An Interview With Dr. Raymond Peat

A Renowned Nutritional Counselor Offers His Thoughts About Thyroid Disease

by Mary Shomon

Raymond Peat, Ph.D. is editor and researcher of a popular and well-known monthly newsletter on nutritiona and health, as well as author of a number of cutting-edge publications that look at aging, nutrition, and hormones from a biochemical perspective. Dr. Peat has a Ph.D. in Biology from the University of Oregon, with specialization in physiology. He has taught at the University of Oregon, Urbana College, Montana State University, National College of Naturopathic Medicine, Universidad Veracruzana, the Universidad Autonoma del Estado de Mexico, and Blake College. He also conducts private nutritional counseling.

I had the privilege to conduct an interview with Ray Peat in November of 2000, touching upon a few of the many interesting points he raises in his various publications.

Mary Shomon: Why do women with treated hypothyroidism frequently still have inappropriately high levels of cholesterol and high triglycerides, and what can they do to help lower these levels?

Dr. Ray Peat: Often it’s because they were given thyroxine, instead of the active thyroid hormone, but hypertriglyceridemia can be caused by a variety of things that interact with hypothyroidism. Estrogen treatment is a common cause of high triglycerides, and deficiencies of magnesium, copper, and protein can contribute to that abnormality. Toxins, including some drugs and herbs, can irritate or stimulate the liver to produce too much triglyceride. T3, triiodothyronine, is the active thyroid hormone, and it is produced (mainly in the liver) from thyroxine, and the female liver is less efficient than the male liver in producing it, as is the female thyroid gland. The thyroid gland, which normally produces some T3, will decrease its production in the presence of increased thyroxine. Therefore, thyroxine often acts as a “thyroid anti-hormone,” especially in women. When thyroxine was tested in healthy young male medical students, it seemed to function “just like the thyroid hormone,” but in people who are seriously hypothyroid, it can suppress their oxidative metabolism even more. It’s a very common, but very serious, mistake to call thyroxine “the thyroid hormone.”

High cholesterol is more closely connected to hypothyroidism than hypertriglyceridemia is. Increased T3 will immediately increase the conversion of cholesterol to progesterone and bile acids. When people have abnormally low cholesterol, I think it’s important to increase their cholesterol before taking thyroid, since their steroid-forming tissues won’t be able to respond properly to thyroid without adequate cholesterol.

Mary Shomon: You feel that progesterone can have anti-stress effects, without harming the adrenal glands. Is progesterone therapy something you feel is useful to many or most hypothyroid patients? How can a patient know if she needs progesterone? Do you recommend blood tests? And if so, at what point in a woman’s cycle?

Dr. Ray Peat: Estrogen blocks the release of hormone from the thyroid gland, and progesterone facilitates the release. Estrogen excess or progesterone deficiency tends to cause enlargement of the thyroid gland, in association with a hypothyroid state. Estrogen can activate the adrenals to produce cortisol, leading to various harmful effects, including brain aging and bone loss. Progesterone stimulates the adrenals and the ovaries to produce more progesterone, but since progesterone protects against the catabolic effects of cortisol, its effects are the opposite of estrogen’s. Progesterone has antiinflammatory and protective effects, similar to cortisol, but it doesn’t have the harmful effects. In hypothyroidism, there is a tendency to have too much estrogen and cortisol, and too little progesterone.

The blood tests can be useful to demonstrate to physicians what the problem is, but I don’t think they are necessary. There is evidence that having 50 or 100 times as much progesterone as estrogen is desirable, but I don’t advocate “progesterone replacement therapy” in the way it’s often understood. Progesterone can instantly activate the thyroid and the ovaries, so it shouldn’t be necessary to keep using it month after month. If progesterone is used consistently, it can postpone menopause for many years.

Cholesterol is converted to pregnenolone and progesterone by the ovaries, the adrenals, and the brain, if there is enough thyroid hormone and vitamin A, and if there are no interfering factors, such as too much carotene or unsaturated fatty acids. Progesterone deficiency is an indicator that something is wrong, and using a supplement of progesterone without investigating the nature of the problem isn’t a good approach. The normal time to use a progesterone supplement is during the “latter half” of the cycle, the two weeks from ovulation until menstruation. If it is being used to treat epilepsy, cancer, emphysema, migraine or arthritis, or something else so serious that menstrual regularity isn’t a concern, then it can be used at any time. If progesterone is used consistently, it can postpone menopause for many years.

Mary Shomon: What supplements do you feel are essential for most people with hypothyroidism?

Dr. Ray Peat: Because the quality of commercial nutritional supplements is dangerously low, the only supplement I generally advocate is vitamin E, and that should be used sparingly. Occasionally, I will suggest limited use of other supplements, but it is far safer in general to use real foods, and to exclude foods which are poor in nutrients. Magnesium is typically deficient in hypothyroidism, and the safest way to get it is by using orange juice and meats, and by using epsom salts baths; magnesium carbonate can be helpful, if the person doesn’t experience side effects such as headaches or hemorrhoids.

Mary Shomon: Do you feel that there are any special considerations, issues, or treatments for men with hypothyroidism?

Dr. Ray Peat: Thyroid supplements can be useful for prostate hypertrophy and some cases of impotence and infertility. Occasionally, a man who can’t put on a normal amount of weight finds that a thyroid supplement allows normal weight gain. Leg cramps, insomnia and depression are often the result of hypothyroidism. Heart failure, gynecomastia, liver disease, baldness and dozens of other problems can result from hypothyroidism.

Mary Shomon: Many people describe how they are clinically hypothyroid, with elevated TSH levels, but have extremely high pulse rates. Do you have any thoughts as to what might be going on in that situation?

Dr. Ray Peat: In hypothyroidism, thyrotropin-release hormone (TRH) is usually increased, increasing release of TSH. TRH itself can cause tachycardia, “palpitations,” high blood pressure, stasis of the intestine, increase of pressure in the eye, and hyperventilation with alkalosis. It can increase the release of norepinephrine, but in itself it acts very much like adrenalin. TRH stimulates prolactin release, and this can interfere with progesterone synthesis, which in itself affects heart function.

I consider even the lowest TSH within the “normal range” to be consistent with hypothyroidism; in good health, very little TSH is needed. When the thyroid function is low, the body often compensates by over-producing adrenalin. The daily production of adrenalin is sometimes 30 or 40 times higher than normal in hypothyroidism. The adrenalin tends to sustain blood sugar in spite of the metabolic inefficiency of hypothyroidism, and it can help to maintain core body temperature by causing vasoconstriction in the skin, but it also disturbs the sleep and accelerates the heart. During the night, cycles of rising adrenalin can cause nightmares, wakefulness, worry, and a pounding heart. Occasionally, a person who has chronically had a heart rate of 150 beats per minute or higher, will have a much lower heart rate after using a thyroid supplement for a few days. If your temperature or heart rate is lower after breakfast than before, it’s likely that they were raised as a result of the nocturnal increase of adrenalin and cortisol caused by hypothyroidism.