Many people may suffer from chronic serotonin syndrome

[TheSir]

That's the idea of C with lysine. Yes. But atherosclerosis is not caused only lack of vitamin C. C does not remove oxidized LDL nor prevent it. Plaque can also be formed by biofilms and remnants of wbc's fighting bacteria, and dormant bacteria.

Vitamin C is not even the antioxidant used when spillover ROS from phagocytosis by neutrophils needs to be neutralized.

The long and short of it is that it's too simplistic to say vitamin C keep arteries young. But of course Dr. Axe would have it sound like that as simple explanations are better in the same way fairy tales and parables are better than novels.

Simplistic or not, it clearly helps. Read the bits I edited into the previous post.

 

[yerrag]

Simplistic or not, it clearly helps. Read the bits I edited into the previous post.

It helps for sure, but it would be a stretch to say it was why the guy has teenager arteries. Come on, the doc was yanking his chain.

 

[TheSir]

It helps for sure, but it would be a stretch to say it was why the guy has teenager arteries. Come on, the doc was yanking his chain.

If you say so!

 

[Birdie]

Problem is that, while vitamin C used to be safe, the modern day production may have problems. Ray said the vitamin C of today is lead tainted. This may have changed lately, I don't know.

 

[mostlylurking]

A very interesting article, which calls out the widespread usage of serotonergic drugs (usually SSRI), and argues that their widespread use may have created an "epidemic" of a chronic, milder version of the (in)famous serotonin syndrome (SS). Currently, mainstream medicine does not recognize chronic SS as a condition, and most ER doctors are inadequately trained how to diagnose even the acute, often-lethal, version of SS. Be that as it may, as the article states, the chronic milder version of SS is far from benign, it does not resolve by itself, and can unpredictably progress into the acute version of SS. In fact, the chronic version of SS may be much more pernicious and relevant for public health due to its prevalence and difficulty of diagnosing even by experienced physicians. Btw, many of the core symptoms of chronic SS mimic those of viral infections, including COVID-19. It has already been recognized that serotonin plays a role in the course of COVID-19 and contributes to both its morbidity and mortality. Considering that almost 20% of the US population takes antidepressants, it may very well be that many of the severe COVID-19 cases, and even deaths associated with the virus, are in fact acute exacerbations of chronic SS.

Chronic serotonin syndrome: A retrospective study
Indian culture, inability to express feelings and depression: explaining the complex relationship.

"...The study serves as an important reminded for psychiatrists to keep an eagle-eye approach for diagnosing chronic SS. SS typically presents within 24h of initiation of change in the dose of serotonergic agents, and it may evolve very rapidly, leading to death within a few hours. However, mild cases of SS (tremor with hyperreflexia and hypertonia) may be ignored by patients and doctors, and patients continue to take serotonergic drugs for a longer period. Such patients may represent the chronic variant of SS."
"...Generalized body pain, stiffness of the limbs, insomnia, dizziness, and irritability were the common presenting features. Such nonspecific symptoms are often ignored by patients, and even physicians do not take these symptoms seriously and attribute such symptoms to underlying primary disorders or associated somatic complaints or nonspecific drug-induced side effects. A diagnosis of SS is important even in mild and indolent form, as it is not supposed to resolve spontaneously as long as serotonergic drugs are administered. Furthermore, it may progress rapidly to death by an inadvertent increase of the dose or addition of another serotonergic agent. Take home message: The incidence of SS is increasing because of the widespread use of serotonergic drugs. There is a need to improve the awareness about SS among the physicians for early recognition and effective management.

There seems to be a connection between serotonin problems and thiamine deficiency. Link: Thiamine deficiency: selective impairment of the cerebellar serotonergic system - PubMed

" Abstract: To explore the role of thiamine deficiency in synaptic transmission, the high-affinity uptake and release systems for putative neurotransmitters were studied in synaptosomal preparations isolated from the telencephalon, hypothalamus, and cerebellum of rats made thiamine deficient by diet or pyrithiamine. There was significant decrease in the uptake of serotonin by the synaptosomal preparations of the cerebellum. Although thiamine and its phosphorylated forms added in vitro did not restore the decreased serotonin uptake, the administration of the vitamin in vivo resulted in a significant reversibility of the inhibition of serotonin uptake, coinciding with dramatic clinical improvement. The study supports the possibility of an important serotonergic innervation of the cerebellum and suggests a selective involvement of this system in the pathogenesis of some of the neurologic manifestations of thiamine deficiency."

also this one: Effect of thiamine deficiency on brain serotonin turnover - PubMed

"Abstract: Serotonin turnover has been investigated in regional brain areas of rats made thiamine deficient by pyrithiamine (PT). Following intracisternal injection of [14C]5-hydroxytryptamine ([14C]5-HT), a marked increase in the accumulation of [14C]5-hydroxyindoleacetic acid ([14C]5-HIAA) was found in the medulla-pons, hypothalamus and cerebral cortex. [14C]5-HT levels were normal in all of the brain areas except the cerebral cortex which had an increase of 58%. The ratio of [14C]5-HIAA/[14C]5-HT was significantly increased in every brain region of PT-treated rats except the cerebral cortex. Part of this increase in [14C]5-HIAA was shown to be due to impairment of active transport of this 5-HT metabolite out of the brain. However, increased 5-HT synthesis in the cerebellum, hypothalamus, striatum, hippocampus and cerebral cortex was demonstrated by measurement of 5-HT accumulation after inhibition of brain monoamine oxidase. PT-induced increase in endogenous 5-HIAA in the medulla-pons occurred simultaneously with the onset of neurological signs and both parameters were reversible by thiamine administration. These results suggest that acute thiamine deficiency, induced by PT, both increases brain 5-HT synthesis and impairs 5-HIAA efflux from the brain. There is a close correlation between neurological manifestations and changes in brain 5-HT metabolism in acute thiamine deficiency."

 

[GreenTrails]

C heals the endothelial wall, inflammation/dysfunction of which lays the foundation to atherosclerosis. In reverse, deficiency in C would lead to overaccumulation of LDL.

Atherosclerosis and the Cholesterol Theory: A Reappraisal

Atherosclerosis is the precedent to ischemic heart disease, which may lead to angina, myocardial infarct, or heart failure; or to ischemic cerebrovascular disease, which may lead to stroke. The prevailing belief underlying conventional approaches to treatment of atherosclerosis and its sequel is...

www.scirp.org

Thank you for the study.

 

[yerrag]

C heals the endothelial wall, inflammation/dysfunction of which lays the foundation to atherosclerosis. In reverse, deficiency in C would lead to overaccumulation of LDL.

Atherosclerosis and the Cholesterol Theory: A Reappraisal

Atherosclerosis is the precedent to ischemic heart disease, which may lead to angina, myocardial infarct, or heart failure; or to ischemic cerebrovascular disease, which may lead to stroke. The prevailing belief underlying conventional approaches to treatment of atherosclerosis and its sequel is...

www.scirp.org

Thanks for the link. It is a nice and a much better written article on the Unified Theory of Human Cardiovascular Disease.

I have no doubt of the usefulness of vitamin C in reducing CVD significantly after reading it once again. I don't know if that the theory suggests it explains everything there is to it, but if it does, I don't agree. There are many other factors which would contribute to it, and taking vitamin C and lysine alone, and some other substances, would not provide an amulet against atherosclerosis caused by other factors such as the intake of PUFAs that cause oxidized LDL, and from the accumulation of detritis from the remnants of immune interaction between white blood cells and pathogens.

The study of the mice removed of the ability to provide endogenous vitamin C proved that there is more Lp(a) produced with having no vitamin C (or less of it) and that vitamin C intake leads to lower plaque formation. There are further studies that can be made. A study can address the impact of feeding PUFA dog foods on dogs who naturally produce their own vitamin C. Would a PUFA fed dog lead to atherosclerosis that is worse compared to a dog fed non-PUFA? Would oxidized LDL from PUFA intake lead to higher mortality or shorter lives for a dog? How much of a difference does eating PUFA food and taking vit C supplementation compare to eating PUFA food without vitamin C supplementation, w/r to severity of artheriosclerosis?

Such questions underlie my reasoning for having a disbelief of the old man having the artery of a teenager, given that he is likely a typical American who eats PUFAs. Note that the proponents of Vitamin C in the Vitamin C Foundation are not Ray Peaters. They are not anti-PUFA.

 

[golder]

Is it necessary to further supplement vitamin C when drinking 4+ glasses of orange juice and a large serving of fruit per day?

 

[TheSir]

There are many other factors which would contribute to it, and taking vitamin C and lysine alone, and some other substances, would not provide an amulet against atherosclerosis caused by other factors such as the intake of PUFAs that cause oxidized LDL, and from the accumulation of detritis from the remnants of immune interaction between white blood cells and pathogens.

Couldn't sufficient vitamin C dosage simply overcome these factors? From what I understand, it doesn't matter how the atherosclerosis would form, as the end result (plaque buildup) would be more or less the same in any case. It is this end result which C/lysine then addresses.

The study of the mice removed of the ability to provide endogenous vitamin C proved that there is more Lp(a) produced with having no vitamin C (or less of it) and that vitamin C intake leads to lower plaque formation. There are further studies that can be made. A study can address the impact of feeding PUFA dog foods on dogs who naturally produce their own vitamin C. Would a PUFA fed dog lead to atherosclerosis that is worse compared to a dog fed non-PUFA? Would oxidized LDL from PUFA intake lead to higher mortality or shorter lives for a dog? How much of a difference does eating PUFA food and taking vit C supplementation compare to eating PUFA food without vitamin C supplementation, w/r to severity of artheriosclerosis?

Yes, these are interesting questions. We know that PUFA attacks liver and thyroid alike, both of which are likely to be important for vitamin C synthesis (even though technically C is made in the liver). So we could hypothesize that PUFA would decrease dog's ability to synthesize C. There's a study in which removing thyroid glands from carnivores led to them developing atherosclerosis, referenced here: Twenty questions on atherosclerosis . Could it be that they stopped producing C?

 

[yerrag]

Couldn't sufficient vitamin C dosage simply overcome these factors? From what I understand, it doesn't matter how the atherosclerosis would form, as the end result (plaque buildup) would be more or less the same in any case. It is this end result which C/lysine then addresses.

It's hard to imagine that one could take vitamin C but take in large amounts of PUFA and still not accumulate plaque and not develop atherosclerosis. The relationship of oxidized LDL to form from PUFA, and for foam cells to to form from macrophages would still remain. And given that the blood vessels are hardly sterile, bacteria, immune complexes, and dead immune cells form a flotsam that adds to the plaque. But if the process of forming plaque is minimized and developing atherosclerosis to crisis poo t is delayed, then vitamin C supplementation could still be called effective.

Yes, these are interesting questions. We know that PUFA attacks liver and thyroid alike, both of which are likely to be important for vitamin C synthesis (even though technically C is made in the liver). So we could hypothesize that PUFA would decrease dog's ability to synthesize C. There's a study in which removing thyroid glands from carnivores led to them developing atherosclerosis, referenced here: Twenty questions on atherosclerosis . Could it be that they stopped producing C?

I didn't think of the effect of PUFA being that of preventing the production of Vitamin C. As that would render useless a study to see the effects of PUFA on the development of atherosclerosis in the presence of vitamin C supplied endogenously.

 

[SlowWalker]

Not sure if this is connected but how come it seems as though many people on carnivore have reduced coronary artery scores when on a diet with low amounts of vitamin C? Does this indicate reduced chances of heart disease?

 

[Rick K]

I believe this. Some years ago I came across a guy who claimed to have had dosed 10grams of vitamin C for years, according to his doctor he had the arteries of a teenager.

That would be me also. 10+ grms daily for over 40 years. BP is 110/80. Constant woodies. I am 60.

 

[golder]

That would be me also. 10+ grms daily for over 40 years. BP is 110/80. Constant woodies. I am 60.

What form of supplemental vitamin C do you use other than food? It’s hard to find a good quality supplement. Thanks!

 

[Mito]

foam cells to to form from macrophages would still remain

L-theanine inhibits foam cell formation via promoting the scavenger receptor A degradation

Abstract Atherosclerosis is one of the most common cardiovascular diseases with highly mortality worldwide. The formation of foam cell plays an important role in the early stage of atherosclerosis pathogenesis. L-theanine is the most abundant free amino acid in tea, which possesses...

raypeatforum.com

 

[Comstock]

Not sure if this is connected but how come it seems as though many people on carnivore have reduced coronary artery scores when on a diet with low amounts of vitamin C? Does this indicate reduced chances of heart disease?

Meat and I think dairy has sufficient Vitamin C. Peat has said that in several interviews.

 

[Rick K]

What form of supplemental vitamin C do you use other than food? It’s hard to find a good quality supplement. Thanks!

sodium or calcium ascorbate

 

[yerrag]

That would be me also. 10+ grms daily for over 40 years. BP is 110/80. Constant woodies. I am 60.

Very nice. Woodies is the new thermometer. How long have you been PUFA - free? Any allergies? Last time you had a fever? Headaches? Gut issues?

Zero would be a hundred.

 

[Rick K]

Very nice. Woodies is the new thermometer. How long have you been PUFA - free? Any allergies? Last time you had a fever? Headaches? Gut issues?

Zero would be a hundred.

I have avoided most oils (save for coconut) since being a teenager. I had chronic allergies and asthma and eczema until I was 15 which is when I took charge of my diet. I have had none of the above mentioned afflictions since that time. When I was 20 I stumbled across a book called Life Extension by Durk Pearson and Sandy Shaw who were scientists practicing what they preached. It was at that time that I adopted the high dose vit. C. I have no gut or fever issues and get headaches about 2 or 3 times a year which seem to be caused by dehydration.

 

[Braveheart]

There seems to be a connection between serotonin problems and thiamine deficiency. Link: Thiamine deficiency: selective impairment of the cerebellar serotonergic system - PubMed

" Abstract: To explore the role of thiamine deficiency in synaptic transmission, the high-affinity uptake and release systems for putative neurotransmitters were studied in synaptosomal preparations isolated from the telencephalon, hypothalamus, and cerebellum of rats made thiamine deficient by diet or pyrithiamine. There was significant decrease in the uptake of serotonin by the synaptosomal preparations of the cerebellum. Although thiamine and its phosphorylated forms added in vitro did not restore the decreased serotonin uptake, the administration of the vitamin in vivo resulted in a significant reversibility of the inhibition of serotonin uptake, coinciding with dramatic clinical improvement. The study supports the possibility of an important serotonergic innervation of the cerebellum and suggests a selective involvement of this system in the pathogenesis of some of the neurologic manifestations of thiamine deficiency."

also this one: Effect of thiamine deficiency on brain serotonin turnover - PubMed

"Abstract: Serotonin turnover has been investigated in regional brain areas of rats made thiamine deficient by pyrithiamine (PT). Following intracisternal injection of [14C]5-hydroxytryptamine ([14C]5-HT), a marked increase in the accumulation of [14C]5-hydroxyindoleacetic acid ([14C]5-HIAA) was found in the medulla-pons, hypothalamus and cerebral cortex. [14C]5-HT levels were normal in all of the brain areas except the cerebral cortex which had an increase of 58%. The ratio of [14C]5-HIAA/[14C]5-HT was significantly increased in every brain region of PT-treated rats except the cerebral cortex. Part of this increase in [14C]5-HIAA was shown to be due to impairment of active transport of this 5-HT metabolite out of the brain. However, increased 5-HT synthesis in the cerebellum, hypothalamus, striatum, hippocampus and cerebral cortex was demonstrated by measurement of 5-HT accumulation after inhibition of brain monoamine oxidase. PT-induced increase in endogenous 5-HIAA in the medulla-pons occurred simultaneously with the onset of neurological signs and both parameters were reversible by thiamine administration. These results suggest that acute thiamine deficiency, induced by PT, both increases brain 5-HT synthesis and impairs 5-HIAA efflux from the brain. There is a close correlation between neurological manifestations and changes in brain 5-HT metabolism in acute thiamine deficiency."

Thanks for this....

 

[Rick K]

I have avoided most oils (save for coconut) since being a teenager. I had chronic allergies and asthma and eczema until I was 15 which is when I took charge of my diet. I have had none of the above mentioned afflictions since that time. When I was 20 I stumbled across a book called Life Extension by Durk Pearson and Sandy Shaw who were scientists practicing what they preached. It was at that time that I adopted the high dose vit. C. I have no gut or fever issues and get headaches about 2 or 3 times a year which seem to be caused by dehydration.

It isn't just the vit. C I take by the way, I just wanted to comment that I read with fascination the health problems so many people experience here. I know that I'm 60 and am reminded by the grey hair but I still weight lift 6 days a week, have 3-4 BM every day and get colds maybe once every 3-5 years, again, only if I've been neglecting my diet. I am fascinated by the mental/emotional/sexual health issues so many experience as I just can't relate. My "gear" works just the same as when I was 15 and I feel profoundly happy, Full head of hair despite many episodes of tweaking testosterone in my lifetime. I just seem oblivious to the health issues at large as I don't experience them apart from the occasional blunt force trauma of a misguided hammer.