Low-carb dieting may be an attractive option if you want to lose weight quickly. However, it’s not all it’s cracked up to be. Before you commit to this type of diet, make sure you are aware of the potential consequences. My last post on The Low-Carb Diet Dilemma noted that one of the many risks of eating a low-carbohydrate diet is hypothyroidism (a.k.a. underactive thyroid). This post will focus specifically on hypothyroidism, its causes, and its effects on the body’s system and functions.
Weight gain is a common symptom of hypothyroidism. So when you adopt a low-carb diet with the goal of losing weight, you may inadvertently bring on a physical state that causes you to do just the opposite.
What Is Hypothyroidism?
Hypothyroidism is a common disorder in which the thyroid gland does not produce enough thyroid hormone. Symptoms include tiredness, constipation, depression, sleep disturbance, and weight gain. There are two major types of this condition. One is primary hypothyroidism, meaning the thyroid itself is impaired in its ability to produce the thyroid hormone. The other is secondary hypothyroidism, meaning peripheral influences of thyroid hormone maintenance are causing a functional deficiency in the hormone.
Interestingly, active thyroid hormone is not primarily produced by the thyroid itself. The liver is actually the primary site of the total conversion of the inactive form (which makes up the majority of hormone released by the thyroid gland). It is also the case that active thyroid hormone is required for the very processes which create the liver’s glycogen release, and that stored glycogen is a major proponent of thyroid conversion (the process in which the inactive form of the thyroid hormone is converted to the active form). The richer your glycogen stores, the higher the rate of thyroid conversion in your liver. Hormones released in a healthy, glycogen-efficient state also increase thyroid reception in the brain. This increased manufacturing of active thyroid in the brain then signals the thyroid gland to start producing less of the hormone.
How Does a Low-Carb Diet Lead to Hypothyroidism?
When you switch to a low-carb diet, your metabolic system shifts and begins using free fatty acids as a primary source of fuel. In the glucose-deficient state brought about by carbohydrate restriction, free fatty acids are brought out of the adipose tissue to reduce glucose dependence, and glycogen is liberated from the liver and used to provide much-needed glucose. This results in a glycogen-deficient state that reduces thyroid conversion, and free fatty acids directly interrupt the thyroid conversion process in the liver. This lowers the level of active thyroid hormone circulating in the blood. And, simultaneously, it causes the pituitary in the brain to begin converting more of the inactive thyroid hormone that the liver has failed to convert. The pituitary cannot provide enough of the active hormone for the body; however, it will provide enough to reduce the thyroid’s production.Thus, the inactive thyroid hormone can remain elevated and being converted at about 20-30% the normal rate. This causes your body to maintain a functional hypothyroid state—in which the common tests will show that your thyroid hormone levels are in the normal range, but your body is still not receiving the hormone it needs to be well. It also means that adding the inactive thyroid hormone via medications like Synthroid (levothyroxin), as commonly prescribed by endocrinologists, will only exacerbate the condition.
What Are the Long-Term Consequences?
It is reasonable to suggest that low-carb dieting will produce the condition of thyroid hormone resistance (a.k.a. hypothyroidism) in as little as a few days to a week, and that extended periods will lead to adaptive changes—making it increasingly more difficult to reintroduce carbs without experiencing a period of glucose intolerance.
The major problem is that a low-carbohydrate diet will never be able to rectify this deranged metabolism. Therefore, you will be forced to maintain strict adherence to the low-carb protocol and condition your lifestyle in a way that slows the inherent degeneration produced by the hypothyroid and hyper-cortisol state. You will likely experience symptoms such as tiredness, constipation, depression, and even rebound weight gain. And you will possibly be at risk for other health conditions, including cognitive decline, type 2 diabetes, abdominal weight gain, obesity, and heart disease.1-5
How Can You Stop the Process and Begin to Heal?
Here are a few quick nutrition tips to help get your metabolism back on track so that you can begin to bring healthy carbs back into your diet:
- Eat fruit with every meal.
- Cook with coconut oil instead of vegetable oil.
- Consume healthy dairy products.
- Limit the amount of polyunsaturated fats (PUFAs) and starches in your diet.
- Eat well-cooked veggies instead of grains, legumes, breads, and pastas until your system has had time to sufficiently heal.
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- Csernansky JG, Dong H, Fagan AM, et al. Plasma cortisol and progression of dementia in subjects with Alzheimer-type dementia. Am J Psychiatry 163, No. 12 (Dec 2006): 2164-2169. http://www.ncbi.nlm.nih.gov/pubmed/17151169
- Siddiqui A, Madhu SV, Sharma SB, Desai NG. Endocrine stress responses and risk of type 2 diabetes mellitus. Stress 13 (Aug 2015): 1-9. http://www.ncbi.nlm.nih.gov/pubmed/26270888
- Wallerius S, Rosmond R, Ljung T, et al. Rise in morning saliva cortisol is associated with abdominal obesity in men: a preliminary report. J Endocrinol Invest 26, No. 7 (Jul 2003): 616-619. http://www.ncbi.nlm.nih.gov/pubmed/14594110
- Westerbacka J, Yki-Järvinen H, Vehkavaara S, et al. Body fat distribution and cortisol metabolism in healthy men: enhanced 5beta-reductase and lower cortisol/cortisone metabolite ratios in men with fatty liver. J Clin Endocrinol Metab 88, No. 10 (Oct 2003): 4924-4931. http://www.ncbi.nlm.nih.gov/pubmed/14557475
- Whitworth JA, Williamson PM, Mangos G, Kelly JJ. Cardiovascular consequences of cortisol excess. Vasc Health Risk Manag 1, No. 4 (Dec 2005): 291-299. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1993964/