Perhaps not ever but this is a very good peice. I think all should read this as it obliterates such myths and theories as the "Don't mix carbs with fat" etc......

Ladies and Gentlement these guys are some of the brightess nutritional minds out there, period.....read on............


Bodybuilder Nutrition Roundtable
By Josh Beaty

The following interview was conducted by Josh Beaty with Layne Norton, Jamie Hale, Alan Aragon and Will Brink. Sit back and enjoy a very informative discussion.

J Beaty: The big focus in hypertrophy research lately has the mtor pathway. What impact does this research have on bodybuilders?

L Norton: The mTOR pathway is a major cellular anabolic pathway that is responsible for much of the anabolic response to nutrient stimulus. In adult subjects, amino acids (specifically leucine) are responsible for triggering mTOR activation. mTOR essentially acts as a 'leucine gage.' If leucine levels increase, mTOR becomes active & activates other components of the protein synthetic pathway because it high leucine levels indicate a fed state and ample amino acids are present
for protein synthesis to occur. If leucine levels drop, mTOR becomes less active as it senses that there are not enough amino acids & energy to continue protein synthesis. mTOR is also sensitive to total energy intake and if total energy drops too low, then mTOR becomes less activated. This research indicates what many bodybuilders have known for sometime: if you're goal is to build muscle mass, make sure you provide a diet with ample calories and ample amino acids.

W Brink: I'm not going to have a great response to this question as it's really not my area of focus or expertise. As far as I know, there is no practical application of the mTOR pathway to athletes at this time. That is to say, I don't know of any particular change an athlete can make to their approach that will profoundly alter this pathway to give any advantages. It may also simply be that the approach we know is optimal for strength and or LBM - loading, volume, tempos, etc - are already the best we can do as far influencing mTOR is concerned. Like so many areas of research that may have applications to wasting diseases and such, such as myostatin, it's more of an intellectual exercise versus having any real practical application to athletes at this time, non pharmacologically speaking at least. There is no doubt that the intensive research going on that examines the signaling events that are activated by aerobics or resistance training will explain how muscle adaptations take place, and pharmaceutical interventions are a focus of many researchers, but I am unaware of any direct application an athlete can incorporate in their training or diet that will be an improvement on what we already know. The other guests on this roundtable may be more up to date on the literature and have a better answer! I'm a bit jaded at this point in that I don't get particularly excited or interested in the latest holy grail of signaling molecules until some real practical application shows itself.

J Hale: The mammalian target of rapamycin (mTOR) is a serine/threonine kinase that plays a key role in anabolism. MTOR stimulates cell growth by phosphorylating p70 ribosomal S6 kinase (S6K) and eukaryote initiation factor 4E-binding protein 1 (4EBP1). mTor is stimulated by resistance training, insulin and Leucine (bcaa). When mentioning mtor pathway it is probably necessary to mention there are also other kinases that inhibit anabolism when activated. In particularly I am referring to the Ampk/ Akt mtor switch. Basically when Ampk is elevated protein synthesis is inhibited. Ampk (5 Amp-activated protein kinase) is a heterotimeric serine/ threonine kinase. Ampk is often referred to as a cellular fuel gauge. Ampk is activated by endurance exercise, elevated levels of cellular AMP, hypoxia, glucose deprivation and ischemia. When Ampk is elevated cellular fuel regenaration is top priority, while pathways the consume energy are inhibited (ex: protein synthesis). This applies to athletes as we know various conditions stimulate these pathways. By optimizing stimulation of anabolic pathways and minimizing catabolic pathways (intensity and duration of) we obviously optimize performance and physique benefits. Does t his really tell us any more than we already knew (proper resistance, protein intake and sufficient cals maximize growth)? For myself and other practical scientists I feel like this info is very helpful with enhancing our knowledge of what’s going on at a cellular level. It also helps with program design and recognizing at a molecular level factors that affect anabolic and catabolic pathways. As far as the typical bodybuilder or trainee is concerned knowledge of mtor pathway may or may not be beneficial. Depends on bodybuilder and how serious he is about furthering his knowledge concerning physique and performance.

A little off the subject alcohol intoxication has also been shown inhibit mtor pathway. Studies involving mtor pathway also are important in treating muscle wasting disease.

A Aragon: First off, I’d like to thank Jamie for inviting me to this roundtable. It’s definitely an honor to be among a carefully chosen few. If I come off too long-winded in this, it’s because I made Jamie wait for months for me to participate, so I figured I might as well show some gratitude and babble for aeons

Ah, the good ol’ phosphatidylinositol 3-kinase-mammalian target rapamycin signaling pathway. There, that should take care of any lack of technical jargon I contribute to this roundtable right off the bat. mTOR research is not likely to have a significant impact on the furthering of what bodybuilders can physically achieve, but it certainly is giving us some understanding of how these achievements occur. Let’s face it, the majority of the biggest, most ripped guys on the planet haven’t even heard of mTOR.

The first thing most folks think about in relation to mTOR and bodybuilding is leucine, and rightly so, since leucine phosphorylates/activates the downstream metabolites of mTOR. But alas, there’s a caveat. A lot of folks who place an excessive focus on leucine will indiscriminately dose the hell up on it. They’ll tank down isolated leucine, BCAA, and/or whey, thinking they’ve found the ticket to net anabolism. There’s also this false implication that whey, being higher in leucine than casein, is superior. Not true, at least according to the current body of research, which indicates that casein, or at the very least, a blend of casein & whey, is superior to whey alone for affecting a number of parameters bodybuilders care about.

What people seem to constantly forget is that net gains in muscle are the result of not just protein synthesis, but the inhibition of protein breakdown. Casein’s antiproteolytic effect is more profound than whey or leucine’s protein-synthetic effect. Hence its lead spot in the current body of research. The name of the game seems to revolve back to the old cliché of mixing things up, and achieving a variety of sources of protein from whey to casein, to flesh, to the range of sea & land flesh, to Asian women. Just kidding, I wanted to make sure everyone was awake. In sum, mTOR activation is just a piece of the puzzle. Thus, the beloved leucine is a mere cog in the complex engine of variables that cause net gains in muscle.

J Beaty: What are your thoughts on the reemergence of the macronutrient food combining theory where carbs shouldn't be mixed with protein/fat meals and fat shouldn't be mixed with protein/carb meals?

L Norton: This is a rather simplistic way of looking at nutrition and focuses mainly on insulin rather than looking at the whole picture. While it probably isn't
a good idea to have a really high carb meal with a really high fat meal, there's nothing wrong with having moderate amounts of both.

W Brink: like many theories, it comes around every few years or decades and gets people all worked up over their food. Problem is, it's no more true today then it was when the book Fit for Life by Harvey and Marilyn Diamond came out. The theory had no scientific support then and it has none now. Humans have been combining fats, carbs, and proteins quite successfully for eons and as omnivores, are perfectly capable of digesting mixed meals.

J Hale: You are probably referring to the theory that assumes insulin and blood levels of fat should never be raised at the same time. This theory assumes that insulin is the key contributor to obesity. There are a few things wrong with this line of thought. One of the key problems is not recognizing something called Acylation Stimulating Protein. Acylation stimulating protein (ASP) is a hormone produced by adipocytes and is of importance for the storage of energy as fat. The consumption of dietary fat alone can increase fat storage. Dietary fat affects fat cell metabolism with NO INCREASE in insulin. Some studies have indicated dietary fat loading found a decrease in HSL (hormone sensitive lipase) and an activation of fat storage despite no increase in insulin. The key reason was activation of acylation stimulating protein (ASP) which is activated by the presence of chylomicrons (basically packaged triglycerides that are found in the bloodstream after the meal). ASP increases glucose uptake into the fat cell, increases insulin release from the pancreas and has been described as 'the most potent stimulator of triglyceride storage' in the fat cells by numerous scientists. Another problem with this line of thought is some proteins causes substantial elevations in insulin. Minimal levels of insulin affect fat cell metabolism. Basal levels can decrease lipolysis by 50%. Another consideration is most bbers are eating every 2-3 hrs so nutrients are still absorbing from previous meals; therefore previous meals interact with the blood levels of nutrients of the present meal.

A study conducted by Golay and colleagues compared a diet with equal macronutrient content and substrate percentages; that differed only in how the substrates were consumed (mixed diet vs. food combining). The results were no difference in weight loss. Here are the exact results reported by the researchers.
“Results: There was no significant difference in the amount of weight loss in response to dissociated (6.2 +/- 0.6 kg) or balanced (7.5 +/- 0.4 kg) diets. Furthermore, significant decreases in total body fat and waist-to-hip circumference ratio were seen in both groups, and the magnitude of the changes did not vary as a function of the diet composition. Fasting plasma glucose, insulin, total cholesterol and triacylglycerol concentrations decreased significantly and similarly in patients receiving both diets. Both systolic and diastolic blood pressure values decreased significantly in patients eating balanced diets. The results of this study show that both diets achieved similar weight loss. Total fat weight loss was higher in balanced diets, although differences did not reach statistical significance. Total lean body mass was identically spared in both groups. CONCLUSION: In summary at identical energy intake and similar substrate composition, the dissociated (or 'food combining') diet did not bring any additional loss in weight and body fat”. Actually looks like a slight increase in fat loss with mixed diet (balanced diet).

We have tons of anecdotal evidence that denies the need for food combining. We have evolved on a mixed diet. With all of that said food combining may be beneficial regarding calorie control. Once you eliminate an entire macronutrient from a meal this can go a long way in decreasing total caloric intake. If this is what you need to do to control energy intake feel free to do so.

A Aragon: I think that the “P+C & P+F = okay but avoid C+F” principle is idiotic when applied across the board without any contingencies or attention to individual situations. For example, is someone is low-carbing for whatever reason you choose (pathological carbophobia included), they might be done with their carb intake by early afternoon, and their meal construction for the rest of the day is gonna be primarily P+F by sheer default. In the latter scenario, I can see the principle being legit.

However, when issued blanketly, it’s usually based upon the wacky idea that you don’t want fat floating around systemically when your insulin levels are high, because this will magically shift your net adipose balance in the positive. That’s false for a number of reasons. First of all, the insulin response generated by CHO + fat generally depends upon the degree of the fat’s saturation. Unsaturated fats tend to either lower insulin response of the coingested carbs, or not affect insulin response at all. Coingested sat fat, on the other hand, tends to raise insulin response, and can do so in a synergistic fashion. But then the question becomes, so what? Others have mentioned the more direct role ASP has in TG synthesis, and indeed, insulin is more of a multi-tasking anabolic/anticatabolic agent in comparison to ASP, which seems to exist solely to pump up the adipocytes. And of course the kicker is that ASP can do its TG-synthesizing magic in the sheer absence of insulin.

And then there’s energy balance… In a negative energy balance, insulinogenesis is wonderful thing, as long as the training stimulus & nutrition is there to work in concert with it to preserve LBM. In the condition of a positive energy balance, trainees in general are gonna have a lot more carbs to throw around, so this makes the whole separation thing even more dicey. Which meals should be carb-free or fat-free in order to pull of this magic separation tactic, and why? The logical answers to this question simply don’t exist. If you were to actually adhere to the mechanics of separation, you’d actually be hard-pressed to maintain a stable insulin profile – which is ironic, since the control of insulin is what “separatists” are aiming for. Regardless of all the previous points, the fundamental shortsight is that digestion/absorption of meals overlap each other when meal frequency is as high as it should be. Therefore, attempting strict separation of the macros = kidding yourself. Not to mention, most foods in nature are a combo of all the macros to begin with.