Why Low Dose DMSO is NOT Safe Part 2
#1
In part one, “Why Low Dose DMSO is NOT Safe”, I covered a number of studies illustrating how even very low dosages of DMSO result in elevated levels of apoptosis in a wide range of tissues including the brain, inhibition of the bodies natural production of hormones, inhibition of mitochondrial respiration, a reduction in body temperature, and increases of intracellular calcium, all while being highly unstable and possessing an extremely long half life which allows the dosage to build up with consistent usage. Here, I will cover the reasoning behind Ray Peat's explicit warning regarding DMSO:

“Its ability to release histamine and nitric oxide and to inhibit cholinesterase (articles below) suggest that its use shouldn’t be prolonged.” (http://raypeatforums.org/showthread.php?tid=15)

Following, Ray Peat explains why even just a tiny amount of MSG can disrupt the whole organism by increasing acetylcholine, thereby activating the production of nitric oxide which leads to cellular apoptosis. DMSO, by inhibiting the enzyme responsible for the break down of acetylcholine, allows acetylcholine to accumulate to higher and higher levels.

“But their theory is so mistaken that it’s hard for them to get off on to a new line of drug treatment because the acetylcholine, it’s essential and part of our conscious regulating – it’s needed for memory, all kinds of biological processes require just the right amount of acetylcholine. But it activates the enzyme that produces nitric oxide. And nitric oxide blocks energy production, and so the process of excitotoxicity, which made monosodium glutamate notorious because a little too much of that activates the production of a little too much acetylcholine and that makes too much nitric oxide. Nitric oxide poisons the ability to oxidize glucose to carbon dioxide, so it increases lactic acid. And the cell has less energy and is more excited by the acetylcholine. So, basically, it becomes susceptible to dying in proportion to the over-stimulation of acetylcholine. (https://l-i-g-h-t.com/transcript-377)

Following, Ray Peat explains how the properties inherent to DMSO, should be expected to result in increased rates of aging and disease including cancer, and actually shift the metabolism away from the oxidation of sugar towards the oxidation of fat:

“ANDREW MURRAY: Oops. So another good case in point of more is not better. In your opinion, do you think most people have enough acetylcholine in their systems?

RAY PEAT: Yeah. Actually, I think that tendency with aging is to have too much of the shock reaction. For over 100 years now, there has been evidence that over-activity of the vagus nerve and parasympathetic nerve system produces shock that it’s the essential factor in shock. And this is the system that acts primarily through acetylcholine producing nitric oxide. Nitric oxide blocks oxygen metabolism. So in shock, your blood stays red and full of oxygen that the tissue can use it. And that happens with aging, heart failure, kidney failure, dementia, all the tissues relatively have a shock-like metabolism that progresses with aging.” (https://l-i-g-h-t.com/transcript-377)

“From more realistic perspectives, nitric oxide is being considered as a cause of aging, especially brain aging. Nitric oxide interacts with unsaturated fats to reduce oxygen use, damage mitochondria, and cause edema.” (http://raypeat.com/articles/aging/corona...rone.shtml)

“Carbon monoxide, and other substances such as nitric oxide which also function as respiratory poisons, suppress energy production by the mitochondria, and this activates enzymes which cut DNA molecules, producing either DNA rearrangement, or apoptotic cell death.”

“Histamine release, nitric oxide, and carbon monoxide are broadly involved in excitotoxic damage, and carbon dioxide tends to be protective against these, too.”

“Nitric oxide, associated with unbalanced excitation, is involved in the nerve damage of epilepsy, amyotrophic lateral sclerosis, Parkinson’s disease, Alzheimer’s disease, and Huntington’s disease.”

“The unsaturated fats and estrogen contribute to the increased release of serotonin and nitric oxide (NO). Nitric oxide is produced during inflammation, and, like ethane, can be detected in the breath when the lungs are inflamed. Nitric oxide, as a pro-inflammatory free radical, stimulates the peroxidation of the unsaturated fats. Both NO and serotonin inhibit mitochondrial respiration, shifting metabolism toward glycolysis.”

“Estrogen, like radiation and oxygen deprivation, increases formation of the nitric oxide (NO) free radical, which has so many harmful effects, ranging from damaging DNA to poisoning mitochondria. One of the consequences of increasing NO formation (and estrogen) is the activation of an enzyme (heme oxygenase) which produces carbon monoxide, in the process of breaking down the heme molecule (which is needed for respiratory enzymes, among other essential functions). In previous newsletters I have discussed the reasons for thinking that endogenously produced carbon monoxide could explain the gradual development of cancer, since it stabilizes cells in the primitive anti-respiratory condition.” (http://www.functionalps.com/blog/2014/02...ric-oxide/)

The latest article on Ray Peat's website, “The dark side of stress (learned helplessness)“ explains in detail how drugs that inhibit cholinesterase or increase nitric oxide, which are properties of DMSO, work in the opposite direction of pro-metabolic compounds including progesterone, resulting in toxicity to the liver and brain along with the creation of learned helplessness:

"In 1997, a group (Pike, et al.) created brain injuries in rats to test the idea that a cholinesterase inhibitor would improve their recovery and ability to move through a maze. They found instead that it reduced the cognitive ability of both the injured and normal rats."

"When the brain is poisoned by an organophosphate insecticide, which lowers the activity of cholinesterase, seizures are likely to occur, and treatment with progesterone can prevent those seizures, reversing the inhibition of the enzyme (and increasing the activity of cholinesterase in rats that weren't poisoned) (Joshi, et al., 2010)."

"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."

"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)."

"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." (http://raypeat.com/articles/articles/dar...ness.shtml)

Further, Ray Peat explains how drugs that inhibit cholinesterase result in liver damage:

“So, they proposed poisoning the enzyme cholinesterase, which was associated in the animal studies with increased intelligence, memory and brain growth. They proposed doing just the opposite, poisoning that enzyme to increase the amount of acetylcholine in the brain. The first drug that was proposed and used according to that theory was Tacrine, was the name of the chemical and several studies, by the late '90s, they were seeing that it did absolutely nothing for the Alzheimer’s dementia but it did cause a terrifically high incidence of liver disease.“ (https://l-i-g-h-t.com/transcript-361)

Lastly, DMSO has been found to increase intracellular calcium. Following, Ray Peat explains why increases of intracellular calcium result in soft tissue calcification and lead to a variety of diseases:

“Magnesium and potassium are mainly intracellular ions, sodium and calcium are mainly extracellular ions. When cells are excited, stressed, or de-energized, they lose magnesium and potassium, and take up sodium and calcium. The mitochondria can bind a certain amount of calcium during stress, but accumulating calcium can reach a point at which it inactivates the mitochondria, forcing cells to increase their inefficient glycolytic energy production, producing an excess of lactic acid. Abnormal calcification begins in the mitochondria.”

“When cells are stressed or dying, they take up calcium, which tends to excite the cells at the same time that it inhibits their energy production, intensifying their stress. A cramp or a seizure is an example of uncontrolled cellular excitation. Prolonged excitation and stress contribute to tissue inflammation and fibrosis.”

“Gross calcification generally follows the fibrosis that is produced by inflammation.
Increased intracellular calcium, in association with excess nitric oxide and excitatory amino acids, is involved in several neurodegenerative diseases, including ALS, Alzheimers disease, Parkinsons disease, Huntingtons chorea, and epilepsy.” (http://raypeat.com/articles/articles/calcium.shtml)
"The true method of knowledge is experiment." -William Blake
#2
Thank you.

I agree, supplements in DMSO are not safe and should not be taken.

Oil, and alcohol solvents are far safer and normal.
  


Possibly Related Threads...
Thread Author Replies Views Last Post
  Why Low Dose DMSO is NOT Safe Sea 0 959 07-01-2017, 10:36 PM
Last Post: Sea

Forum Jump: