@CurmudgeonApple
Ray:
"The normal intestine contains about 95% of the serotonin in the body (and the brain normally contains only about 1%), and in the normal person only about 1% of the dietary tryptophan is converted to serotonin. But in an advanced case of carcinoid, 60% of the tryptophan can be turned into serotonin. Especially if the tumor has invaded the liver, the serotonin won't be destroyed by the liver in the usual way, and will circulate in the bloodstream at high levels, producing symptoms of flushing, sweating (sometimes dark-colored), diarrhea (serotonin stimulates small intestine smooth muscle, but inhibits the large [Bennett & Whitney, 1966]), nausea, anxiety, reduced urination, muscle and joint pains, and, in late stages, very often cardiovascular disease (especially inflammation, fibroma and calcification of the valves in the right side of the heart) and aggressive behavior (Russo, et al., 2004) and psychosis."
The bioenergetic context is not saying there is never a context for serotonin. There is a study in dogs showing high thyroid causes MMC independently of the presumed gut regulating hormones... implying it also has a role in gut regulation - likely a synergism at play.
Ray also stated that in a compromised intestinal state the gut can over produce serotonin, and with weakened gut, the serotonin crosses the intestinal barrier into the blood stream (not just endotoxin does that) - ergo staying away from fermentable starches and including antibiotic foods is crucial in such a state.
Food for Thought
Ray:
"Following the recognition that the SSRI drugs were causing osteoporosis, it was discovered that the serotonin produced in the intestine causes bone loss, and that inhibiting intestinal serotonin synthesis would stop bone loss and produce a bone building anabolic effect (Inose, et al., 2011). One group that had been concentrating on the interactions of genes commented that, recognizing the effects of intestinal serotonin, they had suddenly become aware of 'whole organism physiology' (Karsenty and Gershon, 2011).
"In previous newsletters I have talked about the ability of intestinal irritation and the associated increase of serotonin to cause headaches, asthma, coughing, heart and blood vessel disease, muscular dystrophy, flu-like symptoms, arthritis, inflammation of muscles and nerves, depression, and inflammatory brain diseases."
- Gastroenterology. 2011 Aug;141(2):439-42. The importance of the gastrointestinal tract in the control of bone mass accrual. Karsenty G, Gershon MD
All technical debate aside, I can only assume you've not experimented with thyroid hormone much (or were relatively healthy compared to many extreme cases), as this is a very commonly recognized impact from it's use for a whole lot of people - including myself. To discount that, is to discount the success with digestive function and thyroid use for thousands of people.
Thyroid disorders and gastrointestinal dysmotility: an old association:
Gastrointestinal motility symptoms may be closely related to thyroid diseases. Sometimes, such symptoms are the only thyroid disease-related clue although the degree of the symptoms may vary. The exact mechanism of action of thyroid hormones on gastrointestinal motility is not completely understood, however, a clue lies in the fact that muscle cell receptors can be directly acted upon by thyroxines. Both hypo- and hyperthyroidism can cause impairment of gastrointestinal motility, modifying structure and function of pharynx and esophagus, and regulating esophageal peristalsis through neuro-humoral interaction. In hyperthyroid patients, alterations of postprandial and basic electric rhythms have been observed at gastro-duodenal level, often resulting in slower gastric emptying. Gastric emptying may also be delayed in hypothyroidism, but an unrelated gastric mucosa-affecting chronic modification may also cause such pattern. Hyperthyroidism commonly show malabsorption and diarrhea, while hypothyroidism frequently show constipation. In summary, it can be stated that symptoms of gastrointestinal motility dysfunction can be related to thyroid diseases, affecting any of the gastrointestinal segment. Clinically, the typical thyroid disease manifestations may be missing, borderline, or concealed because of intercurrent sicknesses. Motility-linked gastrointestinal problems may easily conceal a misdetected, underlying dysthyroidism that should be carefully analyzed. Here, we aim to elaborate on the associations between thyroid disorders and GI dysmotility and the common clinical manifestations associated with GI dysmotility.
Introduction
The metabolic activity of most of the body organs is regulated by thyroid hormones (Pirahanchi et al., 2024). Hence, it is quite common to find thyroid diseases in the general population. Iodine-replete communities show spontaneous hypothyroidism prevalence of 1%–2%; it is also 10 times more commonly found in women as compared to men while older women are more likely to be affected (Vanderpump and Tunbridge, 2002). In women, hyperthyroidism prevalence is between 0.5% and 2% in iodine-replete communities; and is nearly 10 times more than in men (Vanderpump and Tunbridge, 2002). Nearly 8% women and 3% men are affected by subclinical hypothyroidism, defined by normal levels of thyroid hormones and high levels of serum thyroid stimulating hormone (TSH) (Fatourechi, 2009). In absence of TSH-secretion inhibitory medication or any diseases (non-thyroidal illness, hypothalamic, or pituitary), almost 3% of the population is affected by subclinical hyperthyroidism, defined by normal levels of thyroid hormones and low levels of serum TSH (Fatourechi, 2009). Thyroid disorders can be linked with gastrointestinal (GI) diseases or GI symptomatology (Kyriacou et al., 2015). Alternatively, non-thyroidal disorders can also be associated with GI diseases, resulting in thyroid function disruption.
Physiology, Thyroid Stimulating Hormone:
Once T3 binds to its receptor in the nucleus, it activates DNA transcription, followed by mRNA translation, and new protein synthesis. These new proteins influence many organ systems, promoting growth as well as bone and central nervous system (CNS) maturation. T3 and T4 act on almost all cells in the body to increase the basal metabolic rate. Specifically, they increase the synthesis of Na?/K?-ATPase, leading to an increase in oxygen consumption and heat production. They also act on B1 receptors in the heart to increase heart rate and contractility through increasing the number of beta-1 receptors on the myocardium such that the myocardium is more sensitive to stimulation by the sympathetic nervous system. Thyroid hormones also activate metabolism, with an increase in glucose absorption, glycogenolysis, gluconeogenesis, lipolysis, and protein synthesis and degradation (net catabolic).[5]
One would infer that proper glucose metabolizing and protein synthesizing intestinal walls, maintain integrity of the barrier between the material in digestive transit, and the bloodstream. That's why I included the above study.
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