensures the proper maintenance of gastrointestinal homeostasis and digestion but is likely to have multiple effects on affect, motivation and higher cognitive functions, including intuitive decision making. Moreover, disturbances of this system have been implicated in a wide range of disorders, including functional and inflammatory gastrointestinal disorders, obesity and eating disorders.

 

-------------------------------------------

 

Diabetes Metab Res Rev. 2011 Feb;27(2):113-9. doi: 10.1002/dmrr.1160.

Gut-brain signalling: how lipids can trigger the gut.

Breen DM, Yang CS, Lam TK.

Source

Toronto General Research Institute, University Health Network, Toronto, Ontario M5G 1L7, Canada.

Abstract

The gut plays a unique role in the metabolic defence against energy excess and glucose imbalance. Nutrients, such as lipids, enter the small intestine and activate sensing mechanisms to maintain energy and glucose homeostasis. It is clear that a lipid-induced gut-brain axis exists and that cholecystokinin and a neuronal network are involved, yet the underlying mechanisms in gut lipid sensing that regulate homeostasis remain largely unknown. In parallel, studies underscore the importance of enzymes involved in lipid metabolism within the brain, such as adenosine monophosphate -activated protein kinase, to maintain homeostasis. In this review, we will first examine what is known regarding the mechanisms involved in this lipid-induced gut-brain neuronal axis that regulate food intake and hepatic glucose production. We will also discuss how enzymes that govern brain lipid metabolism could potentially reveal how lipids trigger the gut, and that both the gut and brain may share common biochemical pathways to sense lipids.

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50. 

Dr Di: What do you know about this company’s supplement lineup? I have a good friend who swears by these, he is diabetic also and thinks these products are the best in the world. I am sure you know the real answer and I think he should be taking your products.

 
The man who is CEO of this the company is a friend of mine and has been for almost 20 years. As a friend, I helped him to formulate some of his supplements. In general his company’s line of supplements is fairly simple as far as formulation and ingredients, first of all to have a perceived large array of supplements even though many have only one or two ingredients, and to satisfy the authorities in the various countries he sells to that don’t allow many of the ingredients I use in my products. Also there’s a lot of hype to his products as he’s pretty aggressive as far as marketing his line to stores, other Internet sites such as Bodybuilding.com, and all his affiliates in various countries, including several countries in Europe that have stringent laws on supplements.
 
For example in Canada L-carnitine is considered a drug. As such, they have L-carnitine in their lineup as a sole supplement for those countries that allow it, mainly the US in this case, and for those in the countries that don’t to try and see if it makes it through customs. Have a look at http://www.mauromd.com/faqs.php and search for Health Canada to see a related Q&A so you can better appreciate what it means as far as supplements that need to sell internationally. 
 
While his line of supplements is relatively simple, his marketing is more like the bigger supplement companies, with a lot of hype and push. I basically have no marketing other than my sites, including my new master site www.MauroMD.com that I’m working on but wont’ be ready for general consumption until some time in October. I’ll also be starting a modest evidence-based marketing campaign this fall but it will be nothing like the clever (read misleading and fraudulent) marketing done be the other supplement companies – see http://www.mauromd.com/det-articles-78-Lies--Lies--and-Damned-Lies.phphttp://www.mauromd.com/det-articles-47-The-Nutritional-Supplement-Industry---Part-1.php and http://www.mauromd.com/det-articles-62-The-Nutritional-Supplement-Industry---Part-2.php.
 
I should also tell you that the CEO of that company, who has dabbled in powerlifting ever since I’ve known him, although never competed, has used and still uses several of my supplements, including MVM, LipoFlush, TestoBoost, GHboost, and Joint Support.
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51. 

Hi Dr Dipasquale, hope your well!

Following on from Carl's announcement on Super Human Radio (SHR) that your taking questions through your e-mail for the SHR show, I would like to ask the following in the hopes that you can clear up a massive source of confusion and frustration I've been feeling regarding post workout (pwo) nutrition:

I've read your article pwo carbs may be counterproductive and listened to several podcasts where you elucidate the same, no problem there and makes a lot of sense and something I've stuck to religiously since starting the Anabolic Diet for powerlifters - Oct'08 - abstain from carbs and keep protein/amino acids and fat high pwo! I’ve seen and heard the Anabolic Diet (the updated version in your Anabolic Solution for Powerlifters) and pwo nutrition etc discussed on several forums and shows and they mainly discuss the role of insulin and they go on to say that it's high insulin levels that should be avoided pwo as well as carbs.

 

Now, the AS booksuggests Power Drink during the workout and Amino immediately pwo. I thought that the whey and amino acids in Power Drink have the ability to spike Insulin pretty darn good and rapid, I'm not sure whether it's of the same magnitude as carbs but I think it might be pretty significant. Therefore, is it glycogen supercompensation in muscle cells and it's detrimental effects on insulin sensitivity (IS) that should be avoided pwo or is it high insulin levels in general that should be avoided; as a result of what I have heard I now see this as carbs=increase in insulin=decrease in IS=bad & Whey/Aminos=increase in insulin=would you get the same decrease in IS as a result just as you would with carbs?

 

I'm slightly worried that I may be short changing the anabolic effects even thoughI'm using your supplements and trying to get better results from training by taking them as you suggest during and after training which provides me with the essential amino acids, and especially the BCAA and Glutamine. But I am worried that I’m stimulating too much insulin and that it will stop me from maintaining prolonged increases in protein synthesis even though I’m sticking to your regimen – and as per your regimen I’m following up an hour later with your MRP LoCarb, which I mix with some raw eggs and a few tablespoons of flax seed and olive oil in order to give me some added protein and fat.

 

Also, you mention several times on podcasts and in some articles off your MetabolicDiet.com site, that whey is not a good source of protein due to it's rapid oxidation/gluconeogenesis rate and suggest if you were to take in powder to take a casein product yet your Power Drink contain whey, mostly as a pure whey isolate. Also your MRP contains both whey and casein, rather than just casein alone, and you've mentioned in one of your books that the absorption rates of different proteins are not affected when taken together. At which point does it become deleterious to use whey, it can't be all bad as it's formulated into your products or should Whey now be avoided indefinately?

Thank you for your time, take care and I look forward to looking over your new master site and also looking forward to when it goes live.

 

There’s a difference between using Power Drink while training compared to using it post workout. First, Power Drink contains much more than just whey protein as you can see by going to http://www.mauromd.com/store/product_info.php?cPath=29_34&products_id=87, and the article at http://www.mauromd.com/det-articles-23-What-to-Use-While-You-re-Training.php. Also, follow the links on the former URL to articles about or mentioning Power Drink.

 

Secondly, I formulated the mix of amino acids in Power Drink as supplied by the whole proteins, glutamine peptides, and individual amino acids, to do among other things, decrease overall muscle breakdown while exercising by providing a stimulus to protein synthesis and decreasing protein breakdown, and to increase anapleurosis (provide Kreb’s/TCA Cycle intermediates) while exercising and thus positively also affect energy metabolism. As such, very little of the amino acid and protein mix actually undergoes gluconeogenesis, thus keeping GH and IGF-1 levels higher, fat burning higher, and keeping insulin levels lower and insulin sensitivity higher while you’re training, as against the close to opposite effects of using carbs (with or without protein) while training. This whole process works even better if you’re on my phase shift diets, such as the Anabolic and Metabolic Diets, including my Anabolic Solutions, which combine updated and enhanced info on the Anabolic Diet, synergized with supplements, for both bodybuilders

 

Optimal post training requires a different tact as there is no exertion and recuperation is the key. As far as skeletal muscle, fatty acids are used preferentially to fuel protein synthesis and to replenish skeletal muscle fibers intramuscular triacylglycerol (IMTG) levels. These processes are more efficient if you’re on my phase shift diet. In order to maximize protein synthesis after training it’s important to have a spike of essential, and some non-essential amino acids – the most effective formulation as far as my knowledge and experience is reflected in Amino. Since the processes involved in protein synthesis are paramount after training, very little of the mix of amino acids in Amino is used for gluconeogenesis or for stimulating insulin release, and thus glycogen synthesis is not significantly elevated resulting in no loss in insulin sensitivity, which can last for many hours (as explained in my articles, for example http://www.mauromd.com/det-articles-48-Maximum-Post-Training-Nutriton.php, http://www.mauromd.com/det-articles-27-Post-Exercise-Nutrition-for-Maximizing-the-Anabolic-Effects-of-Exercise.php, and , and under the info on Max-PTN in my store at http://www.mauromd.com/store/product_info.php?cPath=29_34&products_id=70.

 

Although you’re right about keeping insulin levels down it’s more important to maintain insulin sensitivity since even with lower insulin levels you can be relatively insulin resistant – lower levels of insulin plus insulin resistance won’t give you the beneficial effects of insulin on protein synthesis, something you want to maintain for as long as possible after training. Interestingly enough keeping insulin levels low while keeping insulin sensitivity high will result in less glycogen replenishment (as per your question, it is glycogen supercompensation that you’re trying to delay as once that occurs, then insulin sensitivity decreases and the effects of insulin on increasing protein synthesis is pretty well done) over a certain period of time and paradoxically an increase in fatty acid metabolism.

 

I’ve nothing against whey protein except that it shouldn’t be used before and after training in any significant amounts since excess whey is easily converted to glucose and can be counter productive both before and after training. My MRP LoCarb does contain whey as well as casein and the whey portion acts as an amino acid spike at first, increasing protein synthesis at a time when the amino acid wave from Amino has lessened, with the casein kicking in later on with a lower but sustained increase in amino acids. Most of the amino acids in Amino and MRP LoCarb go toward protein synthesis rather than to glucose via gluconeogenesis or ketones, as is the case with some of the amino acids. The bottom line is that following the advice about no carbs after working out, and using Max-PTN as your post workout nutrition, you prolong the beneficial effects of exercise on protein synthesis and burning off body fat with the end result being more of an improvement in muscle mass and body composition.

 

Mixing in some whole eggs and the flax and olive oil is something that I do as well, but may not be to everyone’s taste. Back in my competitive days I’d make up post exercise shakes that would test anyone’s mettle – I never had to worry that my shakes would disappear from the fridge as few people could stomach them. The MRP LoCarb, while not one of those phony “tasty” shakes that comes in all kinds of frutti tutti flavors, is not bad tasting on its own and way superior to the ones I used to make for myself. Adding some extra ingredients such as you’re doing never hurts.

 

I’ve done some limited testing on several bodybuilders, powerlifters, and a few Olympic track athletes, including myself, on the effects of my Power Drink and Max-PTN, and the results support all that I’ve said above. So it’s not just theoretical info I’m presenting but some actual real world results. Keep in mind that in order to really prove my theories and the effects of my supplements I’d need a much larger sample size, and an independent researcher or team of researchers to validate the results. And of course, I shouldn’t fund the research or be involved in any way so that the results are not biased. That may or may not happen and is beyond my control. Until then I can use the results on present and future studies to provide some evidence based information that backs up what I’m saying.

 

I’m planning to do an article in the very near future that will provide you with a lot more details on the above info and theories, with references to the existing literature where relevant. I’ll also be doing other articles on the best approach to diet and supplements before training. For example, for various reasons which I’ll explain in detail in one of the articles, my approach has always been not to use any whole macronutrients prior to training, and especially not to take in any carbs, to train with some degree of glycogen depletion, and not to take any whey protein unless you’re actually training, which is why I only recommend Resolve and Amino as pre-training supplements – for more info on both as well as Power Drink, used as a complete before, during and after exercise nutritional supplement combo, go to http://www.mauromd.com/store/product_info.php?cPath=29_34&products_id=44. The use of carbs and/or whey protein prior to exercise decreases growth hormone levels, increases insulin, and decreases the use of fat as the major energy source while exercising.

 

BTW, I’m in the process of working on and finessing my new major site www.MauroMD.com and some of the links I’ve provided may not work in the near future. If that’s the case simply go to the Education section to look up articles, Q&A, and my blogs, and to the store to look up info on the various supplements I’ve mentioned.

 

I hope that this info is of some use to you.

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52. 
I’m a drug tested athlete who has been using your LipoFlush for a few years now. It’s a great product as it not only keeps my body fat levels down without me having to lose muscle mass but also gives me loads of energy for training and has improved my performance. However, recently I was told by my coach that LipoFlush contains a substance that is banned by WADA/IOC and will cause a positive drug test. That substance is citrus aurantium. I was at a loss at how to respond as I’ve been tested several times while on LipoFlush and never tested positive. On the other hand even though I’ve never tested positive I need some assurance that I won’t test positive in future drug tests.
 
Let me reassure you that you won’t test positive taking LipoFlush even though it does contain citrus aurantium. Your coach isn’t all wrong but he is wrong about citrus aurantium being banned by WADA and that it causes a positive drug test. As this is an important issue for drug tested athletes I’ll explain in some detail why it’s safe to use LipoFlush and why it won’t cause a WADA/IOC positive drug test. First of all LipoFlush and all my line of nutritional supplements are produced in a lab that is NSF certified, and therefore doesn’t use any ingredients that are banned by WADA. As such, at this time every product in my line of supplements is safe for drug tested athletes to use, even Metabolic, which until I reformulated it contained DHEA, but doesn’t any more. Having said that your coach is misinformed in that citrus aurantium per se is not banned by WADA. The three main ingredients in citrus aurantium are N-methyltyramine (tyramine), octopamine and synephrine. Of the three synephrine, which is by far the most dominant alkaloid, is not banned but is monitored in competition only, as is caffeine and some other stimulants. As per WADA – “The following substances included in the 2014 Monitoring Program (bupropion, caffeine, nicotine, phenylephrine, phenylpropanolamine, pipradol, synephrine) are not considered as Prohibited Substances.” For info go to http://www.wada-ama.org/Documents/World_Anti-Doping_Program/WADP-Prohibited-list/2014/WADA-Monitoring-Program-2014-EN.pdf, http://www.wada-ama.org/en/world-anti-doping-program/sports-and-anti-doping-organizations/international-standards/prohibited-list/monitoring-program/ and http://www.wada-ama.org/Documents/World_Anti-Doping_Program/WADP-Prohibited-list/2014/WADA-prohibited-list-2014-EN.pdf. Octopamine is banned by the IOC (only during competitions but not at other times) as a stimulant but only in significant levels in urine. That’s because octopamine is an endogenous substance (naturally found in the body) and is also found in small amounts naturally in certain foods and ingredients including a wide range of natural 'orange based' food products including freshly squeezed orange juice, marmalades, orange squash, etc. as well as citrus aurantium, also called bitter orange, and in other food types including fish sauce and meat products. Citrus aurantium (bitter orange) is a plant derived ingredient that has extremely low levels of octopamine, and even at many times the dosage not enough to trigger an anti-doping violation. Information from the WADA Science Director confirms that people consuming bitter orange even at relatively high levels will not produce urinary octopamine above the reportable level and this is reflected by the doping lab statistics. The bottom line is that the amount of octopamine in one dose of LipoFlush is less than in a serving of freshly squeezed orange juice and cannot result in a positive drug test. FYI I’ve copied abstracts of a few studies below. The first abstract is a study that found that there was no elevation of urinary octopamine with the use of dietary supplements. Octopamine taken as a drug however, did raise urinary levels above the baseline levels that WADA allows in the urine. ------------------------------------------ Biomed Chromatogr. 2012 May;26(5):610-5. doi: 10.1002/bmc.1705. Epub 2011 Sep 19. Analysis of octopamine in human doping control samples. Thevis M1, Koch A, Sigmund G, Thomas A, Schänzer W. Abstract The biogenic amine octopamine [4-(2-amino-1-hydroxyethyl)phenol] is prohibited in sports owing to its stimulating and performance-enhancing properties. Adverse analytical findings in athletes' doping control samples commonly result from surreptitious applications; however, the occurrence of octopamine in nutritional supplements and in selected invertebrates as well as the assumption that its N-methylated analog synephrine [4-(1-hydroxyethyl-2-methylamino)phenol, not banned by anti-doping authorities but currently monitored in prevalence studies) might be converted in-vivo into octopamine have necessitated a study to investigate the elimination of synephrine and octopamine present in over-the-counter products. Urine samples collected after administration of nutritional supplements containing octopamine and/or synephrine as well as urine samples collected after therapeutic application of octopamine- or synephrine-containing drugs were analyzed using a validated solid-phase extraction-based procedure employing a weak cation exchange resin and liquid chromatographic/tandem mass spectrometric detection with electrospray ionization and multiple reaction monitoring. In the case of therapeutic octopamine application, the urinary concentration of the target compound increased from baseline levels below the lower limit of detection to 142 µg/mL, while urine samples collected after synephrine as well as dietary supplement administration did not yield any evidence for elevated renal excretion of octopamine. ---------------------------------- J Sep Sci. 2011 May 9. doi: 10.1002/jssc.201100186. [Epub ahead of print] Separation of adrenergic amines in Citrus aurantium L. var. amara by capillary electrochromatography using a novel monolithic stationary phase. Chizzali E1, Nischang I, Ganzera M. Abstract This manuscript reports on the use of capillary electrochromatography for the determination of tyramine, (±) synephrine, and (±) octopamine, the major alkaloids in bitter orange peel. A novel methacrylate-based monolithic stationary phase was prepared by UV-photopolymerization in 100?µm id fused-silica capillaries. It facilitated the quantitative assessment of alkaloids with a mobile phase comprising aqueous 10?mM ammonium acetate in ACN and isopropanol. Applied voltage and temperature were 25?kV and 25°C, and samples were injected in electrokinetic mode. The method reported herein revealed adequate sensitivity (LOD =0.6?µg/mL), repeatability (s(rel) =4.1%), accuracy (recovery rates between 95.2 and 102.2%), and precision (intra-day variation =5.7%, inter-day variation =4.1%). The application of the CEC assay on C. aurantium var. amara plant material and dietary supplements, which usually are advertised for slimming properties, indicated that synephrine (0.17-0.82%) is the dominant alkaloid.
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