“Sometimes “antithyroid antibodies” found in the blood are used to diagnose Hashimoto’s disease, but the presence of those antibodies in the blood doesn’t mean that they originated in the thyroid gland, and even though he have very specific names (e.g., “antithyroglobulin,” antithyroperoxidase”) related to the thyroid gland, they aren’t even specific for the thyroid gland. It has been suggested that similarities in molecular structure between thyroglobulin and connective tissue proteins could account for the finding of “antithryoid antibodies” more frequently in rheumatoid arthritis and sjögren’s syndrome than in Hashimoto’s disease and Graves’ disease (Ruggeri, et al, 2002)”
Hashimoto's disease is an epidemic. You have it, your sister has it, and your grandma has it.
The wildly popular book, Why Do I Still Have Thyroid Symptoms When My Lab Tests Are Normal, by Dr Datis Kharrazian states that up to 90% of all people with hypothyroidism is actually undiagnosed Hashimoto's disease.
Friend and former podcasting buddy, Chris Kresser notes that one in eight women have Hashimoto's disease as well as up to 10% of women over 60 have clinical or subclinical hypothyroidism.
This is significant due to the monumental importance of the thyroid gland in producing energy and resisting stress. To borrow another phrase from Chris, "If your thyroid hormones are low, you can't be healthy. Period."
Questions I would like to explore in this article include: why women are more susceptible to Hashimoto's disease (and thyroid disease in general), as well as if the current "evolutionary" model of treatment is adequate.
The Current Alternative Strategy
In his book, Dr. Kharrazian explains the supposed physiological factors behind Hashimoto's disease. In short, thyroid antibodies against thyroid peroxidase (TPO) and thyroglobulin (TGB), which are needed to produce thyroid hormones, are attacked by the immune system, causing a worsening of thyroid function overtime.
Tests to evaluate the presence of antibodies against TPO and TBG (TPO ab and TGB Ab) are used to diagnose Hashimoto's disease.
Corrective approaches range from "balancing the immune system," removing allergenic triggers (especially gluten), increasing vitamin D status, increasing unsaturated fatty acid (omega-3) consumption, and downregulating inflammation with various herbal and nutrient supplements.
Counting The Hits & Ignoring The Misses
Considering the paleosphere's recent track record, which borders on a new breed of conventional wisdom ("metabolic damage," fructose hysteria, fruit makes you fat, sucrose ruins your health, fish oil mega-dosing, calcium isn't important, avoidance of dietary salt, etc.), questioning the "evolutionary model" for treating and diagnosing Hashimoto's seems warranted.
Naturally, turning to Dr. Ray Peat seem appropriate. He's been recommending a consistent dietary philosophy for the last forty years, which is comforting, considering most of paleosphere has completely reversed its theory on dietary carbohydrate in less than five.
In a recent interview, Peat suggested that the whole idea of autoimmune disease was "off the mark":
"The immune system, I think of as a "clean up the mess system". The antibodies help the phagocytes remove debris and if the debris are caused by an infection, they'll get the germs too, but if the germs are caused by low thyroid, causing the connective tissue to swell, the immune system has to come clean out all the junk because of low thyroid."
Peat's thoughts can be better understood in his 2005 newsletter entitled Thyroiditis, some confusion and causes of "autoimmune disease":
"Hashimoto's disease is clearly defined as the infiltration of the gland with lymphocytes causing destruction of the gland's active tissue and leading to hypothyroidism. The only way to know that the gland is being invaded by the large numbers of lymphocytes is by biopsy, but the condition is normally diagnosed by pure guesswork, without any biopsy."
Peat goes on explaining what's wrong with diagnoses based on antibodies:
"Sometimes "antithyroid antibodies" found in the blood are used to diagnose Hashimoto's disease, but the presence of those antibodies in the blood doesn't mean that they originated in the thyroid gland, and even though he have very specific names (e.g., "antithyroglobulin," antithyroperoxidase") related to the thyroid gland, they aren't even specific for the thyroid gland. It has been suggested that similarities in molecular structure between thyroglobulin and connective tissue proteins could account for the finding of "antithryoid antibodies" more frequently in rheumatoid arthritis and sjögren's syndrome than in Hashimoto's disease and Graves' disease (Ruggeri, et al, 2002)."
The "Shock" Hormone
Fitting in with the grand scheme of energy, structure, protective hormones, and degenerative hormones, Peat suggests that a "respiratory defect" is at the root of Hashimoto's disease:
"A generalized inflammatory state, rather than specific 'autoimmunity,' is responsible for thyroiditis and other 'autoimmune degenerative' diseases. A respiratory defect is behind the inflammatory condition."
Peat explains that the colloid, "the viscous protein (thyroglobulin) solution formed in tiny compartments in the thyroid gland" increases during stress, which can be broken down by proteolytic digestive enzymes, forming thyroid hormones.
Estrogen, however, stimulates the production of colloid, but inhibits the proteolytic enzymes that break it down:
"Therefore, when progesterone is deficient or estrogen is present in excess, the colloid tends to accumulate (even to the point of causing visible enlargement of the gland, a "colloid goiter"), at the same time that the person may be hypothyroid, because the hormone isn't being release from the stored colloid, into the blood stream. But, largely because no one wants to suggest that estrogen can be pathogenic, an enlarged thyroid gland is now likely to be diagnosed as "Hashimoto's thyroiditis" (or Hashimoto's stuma, or goiter, or disease)."
Rethinking the concept of estrogen as the "feminine hormone" is an important step in understanding Peat's view towards what Hans Selye labeled the "shock hormone". Peat describes some of the features of excess estrogen:
"These effects of estrogen include interference with oxidative metabolism, formation of lipofuscin (the age-pigment), retention of iron, production of free radicals and lipid peroxides, promotion of excitotoxicity and death of nerve cells, impaired learning ability, increased tendency to form blood clots and to have vascular spasms, increased autoimmunity and atrophy of the thymus, elevated prolactin, atrophy of skin, increased susceptibility to a great variety of cancers, lowered body temperature, lower serum albumin, increased tendency toward edema, and many of the features of shock. In recent years, it has been found to be responsible even for neonatal masculinization and the masculinization of the polycystic ovary syndrome. Although the pharmaceutical industry has often referred to it as "the female hormone," I don't know of any competent scientist who has ever called it that."
Moreover, Constance R. Martin PhD supports many of Peat's conclusions about estrogen (and prolactin) and their roles in the stress response:
"There are indications that the steroids exacerbate preexisting breast disorders, possibly by increasing prolactin levels. (Estrogens can impair B6 metabolism and therefore the synthesis of dopamine, a physiological suppressant of PRL [prolactin] secretion." - Constance R. Martin PhD - Endocrine Physiology 1985
"Estrogens augment PRL secretion in several ways. They lower the sensitivities of lactotrop DA receptors, and they affect DA turnover in the brain." - Constance R. Martin PhD - Endocrine Physiology 1985
"PRL can be released in response to stress. usually, there is a simultaneous discharge of ACTH and b-endorphin." - Constance R. Martin PhD - Endocrine Physiology
"Estrogen levels undergo substantial changes during the course of ovarian cycles. The steroids are potent stimulants for PRL release, and corresponding changes in plasma PRL have been described." - Constance R. Martin PhD - Endocrine Physiology
"Sustained high estrogen concentrations increase both insulin requirements and insulin secretion." - Constance R. Martin PhD - Endocrine Physiology
"Moreover, neurons involved in defeminzation contain aromatase enzymes that convert testosterone (but not DHT) to estrogen. The conclusion that estrogens are the defeminzing agents is supported by several findings." - Constance R. Martin PhD - Endocrine Physiology
Peat's explanation of the genesis of "Hashimoto's disease" dovetails nicely with the statistics that Mr. Kresser gave above. Because thyroiditis is so much more common in women than men, the idea that estrogen, and not some unknown root cause, triggering the onset of Hashimoto's disease is easier to accept.
Experiment
Those currently being treated for Hashimoto's may want to consider getting their PTH, whole blood serotonin, and prolactin measured. From reading Dr. Peat as well as talking to Dr. John Crisler, few estrogen tests are accurate, but the lab work mentioned above can be utilized to asses estrogen status.
