Assumimg I have dysbiosis gut is made worse by any soluable fiber and insoluable
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@Mossy found this:
Some studies show it just about negates the value of the milk you have with it, so you probably have to eat extra milk--more than you think--but two quarts of milk takes care of just about everything. — Ray Peat
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@Mossy
The oat bran, I read that a cup of the cooked stuff--it's fairly filling, so a cup is a big serving--it has only 88 calories, where regular oatmeal has maybe 250 or so for the same thing--so it does provide some carbohydrate, but it's strongly buffered by the presence of the higher fiber content. And studies in animals showed that over a long run, you might have to worry about some of the breakdown products of the soluble fibers that can have an estrogenic effect, but in the short run--up to a year or so--its effect is a matter of the bulk and acceleration of the intestine, so it has an anti-estrogen effect for people who have been re-absorbing the estrogen that their liver tries to excrete. — Ray Peat -
@LetTheRedeemed said in Assumimg I have dysbiosis gut is made worse by any soluable fiber and insoluable:
Elevated estrogen basically causes all skin conditions, and a quick google search yielded this:
Common skin-related die-off symptoms include rashes, itching, redness, increased sensitivity, acne breakouts, dryneStill no let up of redness, when i come out of the shower my has so much dead skin from the redness trying to heal
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@Samyo what were/are you doing?
honestly it warrants a consultation because the variables are so diffuse.
What I know of your symptoms seems to be pointing toward SIBO and poor liver function. I would keep looking for information regarding that.
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@LetTheRedeemed i do not think coffee and sugar is doing me any good?
Whats outside the peat realm that can help my liver ive exchausted the peat ways with no solution
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@Samyo coffee/sugar may not be good right now then. See how you feel with and without them.
I believe Ray said something like until you get the gut fixed, going after liver/thyroid won’t work well because you will have a continued source of estrogen and serotonin elevation via gut health, impacting liver/thyroid.
Things for liver include t3, aspirin, niacinamide, often in that order.
I’d strongly suggest doing a consultation with Danny Roddy. there’s not a lot he hasn’t seen, and has the experience of hundreds of consults, plus all Ray’s inputs from his consulting time.
He put me on the right track after 2 years floundering in my own efforts
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@LetTheRedeemed well coffee sugar make me feel great...
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@Samyo then why did you say:
i do not think coffee and sugar is doing me any good?
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No it doesn't. It relies on MMC function which is controlled by the ENS which is controlled by...dun dun dun dun....serotonin receptors in the gut scary stuff. Just because thyroid provides cellular energy does not mean it is also dictating the functioning of every single biomechanical function in the body.. This is the logical fallacy that a lot of Peat proponents use to insert thyroid function into everything and being the deciding factor in everything. It can be a kink in the chain, but it's not the entirety of the chain
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"I believe Ray said something like until you get the gut fixed, going after liver/thyroid won’t work well because you will have a continued source of estrogen and serotonin elevation via gut health, impacting liver/thyroid"
Ray said lots of things about gut health and very little of it makes sense. Estrogen only has a modulatory role in gut transit and gut function in general. There's no way for it to greatly influence or impact homeostasis in the gut. Again with the serotonin shit..you do know that the very thing that allows the intestines to contract and perform a bowel movement rely almost exclusively on serotonin, right? Both the ENS and MMC rely exclusively on multiple 5-HT receptors given that the gut houses of 95% serotonin receptors and produces 90% of serotonin. it's in everything from the enterocytes to the microvilli. The gut does not and cannot function optimally without it. Cascara anthroquinones, the darling of Peats bowel stimulants retards MMC by down regulating serotonin receptors in the gut and can also damages enteric neurons due to how powerfully it causes contractions in intestines. Those painful cow patties it produces after using it for a while and senna for that matter are because the MMC and ENS are not doing what they are supposed to be doing, and they need serotonin receptors to do it. There's not some magical alternate pathway you can tap into through focussing solely on cellular respiration. That's just how it is
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Hi,
What about a re-initializing process, in a soft way when the natural postprandial contractions occurs through the MMC.
I’ve done it.
Just to be clear about the MMC, being a natural movement but in a sleepy phase.
The migrating motor complex (MMC) is an electrical and contractile activity of digestive motility which takes place in the inter-digestive periods (between two meals), and interrupted by food intake. Each MMC is accompanied by an increase in gastric, pancreatic and duodenal secretions. They are thought to serve to evacuate contents in the small intestine between meals, and also to transport bacteria from the small intestine into the colon. An alteration of this phase notably favors the development of chronic bacterial colonization of the small intestine, a source in particular of bloating, diarrhea, or even steatorrhea, of the majority of food intolerances. When contractile activity is low, we then speak of lazy intestines. Support and rehabilitation is often necessary, with a prokinetic. -
@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.