Genetic Marker for Stroke and Cardiovascular Disease – Folate and Vit B12 pathways

Researchers Discover Underlying Genetic Marker for Stroke and Cardiovascular Disease

NIH-funded findings point to new potential strategies for disease prevention and treatment.

Scientists studying the genomes of nearly 5,000 people have pinpointed a genetic variant tied to an increased risk for stroke, and have also uncovered new details about an important metabolic pathway that plays a major role in several common diseases. Together, their findings may provide new clues to underlying genetic and biochemical influences in the development of stroke and cardiovascular disease, and may also help lead to new treatment strategies.

“Our findings have the potential to identify new targets in the prevention and treatment of stroke, cardiovascular disease and many other common diseases,” said Stephen R. Williams, Ph.D., a postdoctoral fellow at the University of Virginia Cardiovascular Research Center and the University of Virginia Center for Public Health Genomics, Charlottesville.

Dr. Williams, Michele Sale, Ph.D., associate professor of medicine, Brad Worrall, M.D., professor of neurology and public health sciences, all at the University of Virginia, and their team reported their findings March 20, 2014 in PLoS Genetics. The investigators were supported by the National Human Genome Research Institute (NHGRI) Genomics and Randomized Trials Network (GARNET) program.

This image shows a group of people with GTCA written above them.

Researchers supported by NHGRI’s Genomics and Randomized Trials Network (GARNET) program, who have been studying the genomes of nearly 5,000 people, have pinpointed a genetic variant tied to increased risk for stoke and cardiovascular disease. Credit Jonathan Bailey, NHGRI.

Stroke is the fourth leading cause of death and a major cause of adult disability in this country, yet its underlying genetics have been difficult to understand. Numerous genetic and environmental factors can contribute to a person having a stroke. “Our goals were to break down the risk factors for stroke,” Dr. Williams said.

The researchers focused on one particular biochemical pathway called the folate one-carbon metabolism (FOCM) pathway. They knew that abnormally high blood levels of the amino acid homocysteine are associated with an increased risk of common diseases such as stroke, cardiovascular disease and dementia. Homocysteine is a breakdown product of methionine, which is part of the FOCM pathway. The same pathway can affect many important cellular processes, including the methylation of proteins, DNA and RNA. DNA methylation is a mechanism that cells use to control which genes are turned on and off, and when.

But clinical trials of homocysteine-lowering therapies have not prevented disease, and the genetics underlying high homocysteine levels – and methionine metabolism gone awry – are not well defined.

Dr. Williams and his colleagues conducted genome-wide association studies of participants from two large long-term projects: the Vitamin Intervention for Stroke Prevention (VISP), a trial looking at ways to prevent a second ischemic stroke, and the Framingham Heart Study (FHS), which has followed the cardiovascular health and disease in a general population for decades. They also measured methionine metabolism – the ability to convert methionine to homocysteine – in both groups. In all, they studied 2,100 VISP participants and 2,710 FHS subjects.

In a genome-wide association study, researchers scan the genome to identify specific genomic variants associated with a disease. In this case, the scientists were trying to identify variants associated with a trait – the ability to metabolize methionine into homocysteine.

Investigators identified variants in five genes in the FOCM pathway that were associated with differences in a person’s ability to convert methionine to homocysteine. They found that among the five genes, one – the ALDH1L1 gene – was also strongly associated with stroke in the Framingham study. When the gene is not working properly, it has been associated with a breakdown in a normal cellular process called programmed cell death, and cancer cell survival.

They also made important discoveries about the methionine-homocysteine process. “GNMT produces a protein that converts methionine to homocysteine. Of the five genes that we identified, it was the one most significantly associated with this process,” Dr. Williams said. “The analyses suggest that differences in GNMT are the major drivers behind the differences in methionine metabolism in humans.”

“It’s striking that the genes are in the same pathway, so we know that the genomic variants affecting that pathway contribute to the variability in disease and risk that we’re seeing,” he said. “We may have found how genetic information controls the regulation of GNMT.”

The group determined that the five genes accounted for 6 percent of the difference in individuals’ ability to process methionine into homocysteine among those in the VISP trial. The genes also accounted for 13 percent of the difference in those participants in the FHS, a remarkable result given the complex nature of methionine metabolism and its impact on cerebrovascular risk. In many complex diseases, genomic variants often account for less than 5 percent of such differences.

“This is a great example of the kinds of successful research efforts coming out of the GARNET program,” said program director Ebony Madden, Ph.D. “GARNET scientists aim to identify variants that affect treatment response by doing association studies in randomized trials. These results show that variants in genes are associated with the differences in homocysteine levels in individuals.”

The association of the ALDH1L1 gene variant with stroke is just one example of how the findings may potentially lead to new prevention efforts, and help develop new targets for treating stroke and heart disease, Dr. Williams said.

“As genome sequencing becomes more widespread, clinicians may be able to determine if a person’s risk for abnormally high levels of homocysteine is elevated,” he said. “Changes could be made to an individual’s diet because of a greater risk for stroke and cardiovascular disease.”

The investigators plan to study the other four genes in the pathway to try to better understand their potential roles in stroke and cardiovascular disease risk.

NOTES ABOUT THIS GENETICS RESEARCH

In addition to NHGRI, the research was supported by funds from the National Heart, Lung and Blood Institute, the National Institute of Neurological Disorders and Stroke, the National Institute on Aging and the Robert Dawson Evans Endowment of the Department of Medicine at Boston University School of Medicine.

The National Human Genome Research Institute is one of the 27 institutes and centers at the National Institutes of Health. The NHGRI Extramural Research Program supports grants for research and training and career development at sites nationwide.

Contact: Press Office – National Human Genome Research Institute/NIH
Source:National Human Genome Research Institute/NIH press release.


 

Methionine

Although mammals cannot synthesize methionine, they can still use it in a variety of biochemical pathways:

Catabolism

Methionine is converted to S-adenosylmethionine (SAM) by (1) methionine adenosyltransferase.

SAM serves as a methyl-donor in many (2) methyltransferase reactions, and is converted to S-adenosylhomocysteine (SAH).

(3) Adenosylhomocysteinase converts SAH to homocysteine.

There are two fates of homocysteine: it can be used to regenerate methionine, or to form cysteine.

Regeneration

Methionine can be regenerated from homocysteine via (4) methionine synthase in a reaction that requires Vitamin B12 as a cofactor.

Homocysteine can also be remethylated using glycine betaine (NNN-trimethyl glycine, TMG) to methionine via the enzyme betaine-homocysteine methyltransferase (E.C.2.1.1.5, BHMT). BHMT makes up to 1.5% of all the soluble protein of the liver, and recent evidence suggests that it may have a greater influence on methionine and homocysteine homeostasis than methionine synthase.

Reverse-transulfurylation pathway: conversion to cysteine[edit]

Homocysteine can be converted to cysteine.

Ethylene synthesis

This amino acid is also used by plants for synthesis of ethylene. The process is known as the Yang Cycle or the methionine cycle.

The Yang cycle

Chemical synthesis

Racemic methionine can be synthesized from diethyl sodium phthalimidomalonate by alkylation with chloroethylmethylsulfide (ClCH2CH2SCH3) followed by hydrolysis and decarboxylation.[17]

Human nutrition

Requirements

The Food and Nutrition Board (FNB) of the U.S. Institute of Medicine set Recommended Dietary Allowances (RDAs) for essential amino acids in 2002. For methionine combined with cysteine, for adults 19 years and older, 19 mg/kg body weight/day.[18]

Dietary sources

Food sources of Methionine[19]
Food g/100g
Egg, white, dried, powder, glucose reduced 3.204
Sesame seeds flour (low fat) 1.656
Egg, whole, dried 1.477
Cheese, Parmesan, shredded 1.114
Brazil nuts 1.008
Soy protein concentrate 0.814
Chicken, broilers or fryers, roasted 0.801
Fish, tuna, light, canned in water, drained solids 0.755
Beef, cured, dried 0.749
Bacon 0.593
Beef, ground, 95% lean meat / 5% fat, raw 0.565
Pork, ground, 96% lean / 4% fat, raw 0.564
Wheat germ 0.456
Oat 0.312
Peanuts 0.309
Chickpea 0.253
Corn, yellow 0.197
Almonds 0.151
Beans, pinto, cooked 0.117
Lentils, cooked 0.077
Rice, brown, medium-grain, cooked 0.052

High levels of methionine can be found in eggs, sesame seeds, Brazil nuts, fish, meats and some other plant seeds; methionine is also found in cereal grains. Most fruits and vegetables contain very little of it. Most legumes are also low in methionine. However, it is the combination of methionine and lysine which is considered for completeness of a protein.[20] Racemic methionine is sometimes added as an ingredient to pet foods.[21]

Restriction

There is scientific evidence that restricting methionine consumption can increase lifespans in fruit flies.[22]

A 2005 study showed methionine restriction without energy restriction extends mouse lifespan.[23]

A study published in Nature showed adding just the essential amino acid methionine to the diet of fruit fliesunder dietary restriction, including restriction of essential amino acids (EAAs), restored fertility without reducing the longer lifespans that are typical of dietary restriction, leading the researchers to determine that methionine “acts in combination with one or more other EAAs to shorten lifespan.”[22][24][25] Restoring methionine to the diet of mice on a dietary restriction regimen blocks many acute benefits of dietary restriction, a process that may be mediated by increased production of hydrogen sulfide.[26]

Several studies showed that methionine restriction also inhibits aging-related disease processes in mice[27][28] and inhibits colon carcinogenesis in rats.[29] In humans, methionine restriction through dietary modification could be achieved through a vegan diet. Veganism being a completely plant based diet is typically very low in methionine, however certain nuts and legumes may provide higher levels.[30]

A 2009 study on rats showed “methionine supplementation in the diet specifically increases mitochondrial ROS production and mitochondrial DNA oxidative damage in rat liver mitochondria offering a plausible mechanism for its hepatotoxicity“.[31]

However, since methionine is an essential amino acid, it cannot be entirely removed from animals’ diets without disease or death occurring over time[citation needed]. For example, rats fed a diet without methionine and choline developed steatohepatitis (fatty liver), anemia and lost two thirds of their body weight over 5 weeks. Administration of methionine ameliorated the pathological consequences of methionine deprivation.[32] Short-term removal of only methionine from the diet can reverse diet-induced obesity and promotes insulin sensitivity in mice.[33]

Methionine might also be essential to reversing damaging methylation of glucocorticoid receptors caused by repeated stress exposures, with implications for depression.[34]

Health

Loss of methionine has been linked to senile greying of hair. Its lack leads to a buildup of hydrogen peroxide in hair follicles, a reduction in tyrosinase effectiveness, and a gradual loss of hair color.[35]

Methionine is an intermediate in the biosynthesis of cysteinecarnitinetaurinelecithinphosphatidylcholine, and other phospholipids. Improper conversion of methionine can lead to atherosclerosis.[

Lipid Based Diets Effectively Combat Alzheimer’s in Mouse Models of Disease

There is accumulating evidence showing that lifestyle factors like diet may influence the onset and progression of Alzheimer’s disease (AD). Our previous studies suggest that a multi-nutrient diet, Fortasyn, containing nutritional precursors and cofactors for membrane synthesis, viz. docosahexaenoic acid, eicosapentaenoic acid, uridine-mono-phosphate, choline, phospholipids, folic acid, vitamins B6, B12, C, E, and selenium, has an ameliorating effect on cognitive deficits in an AD mouse model. In the present study we analyzed learning strategies and memory of 11-month-old AβPPswe/PS1dE9 (AβPP/PS1) mice in the Morris water maze (MWM) task performed after nine months of dietary intervention with a control diet or a Fortasyn diet to characterize diet-induced changes in cognitive performance. The Fortasyn diet had no significant effect on MWM task acquisition.

To assess hippocampus-dependent learning, the strategies that the mice used to find the hidden platform in the MWM were analyzed using the swim path data. During the fourth day of the MWM, AβPP/PS1 mice on control diet more often used the non-spatial random search strategy, while on the Fortasyn diet, the transgenic animals exhibited more chaining strategy than their wild-type littermates. During the probe trial, AβPP/PS1 mice displayed no clear preference for the target quadrant. Notably, in both transgenic and nontransgenic mice on Fortasyn diet, the latency to reach the former platform position was decreased compared to mice on the control diet. In conclusion, this specific nutrient combination showed a tendency to improve searching behavior in AβPP/PS1 mice by increasing the use of a more efficient search strategy and improving their swim efficiency by decreasing the latency to reach the former platform position.

Researchers have devised several lipid-based diets aimed at slowing down progression and relieving symptoms of Alzheimer’s disease.

Alzheimer´s disease (AD) is the most common disease underlying memory problems and dementia in the elderly. One of the invariable pathologies in AD is degeneration of cholinergic synapses in brain cortex and hippocampus. Despite enormous effort to find out an efficient treatment, current pharmacological interventions are limited to a few drugs that alleviate symptoms but do not slow down the underlying disease processes. These drugs include inhibitors of cholinesterases, enzymes that degrade the neurotransmitter acetylcholine, or memantine, a modulator of glutamate neurotransmission.

It is generally accepted that lifestyle and particularly dietary habits influence mental health, and prevalence and progression of AD. Numerous epidemiological studies have revealed profitable effects of dietary intake of especially fish oil on cognitive decline during aging and dementia.

Within the EU-funded project LipiDiDiet (FP7-211696), therapeutic and preventive impact of nutritional lipids on neuronal and cognitive performance in aging, Alzheimer´s disease and vascular dementia, researchers devised several lipid-based diets aimed at slowing down progression and relieving symptoms of AD. Short-term (3 weeks) feeding of young adult APPswe/PS1dE9 mice (transgenic mouse model of AD) with experimental diets containing fish oil or stigmasterol reversed the decrease in responsiveness of hippocampal muscarinic receptors to acetylcholine compared to their non-transgenic littermates. Only fish oil based diet enriched with nutrients supporting neuroprotection (Fortasyn diet) increased in addition the density of muscarinic receptors and cholinergic synapses in the hippocampus.

Image shows an alzheimer's brain slice.

These findings yield important proof-of-principle evidence that regular intake of specific dietary components may help to prevent some of the key early functional changes that take place in the Alzheimer brain. These findings support viability of the dietary approach in AD.

ABOUT THIS ALZHEIMER’S DISEASE RESEARCH

Source: Faizan ul Haq – Bentham Science Publishers
Image Source: Image is in the public domain
Original Research: Abstract for “Lipid-Based Diets Improve Muscarinic Neurotransmission in the Hippocampus of Transgenic APPswe/PS1dE9 Mice” by Helena Janickova, Vladimir Rudajev, Eva Dolejsi, Hennariikka Koivisto, Jan Jakubik, Heikki Tanila, Esam E. El-Fakahany and Vladimir Dolezal in Current Alzheimer Research. Published online February 2016 doi:10.2174/1567205012666151027130350


Abstract

Lipid-Based Diets Improve Muscarinic Neurotransmission in the Hippocampus of Transgenic APPswe/PS1dE9 Mice

Transgenic APPswe/PS1dE9 mice modeling Alzheimer’s disease demonstrate ongoing accumulation of β-amyloid fragments resulting in formation of amyloid plaques that starts at the age of 4-5 months. Buildup of β-amyloid fragments is accompanied by impairment of muscarinic transmission that becomes detectable at this age, well before the appearance of cognitive deficits that manifest around the age of 12 months. We have recently demonstrated that long-term feeding of trangenic mice with specific isocaloric fish oil-based diets improves specific behavioral parameters. Now we report on the influence of short-term feeding (3 weeks) of three isocaloric diets supplemented with Fortasyn (containing fish oil and ingredients supporting membrane renewal), the plant sterol stigmasterol together with fish oil, and stigmasterol alone on markers of cholinergic neurotransmission in the hippocampus of 5-month-old transgenic mice and their wild-type littermates. Transgenic mice fed normal diet demostrated increase in ChAT activity and attenuation of carbachol-stimulated GTP-γ35S binding compared to wild-type mice. None of the tested diets compared to control diet influenced the activities of ChAT, AChE, BuChE, muscarinic receptor density or carbachol-stimulated GTP-γ35S binding in wild-type mice. In contrast, all experimental diets increased the potency of carbachol in stimulating GTP-γ35S binding in trangenic mice to the level found in wild-type animals. Only the Fortasyn diet increased markers of cholinergic synapses in transgenic mice. Our data demonstrate that even short-term feeding of transgenic mice with chow containing specific lipid-based dietary supplements can influence markers of cholinergic synapses and rectify impaired muscarinic signal transduction that develops in transgenic mice.

“Lipid-Based Diets Improve Muscarinic Neurotransmission in the Hippocampus of Transgenic APPswe/PS1dE9 Mice” by Helena Janickova, Vladimir Rudajev, Eva Dolejsi, Hennariikka Koivisto, Jan Jakubik, Heikki Tanila, Esam E. El-Fakahany and Vladimir Dolezal in Current Alzheimer Research. Published online February 2016 doi:10.2174/1567205012666151027130350

DMSO, hydrogen peroxide and Vit C fight cancer cells

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DMSO

You might ask your oncologist why your chances of survival are only 3% (ignoring all of their statistical gibberish such as “5-year survival rates” and deceptive terms like “remission” and “response”), when your chance of survival would be over 90% if they used DMSO.

It would be better for medical doctors to treat cancer patients with the right treatment than to have patients treat themselves at home. Medical doctors can diagnose better, treat better, watch for developing problems better, etc. Unfortunately, doctors are using treatments that have been chosen solely on the basis of their profitability rather than their effectiveness.

DMSO is a highly non-toxic, 100% natural product that comes from the wood industry. But of course, like so many other potential cancer cures, the discovery was buried. DMSO, being a natural product, cannot be patented and cannot be made profitable because it is produced by the ton in the wood industry. The only side-effect of using DMSO in humans is body odor (which varies from patient to patient).

Your complete DNA sequence will help shape the future of medicine

The FDA took note of the effectiveness of DMSO at treating pain and made it illegal for medical uses in order to protect the profits of the aspirin companies (in those days aspirin was used to treat arthritis). Thus, it must be sold today as a “solvent.” Few people can grasp the concept that government agencies are organized for the sole purpose of being the “police force” of large, corrupt corporations.

While it is generally believed that orthodox medicine and modern corrupt politicians persecute alternative medicine, this is not technically correct. What they do is persecute ANY cure for cancer, it doesn’t matter whether it is orthodox or alternative. The proof of this is DMSO. It appears that orthodox medicine persecutes alternative medicine only because there are far more alternative cancer treatments that can cure cancer than orthodox treatments.

Folic acid

Another substance that targets cancer cells is being researched at Purdue University and other places: folic acid. This too will be buried unless it can lead to more profitable cancer treatments.

But alternative medicine is rightfully not interested in combining DMSO with chemotherapy. DMSO will combine with many substances, grab them, and drag them into cancer cells. It will also blast through the blood-brain barrier like it wasn’t even there.

DMSO has been combined successfully with hydrogen peroxide (e.g. see Donsbach), cesium chloride, MSM (though it may not bind to MSM), and other products.

DMSO – Vitamin C Treatment

Vitamin C is so simlar to glucose, that cells, and especially cancer cells, consume vitamin C the same way they would consume glucose.

Cancer cells are anaerobic obligates, which means they depend upon glucose as their primary source of metabolic fuel. Cancer cells employ transport mechanisms called glucose transporters to actively pull in glucose.

In the vast majority of animals, vitamin C is synthesized from glucose in only four metabolic steps. Hence, the molecular shape of vitamin C is remarkably similar to glucose. Cancer cells will actively transport vitamin C into themselves, possibly because they mistake it for glucose. Another plausible explanation is that they are using the vitamin C as an antioxidant. Regardless, the vitamin C accumulates in cancer cells.

If large amounts of vitamin C are presented to cancer cells, large amounts will be absorbed. In these unusually large concentrations, the antioxidant vitamin C will start behaving as a pro-oxidant as it interacts with intracellular copper and iron. This chemical interaction produces small amounts of hydrogen peroxide.

Because cancer cells are relatively low in an intracellular anti-oxidant enzyme called catalase, the high dose vitamin C induction of peroxide will continue to build up until it eventually lyses the cancer cell from the inside out! This effectively makes high dose IVC a non-toxic chemotherapeutic agent that can be given in conjunction with conventional cancer treatments. Based on the work of several vitamin C pioneers before him, Dr. Riordan was able to prove that vitamin C was selectively toxic to cancer cells if given intravenously. This research was recently reproduced and published by Dr. Mark Levine at the National Institutes of Health.

As feared by many oncologists, small doses may actually help the cancer cells because small amounts of vitamin C may help the cancer cells arm themselves against the free-radical induced damage caused by chemotherapy and radiation. Only markedly higher doses of vitamin C will selectively build up as peroxide in the cancer cells to the point of acting in a manner similar to chemotherapy. These tumor-toxic dosages can only be obtained by intravenous administration.

Over a span of 15 years of vitamin C research, Dr. Riordan’s RECNAC (cancer spelled backwards) research team generated 20 published papers on vitamin C and cancer. RECNAC even inspired its second cancer research institute, known as RECNAC II, at the University of Puerto Rico. This group recently published an excellent paper in Integrative Cancer Therapies, titled “Orthomolecular Oncology Review: Ascorbic Acid and Cancer 25 Years Later.” RECNAC data has shown that vitamin C is toxic to tumor cells without sacrificing the performance of chemotherapy.

Intravenous vitamin C also does more than just kill cancer cells. It boosts immunity. It can stimulate collagen formation to help the body wall off the tumor. It inhibits hyaluronidase, an enzyme that tumors use to metastasize and invade other organs throughout the body. It induces apoptosis to help program cancer cells into dying early. It corrects the almost universal scurvy in cancer patients. Cancer patients are tired, listless, bruise easily, and have a poor appetite. They don’t sleep well and have a low threshold for pain. This adds up to a very classic picture of scurvy that generally goes unrecognized by their conventional physicians.

Because cancer cells consume 15 times more glucose than normal cells, under the right conditions, cancer cells should consume 15 times more vitamin C than a normal cell. While normal cells benefit from vitamin C, the microbes inside of the cancer cells may be killed by vitamin C. It is microbes which are inside of the cancer cells which cause cancer and which force a cancer cell to remain cancerous.
It should be mentioned that two-time Nobel Prize winner Linus Pauling, and an associate, Dr. Ewan Cameron, M.D., were able to extend the lives of cancer patients more than 10-fold using only 10 grams of vitamin C a day by I.V.
This protocol will modify the Pauling/Cameron protocol four different ways:
1) It will include DMSO in the evening dose to help Vitamin C target cancer cells and get inside of cancer cells,
2) It includes a very, very low glucose diet so that the cancer cells will feast on Vitamin C instead of glucose,
3) It includes 15% or less potassium ascorbate, which has a special affinity for cancer cells,
4) It will include as little sodium ascorbate (or other sodium forms of Vitamin C) as possible because these types of Vitamin C do not get inside of cancer cells very well.
Regarding the use of potassium ascorbate, a foundation in Italy has proven that potassium ascorbate can be used to cure cancer (WARNING: no more than 15% of the Vitmain C you take should be a potassium version!!). See: Pantellini Foundation (Italy)

WARNING

Do NOT use potassium ascorbate or any other form of potassium as your primary source of Vitamin C!!! If you use potassium ascorbate work with the vendor of this product to insure you are taking safe doses relative to non-potassium forms of Vitamin C!!! If your vendor does not make a recommendation, then use 15% as the maximum portion of Vitamin C that is a potassium form!!
The second thing this treatment uses is DMSO. DMSO is used to “open” the ports on the cancer cells to assist getting vitamin C inside the cancer cells. DMSO is very well known to target cancer cells and open their ports. To better understand this concept see this article.

In summary, there are three things that help get the vitamin C inside the cancer cells:
1) Cancer cells consume 15 times more glucose than normal cells and cancer cells cannot tell the difference between glucose and vitamin C.
2) The use of potassium ascorbate as a part of the Vitamin C protocol.
3) The use of DMSO.
A fourth unique thing about this protocol is the “cancer diet.” The cancer diet for this treatment focuses on a LOW GLUCOSE cancer diet. In this way, the cancer cells have less glucose to interfere with their consumption of vitamin C!

Possible Swelling and Inflammation

There are two possible results when large amounts of vitamin C get inside of a cancer cell. First, the vitamin C can kill the microbe(s) inside the cancer cell and the cell will safely revert into a normal cell; or second, the vitamin C can kill the cancer cell itself.

While the first of these two options will not cause any swelling or inflammation, the second option may cause swelling and inflammation.
For this reason, anyone on this protocol who would be put at risk by swelling and/or inflammation (e.g. in a tumor), should carefully and slowly build-up to the theraputic dose of vitamin C, watching carefully for any potential swelling or inflammation.

Details of the Treatment

Many people have difficulties working with DMSO. In some cases, when taken transdermally (through the skin) there is a skin rash which is simply too severe to continue the treatment. When you get your bottle of DMSO put one drop on your skin, spread it around a little bit and see if you have an allergic reaction (i.e. severe rash). If not, an hour later put 10 drops on your skin and spread it thin.

If you do have a reaction, you may still be able to take the DMSO orally (added to 4 ounces of water). But if you cannot take the DMSO orally, and you have a skin reaction to the DMSO, you will have to abandon this treatment.

If you want to know more about DMSO, see this website:
http://www.dmso.org/articles/information/muir.htm

The Importance of the DMSO

This treatment uses DMSO (in the evening) and vitamin C (twice a day). The theory of this treatment is that the DMSO will be used first (in the evening dose), either taken orally (with water) or transdermally (through the skin). In about 10 minutes the DMSO will have targeted the cancer cells and will start “opening up” their ports.

In the evening dose, about ten minutes after taking the DMSO, the vitamin C will be taken with water. When the vitamin C gets to the cancer cells the cells natural affinity for consuming vitamin C (because the cancer cells “think” the vitamin C is glucose) should be enhanced by the fact that the cancer cells have been “opened up” by DMSO.

The theory is that the DMSO will allow a larger concentration of vitamin C to get inside the cancer cells than would normally occur.

As already mentioned, once vitamin C can get inside of a cancer cell the cell may revert into a normal cell or it may be killed. If enough cancer cells are killed, some swelling may occur.


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