February, 2000 - (Jon's note: Normal homocysteine levels for adults are currently considered to be about 10 µmol/L) With improved tests to measure homocysteine levels in the 1960s, it was noted that increased levels were associated with coronary artery disease. Recent research has shown that high homocysteine increases the risk for heart disease. Deficiencies of vitamin B6 (pyridoxine), vitamin B12, or folate affect 25-30% of the adult population (Selhub et al, 1993). Elevated homocysteine levels (greater than 14 micromoles/L) often accompany these deficiencies.
Homocysteine levels are usually higher in the elderly, and higher in men than in women. It is now believed that most people get too few vitamins, and that this may be the explanation for high homocysteine levels in the general population. In other words, high homocysteine levels indicate low vitamin intake so in a roundabout way, getting enough vitamins reduces your risk of heart disease. Vitamins B1, B2, B6, B12, folate, niacin, retinol, vitamin C, and vitamin E have all been studied, but the greatest interest is in B6, B12 and folate since they are linked to the way homocysteine is broken down in the body.
Naturally occurring sources of folate in the diet include orange juice and green, leafy vegetables. In 1996, the FDA required American flour and cereal products to be fortified with folate. Cold breakfast cereals are now fortified with folate and have become an important dietary source of it for Americans. About 25% of the adult US population takes vitamin supplements that contain folate. These persons tend to have lower homocysteine levels.
Evidence for the idea that high homocysteine means high risk of heart disease has mainly come from observational studies, but high homocysteine levels (greater than 12 µmol/L) have been seen in those with carotid artery blockages, stroke, and peripheral vascular disease. (Jon's note: Observational evidence is not like clinical trials. Like meta-analysis, it is much less certain because the study was not designed to study this specific effect)
A meta-analysis of previous studies reached the conclusion that a 5-µmol/L rise in homocysteine level was associated with a 1.6-fold risk for coronary artery disease in men and a 1.8-fold risk in women. It should be noted that people with severe kidney disease have very high homocytseine levels (20-30 µmol/L) and folate/vitamin supplements do not lower levels in these patients.
Source: NHLBI's Framingham Heart Study, supported by NIH/NHLBI contract N01-HC-38038
Title: Homocysteine, Vitamins, and Cardiovascular Disease
Author: Peter W.F. Wilson
December, 1999 - Studies have reported high blood levels of homocysteine as a risk factor for coronary artery disease (atherosclerosis). One study - The Cholesterol Lowering Atherosclerosis Study - reported a homocysteine increase in people taking colestipol and niacin. We studied whether niacin treatment raised blood homocysteine levels.
The ADMIT trial (Arterial Disease Multiple Intervention Trial) was a randomized, placebo-controlled trial. It studied the effect of niacin compared with placebo on homocysteine in 52 people with peripheral artery disease. Niacin dose was raised from 100mg to 1000mg daily. After 18 weeks, there was a 55% (absolute, not relative) increase in average blood homocysteine levels in the niacin group and a 7% decrease in the placebo group. This difference remained significant at the end of follow-up at 48 weeks.
We conclude that niacin can raise blood homocysteine levels, which might reduce the expected benefits of niacin, which is taken to reduce cholesterol. However, blood homocysteine levels can be lowered by folic acid supplements. Further studies are needed to know if those taking niacin should also take extra B vitamins.
Title: Niacin Treatment Increases Plasma Homocyst(e)ine Levels
Authors: Rekha Garg, M. Rene Malinow, Mary Pettinger, Barbara Upson, Donald Hunninghake on behalf of the ADMIT Investigators
Source: Am Heart J 138(6):1082-1087, 1999
April, 2002 - Very low dose niacin, taken along with a statin drug (cholesterol-lowering drug like Zocor), raises good cholesterol or HDL, while avoiding niacin's usual side effects. Dr. Jennifer Wink studied 39 patients who had been on stable statin therapy for 3 months. These people took either 50mg niacin twice a day or placebo, for 3 months.
Patients completed questionnaires on current medical problems, meds, and life style before and after niacin therapy. Primary end points were change in HDL cholesterol and patient-reported side effects. Average HDL increased by 2.1 mg/dL in the niacin group; it fell by 0.56 mg/dL in the placebo group.
There were no significant changes in total cholesterol, LDL, or triglycerides in either group. No major side effects were noted and no patients discontinued the niacin due to side effects.
Source: Am Heart J 2002;143:514-518
1996 - People who take vitamin C after angioplasty may be at lower risk for restenosis (having their arteries get plugged up again), according to this study of 119 heart disease patients who had angioplasty. Those who took 500mg of vitamin C per day for 4 months after surgery had a restenosis rate of 24%, compared with a rate of 43% among people who did not take vitamin C after their angioplasty. Twelve percent of patients who took vitamin C needed repeat surgery or stents, compared with 29% of patients not taking vitamin C.
Vitamin C is an antioxidant and may slow reclogging by preventing LDL cholesterol from building up in the blood. "The whole issue with angioplasty is stenosis. Given the increasing use of angioplasty and stents, it would be great if something as simple as vitamin C could prevent this," said Thomas Graboys MD, associate professor of medicine at Harvard Medical School.
Vitamin C and other antioxidants seem to give health benefits without serious side effects, Dr. Graboys added. "They can't hurt you and may help, which is why antioxidants may be an important approach in treating people with heart disease."
Title: Vitamin C Reportedly Prevents Restenosis After Angioplasty
Author: Haruo Tomoda
Journal of the American College of Cardiology(1996;78: 1284-1286)
March 3, 2000 - Vitamin C pills may speed up hardening of the arteries, researchers suggest in a new study that they called a disturbing surprise. The researchers cautioned that trials are needed to know for sure whether megadoses of vitamin C are actually harmful.
Many people load up on vitamin C assuming that it is good for them, even though there is little scientific evidence this is true. In theory, vitamin C and might protect the circulatory system by suppressing the damaging effects of oxygen. "When you extract one component of food and give it at very high levels, you just don't know what you are doing to your system," said Dr. James Dwyer, who directed the study. He presented the findings at an American Heart Association meeting.
Clogged arteries - called atherosclerosis - are the major underlying cause of heart attacks. In this study, doctors looked for early signs of this process by doing ultrasound scans on volunteers' carotid arteries, once at the study's start and again 18 months later.
Dwyer studied 573 outwardly healthy middle-aged men and women who work for an electric utility in Los Angeles. About 30% of them regularly took various vitamins. The study found no clear-cut sign that getting lots of vitamin C from food or a daily multivitamin does any harm. However, those taking additional vitamin C pills had faster thickening of the walls of the big arteries in their necks. In fact, the more vitamin C they took, the faster the buildup.
People taking 500 milligrams of vitamin C daily for at least a year had a thickening rate twice as high as those who avoided supplements. Among smokers, the rate was 5 times higher.
Dr. Shiriki Kumanyika said the research shows the uncertainties of picking out a single vitamin among the huge number of nutrients in a healthy diet. "It's a challenge to sort out what it is in what people eat that makes them live longer," she said. "We have to be careful about recommending foods or nutrients, because if we are wrong, we can do harm."
Source: The Associated Press
September 1996 - A popular theory is that antioxidant vitamins reduce risk of heart disease. One of the regular findings in dietary research is that those who consume higher amounts of fruits and vegetables have lower rates of heart disease and stroke. Recent attention is on the antioxidant content of fruits and vegetables as a possible reason for this protection. Results from several large trials are now available but results are not consistent.
Major trials do not prove or disprove the value of antioxidant vitamins. They suggest that some of the benefits may have been overstated and that there may be some adverse effects. Currently, trial results are not enough to know for sure the risks and benefits of antioxidant supplements. More reliable data should be coming soon, which will better define the role of antioxidants in the prevention of coronary artery disease.
Title: Antioxidants in cardiovascular disease: randomized trials
Author: Gaziano JM.
Source: Nutrition 12 (9): 583-588
ID numbers: PMID: 8878166, MUID: 97032270
December, 1996 - Laboratory studies suggest that antioxidants such as Vitamin C help prevent atherosclerosis (clogged arteries). Most reviews have considered all antioxidants grouped together. This one studies the literature about Vitamin C alone. We used a Medline search for articles from the past 30 years and an EMBASE search for articles published from 1980 to 1996, searching books, reviews and citations in all located articles.
Coronary heart disease 4 of 7 ecological studies, 1 of 4 case-control studies and 3 of 12 cohort studies found significant protection with vitamin C use.
Strokes 2 of 2 ecological studies, zero of 1 case-control study and 2 of 7 cohort studies found significant protection with vitamin C use.
Circulatory disease 2 of 3 cohort studies reported significant protection with vitamin C use.
The evidence, although limited, shows vitamin C having protective effect against stroke, but evidence that vitamin C is protective against coronary heart disease not so strong.
Title: Vitamin C and cardiovascular disease: a systematic review
Authors: Ness AR, Powles JW, Khaw KT
Source: J Cardiovasc Risk 3 (6): 513-521 (Dec 1996)
ID numbers: PMID: 9100087, MUID: 7254677
July 1, 1999 - Taking vitamin C for a long period of time reverses endothelial dysfunction in patients with CAD (coronary artery disease). Endothelium is the layer of cells that line the inside of blood vessels. So say researchers in the June 29th issue of Circulation: Journal of the American Heart Association.
Dr. Joseph Vita randomized 46 patients with CAD to either a single oral dose of 2 grams of vitamin C or placebo. The vitamin C improved dilation of the an artery in the forearm, as measured by ultrasound 2 hours later. The researchers say the effect was sustained among patients who took 500mg of vitamin C daily for 30 days. Dilation did not change in placebo-treated patients.
"In a study about 4 years ago, we showed that if you take a single dose of vitamin C, you see a benefit," said Dr. Vita. "In this follow-up study, we show that if you take vitamin C every day for a month, that benefit is sustained." There was no change in blood pressure or cholesterol levels. The investigators conclude that "long-term ascorbic acid treatment has a sustained benefit on endothelium-derived nitric oxide action."
"Because endothelial dysfunction may add to the development of heart disease, this study indicates that vitamin C treatment might benefit patients with CAD," Dr. Vita concludes.
Source: Circulation 1999;99:3234-3240
March 2, 2001 - A study just published shows that a small increase in vitamin C intake may reduce all-cause mortality. Dr. Kay-Tee Khaw collected data on 19,496 men and women 45 to 79 years of age who were in the EPIC study (European Prospective Investigation into Cancer and Nutrition).
Participants were divided into sex-specific groups based on their blood levels of vitamin C. Across the groups, blood levels of ascorbic acid (vitamin C) for men ranged from a low of 20.9 micromol/L to a high of 73.3 micromol/L. For women the range was 29.2 micromol/L to 86 micromol/L.
They were followed for about 4 years and causes of death were recorded. For both men and women with the highest vitamin C blood levels, risk of mortality from all causes was about 50% less than in those with the lowest vitamin C blood levels.
Overall, a 20% reduction in all-cause mortality risk was seen with an blood level increase in vitamin C of 20 micromol/L. Such an increase could be gotten from an increase of only 50 grams in daily fruit and vegetables. "Our findings suggest that an increase in vitamin C rich foods might have benefits for heart disease and all-cause mortality. This supports the health benefits of eating fruits and vegetables. Small diet improvements could have a large effect," Dr. Khaw said.
Source: Lancet 2001;357:657-663
October 30, 2001 - In CHF patients, vitamin C can suppress the signal that causes cell death in the lining of blood vessels. The lining inside blood vessels is called the endothelium. In heart failure patients, the cells making up the endothelium don't do their job, which can reduce blood supply to their organs. This increases fatigue and shortness of breath. It could be that these endothelial cells are dying too quickly from apoptosis.
Study co-author Dr. Stefanie Dimmeler says, "Evidence suggests that oxidative stress regulates programmed death of endothethial cells. We wondered whether vitamin C could reduce endothelial cell death in CHF patients." (Oxidative stress damages tissue through a chemical reaction)
This randomized, placebo-controlled, double-blind trial of 34 CHF patients studied the effects of vitamin C on cell death. Researchers drew blood samples, then gave a 10-minute infusion of 2.5 grams of vitamin C or placebo. They took another blood sample 15 minutes later. For the next 3 days, patients took vitamin C pills or placebo tablets twice a day. A third blood sample was taken the morning of the fifth day.
Vitamin C reduced blood levels of microparticles (linked to cell death) to just 32% of levels at the study's start. Placebo had no effect. "This study shows that antioxidants inhibit apoptosis of endothelial cells in patients with CHF," Dimmeler says. It's too early to draw conclusions about using vitamin C in CHF patients because of the small number of patients studied, Dimmeler says.
Title: Vitamin C Inhibits Endothelial Cell Apoptosis in Congestive Heart Failure
Authors: Lothar Rossig, Jorg Hoffmann, Benedicte Hugel, Ziad Mallat, Astrid Haase; Jean-Marie Freyssinet, Alain Tedgui, Alexandra Aicher, Andreas Zeiher, Stefanie Dimmeler
Source: Circulation 2001 104: 2182 - 2187
October, 2002 - Okay, try to follow this line of thought:
Add it up and it suggests that nitric oxide is inhibited by oxygen free radicals. Vitamin C is an antioxidant, meaning it fights oxidative stress.This trial studied whether vitamin C improves endothelial function in DCM patients.
In 11 patients, the response of a coronary artery to IV acetylcholine was measured before and after giving 3 grams of IV vitamin C. The response to this should show how well the endothelium works. Artery diameter and average blood flow velocity was measured by catheter.
Dose-dependent acetylcholine reduced artery diameter by 5 to 7%. With vitamin C, however, artery diameter increased from 11% to 15%, peak blood flow velocity increased from 20% to 41%, and blood flow to the heart increased from 38% to 82%. This suggests that vitamin C reverses some endothelium dysfunction in DCM patients.
Title: Reversibility of coronary endothelial vasomotor dysfunction in idiopathic dilated cardiomyopathy: acute effects of vitamin C.
Authors: Richartz BM, Werner GS, Ferrari M, Figulla HR.
Source: Am J Cardiol 2001;88:1001-1005.
June 13, 2003 - In CHFers, high doses of vitamin C can improve what is called "baroreflex sensitivity." That is part of the body's system for controling blood pressure. Receptors in blood vessel walls are connected to the heart by nerves, which carry a message to pump faster or slower in response to blood pressure changes.
As the heart pumps more blood and blood pressure rises, blood vessels expand. That stretches these receptors in blood vessel walls. In response to the stretching, the receptors send a signal to the heart to slow its pumping.
Dr. Gianfranco Piccirillo says that high-dose vitamin C protects against endothelial damage related to chronic heart failure. The endothelium is a layer of cells that lines all blood vessels - it is critical to heart health. The doctor also said that this kind of endothelial damage raises the risk of sudden death related to low baroreflex sensitivity.
In 33 CHFers with EFs under 36% and in 11 healthy controls, the researchers measured baroreflex sensitivity before and after IV doses of placebo and 2.5 mg of vitamin C. In the CHFers, baroreflex sensitivity was much higher after vitamin C than after placebo. In the control group, baroreflex sensitivity did not change.
The researchers point out that if their finding is confirmed in long-term studies, it could help CHFers' bodys fight the onset of dangerous arrhythmias.
Source: Hypertension 2003;41:1240-1245.
I interview some of the best vitamin doctors in the world, read medical journals and nutrition books, and have even written a couple. My diet is generally good, with emphasis on wholesome foods. Until a year ago, I took 1600 IU of vitamin E, 100,000 IU of mixed beta- and alpha-carotene, and about 15 grams of vitamin C every day. These are high doses, I should know what I'm doing, right?
I guess not. With all the attention given to antioxidants, a lot of questions remain unanswered. How much is enough? How much is too much? Are free radicals really all that bad? I began asking these questions because the vitamins I took should have left me feeling energized but over the past 10 years, I've felt far more tired than I should - tired in the morning, tired in the afternoon, tired in the evening.
It wasn't easy finding answers. I finally tracked down the guy who would know: Denham Harman, MD, PhD. He's the fellow who invented the free radical theory of aging back in November of 1954. To my surprise, I discovered that I was doing too good a job crushing those dangerous free radicals we all hear about. I was taking too many antioxidants. With all the talk about the benefits of antioxidants, we forget that free radicals are there for a reason. Free radicals are essential for health. They are molecules with unpaired electrons aggressively looking for a mate. Oxygen free radicals are particularly dangerous because they react easily with other molecules. When they find a mate (just about anything will do <g>) they can oxidize cell membranes and cholesterol, and disrupt DNA in ways that speed aging and may lead to illness.
Cigarette smoke, air pollution, sunlight, radiation, pesticides and some drugs produce free radicals; So do polyunsaturated fats. Even over-exercising generates extra free radicals. The biggest source of free radicals is our own bodies. White blood cells use free radicals to destroy bacteria and virus infected cells. Free radicals help the liver detoxify harmful chemicals. They are also a normal by-product of breathing, in which our bodies use oxygen and generate energy. The process of creating energy is like the childhood game "hot potato." Molecules get passed around, as the cells try to keep the good ones and get rid of the bad ones.
The sheer scale of this activity is mind blowing. Each cell in our body suffers 10,000 free radical "hits" every day. The body's own antioxidants form the foundation of our excellent defense against free radicals, but it isn't perfect. That's why free radical damage - called oxidation - accumulates. It turns good cholesterol bad, causes cataracts, contributes to Alzheimer's disease and leads to cancer. Free radicals also age us, gracefully or not.
The relationship between free radicals and antioxidants is one of balance. I asked Harman which supplements he took. Unlike a lot of doctors who don't want to go on record with this information, he was very up front: 400 IU vitamin E, 2000mg vitamin C, 100 micrograms selenium and 30mg CoQ10 each day and 25,000 IU of beta-carotene every other day. "I'd take more," he said, "but I can't afford to get tired." My ears perked up. He explained that too many antioxidants cause fatigue and muscle weakness. Several years ago, in an experiment, he found that large amounts of BHT, a man-made antioxidant, interfered with the ability of mice to produce energy.
"Too many antioxidants can leave you feeling very weak," Harman said. "BHT decreases ATP and mitochondria function." ATP, or adenosinetriphosphate, is required for energy production in the mitochondria, which is the part of the cell biologists call the energy factory. I asked Harman whether too many natural antioxidants could cause fatigue. I was thinking about the 1600 IU of vitamin E and 100,000 IU of beta-carotene I had been taking for at least 10 years. Harman was positive, "Yes!" There's a point where the stuff turns on you. After hearing what Harman told me, I decided to reduce my vitamin E from 1600 IU to 800 IU daily and my mix of beta- and alpha-carotene to 50,000 IU. Within a day or two, my energy levels were up - way up.
Should you take antioxidants? Yes! How much vitamin E and other antioxidants should you take? There's no simple answer. Last year, the Alliance for Aging Research recommended that healthy people take antioxidant supplements in the following daily ranges:
Do you live in a large, polluted city? Do you smoke or live with a smoker? Do you live at a high altitude or spend a lot of time in the sun? Do you eat refined foods with polunsaturated fats? The more of these questions you answer "yes," your antioxidant intake should probably be higher. Of course, you have to listen to your body and decide what dose actually makes you feel better. Take more if it makes you feel better or if your doctor suggests that you do so. However, if you're really careful about your diet, you may not need a lot of extra antioxidants. Striking a balance between free radicals and antioxidants has benefited my health. It's an important lesson and I'll remember it.
Title: Some Good Things to Say About Free Radicals
Author: Jack Challem
Reproduced from The Nutrition Reporter® newsletter
June 29, 1999 - The jury is still out on the benefits of vitamin E to prevent or treat CAD (coronary artery disease), according to a comprehensive review published in the June 28th Archives of Internal Medicine. "Despite some data supporting the use of vitamin E, findings of controlled trials are limited and inconclusive," Dr. Anne Spencer says in the report. While studies "suggest" that supplemental vitamin E may ward off CAD, several questions have yet to be answered, such as the best dose, how long to take it, and method of consumption.
In the absence of conclusive data, supplemental vitamin E "may be considered" in CAD patients or those at high risk of developing CAD, "but potential benefits should be weighed against possible unknown long-term adverse effects." Editorialist Dr. Gordon Ewy says there are 3 reasons why it might be wise right now to hold off on prescribing vitamin E and other antioxidants.
"It is proven that lowering LDL cholesterol with a statin drug like Zocor decreases CAD and complications," Dr. Ewy concludes. "Antioxidant therapy is far from proven, yet many people take antioxidants, thinking they are protecting themselves from atherosclerosis."
Source: Arch Intern Med 1999;159:1279-1280,1313-1320
December, 1999 - The HOPE trial was a randomized trial of the ACE inhibitor ramipril and vitamin E versus placebo in high-risk heart patients. The primary end point of the study was a combination of heart attack, stroke, or death from cardiovascular causes. Patients with CHF or low EF and patients already on ACE inhibitor or vitamin E were not allowed in the study.
A total of 9297 patients were randomly assigned to take ramipril (10mg per day) or placebo for 5 years. All patients were also randomly assigned to take vitamin E (400 IU a day) or placebo. The study participants stacked up like this:
|Average age||66 years|
|Had coronary artery disease||81%|
|Had a previous heart attack||53%|
|Had peripheral vascular disease||43%|
|Had high blood pressure||47%|
|Had high cholesterol levels||66%|
|Took blood thinners, such as aspirin||76%|
|Took cholesterol-lowering drugs||29%|
The data safety monitoring board stopped the trial early in March of 1999, due to an overwhelming benefit of ramipril.
Vitamin E vs Placebo There were no significant differences in the primary outcome of death, heart attack and stroke (16% in vitamin E group vs 16% in placebo). All-cause mortality was not different between the 2 groups.
Ramipril vs Placebo In the ramipril group, there was a significant reduction in the primary end point from 18% in placebo to 14% in the treatment group. There was also a significant reduction in heart attack, stroke and cardiovascular death. All-cause mortality was reduced by 16% in the ramipril group
Survival curves separated at the 200 day mark and continued to diverge. Ramipril reduced the onset of new congestive heart failure (12% in placebo vs 9% in ramipril - a 23% relative reduction), and reduced need for revascularization procedures like angioplasty by 16%. The benefits of ramipril were seen in all subgroups - patients with or without coronary artery disease, diabetics and nondiabetics, young and old patients, hypertensives and nonhypertensives. Kidney outcomes were also reduced. There was a 25% relative reduction in development of kidney disease from 4% to 3%, and a 10% reduction in development of new microalbuminuria (a sign of kidney failure/disease). Interestingly, the development of diabetes appears to have been reduced by 32% in patients taking ramipril. Ramipril reduced stroke risk by 31% and heart attack risk by 20%.
This provides overwhelming evidence that in high-risk patients, ramipril prevents cardiovascular death, stroke, heart attack, heart failure, and need for revascularization, as well as development of diabetes. The benefits of ramipril are independent of its blood pressure lowering effect. Vitamin E does not have any significant protective effect. The only adverse effect to ramipril was a 5% incidence of cough.
Title: HOPE (Heart Outcomes Prevention Evaluation) Trial
Presented by: Salim Yusuf MD, and Peter Sleight MD
February 7, 2001 - Vitamin E supplements don't seem to improve symptoms of patients with heart failure, scientists reported recently. Their findings add to the long debate over whether antioxidants slow heart disease.
To test whether CHF patients could benefit from vitamin E, researchers gave 56 patients either 500 IU of vitamin E daily or placebo. After 12 weeks, those who took vitamin E had higher levels of the antioxidant in their blood, suggesting that the vitamin had been absorbed. However, their heart function did not improve and their quality of life was no better than that of patients taking placebo.
"It is obvious that any effect of vitamin E on the heart is minor," said Dr. Khursheed Jeejeebhoy, one of the investigators. "Unfortunately, we found that large doses of vitamin E alone will not reduce high oxidative activity in patients with heart failure."
Source: Am J Clin Nutr 2001;73:219-224
March 5, 2001 - High doses of vitamin E may help prevent heart attack and stroke by preventing atherosclerosis from getting worse. Atherosclerosis is the buildup of deposits in the arteries, eventually blocking them. The effect is limited to doses of 300 to 1000mg per day, according to Dr. James Dwyer.
At annual checkups, Dr. Dwyer used ultrasound to measure artery wall thickness in the carotid arteries of 573 men and women who work at the same California company. All of them were free of heart disease when the study began in 1994. The benefit of vitamin E was seen using supplements. Dr. Dwyer said, "We found no effect for dietary vitamin E."
Another antioxidant - vitamin C - showed no benefit. In fact, vitamin C seemed to encourage atherosclerosis to get worse. Dr. Dwyer first reported this negative finding for vitamin C last year, based on 2 years of ultrasound data. "The negative trend for vitamin C continues in the third year," he said.
March 16, 2005 - We studied whether long-term vitamin E use lowered risk of cancer, cancer death, and major heart events. The randomized, double-blind, placebo-controlled HOPE trial was continued to create the HOPE-TOO trial. Patients were at least 55 years old with artery disease or diabetes. HOPE-TOO ran from April of 1999 to May of 2003. Of the HOPE trial's 9500 patients, 3994 agreed to continue with HOPE-TOO. They kept taking the study med or placebo, and 738 more agreed to follow-up but did not keep taking the study med. Average follow-up was a total of 7 years.
Both HOPE and HOPE-TOO gave patients either 400 IU of natural source vitamin E or placebo. HOPE-TOO's primary endpoints were cancer, cancer deaths, and major heart events (heart attack, stroke, and heart-related death). Secondary endpoints included heart failure, unstable angina, and need for angioplasty or bypass procedures.
Heart events, cancer, and cancer deaths were about the same in both groups. However, vitamin E patients had higher risk of heart failure and hospitalization for heart failure. In patients with vascular disease or diabetes, long-term vitamin E use does not prevent cancer or major heart events but may increase risk for heart failure.
Title: Effects of Long-term Vitamin E Supplementation on Cardiovascular Events and Cancer A Randomized Controlled Trial
Authors: The HOPE and HOPE-TOO Trial Invesigators.
Source: JAMA. 2005;293:1388-1347.
September 12, 2002 - For the first 2 to 3 days after a major upper body surgery, most patients have episodes of breathing trouble and low oxygen levels. This increases heart rate and blood pressure, which can eventually damage the heart muscle. Then, a patient who seems fine can suddenly have a heart attack.
Such breathing problems are a side effect of the sedatives and painkillers recovering patients take. It seems that taking vitamins C and E prevents many of these problems.
Thirty-four healthy men were in this trial. One group took sedatives and vitamins C and E. Another group took sedatives but no vitamins. Both groups then got less oxygen than normal for a period of 3 minutes. The vitamin group had better breathing than the other group.
Future trials will see if both vitamins are necessary and will test a variety of sedatives and painkillers.
Source: Netherlands Organization for Scientific Research
January, 2003 - Researchers compared vitamin D levels in 54 CHFers and 34 healthy control participants. The CHF group included 20 patients under 50 years of age and 34 patients older than 50. A peptide in the chain that produces ANP was used to measure how severe each person's CHF was.
Regardless of age, CHFers had higher ANP levels than controls. CHFers also had lower vitamin D levels than controls. The lower the vitamin D levels in CHFers, the higher their ANP levels (the worse their CHF).
"This study provides evidence for a link between low vitamin D and severe CHF," the authors say.
Source: J Am Coll Cardiol 2003;41:105-112
All information on this site is opinion only. All concepts, explanations, trials, and studies have been re-written in plain English and may contain errors. I am not a doctor. Use the reference information at the end of each article to search MedLine for more complete and accurate information. All original copyrights apply. No information on this page should be used by any person to affect their medical, legal, educational, social, or psychological treatment in any way. I am not a doctor. This web site and all its pages, graphics, and content copyright © 1997, 1998, 1999, 2000, 2001, 2002, 2003, 2004, 2005, 2006 Jon C.