So, what is the connection between thyroid dysfunction and metabolic syndrome? The thyroid topic is personal to me due to my challenging journey of living without a thyroid gland from a thyroid cancer history. Thyroid health has been a passion of mine and a focus in my nutrition practice. The thyroid plays a crucial role in a person’s vitality, and I consider it “The Fountain of Youth”. The complete thyroidectomy left me fully dependent on thyroid medications. Two years back, I personally experienced the impact of thyroid hormone (TH) deficiencies on my glucose and lipid metabolism when the medication wasn’t working for me, with its aftermath still lingering to this day.
It is now loud and clear to me that there is a strong association between thyroid function and all the major metabolic pathways. The wide effects of THs on metabolism are exerted mainly by stimulating catabolic and anabolic reactions and by regulating the turnover of fats, carbohydrates, and proteins [1,5]. At a high level looking at these intricate processes, hyperthyroidism promotes a faster-metabolic state characterized by increased resting energy expenditure, reduced cholesterol levels, increased lipolysis, and gluconeogenesis, whereas hypothyroidism induces a slower-metabolic state characterized by all the opposite effects [6].
THs and Carbohydrate Metabolism:
Normal glucose regulation can be disrupted by either an excess or a decreased amount of TH. The studies have shown the dysregulation of carbohydrate metabolism and the derangements in THs are strongly correlated, and an alteration in one can lead to dysregulation in the other. The severity of the metabolic disorder is linearly proportional to the TH derangement, and the effects of the T3 thyroid hormone on glucose metabolism are as substantial as the effects of insulin [2].
So is there any relationship between THs and insulin? The conclusion I obtained from my research is: First, THs can regulate insulin secretion directly and indirectly either by reducing glucose-induced insulin secretion or by reducing beta-cell responsiveness that results from increases in cell mass in hypo- and hyperthyroidism, respectively. Second, both hypo- and hyperthyroidism can induce insulin resistance and dysregulation of carbohydrate metabolism but with different mechanisms. Hypothyroidism induces tissue and cellular level insulin resistance, whereas in hyperthyroidism, this occurs in the liver:
In a hyperthyroid state, glucose depletion often occurs to counteract the loss of energy, and this causes an increase in the demand for insulin in peripheral tissues. This action increases the endogenous glucose production in the liver in the basal state, which leads to the elevated utilization rate resulting in a decreased hepatic insulin sensitivity which then results in glucose intolerance. Hyperthyroidism can also contribute to an increased venous blood flow associated with increased glucose absorption from the GI tract, which leads to hyperglycemia and the subsequent increase in glucose-stimulated insulin secretion [7].
In contrast to hyperthyroidism, hypothyroidism reduces glucose absorption from the GI tract. It is also associated with a reduced level of gluconeogenesis, leading to decreased liver glucose output. However, different studies have shown low production of this has been associated with insulin resistance at the peripheral tissue level. Possible explanations span from the dysregulation of mitochondrial oxidative metabolism to reduced blood flow in muscles and adipose tissues [7]. This slows down the glucose uptake into the cells resulting in excess glucose and insulin circulating in the bloodstream. This was what happened to me two years ago when I was experiencing both hyperglycemia and hyperinsulinemia in a severe hypothyroid state due to the ineffectiveness of the thyroid medication.
THs and Lipid Metabolism:
It’s been well established that thyroid dysfunction has a significant impact on lipids metabolism and cardiovascular risk factors. THs play a great role in regulating lipogenesis, fatty acid β-oxidation, and cholesterol synthesis by stimulating the mobilization and degradation of lipids, as well as hepatic fatty acid synthesis [4,8].
At a deeper level, T3 induces 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase, the first step in cholesterol biosynthesis. T3 also upregulates LDL receptors by controlling the LDL receptor gene activation by T3 directly binding to specific thyroid hormone-responsive elements. Furthermore, T3 controls the sterol regulatory element-binding protein-2 (SREBP-2), which in turn regulates LDL receptor’s gene expression. Lastly, T3 may also protect LDL from oxidation [9].
With the above reasons, hyperthyroidism is associated with acquired hypocholesterolemia and hypobetalipoproteinemia or unexplained improvement of lipid profile in hyperlipidemic patients characterized by a decrease of lipids’ concentration in plasma for triglycerides, phospholipids, and cholesterol. The opposite effects occur in hypothyroidism with increased serum levels of triglycerides and hyperlipidemia as well as non-alcoholic fatty liver disease. These effects progressively increase the risks of cardiovascular disease and potential mortality.
----------------------------
Jenny Noland, MS, CNS, CNGS, CKNS, LDN, MBA
Functional Nutritionist in Eugene, Oregon
Board-Certified Nutrition Specialist
Board-Certified Nutritional Genomics Specialist
Board-Certified Ketogenic Nutrition Specialist
Certified Oncology Nutrition Specialist
Personalized Nutrition Therapy for Metabolic Dysfunction and Cancer Care
To learn more about our services, please visit the Service Offerings page.
To book a discovery call, please visit the Book Consult page or call 541-255-5047.
.===============================================
References:
Cicatiello, A., Di Girolamo, D., & Dentice, M. (2018, September 11). Metabolic Effects of the Intracellular Regulation of Thyroid Hormone: Old Players, New Concepts. Retrieved May 06, 2020, from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6141630/(Links to an external site.) (Links to an external site.)
Martinez, B., & Ortiz, R. M. (2017). Thyroid Hormone Regulation and Insulin Resistance: Insights From Animals Naturally Adapted to Fasting. Physiology, 32(2), 141-151. doi:10.1152/physiol.00018.2016
(2011, September 19). Why Can Insulin Resistance Be a Natural Consequence of Thyroid Dysfunction? Retrieved May 06, 2020, from https://www.hindawi.com/journals/jtr/2011/152850/(Links to an external site.) (Links to an external site.)
Pucci, E., Chiovato, L., & Pinchera, A. (2000). Thyroid and lipid metabolism.International Journal of Obesity, 24(S2). doi:10.1038/sj.ijo.0801292
Stipanuk, M. H., & Caudill, M. A. (2019). Biochemical, physiological, & molecular aspects of human nutrition (pp. 203-228). St. Louis, MI: Elsevier.
Reza Mirbolooki, MD. PhD. Recorded Lecture: Nutrients Metabolism
Brenta, G. (2011). Why Can Insulin Resistance Be a Natural Consequence of Thyroid Dysfunction? Journal of Thyroid Research, 2011, 1-9. doi:10.4061/2011/152850
, L., & Gabriela. (2018, August 15). A Renewed Focus on the Association Between Thyroid Hormones and Lipid Metabolism. Retrieved May 07, 2020, from https://www.frontiersin.org/articles/10.3389/fendo.2018.00511/full (Links to an external site.)
Rizos, C., Elisaf, M., & Liberopoulos, E. (2011). Effects of thyroid dysfunction on lipid profile. Retrieved May 07, 2020, from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3109527/
Comments