When people think about hormone health, they usually think about the organs that produce hormones.
The thyroid produces thyroid hormones. The ovaries produce estrogen and progesterone. The testes produce testosterone. The adrenal glands produce cortisol and other stress hormones.
But producing hormones is only one part of the equation.
Hormones also need to be activated, transported, metabolized, modified, and eventually cleared from the body. Much of that work depends on the liver.
The liver sits at the intersection of metabolism and endocrine function, constantly processing chemical signals according to the body’s needs. It participates in thyroid hormone metabolism, modifies steroid hormones, produces proteins that transport hormones through the bloodstream, and helps prepare used hormones for elimination.
When liver function is compromised, hormone signaling can become less efficient even when the hormone-producing glands themselves are functioning normally.
Your Liver Is Part of Your Endocrine System
The liver is usually discussed in terms of detoxification, digestion, or alcohol metabolism, but its metabolic responsibilities are much broader.
Blood arriving from the digestive tract passes through the liver, where nutrients, hormones, medications, and other compounds can be processed before continuing through circulation. Liver cells contain an enormous collection of enzymes responsible for transforming these compounds into forms the body can use or eliminate.
This makes the liver an important regulator of the hormonal environment.
Steroid hormones such as estrogen, progesterone, testosterone, and cortisol are fat-soluble molecules. After they have performed their functions, they cannot simply be filtered into the urine in their original form. They generally need to undergo enzymatic transformations that make their metabolites easier to eliminate.
The liver performs much of this work through Phase I and Phase II metabolism.
Phase I reactions modify hormone molecules through processes such as oxidation and reduction. Phase II pathways can then conjugate these compounds with molecules such as glucuronic acid or sulfate, increasing their water solubility and facilitating elimination through urine or bile.
These processes require enzymes, nutrients, and cellular energy. Hormone clearance is therefore not a passive process. It is another energy-dependent function of metabolism.
Hormone Production Is Only Half the Equation
Hormone health is often approached as a problem of production.
Low testosterone? Produce more testosterone.
Low thyroid function? Produce more thyroid hormone.
Estrogen symptoms? Reduce estrogen production.
But the concentration of a hormone in circulation reflects several processes occurring simultaneously: how much is produced, how it is transported, how tissues respond to it, how quickly it is metabolized, and how effectively its metabolites are eliminated.
Estrogen provides a useful example.
Estrogens circulate through the body, interact with tissues, and eventually return to the liver for metabolism. The liver converts them into metabolites that can be conjugated and prepared for elimination.
Some of these conjugated metabolites are secreted into bile and enter the intestine. Ideally, they continue through the digestive tract and leave the body in stool.
However, intestinal bacteria can produce enzymes such as beta-glucuronidase that deconjugate some estrogen metabolites, allowing a portion to be reabsorbed through enterohepatic circulation.
This is one reason liver function, bile flow, and intestinal function are interconnected when discussing estrogen metabolism. Producing the right amount of a hormone matters, but so does what happens to that hormone after it has delivered its signal.
The Liver Helps Regulate Thyroid Hormone Activity
The connection between the liver and hormones becomes even clearer with thyroid physiology.
The thyroid gland primarily secretes thyroxine, or T4. T4 is biologically important, but much of thyroid signaling depends on its conversion into the more active hormone triiodothyronine, or T3.
This conversion occurs in several tissues, including the liver.
Deiodinase enzymes remove an iodine atom from T4 to produce T3. The liver therefore participates in determining how much active thyroid hormone is available to influence metabolic activity throughout the body.
The relationship also works in the opposite direction.
Thyroid hormones influence liver metabolism, including carbohydrate and lipid metabolism, mitochondrial activity, and cholesterol handling. Healthy thyroid signaling supports liver function, while the liver contributes to thyroid hormone metabolism.
The liver also produces many of the plasma proteins involved in transporting hormones through the bloodstream, including thyroid-binding globulin and sex hormone-binding globulin. Changes in liver function can therefore influence not only hormone metabolism but also how hormones circulate.
This creates a close relationship between liver health, thyroid signaling, and overall metabolic function.
Steroid Hormones Begin With Metabolism
The liver also plays an important indirect role in steroid hormone production.
Estrogen, progesterone, testosterone, cortisol, and other steroid hormones are synthesized from cholesterol.
Cholesterol is often treated as something the body should minimize, but physiologically it is an essential structural molecule and the raw material for steroidogenesis. The liver is central to cholesterol metabolism, synthesizing cholesterol, packaging it into lipoproteins, converting some of it into bile acids, and helping regulate its movement throughout the body.
Hormone production also requires energy.
Converting cholesterol into steroid hormones involves multiple enzymatic reactions and depends on functioning mitochondria and adequate cellular energy. The endocrine system does not operate separately from metabolism; reproductive and steroid hormone production are metabolically expensive processes.
When the body is chronically under-fueled or heavily reliant on stress hormones to maintain blood sugar, reproductive hormone signaling may be deprioritized.
This is one reason hormone support should not focus exclusively on isolated glands. The liver, thyroid, mitochondria, blood sugar regulation, nutrient availability, and digestive system all contribute to the metabolic environment in which hormones are produced and used.
Liver Glycogen Connects Hormones to the Stress Response
The liver has another hormonal role that receives much less attention: maintaining blood glucose between meals and during sleep.
After carbohydrate is consumed, the liver can store glucose as glycogen. When blood glucose begins to fall, liver glycogen can be broken down and released as glucose to help maintain a stable supply of fuel.
When glycogen stores are inadequate, the body has other ways to maintain blood glucose.
Adrenaline, glucagon, and cortisol help mobilize stored fuel and increase glucose availability. These systems are essential for survival, but chronically depending on stress hormones for basic energy regulation is different from occasionally activating them when needed.
Cortisol itself is a steroid hormone that must eventually be metabolized, with the liver playing a significant role in its clearance.
This creates another connection between liver function and the endocrine system: the liver helps maintain the fuel supply that reduces unnecessary stress signaling while also participating in the metabolism of the hormones involved in that stress response.
Supporting hormone health therefore includes supporting the metabolic conditions that allow the body to produce energy without constantly relying on compensatory stress signals.
Bile Is Part of Hormone Clearance
The liver produces bile continuously.
Most people associate bile exclusively with fat digestion, but bile also serves as an important route through which the liver exports cholesterol, bilirubin, and various metabolized compounds into the digestive tract.
This includes conjugated steroid hormone metabolites.
After the liver processes certain hormone metabolites, they can be secreted into bile, transported into the intestine, and eventually eliminated.
Healthy bile production and flow therefore support more than digestion. They are part of the physical pathway through which the liver moves metabolic waste out of the body.
Bile acids themselves are also metabolically active signaling molecules. Through receptors such as FXR and TGR5, bile acids participate in communication involving glucose metabolism, lipid metabolism, energy expenditure, and aspects of endocrine signaling.
The liver and endocrine system are connected at multiple levels: hormone metabolism, thyroid activation, cholesterol metabolism, glucose regulation, transport proteins, and bile signaling.
Supporting the Liver Supports the Hormonal Environment
Healthy hormones depend on much more than taking supplements designed to increase or decrease individual hormones.
The body needs adequate energy and protein to perform enzymatic reactions. The liver needs nutrients to support detoxification pathways. Thyroid function helps maintain metabolic activity. Carbohydrate availability helps replenish liver glycogen and reduce excessive dependence on stress hormones. Regular bowel function supports the elimination of compounds secreted through bile.
Supporting bile flow can also help the liver perform one of its fundamental jobs: moving processed compounds from the liver into the digestive tract.
This is where TUDCA MAX can fit into a broader metabolic approach.
Tauroursodeoxycholic acid, or TUDCA, is a hydrophilic bile acid that has been studied for its effects on bile acid metabolism, cellular stress, and liver function. By supporting healthy bile flow and normal liver function, TUDCA MAX helps support the systems involved in digestion and the elimination of compounds processed by the liver.
It is not a hormone supplement, nor does it need to be.
The goal is to support the organ doing much of the behind-the-scenes work that allows hormones to be metabolized, transported, converted, and cleared appropriately.
Hormone health depends on the entire metabolic environment in which those signals operate. And the liver is one of the most important parts of that environment.
References
-
Rui L. Energy metabolism in the liver. Comprehensive Physiology. 2014;4(1):177-197. doi:10.1002/cphy.c130024.
-
Mullur R, Liu YY, Brent GA. Thyroid hormone regulation of metabolism. Physiological Reviews. 2014;94(2):355-382. doi:10.1152/physrev.00030.2013.
-
Bianco AC, Kim BW. Deiodinases: implications of the local control of thyroid hormone action. Journal of Clinical Investigation. 2006;116(10):2571-2579. doi:10.1172/JCI29812.
-
Kharbanda KK, McVicker DL, Zetterman RK, MacDonald RG, Donohue TM Jr. Flow cytometric analysis of plasma membrane and intracellular asialoglycoprotein receptor in ethanol-fed rats. Hepatology. 1997;26(4):944-950. doi:10.1002/hep.510260419.
-
Chiang JYL, Ferrell JM. Bile acid metabolism in liver pathobiology. Gene Expression. 2018;18(2):71-87. doi:10.3727/105221618X15156018385515.
-
Chiang JYL, Ferrell JM. Bile acids as metabolic regulators and nutrient sensors. Annual Review of Nutrition. 2019;39:175-200. doi:10.1146/annurev-nutr-082018-124344.
-
Wahlström A, Sayin SI, Marschall HU, Bäckhed F. Intestinal crosstalk between bile acids and microbiota and its impact on host metabolism. Cell Metabolism. 2016;24(1):41-50. doi:10.1016/j.cmet.2016.05.005.
-
Baker JM, Al-Nakkash L, Herbst-Kralovetz MM. Estrogen-gut microbiome axis: physiological and clinical implications. Maturitas. 2017;103:45-53. doi:10.1016/j.maturitas.2017.06.025.
-
Kwa M, Plottel CS, Blaser MJ, Adams S. The intestinal microbiome and estrogen receptor-positive female breast cancer. Journal of the National Cancer Institute. 2016;108(8):djw029. doi:10.1093/jnci/djw029.
-
Russell DW. Fifty years of advances in bile acid synthesis and metabolism. Journal of Lipid Research. 2009;50(Suppl):S120-S125. doi:10.1194/jlr.R800026-JLR200.
-
Trauner M, Claudel T, Fickert P, Moustafa T, Wagner M. Bile acids as regulators of hepatic lipid and glucose metabolism. Digestive Diseases. 2010;28(1):220-224. doi:10.1159/000282091.
-
Amaral JD, Viana RJS, Ramalho RM, Steer CJ, Rodrigues CMP. Bile acids: regulation of apoptosis by ursodeoxycholic acid. Journal of Lipid Research. 2009;50(9):1721-1734. doi:10.1194/jlr.R900011-JLR200.