tag:blogger.com,1999:blog-42729961387850202602024-03-13T02:28:34.813-06:00Vitamin U and Peptic UlcersDisclaimer - 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.Sean Yu McLoughlinhttp://www.blogger.com/profile/03287541681698360493noreply@blogger.comBlogger20125tag:blogger.com,1999:blog-4272996138785020260.post-25257135460728197092023-12-26T17:12:00.001-07:002023-12-26T17:20:54.200-07:00Longevity and Vitamin U<p></p><div class="separator" style="clear: both; text-align: center;"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEjioNCR1nHYQ567r-R-ZfSAVEu6vmmgjVrnPP7uXjcET4enYvaBEb30q-Dg_7AmIL6Wc9srz4zZdq4Mv_Ex_L5MufUjSZT9F7Ah0sQc3PhPQ9cavEd80zSs1usJQkQIpYsxTuFMXOdA7x5w6kaLk-dXp9qicxZ_6uc2RJAxiujLhJQZ43P6fQ3iv-GngvWt/s276/tortoise.jpeg" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img border="0" data-original-height="183" data-original-width="276" height="183" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEjioNCR1nHYQ567r-R-ZfSAVEu6vmmgjVrnPP7uXjcET4enYvaBEb30q-Dg_7AmIL6Wc9srz4zZdq4Mv_Ex_L5MufUjSZT9F7Ah0sQc3PhPQ9cavEd80zSs1usJQkQIpYsxTuFMXOdA7x5w6kaLk-dXp9qicxZ_6uc2RJAxiujLhJQZ43P6fQ3iv-GngvWt/s1600/tortoise.jpeg" width="276" /></a></div><div class="separator" style="clear: both; text-align: center;"><br /></div><p></p><p>We age and die as a result of our body accumulating oxidative damage. For example, smoking creates oxygen radicals that damage lung cells. This damage reduces the function of these cells and when enough cells have been damaged or die, lung tissue fails to function and we die from lung failure. </p><p>The best way to live your healthiest life is to reduce future oxidative damage as much as possible. The key to doing this is to restore and maintain high glutathione levels. Glutathione is the main antioxidant in your body that quenches the radicals that damage cells. </p><p>Healthy glutathione levels have been associated with longevity. Studies have shown that centenarians have similar glutathione levels to that of young people. In contrast, people who die at a younger age almost always have a low level of glutathione, which almost certainly contributes to the degenerate condition. </p><p>Can glutathione levels be restored? Evidence suggests they can. Studies on middle age people showed that taking supplements restored their glutathione levels to that of their younger counterparts in 24 weeks. Studies on mice taking similar supplements found those who received supplements lived 24% longer than those who didn't. Furthermore, biochemical markers of good health improved with supplementation suggesting restoring these biochemical markers is probably a useful predictor of lifespan. </p><p>Does this mean humans taking supplements that restore glutathione levels will live longer lives? As humans aren't mice, we can't extrapolate this data to human longevity, but the results so far are promising.</p><p>What's the best way to restore glutathione levels? Glutathione is made up of cysteine, glycine and glutamic acid. In these studies, NAC and glycine are the two amino acids that improved health and longevity in mice and improved health biochemical markers in people (roughly 7 g per day in people). Note that NAC and glycine levels were low in these middle aged people whereas glutamic acid levels were normal, and that NAC is converted into cysteine before becoming a component of glutathione.</p><p>Can Vitamin U be substituted for NAC? Quite possibly, although this has not been tested directly. Vitamin U is an amino acid (S-methylmethionine) that is produced naturally by all flowering plants and is found in all produce, especially stalky and cruciferous vegetables. Vitamin U is integrated into the human body by specific enzymes in the liver and kidney. One advantage of taking Vitamin U over NAC is that these enzymes in the liver and kidney specifically regulate the integration of Vitamin U, converting it into cysteine-->glutathione when needed without any of the potential side effects of NAC dosing.</p><p>Note that while restoring glutathione levels will minimize further damage from oxidative stress, it won't directly reverse existing damage. However, restoring healthy glutathione levels will allow your body's natural repair systems to heal your body the best they can. </p><div style="text-align: left;"><br /></div><div style="text-align: left;"><a href="https://pubmed.ncbi.nlm.nih.gov/21795440/">https://pubmed.ncbi.nlm.nih.gov/21795440/</a></div><div style="text-align: left;"><a href="https://pubmed.ncbi.nlm.nih.gov/35268089/">https://pubmed.ncbi.nlm.nih.gov/35268089/</a></div><div style="text-align: left;"><div><a href="https://pubmed.ncbi.nlm.nih.gov/12486409/">https://pubmed.ncbi.nlm.nih.gov/12486409/</a></div></div>Sean Yu McLoughlinhttp://www.blogger.com/profile/03287541681698360493noreply@blogger.com0tag:blogger.com,1999:blog-4272996138785020260.post-67911869077116851082023-06-17T20:33:00.000-06:002023-06-17T20:33:16.406-06:00Vitamin U protects against oxidative damage caused by medicines<p><span style="font-family: arial;"><br /></span></p><p><span style="font-family: arial;"></span></p><div class="separator" style="clear: both; text-align: center;"><span style="font-family: arial;"><a href="https://blogger.googleusercontent.com/img/a/AVvXsEhxAamEeCV6d7XEx8XzGjCqU33althLgC20XgotMZ0TyyqwpUxSi02wY-zEDJaSLztZmw7EUTPawhoK-9aNPSn_Ck6XiNVWlsD28uRJ9bUXy3pSDAAqBMHXA_3g6fe3csAk9Mfvottq8VDJ89PJM7KU3vz3zo1lANtBmoXu8hejzTSXSx_KyuvhrAJNcQ" style="margin-left: 1em; margin-right: 1em;"><img alt="" data-original-height="3995" data-original-width="3720" height="240" src="https://blogger.googleusercontent.com/img/a/AVvXsEhxAamEeCV6d7XEx8XzGjCqU33althLgC20XgotMZ0TyyqwpUxSi02wY-zEDJaSLztZmw7EUTPawhoK-9aNPSn_Ck6XiNVWlsD28uRJ9bUXy3pSDAAqBMHXA_3g6fe3csAk9Mfvottq8VDJ89PJM7KU3vz3zo1lANtBmoXu8hejzTSXSx_KyuvhrAJNcQ" width="223" /></a></span></div><span style="font-family: arial;"><br /></span><p></p><p><span style="font-family: arial;">Most drugs we take for medical conditions have side effects. Scientists try to design drugs to react with a target as specifically as possible, and not react with other molecules in the body. This is one of the reasons newly-designed drugs go through clinical trials before they can be prescribed by doctors. However, no drug is perfect. Drugs are very reactive chemicals that often react off-target and can cause side-effects. Some side-effects are tolerable because we might be taking the drugs for a short time or the symptoms are mild. However, plenty of drugs are taken for many years for chronic conditions. Other drugs are actually fairly toxic, but are prescribed for emergency situations </span><span style="font-family: arial;">as a last resort </span><span style="font-family: arial;">to save someone's life. </span></p><p><span style="font-family: arial;">In recent years, scientists in Turkey (Yanardag and Turkyilmaz) have performed a series of studies showing that Vitamin U can have a prophylactic effect when taken before drug administration. Vitamin U prevented oxidative damage caused by amiodarone (<a href="https://acsi-journal.eu/index.php/ACSi/article/view/7899/3654">https://acsijournal.eu/index.php/ACSi/article/view/7899/3654</a>), </span><span style="font-family: arial;">p</span><span style="background-color: white; color: #212121; font-family: arial;">entylenetetrazole (</span><span style="color: #212121; font-family: arial;"><a href="https://pubmed.ncbi.nlm.nih.gov/35833322/">https://pubmed.ncbi.nlm.nih.gov/35833322/</a>)</span><span style="font-family: arial;">, D-</span><span style="background-color: white; color: #212121; font-family: arial;">galactosamine (</span><span style="color: #212121; font-family: arial;"><a href="https://pubmed.ncbi.nlm.nih.gov/35673974/">https://pubmed.ncbi.nlm.nih.gov/35673974/</a>)(<a href="https://pubmed.ncbi.nlm.nih.gov/35670011/">https://pubmed.ncbi.nlm.nih.gov/35670011/</a>), and </span><span style="background-color: white; color: #212121; font-family: arial;">valproic acid </span><a href="https://pubmed.ncbi.nlm.nih.gov/25802006/" style="background-color: white; font-family: arial;">https://pubmed.ncbi.nlm.nih.gov/25802006/</a>.</p><div><span style="font-family: arial;">Vitamin U is a nutrient found in vegetables and fruit, especially cruciferous and stalky vegetables. It is assimilated into the body via the action of the enzyme BHMT-2 and promotes the regeneration of glutathione, the stores of which are rapidly degenerated by taking reactive drugs such as amiodarone. </span></div><p><span style="font-family: arial;">Taking Vitamin U supplements to reduce the side effects of specific drug treatments has not been broadly tested in humans and is not FDA approved, so these findings should not be taken as medical advice. However, this research shows that drugs do cause damage that can lead to long term harm, and that simple, naturally-occurring compounds such as Vitamin U can prevent these side effects.</span></p><p><br /></p>Sean Yu McLoughlinhttp://www.blogger.com/profile/03287541681698360493noreply@blogger.com0tag:blogger.com,1999:blog-4272996138785020260.post-66933555116725452312022-05-17T17:55:00.011-06:002023-06-15T08:07:05.927-06:00Coffee, GERD, stomach ulcers and Vitamin U<div class="separator" style="clear: both; text-align: center;"><div class="separator" style="clear: both;"><br /></div><div class="separator" style="clear: both;"><br /></div></div><div class="separator" style="clear: both; text-align: center;"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEgKcpicLC73-aTKMQR7l0qbO7oy_uRH4OMpLSkLZrynkHy9S6jRDmhyxN51l34NHEDRHRBtOI-oDAXoIenW58m4-GyKgLPgGEVrks6Ntm01yhS9Eh1Ak2ZDnus3XmZMQJmKcyBq-xzK3NuM5Q-9L2oNb-fUxUHtAM8axt3O7B3vQwDT7iOCHiRrpCO_Tg/s4900/drinking%20coffee.jpg" style="margin-left: 1em; margin-right: 1em;"><img border="0" data-original-height="3631" data-original-width="4900" height="237" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEgKcpicLC73-aTKMQR7l0qbO7oy_uRH4OMpLSkLZrynkHy9S6jRDmhyxN51l34NHEDRHRBtOI-oDAXoIenW58m4-GyKgLPgGEVrks6Ntm01yhS9Eh1Ak2ZDnus3XmZMQJmKcyBq-xzK3NuM5Q-9L2oNb-fUxUHtAM8axt3O7B3vQwDT7iOCHiRrpCO_Tg/s320/drinking%20coffee.jpg" width="320" /></a></div><br /><div style="text-align: left;"><br /></div><div style="text-align: left;"><br /></div><div style="text-align: left;">Drinking our morning coffee is one of life's little pleasures. Unfortunately, coffee is notorious for inciting acid reflux, GERD, and worsening peptic ulcers. This is especially the case with more heavily roasted coffees and instant coffee. </div><div style="text-align: left;"><br /></div><div style="text-align: left;">What is it about coffee that makes it so problematic? The underlying reasons for the irritability of coffee are a little mysterious. People often cite the acidity of coffee, and it does seem that coffee that tastes less acidic is less harsh on the stomach. However, considering the stomach has a pH that makes coffee appear comparatively mild, there is likely more to this than meets the eye. Furthermore, there are many foods that taste acidic that don't elicit the same response. Malic acid in green apples is very tart and lemons are barely edible for the amount of citric acid they contain, yet eating these fruits doesn't typically cause acid reflux (they may make ulcers sting, but that's another story).</div><div style="text-align: left;"><br /></div><div style="text-align: left;">The classic stimulant caffeine almost certainly contributes to acid reflux to some extent. Caffeine definitely relaxes the esophageal sphincter, which is a muscle whose function is to separate stomach acid from the esophagus. The stomach is full of concentrated HCl, which would damage the lining of the stomach except for the presence of a thick alkaline mucus bilayer maintained by prostaglandins and certain nutrients such as Vitamin U. However, decaffeinated coffee can still cause acid reflux so there's more to it than just caffeine.</div><div style="text-align: left;"><br /></div><div style="text-align: left;">Stomach acid has several functions, from inhibiting the growth of bacteria to unraveling dietary protein and providing the right pH for the proteolytic actions of pepsin. What isn't widely known is that the stomach isn't full of acid at all times. In fact, eating stimulates the production of the hormone gastrin, which via a chain of events results in the secretion of HCl into the stomach. The key dietary component that stimulates gastrin release is protein. Scientists were curious to understand what is it about protein that triggers this response. Protein consist of 20 types of amino acids that have different properties. The aromatic amino acids phenylalanine and tryptophan were by far the most stimulatory (the other aromatic amino acid tyrosine was not tested due to solubility issues).</div><div style="text-align: left;"><br /></div><div style="text-align: left;">The fact that aromatic amino acids were most stimulatory may be quite revealing. Other amino acids all have an acidic group (in fact, some even have two), so it's not acid per se that is the issue. It would seem that the aromatic side chain is the effector (chemically, aromatic simply means that it has a benzene ring). This is where coffee comes in. Coffee has over 2000 compounds, some of which have benzene rings just like the aromatic amino acids. These are collectively referred to as cinnamic acids, and are present in many vegetables, fruits and other plant-based products. Examples include caffeic acid, <i>p</i>-coumaric acid, ferulic acid, and esters thereof. Though it hasn't been demonstrated conclusively, one may wonder whether some of the adverse gastronomical effects of coffee may in part be due to the fact that coffee is an extract containing a wide array of compounds that bear an uncanny resemblance to known acid producers. As extracts, cinnamic acids in coffee are easily accessible. Furthermore, it has been estimated that coffee is the richest sources of cinnamic acids in the Western diet at up to 1 g per day.</div><div style="text-align: left;"><br /></div><div style="text-align: left;">Can Vitamin U help with acid reflux? As the mode of protective action afforded by Vitamin U is via the stimulation of mucus secretion in the stomach, Vitamin U should protect the lining of the stomach to some extent. There is evidence that Vitamin U can help maintain mucosal integrity in other parts of the alimentary canal such as the esophagus. However, the mucus lining the esophagus is thin and not built to withstand concentrated hydrochloric acid. The protective effects conferred by mucoprotectants such as Vitamin U are most effective when used in conjunction with dietary modification that avoids the worse offenders like coffee. Drinking lightly roasted low-acid coffees still have plenty of caffeine and are less likely to cause problems.</div><div style="text-align: left;"><br /></div><div style="text-align: left;"><br /></div><div style="text-align: left;">Further reading</div><div style="text-align: left;"><br /></div><div style="text-align: left;"><ol style="text-align: left;"><li><a href="https://onlinelibrary.wiley.com/doi/10.1002/(SICI)1097-0010(19990301)79:3%3C362::AID-JSFA256%3E3.0.CO;2-D">https://onlinelibrary.wiley.com/doi/10.1002/(SICI)1097-0010(19990301)79:3%3C362::AID-JSFA256%3E3.0.CO;2-D</a></li><li><a href="https://www.sciencedirect.com/science/article/pii/S2090123219300025">https://www.sciencedirect.com/science/article/pii/S2090123219300025</a></li><li><a href="https://pubmed.ncbi.nlm.nih.gov/6806140/">https://pubmed.ncbi.nlm.nih.gov/6806140/</a></li></ol></div><p><br /></p><p><br /></p>Sean Yu McLoughlinhttp://www.blogger.com/profile/03287541681698360493noreply@blogger.com0tag:blogger.com,1999:blog-4272996138785020260.post-32023942289675978922022-05-17T16:26:00.010-06:002023-06-15T08:07:52.878-06:00Allergies and Vitamin U<div class="separator" style="clear: both; text-align: center;"><br /></div><div class="separator" style="clear: both; text-align: center;"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEiYYgj1LtlKwuoh5DcPlBvtwcwBcaBLuW1VYlbd-xjV8cUiROlN9wWVfra2qy1W8QTAeWKH0EhUKsddzalG_XWGvuLY-JdpSZT8SL82yRPIV938jW8wMGWtL34-TWaBm5aF-QHXfAEro2oiooCWZxeJevSHzOqVYZyc_C5pztiU0gpSo4zpdw4coZM86A/s1023/woman%20blowing%20nose.jpeg" style="margin-left: 1em; margin-right: 1em;"><img border="0" data-original-height="682" data-original-width="1023" height="213" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEiYYgj1LtlKwuoh5DcPlBvtwcwBcaBLuW1VYlbd-xjV8cUiROlN9wWVfra2qy1W8QTAeWKH0EhUKsddzalG_XWGvuLY-JdpSZT8SL82yRPIV938jW8wMGWtL34-TWaBm5aF-QHXfAEro2oiooCWZxeJevSHzOqVYZyc_C5pztiU0gpSo4zpdw4coZM86A/s320/woman%20blowing%20nose.jpeg" width="320" /></a></div><br /><div><br /></div><div><br /></div>At this time of the year, allergies are a seasonal problem for many people. With the coming of pollen also comes itchy eyes, a runny nose, an annoying cough and maybe more serious conditions such as asthma or hives. Cells in our immune system called mast cells produce histamine, which triggers an inflammatory response by binding H1 receptors. Our blood vessels dilate and fill with fluid to help get rid of allergens and to counteract the narrowing causes by the build up of mucus. Unfortunately, our bodies tend to overreact and produce way too much histamine. Antihistamines like loratadine (Claritin), cetirizine (Zyrtec), diphenhydramine (Benadryl) work by blocking the binding of histamine to these receptors.<div><br /></div><div>Our body has a few mechanisms that can remove excess histamine from our body. One of the most important is the enzymatic action of histamine N-methyltransferase. HNMT catalyzes the methylation of histamine using the universal methyl donor S-adenosylmethyltransferase (SAM) as its source of methyl groups. Methylated histamine can no longer bind to the H1 receptor and cannot trigger more inflammation. Methylhistamine is removed from our body in our urine. People with polymorphisms in the gene encoding HNMT often present with a runny nose, hives and peptic ulcer disease.</div><div><br /></div><div>Vitamin U is a natural support for decreases in methylation capacity caused by allergies. Vitamin U carries two methyl groups that contribute to the formation of SAM. Taking Vitamin U in the form of fresh cruciferous or stalky vegetables, or as a supplement, helps replenish methylation capacity when you are struck by allergies. Allergens can have a draining effect on the whole body, with low methylation capacity reducing our ability to maintain good health and can lead to low methylation conditions such as peptic ulcers and histamine intolerance.</div><div><br /></div><div>Vitamin U is not a drug: it will not stop a runny nose dead in its tracks like antihistamines can. <b>Nor will Vitamin U be effective in treating anaphylactic shock. If you have a severe allergic reaction, please immediately rush to the hospital for treatment. </b>Vitamin U simply aids our body's natural mechanism for removing excess histamine. Ensuring your dietary intake of Vitamin U is adequate will complement drugs in your battle with seasonal and persistent allergies.</div><div><br /></div><div>Further reading</div><div><ul style="text-align: left;"><li><a href="https://pubmed.ncbi.nlm.nih.gov/30744146/">https://pubmed.ncbi.nlm.nih.gov/30744146/</a></li><li><a href="https://pubmed.ncbi.nlm.nih.gov/17490952/">https://pubmed.ncbi.nlm.nih.gov/17490952/</a></li></ul></div>Sean Yu McLoughlinhttp://www.blogger.com/profile/03287541681698360493noreply@blogger.com0tag:blogger.com,1999:blog-4272996138785020260.post-56034707895153195942022-01-30T19:35:00.007-07:002023-06-15T08:08:48.073-06:00Neural tube defects and Vitamin U<div style="text-align: left;"><div class="separator" style="clear: both; text-align: center;"><br /></div><div class="separator" style="clear: both; text-align: center;"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEgwygzsi0JlkE2l5a4oS6w5d9qdRvKmpeSVQeOu99f95ikJI_542AjjqaVB4ESOy0RjMETx1qbvy-DXrbrwlCdiRmRBmpMaHkE6EySmTwASNYZFF0gcFDQkK9RYsdtnkhALNpIjZZmuakto/s1731/Spina-bifida.jpg" style="margin-left: 1em; margin-right: 1em;"><img border="0" data-original-height="1396" data-original-width="1731" height="258" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEgwygzsi0JlkE2l5a4oS6w5d9qdRvKmpeSVQeOu99f95ikJI_542AjjqaVB4ESOy0RjMETx1qbvy-DXrbrwlCdiRmRBmpMaHkE6EySmTwASNYZFF0gcFDQkK9RYsdtnkhALNpIjZZmuakto/s320/Spina-bifida.jpg" width="320" /></a></div><br /><div class="separator" style="clear: both; text-align: center;"><span style="font-family: helvetica; font-size: xx-small;">By Centers for Disease Control and Prevention - Centers for Disease Control and Prevention, Public Domain, https://commons.wikimedia.org/w/index.php?curid=30509337</span></div><span style="font-family: helvetica;"><br /></span></div><div style="text-align: left;"><span style="font-family: helvetica;"><br /></span></div><div style="text-align: left;"><span style="font-family: helvetica;"> </span></div><div style="text-align: left;"><span style="font-family: helvetica;"><span style="font-family: helvetica;">Summary - </span><b>Vitamin U may play a supportive role in correct neural tube formation</b><span style="font-family: helvetica;">, a process that depends on the methylation of dUMP to form dTMP via the folate cycle. The folate and methionine cycles work together to meet the methylation needs of the body. Low cellular methylation status diverts methyl groups from the folate cycle to the methionine cycle, thereby decreasing dTMP synthesis and increasing the risk of neural tube defects. Dietary methyl donors that enter the methionine cycle directly (e.g. methionine, betaine, Vitamin U) support neural tube formation by reducing this methyl group drain. While f</span><span style="font-family: helvetica;">olate is the most important factor affecting neural tube formation</span><span style="font-family: helvetica;">, folate intake may not be sufficient in and of itself due to other factors such as polymorphisms within these two pathways and intake of other components that contribute to methylation homeostasis. <b>Talk to your dietitian before conception about designing a diet that reduces the risk of neural tube defects in your baby.</b></span></span></div><div style="text-align: left;"><span style="font-family: helvetica;"><span style="font-family: helvetica;"><b><br /></b></span></span></div><div style="text-align: left;"><span style="font-family: helvetica;"><br /></span></div><div style="text-align: left;"><span style="font-family: helvetica;">Neural tube defects (NTDs) are a collection of medical conditions in which the neural tube of the baby does not form </span><span style="font-family: helvetica;">completely </span><span style="font-family: helvetica;">during early development, exposing the spinal cord and/or brain with permanent disability resulting. Two common neural tube defects are spina bifida (spine) and anencephaly (brain). </span></div><div style="text-align: left;"><span style="font-family: helvetica;"><br /></span></div><div style="text-align: left;"><span style="font-family: helvetica;">What causes NTDs? Like many conditions, NTDs result from a combination of environmental and genetic </span><span style="font-family: helvetica;">factors</span><span style="font-family: helvetica;">. The most common environment factor is the insufficient intake of folate by the mother just before and during the first few weeks of pregnancy. Folate is a vitamin (B9), and is therefore an essential component of one's diet. In the 1950s it was noted that pregnant women taking anti-folate drugs to treat cancer gave birth to babies afflicted with congenital abnormalities like NTDs (</span><a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3415073/#B7" style="font-family: helvetica;" target="_blank">Safi 2012</a>)<span style="font-family: helvetica;">. It was established that folate is essential for embryonic development, that women whose folate levels were low were at greater risk of having babies with NTDs, and that supplementation by the mother-to-be with folate substantially reduced the risk of NTD occurrence </span><span style="font-family: helvetica;">(</span><a href="https://pubmed.ncbi.nlm.nih.gov/6101792/" style="font-family: helvetica;" target="_blank">Smithells 1980</a>; <a href="https://doi.org/10.1016/0140-6736(91)90133-A" style="font-family: helvetica;" target="_blank">Wald 1991</a><span style="font-family: helvetica;">). F</span><span style="font-family: helvetica;">olate supplementation is the most effective way to prevent NTDs, reducing risk by 50-70%. </span><span style="font-family: helvetica;">Consequently, medical authorities recommend young women ensure their diet contains 400 ug of folate per day through food and supplements in case they become pregnant.</span></div><div style="text-align: left;"><span style="font-family: helvetica;"><br /></span></div><div style="text-align: left;"><span style="font-family: helvetica;"><span style="font-family: helvetica;">How does folate prevent neural tube defects? </span><span style="font-family: helvetica;">The function of folate is to transfer methyl groups generated from serine to a range of molecules throughout the cell. In embryos, these methyl groups are essential to make nucleotides required for DNA synthesis. There are many compounds that are methylated as a result of the action of folate. However, there is one for which there is evidence that a shortage of results in neural tube defects - dTMP (deoxythymidylate). There are four nucleotides used to make DNA - abbreviated to A, T, C, G. dTMP is a precursor in the formation of dTTP, usually shortened to T. In humans, the nucleotide dTMP is made from dUMP by the transfer of a methyl group from folate. E</span><span style="font-family: helvetica;">mbryos supplemented with dTTP do not develop neural tube defects despite very low folate levels, indicating that dTMP shortage is the causal factor (<a href="https://pubmed.ncbi.nlm.nih.gov/23935126/" target="_blank">Leung 2013</a>). </span></span><span style="font-family: helvetica;">At conception, nucleotides must be synthesized in utero, and therefore a shortage of folate results in low production of dTMP, which in turn results in NTDs.</span></div><div style="text-align: left;"><span style="font-family: helvetica;"><br /></span></div><div style="text-align: left;"><a href="https://blogger.googleusercontent.com/img/a/AVvXsEglPTtgPkLSSVW0K6XeWHVOBWw-rWMQSABmdyXTqWFVT0iKk-p-H82tXiGFviHn44FP_IOTmMhLiC2tgbidH-ZW8i4qQK1C2raS93NxPCj_RsNh_BLC-CyFIlkM__J4Syk5hpaYlXQAvrHVfUUVAlQSGF05PpTy8rTIjJMM63ggz5yzJtq3Fcry8FKWVw=s1105" style="font-family: helvetica; margin-left: 1em; margin-right: 1em; text-align: center;"><img border="0" data-original-height="725" data-original-width="1105" height="353" src="https://blogger.googleusercontent.com/img/a/AVvXsEglPTtgPkLSSVW0K6XeWHVOBWw-rWMQSABmdyXTqWFVT0iKk-p-H82tXiGFviHn44FP_IOTmMhLiC2tgbidH-ZW8i4qQK1C2raS93NxPCj_RsNh_BLC-CyFIlkM__J4Syk5hpaYlXQAvrHVfUUVAlQSGF05PpTy8rTIjJMM63ggz5yzJtq3Fcry8FKWVw=w538-h353" width="538" /></a></div><div style="text-align: left;"><span style="font-family: helvetica;"><br /></span></div><div style="text-align: left;"><div style="font-family: helvetica;"><div class="separator" style="clear: both; text-align: center;"><span style="font-family: helvetica; font-size: x-small; text-align: left;">Figure 1 - A simplified depiction of the folate cycle. The enzymes responsible for catalyzing each step are -</span></div></div><p style="font-family: helvetica;"></p><p style="font-family: helvetica; line-height: 1.2; margin-bottom: 0pt; margin-top: 0pt;"><span style="color: black; font-size: x-small; font-variant-east-asian: normal; font-variant-numeric: normal; vertical-align: baseline; white-space: pre-wrap;">1. Serine hydroxymethyltransferase</span></p><p style="font-family: helvetica; line-height: 1.2; margin-bottom: 0pt; margin-top: 0pt;"><span style="color: black; font-size: x-small; font-variant-east-asian: normal; font-variant-numeric: normal; vertical-align: baseline; white-space: pre-wrap;">2. Thymidylate synthase</span></p><p style="font-family: helvetica; line-height: 1.2; margin-bottom: 0pt; margin-top: 0pt;"><span style="color: black; font-size: x-small; font-variant-east-asian: normal; font-variant-numeric: normal; vertical-align: baseline; white-space: pre-wrap;">3. Dihydrofolate reductase</span></p><div style="font-family: helvetica;"><span id="docs-internal-guid-2c70d50e-7fff-eac7-3631-95a445598480" style="font-family: helvetica; font-size: x-small;"><p style="line-height: 1.2; margin-bottom: 0pt; margin-top: 0pt;"><span style="white-space: pre-wrap;"><span>4a. 5,10-methylenetetrahydrofolate dehydrogenase NADP+</span></span></p><p style="line-height: 1.2; margin-bottom: 0pt; margin-top: 0pt;"><span style="white-space: pre-wrap;"><span>4b. 5,10-methenyltetrahydrofolate cyclohydrolase</span></span></p><p style="line-height: 1.2; margin-bottom: 0pt; margin-top: 0pt;"><span style="white-space: pre-wrap;"><span>4c. F</span></span><span face="sans-serif" style="background-color: white; color: #202122;">ormate-tetrahydrofolate ligase</span></p><p style="line-height: 1.2; margin-bottom: 0pt; margin-top: 0pt;"><span><span style="white-space: pre-wrap;">5. P</span><span style="background-color: white; color: #202122;">hosphoribosylaminoimidazolecarboxamide formyltransferase</span></span></p><p style="line-height: 1.2; margin-bottom: 0pt; margin-top: 0pt;"><span style="font-variant-east-asian: normal; font-variant-numeric: normal; vertical-align: baseline; white-space: pre-wrap;"><span>6. Methylenetetrahydrofolate reductase</span></span></p><p style="line-height: 1.2; margin-bottom: 0pt; margin-top: 0pt;"><span style="font-variant-east-asian: normal; font-variant-numeric: normal; vertical-align: baseline; white-space: pre-wrap;"><span>7. Methionine synthase</span></span></p><p style="line-height: 1.2; margin-bottom: 0pt; margin-top: 0pt;"><span style="font-variant-east-asian: normal; font-variant-numeric: normal; vertical-align: baseline; white-space: pre-wrap;"><span><br /></span></span></p><p style="line-height: 1.2; margin-bottom: 0pt; margin-top: 0pt;"><span style="font-variant-east-asian: normal; font-variant-numeric: normal; vertical-align: baseline; white-space: pre-wrap;"><span>N.B. 4a-c are three components of MTHFD1</span></span></p></span></div></div><div style="text-align: left;"><br /></div><div style="text-align: left;"><br /></div><div style="text-align: left;"><span style="font-family: helvetica;">Which folate should you take and where should you get it from? </span></div><div style="text-align: left;"><span style="font-family: helvetica;"><br /></span></div><div style="text-align: left;"><span style="font-family: helvetica;">First a note on nomenclature. </span><span style="font-family: helvetica;">The term 'folate' is commonly used to refer to any of the components of this pathway plus other forms like folic acid and folinic acid. Naturally-occurring folate is a mixture of these forms, with the exception of folic acid, which is a non-natural, oxidized version that is relatively stable and therefore used to fortify food in which natural folate has been removed or degraded. Vitamin supplements usually contain either folic acid or 'methyl folate' or 'activated folate', which usually refers to 5-methyltetrahydrofolate.</span></div><div style="text-align: left;"><span style="font-family: helvetica;"><br /></span></div><div style="text-align: left;"><span style="font-family: helvetica;">The best source of natural folates are green leafy vegetables, although all vegetable sources (including fruit and grains) are reasonable sources. Folic acid is a form of folate that is often added to processed grains that have been polished, e.g. wheat flour, white rice.</span><span style="font-family: helvetica;"> For most people, it makes little difference whether their folate is derived from natural or synthetic sources. The important factor is getting the right amount. However, some people do not metabolize synthetic folic acid effectively and as such can actually suffer from a deficiency in functional folate even when their serum levels of folic acid seem sufficient (<a href="https://pubmed.ncbi.nlm.nih.gov/19706381/" target="_blank">Bailey and Ayling 2009</a>). </span><span style="font-family: helvetica;">Sometimes too much folic acid can even cause fertility problems (<a href="https://pubmed.ncbi.nlm.nih.gov/31205715/" target="_blank">Cornet 2019</a>). </span></div><div style="text-align: left;"><span style="font-family: helvetica;"><br /></span></div><div style="text-align: left;"><span style="font-family: helvetica;">There are other components in the folate cycle that also have an effect on neural tube formation, albeit to a lesser extent. For example, vitamin B12 is an essential cofactor for the enzymatic conversion of 5-MTHF to THF, and low B12 levels have been linked to NTDs (</span><a href="https://pubmed.ncbi.nlm.nih.gov/19586788/" style="font-family: helvetica;" target="_blank">Li 2009</a><span style="font-family: helvetica;">). Another example is Vitamin B6, which is a coenzyme for serine hydroxymethylfolate transferase. Cobalt is a component of B12 and therefore is vital for methionine synthase function.</span></div><div style="text-align: left;"><span style="font-family: helvetica;"><div><br /></div><div><div style="font-family: "Times New Roman";"><span style="font-family: helvetica;">Where does genetics fit in? </span><span style="font-family: helvetica;">While folate supplementation reduces risk, unfortunately genetic polymorphisms in the mother are responsible for the majority of NTDs cases </span><span style="font-family: helvetica;">(</span><span style="font-family: helvetica;"><a href="https://pubmed.ncbi.nlm.nih.gov/23790957/" target="_blank">Copp 2013</a>). Mutations of genes in the folate cycle and other branches of one carbon metabolism (methylation) are particularly relevant. </span><span style="font-family: helvetica;">There are many enzymatic steps in the folate cycle, and each enzyme is encoded by a gene. Polymorphisms are nucleotide changes (</span><span style="font-family: helvetica;">mutations</span><span style="font-family: helvetica;">) in these genes </span><span style="font-family: helvetica;">that differ from that found in the majority of people. Most polymorphisms have no significant physiological effect by themselves, but may have an effect in combination. However, there are a few polymorphisms that do correlate with the occurrence of NTDs, such as MTHFR C677T and MTHFD1 R653Q </span><span style="font-family: helvetica;">(</span><span style="font-family: helvetica;"><a href="https://pubmed.ncbi.nlm.nih.gov/23790957/" target="_blank">Copp 2013</a>).</span><span style="font-family: helvetica;"> </span></div><div style="font-family: "Times New Roman";"><span style="font-family: helvetica;"><br /></span></div><div style="font-family: "Times New Roman";"><span style="font-family: helvetica;">Genetic testing is becoming an increasing-popular tool to identify polymorphisms. Though it is tempting to do so, it is important to not assume that polymorphisms necessarily result in reduced physiological function. Human physiology is not fully understood and often contains redundancies that can mask over minor metabolic blocks. The correct way to establish whether there are deficiencies within the folate cycle is through biochemical analysis of the various folate metabolites. Biochemical analysis in combination with genetic analysis is used by specialists to establish whether there is a functional deficit in the mother that results in heightened risk of NTDs in her baby. </span><span style="font-family: helvetica;">Consult with your doctor or dietitian to determine if you have polymorphisms, and if you do, whether these actually affect your metabolism (often they don't) and what measures can be taken to relieve any metabolic blocks.</span></div></div><div><br /></div><div>Aside from the folate cycle, there is another cycle that is even more important in meeting our methylation needs. The methionine cycle is the way in which the methyl donor S-adenosylmethionine (SAM) is generated (<a href="https://www.vitaminuandpepticulcers.com/2020/06/the-methionine-cycle-and-vitamin-u.html" target="_blank">methionine cycle</a>). SAM is the methyl donor for just about all methylation reactions, with the notable exception of those in the folate cycle. It has been shown that a functioning methionine cycle is essential for correct neural tube formation (<a href="https://pubmed.ncbi.nlm.nih.gov/29141214/" target="_blank">Leung 2017</a>). <span style="font-family: helvetica;">When there is a shortage of methyl groups in the methionine cycle (low S-adenosylmethione:S-adenosylhomocysteine), methyl groups are directed from the folate cycle into the methionine cycle. Instead of being used to make nucleotides, </span><span style="font-family: helvetica;">5,10-methylenetetrahydrofolate is reduced by MTHFR to make 5-methyltetrahydrofolate, which donates its methyl group to the methionine cycle in a reaction catalyzed by methionine synthase. The folate molecule is conserved within the folate cycle, but must be remethylated. When maternal folate levels are low and flux through the folate cycle is already slow, this shunt may reduce methylation capacity in the folate cycle to critical levels. </span></div><div><span style="font-family: helvetica;"><br /></span></div><div>The methionine cycle obtains a large amount of its methyl groups from the folate cycle. This shunt operates at moderate levels most of the time - this is actually a normal process. In addition, the methionine cycle obtains methyl groups from methionine, betaine and Vitamin U. Similar to the methionine synthase reaction, betaine and Vitamin U donate methyl groups to homocysteine via enzyme-catalyzed reactions. <span style="font-family: helvetica;">Importantly, methyl groups in the methionine cycle cannot enter the folate cycle. For example, SAM from the methionine cycle cannot substitute for </span>5,10-MeTHF required for <span style="font-family: helvetica;">dTMP synthesis. </span>Low maternal methionine levels pre- and post-conception are associated with a heightened risk of neural tube defects (<a href="https://pubmed.ncbi.nlm.nih.gov/15234930/" target="_blank">Shaw 2004</a>). <span style="font-family: helvetica;">There is evidence that betaine entering the methionine cycle reduces the flow of methyl groups from the folate cycle, which in principle should support 5,10-MeTHF levels (</span><a href="https://pubmed.ncbi.nlm.nih.gov/17413090/" target="_blank">Benevenga 2007</a>)<span style="font-family: helvetica;">.</span></div><div><p><span style="font-family: helvetica;">Where does Vitamin U fit into all this? <b>It should be emphasized that there has not been any scientific research testing whether Vitamin U supplementation can prevent NTDs.</b> 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. </span></p><p></p><ul><li><span style="font-family: helvetica;">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. </span></li></ul><ul><li><span style="font-family: helvetica;">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.</span></li></ul><ul><li><span style="font-family: helvetica;">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.</span></li></ul><ul><li><span style="font-family: helvetica;">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.</span></li></ul><div><br /></div><div>Summary</div><p></p><ul><li><span style="font-family: helvetica;">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.</span></li><li><span style="font-family: helvetica;">Folate requirements may be lowered as long as adequate levels of methyl groups are provided by methionine and betaine from the methionine cycle. </span></li><li><span style="font-family: helvetica;">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.</span></li></ul><p><span style="font-family: helvetica;"><br /></span></p><p><span style="font-family: helvetica;">Further Reading</span></p><p></p><ul style="text-align: left;"><li>Shaw et al 2004 <a href="https://pubmed.ncbi.nlm.nih.gov/15234930/">https://pubmed.ncbi.nlm.nih.gov/15234930/</a></li><li>Zhang et al 2015 <a href="https://pubmed.ncbi.nlm.nih.gov/25466894/">https://pubmed.ncbi.nlm.nih.gov/25466894/</a></li><li>Froese et al 2019 <a href="https://pubmed.ncbi.nlm.nih.gov/30693532/">https://pubmed.ncbi.nlm.nih.gov/30693532/</a></li><li>Halsted et al 2002 <a href="https://pubmed.ncbi.nlm.nih.gov/12122204/">https://pubmed.ncbi.nlm.nih.gov/12122204/</a></li><li>Shin et al 2010 <a href="https://pubmed.ncbi.nlm.nih.gov/20220206/">https://pubmed.ncbi.nlm.nih.gov/20220206/</a></li><li>Bailey and Ayling 2009 <a href="https://pubmed.ncbi.nlm.nih.gov/19706381/">https://pubmed.ncbi.nlm.nih.gov/19706381/</a></li><li>Cornet et al 2019 <a href="https://pubmed.ncbi.nlm.nih.gov/31205715/">https://pubmed.ncbi.nlm.nih.gov/31205715/</a></li><li>Huennekens 1969 <a href="https://pubmed.ncbi.nlm.nih.gov/4891866/">https://pubmed.ncbi.nlm.nih.gov/4891866/</a></li><li>Purohit et al 2007 <a href="https://pubmed.ncbi.nlm.nih.gov/17616758/">https://pubmed.ncbi.nlm.nih.gov/17616758/</a></li><li>Duncan et al 2013 (1) <a href="https://pubmed.ncbi.nlm.nih.gov/23857220/">https://pubmed.ncbi.nlm.nih.gov/23857220/</a> </li><li>Duncan et al 2013 (2) <a href="https://pubmed.ncbi.nlm.nih.gov/23143835/">https://pubmed.ncbi.nlm.nih.gov/23143835/</a></li><li>Teng et al 2012 <a href="https://pubmed.ncbi.nlm.nih.gov/23014492/">https://pubmed.ncbi.nlm.nih.gov/23014492/</a></li><li>Rinehart and Greenberg 1948 <a href="https://pubmed.ncbi.nlm.nih.gov/18859393/">https://pubmed.ncbi.nlm.nih.gov/18859393/</a></li><li>Leung 2013 <a href="https://pubmed.ncbi.nlm.nih.gov/23935126/">https://pubmed.ncbi.nlm.nih.gov/23935126/</a></li><li>Leung 2017 <a href="https://pubmed.ncbi.nlm.nih.gov/29141214/">https://pubmed.ncbi.nlm.nih.gov/29141214/</a></li><li>Blom 2006 <a href="https://pubmed.ncbi.nlm.nih.gov/16924261/">https://pubmed.ncbi.nlm.nih.gov/16924261/</a></li><li>Benevenga 2007 <a href="https://pubmed.ncbi.nlm.nih.gov/17413090/">https://pubmed.ncbi.nlm.nih.gov/17413090/</a></li><li>Bertolo and McBreairity 2013 <a href="https://pubmed.ncbi.nlm.nih.gov/23196816/">https://pubmed.ncbi.nlm.nih.gov/23196816</a></li></ul></div></span></div>Sean Yu McLoughlinhttp://www.blogger.com/profile/03287541681698360493noreply@blogger.com0tag:blogger.com,1999:blog-4272996138785020260.post-50284947304433340162021-06-17T00:02:00.006-06:002023-06-15T08:09:40.233-06:00Blood glucose test and Vitamin U<p></p><div class="separator" style="clear: both; text-align: center;"><br /></div><div class="separator" style="clear: both; text-align: center;"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEjDoYj_b1UkQ365S9P9w9wRnXKolbln_zhQ5l5Sk39rwHv_F__T5C_WN5m9vcsiU5mutmh0iVEV4AODSmg4yCATUj6QH1YFBSq7zWk8xgeM145SmI76yQhae6L66Ksh830mqYurqvzGmc7L/s1920/Blood+drawn.jpeg" style="margin-left: 1em; margin-right: 1em;"><img border="0" data-original-height="1280" data-original-width="1920" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEjDoYj_b1UkQ365S9P9w9wRnXKolbln_zhQ5l5Sk39rwHv_F__T5C_WN5m9vcsiU5mutmh0iVEV4AODSmg4yCATUj6QH1YFBSq7zWk8xgeM145SmI76yQhae6L66Ksh830mqYurqvzGmc7L/s320/Blood+drawn.jpeg" width="320" /></a></div><p>Summary - Taking particular supplements may produce a blood glucose reading that is erroneously higher than the actual glucose concentration due to the non-specificity of the various tests. False high readings can be misdiagnosed as high glucose levels, a result that can have dangerous repercussions. Prescription of medication that reduces actual blood glucose levels in people with false high readings can result in hypoglycemia and death. If you are having a blood glucose test and are taking supplements that can increase the concentration of reducing agents in your blood (e.g. Vitamin C, N-acetylcysteine, glutathione, Vitamin U), be sure to mention it to your medical practitioner.</p><p></p><p>Quantifying blood sugar levels is a standard medical procedure that is commonly used to diagnose diabetes. There are many different tests used to quantify glucose. The tests typically use an enzyme to catalyze the oxidation of glucose. This reaction usually involves a cofactor that is reduced during the process. A third molecule reacts with the reduced cofactor to produce a colored product which can be readily measured and the concentration of glucose deduced. </p><p>If you have looked at your lab results, you may have seen a note that taking supplements such as Vitamin C, N-acetylcysteine or glutathione may affect blood glucose test results. These chemicals are reducing agents and act as antioxidants in your body. In their reduced form, these chemicals have a similar reactivity to that of the reduced cofactor in the reaction coupled with glucose oxidation. Consequently, when moderate amounts of these supplements show up in the blood, they will also react with the indicator to produce a color. <a href="https://pubmed.ncbi.nlm.nih.gov/33766514/" target="_blank">Grzych et al (2021)</a> showed that even modest amounts of these supplements in the blood can lead to a false positive result for diabetes based on seven commonly used glucose test kits.</p><p>If your medical practitioner is unaware you are taking these or similar supplements, they may mistakenly think you have elevated blood glucose and prescribe medication to decrease your sugar levels. Such measures are very dangerous in people with normal blood glucose levels as medication that stimulates the removal of glucose will result in hypoglycemia (low blood glucose). Accidental death has unfortunately occurred from this very problem. When your medical practitioner asks whether you are taking supplements, it is certainly in your best interest to list everything you take so they may interpret lab results in a fuller context. </p><p>Vitamin U is not a reducing agent, so it will not directly react with the indicator. However, Vitamin U is metabolized into compounds that are reducing agents, such as S-adenosylmethionine (SAM), homocysteine, cysteine and glutathione. Therefore, if you are getting a blood glucose test and are taking Vitamin U, it would be wise to tell your medical practitioner about this supplement.</p><p><br /></p>Sean Yu McLoughlinhttp://www.blogger.com/profile/03287541681698360493noreply@blogger.com0tag:blogger.com,1999:blog-4272996138785020260.post-56140571962975066092021-04-21T20:02:00.010-06:002023-06-15T08:10:25.972-06:00Vitamin U is metabolized by the enzyme BHMT2<div style="text-align: center;">
<div style="text-align: left;"><div class="separator" style="clear: both; text-align: center;"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEh2FV7svdh8ehBFpilMae2KzY70tKZ8Ze7KXrH2AVyV-0n8UYo9E-FhaoFMuUJiiaODuGwqbVFajD5c7NnjyXqGS6upqfDkE9EPklsEnmdsQYviFgf-tnn1wm-IRj677STNoFCPnyLF5xNn/s823/Anatomy_Abdomen_Tiesworks.jpg" style="margin-left: 1em; margin-right: 1em;"><img border="0" data-original-height="768" data-original-width="823" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEh2FV7svdh8ehBFpilMae2KzY70tKZ8Ze7KXrH2AVyV-0n8UYo9E-FhaoFMuUJiiaODuGwqbVFajD5c7NnjyXqGS6upqfDkE9EPklsEnmdsQYviFgf-tnn1wm-IRj677STNoFCPnyLF5xNn/s320/Anatomy_Abdomen_Tiesworks.jpg" width="320" /></a></div></div>
<div style="text-align: left;"><span face=""><div><span face=""><br /></span></div><div><br /></div><div>Summary - BHMT2 is the enzyme that catalyzes the assimilation of Vitamin U into our body. Made at high levels in the liver and kidneys, BHMT2 catalyzes the transfer of a methyl group from Vitamin U to homocysteine. This reaction plays an important role in the maintenance of healthy glutathione levels by contributing to an optimal methylation state, which drives existing and newly-formed homocysteine into the transsulfuration pathway and towards glutathione synthesis.</div><div><br /></div><div><br /></div><div>Vitamin U is a nutrient that is ubiquitous and abundant in vegetables and fruit. It is a noted dietary mucin secretagogue that has been shown to play an important role in healing and preventing peptic ulcers. It appears that Vitamin U interacts directly with the cells lining the stomach and induces secretion through a non-receptor mediated mechanism, different to that used by other secretagogues (<a href="https://pubmed.ncbi.nlm.nih.gov/10719747/" target="_blank">more</a>). </div><div><br /></div><div>Vitamin U doesn't just interact with the stomach. In fact, much of Vitamin U is absorbed by the small intestine and taken to the liver where it is metabolized. It is assimilated into our body via the methionine cycle (<a href="https://www.vitaminuandpepticulcers.com/p/vitamin-u-summary.html" target="_blank">more</a>). The enzyme that is responsible for Vitamin U assimilation is BHMT2 (Betaine Homocysteine Methyl Transferase 2). BHMT2 catalyzes the transfer of a methyl group from Vitamin U to homocysteine to produce two molecules of methionine. These products enter the methionine cycle where they donate methyl groups to form the universal methyl donor SAM and eventually are converted back into homocysteine. The fate of homocysteine is determined by the methylation status in the cell. A low SAM:SAH ratio results in homocysteine awaiting the appearance of new methyl donors in the form of Vitamin U, betaine and methyl folate for reentry into the methionine cycle. A high SAM:SAH ratio results in homocysteine entering the transsulfuration pathway, eventually forming cysteine and glutathione.</div><div><br /></div><div>BHMT2 is well-expressed in the liver and kidneys (top 5% of proteins in these organs by abundance) (<a href="https://pax-db.org/protein/1844362" target="_blank">more</a>) and is expressed at low levels in many other tissues throughout our body (<a href="https://www.proteinatlas.org/ENSG00000132840-BHMT2/tissue/primary+data" target="_blank">more</a>). </div><div><br /></div><div><div><u>High expression</u> kidney, liver</div><div><br /></div><div><u>Moderate expression</u> thyroid, adrenal, pancreas, gallbladder, ovaries, rectum</div><div><br /></div><div><u>Low expression</u> nasopharynx, bronchus, stomach, duodenum, small intestine, colon, testis, epididymis, prostate, endometrium, fallopian tubes, heart muscle, skeletal muscle</div></div><div><br /></div><div><div><span face=""><u>Examples</u></span></div><div><span face=""><br /></span></div><div><span face="">BHMT2 is expressed at low, but measurable levels in the gastric glands. Not expressed in the gastric pits or muscle layer (<a href="https://www.proteinatlas.org/ENSG00000132840-BHMT2/tissue/stomach#img" target="_blank">more</a>). </span></div><div><br /></div><div>BHMT2 is expressed at moderate levels in the thyroid gland (<a href="https://www.proteinatlas.org/ENSG00000132840-BHMT2/tissue/thyroid+gland#img" target="_blank">more</a>).</div><div><br /></div><div>BHMT2 is expressed at moderate levels in the mucosa lining the gallbladder (<a href="https://www.proteinatlas.org/ENSG00000132840-BHMT2/tissue/gallbladder#img" target="_blank">more</a>).</div><div><br /></div><div>BHMT2 is expressed at high levels in the renal tubules, but not in the renal glomeruli (<a href="https://www.proteinatlas.org/ENSG00000132840-BHMT2/tissue/kidney" target="_blank">more</a>).</div><div><br /></div><div>BHMT2 is expressed at high levels in hepatocytes, but not in bile duct cells (<a href="https://www.proteinatlas.org/ENSG00000132840-BHMT2/tissue/liver" target="_blank">more</a>).</div></div><div><br /></div><div>To what extent these antibody stains indicate function of BHMT2 remains an open question. If the low expression of BHMT2 in the stomach is actually responsible for the protection afforded by Vitamin U, then the similar levels of expression in other tissues may indicate that Vitamin U has a physiological function in those tissues too. <b>However, this remains to be scientifically investigated and does not constitute medical advice.</b></div><div><br /></div><div><br /></div><div>How was BHMT2 discovered?</div><div><br /></div><div><div>Around 1940, scientists at the Lankenau Hospital Research Institute in Philadelphia were investigating the effects of oxidation on the uptake and metabolism of proteins. Gerrit Toennies was a chemist focusing on making forms of methionine and cysteine that had undergone oxidation to varying degrees. Mary Bennett fed these oxidized amino acids to rats to further our understanding of how animals use sulfur amino acids. They found that when the milk protein casein was chemically oxidized, it was no longer a viable source of protein for rats. Most proteins are made up of 20 types of amino acids. The scientists discovered that methionine and tryptophan were the two types of amino acid that were irreversibly oxidized (<a href="https://www.sciencedirect.com/science/article/pii/S0021925818513090" target="_blank">more</a>).</div><div><br /></div><div>During these studies, Toennies made a methionine derivative that was a little different. By reacting methionine with methyl iodide, methionine was methylated at the sulfur again, converting the sulfur into a sulfonium. Bennett fed this methionine sulfonium to rats in place of methionine. For 5 days, the rats did not grow. On the 6th day, the rats suddenly started growing at the same rate as the control rats being fed methionine (<a href="https://www.jbc.org/content/141/2/573.full.pdf" target="_blank">more</a>).</div><div><br /></div><div>What happened to the rats? Bennett suggested that the rats "may have developed a special mechanism for taking care of the extra methyl group" that allowed the sulfonium to be converted into methionine. This special mechanism was probably an enzyme that at that time had yet to be discovered. In 1959, Shapiro and Yphantis revealed that the liver expresses an enzyme that converts Vitamin U into methionine by methyl transfer to homocysteine (<a href="https://pubmed.ncbi.nlm.nih.gov/14445542/" target="_blank">more</a>). The gene encoding this activity was characterized in 2000 by Chadwick and named BHMT2 due to its resemblance to another liver enzyme BHMT1 (<a href="https://pubmed.ncbi.nlm.nih.gov/11087663/" target="_blank">more</a>). It was shown by the Garrow lab in 2008 that purified BHMT2 enzyme catalyzed the reaction between Vitamin U and homocysteine (<a href="https://pubmed.ncbi.nlm.nih.gov/18230605/" target="_blank">more</a>). </div><div><br /></div></div><div>It was hypothesized by Toennies that sulfoniums could have a biological role and it was speculated that methylmethionine sulfonium could exist naturally. In 1954, this hypothesis was confirmed by McRorie and others, extracting this compound from cabbage. Interestingly, the latter linked the chemical properties of their newly-discovered compound with those of a recently-discovered Vitamin U, and proposed that this compound was a source of methionine as well as a methyl donor (<a href="https://pubs.acs.org/doi/abs/10.1021/ja01630a032" target="_blank">more</a>). </div><div><br /></div><div>Does expression of BHMT2 depend on the presence of Vitamin U? From the studies of Bennett, it would seem that a lack of methionine might induce BHMT2 expression in rats rather than the presence of Vitamin U. For comparison, expression of the related enzyme BHMT1 in rat liver is induced 4-fold when methionine levels are low/choline normal and an additional 2-fold in the presence of betaine (<a href="https://www.sciencedirect.com/science/article/abs/pii/S0955286397001010" target="_blank">more</a>). However, not much research has gone into addressing BHMT2 expression, especially in humans. </div></span></div>
</div>
Sean Yu McLoughlinhttp://www.blogger.com/profile/03287541681698360493noreply@blogger.com0tag:blogger.com,1999:blog-4272996138785020260.post-71605763820773855612020-12-29T22:01:00.033-07:002023-06-15T08:11:55.529-06:00Mouth ulcers and Vitamin U<div><div class="separator" style="clear: both; text-align: center;"><br /></div><div class="separator" style="clear: both; text-align: center;"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEjXgf0E-KegRlNnUT6CEqzqL64wSKrrgRFLHh2Mjen4aGo1ZVw89WGPOhphKP53Ew0zZNrfKdVU2mO0ksUrsq-sK-_AoX1xT6tnD6asLkvuyGQN7XctNJluvt5uNZRn5nxRE3VyfTKhXbd4/s1375/Aphthe_Unterlippe.jpg" style="margin-left: 1em; margin-right: 1em;"><img border="0" data-original-height="1339" data-original-width="1375" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEjXgf0E-KegRlNnUT6CEqzqL64wSKrrgRFLHh2Mjen4aGo1ZVw89WGPOhphKP53Ew0zZNrfKdVU2mO0ksUrsq-sK-_AoX1xT6tnD6asLkvuyGQN7XctNJluvt5uNZRn5nxRE3VyfTKhXbd4/s320/Aphthe_Unterlippe.jpg" width="320" /></a></div><div style="text-align: center;"><br /></div><span style="font-family: helvetica;"><br /></span></div><div><span style="font-family: helvetica;">Summary - Mouth ulcers result from a breach of the mucous layer that protects the lining of the mouth and an underlying inability to repair the mucous layer quickly. Taking Vitamin U in the form of fresh vegetable juice and/or supplements is a great way to naturally heal mouth ulcers. Talk to your doctor or dentist.</span></div><div><br /></div><div><span style="font-family: helvetica;">Mouth ulcers (aphthous ulcers or stomatitis) are small, painful, circular sores that form in the lining of the mouth. They are very common. </span><span style="font-family: helvetica;">Right this minute, 1-2% of people have a mouth ulcer. Over a lifetime, about half of the US population will get at least one if not many. They mainly afflict teenagers.</span><span style="font-family: helvetica;"> Ulcers normally heal spontaneously in one to two weeks, although they can reoccur many times. Recurrent ulcers indicate an underlying health problem. </span><span style="font-family: helvetica;">Sores in the corner of the mouth or outside the mouth are not ulcers and should be treated differently.</span><span style="font-family: helvetica;"> </span></div><div><span style="font-family: helvetica;"><br /></span></div><div><span style="font-family: helvetica;">Why do I have a mouth ulcer? </span></div><div><span style="font-family: helvetica;"><br /></span></div><div><span style="font-family: helvetica;">The lining of your mouth is covered by a thin layer of mucus. The main purposes of this mucus is to protect the lining of the oral cavity from physical and chemical damage, infection, and to help digest food.</span><span style="font-family: helvetica;"> M</span><span style="font-family: helvetica;">outh ulcers develop when the protective mucus layer is breached and the body shows a delayed repair response with non-specific oral bacteria infecting. The integrity of the mucus layer is a function of constructive vs destructive factors. </span></div><div><span style="font-family: helvetica;"><br /></span></div><div><span style="font-family: helvetica;">Destructive factors</span></div><div><span style="font-family: helvetica;"><br /></span></div><div><span style="font-family: helvetica;">Biting your mouth while eating or from a nervous habit is probably the most common way ulcers start. Physical or chemical damage from food is another very common cause - </span></div><div><ul style="text-align: left;"><li><span style="font-family: helvetica;">Crusty food like bread or toast</span></li><li><span style="font-family: helvetica;">Crispy food like chips</span></li><li><span style="font-family: helvetica;">Salty food like pretzels</span></li><li><span style="font-family: helvetica;">Sweet food like candy</span></li><li><span style="font-family: helvetica;">Sticky food like cookies</span></li><li><span style="font-family: helvetica;">Sour food like vinegar</span></li><li><span style="font-family: helvetica;">Hot food like coffee</span></li></ul></div><div><span style="font-family: helvetica;">Abrasive, salty and hot foods/drinks physically damage the mouth. Sour foods/drinks chemically burn the mouth instantly. Sweet and sticky foods burn slowly by feeding oral bacteria, which metabolize sugars to produce corrosive acids. </span></div><div><span style="font-family: helvetica;"><br /></span></div><div><span style="font-family: helvetica;">Drugs are another destructive factor. Alcohol is oxidized by oral bacteria to acetaldehyde, which is toxic and a carcinogen (<a href="https://pubmed.ncbi.nlm.nih.gov/31320675/" target="_blank">Tagaino et al, 2019</a>). Some acetaldehyde is even produced from sugar by oral bacteria. Acetaldehyde is also found in cigarette smoke (<a href="https://pubmed.ncbi.nlm.nih.gov/1171591/" target="_blank">Sprince et al, 1975</a>). As with peptic ulcers, NSAIDs like aspirin inhibit prostaglandin E2 synthesis which reduces mucin secretion. People swishing aspirin in their mouth to quell inflammation are actually slowing down ulcer healing (</span><span style="font-family: helvetica;"><a href="https://iubmb.onlinelibrary.wiley.com/doi/epdf/10.1080/713803747" target="_blank">Slomiany and Slomiany, 2000).</a></span></div><div><span style="font-family: helvetica;"><br /></span></div><div><span style="font-family: helvetica;">Poor dental hygiene is yet another destructive factor. Harsh brushing makes tiny holes through which corrosive agents can meet the cell surface. Ineffectual or nonexistent brushing leaves food and bacteria in position to generate more organic acids and acetaldehyde.</span></div><div><span style="font-family: helvetica;"><br /></span></div><div><span style="font-family: helvetica;">Constructive factors</span></div><div><span style="font-family: helvetica;"><br /></span></div><div><span style="font-family: helvetica;">The major factor protecting the mouth is mucus. </span><span style="font-family: helvetica;">There are five kinds of mucin produced in the mouth - MUC5B and MUC7 being the most important (</span><a href="https://pubmed.ncbi.nlm.nih.gov/26701274/" style="font-family: helvetica;" target="_blank">Frenkel and Ribbeck, 2015</a><span style="font-family: helvetica;">). MUC5B is a very long protein rich in serine and threonine amino acids to which glycans attach. </span><span style="font-family: helvetica;">These glycans attract water to form a gel and gives your mouth that slippery feeling. </span><span style="font-family: helvetica;">The protein overall looks likes a bottle brush with one end attached to the cell. MUC7 is similar, but is unattached and therefore flows freely aiding in formation of the soft bolus from food. </span><span style="font-family: helvetica;">MUC5B proteins form polymers via disulfide bonds. Cysteine is unusually common in MUC5B and is essential for disulfide bond formation.</span></div><div><span style="font-family: helvetica;"><br /></span></div><div><span style="font-family: helvetica;"><div style="font-family: Times;"><span style="font-family: helvetica;">A shortage of many dietary factors have been suggested to cause mouth ulcers. Examples include vitamin B9 (folate), vitamin B12, vitamin C, vitamin E, selenium. All play a role in antioxidation, and it makes sense that these nutrients are low in ulcers as the environment shows signs of oxidative stress (elevated malondialdehyde and depressed glutathione)</span><span style="font-family: helvetica;">(</span><span style="font-family: helvetica;"><a href="https://pubmed.ncbi.nlm.nih.gov/19761497/" target="_blank">Arikan et al, 2009</a>). </span></div><div style="font-family: Times;"><span style="font-family: helvetica;"><br /></span></div><div style="font-family: Times;"><span style="font-family: helvetica;">Despite this speculation, however, the evidence has been inconclusive. There are certainly some patients who respond well to supplementation with one or another of these micronutrients. However, many times mouth ulcers occur in people with no apparent deficiency and/or supplementation has no effect. Considering that some of these micronutrients work in some cases, it's possible that they help in an indirect way, or that chronic mouth ulcers are indicative of a systemic redox imbalance. For example, c</span><span style="font-family: helvetica;">hronic ulcers are more prevalent in those with other problems in their digestive tract (</span><a href="https://pubmed.ncbi.nlm.nih.gov/17489510/" style="font-family: helvetica;" target="_blank">Brailo et al, 2007</a><span style="font-family: helvetica;">).</span></div></span></div><div><span style="font-family: helvetica;"><br /></span></div><div><span style="font-family: helvetica;">Can Vitamin U help heal and prevent mouth ulcers?</span></div><div><div><span style="font-family: helvetica;"><br /></span></div><div><span style="font-family: helvetica;">The use of Vitamin U to treat or prevent mouth ulcers has undergone little investigation (<a href="https://pubmed.ncbi.nlm.nih.gov/14454299/" target="_blank">Kato and Takayasu, 1961</a>). </span><span style="font-family: helvetica;">Vitamin U has been shown to be a useful treatment for</span><span style="font-family: helvetica;"> gum disease (</span><span style="font-family: helvetica;"><a href="https://dental-almanac.org/index.php/journal/article/view/135" target="_blank">Sulym, 2016</a>), an</span><span style="font-family: helvetica;">d </span><span style="font-family: helvetica;">sulfur compounds like cysteine are effective in quenching the damaging effects of acetaldehyde in the mouth, particularly when combined with vitamins B1 and C (<a href="https://pubmed.ncbi.nlm.nih.gov/1171591/" target="_blank">Sprince et al, 1975</a>; <a href="https://pubmed.ncbi.nlm.nih.gov/27127136/" target="_blank">Syrjanen et al, 2016</a>).</span></div></div><div><span style="font-family: helvetica;"><br /></span></div><div><span style="font-family: helvetica;">The fact that Vitamin U has been shown to heal and prevent peptic ulcers by stimulating the release of mucin suggests that it may also have this function in other pa</span><span style="font-family: helvetica;">rts of the digestive tract which also secrete mucin (<a href="https://pubmed.ncbi.nlm.nih.gov/10719747/" target="_blank">Watanabe et al, 2000</a>). </span><span style="font-family: helvetica;">One can't help but wonder whether mouth ulcers have a similar etiology to its more dangerous relatives.</span><span style="font-family: helvetica;"> </span><span style="font-family: helvetica;">If this is indeed the case, one may speculate as to whether Vitamin U or a metabolic derivative could have this effect on the release of mucin from not only the mouth or other parts of the alimentary canal, but even other epithelial tissues, including the lungs, trachea, nose and eyes.</span><span style="font-family: helvetica;"> </span><span style="font-family: helvetica;"> </span></div><div><span style="font-family: helvetica;"><br /></span></div><div><span style="font-family: helvetica;">Vitamin U may also support mucosal function i</span><span style="font-family: helvetica;">n indirect ways</span><span style="font-family: helvetica;">. Firstly, Vitamin U yields cysteine, which is the rate-limiting component of glutathione, the master antioxidant that fights oxidative stress. Secondly, t</span><span style="font-family: helvetica;">he relatively large amount of cysteine required to tether mucin to the epithelial tissue means that extra cysteine in the form of Vitamin U may prove useful. Thirdly, much of the glycans that attach to mucins are themselves sulfated, requiring more sulfur. </span></div><div><span style="font-family: helvetica;"><br /></span></div><div><span style="font-family: helvetica;">M</span><span style="font-family: helvetica;">any people, especially those whose diet is low in the sulfur amino acids methionine and cysteine, have limited antioxidant capacity due to having low levels of glutathione. For those people, alternative sources of sulfur amino acids like Vitamin U are an important alternative source. </span><span style="font-family: helvetica;">Drinking freshly-made vegetable juice or taking Vitamin U supplements in combination with the cessation of destructive practices will probably help clear up your current mouth ulcer and help prevent future ulcers.</span></div>Sean Yu McLoughlinhttp://www.blogger.com/profile/03287541681698360493noreply@blogger.com0tag:blogger.com,1999:blog-4272996138785020260.post-30411719141034748922020-12-22T09:07:00.017-07:002023-06-15T08:12:35.786-06:00Vitamin U complements H2 blockers<p></p><div class="separator" style="clear: both; text-align: center;"><br /></div><div class="separator" style="clear: both; text-align: center;"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEjVgj1PLPLY47jJD0YoAuuqCKD3dbg5B3GAInZfoARqLLoPHNNGUQ013kiUMA-lu4Qs6Khc4j3D4X_juAkRyZBtWYa4LlUYxIzuzfTatx7hjP6Bt2o7o6JYvVbbNvaSmnxWqLqcTbqa1poD/s500/unnamed.png" style="margin-left: 1em; margin-right: 1em;"><img border="0" data-original-height="265" data-original-width="500" height="213" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEjVgj1PLPLY47jJD0YoAuuqCKD3dbg5B3GAInZfoARqLLoPHNNGUQ013kiUMA-lu4Qs6Khc4j3D4X_juAkRyZBtWYa4LlUYxIzuzfTatx7hjP6Bt2o7o6JYvVbbNvaSmnxWqLqcTbqa1poD/w400-h213/unnamed.png" width="400" /></a></div><p><span style="font-family: helvetica;">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.</span></p><p><span style="font-family: helvetica;"><br /></span></p><p><span style="font-family: helvetica;">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. </span></p><p><span style="font-family: helvetica;">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 </span><span style="font-family: helvetica;">in the stomach </span><span style="font-family: helvetica;">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.</span></p><p><span style="font-family: helvetica;">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). </span></p><p><span style="font-family: helvetica;">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 </span><span style="background-color: white; color: #202122; font-family: helvetica;">omeprazole (e.g. Prilosec), </span><span style="font-family: helvetica;">famotidine (e.g. Pepcid) and cimetidine (e.g. Tagamet). Ranitidine (e.g. Zantac) was the most prescribed drug in the US during the 1980s, but the FDA has recently banned its sale due to carcinogenic impurities. </span></p><p><span style="font-family: helvetica;">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.</span></p><p><span style="font-family: helvetica;">One unfortunate problem with taking H2 blockers for stomach ulcers is that they reduce the secretion of mucin (<a href="https://pubmed.ncbi.nlm.nih.gov/19175830/" style="background-color: white; color: #cc1177; text-decoration-line: none;" target="_blank">Ichikawa et al.</a>, <a href="https://pubmed.ncbi.nlm.nih.gov/22000186/" target="_blank">Diebel et al</a>). So while they reduce pain by reducing the amount of acid produced, they also increase the risk of pain by weakening the mucous bilayer. </span></p><p><span style="font-family: helvetica;">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. </span></p><p><span style="background-color: white; color: #222222;"><span style="font-family: helvetica;">Can Vitamin U be combined with H2 blockers? </span></span></p><p><span style="font-family: helvetica;"><span style="background-color: white; color: #222222;">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. </span><span style="color: #222222;">The evidence suggests yes. <b>In 2009, </b></span><b><a href="https://pubmed.ncbi.nlm.nih.gov/19175830/" style="color: #cc1177; text-decoration-line: none;" target="_blank">Ichikawa et al.</a><span style="color: #222222;"> showed that </span><span style="color: #222222;">co-administration of Vitamin U with famotidine reversed the mucin-blocking effects of famotidine without affecting the acid-suppression effects.</span></b><span style="color: #222222;"><b> </b>These results suggest that Vitamin U can add another level of protection to the gut in those taking H2 blockers.</span></span></p><div style="background-color: white; color: #222222;"><span style="font-family: helvetica;">Considering these findings, drinking fresh vegetable juice daily or taking Vitamin U supplements may help restore your mucous bilayer, ease discomfort and heal your ulcers.</span></div>Sean Yu McLoughlinhttp://www.blogger.com/profile/03287541681698360493noreply@blogger.com0tag:blogger.com,1999:blog-4272996138785020260.post-74705424685476777882020-12-08T21:10:00.047-07:002023-06-15T08:13:05.386-06:00High salt consumption may cause stomach ulcers<div class="separator" style="clear: both; text-align: center;"><br /></div><div class="separator" style="clear: both; text-align: center;"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEidDpk01HyxCfyFimo06CaMbbdE-ovPrRLKPVAaf1BF2qz3yqT5Jg8YOwHrigerDTIFjAtML7CNj8Akjq3ibcu8DH3R1rpgXNvS9FPMROEOyZ-QEUkbeSIY78sCl1iR6Jx6WanBHMJye6Uu/s1920/salt-1884166_1920.jpg" style="margin-left: 1em; margin-right: 1em;"><img border="0" data-original-height="1280" data-original-width="1920" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEidDpk01HyxCfyFimo06CaMbbdE-ovPrRLKPVAaf1BF2qz3yqT5Jg8YOwHrigerDTIFjAtML7CNj8Akjq3ibcu8DH3R1rpgXNvS9FPMROEOyZ-QEUkbeSIY78sCl1iR6Jx6WanBHMJye6Uu/s320/salt-1884166_1920.jpg" width="320" /></a></div><div><br /></div><div><span style="font-family: helvetica; font-size: medium;"><u><br /></u></span></div><div><span style="font-family: helvetica;">Summary - High salt consumption is a risk factor for the development of gastritis, gastric ulcers and gastric adenocarcinoma. If you have a stomach ulcer and your salt consumption is high, reducing the amount of salt you eat might help heal your ulcer, especially in combination with other treatments like antibiotics and Vitamin U. Talk to you doctor about your options.</span></div><div><span style="font-family: helvetica;"><br /></span></div><div><span style="font-family: helvetica;"><span style="font-family: helvetica;">(For clarification, "p</span><span style="font-family: helvetica;">eptic ulcer" usually refers to ulcers in either the stomach or the duodenum. A "g</span><span style="font-family: helvetica;">astric ulcer" is another name for a stomach ulcer.)</span></span></div><div><span style="font-family: helvetica;"><br /></span></div><div><span style="font-family: helvetica;"><span><span><span><span><span><span><span>The two most cited risk factors for the development of stomach ulcers are infection with <i>Helicobacter pylori</i> and taking NSAIDs (<a href="https://www.mayoclinic.org/diseases-conditions/peptic-ulcer/symptoms-causes/syc-20354223" target="_blank">Mayo Clinic, 2020a</a>). High dietary salt is another risk factor that is lesser known, though it has long been considered a risk factor in the development of stomach cancer (<a href="https://www.mayoclinic.org/diseases-conditions/stomach-cancer/symptoms-causes/syc-20352438" target="_blank">Mayo Clinic, 2020b</a>; <a href="https://pubmed.ncbi.nlm.nih.gov/15393737/" target="_blank">Cromer et al, 1949</a>). </span></span></span></span></span></span></span></span><span><b>Stomach ulcers and stomach cancer are two different conditions, and ulcers do not automatically lead to stomach cancer. </b>However, these two conditions result from a similar set of risk factors, include high salt intake. What determines whether you develops ulcers or cancer may lie in genetics, diet, and to a certain extent, luck.</span></div><div><span style="font-family: helvetica;"><span><span><span> </span></span></span></span></div><div><span style="font-family: helvetica;"><span><span><span>It has been long noted that at times when salt consumption within a population </span></span></span>is low, stomach ulcers are rare (<a href="https://pubmed.ncbi.nlm.nih.gov/3781325/" target="_blank">Sonnenberg 1986</a> and references within). For example, p<span><span>rior to the French Revolution, salt was heavily taxed in France as a means of raising crown revenue. Salt consumption was light among the general population. and the incidence of stomach ulcers was low. As salt taxes were repealed, salt consumption especially via its use as a food preservative increased. Salt consumption in the Western world peaked in the early 20th century, declining with the invention of alternative forms of preservation like canning and refrigeration. </span><span>Throughout this period, mortality due to stomach ulcers rose, peaked, then declined in lockstep with salt use. </span></span></span></div><div><span style="font-family: helvetica;"><br /></span></div><div><span><span style="font-family: helvetica;">Another way to show a relationship between salt intake and stomach ulcer prevalence is to look at these factors in different countries at a given time. Countries in which salt intake is high (e.g. Japan, Portugal, Spain) tend to have higher mortalities from stomach ulcers than those in which salt intake is low (<a href="https://pubmed.ncbi.nlm.nih.gov/3781325/" target="_blank">Sonnenberg 1986</a>)</span><span style="font-family: helvetica;">. </span></span></div><div><span style="font-family: helvetica;"><br /></span></div><div><span style="font-family: helvetica;"><span style="font-family: helvetica;">Does this mean your stomach ulcer is caused by eating too much salt? On the one hand, your ulcer is caused by something, and if your diet is heavy in salt, it might be a contributing factor. </span><span style="font-family: helvetica;">On the other hand</span><span style="font-family: helvetica;">, while the</span><span style="font-family: helvetica;"> evidence is quite suggestive,</span><span style="font-family: helvetica;"> it's important to take these findings with a grain of salt (so to speak). </span><span style="font-family: helvetica;">If you have a stomach ulcer and eat a lot of salt, reducing dietary salt for a couple of weeks and seeing whether the pain goes away might be worth trying. Even better, talk to your doctor as a combination of reduced salt intake and other treatments might be even more effective.</span></span></div><div style="text-align: left;"><div><span style="font-family: helvetica;"><br /></span></div><div><span style="font-family: helvetica;"><br /></span></div><div><span style="font-family: helvetica;">How does a high-salt diet cause stomach ulcers? </span></div><div><span style="font-family: helvetica;"><br /></span></div><div><span style="font-family: helvetica;"><span><span><span>B</span>y itself, h<span>igh salt intake can </span>cause a non-inflammatory atrophic gastritis (<a href="https://pubmed.ncbi.nlm.nih.gov/12757158/" target="_blank">Bergin et al, 2003</a>). Concentrated salt strips off the mucous bilayer by inducing edema, increasing the percentage of replicating cells susceptible to mutagenesis, and exposing the underlying epithelial cells to damaging stomach acid <a href="https://pubmed.ncbi.nlm.nih.gov/4053034/" target="_blank">(Charnley and Tannenbaum, 1985)</a>. </span></span><span>The</span><span> heightened cell turnover especially in combination with mutagens increases the chances of a cancer-causing mutation occurring. Acidic</span><span> damage reduces production of mucus and acid required for digestion, with chronic damage resulting in low stomach acid (hypochlorhydria) </span><span>(</span><a href="https://pubmed.ncbi.nlm.nih.gov/15393737/" target="_blank">Cromer et al, 1949</a><span>) </span><span>and predisposes to ulcer formation</span><span>. </span></span></div><div><span style="font-family: helvetica;"><br /></span></div><div><span style="font-family: helvetica;"><span>Like salt, </span><span><i>H. pylori</i> </span><span>can induce atrophic gastritis in and of itself, while also inducing an inflammatory response. </span><b>However, it seems that a combination of <i>H. pylori</i> infection and a high-salt environment leads to a much greater chance of developing stomach ulcers and/or cancer. </b><span>Damaging the mucous bilayer with salt enables <i>H. pylori</i> to directly contact the epithelial cells. </span><span>Low stomach acid allows <i>H. pylori </i>to more easily survive in the stomach, especially in parts prone to ulceration/cancer such as the corpus. </span><span>I</span><span>nflammation generates reactive oxygen species that damage the DNA of epithelial cells, resulting in immediate reduction in function as well as debilitating mutations. </span><span>Reactive oxygen species generate mutations in the cells lining the stomach that are then enriched by heightened cell turnover. Most mutations result in reduced cell function, which often shows up as cells that produce less mucus or less gastric acid on a permanent basis. However, some mutations are in genes that when damaged result in the cells reproducing at an inappropriately increased rate, oftentimes producing cancer. </span></span></div><div><b><span style="font-family: helvetica;"><br /></span></b></div><div><span style="font-family: helvetica;">A high-salt environment also seems to induce physiological changes in <i>H. pylori</i> that enable the bacterium to survive under the unusual conditions. When the salt concentration in the stomach increases above a certain level, <i>H. pylori</i> becomes stressed and its growth slows. It changes its shape from its regular spiral to an elongated filamentous form (<a href="https://pubmed.ncbi.nlm.nih.gov/18375562/" target="_blank">Gancz et al, 2008</a>). Virulence factors (e.g. cagA, vacA, adherins) may be induced depending on the strain of <i>H. pylori </i>present, which enable the bacterium to invade the cells lining the stomach (<a href="https://pubmed.ncbi.nlm.nih.gov/17510398/" target="_blank">Loh et al, 2007</a>).</span></div><div><span style="font-family: helvetica;"><br /></span></div><div><span style="font-family: helvetica;"><span>What constitutes high salt? </span><a href="https://pubmed.ncbi.nlm.nih.gov/4053034/." target="_blank">Charnley and Tannenbaum (1985)</a> stated that frequent consumption of foods rich in salt such as soy sauce (18%), dried fish (20%), and pickles (13-25%) would probably lead to increased gastric cell proliferation. Chips and pretzels are similarly salt-rich, and in large and regular amounts would be expected to have similar effects on the gastric lining. The best measure of whether you are taking in too much salt is by having your doctor measure your 24 h urinary sodium output (<a href="https://pubmed.ncbi.nlm.nih.gov/3781325/" target="_blank">Sonnenberg 1986</a>).</span></div></div><div><span style="font-family: helvetica;"><br /></span></div><div><span style="font-family: helvetica;">Stomach ulcers result from an imbalance between destructive factors such as high salt intake and <i>H. pylori</i> infection, and constructive factors such as the mucus-stimulating ability of prostaglandin E2 and Vitamin U. Taking Vitamin U in the form of fresh vegetable juice or supplements will to some extent counteract the negative effects resulting from high salt consumption by rebuilding the protective mucous bilayer lining the stomach. Recall the pioneering cabbage juice studies of Cheney from 70 years ago (<a href="https://pubmed.ncbi.nlm.nih.gov/18104715/" target="_blank">more</a>). The role of <i>H. pylori </i>infection was unknown at the time, yet cabbage juice in the absence of supporting antibiotics was effective in healing peptic ulcers. </span></div><div><span style="font-family: helvetica;"><br /></span></div><div><span style="font-family: helvetica;">Whatever means you take to treat your stomach ulcer, it would be wise to reduce exposure to the causative agent(s), whether that be infection with <i>Helicobacter pylori,</i> NSAIDs, a stressful job, the morning donuts, or in this case, a high-salt diet. If you have stomach issues but are not sure what condition you have, visit your doctor for a diagnosis. </span></div><div><span style="font-family: helvetica;"><br /></span></div><div><span><span style="font-family: helvetica;"><b>Please don't treat stomach cancer with vegetable juice or Vitamin U supplements. </b></span><span style="font-family: helvetica;">The primary role of nutrients is to promote good health and reduce the risk of developing cancer in the first place. </span><span style="font-family: helvetica;">Once a cancer has formed, it should be treated with chemotherapy, radiation and/or surgery. </span></span></div><div>
<br /></div>Sean Yu McLoughlinhttp://www.blogger.com/profile/03287541681698360493noreply@blogger.com0tag:blogger.com,1999:blog-4272996138785020260.post-40820464053152538222020-11-16T19:25:00.015-07:002023-06-15T08:13:39.761-06:00Vitamin U may help combat the ulcergenic effects of NSAIDs<div><div class="separator" style="clear: both; text-align: center;"><br /></div><div class="separator" style="clear: both; text-align: center;"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEgwx5I0-5104UYxAGsIzX2DO-6CeR8FterUv_GNcbJCWUBgkNMt-OO-MoK6D0SvVlyArKF3_mV_OcmJnpPc6vRsbqdlUUROa9WpNSVdPDjh6kinnKf324A0UxvcnE9MzhgUjskdd2Dqk4vX/s1920/pharmacy-3087596_1920.jpg" style="margin-left: 1em; margin-right: 1em;"><img border="0" data-original-height="1276" data-original-width="1920" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEgwx5I0-5104UYxAGsIzX2DO-6CeR8FterUv_GNcbJCWUBgkNMt-OO-MoK6D0SvVlyArKF3_mV_OcmJnpPc6vRsbqdlUUROa9WpNSVdPDjh6kinnKf324A0UxvcnE9MzhgUjskdd2Dqk4vX/s320/pharmacy-3087596_1920.jpg" width="320" /></a></div><br /><font face="helvetica"><br /></font></div><div><font face="helvetica">Summary - Taking NSAIDs increases the risk of you developing stomach ulcers by inhibiting your natural protective system. There are several measures you can take to help get rid of stomach ulcers due to NSAIDs -</font></div><div><span style="font-family: helvetica;"><br /></span></div><div><span style="font-family: helvetica;"><span> </span>1) reduce the dose</span></div><div><font face="helvetica"><span> 2) </span></font><span style="font-family: helvetica;">change the NSAID to one less irritating</span><span style="font-family: helvetica;"> </span></div><div><font face="helvetica"><span> 3</span>) counteract with other drugs</font></div><div><font face="helvetica"><span> </span>4) switch from NSAIDs to other pain relievers</font></div><div><font face="helvetica"><span> 4) take </span>Vitamin U</font></div><div><font face="helvetica"><br /></font></div><div><span style="font-family: helvetica;">Vitamin U in the form of fresh vegetable juice or supplements </span><span style="font-family: helvetica;">can be used in combination with other measures to combat ulcers. However, Vitamin U will not</span><span style="font-family: helvetica;"> counteract </span><span style="font-family: helvetica;">all</span><span style="font-family: helvetica;"> of these negative effects as NSAIDs are powerful drugs. If you have an ulcer and are taking NSAIDs, talk to your doctor as there may be a solution.</span></div><div><span style="font-family: helvetica;"><br /></span></div><div><span style="font-family: helvetica;">-----------------------------------------------------------------------------------------------------------------------------</span></div><div><font face="helvetica"><br /></font></div><div><font face="helvetica"><br /></font></div><div><font face="helvetica">Stomach ulcers result from an imbalance between protective and destructive factors. There are several destructive factors including infection with <i>Helicobacter pylori</i>, overproduction of stomach acid, overeating salt, alcohol and sugar, and taking NSAIDs. Ulcers often result from a combination of these factors. The focus of this post is the role NSAIDs play in causing your ulcer.</font></div><div><span style="font-family: helvetica;"><br /></span></div><div><span style="font-family: helvetica;">NSAIDs (</span><font face="helvetica">N</font><span style="font-family: helvetica;">on-Steroidal Anti-Inflammatory Drugs) </span><span style="font-family: helvetica;">are widely used to reduce pain and inflammation.</span><span style="font-family: helvetica;"> </span><span style="font-family: helvetica;">The most commonly taken NSAIDs are aspirin (e.g. Bayer), ibuprofen (e.g. Advil, Motrin), naproxen (e.g. Aleve), mefenamic acid (e.g. Ponstal), diclofenac (e.g. Voltaren), piroxicam (e.g. Feldene). A more complete list is linked </span><a href="https://www.healthline.com/health/osteoarthritis/medications-list#nsaids" style="font-family: helvetica;" target="_blank">here</a><span style="font-family: helvetica;">.</span></div><div><span style="font-family: helvetica;"><br /></span></div><div><span style="font-family: helvetica;">NSAIDs reduce inflammation and pain by inhibiting the enzyme COX-2. COX-2 is part of your body's inflammatory response. A certain amount of inflammation is good and necessary for healing. However, too much inflammation causes pain and further damage, which is why we take NSAIDs.</span></div><div><span style="font-family: helvetica;"><br /></span></div><div><span style="font-family: helvetica;"><br /></span></div><div><span style="font-family: helvetica;">How do NSAIDs cause stomach ulcers? </span></div><div><span style="font-family: helvetica;"><br /></span></div><div><span style="font-family: helvetica;">In addition to inhibiting COX-2, NSAIDs also inhibit the related enzyme COX-1, albeit </span><span style="font-family: helvetica;">to a lesser extent. COX-1 catalyzes the same reaction as COX-2, that being the synthesis of prostaglandins from arachidonic acid. However, COX-1 and COX-2 have different functions due to their different expression patterns. COX-1 is expressed throughout the body </span><span style="font-family: helvetica;">continuously</span><span style="font-family: helvetica;">, in contrast to COX-2 which is only expressed during inflammation. In the gastrointestinal tract, the continuous production of prostaglandin E2 catalyzed by COX-1 stimulates mucin production. Mucin forms a mucus bilayer in the stomach that protects the lining against corrosive agents such as stomach acid. The inadvertent inhibition of COX-1 by NSAIDs reduces mucin production, leaving the stomach wall vulnerable. To compound the problem</span><span style="font-family: helvetica;">, NSAIDs also have a multitude of other negative effects including increasing the production of stomach acid and increasing oxidative stress (<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3045681/" target="_blank">Matsui et al, 2011</a>), which for people with an ulcer will cause more discomfort and make the ulcer worse.</span></div><div><span style="font-family: helvetica;"><br /></span></div><div><span style="font-family: helvetica;">Fortunately, n</span><span style="font-family: helvetica;">ot all NSAIDs inhibit COX-1 equally. </span><span style="font-family: helvetica;">Some NSAIDs are more ulcergenic than others.</span><span style="font-family: helvetica;"> For example, some of the early NSAIDs like aspirin are notorious for upsetting the stomach. More recently, scientists have developed NSAIDs that don't inhibit COX-1 as much as their predecessors and while still inhibiting COX-2 strongly, so-called COX-2 inhibitors, e.g. celecoxib (Celebrex). Consequently, these newer NSAIDs may reduce ulcer formation while still providing pain relief elsewhere in your body. </span><span style="font-family: helvetica;"><b>If you have an ulcer and are taking NSAIDs, talk to your doctor about alterative NSAIDs. Be warned that these new generation NSAIDs are not without other side effects.</b></span></div><div><span style="font-family: helvetica;"><div><br style="font-family: "Times New Roman";" /></div></span></div><div><span style="font-family: helvetica;"> </span></div><div><span style="font-family: helvetica;">Can Vitamin U help?</span></div><div><span style="font-family: helvetica;"><br /></span></div><div><span style="font-family: helvetica;">The short answer is probably. Vitamin U is a naturally-occurring nutrient found in all vegetables, fruit and grains. One of its functions is to stimulate the secretion of mucin onto the walls of the stomach. How it does this is not well understood, but it is doesn't seem to have anything to do with COX-1/2 and prostaglandins. As a result, Vitamin U can be used to counteract the mucus-depleting effects of NSAIDs.</span></div><div><span style="font-family: helvetica;"><br /></span></div><div><span style="font-family: helvetica;"><br /></span></div><div><span style="font-family: helvetica;">Are there any studies supporting the use of Vitamin U to counteract the ulcergenic effects of NSAIDs?</span></div><div><span style="font-family: helvetica;"><br /></span></div><div><span style="font-family: helvetica;">Yes. In 1993, <a href="https://pubmed.ncbi.nlm.nih.gov/8443719/" target="_blank">Salim reported</a> the findings of a clinical trial in which Vitamin U was found to accelerate healing of patients hospitalized for erosive gastritis (bleeding from the stomach) caused by NSAID intake. Erosive gastritis is a common precursor to stomach ulcers. The majority of the patients had been taking NSAIDs for either osteo- or rheumatoid arthritis for less than 3 months. The NSAIDs used included diclofenac, piroxicam, mefenamic acid, naproxen and ibuprofen. The double-blind study found that the patients who received 4 x 500 mg of Vitamin U (DL-methylmethionine sulfonium chloride) per day had significantly less bleeding than the negative controls. Similarly to Vitamin U, patients given the sulfhydryl amino acid L-cysteine were also found to have significantly reduced bleeding, demonstrating the action of Vitamin U is likely via its conversion to a sulfhydryl. Endoscopies performed two days after treatment revealed significantly greater healing in those who were given either Vitamin U or cysteine. Of the 57 patients who were not treated with either Vitamin U or cysteine, 4 died from their condition. In contrast, there were no fatalities in those who were treated with either of these compounds. </span></div><div><span style="font-family: helvetica;"><br /></span></div><div><span style="font-family: helvetica;">Currently, it is standard medical practice in cases of erosive gastritis to get the patient to stop taking NSAIDs, or at least take less irritating types, and/or to suppress stomach acid production. For a person who is taking NSAIDs for arthritic pain, reducing the amount of NSAIDs taken is clearly not desirable. Switching to less irritating NSAIDs is an option. Talk to your doctor.</span></div><div><span style="font-family: helvetica;"><br /></span></div><div><span style="font-family: helvetica;">Suppressing acid production will reduce irritation of the stomach, but at what cost? Unless you are producing too much stomach acid (a rare condition), reducing stomach acid will have side effects. The major role of stomach acid is to digest protein in our food. </span><span style="font-family: helvetica;">Dietary protein must be unraveled then enzymatically chopped up by pepsin to produce peptides.</span><span style="font-family: helvetica;"> </span><span style="font-family: helvetica;">Without an acidic environment, protein passes through to the duodenum half digested. Enzymes in the duodenum that further digest protein into tiny peptides or amino acids can only do so much, leaving a significant portion of protein to pass into the colon. Consequently, low stomach acid can result in inadequate protein absorption as well as colonic fermentation (smelly gas). Furthermore, long-term suppression of stomach acid production promotes the growth of <i>Helicobacter pylori</i>, a known carcinogen (<a href="https://www.vitaminuandpepticulcers.com/2019/06/salt-and-gastric-ulcers.html" target="_blank">more</a>).</span></div><div><span style="font-family: helvetica;"><br /></span></div><div><span style="font-family: helvetica;">While the results of this clinical trial are promising, Vitamin U is not infinitely powerful. There is only a certain amount Vitamin U can do to reverse or prevent damaged induced by NSAIDs. Large doses of NSAIDs will probably damage the stomach faster than Vitamin U can reverse this damage. However, these findings suggest that Vitamin U may be of some use in counteracting some of the negative effects caused by NSAIDs. Drinking freshly-made vegetable juice on a daily basis provides Vitamin U as well as other beneficial nutrients such as folate. </span></div>Sean Yu McLoughlinhttp://www.blogger.com/profile/03287541681698360493noreply@blogger.com0tag:blogger.com,1999:blog-4272996138785020260.post-44678980421119438622020-08-09T09:06:00.013-06:002023-06-15T08:14:12.126-06:00Vitamin U and acne, dandruff and eczema<p></p><div class="separator" style="clear: both; text-align: center;"><br /></div><div class="separator" style="clear: both; text-align: center;"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEhovg3eARWWfp_AXzD0O4mtlsJqQYw2c6lPSNVuB349hwHz2Q5h0H7RydIjnIYpinhZ7fgKT8Z0wqqpYw3_WaOj8Qyapw2aWv1ZDrp_DwL31rKmRLQ0WF20z1gXAfG9ZoqXrATer5TqT-iN/s1920/acne-1606765_1920.jpg" style="margin-left: 1em; margin-right: 1em;"><img border="0" data-original-height="1280" data-original-width="1920" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEhovg3eARWWfp_AXzD0O4mtlsJqQYw2c6lPSNVuB349hwHz2Q5h0H7RydIjnIYpinhZ7fgKT8Z0wqqpYw3_WaOj8Qyapw2aWv1ZDrp_DwL31rKmRLQ0WF20z1gXAfG9ZoqXrATer5TqT-iN/s320/acne-1606765_1920.jpg" width="320" /></a></div><span style="font-family: helvetica;"><br /></span><p></p><p><span style="font-family: helvetica;">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. </span></p><p><span style="font-family: helvetica;">There are three main causes of low glutathione - </span></p><p><span style="font-family: helvetica;">1. A medical condition that drains large amounts of glutathione</span></p><p><span style="font-family: helvetica;">2. A genetic block that prevents the biosynthesis or regeneration of glutathione</span></p><p><span style="font-family: helvetica;">3. Not enough glutathione precursors in our diet</span></p><p><span style="font-family: helvetica;">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 </span><span style="font-family: helvetica;">suddenly</span><span style="font-family: helvetica;"> </span><span style="font-family: helvetica;">and worsen quickly, particularly under stress. At other times, symptoms can persist chronically for years.</span></p><p><span style="font-family: helvetica;">I</span><span style="font-family: helvetica;">rrespective of the root cause, </span><span style="font-family: helvetica;">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. </span></p><p><span style="font-family: helvetica;">Vitamin U is S-methylmethionine, a soluble nutrient abundant in vegetables and fruit that is converted into methionine by the enzyme BHMT2. </span><span style="font-family: helvetica;"><b>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. </b>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, <b>especially in combination with the identification and removal of triggers of these conditions in you. </b></span></p><p><span style="font-family: helvetica;">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.</span></p>Sean Yu McLoughlinhttp://www.blogger.com/profile/03287541681698360493noreply@blogger.com0tag:blogger.com,1999:blog-4272996138785020260.post-5768883370408118552020-06-30T14:43:00.032-06:002023-06-15T08:14:43.670-06:00The methionine cycle and Vitamin U<div class="separator" style="clear: both; text-align: center;"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEg0I-YBP4f4pHC6Ifq_O4Jl6Gd7cQkctwx9W3zQoqmwtzzwuTK87pmzB9G-EwYPmSjoMEMjw38UweAJmQG1Fzf1cXyB2WUtjonEG_B4Jd7F_6optBAiM2MzfX2ssxWuYL_KboNOyOvTefZP/s960/Methionine+cycle+%25287%2529.jpg" style="margin-left: 1em; margin-right: 1em;"><img border="0" data-original-height="720" data-original-width="960" height="469" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEg0I-YBP4f4pHC6Ifq_O4Jl6Gd7cQkctwx9W3zQoqmwtzzwuTK87pmzB9G-EwYPmSjoMEMjw38UweAJmQG1Fzf1cXyB2WUtjonEG_B4Jd7F_6optBAiM2MzfX2ssxWuYL_KboNOyOvTefZP/w625-h469/Methionine+cycle+%25287%2529.jpg" width="625" /></a></div><div class="separator" style="clear: both; text-align: center;"><br /></div><div><span style="font-family: helvetica;">Summary - The methionine cycle is a multistep enzymatic process than enables Vitamin U to be used as a source of methyl groups vital for gene regulation and the regeneration of creatine/ATP in muscles, as well as its use as a precursor of glutathione required to fight oxidative stress and inflammation.</span></div><div><font face="helvetica"><br /></font></div><div><font face="helvetica">This is a simple depiction of the four-step methionine cycle in our body. In the first step, the adenosyl group of ATP is transferred to methionine to form S-adenosylmethionine (SAM), thereby activating the methyl group of methionine. In the second step, SAM donates its methyl group to a range of acceptor molecules (notably DNA, guanidinoacetate, and phosphatidylethanolamines), also yielding S-adenosylhomocysteine (SAH). In the third step, the adenosyl group SAH is removed by hydrolysis leaving homocysteine. In the fourth step, homocysteine is either remethylated using one of three methyl donors to reform methionine (step 4a) or is directed into the transsulfuration pathway to form cystathionine (step 4b).</font></div><div><font face="helvetica"><br /></font></div><div><font face="helvetica">The methionine cycle has a myriad of functions including -</font></div><div><font face="helvetica"><br /></font></div><div><font face="helvetica">1. The generation of methylation capacity, </font></div><div><font face="helvetica">2. The biosynthesis of cysteine as a component of proteins and glutathione, and as a precursor to taurine and hydrogen sulfide, </font></div><div><font face="helvetica">3. The biosynthesis of polyamines from SAM. </font></div><div><font face="helvetica"><br /></font></div><div><font face="helvetica">The most important function of the methionine cycle is to generate methylation capacity. </font><span style="font-family: helvetica;">A measure of our body's methylation capacity is the SAM:SAH ratio, i.e. the relative amounts of the two intermediates. If this ratio is low (below 4), the first enzyme in transsulfuration (cystathionine beta synthase) will have low activity and homocysteine will be remethylated to reenter the methionine cycle (step 4a). This tendency will continue until the ratio is above 4, at which point the relatively high concentration of SAM activates cystathionine beta synthase (CBS) resulting in excess homocysteine being funneled into the transsulfuration pathway. </span></div><div><font face="helvetica"><br /></font></div><div><font face="helvetica">Another important function of the methionine cycle is the biosynthesis of cysteine via transsulfuration. Transsulfuration adds cysteine to that obtained from our diet as a component of protein (~50%). Cysteine is used as a building block in human proteins, is the catalytic center of the master antioxidant glutathione as well as acting as a precursor to molecules such as taurine and hydrogen sulfide. Increased oxidative stress will result in activation of CBS activity via allosteric binding by glutathione and transcriptional upregulation by hydrogen sulfide, nitric oxide and carbon monoxide. However, despite the negative health effects of high homocysteine levels (associated with cardiovascular disease) and low glutathione levels (associated with inflammation), the maintenance of methylation capacity trumps that of the provision of transsulfuration products.</font></div><div><font face="helvetica"><br />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.</font></div><div><font face="helvetica"><br /></font></div><div><font face="helvetica">There are several nutrients that can contribute methyl groups to the methionine cycle. Aside from methionine, which enters the methionine cycle directly, the other dietary methyl donors enter the methionine cycle via methylation of homocysteine. There are three enzymes known to catalyze this reaction in humans, with each enzyme acting upon a single methyl donor molecule. Other molecules that can contribute methyl groups must do so indirectly. Consequently, the three classes of dietary methyl donor are characterized by the enzyme that catalyzes the reaction with homocysteine and its substrate -<br /><br />1. Betaine:homocysteine methyltransferase 1 (BHMT1) and <b>betaine</b> (trimethylglycine or TMG)<br />2. Methionine synthase (MS) and <b>folate</b> (5'-methyltetrahydrofolate or MTHF)</font><div><font face="helvetica">3. Betaine:homocysteine methyltransferase 2 (BHMT2) and <b>Vitamin U</b> (S-methylmethionine)</font><div><font face="helvetica"><br />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.</font><div><font face="helvetica"><br /></font></div><div><font face="helvetica">Betaine is plentiful in whole grains, with the notable exception of rice (betaine is an osmoprotectant in plants and it appears that under the wet conditions in which rice is usually grown betaine formation is suppressed). Betaine is also produced in our body from choline, which is abundant in the fatty component of food as phosphatidylcholine. Consequently, food with more naturally occurring fat such as meat, eggs, dairy and nuts are the richest sources of choline, with produce and grains contributing a lesser amount.</font></div><div><font face="helvetica"><br /></font></div><div><font face="helvetica">The active form of folate (Vitamin B9) is 5'-methyltetrahydrofolate, which supplies a methyl group to homocysteine to yield methionine and tetrahydrofolate. Once folate has donated its methyl group, it must be remethylated in the folate cycle to be reused. The primary source of these methyl groups is serine. Contrary to popular belief, folate itself is a minor dietary source of methyl groups. Even taking supplements labelled "methyl folate" or "activated folate" or eating green leafy vegetables provides minimal extra methylation substrate. With regards to its role in methylation, folate is better thought of as a carrier molecule analagous to homocysteine rather than as a methyl source.</font></div><div><font face="helvetica"><br />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 <a href="https://pubmed.ncbi.nlm.nih.gov/32503840/" target="_blank">rarely</a> 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.<br /><br />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.</font></div><div><br /></div><div><font face="helvetica"><br /></font></div><div><font face="helvetica"><br /></font></div><div><font face="helvetica">References</font></div><div><font face="helvetica"><br /></font></div><div><ol style="text-align: left;"><li><span style="font-family: helvetica;">Finkelstein (1990) <a href="https://pubmed.ncbi.nlm.nih.gov/15539209/">https://pubmed.ncbi.nlm.nih.gov/15539209/</a></span></li><li><span style="font-family: helvetica;">Mudd and Poole (1975) </span><a href="https://www.blogger.com/#" style="font-family: helvetica;">https://pubmed.ncbi.nlm.nih.gov/1128236/</a></li><li><span style="font-family: helvetica;">Benevenga (2007) </span><a href="https://www.blogger.com/#" style="font-family: helvetica;">https://pubmed.ncbi.nlm.nih.gov/17413090/</a></li><li><span style="font-family: helvetica;">Bertolo and McBrearity (2013) </span><a href="https://www.blogger.com/#" style="font-family: helvetica;">https://pubmed.ncbi.nlm.nih.gov/23196816/</a></li><li><span style="font-family: helvetica;">Olszewski (1989) </span><a href="https://pubmed.ncbi.nlm.nih.gov/2930611/"><font face="helvetica">https://pubmed.ncbi.nlm.nih.gov/2930611/</font></a></li><li><span style="font-family: helvetica;">Reed (2008) </span><a href="https://pubmed.ncbi.nlm.nih.gov/18442411/" style="font-family: helvetica;">https://pubmed.ncbi.nlm.nih.gov/18442411/</a><br style="font-family: helvetica;" /></li><li><span style="font-family: helvetica;">Filipcev (2018) </span><a href="https://www.blogger.com/#" style="font-family: helvetica;">https://pubmed.ncbi.nlm.nih.gov/29596314/</a></li><li><span style="font-family: helvetica;">Dai (2020) </span><a href="https://pubmed.ncbi.nlm.nih.gov/32503840/" style="font-family: helvetica;">https://pubmed.ncbi.nlm.nih.gov/32503840/</a></li></ol></div></div></div></div>Sean Yu McLoughlinhttp://www.blogger.com/profile/03287541681698360493noreply@blogger.com0tag:blogger.com,1999:blog-4272996138785020260.post-70373981493150374462020-06-20T19:19:00.039-06:002023-06-15T08:16:26.285-06:00Vitamin U is a mucin secretagogue<p style="text-align: left;"></p><div class="separator" style="clear: both; text-align: center;"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEiSXmyT5TAYLuAMgtRz1-iHukpOFTeXJthLclWCqCklWTMiRf7MifFf9OgCnQcBapa2K_q0BTDNuScBPInSPpXB66y0cqgTv2uiqvhtXgdGiDFplM34q7G_2Pjy-_XqppxBOa0axSj2M0y7/s1920/abdomen-1698565_1920.png" style="margin-left: 1em; margin-right: 1em;"><img border="0" data-original-height="1490" data-original-width="1920" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEiSXmyT5TAYLuAMgtRz1-iHukpOFTeXJthLclWCqCklWTMiRf7MifFf9OgCnQcBapa2K_q0BTDNuScBPInSPpXB66y0cqgTv2uiqvhtXgdGiDFplM34q7G_2Pjy-_XqppxBOa0axSj2M0y7/s320/abdomen-1698565_1920.png" width="320" /></a></div><span style="font-family: helvetica;"><p style="text-align: left;"><span style="font-family: helvetica;"><br /></span></p>Summary - Vitamin U is a nutrient abundant in vegetables and fruit whose main function is to stimulate the secretion of mucin and enable the formation of the mucous bilayer that protects the stomach from acid and </span><i style="font-family: helvetica;">Helicobacter pylori</i><span style="font-family: helvetica;">.</span><div><span style="font-family: helvetica;"><br /></span><p></p><p style="text-align: left;"><span style="font-family: helvetica;">In the human body, Vitamin U heals and protects against peptic ulcers. It does so by stimulating the secretion of mucins onto the walls of the digestive tract, acting as a precursor to the biosynthesis of the master antioxidant glutathione, and supplies methyl groups for gene regulation, polyamine biosynthesis and a range of other molecules. Of these three functions, stimulating mucin secretion is the most direct way in which Vitamin U works.</span></p><p style="text-align: left;"><font face="helvetica"><span>In the stomach, there is</span><span> an alkaline mucous bilayer gel that protects the stomach from gastric acid, pepsin digestion and bacterial infection. </span><span>Mucus consists of two layers - a deep gel-like layer attached to cells and a superficial loosely-attached layer on top.</span><span> The proteins that make up mucus are called mucins (<a href="https://pubmed.ncbi.nlm.nih.gov/22969235/" target="_blank">MUC1, MUC5AC, MUC6</a>), which are</span><span> heavily-glycosylated proteins that attract water, thereby forming a gel. Mucins are made in foveolar cells lining the stomach and are stored in vesicles awaiting summons to the lumen. At the surface, some mucins stay attached</span><span> to the cells and act as an anchor for the loosely-bound mucins to attach by disulfide bonds.</span><span> </span><span>When this mucous bilayer is disrupted, gastric juice can reach the lining of the stomach causing irritation and inflammation. Left long enough, a peptic ulcer may form.</span></font></p><p style="text-align: left;"><span style="font-family: helvetica;">Your body has a number of different ways to stimulate the secretion of mucin. The molecules that trigger secretion are called mucin secretagogues. The prime mucin secretagogue is prostaglandin E2, a hormone-like molecule that has many functions in the human body. It has a protective role in stomach function, suppressing production of gastric acid and pepsin, while at the same time promoting secretion of mucin and the alkaline molecule bicarbonate (<a href="https://pubmed.ncbi.nlm.nih.gov/1477025/" target="_blank">Park et al</a>). NSAIDs reduce prostaglandin E2 synthesis by inhibiting COX-1, leading to less mucin, less protection and a greater risk of ulcers.</span></p><div><span><font face="helvetica">Vitamin U (S-methylmethionine) is a nutrient found in all vegetables and fruit, and especially members of the cabbage family. Vitamin U protects the digestive tract by stimulating the secretion of mucin from the foveolar cells. In 1996, <a href="https://pubmed.ncbi.nlm.nih.gov/8565766/" target="_blank">Watanabe et al.</a> showed that exposing gastric mucous cells to L-cysteine or methylmethionine sulfonium chloride (MMSC or Vitamin U) prevented the formation of stomach ulcers caused by exposure to 50% ethanol. They demonstrated that Vitamin U and cysteine work in a similar manner via a sulfhydryl group. Interestingly, Vitamin U does not have a sulfhydryl group, but rather a sulfonium group. Consequently, Vitamin U is usually described as a latent sulfhydryl. The fact that Vitamin U and L-cysteine activities were inhibited by the pre-administration of the sulfhydryl inhibitor N-ethylmaleimide suggests that Vitamin U is active as a sulfhydryl. Vitamin U is stable at acid pH, so activation probably takes place in foveolar cells. </font></span></div><div><span><font face="helvetica"><br /></font></span></div><div><font face="helvetica">In a follow up study, <a href="https://pubmed.ncbi.nlm.nih.gov/10719747/" target="_blank">Watanabe et al.</a> (2000) found that Vitamin U and cysteine induced the transport of vesicles containing mucin from deep within the cytosol to the cell surface for release into the stomach lumen, thereby forming a protective barrier. Interestingly, the movement they observed was independent of Ca2+ and cAMP. When signal transduction occurs via an endogenous molecule like prostaglandin-E2, there is a rise in the concentration of cAMP. When the P2 purinergic receptor is activated by ATP, there is an accompanying rise in Ca2+. Yet sulfhydryl-instigated movement did not induce a change in Ca2+ or cAMP levels. The authors suggested sulfhydryls promote mucus movement by a non-receptor mediated process.</font></div><div><font face="helvetica"><br /></font></div><div><span><font face="helvetica">Irrespective of how Vitamin U works, there's good evidence that drinking fresh vegetable juice or taking Vitamin U supplements may help restore your mucous bilayer, ease discomfort and heal your ulcers.</font></span></div><div><div><div style="background-color: white;"><div style="margin-bottom: 0.5em;">
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<span><br /></span><span>Nutritionists have responded that while celery juice can be part of a well-rounded diet, it should not be considered the cure-all being touted. Some are concerned by the removal of fiber. Some consider the positive effects result primarily from the water content rather than any nutrient in the juice. Others generally state that celery juice is nothing special and won't cure anything. </span></font><span style="font-family: helvetica;">There are also </span><a href="https://sciencebasedmedicine.org/the-medical-mediums-thyroid-pseudoscience/" style="font-family: helvetica;" target="_blank">skeptics</a><span style="font-family: helvetica;"> who question William's conflation of the scientifically-backed benefits of eating vegetables with the nonscientific rationale for how this improves health.</span><div><font face="helvetica">
<span><br /></span><span>Drinking celery juice is most likely good for us. From a scientific standpoint, celery juice contains lots of vitamins, minerals and other nutrients that will improve our health if we are not getting enough from our regular diet. Celery juice is also low in calories, unlike most fruit juices. Celery juice might help people psychologically in helping people make healthy lifestyle choices like avoiding bad foods and getting regular exercise.</span></font></div><div><font face="helvetica"><span><br /></span></font></div><div><font face="helvetica"><span>It is quite likely that some of the health benefits resulting from drinking celery juice daily can be ascribed to boosting one's intake of Vitamin U. For those unfamiliar with Vitamin U (S-methylmethionine), it was discovered as an anti peptic ulcer factor during the <a href="https://pubmed.ncbi.nlm.nih.gov/18104715/" target="_blank">1940s</a>-<a href="https://pubmed.ncbi.nlm.nih.gov/13276831/" target="_blank">1950s</a> by Dr Garnett Cheney. Patients with peptic ulcer disease were cured by drinking 1 liter of fresh cabbage juice every day for 7-10 days. Cheney found that other vegetables like celery also worked and increased the palatability of the treatment. Later research found that all vegetables and fruit have Vitamin U, especially in the stalky part. One of its functions in plants is to facilitate the movement of methionine between roots and leaves/fruit. Being mostly stalk, celery makes large amounts of Vitamin U to function. </span><br />
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<span>Most people have chronically low levels of glutathione, which results in chronically high levels of inflammation. People differ in their susceptibility to inflammation according to their genetic makeup, their diet and lifestyle. Vitamin U in celery juice probably improves the function of every body part by helping to restore glutathione levels, thereby reducing inflammation.</span><br /></font></div>Sean Yu McLoughlinhttp://www.blogger.com/profile/03287541681698360493noreply@blogger.com0tag:blogger.com,1999:blog-4272996138785020260.post-68830364430172671112019-12-28T18:20:00.029-07:002023-06-15T08:18:47.673-06:00Vitamin U - A possible natural alternative to N-acetylcysteine (NAC)<div><div class="separator" style="clear: both; text-align: center;"><br /></div><div class="separator" style="clear: both; text-align: center;"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEjdTpOTkdx32TW-sw9GXlkzS8izcCcxVouoELyXT2NBTfXBcMeiwbtGy6NRYzbwZu4-7KLncRIj9mwjcqPNyV42HRLeaWeJPPhq9Fbf02PIrvOItxdxFVx7z_q3s_qOzbbJBJ2J9pwjdKBP/s1920/virus-4937553_1920.jpg" style="margin-left: 1em; margin-right: 1em;"><img border="0" data-original-height="1025" data-original-width="1920" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEjdTpOTkdx32TW-sw9GXlkzS8izcCcxVouoELyXT2NBTfXBcMeiwbtGy6NRYzbwZu4-7KLncRIj9mwjcqPNyV42HRLeaWeJPPhq9Fbf02PIrvOItxdxFVx7z_q3s_qOzbbJBJ2J9pwjdKBP/s320/virus-4937553_1920.jpg" width="320" /></a></div><br /><font face="helvetica"><br /></font></div><div><font face="helvetica">The current coronavirus pandemic has changed our lives forever. One of the hallmarks of coronavirus (COVID-19) infection is acute oxidative stress, and as a consequence, life-threatening damage to the endothelial cells lining our blood vessels. It has been proposed that to counter this oxidative stress one may take N-acetylcysteine (NAC) as part of an array of treatment options that may allay this frightening illness.</font></div><div><font face="helvetica"><br /></font></div><div><font face="helvetica">Dr Roger Seheult </font></div><div><font face="helvetica"><a href="https://www.youtube.com/watch?v=Dr_6w-WPr0w">https://www.youtube.com/watch?v=Dr_6w-WPr0w</a></font></div><div><a href="https://www.youtube.com/watch?v=kK-DNyKnb5c"><font face="helvetica">https://www.youtube.com/watch?v=kK-DNyKnb5c</font></a></div><div><font face="helvetica"><br /></font></div><div><font face="helvetica">Dr Chris Martenson </font></div><div><a href="https://youtu.be/lIkXmAI6A0o?list=PLRgTUN1zz_oeQpnJxpeaEkFimDeepqyWf&t=1494" target="_blank"><font face="helvetica">https://youtu.be/lIkXmAI6A0olist=PLRgTUN1zz_oeQpnJxpeaEkFimDeepqyWf&t=1494</font></a></div><div><font face="helvetica"><br /></font></div><div><span><font face="helvetica">N-acetylcysteine (NAC) is a popular supplement invented in the 1960s used primarily to optimize glutathione levels. It is normally used in hospitals in emergency situations to treat overdoses of acetaminophen (e.g. Tylenol), which results in an acute and deadly shortage of glutathione in the liver. When acetaminophen is taken as directed, it is safely metabolized by the liver enzymatically. A small amount is oxidized to form N-acetyl-p-benzoquinone imine (NAPQI), which is highly toxic. NAPQI is detoxified in the liver by conjugation with glutathione. However, in overdoses of acetaminophen, NAPQI levels rise dramatically as the regular detoxification processes are overwhelmed. The liver literally cannot regenerate glutathione fast enough to quench the toxic NAPQI. Extensive liver damage and death often ensues. NAC helps by being quickly converted into cysteine, which enables the production of fresh glutathione.</font></span></div><span><font face="helvetica"><br />NAC is also sold as a dietary supplement as a means of optimizing glutathione levels on an everyday basis. Glutathione is the master antioxidant in the human body, responsible for detoxifying compounds in the liver as well as reacting with reactive oxygen species that are harmful in large amounts. Glutathione differs significantly to other antioxidants (such as Vitamin C) in that it is made by humans. Our body makes glutathione from three amino acids - glutamate, cysteine and glycine. Levels can get low when our diet is short of these amino acids. The rate-limiting amino acid is usually cysteine, which the body can obtain from the diet following the digestion of protein, and also enzymatically from methionine. When cysteine levels in the diet are inadequate, glutathione levels in the body become inadequate, resulting in general inflammation. Most chronic illnesses are characterized as having low glutathione levels and restoring glutathione levels may help reduce inflammation, if not actually reverse the underlying problem. </font></span><div><span><font face="helvetica"><br /></font></span></div><div><font face="helvetica"><span>Vitamin U (S-methylmethionine) is a naturally abundant nutrient found in vegetables and fruits, especially cruciferous (e.g. cabbage, kale) and stalky vegetables (e.g. celery, asparagus). Like NAC, one of the functions of Vitamin U is to facilitate glutathione biosynthesis via its conversion to cysteine. Its use as an alternative to NAC in the treatment of acetaminophen overdose has been proposed and remains under investigation. One of the advantages of Vitamin U is that unlike NAC, </span><span>Vitamin U is already found in many of the foods available in the fresh market, and is therefore unlikely to cause side effects. </span></font></div><div><span><font face="helvetica"><br /></font></span></div><div><font face="helvetica"><span>While </span><span>Vitamin U should not be used in an emergency situation as its efficacy has not been tested, Vitamin U may serve as an alternative to NAC by those looking for a natural choice to boost their glutathione levels and restore their redox balance on an everyday basis. </span></font></div><div><div><span><b><font face="helvetica"><br /></font></b></span></div><div><span><b><font face="helvetica">It should be emphasized that any possible overdose of paracetamol/acetaminophen should be treated at a hospital by a doctor and not self-treated with NAC or Vitamin U. </font></b></span></div><div><span><font face="helvetica"><br /><br />References<br /><br /><a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2798828/">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2798828/</a><br /><br /><a href="https://www.webmd.com/vitamins-supplements/ingredientmono-1018-N-ACETYL+CYSTEINE.aspx?activeIngredientId=101">https://www.webmd.com/vitamins-supplements/ingredientmono-1018-N-ACETYL+CYSTEINE.aspx?activeIngredientId=101</a></font></span></div></div>Sean Yu McLoughlinhttp://www.blogger.com/profile/03287541681698360493noreply@blogger.com0tag:blogger.com,1999:blog-4272996138785020260.post-25767543537550830392019-12-28T18:19:00.040-07:002023-06-15T08:19:38.387-06:00Food sources of Vitamin U<div><div class="separator" style="clear: both; text-align: center;"><br /></div><div class="separator" style="clear: both; text-align: center;"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEjGr0rZPLdXOPJd-mcXWbtHj_OFLy04plAUb8cEnheo-xvUbsmfg9HBtAC2UwLsESXg1znyDNXfhAcw1CSuZ1iF7acuWIj2xrR3ZNq2ObJ7_6SKyYKPfn2On0Ow2sKfyfKl_lSSoeRGzGXW/s2048/Veggies.jpg" style="margin-left: 1em; margin-right: 1em;"><img border="0" data-original-height="1380" data-original-width="2048" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEjGr0rZPLdXOPJd-mcXWbtHj_OFLy04plAUb8cEnheo-xvUbsmfg9HBtAC2UwLsESXg1znyDNXfhAcw1CSuZ1iF7acuWIj2xrR3ZNq2ObJ7_6SKyYKPfn2On0Ow2sKfyfKl_lSSoeRGzGXW/s320/Veggies.jpg" width="320" /></a></div><br /></div><font face="helvetica">Vitamin U is produced by all flowering plants (angiosperms). Pretty much any vegetable and fruit we eat comes from a flowering plant, so pretty much anything we eat that comes from a plant has some Vitamin U, at least before it is processed. In fact, the only plants or plant-like organisms that don't make Vitamin U are conifers, ferns, mosses, algae and fungi.<br /><br />In general, vegetables belonging to the Brassicacea family are the best source of Vitamin U. This family includes cabbages, kale, broccoli, kohlrabi, collards and turnips. Other vegetables such as spinach, asparagus and celery also produce abundant amounts of Vitamin U. Fruit are also good sources, but not as good as vegetables. In general, there is more Vitamin U in the leaves and stalks than in the fruit, roots and seeds. Grains seem to have little when fresh, but Vitamin U is made during sprouting. Animal products have little to no Vitamin U as it is not synthesized nor stored in significant amounts in animals.<br /><br />Several studies have measured the concentration of Vitamin U in various foods. Tables listing some of these results are included below. Many factors affect the amount of Vitamin U in a given vegetable. These factors include storage conditions, storage duration, harvest time, regional variations and species variations. For example, cabbages have more Vitamin U during spring and summer when freshly harvested, with the nutrient slowly degrading with storage. After six months in the fridge, the concentration drops by one third, with faster losses at room temperature. In contrast, when barley is germinated for making beer, the amount of Vitamin U rises over time, affecting the flavor of the end product. In some cases, there are varieties of fruit that produce less Vitamin U. Oranges that have been selected to produce less Vitamin U are used to make juice because Vitamin U breaks down with extended storage and pasteurisation to form dimethyl sulfide, a compound that negatively affects the taste of the product (Sakamoto et al </font><a href="https://pubmed.ncbi.nlm.nih.gov/8987599/"><font face="helvetica">https://pubmed.ncbi.nlm.nih.gov/8987599/</font></a><font face="helvetica"><span>.) </span><br />
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<font face="helvetica"><span>--------------------------------------------------------------------------------------------------------------------------<br /><br />Song, Ji-Hoon, Hae-Rim Lee, and Soon-Mi Shim. 2016. “Determination of S-Methyl-L-Methionine (SMM) from Brassicaceae Family Vegetables and Characterization of the Intestinal Transport of SMM by Caco-2 Cells.” Journal of Food Science 82 (1): 36–43.<br /><br /><a href="https://www.ncbi.nlm.nih.gov/pubmed/27883364">https://www.ncbi.nlm.nih.gov/pubmed/27883364</a></span><br />
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<u><span>Food (Vitamin U concentration (</span><span>mg/kg dry weight</span><span>))</span></u><span><br /><br />Radish (129-139)<br />Cabbage (535)<br />Kimchi cabbage (89-116)<br />Broccoli (150-350)<br /><br />--------------------------------------------------------------------------------------------------------------------------</span></font></div>
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<span><font face="helvetica">Scherb, J., Kreissl, J., Haupt, S. & Schieberle, P. Quantitation of S-methylmethionine in raw vegetables and green malt by a stable isotope dilution assay using LC-MS/MS: comparison with dimethyl sulfide formation after heat treatment. J. Agric. Food Chem. 57, 9091–9096 (2009).<br /><br /><a href="https://www.ncbi.nlm.nih.gov/pubmed/19754146">https://www.ncbi.nlm.nih.gov/pubmed/19754146</a></font></span></div>
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<font face="helvetica"><span><br /><u>Food (Vitamin U concentration (</u></span><span><u>mg/kg wet weight</u></span><span><u>))</u><br /><br />Celery (176)<br />Kohlrabi (124)<br />Leek (94)<br />Beetroot (89)<br />Cabbage (81)<br />White asparagus - Peru spears (161)<br />White asparagus - Peru stalks (86)<br />White asparagus - Germany spears (252)<br />White asparagus - Germany stalks (68)<br />White asparagus - Greece spears (113)<br />White asparagus - Greece stalks (101)<br />Green asparagus - Peru spears (234)<br />Green asparagus - Peru stalks (109)<br />Green asparagus - Germany spears (94)<br />Green asparagus - Germany stalks (53)<br />Green asparagus - Mexico spears (134)<br />Green asparagus - Mexico stalks (64)<br />Tomato (2.8)<br />Commercial orange juice (0.9)<br />Commercial strawberry juice (1.8)</span><br />
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<span><font face="helvetica">Freshly-squeezed orange juice (1.2)<br />Barley - unprocessed (0.9)<br />Barley - after 4 days of germination (24)</font></span></div>
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<font face="helvetica"><span>--------------------------------------------------------------------------------------------------------------------------<br /><br />Kim, G.-H. Determination of Vitamin U in Food Plants. Food Sci. Technol. Res. 9, 316–319 (2003).<br /><br /><a href="https://www.jstage.jst.go.jp/article/fstr/9/4/9_4_316/_pdf">https://www.jstage.jst.go.jp/article/fstr/9/4/9_4_316/_pdf</a><br /><br /><u>Food (Vitamin U concentration (mg/100g dry weight))</u><br /><br />Spinach (45.2)<br />Pak-choy (34.3)<br />Kale (23.4)</span><br />
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<span><font face="helvetica">Sumssukbujaengi - a wild korean leafy vegetable (19.8)<br />Leaf mustard (19.6)<br />Bud of aralia (19.3)<br />Broccoli (18.9)<br />Asparagus (18.7)<br />Sanmanul - a wild garlic (14.4)<br />Crown daisy (11.1)<br />Burdock (11.0)<br />Celery (8.3)<br />Komchi (4.7)<br />Wasabi (4.7)<br />Chamchi - a wild korean plant (4.0)<br />Shepherd’s purse (3.4)<br />Garlic (2.8)<br />Onion (2.7)<br />Green onion (2.6)<br />Laver (2.2)<br />Nurukchi (0.8)<br />Green tea (0.1)<br />Ginger (not detected)<br />Seaweed (not detected)<br />Red chilli (not detected)<br />Miscellaneous wild korean vegetables (not detected)</font></span></div>
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<font face="helvetica"><span>--------------------------------------------------------------------------------------------------------------------------<br /><a href="https://www.blogger.com/null"></a><br />Kovatscheva, E. G. & Popova, J. G. [S-Methylmethionine content in plant and animal tissues and stability during storage]. Nahrung 21, 465–472 (1977).</span><br />
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<a href="https://www.ncbi.nlm.nih.gov/pubmed/927476"><font face="helvetica">https://www.ncbi.nlm.nih.gov/pubmed/927476</font></a></div>
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<u><span>Food (</span><span>Vitamin U concentration </span><span>(mg/kg wet weight))</span></u><span><br /></span><br />
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<font face="helvetica"><span><br />Cabbage (50-104)<br />Kohlrabi (81-110)</span><br />
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<font face="helvetica"><span>Turnip (51-72)<br />Tomato (45-83)</span><br />
</font><div><span style="font-family: helvetica;">Celery (38-78)</span></div><div><font face="helvetica"><span>Leeks (66-75)<br />Garlic leaves (44-64)</span><br />
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<span><font face="helvetica">Beet (22-37)<br />Raspberries (27)<br />Strawberries (14-25)</font></span></div><div><span><font face="helvetica"><br /></font></span></div><div><span><font face="helvetica">-----------------------------------------------------------------------------------------------------------------------------</font></span></div></div><div><div><span><font face="helvetica"><br /></font></span></div><div><font face="arial">Other references</font></div><div><font face="arial"><br /></font></div><div><font face="arial">1. 100-600 mg/kg dry weight (Bourgis et al and references within.)</font></div><div><font face="arial"> </font></div><div><font face="arial"><a href="https://pubmed.ncbi.nlm.nih.gov/10449582/">https://pubmed.ncbi.nlm.nih.gov/10449582/</a></font></div>
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Sean Yu McLoughlinhttp://www.blogger.com/profile/03287541681698360493noreply@blogger.com0tag:blogger.com,1999:blog-4272996138785020260.post-87909587225762552472019-12-28T18:19:00.039-07:002023-06-15T08:06:22.171-06:00How much Vitamin U do you need to heal ulcers?<div><font face="helvetica"><span><div class="separator" style="clear: both; text-align: center;"><br /></div><div class="separator" style="clear: both; text-align: center;"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEggxM2mnDLA1SceCoVBSHzewIN2iGXXyRuAICD9IWXOreXYvDbhQ7kEUaiYTKNnWUbpPZn4g4tkQcmx8O6tGkjGNhXwNFW4uhKWTfr-KQeEAHQcAbuPqU-1IngiUMly5l0iHyhKXGMEQDgA/s1920/medicine-4097308_1920.jpg" style="margin-left: 1em; margin-right: 1em;"><img border="0" data-original-height="1280" data-original-width="1920" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEggxM2mnDLA1SceCoVBSHzewIN2iGXXyRuAICD9IWXOreXYvDbhQ7kEUaiYTKNnWUbpPZn4g4tkQcmx8O6tGkjGNhXwNFW4uhKWTfr-KQeEAHQcAbuPqU-1IngiUMly5l0iHyhKXGMEQDgA/s320/medicine-4097308_1920.jpg" width="320" /></a></div><br /><b><br /></b></span></font></div><div><font face="helvetica"><span><b>Summary - Hospitalized peptic ulcer patients were cured by drinking cabbage juice containing 42-162 mg of Vitamin U per day for 7-10 days when eating a bland diet and getting bed rest.</b></span></font></div><font face="helvetica"><span><div><font face="helvetica"><span><br /></span></font></div>A recommended dietary allowance (RDA) for Vitamin U has not been established by the US National Academy of Medicine. However, an estimate of how much Vitamin U you could try can be made by calculating the amount of Vitamin U used in <a href="https://pubmed.ncbi.nlm.nih.gov/18104715/" target="_blank">Dr Cheney's studies</a>. Cheney healed ulcer patients with 1 liter of cabbage juice per day over 7-10 days. At the time, Cheney didn't know exactly how much Vitamin U was in the juice. He just knew this much juice in combination with a bland diet and rest was enough. In more recent years, Vitamin U was identified as S-methylmethionine, and there have been several studies in which the amount of this amino acid has been quantified in cabbages. From these studies we can approximate how much supplemental Vitamin U is required to heal ulcers.<br /><br />In 2003, <a href="https://www.jstage.jst.go.jp/article/fstr/9/4/9_4_316/_article" target="_blank">Kim reported</a> 26-46 mg/100 g of dry weight, which given that a cabbage is ~92% water, works out as 21-37 mg/kg of fresh cabbage. In 2009, <a href="https://pubmed.ncbi.nlm.nih.gov/19754146/" target="_blank">Scherb and others</a> found that cabbages have 81 mg of Vitamin U per kg of fresh cabbage. In 2017, <a href="https://pubmed.ncbi.nlm.nih.gov/27883364/" target="_blank">Song et al</a> determined that cabbages contain 50 mg/kg of Vitamin U. So we can estimate that there is roughly 21-81 mg Vitamin U per kg of cabbage.</span></font><div><font face="helvetica"><span><br /></span></font></div><div><font face="helvetica"><span>Why this variation? There are several probable explanations. O</span></font><span style="font-family: helvetica;">ne possibility is that different parts of the cabbage were analyzed by the various researchers.</span><span style="font-family: helvetica;"> </span><span style="font-family: helvetica;">Kim found that the concentration of Vitamin U in the core, middle and outside leaves varied by 2-fold, with the middle leaves having the most. Scherb found that vegetables grown in different countries had different amounts of Vitamin U, suggesting that some of the variation may be due to geography. Another possibility is that the cabbages were not all of equal freshness or picked at the same time of the year. In an older study, <a href="https://pubmed.ncbi.nlm.nih.gov/927476/" target="_blank">Kovatscheva and Popova noted</a> that cabbages lose 62% of their Vitamin U during six months of storage without refrigeration and 34% with refrigeration. Cabbages harvested in spring /summer have the highest Vitamin U content. Finally, it is possible that the various extraction procedures used in the studies resulted in slightly different yields of Vitamin U. </span></div><div><font face="helvetica"><span><br />1 liter of juice is typically extracted from about 2 kg of cabbage. Cheney arrived at 1 liter from prior studies in which various volumes of cabbage juice were given to guinea pigs subjected to chemically-induced ulceration. 100% of the guinea pigs responded to the guinea-pig equivalent of 720 ml of juice. The volume used in the clinical study was rounded up to 1 liter to take into consideration variations in body weight and unexpected factors. </span></font><div><font face="helvetica"><span><br /></span></font></div><div><font face="helvetica"><span>Taking all this data together, it can be estimated that 1 litre of juice contains 42-162 mg of Vitamin U, which probably represents a maximum daily requirement.</span></font></div></div>Sean Yu McLoughlinhttp://www.blogger.com/profile/03287541681698360493noreply@blogger.com0tag:blogger.com,1999:blog-4272996138785020260.post-73556441174093562522019-12-28T18:17:00.031-07:002023-06-15T08:04:04.712-06:00Issues with drinking 1 liter of cabbage juice<div><div class="separator" style="clear: both; text-align: center;"><br /></div><div class="separator" style="clear: both; text-align: center;"><br /></div><div class="separator" style="clear: both; text-align: center;"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEiHGRse2cUpbgjoqNt_-Un-GJOB_oi1lMNvJmkZrxPqJmIvH4H3WrHA8lLPiuNreTOhpdG-MWSncLMdKfOfgRwgrUKBeAy8nSg0dov3zot_V4PUHorPXqUiGc6uDQj8Wu2pOjycTcdOmEyW/s1920/top-view-1248949_1920.jpg" style="margin-left: 1em; margin-right: 1em;"><img border="0" data-original-height="1280" data-original-width="1920" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEiHGRse2cUpbgjoqNt_-Un-GJOB_oi1lMNvJmkZrxPqJmIvH4H3WrHA8lLPiuNreTOhpdG-MWSncLMdKfOfgRwgrUKBeAy8nSg0dov3zot_V4PUHorPXqUiGc6uDQj8Wu2pOjycTcdOmEyW/s320/top-view-1248949_1920.jpg" width="320" /></a></div><span style="font-family: helvetica;"><br /></span></div><div><span style="font-family: helvetica;"><br /></span></div><div><span style="font-family: helvetica;">In the 1940s and 1950s, Stanford doctor <a href="https://pubmed.ncbi.nlm.nih.gov/18104715/" target="_blank">Garnett Cheney</a> healed his peptic ulcer patients by having them drink 1 liter of cabbage juice daily for a couple of weeks. Cabbage juice is not only rich in Vitamin U, but is also rich in folate, vitamin C, vitamin K and potassium among other nutrients. It's well worth trying this treatment for peptic ulcers rather than taking supplements. However, there may be some drawbacks. </span></div><div><b style="font-family: helvetica;"><br /></b></div><font face="helvetica"><span><div><span><br /></span></div>Taste<br /><br />Many people find cabbage juice to be</span><span> d</span><span>istasteful. The chemicals responsible for this bitterness are called isothiocyanates. These compounds are produced in the cabbage when the leaves are physically damaged during chewing or juicing. Glucosinolates are enzymatically converted by myrosinases to form the bitter isothiocyanates. Some people are lucky in that can't taste isothiocyanates all that well so they can readily drink cabbage juice. One way to prevent the formation of isothiocyanates is by boiling unbroken cabbage leaves before juicing to kill the enzymes. That's why boiled cabbage has a mild taste compared to raw cabbage. However, the problem with this approach is that Vitamin U is also unstable to boiling, negating any beneficial effects. </span></font><div><font face="helvetica"><span><br /></span></font></div><div><font face="helvetica"><span>One solution is to drink the one liter of juice as 4 cups throughout the day instead of all at once. Another solution is to mix in better tasting vegetables that contain Vitamin U such as celery. Cheney used mixes containing a 3:1 cabbage-to-celery to good effect.<br /><br /><br />Gas<br /><br />A second issue is gas. Cabbage has a significant amount of raffinose, a sugar that is notorious for producing gas when eaten. The human small intestine lacks the enzyme required for the digestion of raffinose. Unfortunately, some types of bacteria in our large intestine do have such an enzyme and will ferment raffinose quite readily to form gases. These gases produced in the colon have only one way out and will cause bloating and discomfort until discharged. Ingesting one liter of cabbage juice will cause problems for most people. In principle, a possible solution is to treat the cabbage juice with Beano before drinking it. Beano is basically alpha-galactosidase, an enzyme that will break down raffinose into sucrose and galactose, both of which we can easily break down and absorb. I'm not sure whether anyone has tested this idea, though taking Beano along with the juice as recommended should help. Drinking several cups spread throughout the day should also reduce bloating.<br /><br /><br />Smell<br /><br />A third issue is smell. Fresh cabbage juice smells fine - old juice does not. Vitamin U is degraded to homoserine and dimethylsulfide by enzymes found in cabbage. Dimethylsulfide has a disagreeable sulfur odor a little like that found in rotten eggs, though without the toxicity. These enzymes don't work as quickly as myrosinases, but leaving cabbage juice sitting around for a few hours will allow plenty of time for dimethylsulfide to form. Putting the juice in the fridge will slow the reaction somewhat, but after 24 h the juice still tastes terrible. Even if a person could stomach the old juice, there would not be much point as by this stage most of the Vitamin U would have been degraded. Cabbages also have other compounds that contain sulfur that when broken down produce disagreeable odors. The solution is to drink cabbage juice fresh before it has had a chance to go off.</span></font></div><div><div>
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</div>Sean Yu McLoughlinhttp://www.blogger.com/profile/03287541681698360493noreply@blogger.com0tag:blogger.com,1999:blog-4272996138785020260.post-80178200698859937852017-01-09T10:53:00.041-07:002023-06-15T08:03:26.054-06:00Cabbage Juice Heals Peptic Ulcers<div style="text-align: center;">
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</div><div><div><div style="font-style: normal; letter-spacing: normal;"><div class="separator" style="clear: both; text-align: center;"><br /></div><div class="separator" style="clear: both; text-align: center;"><br /></div><div class="separator" style="clear: both; text-align: center;"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEi6vp_YTnQdxRSU1o2FsjfV2idwAIR3cHKO3MpLT6jaHNsrrxAEMk_YmRjS_JRgozyyl2a90mDeYfiKEvULy2C1zON-2_CB-E1YTJui1HUgqjEMwEAMu_HhNv4YUaLZcZtWJmmFeLnM0CER/s1920/white-cabbage-2705228_1920.jpg" style="margin-left: 1em; margin-right: 1em;"><img border="0" data-original-height="1440" data-original-width="1920" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEi6vp_YTnQdxRSU1o2FsjfV2idwAIR3cHKO3MpLT6jaHNsrrxAEMk_YmRjS_JRgozyyl2a90mDeYfiKEvULy2C1zON-2_CB-E1YTJui1HUgqjEMwEAMu_HhNv4YUaLZcZtWJmmFeLnM0CER/s320/white-cabbage-2705228_1920.jpg" width="320" /></a></div><br /></div><div style="font-style: normal; letter-spacing: normal;"><font face="helvetica"><br /></font></div><div style="font-style: normal; letter-spacing: normal;"><font face="helvetica">In the 1940s and 1950s, Dr Garnett Cheney from Stanford discovered that having his peptic ulcer patients drink one liter of fresh cabbage juice every day healed their stomach and duodenal ulcers 3-6 times faster than a bland diet alone. Chronic ulcers disappeared in 1-2 weeks depending on their severity. Dr Cheney was of the opinion that peptic ulcers resulted from a deficiency of a nutritional factor he termed Vitamin U, later identified as the amino acid S-methylmethionine. While cabbages are a particularly rich source of Vitamin U, Cheney found that all raw vegetables, and to a lesser extent, fruit, contain Vitamin U. In addition to healing existing ulcers, Dr Cheney found that Vitamin U also prevented the formation of new ulcers.<br /><br />Why do we get ulcers? <b>Ulcers result from an imbalance in the digestive system between protective and destructive factors. </b>An alkaline bilayer of mucus containing mucin protects the wall of the digestive tract from harsh elements such as stomach acid, infection by bacteria living in the digestive system, NSAIDs, and dietary factors like high salt and alcohol. In modern times, NSAIDs increasingly contribute to ulcer formation by</font><span style="font-family: helvetica;"> inhibiting the mucus-stimulating function of our body's prostaglandins. </span><span style="font-family: helvetica;">When the mucus layer is depleted, these harsh elements irritate the epithelial cells lining the digestive tract causing inflammation and enabling deep infection. </span></div><div style="letter-spacing: normal;"><font face="helvetica" style="font-style: normal;"><br />Ulcers are usually treated with proton pump inhibitors or </font><span style="font-family: helvetica; font-style: normal;">H2 blockers </span><span style="font-family: helvetica; font-style: normal;">to reduce acid production, antibiotics to treat bacterial infections (particularly </span><i style="font-family: helvetica;">Helicobacter pylori</i><span style="font-family: helvetica;"> in the stomach), antacids to neutralize acid, and mucosal protectants such as prostaglandin mimics. </span><span style="font-family: helvetica;">Unfortunately, these only provide a temporary solution to the problem. Ulcers return soon after cessation of treatment. E</span><span style="font-family: helvetica;">xcessive stomach acid is usually not the root problem, nor is </span><i style="font-family: helvetica;">H. pylori </i><span style="font-family: helvetica;">infection. M</span><span style="font-family: helvetica;">ost people with ulcers produce a normal amount of stomach acid, and h</span><span style="font-family: helvetica;">alf the world's population has </span><i style="font-family: helvetica;">H. pylori </i><span style="font-family: helvetica;">yet remain ulcer-free. These facts indicate that while acid and infection contribute to the formation of ulcers, other factors are at play.</span></div><div style="font-style: normal; letter-spacing: normal;"><font face="helvetica"><br />Given the findings of Dr Cheney, it's easy to see that eating a balanced diet rich in sources of Vitamin U is beneficial. But how does Vitamin U work? In later studies, it was shown that Vitamin U has three properties that help maintain a healthy gut.<br /><br /></font><ol><li><font face="helvetica">Stimulating the release of mucin into the mucus layer, thereby protecting the walls from acid and bacterial infection <b>(most important)</b>.</font></li><li><font face="helvetica">Reducing inflammation by acting as a precursor to glutathione, the master antioxidant of the human body via its conversion to cysteine.</font></li><li><font face="helvetica">Coordinating with other nutrients such as methionine, folate, B12, betaine, choline, SAMe and B6 to supply vital methyl groups required for optimal health.</font></li></ol><font face="helvetica"><br />Increasing the Vitamin U content of one's diet in combination with reducing the intake of foods that deplete the protective mucus layer has been shown to improve ulcerative conditions in the digestive system. <b>A diet rich in fresh vegetables, vegetable juice and fruit, and low in salt, alcohol and sugars is a good approach for restoring the mucus bilayer in most patients.</b></font></div><div style="font-style: normal; letter-spacing: normal;"><font face="helvetica"><br /><br />References</font></div><div style="font-style: normal; letter-spacing: normal;"><font face="helvetica"><br /><a href="https://www.ncbi.nlm.nih.gov/pubmed/18104715">http</a><a href="goog_1746659184">s://www.ncbi.nlm.nih.gov/pubmed/18104715</a></font></div><div style="font-style: normal; letter-spacing: normal;"><span style="font-family: helvetica;"><a href="goog_1746659184"><br /></a></span></div><div><div style="font-style: normal; letter-spacing: normal;"><font face="helvetica"><a href="goog_1746659184">https://www.ncbi.nlm.nih.gov/pubmed/10719747</a></font></div><div style="font-style: normal; letter-spacing: normal;"><span style="font-family: helvetica;"><a href="goog_1746659184"><br /></a></span></div><div><span style="font-family: helvetica;"><a href="https://pubs.acs.org/doi/pdf/10.1021/ja01630a032">https://pubs.acs.org/doi/pdf/10.1021/ja01630a032</a></span></div><ol style="font-style: normal; letter-spacing: normal;"><font face="helvetica"></font></ol><div style="font-style: normal; letter-spacing: normal;"><font face="helvetica"></font></div><div style="font-style: normal; letter-spacing: normal;"><span style="font-family: times, "times new roman", serif;"><font face="arial" size="5"><br /></font></span></div></div><div style="font-style: normal; letter-spacing: normal;"><div><span style="font-family: times, "times new roman", serif;"><font face="arial"><br /></font></span></div></div></div>
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Sean Yu McLoughlinhttp://www.blogger.com/profile/03287541681698360493noreply@blogger.com4