Disclaimer - While Vitamin U has been shown to have value as a nutrient, it has not been approved by the FDA as a treatment for any disease. Talk to your doctor or dietitian about your medical condition.
Coffee, GERD, stomach ulcers and Vitamin U
Allergies and Vitamin U
Neural tube defects and Vitamin U
1. Serine hydroxymethyltransferase
2. Thymidylate synthase
3. Dihydrofolate reductase
4a. 5,10-methylenetetrahydrofolate dehydrogenase NADP+
4b. 5,10-methenyltetrahydrofolate cyclohydrolase
4c. Formate-tetrahydrofolate ligase
5. Phosphoribosylaminoimidazolecarboxamide formyltransferase
6. Methylenetetrahydrofolate reductase
7. Methionine synthase
N.B. 4a-c are three components of MTHFD1
Where does Vitamin U fit into all this? It should be emphasized that there has not been any scientific research testing whether Vitamin U supplementation can prevent NTDs. The studies have simply not been done. However, there is some genetic evidence that suggests that Vitamin U may play a role in correct neural tube formation.
- Vitamin U supplies methyl groups to mammals via its reaction with homocysteine to form methionine catalyzed by the enzyme BHMT2. This is very similar to that of betaine, though whether Vitamin U plays this role in embryonic tissue has not been investigated.
- Vitamin U is abundant in vegetables, the benefits of which have been long known in preventing neural tube defects. While the presence of folate is most likely the primary factor, it is possible that some of the benefits conferred by eating vegetables are due to the provision of methyl groups from Vitamin U.
- A preconception diet rich in methionine reduces the prevalence of neural tube defects. Vitamin U is essentially methionine with an extra methyl group. One molecule of Vitamin U actually supplies two molecules of methionine, one being the newly-methylated homocysteine, the other being the demethylated Vitamin U.
- Studies have shown that methylation in the embryo is supplied by methyl groups from both the folate cycle and betaine. If we assume that methionine synthase and BHMT1 contribute to embryonic methylation, then Vitamin U is also likely to make a contribution. It is logical that the benefits of green vegetables in preventing neurological abnormalities is due to the combined effects of folate, betaine and Vitamin U, with the emphasis on folate.
- Folate is absolutely necessary at some level to provide the embryo nucleotides during the first weeks following conception. It cannot be replaced by other molecules.
- Folate requirements may be lowered as long as adequate levels of methyl groups are provided by methionine and betaine from the methionine cycle.
- Though its role in fetal development has not been investigated, it is likely that Vitamin U has a similar role to that of methionine and betaine, and would be of greater importance for people whose diet is low in protein and fat such as vegans.
- Shaw et al 2004 https://pubmed.ncbi.nlm.nih.gov/15234930/
- Zhang et al 2015 https://pubmed.ncbi.nlm.nih.gov/25466894/
- Froese et al 2019 https://pubmed.ncbi.nlm.nih.gov/30693532/
- Halsted et al 2002 https://pubmed.ncbi.nlm.nih.gov/12122204/
- Shin et al 2010 https://pubmed.ncbi.nlm.nih.gov/20220206/
- Bailey and Ayling 2009 https://pubmed.ncbi.nlm.nih.gov/19706381/
- Cornet et al 2019 https://pubmed.ncbi.nlm.nih.gov/31205715/
- Huennekens 1969 https://pubmed.ncbi.nlm.nih.gov/4891866/
- Purohit et al 2007 https://pubmed.ncbi.nlm.nih.gov/17616758/
- Duncan et al 2013 (1) https://pubmed.ncbi.nlm.nih.gov/23857220/
- Duncan et al 2013 (2) https://pubmed.ncbi.nlm.nih.gov/23143835/
- Teng et al 2012 https://pubmed.ncbi.nlm.nih.gov/23014492/
- Rinehart and Greenberg 1948 https://pubmed.ncbi.nlm.nih.gov/18859393/
- Leung 2013 https://pubmed.ncbi.nlm.nih.gov/23935126/
- Leung 2017 https://pubmed.ncbi.nlm.nih.gov/29141214/
- Blom 2006 https://pubmed.ncbi.nlm.nih.gov/16924261/
- Benevenga 2007 https://pubmed.ncbi.nlm.nih.gov/17413090/
- Bertolo and McBreairity 2013 https://pubmed.ncbi.nlm.nih.gov/23196816
Vitamin U is metabolized by the enzyme BHMT2
Mouth ulcers and Vitamin U
- Crusty food like bread or toast
- Crispy food like chips
- Salty food like pretzels
- Sweet food like candy
- Sticky food like cookies
- Sour food like vinegar
- Hot food like coffee
Vitamin U complements H2 blockers
Image - http://www.vivo.colostate.edu/hbooks/pathphys/digestion/stomach/parietal.html
Summary - H2 blockers are drugs used to reduce stomach acid in people who have pain due to stomach ulcers. Vitamin U in the form of fresh vegetable juice or supplements can be used alongside H2 blockers to speed up the restoration of the protective mucous bilayer.
The human stomach is a very acidic environment. The pH of a correctly-functioning stomach is 1.5 - 3. The acidity of gastric juice is due to hydrochloric acid (HCl), which is produced by parietal cells in the upper parts of the stomach (fundus and cardia). Parietal cells produce acid using enzymes called proton pumps (H+/K+ ATPase), which use the energy derived from the hydrolysis of ATP to pump H+ into the stomach. It is the protons (H+) that cause acidity.
The parietal cells pump acid into the stomach in response to signal molecules binding receptors. There are numerous kinds of receptors that respond to different stimuli, either positively or negatively. The most important for acid production are the H2 histamine receptors. Protein in food is broken down in the stomach by acid and the enzyme pepsin to form peptides. These peptides stimulate the release of the hormone gastrin from G cells in the stomach and duodenum. Gastrin stimulates the release of histamine from ECL cells. Histamine binds receptors in the base of parietal cells where it stimulates the movement of proton pumps to the apical surface, where they pump acid into the stomach cavity (lumen). This acid accelerates this whole cycle, breaking down more proteins in food by hydrolysis as well as activating pepsin.
H2 blockers bind to the H2 receptors, which stops histamine from binding. If histamine can't bind, the levels of acid in the stomach remain fairly low and the corresponding pH relatively high. (H2 blockers are often referred to as H2 antagonists because they block the binding of histamine without itself stimulating the function of the receptor, an important distinction from agonists).
H2 blockers were invented in the 1960s and have to a large extent been superseded by proton pump inhibitors due to the latter's more potent acid-suppressing abilities. Commonly used H2 blockers include famotidine (Pepcid) and cimetidine (Tagamet). Ranitidine (Zantac) was the most prescribed drug in the US during the 1980s, but the FDA has recently banned its sale due to carcinogenic impurities.
Stomach ulcers and gastroesophageal reflux (GERD) are conditions characterized by pain caused by stomach acid coming into direct contact with the lining of the stomach and esophagus, respectively. Contrary to popular opinion, these conditions are rarely caused by excessive production of stomach acid. In fact, the acidity in the stomach of those with stomach ulcers is typically low (i.e. relatively high pH). GERD is caused by normal stomach acid coming into contact with the esophagus, an organ that is not designed to withstand such exposure. Unlike the stomach, the esophagus is not coated with a protective alkaline mucous bilayer and is very sensitive to contact from even small amounts of gastric juice.
One unfortunate problem with taking H2 blockers for stomach ulcers is that they reduce the secretion of mucin (Ichikawa et al., Diebel et al). So while they reduce pain by reducing the amount of acid produced, they also increase the risk of pain by weakening the mucous bilayer.
Vitamin U is a nutrient abundant in vegetables and fruit that stimulates the secretion of mucin in the stomach. As fresh vegetables and fruit have been a major component of our diet for a very long time, it is reasonable to conclude that dietary Vitamin U plays an important role in the maintenance of optimal stomach function.
Can Vitamin U be combined with H2 blockers?
Considering Vitamin U stimulates mucin secretion and H2 blocker reduce it, one may wonder whether Vitamin U can be taken with H2 blockers to negate the negative effects. The evidence suggests yes. In 2009, Ichikawa et al. showed that co-administration of Vitamin U with famotidine reversed the mucin-blocking effects of famotidine without affecting the acid-suppression effects. These results suggest that Vitamin U can add another level of protection to the gut in those taking H2 blockers.
Take care and good luck,
High salt consumption may cause stomach ulcers
Vitamin U may help combat the ulcergenic effects of NSAIDs
Vitamin U and acne, dandruff and eczema
Acne, dandruff and eczema are skin conditions the origins of which are often idiosyncratic and mysterious. However, one characteristic shared by all three conditions is low glutathione levels. Glutathione is by far the most important antioxidant in the human body, yet we absorb little of it from our food- that's why our body makes it.
There are three main causes of low glutathione -
1. A medical condition that drains large amounts of glutathione
2. A genetic block that prevents the biosynthesis or regeneration of glutathione
3. Not enough glutathione precursors in our diet
Identifying the root cause of your skin condition is an important first step in the healing process. However, this is easier said than done. Often we just don't know why these conditions happen. Sometimes they can break out suddenly and worsen quickly, particularly under stress. At other times, symptoms can persist chronically for years.
Irrespective of the root cause, restoring your glutathione levels is a vital part of this rebalancing act. Glutathione is a tripeptide comprised of cysteine, glutamate and glycine. Of these amino acids, cysteine is most commonly in short supply. If glutathione levels are low due to dietary factors, it is usually due to a shortage of cysteine. Cysteine is found in protein, especially that derived from animals. Cysteine is also made from methionine, again abundant in animal proteins. These sulfur amino acids are also plentiful in grain proteins. However, some people find that meat/dairy/grain are inflammatory for other reasons like hormones or allergens.
Vitamin U is S-methylmethionine, a soluble nutrient abundant in vegetables and fruit that is converted into methionine by the enzyme BHMT2. There have not been any direct studies into whether Vitamin U has any effect on these three conditions, whether taken internally in the diet or as a supplement, or when applied topically as an active component of a lotion. However, taking Vitamin U can help restore glutathione levels which are low in the tissues affected by acne, dandruff and eczema, so it is quite likely that increasing your intake of Vitamin U will help with these conditions, especially in combination with the identification and removal of triggers of these conditions in you.
A glass of freshly-made vegetable juice every day is an excellent way to boost your Vitamin U intake along with a slew of vitamins and minerals essential for good skin health. For those who prefer a supplement, one capsule per day of Bioremediation's Vitamin U may be a useful alternative.
Take care and good luck,
The methionine cycle and Vitamin U
The most common cause of a low SAM:SAH is a shortfall in the supply of dietary methyl donors. Other causes of low flux include shortages in vitamins that help catalyze reactions (e.g, folate, B12, B6), mutations in genes that encode enzymes involved in catalysis (e.g. MTHFR, CBS), and very low calorie diets.
1. Betaine:homocysteine methyltransferase 1 (BHMT1) and betaine (trimethylglycine or TMG)
2. Methionine synthase (MS) and folate (5'-methyltetrahydrofolate or MTHF)
Betaine (trimethyl glycine) has three methyl groups, one of which is transferred to homocysteine to form methionine and dimethyl glycine. The other two methyl groups contribute to methylation, though via assimilation through the folate cycle. Dimethyl glycine dehydrogenase catalyzes the transfer of a methyl group from dimethyl glycine to tetrahydrofolate to produce 5, 10-methylenetetrahydrofolate. The other product, methyl glycine (sarcosine) yields the last methyl group to tetrahydrofolate in a similar reaction catalyzed by the homologue sarcosine dehydrogenase.
Most methionine in our diet is found as a component of protein, which requires extensive digestion by a slew of enzymes to release methionine as an amino acid before it can enter the methionine cycle. Vitamin U (S-methylmethionine) is methionine with an extra methyl group, although unlike methionine, Vitamin U is rarely a component of proteins. It supplies a methyl group to homocysteine yielding two molecules of methionine. Vitamin U is abundant in vegetables and fruits, especially cruciferous (e.g. cabbage, kale) and stalky (e.g. celery, asparagus) vegetables.
The degree to which these methyl donors contribute to the methionine cycle is dependent upon our diet. In a diet rich in protein and fats, methionine and choline will be major sources. In a diet in which more calories are gleaned from whole grains, betaine will make a greater contribution. Folate and Vitamin U will make larger contributions in diets rich in fresh produce.
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- Mudd and Poole (1975) https://pubmed.ncbi.nlm.nih.gov/1128236/
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