Estrogen is the Problem

Elevated estrogen in men and women is associated with obesity and metabolic syndrome. The pro-metabolic hormones like progesterone for women and testosterone for men are both lowered by estrogen dominance. And unlike those pro-metabolic hormones, estrogens continue to be produced by men and postmenopausal until end of life.

Today we’re going to investigate how estrogen blocks T3 conversion in the liver as do the other major inhibitors like CORTISOL, PUFA and PLASTIC.

There are a few types of estrogen but the most important for our purposes is Estradiol. It’s the most potent estrogen and the one associated with hormone-based cancers. For cycling women its directly produced in the ovaries and for men and postmenopausal women its produced by the aromatase enzyme from testosterone.

The aromatase enzyme resides in many tissue but is in highest concentration is in fat cells. This is why obesity is associated with estrogen dominance (and hypothyroidism).

Estradiol is associated with hormone-sensitive cancers, particularly breast and endometrial cancers in women. In men, it is a driver of prostate cancer.

Birth control pills and IUDs contain synthetic estrogen and/or progestin and are a major cause of hypothyroidism via estrogen dominance. This is achieved in two ways: firstly by blocking ovulation endogenous progesterone production stops massively increasing estradiol (estrogen dominance). Secondly, Progestin isn’t biodentical progesterone and as such also binds to estrogen and testosterone receptors causing further escalation of estrogen while also expressing androgenic effects. I have personally seen how IUDs and the pill skyrocket TSH and thyroid antibodies creating both hypothyroidism and Hashimoto’s.

The liver is the organ responsible for metabolizing estrogen for excretion in the urine. It is because excess estrogen is so damaging to the body that the liver prioritizes estrogen detoxification over T3 conversion. Additionally, excess estrogen lowers glucose availability to the deiodinsase ezymes that convert T4 to T3 thus down-regulating them.

The next major inhibitor of thyroid conversion is the stress hormone cortisol. Excess estradiol increases cortisol and cortisol directly inhibits the deiodinases in the liver.

Another way of thinking about stress hormones is that they function as emergency power while the pro-metabolic hormones (like thyroid) are the primary power. When the primary power supply is offline due to scarcity of fuel, emergency power steps in. Excessive stress hormones can also shut down the primary power supply. As a result cortisol and thyroid hormones are usually opposed to one another. High cortisol means low active T3 and vice versa.

Elevated cortisol depletes progesterone (the true female hormone) in women creating estrogen dominance. In men, elevated cortisol leads to loss of testosterone (the male hormone).

In the context of gut health, leaky gut triggers cortisol and pro-inflammatory cytokines like IL-6 which increases aromatase activity, producing more estradiol. If you have gut dysbiosis, there is a high likelihood its driven by pathogenic bacteria containing the enzyme beta-glucuronidase. This enzyme reverses the glucuronidation performed by the liver returning the estradiol back into active form to do more damage.

Polyunsaturated fats (PUFA) found in seed oils are another surprising source of thyroid conversion inhibition. PUFA increase inflammatory molecules called prostaglandins. For reference, Prostaglandins are targeted by NSAIDS like aspirin, Advil and Motrin which block the COX enzyme that creates them. Prostaglandins are widely known to increase to increase aromatase activity, producing more estradiol.

The last major source of inhibition that are increasing daily in our environment are Xenoestrogens. These are exogenous estrogen-like chemicals from plastics and forever chemicals that have estrogenic effects in the body. The most ubiquitous Xenoestrogens are BPA, phthalates and flame retardants.

The liver also has to detoxify these chemicals which directly and indirectly slow thyroid conversion in the liver (through the same mechanisms as estrogen).

Fortunately you can mitigate the input of xenoestrogens by using less plastic and less recycled paper and buying natural beauty products. Plastics also increase pathogenic bacteria and fungi in the gut because some microbes can eat it.

You can also speed the detoxification of Xenoestrogens through sweating as demonstrated in BUS studies.

But just so we’re clear, excess estrogen is negatively effecting BOTH women and men. It’s causing early puberty in females, feminization of males, infertility in the adult population and it’s a major source of metabolic dysfunction for everyone by lowering thyroid function.

Jonathan