A few forum members have pointed out that very low carbohydrate diets cause an elevation in reverse T3 (inactive T3 thyroid hormone). Apparently this is the reason everyone MUST EAT 50 grams of carbohydrates a day.

I will state here, I am not an expert and I don't pretend to be. My point of interest is that zero-carbers have a high success rate. The proclaimed crashing of the metabolism due to elevated rT3 does not jive with the real life results. I also reject the idea that low-carbers need to take thyroid pharmaceuticals to be healthy.

Here is a snippet of the study that's being tossed around.

Starvation has a profound effect on thyroid function, causing a decrease in serumT3 concentration and a reciprocal increase in rT3 level. These changes are due to aselective inhibition of the 5’-monodeiodination of iodothyronines by peripheral tis-sues. Reduction in carbohydrate intake rather than total calorie deprivation appearsto be the determinant factor. These alterations in thyroid function are believed to re-duce the catabolic activity of the organism and thus to conserve energy in the faceof decreased calorie intake. Chronic malnutrition is accompanied by similar changes.Overfeeding has opposite although transient effects.

But wait, there's more.

To evaluate the effect of caloric restriction and dietary composition on circulating T3 and rT3 obese subjects were studied after 7-18 days of total fasting and while on randomized hypocaloric diets (800 kcal) in which carbohydrate content was varied to provide from 0 to 100% calories. As anticipated, total fasting resulted in a 53% reduction in serum T3 in association with reciprocal 58% increase in rT3. Subjects receiving the no-carbohydrate hypocaloric diets for two weeks demonstrated a similar 47% decline in serum T3 but there was no significant change in rT3 with time. In contrast, the same subjects receiving isocaloric diets containing at least 50 g of carbohydrate showed no significant changes in either T3 or rT3 concentration. The decline in serum T3 during the no-carbohydrate diet correlated significantly with blood glucose and ketones but there was no correlation with insulin or glucagon. We conclude that dietary carbohydrate is an important regulatory factor in T3 production in man. In contrast, rT3 concentration is not significantly affected by changes in dietary carbohydrate. Our data suggest that the rise in serum rT3 during starvation may be related to more severe caloric restriction than that caused by the 800 kcal diet.

What we have here is two seemingly good studies, in complete opposition of each other. The later was specifically conducted with individuals eating a zero carb diet.

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My renewed interest in caloric consumption started with my review of my first year on the all carnivorous diet. I gained about ~15 lbs, by not counting calories and stuffing myself at each meal (when I started, I ate 2-3 meals). It's unclear to me whether this weight was put on because I was eating too much protein, too much fat, too much food (too many calories) or or even too many meals (fasting has a fat burning hormonal effect).

There are so many different schools of thought on caloric consumption (sometimes called "volume", other times called "too much fat") that entertaining the idea enters the mind into a world of cerebral gymnastics. Now, I want to be very clear that I believe that hormones are driving fat accumulation, not the quantity of calories, but the question I'm interested in is:

When insulin levels are low, what is responsible if fat is still not being mobilized?

Who is to blame here? Is it volume (calories), meal timing, or a macro nutrient? And if it's a macro nutrient, which one?

We learned from GCBC that whatever makes you fat also makes you sick. This conversation is extremely relevant to obtaining optimal health. Here are some accepted theories as well as points of contention when it comes to what the body does with specific macro nutrients.

• Carbohydrates are converted into glucose and raise blood sugar potentiating the release of  insulin.
• Protein is converted into amino acids. When there is a long term deficit of glucose, gluconeogenesis is initiated, which is the manufacturing of glucose from amino acids. Short term deficits of glucose are covered by dipping into your bodies store of glycogen (stored glucose) in your liver, not by breaking down proteins. (thanks to Dr. Kurt Harris of The PaNu Weblog - read the comments for more info). The second school of thought on the protein to glucose issue is brought to us by my good friend Lex Rooker. Evidenced by his meticulous BG tracking in his wildly popular journal, Lex's data showed a different story on the conversion of protein to glucose. Lex's self experimentation indicated that glucose rises higher after eating a meal containing more protein than when eating a meal containing less protein. This rise in BG happens even when blood glucose before the meal is already at 100 mg/dl. This would suggest that at least some protein is converted to glucose independent of blood glucose levels, glycogen stores, or a "metabolic emergency". For all the details, make sure to stop by the raw paleo forum and give his incredible journal a read.
• Fat does not have a noticeable effect on insulin. Fat can be stored independently of insulin by the enzyme Acylation Stimulating Protein (ASL) - which is influenced by insulin. A very small amount of fat is converted into glucose, but is done so inefficiently by the liver. 

Let's look at some of the greats in the low carb universe and see what they think about calories (and for some, meal timing). I took all of their quotes completely out of context, mostly from message boards, so if they seem a little out of place, they are. I tried my best to represent each all-star's view accordingly. Here they are in no particular order:

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Updated on Thursday, August 27, 2009 at 2:18AM by Danny Roddy

I was shocked at the popularity of my post chronicling my first year on the all carnivorous diet. In this post I make some wild, embarrassing claims such as; too much fat made me fat, and even worse that I was experiencing a protein deficiency. I ask my dear reader to forgive me for these junior high errors. I promise in the future I will not jump to such conclusions. In reality, as we learned from Good Calories, Bad Calories, hormones are to blame, which brings us to the the point of this post.

Recently I had the pleasure of meeting up with my 5 year carnivore friend Lex Rooker. We sat down and Lex instantly started to shift my paradigm with his new found knowledge. Here's a link to Lex Rooker's famous journal, in which Lex explains Peter's (from the popular Hyperlipid blog) theory on weight gain. His post embodies most of what we discussed.

It appears that my conjecture on gaining weight and putting on body fat while on a Zero Carb or Very Low Carb diet is not all there is to the story, and may even be just incidental in the whole weight gain issue on a ZC/VLC diet. Most of my ideas have been based on excess glucose created from protein and/or the left over glycerol from fat metabolism. Seems there’s another metabolic pathway at work here. An enzyme called ASP (Acylation Stimulating Protein). This little jewel has the ability to directly store fat in the fat cells completely bypassing the glucose and insulin pathways.

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