Omega-6 Linoleic Acid Suppresses Thyroid Signaling

The thyroid gland controls the body's metabolic rate, among other things. It does this by secreting the thyroid hormones triiodothyronine (T3) and thyroxine (T4). As with any other hormone, the tissue response depends on the amount of hormone and the tissue's sensitivity to the hormone.

For example, in type I diabetes, the pancreas doesn't produce enough insulin to move glucose from the blood into tissues. In type II diabetes, often the tissues are so resistant to the action of insulin that glucose is not effectively transported from the blood into tissues, despite high levels of insulin. Both result in excessively high blood glucose after a meal containing carbohydrate.

In the last post, I discussed a study in which rats on different diets, fed equal amounts of calories and omega-3, gained weight in proportion to the omega-6 linoleic acid content of their diets. 1960s men fed a diet high in linoleic acid also gained weight relative to a more typical control diet containing the same number of calories. Rats deficient in linoleic acid develop an abnormally high metabolic rate. This suggests that the metabolic rate may be supressed by linoleic acid, and leads us to the question: does linoleic acid suppress thyroid signaling?

I was first introduced to the idea by Dr. Ray Peat, who suggests that all polyunsaturated fats (PUFA) suppress thyroid signaling (and should be avoided as much as possible). I couldn't find any credible references in his articles, so I went digging around PubMed myself. It turns out, he's right, and it's been known since at least the 1970s.

The first thing I searched for is whether or not linoleic acid reduces the secretion of T3 or T4 by the thyroid gland. It doesn't seem to, although one study I found used Crisco as the "saturated fat" control group (I'm not making this up!). Next, I looked for studies that evaluated the effect of linoleic acid on tissue sensitivity to thyroid hormones. Here's what I found:

• A corn oil diet greatly suppresses the liver's response to T4 when compared with an equal amount of lard (5% by weight).
  
• A safflower oil diet suppresses the liver's response to T3 when compared with an equal amount of beef tallow (10% by weight).
• A diet high in linoleic acid (undisclosed source) suppresses the response of brown fat and liver to T3.
  

This is highly significant, since the liver is one of the major sites of thyroid hormone-responsive heat production. The liver and other visceral organs generate heat largely by activating a pump that pushes ions back and forth across the cell membrane, called the sodium-potassium ATPase. It's basically a way to create heat from chemical energy, like rubbing your hands together.

In another study, investigators showed that rats eating a diet containing 20% beef tallow ad libitum ate more, weighed less and carried less fat than rats eating 20% safflower oil. The liver sodium-potassium ATPase activity of the safflower group was 26% lower, although the result was not considered statistically significant. Serum leptin was much higher in the safflower oil group. High leptin plus low energy expenditure suggests leptin resistance. The safflower group was eating less food, and gaining more weight, probably because linoleic acid was suppressing its ability to generate heat. This may be partly due to inhibition of the sodium-potassium ATPase, as well as the effects of leptin resistance.

In the 1970s, linoleic acid was being considered as a treatment for hyperthyroidism:

Further studies should reveal the extent to which observed effects of excess thyroid hormone are amenable to control by dietary polyunsaturated fat.

Linoleic acid may interfere with thyroid signaling by inhibiting thyroid hormone binding to its receptor. Not all PUFA are equal in their ability to promote weight gain. Growing mice fed 15% corn oil develop more fat mass than mice fed 10% corn oil plus 5% perilla oil (rich in omega-3 alpha-linolenic acid). The effect can be blocked by knocking out the prostacyclin receptor, which shows that omega-6 derived eicosanoid signaling is responsible for the "excessive adipose [fat] tissue development" in growing mice. This mechanism is different from thyroid signaling.

Add gluten-induced autoimmune hypothyroidism, goitrogens (thyroid inhibitors) in soy, and endocrine disruptors from plastic like bispheonl-A, and you have potent brew that may strongly promote obesity in Western industrial nations.

The treatment? Dump the vegetable oil, wheat, soy, sugar and processed food in favor of the things the human body is equipped to handle: animal fats, root vegetables, vegetables, fruit, meats, organs, seafood, eggs, nuts and soaked or fermented non-gluten grains and legumes. Throw in some bugs if you're feeling adventurous.

Coconut oil can be particularly helpful because it's almost exclusively saturated, so it doesn't interfere with thyroid signaling. That may be why it increases energy expenditure and aids weight loss. Coconut has a long history of use by healthy non-industrial cultures in tropical areas. The medical literature likes to use the euphemism "medium-chain triglycerides" when referring to the saturated fat in coconut oil because it conceals the fact that it's saturated. Low-carbohydrate diets are also very helpful for weight loss, but I'm not sure it's really due to the carbohydrate itself rather than restricting wheat and sugar. I discussed that concept in this post.

Thanks to Wikipedia for the CC photo.