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Thyroid Function and Gut

Gut or digestive function is essential. It enables us to absorb nutrients so we regenerate tissue and metabolize energy. Our digestion turns what we eat into what we need to make energy and vital...
Author
Dr. Elizabeth Bright, , DO, ND, MICO
Published on
September 23, 2024

Gut or digestive function is essential. It enables us to absorb nutrients so we regenerate tissue and metabolize energy. Our digestion turns what we eat into what we need to make energy and vital nutrients. However, just as we see hormones monetized into hormone replacement therapy, the mechanics of our digestion are being isolated, made in laboratories, packaged, and sold back to us. How wonderful that the contents contain countless individual species of bacteria, not to mention acids and peptides that can quickly end up in a bottle. Our digestive function evolved to digest our food and eliminate waste without the help of intestinal isolates and factorymade "good" bacteria.So why do so many people have gut issues? A lot of it has to do with what we eat or don't eat. Some people have gastrointestinal problems, not because they lack certain bacteria or acids, like butyrate acid, that thrive on high-fiber foods, but because they have low thyroid function. Humans didn't evolve to eat fiber. Many have gut issues because they have low thyroid function. It may be because they haven't been giving their thyroid the nutrients it needs, like cholesterol and iron. There are many reasons why a person can have irregular thyroid function.

Just as healthy skin depends on adequate thyroid hormone, gut function does too. One of the classic gut function problems with low thyroid function is constipation. Many people address this with laxatives. After a while, laxatives no longer work. This usually happens because chronic laxative use irritates intestinal tissue so much that the last thing intestinal epithelial tissue, scratched and lesioned as it is by intestinal irritants, wants to keep the irritants near the tissue. The bowels expel their contents because the tissues are irritated. People then resort to other "aids," like colonics. These also irritate intestinal tissue. They may also resort to adrenal stimulants, like caffeine and nicotine, which also irritate intestinal tissue, this time via adrenal stimulation. This way lies diverticulitis and colon inflammation, and eventually, something worse. Sometimes, they resort to colectomy for "slow transit constipation." They have their colon removed, not because the organ is diseased, but because it is not getting adequate stimulation. The stuff sitting in the bowels rarely becomes toxic. It is far better to wait for stimulation, muscle function, and proper mechanics to return than to force the colon to empty. Imagine having organs removed because low thyroid function has not been diagnosed. That is precisely why so many women have their gallbladders removed. 80% of cholecystectomies occur in women.

Compromised gut health—from nutrient malabsorption to other digestive issues such as IBS and dysbiosis, can eventually cause autoimmunity. So what does reduced thyroid function, specifically low T3 hormone, have to do with this? Motility, for one. There isn't any. These issues come with abdominal pain and bloating. Colon tissue itself will get lesioned. There is rectal prolapse, a twisted colon, the sensation that something is blocking the colon, decreased intestinal and colonic mucus, and reduced adrenergic peristaltic stimulation. Decreased adrenergic stimulation results from the adrenal glands, through the chemical messengers epinephrine and norepinephrine, trying to send a neurohormonal stimulus to the smooth muscle tissue of the intestines, but it isn't getting there.

The amplitude and velocity of muscular peristaltic action are reduced. There will be fewer contractions of the digestive muscles in the sigmoid colon and the rectum. Food takes a much longer time to pass through the intestines. The gastroparesis associated with diabetes is just plain ordinary in the digestive system without T3 doing its job.

The glycosaminoglycan accumulation due to low T3, which I discussed in the skin video, also affects intestinal tissue. There can be swelling that interferes with motility and absorption. Calcium absorption decreases greatly, which can affect bone health. Due to tissue irritation or swelling, the intestines react less to stimuli from a vasoactive intestinal polypeptide, the neurotransmitter important to gastric health. VIP regulates gastric acid secretion in the stomach, water and ion absorption in the colon, and peristalsis and mucus secretion. VIP is a massive part of gastrointestinal function! VIP also maintains the intestinal epithelial cells, which are crucial to prevent a leaky gut. It stimulates sensory nerves and is essential in preserving microbiota balance and biodiversity. You can get it in a supplement, but wouldn't it be better to make your own?

While constipation is common, there may be diarrhea because no motility means some bacteria grow more than others. You can buy some of those. You can also get some plant extracts in a bottle to rein in the ones you don't want too much of. But are my intestines in need of plant antibiotics?

I'm not a plant-eater. People with digestive issues often take medication or supplements that can irritate epithelial tissue and reduce T4 conversion and T3 absorption. Thyroid hormones go to the liver, are secreted into bile, and then return to the intestines. If the hormones are not absorbed, they end up in the stool. More intestinal inflammation means less thyroid absorption.

What else does T3 do for gut function? T3 increases sensitivity to aldosterone, which regulates the absorption of sodium and potassium in the small intestine. An imbalance here will affect blood pressure. You can have much sodium, too little and too much potassium, and too little. Again, you can take supplements, drink electrolytes, or eat celery. Please don't eat celery. T3 down-regulates lactase, making lactose digestion difficult. It stimulates alkaline phosphatase,

which is essential to absorb minerals. Low T3 causes low gastrin and low hydrochloric acid. Hence, less food is broken down, causing acid reflux, malabsorption, bloating, and pain.

Heliobacter pylori infection is related to low T3 because low T3 means fewer good bacteria in the gut. You can take all the probiotics and healthy fecal matter you want, but how well will these work with low T3? What percentage of these will remain in the gut and work? Another organ that so many middle-aged women have had removed is the gallbladder. In the presence of low T3, there is a decrease in bile flow, a reduction of bile salts, and a reduced cholesterol synthesis. Then, a person will have high triglycerides. The gallbladder will become hypotonic or stuck full of gallstones. Here we have the reason, so many women had theirs removed. I'm not saying this is why your digestion is bad. I'm just suggesting you look into it. The best diet for optimum digestion function is a high-fat carnivore diet. If that doesn't help, look to stress and thyroid function before spending much money on supplements and having surgery.

References:

Layden TJ, Boyer JL. The effect of thyroid hormone on bile salt-independent bile flow and Na+, K+ -ATPase activity in liver plasma membranes enriched in bile canaliculi. J Clin Invest. 1976 Apr;57(4):1009-18.

Pácha J, Pohlová I, Zemanová Z. Hypothyroidism affects the expression of electrogenic amiloridesensitive sodium transport in rat colon. Gastroenterology. 1996 Dec;111(6):1551-7.

Crowe JP, Christensen E, Butler J, Wheeler P, Doniach D, Keenan J, Williams R. Primary biliary cirrhosis: the prevalence of hypothyroidism and its relationship to thyroid autoantibodies and sicca syndrome. Gastroenterology. 1980 Jun;78(6):1437-41.

Zeniya M. Thyroid disease in autoimmune liver diseases. Nippon Rinsho 1999;57(8):1882.


67. Borgaonkar MR, Morgan DG. Primary biliary cirrhosis and type II autoimmune polyglandular syndrome. Can J Gastroenterol 1999;13(9):767.

Hoogenbrugge van der Linden H, Jansen H, Hulsmann WC, et al. Relationship between insulinlike growth factor-I and low density lipoprotein cholesterol levels in primary hypothyroidism in women. J Endocrinol 1989;123:341.

Hays MT. Thyroid hormone and the gut. Endocr Res. 1988;14(2-3):203-24.

Molinero P, Calvo JR, Jimenez J, et al. Decreased binding of vasoactive intestinal peptide to intestinal epithelial cells from hypothyroid rats. Biochem Biophys Res Commun 1989;162: 701.


Goldin E, et al. Diarrhea in hypothyroidism: Bacterial overgrowth as a possible etiology. J Clin Gastroenterol 1990;12:98.

Kahraman H, Kaya N, Demirçali A, Bernay I, Tanyeri F. Gastric emptying time in patients with primary hypothyroidism. Eur J Gastroenterol Hepatol. 1997 Sep;9(9):901-4.

Song Y, Zhao M, Zhang H, Zhang X, Zhao J, Xu J, et al. Thyroid-stimulating hormone levels are inversely associated with serum total bile acid levels: a cross-sectional study. Endocr Pract Off J Am Coll Endocrinol Am Assoc Clin Endocrinol. (2016) 22:420–6.

Zhao F, Feng J, Li J, Zhao L, Liu Y, Chen H, et al. Alterations of the gut microbiota in Hashimoto's thyroiditis patients. Thyroid Off J Am Thyroid Assoc. (2018) 28:175–86.

Su X, Zhao Y, Li Y, Ma S, Wang Z. Gut dysbiosis is associated with primary hypothyroidism with interaction on gut-thyroid axis. Clin Sci Lond Engl. (1979) (2020) 134:1521–35.

Patil AD. Link between hypothyroidism and small intestinal bacterial overgrowth. Indian J Endocrinol Metab. (2014) 18:307–9. doi: 10.4103/2230-8210.131155

Braverman, L.D. Utinger, R.D. Werner and Ingbar’s The Thyroid. Lippincott, 1991

Shilling Bailey K, Marsh W, Daughtery L, Hobbs G, Borgstrom D. Gender Disparities in the Presentation of Gallbladder Disease. Am Surg. 2019 Aug 1;85(8):830-833.

Ravi PC, Thugu TR, Singh J, Dasireddy RR, Kumar SA, Isaac NV, Oladimeji A, DeTrolio V, Abdalla R, Mohan V, Iqbal J. Gallstone Disease and Its Correlation With Thyroid Disorders: A Narrative Review. Cureus. 2023 Sep 12;15(9):e45116.

Lekkerkerker JF, Van Woudenberg F, Beekhuis H, et al. Enhancement of calcium absorption in hypothyroidism. Isr J Med Sci 1971;7:399.

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