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Medical Forum / General / General / March 2005stroke, homocysteine and B 12
This was given to me by my physician because my homocysteine level is not responding to 3 mg folate and one B50 complex. It came from the stroke prevention clinic at my provincial university medical school. "It has come to our attention that your patient has an elevated homocysteine level. Although clinical trials of treatment of hyperhomocysteinemia to prevent vascular disease have not been positive to date, definitive trials in stroke prevention are still pending. Given the theoretical advantage of lowering homocysteine and the relative safety of vitamin therapy we recommend treatment with vitamin B75 one tablet daily, and "Swiss" brand Vitamin B12 plus Folic Acid sublingual one tablet daily. This combination allows 75 mg of B6, 1.0 mg of folic acid and 1075 mg of B12, which is an approprate combination for lowering elevated homocysteine. This is a suggestion only as more firm recommendations await the results of clinical trials currently underway. ...". Zee > This was given to me by my physician because my homocysteine level is > not responding to 3 mg folate and one B50 complex. It came from the [quoted text clipped - 14 lines] > > Zee I'd say this is wishful thinking by the stroke prevention clinic. While there may be some suggestion of benefit in treating some people with vitamins to lower homocysteine levels, the evidence on stroke is pretty negative. There was a trial of more than 3600 people with a stroke that found no decrease in recurrent stroke or in cardiac events or death in people who were treated with B-vitamin supplements. It would be surprising for a primary prevention trial to show an effect when a secondary prevention trial showed no benefit, so it's hard to accept their implication that the evidence isn't in yet.  SignatureDavid Rind drind@caregroup.harvard.edu > > This was given to me by my physician because my homocysteine level is > > not responding to 3 mg folate and one B50 complex. It came from the [quoted text clipped - 28 lines] > David Rind > drind@caregroup.harvard.edu I was hoping you would comment. I am being told I *must* lower my homocysteine. It has not responded to folate. I am also told my physcians are "very worried" about my ldl cholesterol. These comments are usually followed by my getting a "non-compliant patient" talk followed by a sign-off as patient letter cc'd to my general practitioner. Did you see the recent post about pantethine to lower cholesterol? Do you have any thoughts on that? I would welcome your opinion. Zee > I was hoping you would comment. I am being told I *must* lower my > homocysteine. It has not responded to folate. I am also told my [quoted text clipped - 7 lines] > > Zee I'm not sure my comments will be too helpful for a couple of reasons: First, it's hard for me to make useful comments about for an individual over the Net -- it's just not similar to the information available when seeing a patient. Second, my approach to high risk cardiac situations is the one you like least. If I were really worried that someone's homocysteine level (plus some number of other risk factors) placed them at too high a risk for cardiovascular disease, my approach would be to have them take a statin. High homocysteine levels do seem to correlate some with cardiovascular risk, but we really don't know that lowering those levels with folate (or with folate plus other vitamins) really has any important impact on that risk. I don't know of any evidence that anyone "must" lower their homocysteine level, since we don't actually know that doing so has any beneficial effect. In contrast, statins clearly lower cardiovascular risk. I didn't notice the post on pantethine (is this pantothenic acid?), but in the absence of any specific information my take would be similar to what I posted a while ago about ezetimibe (and also similar to what I wrote about lowering homocysteine levels above). Knowing that something lowers cholesterol levels in and of itself isn't that convincing to me that it will show clinical benefit. It is really not at all clear that the benefit of statins doesn't have a lot to do with effects separate from lowering cholesterol levels. I believe we really need trials with clinical endpoints for any drug intended to treat hypercholesterolemia. SignatureDavid Rind drind@caregroup.harvard.edu > I didn't notice the post on pantethine (is this pantothenic acid?), > David Rind > drind@caregroup.harvard.edu Pantethine is the activated form of of vitamin B-5. Its properties maybe somewhat different form pantothenic acid. For example, a large dose of pantethine is said to lower cholesterol. I believe this has been shown in research. I never read this claim made for pantothenic acid that I can recall on the spur of this moment. > > I didn't notice the post on pantethine (is this pantothenic acid?), > [quoted text clipped - 7 lines] > pantothenic > acid that I can recall on the spur of this moment. John Here is what I saw on pantethine: http://tinyurl.com/6sr5h Zee > Here is what I saw on pantethine: > http://tinyurl.com/6sr5h > > Zee So, in a quick glance at those abstracts, despite all those studies, only one of the human studies had a control group, and no study looking at effects on cholesterol had a control group. Hard to know from that if pantethine has any effect greater than placebo. SignatureDavid Rind drind@caregroup.harvard.edu > > Here is what I saw on pantethine: > > http://tinyurl.com/6sr5h [quoted text clipped - 9 lines] > David Rind > drind@caregroup.harvard.edu I posted the abstracts, and as an n of one can tell you that my LDL dropped 70 points on 450mg twice per day when tested 3 mos. after commencing it. My HDL happened to hit a high of 70 at the same test, though it had gotten to 68 in the past, from a decade of 34, when I began low carbing, then my numbers began to worsen some. I am of the (admittedly lay)opinion that statin drugs do more harm than good, overall, and that they pose an unnecessary risk. Susan > > I was hoping you would comment. I am being told I *must* lower my > > homocysteine. It has not responded to folate. I am also told my [quoted text clipped - 13 lines] > over the Net -- it's just not similar to the information available when > seeing a patient. I know, for me specifically. But I meant, about substance generally, and if you had knowledge of it. > Second, my approach to high risk cardiac situations is the one you like > least. If I were really worried that someone's homocysteine level (plus > some number of other risk factors) placed them at too high a risk for > cardiovascular disease, my approach would be to have them take a statin. And I would be happy to take statins were I not still suffering from my previous statin use and quite certain I would kill myself by taking one again. Over and over I was talked into going on yet a different one, or back on a previous one, because I AM AFRAID. I hoped, like anyone else, they would help me. My physicians would love for me to take Crestor and would write the script immediately, not because there is any evidence of overall efficacy--in me--but because it lowers numbers. A physician friend (who does not treat me) referred to it as: "My profession is notoriously numerically fixated (it's easier to be quick and dirty - and linear - that way). Numerical endpoints and standards make us slaver like caged vampires." http://tinyurl.com/3ku3r > High homocysteine levels do seem to correlate some with cardiovascular > risk, but we really don't know that lowering those levels with folate > (or with folate plus other vitamins) really has any important impact on > that risk. I am well aware of that. And so are my physicians. I suspect they are grasping at straws with me and others like me. I know there are several on this newsgroup taking folate et al to lower homocysteine. I don't know of any evidence that anyone "must" lower their > homocysteine level, since we don't actually know that doing so has any > beneficial effect. In contrast, statins clearly lower cardiovascular risk. So you say. I think it is one of those u shaped curves, for many. Me. > I didn't notice the post on pantethine (is this pantothenic acid?), but > in the absence of any specific information my take would be similar to > what I posted a while ago about ezetimibe (and also similar to what I > wrote about lowering homocysteine levels above). Knowing that something > lowers cholesterol levels in and of itself isn't that convincing to me > that it will show clinical benefit. Right. It may lower cholesterol. And so? {shrug}. Merely wondered; had you used it...heard of it. It is really not at all clear that > the benefit of statins doesn't have a lot to do with effects separate > from lowering cholesterol levels. Aspirin. I believe we really need trials with > clinical endpoints for any drug intended to treat hypercholesterolemia. Zee > And I would be happy to take statins were I not still suffering from my > previous statin use and quite certain I would kill myself by taking one [quoted text clipped - 9 lines] > standards make us slaver like caged vampires." > http://tinyurl.com/3ku3r As mentioned in the past, I don't disagree with this. I think lots of people end up with their cholesterol numbers treated simply because we have drugs that affect the numbers. Have you or someone else calculated your ten year risk for a cardiac event? Is that number so high that a 30% reduction in relative risk (about what you might see with a statin) is worth lots of effort to try to achieve? SignatureDavid Rind drind@caregroup.harvard.edu > > And I would be happy to take statins were I not still suffering from my > > previous statin use and quite certain I would kill myself by taking one [quoted text clipped - 11 lines] > > As mentioned in the past, I don't disagree with this. I think lots of > people end up with their cholesterol numbers treated simply because we > have drugs that affect the numberou. > Have you or someone else calculated your ten year risk for a cardiac > event? Yes it is around 3 per cent, with a TC of 9.7 and HDL 68. Physicians I have encountered say such numbers should be treated. Many persons with similar numbers are told such numbers require treatment. We hear little about using ten-year risk or even ratios as the determining factor for medicating. The latest is: ldl below 100. No? Is that number so high that a 30% reduction in relative risk > (about what you might see with a statin) is worth lots of effort to try > to achieve? Definitely worth lots of effort; with diet, exercise, and what may help but not harm such as salmon oil and perhaps folate/Bs. I do know the jury isn't in yet on this. It certainly hasn't worked for me, so far, and there are other posters here who have not lowered homocysteine with folate/Bs. I am checking that suggestion from the stroke clinic, by the way. I want to know what the study is they reference and what they think about the study you mentioned. What was the name of it, where done, by whom? Zee > Yes it is around 3 per cent, with a TC of 9.7 and HDL 68. Physicians I > have encountered say such numbers should be treated. Many persons with > similar numbers are told such numbers require treatment. We hear little > about using ten-year risk or even ratios as the determining factor for > medicating. The latest is: ldl below 100. No? > I am checking that suggestion from the stroke clinic, by the way. I > want to know what the study is they reference and what they think about [quoted text clipped - 3 lines] > > Zee LDL below 100 is the goal in secondary prevention. It could conceivably be a primary prevention goal in someone at high risk. If someone really has a ten-year risk of 3 percent, about the best you could hope for with statins is to decrease that to 2 percent. I'm somewhat surprised that doctors would be pushing hard to get someone to take a statin to get an absolute 1 percent decrease in the ten-year risk of cardiac events. There's no reason to think that B-complex vitamins to reduce homocysteine levels accomplish even this much of a decrease in absolute risk. Study was: Lowering homocysteine in patients with ischemic stroke to prevent recurrent stroke, myocardial infarction, and death: the Vitamin Intervention for Stroke Prevention (VISP) randomized controlled trial. AU - Toole JF; Malinow MR; Chambless LE; Spence JD; Pettigrew LC; Howard VJ; Sides EG; Wang CH; Stampfer M SO - JAMA 2004 Feb 4;291(5):565-75. SignatureDavid Rind drind@caregroup.harvard.edu > > Yes it is around 3 per cent, with a TC of 9.7 and HDL 68. Physicians I > > have encountered say such numbers should be treated. Many persons with [quoted text clipped - 12 lines] > LDL below 100 is the goal in secondary prevention. It could conceivably > be a primary prevention goal in someone at high risk. Well who exactly isn't at high risk? Everyone it seems. The latest campaign admits there is no evidence for women, but prescribe them to her anyway. There seem to be few who do not qualify, somehow or other. People who have total cholesterol levels of 6, people who have diabetes, people who are over 60, people who had a parent with heart disease, people who simply believe to take them is to be prudent and...people who are continually inundated with such dreck as...how did it go... "The objective of our advertising is to break through barriers people have to taking action around their health and to encourage appropriate patients to speak to their doctors," said Dorothy Wetzel, Pfizer vice president for consumer marketing. If someone really > has a ten-year risk of 3 percent, about the best you could hope for with > statins is to decrease that to 2 percent. I'm somewhat surprised that > doctors would be pushing hard to get someone to take a statin to get an > absolute 1 percent decrease in the ten-year risk of cardiac events. That was on the NIH scale. The Harvard scale wouldn't let me in. Told me to enter a number under 300. <chortle> > There's no reason to think that B-complex vitamins to reduce > homocysteine levels accomplish even this much of a decrease in absolute > risk. It seemed like something I could do David. My endocrinologist's poor litte face just fell with disappointment when I told him I wasn't going to be taking Zetia. > Study was: Thank you. I will call tomorrow. Zee > Lowering homocysteine in patients with ischemic stroke to prevent > recurrent stroke, myocardial infarction, and death: the Vitamin > Intervention for Stroke Prevention (VISP) randomized controlled trial. > AU - Toole JF; Malinow MR; Chambless LE; Spence JD; Pettigrew LC; Howard > VJ; Sides EG; Wang CH; Stampfer M > SO - JAMA 2004 Feb 4;291(5):565-75. David Rind <drind@caregroup.harvard.edu> wrote in part: >> And I would be happy to take statins were I not still suffering from my >> previous statin use and quite certain I would kill myself by taking one [quoted text clipped - 18 lines] >(about what you might see with a statin) is worth lots of effort to try >to achieve? That's certainly the right way to think about it. I am also slightly hyperhomocystemic...around 12.9 or so. And it responds very little to B vitamins. It seems that Hcy is *associated* with a lot of bad stuff: atherosclerosis, stroke, cancer, Alzheimer's--the latest appears to be fractures... The usual view I hear is that folate and such will drop it, so it's a non problem. But that's apparently not true--at least in my case and Zee's case. And it's also not true that the data (taken as a whole) show that reducing Hcy with folate does any good. Since there are theoretical reasons why homocysteine might be causal in some of the bad stuff it's associated with, my personal view is that it might be wise to try to reduce it via means other than B-vitamins. One such approach might be to replace animal protein high in methionine with plant protein. I don't know that that will reduce my Hcy--or that doing so in that way would help--but I'm doing a bit of it anyway. There is very little good research on this issue. Back to the topic in the quoted post: I think there are some variables that serve to warn of cardiac events and strokes. In my opinion, LDL in isolation is a very weak predictor. Total non-HDL cholesterol divided by HDL may be the strongest based on the usual lipid measures. Apparently, predictability is improved if you know your LDL particle distrribution type, your Lp(a) level, your hsCRP, and maybe your Hcy... Then there's personal history, family history, gender, age, CT scans or IMT measures, etc. Doesn't it seem that doctors who are pushing statins on someone whose risk might be pretty darn low when all predictors are considered are doing a disservice to their patients? -- Jim Chinnis Warrenton, Virginia, USA :: I am also slightly hyperhomocystemic...around 12.9 or so. And it :: responds very little to B vitamins. [quoted text clipped - 14 lines] :: that will reduce my Hcy--or that doing so in that way would :: help--but I'm doing a bit of it anyway. Sounds a good idea. In addition to that in the VISP-study (Lowering Homocysteine in Patients With Ischemic Stroke to Prevent Recurrent Stroke, Myocardial Infarction, and Death. The Vitamin Intervention for Stroke Prevention (VISP) Randomized Controlled Trial) it was suggested very briefly that betaine might also help. SignatureJuhana > Back to the topic in the quoted post: I think there are some > variables that serve to warn of cardiac events and strokes. In my [quoted text clipped - 10 lines] > -- > Jim Chinnis Warrenton, Virginia, USA Jim Thank You! Saw my PCP today. She did not like my numbers but we spoke about quality of life. EG Dealing with side effects . My Total is 215 LDL is 160 HDL is 69 Ratio 3.9 BP 135/85 on a good day. I'm getting tired of drugs otherwise I can still kick lower extremities. Lipitor 40 and this after I said no to 80. Had a 4 bypass. 48 & 49 again? Bill SignatureZone 5 S Jersey USA Shade --> http://www.ocutech.com/ For vision problems http://www.truemajorityaction.org/site/pp.asp?c=jvLUJdP8H&b= 315914&msource=ustack > David Rind <drind@caregroup.harvard.edu> wrote in part: > [quoted text clipped - 58 lines] > -- > Jim Chinnis Warrenton, Virginia, USA Yes they are (unless they believe there might be perhaps other factors for which taking a statin may help overall cardiovascular health?). But I will say that I meet people every week who are *not* on a statin for that very reason - their numbers are within or below range. As a matter of fact, I personally have not met someone who said (something to the effect) "...my cholesterol is low, I'm in good health, I feel great and my doctor is forcing me to take a statin anyway." L. :: David Rind wrote: ::: Zee wrote: [quoted text clipped - 44 lines] :: :: Zee Here are some studies related to homocysteine lowering therapy that you might find interesting: O'Connor JJ, Meurer LN. Should patients with coronary disease and high homocysteine take folic acid? J Fam Pract. 2003 Jan;52(1):16-8. "All patients with known coronary artery disease should take prescription strength (1 mg/d) folic acid, vitamin B12 (400 microg/d), and vitamin B6 (10 mg/d), which have few if any known adverse effects. In this study, therapy to reduce homocysteine levels with prescription strength folic acid (1 mg) and vitamins B12 and B6 for 6 months following coronary angioplasty reduced the risk of need for revascularization of target lesions and of overall adverse cardiac events at least 6 months following cessation of therapy. Based on this study, it is unknown whether the benefit is related to baseline homocysteine levels or whether there is further benefit to continuing treatment beyond 6 months. Over-the-counter folic acid supplements (800 microg or less) were not studied and may not be as beneficial. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1 2540303&dopt=Abstract Schnyder G et al, Effect of homocysteine-lowering therapy with folic acid, vitamin B12, and vitamin B6 on clinical outcome after percutaneous coronary intervention: the Swiss Heart study: a randomized controlled trial. JAMA. 2002 Aug 28;288(8):973-9. "RESULTS: After a mean (SD) follow-up of 11 (3) months, the composite end point was significantly lower at 1 year in patients treated with homocysteine-lowering therapy (15.4% vs 22.8%; relative risk [RR], 0.68; 95% confidence interval [CI], 0.48-0.96; P =.03), primarily due to a reduced rate of target lesion revascularization (9.9% vs 16.0%; RR, 0.62; 95% CI, 0.40-0.97; P =.03). A nonsignificant trend was seen toward fewer deaths (1.5% vs 2.8%; RR, 0.54; 95% CI, 0.16-1.70; P =.27) and nonfatal myocardial infarctions (2.6% vs 4.3%; RR, 0.60; 95% CI, 0.24-1.51; P =.27) with homocysteine-lowering therapy. These findings remained unchanged after adjustment for potential confounders. CONCLUSION: Homocysteine-lowering therapy with folic acid, vitamin B12, and vitamin B6 significantly decreases the incidence of major adverse events after percutaneous coronary intervention." http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstra ct&list_uids=12190367 There is also some evidence that vitamin treatment is beneficial in the primary prevention: Vermeulen EGJ et al, Effect of homocysteine-lowering treatment with folic acid plus vitamin B6 on progression of subclinical atherosclerosis: a randomised, placebo-controlled trial. Lancet 2000; 355: 517-22. "INTERPRETATION: Homocysteine-lowering treatment with folic acid plus vitamin B6 in healthy siblings of patients with premature atherothrombotic disease is associated with a decreased occurrence of abnormal exercise electrocardiography tests, which is consistent with a decreased risk of atherosclerotic coronary events." http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstra ct&list_uids=10683000 In addition to vitamin B, *betaine* can also be used to lower homocysteine: Craig S, Betaine in human nutrition. American Journal of Clinical Nutrition, Vol. 80, No. 3, 539-549, September 2004 "Inadequate dietary intake of methyl groups leads to hypomethylation in many important pathways, including 1) disturbed hepatic protein (methionine) metabolism as determined by elevated plasma homocysteine concentrations [...]" http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstra ct&list_uids=15321791 Zeisel, SH et al, Concentrations of Choline-Containing Compounds and Betaine in Common Foods. J. Nutr. 133:1302-1307, May 2003 "Choline is important for normal membrane function, acetylcholine synthesis and methyl group metabolism; the choline requirement for humans is 550 mg/d for men (Adequate Intake). Betaine, a choline derivative, is important because of its role in the donation of methyl groups to homocysteine to form methionine. In tissues and foods, there are multiple choline compounds that contribute to total choline concentration (choline, glycerophosphocholine, phosphocholine, phosphatidylcholine and sphingomyelin). In this study, we collected representative food samples and analyzed the choline concentration of 145 common foods using liquid chromatography-mass spectrometry. Foods with the highest total choline concentration (mg/100 g) were: beef liver (418), chicken liver (290), eggs (251), wheat germ (152), bacon (125), dried soybeans (116) and pork (103). The foods with the highest betaine concentration (mg/100 g) were: wheat bran (1339), wheat germ (1241), spinach (645), pretzels (237), shrimp (218) and wheat bread (201). A number of epidemiologic studies have examined the relationship between dietary folic acid and cancer or heart disease. It may be helpful to also consider choline intake as a confounding factor because folate and choline methyl donation can be interchangeable." http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstra ct&list_uids=12730414 SignatureJuhana > :: David Rind wrote: > ::: Zee wrote: [quoted text clipped - 140 lines] > > http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstra ct&list_uids=12730414 Why did you post an abstract from the study showing that treatment reduces progression after PTCA, but not post the abstract from the study showing that it sped progression after coronary stenting? SignatureDavid Rind drind@caregroup.harvard.edu :: Juhana Harju wrote: ::::: David Rind wrote: [quoted text clipped - 55 lines] :: reduces progression after PTCA, but not post the abstract from the :: study showing that it sped progression after coronary stenting? Because for some reason you were referring only to the negative studies. To balance it I wanted to post some positive results to give a more complete picture of the results of homocysteine lowering vitamin therapy. I would say that for some reason supplementing with vitamin B:s might not be helpful in preventing strokes, but folic acid, B6 and B12 seem to offer some protection from other cardiovascular diseases and they also seem to reduce mortality a bit. SignatureJuhana > Because for some reason you were referring only to the negative studies. > To balance it I wanted to post some positive results to give a more [quoted text clipped - 5 lines] > offer some protection from other cardiovascular diseases and they also > seem to reduce mortality a bit. Well, you can say this if you like, but there is essentially no evidence from randomized, contolled trials to support that. There are no RCTs showing benefit in primary prevention, there are two negative RCTs in patients with CHD, a negative RCT in patients after stroke, an RCT in patients undergoing stenting that showed actual harm, and the single positive RCT in patients undergoing PTCA. So claiming that supplementation "seems to offer some protection from other cardiovascular disease" or that supplementation reduces mortality seems to me to be ignoring the evidence from randomized trials. Other than the trial in patients after PTCA, do you know of a single RCT of lowering homocysteine with vitamins that showed a benefit on an important clinical outcome? By the way, I have no problem with people taking a daily multivitamin with folate with the intent of lowering homocysteine levels. It's unlikely to be harmful and could conceivably turn out to be benefitical. But we don't have any decent data at this point to support such a strategy. SignatureDavid Rind drind@caregroup.harvard.edu Thanks Juhana. I began the folate therapy, rather tentatively, at one mg, then moved to five, and back down to three, after having read other posters here say they had lowered hcy with folate therapy. But it doesn't seem to work for me. I know I am not deficient in B12 (tested at almost twice normal before I began supplementing) nor do I have high CRP. And, I do not eat much meat. Still, at last bloodwork, while taking one mg folate, my hcy was 14. It had gone from 8 to 11 to 14 in just under one year. Zee :: Thanks Juhana. I began the folate therapy, rather tentatively, at one :: mg, then moved to five, and back down to three, after having read [quoted text clipped - 8 lines] :: :: Zee Here is some additional information about betaine and homocysteine. "An additional mechanism for reconverting homocysteine to methionine is provided by the enzyme betaine homocysteine methyltransferase (BHMT). Human BHMT is found almost exclusively in the liver and kidney. High intakes of betaine (6 grams or more daily) have been used successfully to treat genetic homocystinuria in humans, and betaine fed to rats given alcohol or carbon tetrachloride has been shown to boost hepatic SAM levels. However, there has been relatively little interest in medical applications of betaine, and, in particular, only a few investigators have examined its potential utility for decreasing modestly elevated homocysteine levels. For example, Dr. K. Franken and colleagues used betaine (6 grams daily) and vitamins in several patients with mild hyperhomocysteinemia who were not optimally responsive to vitamins alone. The specific response to betaine was not reported, though. Dr. N. Dudman and colleagues gave 840 mg of betaine, twice daily, to patients with CBS deficiency. They reported reductions of homocysteine in the blood of about 30%. Since there are two mechanisms for reconverting homocysteine to methionine, one would expect that stimulation of both of these mechanisms should produce the most profound reductions in homocysteine. Supplementation with vitamins B6, B12, and folic acid, as well as betaine, may, through their influence on homocysteine levels, help reduce the risk of heart disease and other vascular diseases." http://lpi.oregonstate.edu/f-w99/vascular.html SignatureJuhana > This was given to me by my physician because my homocysteine level is > not responding to 3 mg folate and one B50 complex. It came from the [quoted text clipped - 14 lines] > > Zee Is anyone using folate/Bs taking this much B12? Zee + > > This was given to me by my physician because my homocysteine level is > > not responding to 3 mg folate and one B50 complex. It came from the [quoted text clipped - 21 lines] > > Zee 1075 milligrams .... no way. That has to be a mistake. The subjects are taking one of those silly 75 mg/75mcg formulations plus a 1000 microgram B-12 supplement which is likely cyanocobalamin. Some days I take more B-12, some the same, and some days less. I take 5 to 6 milligrams of folic acid, often several grams of betaine, and 50 to ~80 mgs of B-6 per day. "John Que" <123456789travelguide@hotmail.com> wrote in news:4226afab$0 $26194$a32e20b9@news.nntpservers.com: > + >> [quoted text clipped - 32 lines] > grams of betaine, and 50 to ~80 mgs of > B-6 per day. Probably should be "mcg", not "mg". I take 3.2mg of Folic, 100mg of B6 and 500mcg of B12, powdered capsule form about 20 minutes before breakfast. That regime cut my homocysteine level from 22 to 9. L. >This was given to me by my physician because my homocysteine level is >not responding to 3 mg folate and one B50 complex. It came from the [quoted text clipped - 14 lines] > >Zee Zee, so far the trials on lowering homocysteine with diet and impacting risk of cardiovascular events is negative. Although people with higher homocysteine levels are at increased risk, the vitamins don't seem to translate into clinical benefit (in this particular area). H2 |
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