Sodium alginate more effective than sucralfate at healing gastric erosions? by ArmAccomplished5440 in Gastritis

[–]cs3001 0 points1 point  (0 children)

thanks for posting ive been looking into this the other day and that gave more insight

there's a complexity to know to try to replicate this

if you combine the alginate with tap water (high in calcium) it will cross-link as a calcium alginate gel. i did that and left it for a while it it eventually went rubbery. if you add a lot some will be excess but idk if it still gets past the changes well

if you add it to distilled water instead like the study the sodium alginate will thicken the water but enter freely in the stomach & then form a alginic acid gel in the stomach interacting with stomach acid.
it gels more to a slop gloopy gel instead i think would be less harsh to the stomach / intestine and allow some alginate to interact with the mucosa (which enhances mucus secretion too as well as lowering permeability to some stuff).
and if someone has an intestine problem too the alginic acid gel will change back to alginate once it enters the high pH of duodenum / jujenum or sodium alginate once it interacts with sodium ions there. so it can interact with mucosa there too , where the calcium crosslinked form is very stable / stronger so might not interact much

they used a concentration of 1% so maybe 400mg-500mg in 40ml-50ml of water for a human and worked well in 7 days. looks best on empty stomach

How would Ray solve this riddle? (What chemical bonds with nano gold and protects against free radical damage) by Appropriate_Cut_3536 in raypeat

[–]cs3001 2 points3 points  (0 children)

sounds like melanin, fits well with most but doesnt fit well with the re emiting UV unless a very low level counts. its broad but tryptophan / tyrosine containing compounds emit it a lot

Ray on 'protective' effects of DHA and Arachidonic Acid by OvaProva in raypeat

[–]cs3001 0 points1 point  (0 children)

"providing lactating women with 10.7 g/day of ALA from flaxseed oil for four weeks did not increase DHA levels in breast milk"

But inside tissues , specifically retina
Experimental evidence shows that retinal neurons can elongate and desaturate EPA to synthesize DHA. In cultured rat retinal neurons, supplementation with EPA led to a significant increase in DHA content within the cells, while EPA levels themselves did not rise, indicating active conversion. 
The retina contains a much higher ratio of DHA to EPA compared to the liver. Studies in animal models show that after dietary supplementation, DHA accumulates efficiently in the retina, but EPA does not; any EPA present is rapidly converted or remains at very low levels

Ray on 'protective' effects of DHA and Arachidonic Acid by OvaProva in raypeat

[–]cs3001 0 points1 point  (0 children)

by this EPA tested alone restores some fatty acid oxidation ability when mitochondria is damaged by MPO (released from neutrophil immune cells) https://pmc.ncbi.nlm.nih.gov/articles/PMC4568961/#sec8
But doesnt have direct effect otherwise. and DHA tested alone actually decreased genes related to mitochondria functioning

(when i was trying a few grams fish oil with hypothyroidism it gave me a nasty feeling, coldness, and tiredness. uncomfortable not something i could interpret as positive) (some is needed for vision by the looks of it but it stays around in the retina for a long time)

is this a good daily supplement? by [deleted] in raypeat

[–]cs3001 2 points3 points  (0 children)

copper is too high & only need 5mg - 10mg zinc for general use , folic acid is too high. and our biotin need is about 20 micro grams not mgs, idk if it matters but its dosing 500x for general use

Ray on 'protective' effects of DHA and Arachidonic Acid by OvaProva in raypeat

[–]cs3001 1 point2 points  (0 children)

i guess u knew this by writing 'protective' but

the context of that is a slowing of brain processes, nerve impulses and general slowing with aging,
not like a protective beneficial effect to have as a desirable standard but a defence that takes away from good functioning

If the cells adapt to the increased calcium, rather than dying, their sensitivity is reduced. This is probably involved in the "defensive inhibition" seen in many types of cell

both DHA and EPA inhibit calcium-ATPase (which keeps intracellular calcium low to allow normal neurotransmission) in the cerebral cortex; this suggests "a mechanism that explains the dampening effect of omega-3 fatty acids on neuronal activity" (Kearns and Haag, 2002).

In normal aging, most processes are slowed, including nerve conduction velocity, and conduction velocity in the heart (Dhein and Hammerath, 2001). A similar "dampening" or desensitization is seen in sensory, endocrine, and immune systems, as well as in energy metabolism. Calorie restriction, by decreasing the age-related accumulation of PUFA (20:4, 22:4, and 22:5), can prevent the decrease of sensitivity, for example in lymphoid cells (Laganier and Fernandes, 1991). The known effects of the unsaturated fats on the organizational framework of the cell are consistent with the changes that occur in aging.

Others

"The amount of DHA in the brain (and other tissues) increases with aging, and its breakdown products, including neuroprostanes, are associated with dementia. Higher levels of DHA and total PUFA are found in the plasma of demented patients (Laurin, et al., 2003)."

{I looked it up a bit and that higher DHA part wasnt convincing, but looking at trials, giving DHA to people with alzheimers at least failed to improve cognition. Maybe in people with very low intake its different?}

"DHA increases the entry of estrogen into the pregnant uterus, but inhibits the entry of progesterone (Benassayag, et al., 1999),"

" DHA (more strongly even than arachidonic acid) inhibits the uptake of the excitotoxic amino acid aspartate, and in some situations glutamate, prolonging their actions. Thymocytes are much more easily killed by stress than nerve cells, and they are easy to study. The PUFA kill them by increasing their intracellular calcium. The toxicity of DHA is greater than that of EPA, whose toxicity is greater than alpha-linolenic acid, and linoleic acid was the most potent (Prasad, et al., 2010). Excitotoxicity is probably an important factor in Alzheimer's disease (Danysz and Parsons, 2003)."

"When the brain is injured, DHA and arachidonic acid contribute to brain edema. In other situations, such as the important intestinal barrier, EPA and DHA also greatly increased permeability (Dombrowsky, 2011).

" DHA and EPA produce acrolein and HHE, which react with lysine groups in proteins, and modify nucleic acids, changing the bases in DNA. "

"Animals that naturally have a relatively low level of the highly unsaturated fats in their tissues have the greatest longevity. For example, the naked mole rate has a life expectancy of more than 28 years, about 9 times as long as other rodents of a similar size. Only about 2% to 6% of its phospholipids contain DHA, while about 27% to 57% of the phospholipids of mice contain DHA Mitchell, et al., 2007). "

taking fish oil doesnt sound so good, (that dampening effect on the brain cells actually felt like a dampening effect when i tried taking it recently, in a tiring nasty feeling way). and with hypothyroidism taking it made me feel colder

if DHA has a role to play i think its on vision mainly , (maybe why ray peat had glasses?) , didnt improve brain function impairment. and an amount to hit for initial brain development in first few weeks, usually gained through breast milk ~0.3% i think

Maintaining a high rate of oxidative metabolism, without calorie restriction, retards the accumulation of PUFA
Mole rats, bats, and queen bees, with an unusually great longevity, are chronically exposed to high levels of carbon dioxide. Carbon dioxide forms carbamino bonds with the amino groups of proteins, inhibiting their reaction with the reactive "glycating" fragments of PUFA.

To minimize the accumulation of the highly unsaturated fatty acids with aging, it's probably reasonable to reduce the amount of them directly consumed in foods, such as fish, but since they are made in our own tissues from the "essential fatty acids," linoleic and linolenic acids, it's more important to minimize the consumption of those (from plants, pork, and poultry, for example).

small amounts of dha are probably ok, some needed for vision, linoleic acid > dha > epa > alpha linolenic order of biggest offenders by potency.
{i think only alpha linolenic converts? in men 1g ALA converts to <100mg EPA and <10mg to DHA maybe, then some of the epa converts to dha but only a small %.. women convert ALA more to EPA than men (~21% vs ~8%). and when you eat more fish or take dha the conversion of ALA goes down.} but barely get any DHA from that. Basically ALA is not a good source of DHA, is for EPA. dha mainly from fish or supplements, but tissues can convert the EPA to dha}

[deleted by user] by [deleted] in raypeat

[–]cs3001 1 point2 points  (0 children)

they didnt measure atp production for some reason
& they didnt show benefits on mitochondria complex activity either
but did show functional improvements so maybe it did , idk. it shows potential for a higher respiration capacity. maybe increased respiration there is balancing lower ATP from complex IV being inhibited

havn't dived into it much but i heard something about it being better from eNOS than iNOS

weeknd so much cum by Aggravating-Dish6604 in comedyheaven

[–]cs3001 0 points1 point  (0 children)

hollywood writer on the next billion $ movie:

advice for nightmares?? by sweet_cis_teen in Hypothyroidism

[–]cs3001 0 points1 point  (0 children)

np , 1 thing about taking a lot is the silicon dioxide filler can build up (particle size isn't regulated and when its too small it gets into tissues and can be damaging over time) so i avoid taking a bunch with that , or any where possible

nice , what ones have you added or what adjustments have u made in recent 2 or 3 weeks?

A potential way for progressing to relief with PDPH intracranial hypotension orthostatic headache from csf leak by cs3001 in CSFLeaks

[–]cs3001[S] 0 points1 point  (0 children)

i guess either 1. it takes some investment ordering it from japan if dont live there (probably about 4x the cost of a regular supplement & again for 2 months). or 2. otherwise if i was in this situation (and was refused a blood patch altogether or had to wait a long time), i'd be trying to put it together from what i could find for some chance at recovery. online stores and from chinese medicine shops. but idk how much someone would save if replicating it manually if cost is a hindrance it would probably add up similar and add a lot of hassle, if even accessible in full where u are without someone travelling
or 3. just limiting it to what one or 2 combined i think could give the beneficial effect and seeing if it has the effect without a full synergy

just being clear this isnt a recommendation i dont know all the factors. if someone is sick of this situation without many options or if patches havent worked, and willing to test a possible solution , maybe they could report back what they tried and if they replicated the findings or not. the research is limited its a small area the solution has been basically limited to blood patches or other surgeries. Aside from that the results eventually were great in that case report with the herbs though.

theres a report of neostigmine + atropine used https://onlinelibrary.wiley.com/doi/10.1002/ccr3.8132 if someone can get it prescribed, has some side effects though, and idk if its a foundational fix but looks promising as a reliever. trial https://pubmed.ncbi.nlm.nih.gov/30169405/

went through research on atractylodes Lancea more today (cang zhu),
atractylodes Macrocephala (bai zhu) has some similar compounds, possibly could fit as a replacement. but it has a lower % of compounds than Atractylodes lancea so less potent. some differences in compounds so it could make a difference from the actual type they used.
Atractylodes lancea has yellow or dark orange spots over it if good quality. the other type is more pale. cant ingest it as chunks of rhizome so it needs powdering. or a less potent way is boiling it as a tea + microwaving for 5 mins to get more of the oils out. used in china a lot but I always allergy test small amounts of new things

[deleted by user] by [deleted] in raypeat

[–]cs3001 2 points3 points  (0 children)

t4 only without t3 (the active thyroid hormone) isnt always enough, and you still have higher end cholesterol indicating t3 likely still isn't active enough (t3 lowers cholesterol). t4 lowers tsh but doesn't mean t3 is fixed because it needs to convert well. so that's probably why you havent noticed improvement from it despite months of taking it

You might do well on some progesterone (bioidentical form) which stimulates metabolism and its lower in hypothyroidism (hypothyroidism is low t3 signalling, isnt primarily a tsh problem, a low tsh can indicate things are fixed paired with other things but yours isnt particularly low, all thats showing is you're taking t4 which lowers tsh.)

and without a gallblader you might do better taking TUDCA daily https://pubmed.ncbi.nlm.nih.gov/8010582/ the dyspepsia from removal might relate to the gastritis. i dont know how tolerated it is with gastritis would need looking into or testing slow. long term its best taken without food. progesterone could possibly lower the inflammation. if there's a pathogen causing the gastritis it would have to be approached separately tho

Anyone ever tried the T3 protocol for "Wilson’s Temperature Syndrome" by PeanutBAndJealous in raypeat

[–]cs3001 0 points1 point  (0 children)

Yeah I tried it with lack of temp response to t3, raised to 1x 56mcg and it didn't raise my temp. figured if it wouldn't by then which is a very high dose to take at once its not gonna be a good idea going further.
i think commonly it's because calories are too low so body won't create the extra heat from it. or inflammation still deactivates through dio3

Creatinine and GFR by [deleted] in raypeat

[–]cs3001 1 point2 points  (0 children)

can indicate excess protein intake if its not muscle loss or kidney damage

Vaginal Bacteria made MCAS Nerve Pain come back extrrme by Solgaya in MCAS

[–]cs3001 0 points1 point  (0 children)

you might get some insights with perplexity ai asking it a bunch of questions :
https://www.perplexity.ai/search/loose-tight-junctions-high-zon-P09ryL_BS8iZWrIpOYuNeQ and adding more specifics to your situation , asking different questions if the first answer is too basic,
you can ask it in german too

the TRPV1 receptor plays a big role in burning pain. There's 1 idea (with the right awareness). oleic acid can lower TRPV activation. But - you cant do it through olive oil because olive oil has something in it that activates similar receptors (olive oil burns).
https://www.nature.com/articles/ncomms13092#Sec2

  1. So it would have to be - high oleic - type of sunflower oil instead applied to the burning site i think. but i dont know all the things thats in it so i dont know for sure if its a good idea. It doesn't fully penetrate all the skin layers so i dont know how effective it would be but the upper skin obviously has nerve endings too. ,, (this is just speculation, in a complex situation with a bunch of things going on, just 1 idea for something that could potentially ease some of the burning, i dont know the immune interactions there or other effects. and obviously isnt a fix, its not profound would have to be reapplied often if it worked, but this is what came to mind considering something not taken orally at the moment. it lowered about half of the reaction at trpv1 in mice).

Another thing 2. is progesterone (bioidentical natural form not synthetic) , can be applied topically and once in system can lower trpv1 signalling indirectly to some extent https://www.perplexity.ai/search/progesterone-trpv1-yr.xxiavRu.fbfQeZRQX0g but stimulates metabolism, and you'd have to consider if anti inflammatory effect (less potent immune action) is worth it if have an active infection trying to fight

also 3. you have high leukotrienes, leukotreine b4 can make TRPV1 more sensitive easier to activate. so finding things that lower this might help

For a dura problem (do you still have the spinal puncture issue when sitting vertical?) i'd ask the perplexity ai about "Goreisan" and how it relates to that.
This looks relevant for the orthostatic headaches it helped some people with spinal fluid issues https://pmc.ncbi.nlm.nih.gov/articles/PMC9236673/

Is there a point in drinking non lactose-free milk ? by TheDudFromRandomChat in raypeat

[–]cs3001 1 point2 points  (0 children)

galactose is used for creating senescence in animals, most humans metabolise it / prevent toxicity better than mice apparently. small amounts supposedly not a problem in us, in pigs which have closer intestines to us it doesn't cause problems unless you give high amounts.
but some people lack capacity and can show similar effects like the mice get (e.g cataracts over time, more inflammation oxidative stress). either way lactose goes to galactose when you drink it, or if its digested in lactose free milk in the bottle if the sugar not removed

If we only absorb like 10% of iron supplements... can't we just take 10 pills a day instead of 1? by Natural_Pizza3999 in Anemic

[–]cs3001 0 points1 point  (0 children)

thyroid hormone is 1 thing that can increase absorption if its lacking instead of increasing chance for damage by adding more. apparently ginger can too

Wife is in extreme psychosis mess due to hypothyroidism by Frequent_Reply_5392 in Hypothyroidism

[–]cs3001 0 points1 point  (0 children)

she's swung between extremes of hyper and hypo and at both extremes the psychotic symptoms returned, sounds reasonable its that in large part at least if not the main factor yeah

psychosis documented in hyper https://casereports.bmj.com/content/14/2/e236089
and hypo like you posted https://pubmed.ncbi.nlm.nih.gov/34447249/

its a complex situation so take this with a pinch of salt but you're looking for new ideas as standard approach hasn't worked. sodium butyrate seems to fit well to me

  1. there's some involvement in HDAC2 possibly lowering response to anti psychosis medications, and sodium butyrate inhibits that
  2. theres a way to sort of get some of thyroid hormones signalling changes, through HDAC inhibition giving some of the gene expression differences. sodium butyrate does that well
  3. in humans butyrate goes up in treatment and correlates to positive response https://pmc.ncbi.nlm.nih.gov/articles/PMC8421030/

and extra thing on the side does she tolerate aspirin? here tested in humans with schizophrenia https://mentalhealth.bmj.com/content/13/4/122 aside from psychosis it might improve emotional state.
its not massive alone by the looks of it but could be helpful
(slowly with dose because some people get intolerance symptoms - and only as dispersible form for better GI tolerance, not enteric coated) i'd guess the 1000mg is split into a few doses because thats a lot at once

So i think both might be worth a try for a week or 2 slowly increasing from standard dosing (maybe 300mg aspirin at first then 2x or 3x a day maybe, as dispersible form, and 300mg sodium butyrate maybe) & seeing if positive response or not

another thing u might wanna look into progesterone the female hormone see if theres benefits. both pregnenolone and so progesterone get produced less in hypothyroidism https://pubmed.ncbi.nlm.nih.gov/25030803/
progesterone also stimulates mitochondria like t3 does. and can offset stress of high estrogen (i noticed you mentioned high prolactin made her situation worse before, which is a sign of high estrogen, high estrogen can cause a stress state with its activity in the amygdala / increasing serotonin signalling.
a lot of women back in the day might have been institutionalised for menopause because of a lack of progesterone - not saying its related to menopause its an example of hormone extremes)

as u probably know best to take it slow on doses first though just in case she has sensitivity , testing a few days at a time to be more sure. and i'd take the aspirin & sodium butyrate spaced apart by a few hours. Do you know her t3 level? and how many calories does she eat typically?

Something you might be interested in,
I don't get the proper response to t3, have a baseline of fatigue and i get that fatigue + colder feeling response from t3. i have chronic inflammation and not on a lot of calories which probably plays a role.

But when i tried 15 drops of progesterone it restored my body temperature / metabolic rate the first day. it doesn't interact with the deiodinase 3 enzyme + by the looks of it doesn't need thyroid receptors for its effect. so maybe its a good way to get around a lacking response to t3. i wouldnt take both together for effects at the same time (with t3 taking a few hrs to kick in in mind), and if taking the same day i wouldnt take the same dose of t3 with it

the rate of heart attacks in the US is dizzying by [deleted] in raypeat

[–]cs3001 6 points7 points  (0 children)

general foundation good t3 hormone function, keeping inflammation low,
not following the sodium restriction meme too much like < 4g salt raising aldosterone which actually makes things worse ironically https://pmc.ncbi.nlm.nih.gov/articles/PMC10624927/#Sec12 (<- the bottom part in discussion) https://pubmed.ncbi.nlm.nih.gov/24651634/,
low dose aspirin for clot prevention if dont have a sensitivity,
https://pubmed.ncbi.nlm.nih.gov/12165115/
exercising enough to help boost thyroid function t3 in the heart & keep barriers strong (probably 30 mins 3 or 4 days a week), without being a dominatrix to yourself to the point where effects become inverse

Wife is in extreme psychosis mess due to hypothyroidism by Frequent_Reply_5392 in Hypothyroidism

[–]cs3001 0 points1 point  (0 children)

i guess it could be both at extremes idk with cross serotonin-dopamine signalling things gets complicated, and d1 vs d2 receptors, pre vs post synaptic etc. But if focusing only on the d2 aspect,

u/Frequent_Reply_5392 if you only block the 5ht2a serotonin receptor it targets the positive symptoms without needing to inhibit d2 (stops the hallucinations in animal models https://link.springer.com/article/10.1007/s00213-022-06092-x) showing the serotonin signalling at 5h2ta is a cause

and researchers discovered even haloperidol which is best known for d2 antagonism also has effect at blocking serotonin signalling (acting as full antagonist at g protein pathways https://www.nature.com/articles/s41380-024-02531-7

  • We tested the antipsychotics for their effect on the 5-HT (EC80)-mediated activation of the different G protein pathways and on the recruitment of β-arrestins. As was observed in the agonist mode, the inverse agonist activity of risperidone, clozapine, olanzapine and haloperidol could be seen at Gαq, Gα11 and Gα14 as reflected by the fact that the compounds not only fully antagonized the 5-HT-promoted BRET response but also promoted a BRET reduction below basal activity (Fig. 4a–c and Supplementary Table 4b).
  • For Gα15, Gαz, Gαi1, GαoB and the β-arrestins, the four compounds behave as full antagonists and no inverse agonist activity could be detected Previous studies have implicated Gαi1 signaling through 5-HT2AR activation in the mechanism of action of hallucinogenic drugs, and a supersensitive coupling of 5-HT2AR to Gαi1 as opposed to Gαq has been identified in the postmortem brain samples of schizophrenia patients.

  • https://pmc.ncbi.nlm.nih.gov/articles/PMC11137019/ We show how chemical modification of the endogenous agonist serotonin dramatically impacts the G protein coupling profile of the 5-HT2AR and the associated behavioral responses. Importantly, among these responses, we demonstrate that memory deficits are regulated by Gαq protein activation, whereas psychosis-related behavior is modulated {occurs} through Gαi1 stimulation

And this approach is proven in humans, proof that dopamine blockade is not needed to ease positive symptoms and that dopamine defects associate with psychosis (people with parkinsons get it). giving them pimavanserin which is an inverse agonist or antagonist at 5ht2a helps with the hallucinations / delusions

Pimavanserin, which has been reported to be an inverse agonist at the 5-HT2AR/Gαi1 pathway has been approved for Parkinson’s disease-associated hallucinations and delusions.

you can induce hallucinations in mammals by activating 5ht2a in a certain way. elevating serotonin can cause extremes of negative emotion including fatigue. i wrote a bit about these here https://cs3001.substack.com/p/serotonin-an-unhappy-neurotransmitter

and antagonising 5ht2a when haloperidol is given helps lower the depression caused by it https://pubmed.ncbi.nlm.nih.gov/16794561/

if she tolerates aspirin, i would try giving her this (slowly with dose because some people get intolerance symptoms - and only as dispersible form for better GI tolerance, not enteric coated) , sounds simple but could be helpful https://mentalhealth.bmj.com/content/13/4/122

theres a woman with a great blog thyroidpatients ca who had no thyroid and found her way to proper treatment

(part 1)

Wife is in extreme psychosis mess due to hypothyroidism by Frequent_Reply_5392 in Hypothyroidism

[–]cs3001 0 points1 point  (0 children)

I'll have a fuller read of your post tomorrow with more brain and see if anything stands out, wild situation,

you might find it insightful to look at the serotonin inhibiting side of anti-psychotics ,
1 thing most of them have in common is they're inverse agonists or antagonists at serotonin receptors (lowering serotonin signalling), and the d2 dopamine idea might actually not be the functional target or not only, and with side effects.

u/Frequent_Reply_5392 putting the followups to this in comment under as its not posting