Thyroid hormones have an important role in regulating metabolic rate. When some people adopt a low-carbohydrate lifestyle, their thyroid hormone levels may change. Several factors may contribute to the thyroid response.
Firstly,eating fewer calories than you expend, causing weight loss, prompts the body to reduce thyroid function to slow its metabolism. That’s because the body interprets any form of energy restriction from any cause as a sign of famine, leading it to reduce metabolism by 5-15% to conserve energy stores.
Secondly,even when energy is not restricted, a ketogenic diet seems to result in improved thyroid hormone sensitivity (i.e., it takes less hormone to produce the same effect), and puts less of a burden on thyroid hormone (T4) production in the thyroid gland and its conversion to T3 in the liver.
It has been repeatedly demonstrated that a well-formulated ketogenic diet (WFKD) improves insulin sensitivity, often dramatically so in people with insulin resistance or type 2 diabetes. There is also strong evidence that the brain’s sensitivity to the satiety hormone leptin is improved during nutritional ketosis as well. Thus an improved thyroid hormone response during a low-carb, high-fat eating diet would be quite consistent with these other documented improvements in hormone sensitivity.
How many published studies from well designed, prospective human trials have shown that impaired thyroid function (i.e., hypothyroidism) occurs on a ketogenic diet? The answer to this question is quick and simple – NONE!
It is common to find recommendations on the internet for daily carb intakes at or above 100 grams per day to maintain “normal thyroid function.” But here’s the key question: are these higher thyroid hormone levels really normal, or is this a relatively hyperthyroid state (compared to nutritional ketosis) driven by excess dietary carbohydrates?What if the lower T3 levels associated with a WFKD are indicative of optimum T3 sensitivity and thus the true physiologic norm for humans?
The other proposed “cure” for this “problem” is to intermittently eat lots of carbs. What sense does it make to be jerking the body back to deal with the disposal of high carbohydrate loads? Given that blood beta-hydroxybutyrate levels characteristic of nutritional ketosis reduce oxidative stress and inflammation, why would you want to shut down this beneficial effect even part of the time?
If carbohydrate-restricted diets were having a negative effect on thyroid function, it would be predicted that a disproportionate number of people would develop clinically obvious cases of thyroid failure (hypothyroidism) while following a ketogenic diet.Let’s look and see how many new cases of low-carb-induced hypothyroidism were reported in a number of large randomized studies published in the last decade. Please see the CHART
While these studies were not purposefully designed to look for thyroid dysfunction, overt hypothyroidism is hard to miss. These studies were all run by (or involved monitoring by) top-notch physicians, so a new case of hypothyroidism would definitely have been reported as a “serious adverse event” associated with the LCHF diet. And yet, out of 350 closely monitored patients, there were none!
Studies:Along with his early mentors and collaborators, Dr. Phinney was involved in three studies of ketogenic diets in which they measured one or more parameters of thyroid hormone response. The first study involved six subjects on a very low-calorie ketogenic diet (VLCKD) for six weeks, the second evaluated nine men given a weight-maintenance ketogenic diet for 4 weeks, and the third studied 12 adults given a VLCKD with or without exercise training for 4-5 weeks.
In addition, in 2005 Yancy et al. published a study (Nutr & Metab) of 28 diabetics given a LCHF diet for four months, during which their mean TSH values did not change significantly (1.6 to 1.4 uU/L).
So let’s query these data from three perspectives:
1) failure of the thyroid to make enough T4,
2) failure of the liver to turn enough T4 into T3, and
3) markedly improved T3 sensitivity.
Starting with the latest data from Yancy et al. first, if either the thyroid gland or the liver were failing to maintain adequate thyroid hormone effect, TSH should increase. It does not, but this was only measured in one study. Second, if the liver is failing to make enough T3, then TSH and T4 values should rise. In both our 1980 and 1988 reports, T4 went down slightly. And third, in all three studies blood T3 levels went down sharply (from a mean of 151 to 92) but clinical signs and symptoms were not indicative of overt hypothyroidism.
Case in point: Dr. Volek ran some thyroid tests on 14 overweight/obese men whose other results were reported in a 2004 study. Eight of these men consumed a reduced energy ketogenic diet for six weeks and then switched to a low-fat diet for another six weeks. Six other men consumed the low-fat diet first and then switched to a ketogenic diet. Average free T3 concentrations in the 14 individuals were significantly lower after the ketogenic plan than the low-fat diet (3.5 vs 4.2 pmol/L). Regardless of diet order, free T3 concentrations were lower during the ketogenic diet in 13 out of 14 men (see figure). However, despite the lower free T3 levels, the measured resting metabolic rates of these subjects were not different between diets.
And finally, although it was a relatively short 11-day study, Bisschop et al. fed six men weight-maintaining diets containing 85%, 44%, and 2% of energy as carbohydrates. Although TSH and REE did not decline, serum T3 values plummeted, these results again show a disconnect between circulating T3 and REE in the context of a ketogenic diet.
The only viable interpretation of these data is that ketogenic diets markedly increase tissue sensitivity to T3, and thus serum T3 levels decline while the physiological response to T3 remains normal. In this scenario, both the thyroid and the liver have to do far less “work” to maintain a normal thyroid physiologic response. Taking this one step further, why would anyone want to force their thyroid or liver to greater levels of thyroid hormone production by eating lots more carbohydrates? Forcing the pancreas to make more insulin by eating more carbs clearly doesn’t do a lot of good for type 2 diabetics, and we think the same logic applies here for thyroid function.
It’s understandable why some people may be concerned or misled by the changes in thyroid hormones that occur when one adopts a low-carb high-fat lifestyle. Don’t be pressured into eating more carbs than you really need on the mistaken assumption that they are required to maintain normal function of your thyroid gland.
SOURCE: Does Your Thyroid Need Dietary Carbohydrates?by Stephen Phinney, MD, PhD on May 3, 2017
To learn more about Hypothyroidism please read:
- Metabolic Syndrome X and Hypothyroidismhttps://2healthyhabits.wordpress.com/2018/03/09/metabolic-syndrome-x-and-hypothyroidism/
- The Ketogenic Diet for Healthhttp://www.ketotic.org/2014/12/the-effect-of-ketogenic-diets-on.html
Conclusion: There is no evidence that we are aware of indicating that ketogenic diets cause hypothyroid, or negatively impact thyroid function. The fact that T₃is lower in ketogenic dieters is probably part of the mechanism that protects lean mass when fat is being lost. Moreover, low T₃may possibly even be an indicator of a life extending effect, an effect we have suggested elsewhere when examining the cortisol profile of ketogenic dieters.
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