
Progesterone and Thyroid hormone
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Though each hormone is unique, hormone balanceinvolves a complex harmonious blend of all hormones. I tend to think or hormones asinstruments in an orchestra - the harmony we seek is the proper contribution of all theinstruments together not only in pitch but also in volume and rhythm. The same is true ofsex hormones and thyroid hormone.
In my medical practice, I was impressed with the much greater number of women takingthyroid supplements for hypothyroidism (low thyroid) than men. Thyroid is the hormone thatregulates metabolic rate. Low thyroid tends to cause low energy levels, cold intolerance,and weight gain. Excess thyroid causes higher energy levels, feeling, feeling too warm andweight loss.
The thyroid gland makes from tyrosine, one of the amino acids and iodine, two versionsof thyroid hormone, one containing four atoms of iodine (thyroxine, T4) and anotherversion containing three atoms of iodine (triiodothyronine, T3) Both versions are thenenveloped in a relatively large glycoprotein complex called thyroglobulin and stored inthe thyroid gland.
To be released into the bloodstream for circulation throughout the body, the hormonesare separated from thyroglobulin and bound to a much smaller globulin (thyroxine-bindingglobulin) or albumin. However, only 0.5 percent of thyroid hormone is "free" tobe biologically active. It is the "free" hormone that can leave the bloodstreamand enter body cells, where it meets with a special receptor and thereby modulates thecells metabolic rate. Thyroids actions in the cell is to increase thebiosynthesis of enzymes, resulting in heat production, oxygen consumption, and elevatedmetabolic rate. Thyroid stimulates the release of free fatty acids from adipose (fat)tissue, stimulates the oxidation of fatty acids (energy production), and reducescholesterol by oxidizing it into bile acids. Thyroid also stimulates enzymes for proteinsynthesis and, when present in excessive amounts, can catabolize (destroy) muscle protein.
As with the sex hormones, a neural center in the hypothalamus monitors the blood levelof T3 and T4. If the levels are low, the hypothalamus sends a message,thyrotropin-releasing hormone (TRH), to the pituitary, which then sends its message,thyrotropin, also known as thyroid-stimulating hormone (TSH), through the bloodstream tothe thyroid gland to stimulate it to make more thyroid hormone. If the thyroid levels risetoo high, the hypothalamus detects this and reduces or stops its TRH, which results inlower TSH and the consequent diminished production of thyroid hormone. This is the samenegative feedback system our body uses to regulate sex hormone levels. What differenceshould gender make to the incidence of hypothyroidism? As I became aware of estrogendominance syndrome, I noticed that the taking of thyroid supplements was especially commonin women with this condition. When I attempted to correct their estrogen dominance byadding progesterone, it was common to see that their need for thyroid supplementsdecreased and could often be successfully eliminated. Thus I became aware that estrogen,progesterone, and thyroid hormones are interrelated.
Many of these women had come to me from other doctors offices for PMS orosteoporosis prevention and/or treatment. On reviewing the laboratory studies that had ledto their presumed diagnosis of hypothyroidism, I often found that their T3 and T4 levelshad been normal and their TSH levels only slightly elevated. Their thyroid supplement hadbeen prescribed on the basis of hypothyroid-like symptoms such as feeling tired orsluggish, a little cold intolerance, and thinning hair, for example. While the thyroidmedication had improved their tiredness a bit it had not corrected the symptoms I hadlearned to associated with estrogen dominance such as fat and water retention, beastswelling, headaches, and loss of libido. When their hormones were balanced, meaningprogesterone deficiency was adequately treated, not only did their estrogen dominancesymptoms decrease or disappear but sop did their presumed hypothyroidism!
Let us look at this situation again. Estrogen causes food calories to be stored as fat.Thyroid hormone causes fat calories to be turned into usable energy. Thyroid hormonecauses fat calories to be turned into usable energy. Thyroid hormone and estrogen haveopposing actions. The "central command post" of this opposition may be in thehypothalamus, the pituitary, they thyroid gland, or the body cells where the hormonesenact their destined roles. My hypothesis is that estrogen inhibits thyroid action in thecells, probably interfering with the binding of thyroid to its receptor. Both hormoneshave phenol rings at the corner of their molecule. Estrogen may compete with thyroidhormone may never complete its mission, creating the hypothyroid symptoms despite normalserum levels of thyroid hormone. Progesterone, on the other had, increases the sensitivityof estrogen receptors for estrogen and yet at the proper level, inhibits many ofestrogens side effects. That is what is meant when we say that progesterone opposesestrogen: The lack of progesterone in a woman still making estrogen or taking estrogensupplements leads to the condition of unopposed estrogen.
I will leave the exact mechanism of action to the biochemists, but it is clear to methat symptoms of hypothyroidism occurring in patients with unopposed estrogen(progesterone-deficient) become less so when progesterone is added and hormone balance isattained.
Another common thyroid dysfunction is Hashimotos thyroiditis, which is anautoimmune inflammatory process of the thyroid gland. That means the body is creatingantibodies against the cells unknown. However, inhibitory antibodies bind to TSH receptorsby which this disorder results in inefficient production of thyroid hormone. As thedisease progresses, cells of the thyroid gland are destroyed and inflammation occurs,along with fibrous deterioration of the entire gland.
Autoimmune disorder in general are thought to be triggered by transient viruses insusceptible people; the virus triggers antibodies against some protein component of thevirus. By some probably minor fluke, the antibodies attack similar proteins in certainbody tissues, in this case the thyroid. Corticosteroids block this attack by onesown antibodies. Diagnosis is made by detecting the presence and serum levels of theparticular antibody. In some people, Hashimotos thyroiditis also causes leakage ofexcess T3 and T4 into the serum, resulting in a hyperthyroid state(thyroidtoxicosis)usually of short duration. The usual treatment of Hashimotosthyroiditis is suppression of gland function by full doses of thyroid medication, such asthyroxine and /or triiodothyronine.
It has been my experience in practice that when a woman with Hashimotosthyroiditis is given progesterone for osteoporosis, for example, there results a gradualdiminution in the severity and sometimes a complete resolution of the thyroiditis problem.One can hypothesize that estrogen dominance may have had a hand in triggering the errantantibodies and thus correcting the estrogen dominance leads to gradual correction of theproblem. Progesterone is also the main precursor of corticosteroids and inprogesterone-deficient women, restoration of normal progesterone levels may enhance normalcorticosteroid production, thus suppressing the autoimmune attack. Hope it helps.
This is long but may explain some things for you. It isfrom the book "What Your Doctor May Not Tell You About Menopause"
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