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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