Supplementary Choline Raises Risk Of Blood Clots; Aspirin To The Rescue

InChristAlone

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Not to mention coffee is cholinergic.
 

Amazoniac

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Eggs (again) are also capable of this effect:

Effect of egg ingestion on trimethylamine-N-oxide production in humans: a randomized, controlled, dose-response study

"Free sucholine is absorbed in the small intestine via mediated transport (6), whereas phosphatidylcholine is not converted to choline within the intestinal lumen [it is absorbed intact via the lymphatic system or is hydrolyzed by pancreatic lipases and absorbed as glycerophosphocholine (7)]. On the basis of these differences, dietary free choline (the substrate for trimethylamine formation by bacteria) but not dietary phosphatidylcholine should result in TMAO formation. Although the bacterial degradation of choline in the human gastrointestinal tract has been well documented (8), we previously reported that phosphatidylcholine was not readily used as a substrate for the formation of trimethylamine by gut microbes (9). Furthermore, clinicians who used supplemental choline to treat Huntington’s disease noted that patients developed fishy body odor (the odor of trimethylamine) when given large doses of choline (10) but did not develop this fishy odor when molar-equivalent doses of phosphatidylcholine (lecithin) were administered (11)."

"Tang et al (3) and Wang et al (4) reported that dietary choline is in part converted to trimethylamine and oxidized by liver to form TMAO. Although it was well documented that bacterial metabolism of choline to form trimethylamine occurs in the human gastrointestinal tract (8), we previously thought that phosphatidylcholine was not a substrate for TMA-forming bacteria (9). Therefore, eggs, which are a major dietary source of choline in the form of phosphatidylcholine (5), were not expected to result in the formation of TMAO. Recently, Tang et al (3) reported that people who ate 2 eggs formed TMAO. In the current study, we confirmed this finding and current additional information on effects of a range of egg doses on plasma and urinary TMAO concentrations and the variability in TMAO responses in individuals. We showed that ~11–15% of dietary total choline is converted into TMAO after consumption of meal that contained eggs."

"TMAO is excreted into urine via the kidney, and thus, the plasma TMAO concentration may be a marker for decreased renal function associated with atherosclerosis of the renal vasculature rather than a direct cause of atherosclerosis in humans."

"In our study, the amount of TMAO in plasma or urine varied between individuals by 4-fold from the equivalent dietary choline intake. People are different from one another in types of microbes that live in the gastointestinal tract (22), as were our subjects (see Supplementary Figure 1 under “Supplemental data” in the online issue), which is a characteristic that can profoundly affect metabolism (23) and may mediate differences in the trimethylamine formation from dietary choline. Alternatively, these differences in TMAO formation from dietary eggs may be due to differences in hepatic oxidation of trimethylamine mediated by 2 flavin-containing monooxygenase (FMO) family members FMO1 and FMO3 (1). Hepatic FMO3 expression in mice is reduced in males compared with females because of downregulation by androgens (1). In our study, men (subjects 3 and 4) produced more TMAO than did women after each egg dose (Figures 2 and 3), which perhaps indicated a profound difference in the regulation of FMO3 activity in humans."

"We observed that increased plasma TMAO concentrations in subjects seen after a single dose of eggs, ranging from 1 to 6 eggs, was not associated with an increase in hsCRP (which is a measure of inflammation) or oxidized LDL."

"[Two different] studies suggested that, although the consumption of eggs may increase the generation of TMAO, this increase is not necessarily associated with an increase in cardiovascular risk markers."
 

ddjd

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Haidut do you know whether this study about the effects of Riboflavin in reversing the fishy odour caused by betaine/TMG supplementation, might also point to the possibility of Riboflavin reversing the damage caused by TMAO ?

Riboflavin-Responsive Trimethylaminuria in a Patient with Homocystinuria on Betaine Therapy

"A 17-year-old female patient with pyridoxine non-responsive homocystinuria, treated with 20 g of betaine per day, developed a strong body odour, which was described as fish-like. Urinary trimethylamine (TMA) was measured and found to be markedly increased. DNA mutation analysis revealed homozygosity for a common allelic variant in the gene coding for the TMA oxidising enzyme FMO3. Without changing diet or betaine therapy, riboflavin was given at a dose of 200 mg per day. An immediate improvement in her odour was noticed by her friends and family and urinary TMA was noted to be greatly reduced, although still above the normal range.

Gradual further reductions in TMA (and odour) have followed whilst receiving riboflavin. Throughout this period, betaine compliance has been demonstrated by the measurement of dimethylglycine (DMG) excretion, which has been consistently increased. Marked excretions of DMG when the odour had subsided also demonstrate that DMG was not the source of the odour.

This patient study raises the possibility that betaine may be converted to TMA by intestinal flora to some degree, resulting in a significant fish odour when oxidation of TMA is compromised by FMO3 variants. The possibility exists that the body odour occasionally associated with betaine therapy for homocystinuria may not be related to increased circulating betaine or DMG, but due to a common FMO3 mutation resulting in TMAU. Benefits of riboflavin therapy for TMAU for such patients would allow the maintenance of betaine therapy without problematic body odour."
 

ddjd

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another peaty substance apart from aspirin which can reduce TMAO

Meldonium
Meldonium is an anti-ischemic medication that increases blood flow and oxygen supply to the body.

This drug decreased blood TMAO levels in eight healthy adults on TMA-rich diets by increasing the elimination of TMAO through urine [68].

In rats, meldonium reduces the production of TMA from L-carnitine and, thus, decreases TMAO levels. Twenty-four hours after meldonium treatment, the TMAO levels in urine were 3.6 times lower [69].
 

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Not to mention coffee is cholinergic.
"Caffeine has anticholinergic effects by its antagonism of adenosine receptors, and thus potential effect on the lacrimal gland formation. The reduction of glandular secretion induced by caffeine is one of its many anticholinergic effect . Among agents that frequently reduce tear secretion are the anticholinergics, antihistamines and antianxietydrugs."

This was shown by AMAECHI, O. U. AND SAVIA, J. in THE EFFECT OF CAFFEINE ON TEAR FORMATION.

https://pdfs.semanticscholar.org/c170/e2fc51ce815b61b1e45d0f11efc9a6ef1dc7.pdf
 
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haidut

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"Caffeine has anticholinergic effects by its antagonism of adenosine receptors, and thus potential effect on the lacrimal gland formation. The reduction of glandular secretion induced by caffeine is one of its many anticholinergic effect . Among agents that frequently reduce tear secretion are the anticholinergics, antihistamines and antianxietydrugs."

This was shown by AMAECHI, O. U. AND SAVIA, J. in THE EFFECT OF CAFFEINE ON TEAR FORMATION.

https://pdfs.semanticscholar.org/c170/e2fc51ce815b61b1e45d0f11efc9a6ef1dc7.pdf

And here is a thread that shows caffeine specifically to be anticholinergic.
Caffeine Is A Serotonin Receptor Antagonist
 

DaveFoster

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And here is a thread that shows caffeine specifically to be anticholinergic.
Caffeine Is A Serotonin Receptor Antagonist
Interesting, thank you. So many who take the SSRIs drink coffee because of the sedation, and, given the fibrotic effects of these drugs, it's extremely disconcerting to see the public campaigns against caffeine in citation of mental health.
 

InChristAlone

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Interesting, thank you. So many who take the SSRIs drink coffee because of the sedation, and, given the fibrotic effects of these drugs, it's extremely disconcerting to see the public campaigns against caffeine in citation of mental health.
Unfortunately many cannot use coffee due to panic attacks. Panic disorder is not a small mental health disorder and can completely destroy someone's life. I no longer have any mental health disorder other than some obsessiveness thanks to avoiding caffeine.
 

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Unfortunately many cannot use coffee due to panic attacks. Panic disorder is not a small mental health disorder and can completely destroy someone's life. I no longer have any mental health disorder other than some obsessiveness thanks to avoiding caffeine.
It's debilitating, definitely, but the point of my post rested on the use of SSRIs, which have fibrotic effects, to treat it. Dozens of different drugs and hormones have been used clinically to treat panic disorder.

What did you find worsened from caffeine besides anxiety?
 

InChristAlone

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It's debilitating, definitely, but the point of my post rested on the use of SSRIs, which have fibrotic effects, to treat it. Dozens of different drugs and hormones have been used clinically to treat panic disorder.

What did you find worsened from caffeine besides anxiety?
IBS was worse for sure. Inability to do anything until I got the caffeine hit, which is a sign of dependency. I also had hypomania at times. I admit my metabolism was higher, but with it came the extreme sensitivity to adrenaline and the blood sugar rollercoaster. The constant need to medicate all the side effects. I don't have to medicate anything anymore. That's true freedom.
 

DaveFoster

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IBS was worse for sure. Inability to do anything until I got the caffeine hit, which is a sign of dependency. I also had hypomania at times. I admit my metabolism was higher, but with it came the extreme sensitivity to adrenaline and the blood sugar rollercoaster. The constant need to medicate all the side effects. I don't have to medicate anything anymore. That's true freedom.
Thank you. How do you react to progesterone?
 

InChristAlone

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Thank you. How do you react to progesterone?
I am not sure anymore. I stopped taking it. I might start back up again depending on my reaction. I have been continually trying to get to a place of balance. I want my body to re learn how to balance itself. I had felt like taking progesterone was pushing my body to do what I wanted instead of allowing it to do what it needed to. I am not against therapies when things are very bad, but in general I am learning to trust my body more. I think I lost that when I got into all this.
 

DaveFoster

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I am not sure anymore. I stopped taking it. I might start back up again depending on my reaction. I have been continually trying to get to a place of balance. I want my body to re learn how to balance itself. I had felt like taking progesterone was pushing my body to do what I wanted instead of allowing it to do what it needed to. I am not against therapies when things are very bad, but in general I am learning to trust my body more. I think I lost that when I got into all this.
I can relate to that. Dr. Peat's very conservative, anyway, which has been lost on this forum, I think. He often recommends dietary changes and then thyroid. He'll suggest progesterone, vitamin E and, for short-term use, niacinamide in some cases. He only recommends other things for acute use like during an infection and so on.
 

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I searched through all the transcripts I have of Rays work and I only found two instances where "choline" is discussed separate from "acetylcholine". Most of his exploration was around acetylcholine. However is it super obvious that just because you consume plenty of choline, doesn't mean you are going to make heaps of acetylcholine as it would be a high regulated process, especially with how important it is for neurotransmission.

I think this is a good area to explore. Lots of new studies are showing correlation between low dietary choline and dementia/AD. It could be that the failure of the cholinergic drugs to treat AD that haidut mentioned was through trying to force acetylcholine activity. But that shouldn't say anything about dietary choline right?

In my own personal experience I seem deficient in acetylcholine type activity and when ever I have increased it, my quality of life has only improved. It could be that there is a lot of biochemical individuality around acetylcholine. It is known for example that creative types are acetylcholine dominant. Low choline seems to be associated with dry mucus membranes, low secretions generally, which I am constantly dealing with. Coffee makes this worse for me, which makes sense if it is an anti-cholinergic.

Another point. Apparently bile is made of 90% phosphatidylcholine (PC) and 10% cholesterol. But if someones dietary choline drops too low, then the bile is made up mostly of cholesterol which is much more solid and stickier than PC, the end result are gallstones. I searched RP transcripts for gallstones and I did not see one mention. Both my parents had to have them removed.

I am homozygeous for C677T and have other methylation SNPs so I'm particularly interested in this.

An interesting summary here:
View: https://www.youtube.com/watch?v=sucrtrVcow0
 

PowerPlayer

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There's a doctor on YouTube named Dr. Rand Mcclain, he specializes in regenerative medicine and TRT but he has a pretty solid bodybuilding audience. One of his recommendations to keep fat off your liver is to take 3 grams of choline, 3 grams of inositol and 1.5 grams of methionine for 30 days. And you'll have no more fat on your liver. This was brought to his attention by Franco Columbu a golden era bodybuilding legend. He said out of curiosity he checked the science and saw there was validity.

This worked for guys who were on oral steroids with known liver toxicity risks, and the combination had no problem reversing it even without adding aspirin.

Maybe it's extended choline supplementation that is problematic if short therapeutic protocols like this are so effective.

Although, from a Peat standpoint it might be wise to switch to glycine instead of methionine since glycine was shown to have NAFLD reversing properties on it's own.

After the 30 days you can maintain a spotless liver with taurine and glycine, and (maybe aspirin).

Also, if you're looking to boost acetylcholine one of the best ways is with pantothenic acid (B5).
 

AinmAnseo

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Ray has written about the dangers of choline and its close relationship with estrogen. The histamine and acetylcholine receptors are perhaps the two main systems through which estrogen negatively affects the systemic health of the organism. As such, antihistamine and antocholinergic drugs can help block the effects of estrogen. Peat has even written separate articles on both systems and their role in disease, as well as the failure of choline and cholinergic drugs in treating brain conditions like Alzheimer and other dementias.
Now, we can add increased risk of blood clots to the list of negative effects of (excess) dietary choline. It seems that the mechanism is the same as the one for dietary carnitine raising CVD risk - i.e. increased synthesis of the substance TAMO.
Trimethylamine N-oxide - Wikipedia

It should be noted that choline and carnitine by themselves do not raise TMAO. It is gut bacteria that makes that metabolic conversion, so the role of gut bacteria in vascular health is once again very prominent and finally starting to be recognized by mainstream medicine. Be that as it may, the study found that (possibly excessive) dietary choline in the form of a supplement raised TMAO levels, and platelet aggregation in humans and a low dose aspirin reversed not only the platelet aggregation but also the increase in TMAO levels. The reduction of platelet aggregation by aspirin is not novel, it is a soidly established benefit. But the reduction in TMAO levels is a new and previously unknown benefit of aspirin, and as such it may explain at least one of the mechanism by which aspirin prevents CVD. So, for diets heavy in eggs and meat proteins, taking aspirin 2-3 times a week may be a good idea. Keeping the gut as clean of bacteria as possible should also help, and aspirin may actually be lowering TMAO levels through its antibacterial effects I posted about in the past.

Gut Microbe-Generated Trimethylamine N-Oxide From Dietary Choline Is Prothrombotic in Subjects | Circulation
Diet and gut bacteria linked with blood clots

"...Consuming too much choline, a nutrient sold in over-the-counter dietary supplements, can boost the risk for blood clots, researchers warn. That’s because bacteria in the intestines interact with choline to produce a compound that encourages platelets to clump together and form clots. Choline is found in a variety of foods including meat, eggs and milk. It’s what’s known as an essential nutrient, which means the body can’t make enough choline on its own and so it must be provided in food. But “unless prescribed by your doctor, avoid supplements with choline,” said senior study researcher Dr. Stanley L. Hazen of the Cleveland Clinic in Ohio, in a statement. Hazen and colleagues had previously shown that bacteria in the intestines interact with choline and other dietary nutrients to produce a substance called TMAO, and they linked high levels of TMAO in the blood to an increased risk of cardiovascular diseases. Also, in studies in animals, they linked higher levels of TMAO to a higher risk for blood clots. Their latest research, reported in the American Heart Association’s journal Circulation, shows that choline in food can affect blood clotting risk in humans, and in some cases, that risk can be minimized by taking low-dose aspirin."

"...Aspirin, which reduces the stickiness of platelets, reduced both the increases in TMAO and the increases in platelet clotting associated with choline, but it didn't completely eliminate them, the researchers found. The findings are of particular concern in people at high cardiovascular risk, whose increased risk of blood clots may not be overcome by low-dose aspirin. The researchers recommend further study. They also say it's worth exploring whether low-dose aspirin is beneficial in otherwise healthy people with high TMAO in the blood – although at this point, they can’t explain why the aspirin seemed to bring down TMAO levels. Dr. Herbert Tilg from Medical University Innsbruck, Austria, who has studied the link between gut microbes and blood clots, told Reuters Health by email, “This and earlier studies show that we now definitely have to consider dietary aspects in this context, i.e., diet drives thrombosis risk.” “These associations are totally new and unexpected: a link between diet - gut microbiota - and thromboembolic events,” he said. “They are extremely relevant for the public and in medicine,” given that clots are “very, very common” and can be fatal, he said."
Haidut,
Where has Ray written about the dangers of choline and its close relationship with estrogen?
Thanks.
 
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@ainmBob I remember that if your estrogen level is low you are probably low on choline, I just remember this correlation.
 

David PS

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Haidut,
Where has Ray written about the dangers of choline and its close relationship with estrogen?
Thanks.
I asked Peatbot this question.

User: dangers of choline and its close relationship with estrogen?

Peatbot: There is no mention of choline or its relationship with estrogen in the provided context. Therefore, I don't have any information on the dangers of choline or its relationship with estrogen.

I also asked:

User: dangers of choline?

Peatbot: Choline is an essential nutrient that plays a crucial role in various bodily functions, including brain development, nerve function, and metabolism. However, excessive intake of choline or certain forms of choline can have potential dangers and side effects. Here are some potential dangers of choline:

1. Increased risk of cardiovascular disease: High levels of choline in the body can lead to the production of a compound called trimethylamine N-oxide (TMAO), which has been associated with an increased risk of cardiovascular disease, including heart attacks and strokes.

2. Increased risk of certain cancers: Studies have suggested that high choline intake, particularly from animal sources, may be associated with an increased risk of certain cancers, such as colorectal and prostate cancer. However, more research is needed to establish a definitive link.

3. Gastrointestinal distress: Excessive intake of choline or certain forms of choline, such as choline bitartrate, can cause gastrointestinal side effects like diarrhea, nausea, and stomach cramps.

4. Fishy body odor: Some individuals may experience a fishy body odor when consuming large amounts of choline-rich foods or supplements. This is due to the breakdown of choline into trimethylamine (TMA), which is then converted to trimethylamine N-oxide (TMAO) in the liver.

5. Interference with certain medications: Choline supplements can interact with certain medications, such as anticholinergic drugs, and may reduce their effectiveness. It is important to consult with a healthcare professional before taking choline supplements if you are on any medications.

It is worth noting that choline is an essential nutrient, and most people can safely consume adequate amounts of choline through a balanced diet without experiencing any adverse effects. However, if you have any concerns or specific health conditions, it is always best to consult with a healthcare professional before making any significant changes to your diet or taking choline supplements.

Sources
Insecticide exposure has been suspected to be a factor in the increased incidence of Alzheimer's disease (Zaganas, et al., 2013), but it could be contributing to many other problems, involving inflammation, edema, and degeneration. Another important source of organophosphate poisoning is the air used to pressurize airliners, which can be contaminated with organophosphate fumes coming from the engine used to compress it.

Possibly the most toxic component of our environment is the way the society has been designed, to eliminate meaningful choices for most people. In the experiment of Freund, et al., some mice became more exploratory because of the choices they made, while others' lives became more routinized and limited. Our culture reinforces routinized living. In the absence of opportunities to vary the way you work and live to accord with new knowledge that you gain, the nutritional, hormonal and physical factors have special importance.

Supplements of thyroid and progesterone are proven to be generally protective against the cholinergic threats, but there are many other factors that can be adjusted according to particular needs. Niacinamide, like progesterone, inhibits the production of nitric oxide, and also like progesterone, it improves recovery from brain injury (Hoane, et al., 2008). In genetically altered mice with an Alzheimer's trait, niacinamide corrects the defect (Green, et al., 2008). Drugs such as atropine and antihistamines can be used in crisis situations. Bright light, without excess ultraviolet, should be available every day.

The cholinergic system is much more than a part of the nervous system, and is involved in cell metabolism and tissue renewal. Most people can benefit from reducing intake of phosphate, iron, and polyunsaturated fats (which can inhibit cholinesterase; Willis, et al., 2009), and from choosing foods that reduce production and absorption of endotoxin. And, obviously, drugs that are intended to increase the effects of nitric oxide (asparagine, zildenafil/Viagra, minoxidil/Rogaine) and acetylcholine (bethanechol, benzpyrinium, etc.) should be avoided.

References

Acta Biochim Pol. 2011;58(4):513-20.Neuroprotective effects of dehydroepiandrosterone (DHEA) in rat model of Alzheimer's disease.Aly HF, Metwally FM, Ahmed HH.

Psychopharmacology (Berl). 1981;74(1):81-7.Cholinergic influences on escape deficits produced by uncontrollable stress.Anisman H, Glazier SJ, Sklar LS.

Biochim Biophys Acta. 2001 Nov 1;1506(3):204-11.Endothelial- and nitric oxide-dependent effects on oxidative metabolism of intact artery.Barron JT, Gu L, Parrillo JE.

Psychiatry Res. 1987 Jul;21(3):267-75.Triiodothyronine potentiation of antidepressant-induced reversal of learned helplessness in rats.Brochet DM, Martin P, Soubrié P, Simon P.

Behav Brain Res. 2013 Aug 12. pii: S0166-4328(13)00482-8.Increased nitric oxide-mediated neurotransmission in the medial prefrontal cortex is associated with the long lasting anxiogenic-like effect of predator exposure.Campos AC, Piorino EM, Ferreira FR, Guimarães FS.

J Biomed Sci. 2001 Nov-Dec;8(6):475-83.Engagement of inducible nitric oxide synthase at the rostral ventrolateral medulla during mevinphos intoxication in the rat.Chang AY, Chan JY, Kao FJ, Huang CM, Chan SH.

Science. 1984 Jan 6;223(4631):61-3.Coexistence of acetylcholinesterase and somatostatin-immunoreactivity in neurons cultured from rat cerebrum.Delfs JR, Zhu CH, Dichter MA.

Neurosci Bull. 2011 Dec;27(6):366-82.Nitric oxide in neurodegeneration: potential benefits of non-steroidal anti-inflammatories.Doherty GH.18.

Brain Inj. 2007 Sep;21(10):1031-7.Alterations of acetylcholinesterase activity after traumatic brain injury in rats.Donat CK, Schuhmann MU, Voigt C, Nieber K, Schliebs R, Brust P.
Source: the-dark-side-of-stress-learned-helplnessness.html

The increase of cholinesterase by enriched living serves to protect tissues against an accumulation of acetylcholine. The activation of nitric oxide synthesis by acetylcholine tends to block energy production, and to activate autolytic or catabolic processes, which are probably involved in the development of a thinner cerebral cortex in isolated or stressed animals. Breaking down acetylcholine rapidly, the tissue renewal processes are able to predominate in the enriched animals.

Environmental conditions that are favorable for respiratory energy production are protective against learned helplessness and neurodegeneration, and other biological problems that involve the same mechanisms. Adaptation to high altitude, which stimulates the formation of new mitochondria and increased thyroid (T3) activity, has been used for many years to treat neurological problems, and the effect has been demonstrated in animal experiments (Manukhina, et al., 2010). Bright light can reverse the cholinergic effects of inescapable stress (Flemmer, et al., 1990).

During the development of learned helplessness, the T3 level in the blood decreases (Helmreich, et al., 2006), and removal of the thyroid gland creates the "escape deficit," while supplementing with thyroid hormone before exposing the animal inescapable shock prevents its development (Levine, et al., 1990). After learned helplessness has been created in rats, supplementing with T3 reverses it (Massol, et al., 1987, 1988).

Hypothyroidism and excess cholinergic tone have many similarities, including increased formation of nitric oxide, so that similar symptoms, such as muscle inflammation, can be produced by cholinesterase inhibitors such as Tacrine, by increased nitric oxide, or by simple hypothyroidism (Jeyarasasingam, et al., 2000; Franco, et al., 2006).

Insecticide exposure has been suspected to be a factor in the increased incidence of Alzheimer's disease (Zaganas, et al., 2013), but it could be contributing to many other problems, involving inflammation, edema, and degeneration. Another important source of organophosphate poisoning is the air used to pressurize airliners, which can be contaminated with organophosphate fumes coming from the engine used to compress it.

Possibly the most toxic component of our environment is the way the society has been designed, to eliminate meaningful choices for most people. In the experiment of Freund,et al., some mice became more exploratory because of the choices they made, while others' lives became more routinized and limited. Our culture reinforces routinized living. In the absence of opportunities to vary the way you work and live to accord with new knowledge that you gain, the nutritional, hormonal and physical factors have special importance.

Supplements of thyroid and progesterone are proven to be generally protective against the cholinergic threats, but there are many other factors that can be adjusted according to particular needs. Niacinamide, like progesterone, inhibits the production of nitric oxide, and also like progesterone, it improves recovery from brain injury (Hoane, et al., 2008). In genetically altered mice with an Alzheimer's trait, niacinamide corrects the defect (Green, et al., 2008). Drugs such as atropine and antihistamines can be used in crisis situations. Bright light, without excess ultraviolet, should be available every day.

The cholinergic system is much more than a part of the nervous system, and is involved in cell metabolism and tissue renewal. Most people can benefit from reducing intake of phosphate, iron, and polyunsaturated fats (which can inhibit cholinesterase; Willis, et al., 2009), and from choosing foods that reduce production and absorption of endotoxin. And, obviously, drugs that are intended to increase the effects of nitric oxide and acetylcholine should be avoided.
Source: The dark side of stress (learned helplessness) — Chadnet
 

moa

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User: reduce nitric oxide in the colon

Peatbot: According to a study published in Nitric Oxide, inhibiting nitric oxide synthase (NOS) activity can promote carcinogen-induced preneoplastic changes in the colon of rats. The study used N(G)-nitro-l-arginine methyl ester (l-NAME), an inhibitor of NOS, to reduce nitric oxide levels in the colon. The results showed that in l-NAME-treated rats, the number of aberrant crypt foci (ACF), which are considered preneoplastic changes, was higher compared to the control group. Additionally, the study found that l-NAME treatment increased ornithine decarboxylase (ODC) activity, which is involved in polyamine biosynthesis. Polyamines are known to be high in tumor cells. Therefore, inhibiting NOS activity with l-NAME not only reduced nitric oxide levels but also stimulated polyamine biosynthesis, potentially promoting carcinogenesis in the colo
n.

???
 

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