Here's what I wrote in MD magazine in response to BROSER's first Anti-Keto Diet article...the same article that Blechman said was his best work to date!
QUESTION:
In the December issue of MD, Eric Broser wrote an article that listed 7 reasons why a zero carbohydrate diet is bad for bodybuilders. In it, he claimed that low carb diets result in no insulin production, high cortisol, low thyroid, low GH, low IGF-1, a compromised immune system, and impaired gene expression for muscle hypertrophy. What’s the deal with these claims?
ANSWER:
I really don’t want this to turn into a bash Eric Broser response because I really like the guy and respect what he’s doing in the industry. However, when people make bold statements like this, I feel they must be held accountable for what they say. Let’s start by addressing the statement, “Without any carbs there will be no insulin!” Eric then goes on to explain that without insulin secretion pre- and post-workout, you won’t transport vital nutrients into muscle cells. Anyone who knows anything about biochemistry will realize this statement is completely ludicrous since glucose is constantly being made in the liver via gluocneogenesis (Remember, 80% of the glucose you use during weight training comes from amino acids). In order to shuttle this glucose into the working muscle cells, insulin in required. Likewise, it's important to understand that in a low insulin environment, GH and IGF-1 levels are elevated. IGF-1 can do everything insulin can do (except store fat); and it does it better!
With regard to the statement that low insulin leads to increased cortisol, I have to remind Mr. Broser that when consuminga high protein/moderate fat/low carb ketogenic diet, cortisol levels will be low (not high) because the brain is feeding on fats. Contrary to what he’s thinking, cortisol levels are much more elevated when on a high protein/moderate carb/low fat because the brain is constantly looking for glucose to feed itself. When blood glucose dips (especially in-between meals), cortisol (a stress hormone) is released and it helps to raise blood sugar by telling the liver to turn amino acids (possibly coming from muscle) into glucose.
Given the fact that we now know that cortisol levels are low when following a high protein/moderate fat/low carb ketogenic diet, Brosers’ statement, “With more cortisol there will be decreased thyroid function” becomes much more relevant to his high protein/moderate carb/low fat diet. However, what he may have meant to say was thatlow insulin levels can decrease T4 (inactive thyroid hormone) to T3 (active thyroid hormone) thus reducing the output of functional thyroid hormone. This is certainly true and it’s why I recommend a weekly insulin-spiking cheat meal once a week!
When addressing Broser’s statement that attempts to correlate elevated cortisol with low levels of GH and IGF-1, I have to, once again, remind him that cortisol will be much higher on a diet where the brain is dependent on glucose (i.e. his high protein/moderate fat/low carb diet). While on high protein/moderate fat/low carb ketogenic diets, insulin levels are low, GH levels are high, and IGF-1 levels are also elevated.
Will the exclusion of carbs pre- and post-workout result in a suppressed immune system? No way! Remember, immune cells are made from protein and fat; therefore, it's insane to think that no pre- or post-workout carbs would have any effect, whatsoever. More likely, the immune system will suffer on a diet that is deficient in essential fatty acids. When Dr Scott Connelly was doing his initial research on burn patients, he found that diets as high as 10,000 calories of carbs per day wouldn't stop patients from withering away and dying of wasting and immune system failure. However, when amino acids and essential fats where added to the IV bags (at a mere 3000 calories) the patients began gaining weight and resisting infection.
Finally, I’d love for Broser to show me one stitch of research that demonstrates that bodybuilders, who follow a high protein/moderate fat/low carb ketogenic diet, have compromised muscle hypertrophy genes. That’s one study I’d like to read. The problem is that it doesn’t exist.