MEDICATION SHORTAGE

Lollipop2

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Selenium for Mercury Toxicity

 
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The effects of dietary lysine on the gut and/or brain-gut function in marginally deficient diets are not fully understood. Rodent models show that lysine deficiency contributes to serotonin-mediated anxiety and diarrhea through a direct effect on serotonin receptors (20, 21). Diarrheal incidence could also be affected through enhanced intestinal repair or through effects on the sodium- and chloride-dependent opioid peptide transport systems (22). Whereas the mechanism may not be understood, the need to investigate the concomitant effects of dietary lysine on stress, diarrhea, growth, and morbidity in developing countries is based on lysine being reported effective in 1) protecting the gut irrespective of the diarrhea trigger (stress, bacterial, or viral infection) (17, 18, 20), 2) alleviating chronic anxiety across different populations (6, 19), and 3) potentially enhancing growth in children with poor-quality diets (13, 14, 23, 24) while potentially playing a role in body composition (10, 11).
 
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Excess nicotinamide increases plasma serotonin and histamine levels


Methylation, a methyl group-consuming reaction, plays a key role in the degradation (i.e., inactivation) of monoamine neurotransmitters, including catecholamines, serotonin and histamine. Without labile methyl groups, the methylation-mediated degradation cannot take place. Although high niacin (nicotinic acid and nicotinamide) intake, which is very common nowadays, is known to deplete the body's methyl-group pool, its effect on monoamine-neurotransmitter degradation is not well understood.

The aim of this article was to investigate the effect of excess nicotinamide on the levels of plasma serotonin and histamine in healthy subjects. Urine and venous blood samples were collected from nine healthy male volunteers before and after oral loading with 100 mg nicotinamide. Plasma N(1)-methylnicotinamide, urinary N(1)-methyl-2-pyridone-5-carboxamide (2-Py), and plasma betaine levels were measured by using high-performance liquid chromatography (HPLC). Plasma concentrations of choline, serotonin and histamine were measured using commercial kits.

The results showed that the plasma N(1)-methylnicotinamide level and the urinary excretion of 2-Py significantly increased after oral loading with 100 mg nicotinamide, which was accompanied with a decrease in the methyl-group donor betaine. Compared with those before nicotinamide load, five-hour postload plasma serotonin and histamine levels significantly increased.

These results suggest that excess nicotinamide can disturb monoamine-neurotransmitter metabolism. These findings may be of significance in understanding the etiology of monoamine-related mental diseases, such as schizophrenia and autism (a neurodevelopmental disorder.

Posted elsewhere by @fico
 
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Thiamine and Riboflavin for Chronic Fatigue

Here was young man (30 years old) who, six months after surviving infective endocarditis of the native valve that necessitated, not only the use of some pretty powerful antibiotics, but also, an aortic valve replacement and oral anticoagulation therapy, developed profound and unremitting fatigue. Several years and conventional treatments later, physicians considered the mitochondria and the prospect that mitochondrial damage might be behind the fatigue and other symptoms. Mitochondrial testing ensued and upon confirmation, treatment with vitamins, 300mg of thiamine (vitamin B1) and 300mg of riboflavin (vitamin b2) commenced. Within a month, there was significant improvement that was maintained at the five year followup. Effectively, vitamins treated what medicine could not.

 
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Vitamin Therapy with Chronic Deficiency: Expect a Decline before Improving

Physicians who practice Alternative Medicine have found that it is possible sometimes to retrieve function at this late stage of development by the use of a course of vitamins given intravenously. They have also learned that the symptoms of the patient actually get worse (paradox) in the initial stages of intravenous treatment but begin to get better following an unpredictable period of worsening. Naturally, the patient concludes that the treatment is bad or that it is causing side effects as in the use of pharmaceuticals. That is why I have christened it paradox, meaning that the unexpected happens.

Over the years of administering intravenous vitamin therapy for all kinds of conditions, irrespective of conventional diagnosis, I quickly learned to inform a patient about paradox before instituting treatment. Surprisingly, this paradoxical response usually heralds a good outcome. I do have some ideas about the cause of paradox, but it is so technical that I cannot attempt it here, perhaps in future posts. Intravenous vitamins are tremendously effective in the improvement of most chronic diseases, an effect that is almost impossible to achieve with the standard treatment of drugs as used in modern medicine today.


To summarize, the initial cellular processing of TTFD requires adequate levels of reduced glutathione. Glutathione becomes oxidized, and so TTFD has can have a depleting effect on GSH and increase the requirement for recycling. If there is insufficient active B2 (as FAD) or NADPH levels, glutathione is not likely to be recycled sufficiently and may lead to GSSG radical formation.
It is therefore possible that the glutathione-depleting effect of TTFD could be responsible for some of the side effects associated with supplementation. This is probably most applicable in individuals with poor glutathione recycling and underlying oxidative stress. Therefore, nutrient therapies that may support this initial phase of TTFD metabolism include:
  • Selenium (improve GSH levels)
  • Riboflavin (improve GSSG-GSH recycling)
  • Niacin (increase NADPH)
  • Ordinary thiamine (increase NAPH via PPP)
  • NAC, glycine and/or glutathione TAKEN HOURS AWAY from TTFD (GSH precursors)
 
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Death by Medicine
By Gary Null, PhD; Carolyn Dean MD, ND; Martin Feldman, MD; Debora Rasio, MD; and Dorothy Smith, PhD​

Something is wrong when regulatory agencies pretend that vitamins are dangerous, yet ignore published statistics
showing that government-sanctioned medicine is the real hazard.

 
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Drug-Induced Serotonin Syndrome


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Treatment​

In general, treatment of SS first involves discontinuing the offending drug(s) and providing the patient with supportive care. Many mild-to-moderate SS cases are self-limiting and usually resolve within 24 to 72 hours.19 Resolution of more severe cases will likely take much longer. In such cases, supportive care, drug discontinuation, and administration of medication (e.g., diazepam 5 mg IV to reduce hypertonicity and neurologic excitability) may be sufficient to resolve mild symptoms.2,13,36 Patients with severe symptoms may need sedation, paralyzation, and intubation.

Administration of drugs with serotonin antagonist properties, such as cyproheptadine and chlorpromazine, has been utilized in a few patients.4,16,18 Cyproheptadine 4 mg orally is the most widely used antidote for SS.36 Although increased body temperature is common in patients with severe SS, antipyretic therapy usually is not recommended. This is because the fever that occurs with SS is caused by excessive muscular activity, not a change in the hypothalamic temperature set point.2
 
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A parasitological evaluation of edible insects and their role in the transmission of parasitic diseases to humans and animals​

 
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Adaptive decreases in amino acids (taurine in particular), creatine, and electrolytes prevent cerebral edema in chronically hyponatremic mice: rapid correction (experimental model of central pontine myelinolysis) causes dehydration and shrinkage of brain.

 
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@Trullo posted this elsewhere


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Lactate levels during the first 24 hours. IV, intravenous.

Oral or intravenous thiamine in the emergency department?


CLINICAL BOTTOM LINE

Oral thiamine administration is as effective as parenteral administration after five days. In compliant alcoholics without encephalopathy oral administration is the route of choice.
 
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Thank you. Looks like significant cholesterol in lamb's liver. Something I'm trying to reduce. I find beef liver crunchy - awful texture!
Beef liver is high cholestrol too. If you don't mind me asking how high is your cholestrol - it might not be a big deal according to peat.
 

Lizb

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Beef liver is high cholestrol too. If you don't mind me asking how high is your cholestrol - it might not be a big deal according to peat.
I could be brave and get it tested!

It was 7.4 LDL.
HDL 1.97
that was in 2017

My husband's was 8 in 2019.

I now have those cholesterol lumps on my eyes. I can see them developing on my husband's too. He has dementia. I heard Ray say recently that dementia patients have too much cholesterol in their brains.......
I've just started T3 (low dose with food). I'm told that'll lower it. But will it stop the development or eradicate those unsightly lumps?....
 
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I could be brave and get it tested!

It was 7.4 LDL.
HDL 1.97
that was in 2017

My husband's was 8 in 2019.

I now have those cholesterol lumps on my eyes. I can see them developing on my husband's too. He has dementia. I heard Ray say recently that dementia patients have too much cholesterol in their brains.......
I've just started T3 (low dose with food). I'm told that'll lower it. But will it stop the development or eradicate those unsightly lumps?....
I lowered my cholestrol - I will PM you.
 
EMF Mitigation - Flush Niacin - Big 5 Minerals

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