Previously, I’ve posted studies showing the negative hormonal effects of many pharmaceutical antidepressants. Particularly, the SSRI class tends to lower androgens (hormones associated with masculine behaviors, such as confidence, relaxation and motivation), but their effects in the brain oppose their peripheral effects.
Antidepressants almost universally raise allopregnenolone (a neurosteroid, low levels of which appears in depression) and antagonize the 5-HT3 receptor (a serotonin receptor.) The “antagonism” of a serotonin receptor means they act in a manner opposite to serotonin in the brain: so these drugs have anti-serotonin effects in the brain, but not in the body, where they often cause permanent sexual dysfunction and accelerate the aging process.
The active thyroid hormone, liothyronine (also known as T3) speeds the breakdown of serotonin in the body and effectively treats depression. Hypothyroidism also appears in anxiety disorders.
It’s interesting to note the co-morbidity among fibromyalgia, irritable-bowel syndrome (IBS) and anxiety disorders. T3 itself promotes peristalsis (the contraction and movement of digested food along the intestine, eventually in a bowel movement.) Hypothyroidism (or a lack of T3) often results in chronic constipation, but some individuals adapt to the decreased level of thyroid hormone.
Without adequate T3, waste ferments in the intestine, causing inflammation and releasing endotoxin ( a nasty metabolic by-product of a certain type of bacteria in the gut, specifically negative-gram bacteria.) Endotoxin causes a cascade of inflammatory reactions.
Starch (such as grains, legumes, beans and even tubers) feed bacteria and amplify the production of endotoxin, but the starch particles themselves can move through the intestinal wall (called presorbtion) and into the blood, where they activate the immune system (much like endotoxin.) Consumed starch both contributes to endotoxin and directly presorbs through the intestine, thus causing an immune reaction.