Body, Mind, Spirit Magazine

Fasting, Carbohydrate Consumption, and the Thyroid Gland

By Jamie Koonce @charcuterielove

Recently, there has been a debate throughout the blogosphere about the role of carbohydrates in thyroid function.  Bloggers and health practitioners alike claim that low carbohydrate diets cause reduced thyroid function, and there is some reference to “scientific studies” proving this fact.  However, no references to such studies are given.  Because of the rumors that low carb may cause hypothyroidism, some people have started adding potatoes, orange juice, and even rice krispies to their diet in hopes that this will improve their thyroid function and get them over a weight loss plateau.

I’m not trying to say that potatoes, orange juice, and rice krispies are “bad,” and I’m not trying to personally criticize anyone who has blogged about this and claimed that consuming these foods has helped them in some way.  However, I would like to point out that when I went digging for the science behind the claim that low carb causes hypothyroidism, I actually found the opposite.  Low carb may prevent decreased thyroid function during long-term calorie restriction.

Below, you can see what I found.  The bold print is my emphasis, and the red is my own personal remarks.


Healthy, lean people on a nutrient dense, calorie restricted diet show a slight decrease in T3 hormone, but no increase in rT3.  These people were eating 250 grams of carbohydrates per day!  Some studies suggest that a low-carb calorie restricted diet may prevent having reduced T3 hormone. Patients who have chronic systemic inflammation have a reduction in serum T3 levels, and it is suspected that inflammation — rather than a low-carb diet — is to blame for long-term reduction in T3 hormone.

Mean serum T3 concentration was significantly lower in the CR group than the EX or WD groups, whereas serum T4 and FT4, and TSH concentrations were not significantly different among groups (Table 1⇑). Mean serum free T3 concentration (normal range 1.45–3.48 pg/dl) was significantly lower in 10 CR subjects who had the lowest serum total T3 concentrations than in 10 age- and sex-matched sedentary WD subjects (1.08 ± 0.46 vs. 1.68 ± 0.72 pg/ml; P = 0.04). However, serum rT3 concentration (normal range 19–46 ng/dl) in 10 CR subjects who had the lowest serum total T3 concentrations was normal and not significantly different from 10 age- and sex-matched sedentary WD subjects (26 ± 11 vs. 19 ± 4 ng/dl, respectively).

Data from a series of studies have shown that short-term (2 wk to 6 months) fasting or severe CR decreases serum T3 and transiently increases serum rT3 concentrations in obese subjects who are actively losing weight (9). Similar findings have been reported in a study of eight nonobese individuals who unintentionally underwent moderate CR and intense physical labor (70–80 h/wk) for 21 months (3). In addition, the results from some studies (9, 10, 11) suggest that a low-carbohydrate intake (50–120 g/d) can prevent the fall in serum T3 and particularly the rise in serum rT3 concentration induced by CR. Carbohydrate intake in our CR subjects was approximately 250 g/d, which may have contributed to their normal serum rT3concentrations. Therefore, our findings provide evidence that long-term CR in sedentary lean, weight-stable subjects causes similar but persistent changes in thyroid hormones as previously reported during short-term fasting or CR in obese subjects who were continuing to experience active diet-induced weight loss.

Patients who have the sick euthyroid syndrome also have low serum T3 concentrations (12). However, these patients have systemic nonthyroidal illnesses, such as cancer, myocardial infarction, severe infections, and major injuries (6, 12). Therefore, it is likely that inflammation, rather than decreased calorie intake, is responsible for the reduction in serum T3 concentrations in patients with sick euthyroid syndrome (13). In fact, infusion of proinflammatory cytokines in human subjects decreases serum T3 concentration (14, 15). Moreover, the decline in serum T3 concentration induced by illness is blunted in IL-6 knockout mice, which supports the notion that cytokines are involved in the pathogenesis of the sick euthyroid syndrome (16). The mechanism responsible for this response is probably related to a cytokine-induced reduction in type I iodothyronine-5′-monodeiodinase expression, which results in decreased conversion of T4 to T3 in extrathyroidal tissues and decreased serum T3 concentrations (6, 13, 14, 15, 16). In contrast, low serum T3 concentration was not associated with an increase in inflammatory cytokines in our CR subjects. In fact, markers of systemic inflammation, serum CRP and TNFα concentrations, were low in our CR subjects. These findings are consistent with data from CR studies conducted in rodents and monkeys, which showed that CR caused a marked decrease in markers of inflammation and a reduction in serum T3 concentration (7, 8, 17, 18). The combination of decreased serum T3 and reduced systemic inflammation could alter the aging process by reducing metabolic rate, oxidative stress, and systemic inflammation (1, 19, 20).


In this study, the low carb participants lost significantly more weight than the high carb participants even though all particiants were consuming a 1,000 calorie diet.  Serum T3 decreased more in the low carb group than in the high carb group, but the low carb group still lost the most weight.  Serum T3 and serum rT3 also returned to baseline following one week of the diet.

Twelve obese women were studied to determine the effects of the combination of an aerobic exercise program with either a high carbohydrate (HC) very-low-caloric diet (VLCD) or a low carbohydrate (LC) VLCD diet on resting metabolic rate (RMR), serum thyroxine (T4), 3,5,3′-triiodothyronine (T3), and 3,5,3′-triiodothyronine (rT3). The response of these parameters was also examined when subjects switched from the VLCD to a mixed hypocaloric diet. Following a maintenance period, subjects consumed one of the two VLCDs for 28 days. In addition, all subjects participated in thrice weekly submaximal exercise sessions at 60% of maximal aerobic capacity. Following VLCD treatments, participants consumed a 1,000 kcal mixed diet while continuing the exercise program for one week. Measurements of RMR, T4, T3, and rT3 were made weekly. Weight decreased significantly more for LC than HC. Serum T4 was not significantly affected during the VLCD. Although serum T3 decreased during the VLCD for both groups, the decrease occurred faster and to a greater magnitude in LC (34.6% mean decrease) than HC (17.9% mean decrease). Serum rT3 increased similarly for each treatment by the first week of the VLCD. Serum T3 and rT3 of both groups returned to baseline concentrations following one week of the 1,000 kcal diet. Both groups exhibited similar progressive decreases in RMR during treatment (12.4% for LC and 20.8% for HC), but values were not significantly lower than baseline until week 3 of the VLCD. Thus, although dietary carbohydrate content had an influence on the magnitude of fall in serum T3, RMR declined similarly for both dietary treatments.


In this study, the subjects consumed only 800 calories per day during the non-fasting period of the study.  Those consuming ZERO carbohydrates did show a decline in T3 hormone, but no increase in rT3.  Those consuming 50 grams of carbohydrates per day did not show a decline in T3 or increase in rT3.

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 a 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. 

I think the main thing that people want to know is if a low carb diet will cause thyroid problems for them, and if adding carbohydrates to a low carb diet will assist in weight loss.  Based on the studies and based on what I have seen clinically, a zero carb diet may be problematic for many reasons besides just a decrease in thyroid hormone.  A low carb diet containing at least 50 grams of carbs per day might reduce serum T3 for about a week, but over the long-term it will probably not affect T3 or rT3 to the point of hindering weight loss or sense of well-being.  If a person does experience a reduction in T3 and a rise in rT3 while consuming a low carb diet, it would be a good idea to investigate whether it is chronic inflammation — rather than the diet — that is causing the altered thyroid hormones. 

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