Is your hypothyroidism causing fatty liver?

I came across a study called Hypothyroidism-Induced Nonalcoholic Fatty Liver Disease (HIN): Mechanisms and Emerging Therapeutic Options by Tanase et al 2020 that had some interesting info about the relationship between NAFLD and hypothyroidism, particularly if you are either subclinically hypothyroid or if your medication is not optimized.

Many people are being diagnosed with a fatty liver that are not alcoholics which is how people used to get a fatty liver. Excessive and chronic alcohol consumption will do that. What happens in fatty liver disease is basically an accumulation of fat deposits in the liver that can lead to cirrhosis and liver cancer if not treated.

NAFLD is also sometimes called NASH or non alcoholic steatohepatitis but it is actually under the umbrella of NAFLD with cirrhosis and cancer. It is actually one of the main causes of the need for a liver transplant and for the most part is totally preventable. Chronic conditions that are causal of NAFLD include T2D, chronic kidney disease, gallstones, CVD, metabolic disorders, hypothyroidism, PCOS and more.

When you are dealing with subclinical hypothyroidism or perhaps your doctor believes you are good to go with a TSH of 4-5, you are at risk for metabolic syndrome, obesity, atrial fibrillation and cancer.

These researchers state that other studies have shown that patients with over 10 years of dysfunction of the thyroid have a much higher chance of developing liver cancer. People who had NASH or chronic Hep B infections also had a higher rate of thyroid dysfunction than the control group in one study.

Hypothyroidism induced NAFLD has become its own disease entity. This means that it’s a disease by itself and this is really sad because so many people are walking around with subclinical hypothyroidism and their doctors are told that a TSH of 4-5 and sometimes even higher is normal. It’s maddening to me.

Hypothyroidism on labs would look like a high TSH with FT4 within the reference range and no real clinical symptoms (aside from the ones your doctor just writes off as either in your head or related to laziness and depression) or with low FT4 with any of the clinical symptoms.

According to this paper the cut off for TSH labs is between 4.0 and 4.5 mIU/l

NAFLD is defined as an accumulation of fat in the liver in over 5% of liver cells with no secondary causes or by 5.6% in an MRI. The gold standard for diagnosis is a liver biopsy which is invasive and has some potential severe side effects.

These two problems are occurring in children now with obese children and abnormal thyroid hormone levels had a higher risk of having fatty liver and in obese children with normally working thyroids, there was around a 30% prevalence of fatty liver. Those with fatty liver had a much higher TSH level than those without a fatty liver but T3 and T4 remained the same for both groups studied.

Many studies have been done on adults showing hypothyroid patients, both subclinical and overt hypothyroidism, had a higher prevalence of NAFLD. Said another way, the subjects with hypothyroidism were more likely to have fatty liver than those who didn’t have hypothyroidism.

There was also an association between the level of TSH and a higher risk of fatty liver. The Ft3/Ft4 ratio, insulin resistance, waist circumference, and high triglycerides were also risk factors for fatty liver in both hypothyroid and euthyroid people.

Having low FT3 was also associated with scarring on the liver called liver fibrosis.

There have been a lot of studies on this topic according to this one paper and they suggest that women with fatty liver disease had significantly higher TSH levels than control groups, low FT4, higher triglycerides, and were obese. In addition, and a high AST (liver enzyme marker on basic labs).

The authors did make it clear that there is no clear cause and effect relationship here but that there is some kind of relationship. They don’t really understand physiologically how this is happening though speculation has to do with the weight gain, poor blood sugar regulation, and inability to lose fat that many have due to hypothyroidism.

All of these things also occur in NAFLD which is known to be related to fat accumulation in the liver, inflammation due to oxidative stress and the livers inability to repair itself.

The thyroid gland is hugely responsible for heat production, creation of fat cells, fat distribution, overall energy, fat, carb, and protein metabolism as well as cell metabolism. Metabolism in this case is just referring to all the chemical processes it takes to break down fat, carbs, and protein into the substrate that the body uses for everyday functions. Cell metabolism is referring to all the chemical reactions that take place inside of the cell.

We need T3 and T4 so our tissues can repair themselves, so our cells can communicate and helps with cell differentiation. This is when a cell changes into another kind of cell such as immune cells or when a cell is destroyed.

In fatty liver, it is thought that there is some thyroid hormone resistance (similar to insulin resistance) where the cells are resisting letting the hormone enter. There is a direct relationship to T3’s ability to function in the cells and liver cancer. In addition, T3 is suppressed in injury to muscle, heart attacks and in partial removal of the liver. According to this paper, many chronic diseases result in low T3. This doesn’t mean you need to up your T3, it means you need to figure out what is causing the low T3 in the first place.

Thyroid hormones and your TSH level in particular have direct affects on liver cell membranes and can create blood sugar issues and affect bile production. Low bile production means poor fat digestion and the potential for gallbladder issues like gallstones.

Thyroid hormones play a role in cholesterol: VLDL, LDL, HDL, ApoB as well. So pretty important that the darn gland is working properly or your hormone replacement is good.
These are not necessarily things you would notice right away either, it could be negative changes over time if you are dealing with subclinical hypothyroidism.

The good news in all of this is that thyroid hormones can help prevent all of this given and healthy diet and lifestyle. The problem is finding the right medication for you and getting your doctor to agree to give you a dose that puts your TSH in a better place.

The rest of this particular study goes in to great scientific detail about how and why these two things are tied together and discusses some studies where thyroid hormone treatment improved both.

If you are concerned about fatty liver there is a fatty liver index calculator I use with my clients that takes your trigylceride levels, BMI, a marker called GGT, and your wait circumference and it will come up with a calculation of how close you are to fatty liver.

In addition, looking at an elevated BUN (blood urea nitrogen) level can indicate a potential for fatty liver. AST and ALT are the common markers on basic blood labs your doctor would run. They are enzymes made in the liver and AST will be high when there is active tissue and cell destruction happening. ALT will usually be higher than AST when there is something wrong in the liver. My ranges for these are from my mentor Dr. Bryan Walsh and are much tighter ranges than will be on your labs from your doctor. He combed the research to find healthy controls where liver enzymes were measured and found the healthy range to be much smaller than the lab range.

Alkaline phosphatase will be high when there is some kind of liver issue along with GGT and bile acids. These markers are cheap and easy to get. If your doctor won’t order them, you can order them yourself using my link to Ulta Labs or you can have me order through other agencies and we can go over your labs and make a plan for getting you off the sidelines. Around 30% of the population has fatty liver and 90% of obese people have it. You can have a lab normal ALT level and already have liver damage.

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Tanase DM, Gosav EM, Neculae E, Costea CF, Ciocoiu M, Hurjui LL, Tarniceriu CC, Floria M. Hypothyroidism-Induced Nonalcoholic Fatty Liver Disease (HIN): Mechanisms and Emerging Therapeutic Options. International Journal of Molecular Sciences. 2020; 21(16):5927. https://doi.org/10.3390/ijms21165927