Tuesday, June 30, 2015
Five modifiable risk factors continue to account for half of cardiovascular deaths in U.S.
Despite decades of progress in reducing cardiovascular mortality, preventable risk factors continue to account for half of heart disease deaths. The findings from national survey data are published in Annals of Internal Medicine.
Cardiovascular disease remains a leading cause of death nationally. The top five leading preventable risk factors for heart disease are elevated cholesterol, diabetes, hypertension, obesity, and smoking. Researchers studied data from Behavioral Risk Factor Surveillance System (BRFSS) national surveys from 2009 to 2010 to determine the extent to which national cardiovascular mortality could be expected to decrease if all states were successful at reducing those modifiable risk factor levels to specified target levels. The author report the fraction of cardiovascular deaths that could have been prevented in 2009 to 2010 under two scenarios: complete elimination of risk factors, and reduction of risk factors to the best achieved levels in U.S. states in 2009-2010 (a more realistic goal).
The data showed that about half of deaths could be prevented if the modifiable risk factors were completely eliminated. Fewer than 10 percent of cardiovascular deaths could be prevented if all states were to achieve risk factor levels observed in the best-performing states. The authors conclude that all states could benefit from more aggressive policies and programs to help reduce risk of death from heart disease.
Consumption of sugary drinks may lead to an estimated 184,000 adult deaths each year worldwide, according to research published today in the journal Circulation and previously presented as an abstract at the American Heart Association Council on Epidemiology and Prevention in 2013.
"Many countries in the world have a significant number of deaths occurring from a single dietary factor, sugar-sweetened beverages. It should be a global priority to substantially reduce or eliminate sugar-sweetened beverages from the diet," said Dariush Mozaffarian, M.D., Dr.P.H., senior author of the study and dean of the Friedman School of Nutrition Science & Policy at Tufts University in Boston.
In the first detailed global report on the impact of sugar-sweetened beverages, researchers estimated deaths and disabilities from diabetes, heart disease, and cancers in 2010. In this analysis, sugar sweetened beverages were defined as any sugar-sweetened sodas, fruit drinks, sports/energy drinks, sweetened iced teas, or homemade sugary drinks such as frescas, that contained at least 50 kcal per 8oz serving. 100 percent fruit juice was excluded.
Estimates of consumption were made from 62 dietary surveys including 611,971 individuals conducted between 1980 and 2010 across 51 countries, along with data on national availability of sugar in 187 countries and other information. This allowed capture of geographical, gender and age variation in consumption levels of sugar-sweetened beverages in different populations. Based on meta-analyses of other published evidence on health harms of sugar-sweetened beverages, the investigators calculated the direct impact on diabetes and the obesity-related effects on cardiovascular disease, diabetes and cancer.
In 2010, the researchers estimate that sugar-sweetened beverages consumption may have been responsible for approximately:
- 133,000 deaths from diabetes
- 45,000 deaths from cardiovascular disease
- 6,450 deaths from cancer
The impact of sugar-sweetened beverages varied greatly between populations. At the extremes, the estimated percentage of deaths was less than 1 percent in Japanese over 65 years old, but 30 percent in Mexican adults younger than 45.
Of the 20 most populous countries, Mexico had the highest death rate attributable to sugar-sweetened beverages with an estimated 405 deaths per million adults (24,000 total deaths) and the U.S. ranked second with an estimated 125 deaths per million adults (25,000 total deaths).
About 76 percent of the estimated sugar-sweetened beverage-related deaths occurred in low- or middle-income countries.
In nations of the Caribbean and Latin America, such as Mexico, homemade sugary drinks (e.g. frescas) are popular and consumed in addition to commercially prepared sugar-sweetened beverages. "Among the 20 countries with the highest estimated sugar-sweetened beverage-related deaths, at least 8 were in Latin America and the Caribbean, reflecting the high intakes in that region of the world," said Gitanjali Singh, Ph.D., lead author of the study and a research assistant professor at the Friedman School.
Overall, in younger adults, the percent of chronic disease attributed to sugar-sweetened beverages was higher than the percent in older adults.
"The health impact of sugar-sweetened beverage intake on the young is important because younger adults form a large sector of the workforce in many countries, so the economic impact of sugar-sweetened beverage-related deaths and disability in this age group can be significant. It also raises concerns about the future. If these young people continue to consume high levels as they age, the effects of high consumption will be compounded by the effects of aging, leading to even higher death and disability rates from heart disease and diabetes than we are seeing now," Singh said.
A new study (1) reveals that drinking low-calorie cranberry juice cocktail may help lower the risk of chronic diseases that rank among the leading causes of death worldwide, including heart disease, diabetes and stroke. The finding is welcome news considering the World Health Organization estimates the trio of diseases annually claim 15.6 million lives around the globe (2). These illnesses are among the most common and costly health conditions, but fortunately, they are also among the most preventable through dietary intervention. That's where this research comes in. It shows that cranberries provide a rich source of protective compounds - called polyphenols - that support our body's natural defenses and help us achieve a balanced lifestyle to improve health.
Sipping Your Way to Better Health
To discover the extent to which polyphenol-rich cranberries can bolster whole-body health, researchers from the United States Department of Agriculture (USDA) provided eight weeks' worth of meals to 56 healthy adult volunteers (average 50 years of age). One group drank a glass (8 oz) of low-calorie cranberry juice twice daily (16 oz total). Meanwhile, the other group drank a placebo beverage with a similar color and flavor.
"At the start and end of the experiment, the researchers measured things like blood pressure, blood sugar levels, blood lipids, as well as C-reactive protein, a marker of inflammation," explained Christina Khoo, PhD, Director of Research Sciences at Ocean Spray. "All of these measurements come together to tell a story. The worse off these numbers are in an individual, the more likely he or she will face a health condition like diabetes, heart disease or stroke in the future."
Individuals drinking two glasses of low-calorie cranberry juice a day improved across all these measures. It's a change that adds up, and could be associated with a 10 percent lower risk of heart disease and a 15 percent lower risk of stroke (3). Of note, the reductions in blood pressure numbers alone matched those achieved from top-rated diets such as DASH (Dietary Approaches to Stop Hypertension) (4); an eating pattern established as the gold standard for lowering blood pressure after several successful studies by the National Institutes of Health.
Power-Packed with Polyphenols
"These findings suggest that polyphenols help to protect our bodies, and may be adept at keeping a large number of ailments at bay," said Dr. Khoo. "Luckily for us, a rich source of polyphenols is only a glass of cranberry juice away. Among the commonly consumed fruits in our diets, cranberries boast some of the highest levels of polyphenols - more than apples, blueberries, grapes or cherries."
Incorporating these tart-tasting berries into our daily diets is a sustainable and practical lifestyle approach that holds notable promise for improving health. In addition to the cardiometobolic effects of polyphenols, cranberries also contain unique proanthocyanidins (PACs) that may help prevent certain bacteria from sticking inside the body.
Track Record of Whole-Body Health
The findings by the team of USDA researchers that drinking cranberry juice could lower disease risk comes on the heels of supporting research that further espouses cranberry products as part of a healthy diet and balanced lifestyle. Two recent studies (5,6) analyzing four years' worth of data from the Center for Disease Control's National Health and Nutrition Examination Survey (NHANES), found that those who regularly drink cranberry juice are more likely to be normal weight, have significantly lower waist circumference and showcase improved heart health characteristics.
At least 14 deaths of marathon runners, football players and other athletes have been attributed to a condition called exercise-associated hyponatremia, which results from drinking too much water or sports drinks.
But there's an easy way to prevent hyponatremia, according to new guidelines from an international expert panel: Simply put, drink only when you're thirsty.
"Using the innate thirst mechanism to guide fluid consumption is a strategy that should limit drinking in excess and developing hyponatremia while providing sufficient fluid to prevent excessive dehydration," according to the guidelines, published in the Clinical Journal of Sport Medicine.
Loyola University Medical Center sports medicine physician James Winger, MD, is a member of the 17-member expert panel that wrote the guidelines. Dr. Winger, who has published studies on hyponatremia in athletes, is an associate professor in the Department of Family Medicine of Loyola University Chicago Stritch School of Medicine. Corresponding author of the guidelines is Tamara Hew-Butler, DPM, PhD, of Oakland University in Rochester, Mi.
Exercise-associated hyponatremia (EAH) occurs when drinking too much overwhelms the ability of the kidneys to excrete the excess water load. Sodium in the body becomes diluted. This leads to swelling in cells, which can be life-threatening.
Symptoms of mild EAH include lightheadedness, dizziness, nausea, puffiness and gaining weight during an athletic event. Symptoms of severe EAH include vomiting, headache, altered mental status (confusion, agitation, delirium, etc.), seizure and coma.
EAH has occurred during endurance competitions such as marathons, triathlons, canoe races and swimming; military exercises; hiking; football; calisthenics during fraternity hazing; and even yoga and lawn bowling, the guidelines said.
Athletes often are mistakenly advised to "push fluids" or drink more than their thirst dictates by, for example, drinking until their urine is clear or drinking to a prescribed schedule. But excessive fluid intake does not prevent fatigue, muscle cramps or heat stroke.
"Muscle cramps and heatstroke are not related to dehydration," Dr. Winger said. "You get heat stroke because you're producing too much heat."
Modest to moderate levels of dehydration are tolerable and pose little risk to otherwise healthy athletes. An athlete can safely lose up to 3 percent of his or her body weight during a competition due to dehydration without loss of performance, Dr. Winger said.
The guidelines say EAH can be treated by administering a concentrated saline solution that is 3 percent sodium - about three times higher than the concentration in normal saline solution.
The guidelines are published in an article titled "Statement of the Third International Exercise-Associated Hyponatremia Consensus Development Conference, Carlsbad, California, 2015."
Although vitamin A supplementation can have profound health benefits when someone is deficient, new evidence is emerging to show that vitamin A supplementation above and beyond normal levels may have negative health consequences. A new research report published in the July 2015 issue of the Journal of Leukocyte Biology may help to explain why too much vitamin A can be harmful. Too much vitamin A shuts down the body's trained immunity, opening the door to infections to which we would otherwise be immune. This study adds to the arguments that vitamin A supplementation should only be done with clear biological and clinical arguments. Furthermore, it also suggests that low vitamin A concentrations in certain situations may even be "normal."
"This study helps to explain the mechanisms of anti-inflammatory effects of vitamin A and by doing so opens the door to identifying novel ways to modulate the immune response and restore its function in situations in which it is dysregulated," said Mihai G. Netea, M.D., Ph.D., a researcher involved in the work from the Department of Internal Medicine at Radboud University Medical Center in Nijmegen, The Netherlands.
To make this discovery, Netea and colleagues stimulated immune cells, isolated from volunteers, with Vitamin A and saw that the cells produced fewer cytokines, key proteins that help ward off microbes, upon stimulation with various mitogens and antigens. Furthermore, the cells were also stimulated with various microbial structures, which resulted in long-term activation or training of the cells. When the same experiments were performed in the presence of vitamin A, the microbial structures were no longer able to activate the immune cells.
"The interface of nutrition and immunity is an area of considerable importance, especially in an age when dietary supplements and vitamins are quite common," said John Wherry, Ph.D., Deputy Editor of the Journal of Leukocyte Biology. "These new findings shed light on an importance balance in vitamin A levels for optimal immunity. These studies have implications for how we think about daily vitamins, but also for the developing world, where improving diet could have dramatic benefits on how the immune system is trained to respond to different infections."
Tree nut consumption associated with lower body weight and lower risk of metabolic syndrome and cardiovascular disease
In a study published this week in Nutrition Journal*, researchers compared risk factors for heart disease and metabolic syndrome of tree nut consumers versus those who did not consume tree nuts. Tree nut (almonds, Brazil nuts, cashews, hazelnuts, macadamias, pecans, pine nuts, pistachios and walnuts) consumption was associated with lower body mass index (p=0.004), systolic blood pressure (p=0.001), insulin resistance (p=0.043) and higher levels of high-density lipoprotein-cholesterol (good cholesterol) (p=0.022). In addition, tree nut consumers were 25% less likely to be obese and 21% less likely to have an elevated waist circumference than those who did not consume tree nuts.
The study looked at 14,386 men and women (19+ years) participating in the 2005-2010 National Health and Nutrition Examination Surveys (NHANES). Intake was from 24-hour recall data and tree nut consumers were defined as those who consumed ¼ ounce or more per day. "Approximately 6.8% of the study population consumed tree nuts," stated Carol O'Neil, PhD, MPH, RD, lead author on the paper and Professor at Louisiana State University Agricultural Center. "While that may sound small, it actually represents over 12 million individuals--a significant number." She added, "Those who consumed nuts ate about 1.5 ounces (44.3 grams) of tree nuts per day--similar to the amount recommended in the FDA qualified health claim for nuts and heart disease."
Research has shown that nuts can help reduce the risk of cardiovascular disease and metabolic syndrome (MetS). The latter is a cluster of risk factors for cardiovascular disease and type 2 diabetes and includes elevated blood lipids, blood pressure, blood sugar, insulin resistance and abdominal obesity. Obesity is also a risk factor for these two diseases and although tree nuts contain fat and calories, numerous studies have shown that diets "enriched with nuts" do not increase weight
Here's more evidence that fish oil supplementation and antioxidants might be beneficial for at least some people facing Alzheimer's disease: A new report published in the July 2015 issue of The FASEB Journal describes the findings of a very small study in which people with mild clinical impairment, such as those in the very early stages of the disease, saw clearance of the hallmark amyloid-beta protein and reduced inflammation in neurological tissues. Although the findings involved just 12 patients over the course of 4 to 17 months, the findings suggest further clinical study of this relatively inexpensive and plentiful supplement should be conducted.
"Prevention of mild cognitive impairment progression is one of the best hopes," said Milan Fiala, M.D., Research Professor at the University of California's Department of Surgery in Los Angeles. "In addition to physical and mental exercises recommended by experts, this study suggests that nutrition is equally important."
To make their discovery, Fiala and colleagues investigated the effects of 4 to 17 months of supplementation with omega-3 fatty acids and antioxidants in 12 patients with minor cognitive impairment, 2 patients with pre-mild cognitive impairment, and 7 patients with Alzheimer disease. They measured the phagocytosis of amyloid-beta 1-42 by flow cytometry and microscopy, the transcription of inflammatory genes by RT-PCR, the production of resolvin D1 by enzyme immunoassay, and the cognitive status by MMSE.
In patients with mild clinical impairment and pre-mild clinical impairment, phagocytosis of amyloid-beta by monocytes increased from 530 to 1306 mean fluorescence intensity units. The increase in patients with Alzheimer's disease was not significant. The lipidic mediator resolvin D1, which stimulates amyloid-beta phagocytosis in vitro, increased in macrophages in 80 percent of patients with mild clinical impairment and pre-mild clinical impairment. The transcription of inflammatory genes' mRNAs was increased in a subgroup of patients with low transcription at baseline, whereas it was not significantly changed in patients with high transcription at baseline.
"We've known for a long time that omega-3 fatty acids and some antioxidants can be beneficial to people with a wide range of health problems, as well as protective for healthy people," said Gerald Weissmann, M.D., Editor-in-Chief of The FASEB Journal. "Now, we know that the effects of these supplements may extend to Alzheimer's disease as well. Although these supplements are considered to be generally safe and are very easy to obtain, full-scale clinical trials are necessary to verify the findings of this research and to identify who might benefit the most."
People on a vegetarian diet, and especially those following a vegan one that includes no animal products, see better results than dieters on other weight-reducing plans. In fact, they can lose around two kilograms more on the short term, says Ru-Yi Huang of E-Da Hospital in Taiwan after reviewing the results of twelve diet trials. The findings¹ appear in the Journal of General Internal Medicine², published by Springer.
Huang's review includes twelve randomized controlled trials, involving 1,151 dieters who followed a specific eating regime for between nine and 74 weeks. It is the first study to combine the findings from various independent projects that weighed up the results of vegetarian diets against other eating plans. These include the Atkins diet, and ones recommended by the American Diabetes Association or the US National Cholesterol Education Program.
Overall, individuals assigned to the vegetarian diet groups lost significantly more weight (around 2.02 kilograms) than dieters who ate meat and other animal products. Vegetarians who followed a vegan diet lost even more weight. Comparatively, they lost around 2.52 kilograms more than non-vegetarian dieters. Vegetarians who do consume dairy products and eggs lost around 1.48 kilograms more than those on a non-vegetarian diet. People following vegetarian diets that prescribe a lower than normal intake of calories (so-called energy restriction) also shed more kilograms than those without any such limitations being placed on their eating habits.
According to Huang, the abundant intake of whole grains, fruits and vegetables might play a role in the favorable results seen in vegetarian diets. Whole-grain products and vegetables generally have low glycemic index values and don't cause blood sugar levels to spike. Fruits are rich in fiber, antioxidants, minerals and protective chemicals that naturally occur in plants. Whole-grain products contain soluble fiber. Such so-called good fiber helps to delay the speed by which food leaves the stomach and ensures good digestion. It also allows enough nutrients to be absorbed while food moves through the intestines. Several studies have reported that fiber consumption helps with weight loss.
"Vegetarian diets are more effective than non-vegetarian diets for weight loss," says Huang, who added that longer term intervention trials are needed to investigate the effect of vegetarian diets on weight control and cardio-metabolic risk.
Friday, June 26, 2015
A new study suggests that people with a genetic predisposition to high blood pressure have a lower risk for Alzheimer's disease.
However, authors conclude the connection may have more to do with anti-hypertension medication than high blood pressure itself.
"It's likely that this protective effect is coming from antihypertensive drugs," said co-author John Kauwe, associate professor of biology at Brigham Young University. "These drugs are already FDA approved. We need to take a serious look at them for Alzheimer's prevention."
The study, published this month in PLOS Medicine, analyzed genetic data from 17,008 individuals with Alzheimer's and 37,154 people without the disease. Data came from the Alzheimer's Disease Genetics Consortium and the International Genomics of Alzheimer's Project.
BYU researchers worked with scholars from the University of Cambridge, Aarhus University in Denmark and the University of Washington on the massive study. BYU's role was to flex its muscles in supercomputing and bioinformatics. With the help of BYU's supercomputer, Kauwe and undergraduate student Kevin Boehme pieced together 32 data sets for the analysis.
The research team looked for links between Alzheimer's disease and a number of health conditions -- including diabetes, obesity, and high cholesterol -- but only found a significant association between higher systolic blood pressure and reduced Alzheimer's risk. (A weak connection between smoking and Alzheimer's also surfaced.)
"Our results are the opposite of what people might think," said fellow co-author Paul Crane, a University of Washington associate professor of internal medicine. "It may be that high blood pressure is protective, or it may be that something that people with high blood pressure are exposed to more often, such as antihypertensive medication, is protecting them from Alzheimer's disease."
University of Cambridge senior investigator scientist Robert Scott led the study, which used "Mendelian randomization" to find if the risk factors (BMI, insulin resistance, blood pressure, cholesterol, diabetes) for Alzheimer's had a causal impact. Mendelian randomization uses subjects' genetics as a proxy for a randomized clinical trial.
"This is to date the most authoritative paper looking at causal relationships between Alzheimer's disease and these potentially modifiable factors," Kauwe said. "In terms of the number of samples, it can't get bigger at this point."
New research reveals that it only takes two weeks of not using their legs for young people to lose a third of their muscular strength, leaving them on par with a person who is 40-50 years their senior. The Center for Healthy Aging and the Department of Biomedical Sciences at the University of Copenhagen conducted the research.
Time and again, we are told that we need to stay physically active and exercise daily. But how quickly do we actually lose our muscular strength and muscle mass if we go from being averagely active to being highly inactive? For example when we are injured, fall ill or simply take a very relaxing holiday. Researchers from the University of Copenhagen have examined what happens to the muscles in younger and older men after a period of high inactivity, by way of so-called immobilization with a leg pad.
Both older and younger people lose muscular strength
"Our experiments reveal that inactivity affects the muscular strength in young and older men equally. Having had one leg immobilized for two weeks, young people lose up to a third of their muscular strength, while older people lose approx. one fourth. A young man who is immobilized for two weeks loses muscular strength in his leg equivalent to ageing by 40 or 50 years," says Andreas Vigelsoe, PhD at the Center for Healthy Aging and the Department of Biomedical Sciences at the University of Copenhagen.
Young people lose twice as much muscle mass
With age, our total muscle mass diminishes, which is why young men have approx. one kilogram more muscle mass in each leg than older men. Both groups lose muscle mass when immobilized for two weeks - young men lose 485 grams on average, while older men lose approx. 250 grams. The participants' physical fitness was also reduced while their one leg was immobilized in a pad.
"The more muscle mass you have, the more you'll lose. Which means that if you're fit and become injured, you'll most likely lose more muscle mass than someone who is unfit, over the same period of time. But even though older people lose less muscle mass and their level of fitness is reduced slightly less than in young people, the loss of muscle mass is presumably more critical for older people, because it is likely to have a greater impact on their general health and quality of life," says Martin Gram, researcher at the Center for Healthy Aging and the Department of Biomedical Sciences, explains.
Cycling is not enough
After two weeks of immobilization, the participants bicycle-trained 3-4 times a week for six weeks.
"Unfortunately, bicycle-training is not enough for the participants to regain their original muscular strength. Cycling is, however, sufficient to help people regain lost muscle mass and reach their former fitness level. If you want to regain your muscular strength following a period of inactivity; you need to include weight training," Andreas Vigelsoe states.
"It's interesting that inactivity causes such rapid loss of muscle mass, in fact it'll take you three times the amount of time you were inactive to regain the muscle mass that you've lost. This may be caused by the fact that when we're inactive, it's 24 hours a day," Martin Gram concludes.
I take Coenzyme Q10 for its prevention of muscle pain for statin users:
Treatment of statin adverse effects with supplemental Coenzyme Q10 and statin drug discontinuation
According to study published in Biofactors in 2005, fifty consecutive new cardiology clinic patients who were on statin drug therapy (for an average of 28 months) on their initial visit were evaluated for possible adverse statin effects (myalgia, fatigue, dyspnea, memory loss, and peripheral neuropathy). All patients discontinued statin therapy due to side effects and began supplemental CoQ(10) at an average of 240 mg/day upon initial visit.
The patients were then followed for an average of 22 months with 84% of the patients followed now for more than 12 months. The prevalence of patient symptoms on initial visit and on most recent follow-up demonstrated a decrease in fatigue from 84% to 16%, myalgia from 64% to 6%, dyspnea from 58% to 12%, memory loss from 8% to 4% and peripheral neuropathy from 10% to 2%. There were two deaths from lung cancer and one death from aortic stenosis with no strokes or myocardial infarctions. Measurements of heart function either improved or remained stable in the majority of patients.
The researchers concluded that statin-related side effects, including statin cardiomyopathy, are far more common than previously published and are reversible with the combination of statin discontinuation and supplemental CoQ(10).
But Coenzyme Q10 has lots of other benefits as well:
Coenzyme Q10 Improves Heart Failure Mortality
Coenzyme Q10 decreases all cause mortality by half, according to the results of a multicentre randomised double blind trial presented at Heart Failure 2013 congress. It is the first drug to improve heart failure mortality in over a decade and should be added to standard treatment, according to lead author Professor Svend Aage Mortensen (Copenhagen, Denmark).
Heart Failure 2013 was held from 25-28 May in Lisbon, Portugal. It is the main annual meeting of the Heart Failure Association of the European Society of Cardiology.
Coenzyme Q10 (CoQ10) occurs naturally in the body and is essential to survival. CoQ10 works as an electron carrier in the mitochondria, the powerhouse of the cells, to produce energy and is also a powerful antioxidant. It is the only antioxidant that humans synthesise in the body.
CoQ10 levels are decreased in the heart muscle of patients with heart failure, with the deficiency becoming more pronounced as heart failure severity worsens. Statins are used to treat many patients with heart failure because they block the synthesis of cholesterol, but these drugs also block the synthesis of CoQ10, which further decreases levels in the body.
Double blind controlled trials have shown that CoQ10 improves symptoms, functional capacity and quality of life in patients with heart failure with no side effects. But until now, no trials have been statistically powered to address effects on survival.
The Q-SYMBIO study (2) randomised 420 patients with severe heart failure (New York Heart Association (NYHA) Class III or IV) to CoQ10 or placebo and followed them for 2 years. The primary endpoint was time to first major adverse cardiovascular event (MACE) which included unplanned hospitalisation due to worsening of heart failure, cardiovascular death, urgent cardiac transplantation and mechanical circulatory support. Participating centres were in Denmark, Sweden, Austria, Slovakia, Poland, Hungary, India, Malaysia and Australia.
CoQ10 halved the risk of MACE, with 29 (14%) patients in the CoQ10 group reaching the primary endpoint compared to 55 (25%) patients in the placebo group (hazard ratio=2; p=0.003). CoQ10 also halved the risk of dying from all causes, which occurred in 18 (9%) patients in the CoQ10 group compared to 36 (17%) patients in the placebo group (hazard ratio=2.1; p=0.01).
CoQ10 treated patients had significantly lower cardiovascular mortality (p=0,02) and lower occurrence of hospitalisations for heart failure (p=0.05). There were fewer adverse events in the CoQ10 group compared to the placebo group (p=0.073).
Professor Mortensen said: "CoQ10 is the first medication to improve survival in chronic heart failure since ACE inhibitors and beta blockers more than a decade ago and should be added to standard heart failure therapy."
He added: "Other heart failure medications block rather than enhance cellular processes and may have side effects. Supplementation with CoQ10, which is a natural and safe substance, corrects a deficiency in the body and blocks the vicious metabolic cycle in chronic heart failure called the energy starved heart."
CoQ10 is present in food, including red meat, plants and fish, but levels are insufficient to impact on heart failure. CoQ10 is also sold over the counter as a food supplement but Professor Mortensen said: "Food supplements can influence the effect of other medications including anticoagulants and patients should seek advice from their doctor before taking them."
Patients with ischaemic heart disease who use statins could also benefit from CoQ10 supplementation. Professor Mortensen said: "We have no controlled trials demonstrating that statin therapy plus CoQ10 improves mortality more than statins alone. But statins reduce CoQ10, and circulating CoQ10 prevents the oxidation of LDL effectively, so I think ischaemic patients should supplement statin therapy with CoQ10."
Cardiologists examine alternatives to halt high blood pressure
Hypertension expert John Bisognano, M.D., Ph.D. and Kevin Woolf, M.D., a cardiology fellow at the Medical Center, conducted the most comprehensive review to date of the evidence behind a wide range of non-drug interventions for the treatment of high blood pressure. The review is featured in the September 2011issue of the Journal of Clinical Hypertension.
The shining star among supplements is coenzyme Q10, an enzyme involved in energy production that also acts as an antioxidant. Patients with hypertension tend to have lower levels of the enzyme, and a meta-analysis – an overarching analysis of past studies – found that treatment with coenzyme Q10 supplements significantly reduced blood pressure.
Woolf noted that "Coenzyme Q10 has a pretty profound effect on blood pressure, but whenever research is based on a collection of other data you have to have some skepticism." Woolf said he still thinks the compound is promising.
Study shows coenzyme Q10 may prevent migraine
A popular supplement, coenzyme Q10 (CoQ10), may help prevent migraine, according to research presented at the American Academy of Neurology 56th Annual Meeting in San Francisco, Calif., April 24 – May 1, 2004.
Migraine patients who took 100 mg three times a day of CoQ10--which acts as the body's energy producer--had fewer attacks in three months than those who took a placebo. The participants taking CoQ10 also had fewer days with a headache and fewer days with nausea.
"A lack of cell energy in the brain may be a cause of migraine," said study author Peter S. Sandor, MD, University Hospitals Zurich, Switzerland. "CoQ10 may give a boost to those cells and help prevent migraine."
The study involved 42 people who suffered an average 4.4 migraine attacks per month. Approximately 48 percent of those who took CoQ10 had half as many attacks during the three-month study, while this occurred in only about 14 percent of those taking a placebo.
"We found that coenzyme 10 had a significant effect on reducing migraine," said Sandor. "We also found that the only side effect appeared to be an allergic skin rash in one patient. This compares with side effects of fatigue, weight gain, dry mouth, and other side effects found with other methods to prevent migraine."
Supplemental co-enzyme Q may prevent heart disease in some individuals
New research in The FASEB Journal suggests that low birth weight in rats leads to a reduction in co-enzyme Q in the aorta and that supplemental dosage prevents age-associated damage leading to heart disease
New research involving rats, and published in the December 2014 issue of The FASEB Journal, suggests that if you were born at a low birth weight, supplemental co-enzyme Q (CoQ) may lower your risk for heart disease. This enzyme, which is naturally made in the body, is required to ensure the proper functioning of cell mitochondria and also protects cells from oxidative damage. Feeding low birth weight rat offspring extra CoQ prevented the age-associated damage that causes heart disease. Additionally, the reports shows that CoQ is reduced in white blood cells from low birth weight offspring, and levels of CoQ in the blood can be an indicator of how much damage to the aorta has already occurred.
"We believe our study provides the first steps in the development of a routine diagnostic test for blood coenzyme Q levels which can be used to identify individuals who are at risk of cardiovascular disease later in life," said Jane L. Tarry-Adkins, a researcher involved in the work from the Institute of Metabolic Science at the University of Cambridge Metabolic Research Laboratories in the United Kingdom. "Additionally, simple co-enzyme Q supplements may be able to lower these individuals risk."
To make their discovery, Tarry-Adkins and colleagues fed pregnant rats either a control diet or a diet that had the same total calories but contained less protein and more carbohydrates. The mothers fed the low protein diet had pups which had a low birth weight but grew quickly when suckled by a control fed mother. Researchers examined the aorta from the rats which were born small and grew very quickly after birth and showed that their cells aged more quickly than those from the normal birth weight offspring and that this was associated with a deficit in co-enzyme Q, in both the aorta and in the blood compared to the normal birth weight rats. Administering extra coenzyme Q in their diet from weaning prevented the accelerated aging of and damage to their aortas.
"Coenzyme Q is in the drug store now, but if you think that what you buy is going to keep you from having a heart attack or stroke, don't get your hopes up just yet," said Gerald Weissmann, M.D., Editor-in-Chief of The FASEB Journal. "This promising research was conducted in rats, and if it also applies to people, still doesn't tell us how much to take, for how long, and if it's safe for these purposes. We've got a long way to go on this one, but so far, so good!"
Coenzyme Q10 helps veterans battle Gulf War illness symptoms
Eighty percent of treated veterans improved physical function
Roughly one-third of the 700,000 United States troops who fought in the 1990-1991 Persian Gulf War have subsequently developed a distinct set of chronic health problems, dubbed Gulf War illness. Their symptoms, from fatigue, muscle pain and weakness to decreased cognitive function and gastrointestinal and skin problems, persist decades after the conflict.
In a study published in the Nov. 1 issue of Neural Computation, researchers at the University of California, San Diego School of Medicine report that a high quality brand of coenzyme Q10 (CoQ10) – a compound commonly sold as a dietary supplement – provides health benefits to persons suffering from Gulf War illness symptoms.
Forty-six United States Gulf War veterans participated in the randomized, double-blind, placebo-controlled study. Each veteran had been diagnosed with Gulf War illness.
"Gulf War illness is not the same as post-traumatic stress disorder or traumatic brain injury, signature illnesses of later deployments, which are caused by psychological and mechanical injury, respectively," said Beatrice Golomb, MD, PhD, professor of medicine at UC San Diego School of Medicine and principal investigator on the study. "Evidence instead links Gulf War illness to chemical exposures, such as pesticides or pills given to soldiers to protect them from possible nerve agents. These chemicals can damage mitochondria, which generate the energy our cells need to do their jobs. When these powerhouses of the cells are disrupted, it can produce symptoms compatible with those seen in Gulf War illness."
The connection to chemical and toxin exposures is fortified by evidence of mitochondrial problems in affected veterans, said Golomb, as well as evidence showing those veterans who became ill are significantly more likely than others to harbor genetic variants that render their enzymes less effective at detoxifying these chemicals.
CoQ10 is a fat-soluble antioxidant made by the body to support basic cell functions, including directly assisting mitochondrial energy production. Over a course of three and a half months, the veterans in the study received a pill form of either CoQ10 or a placebo. Researchers found 80 percent of those who received 100mg of CoQ10 had improvement in physical function. The degree of improvement correlated to the degree in which CoQ10 levels in the blood increased.
The researchers reported that Gulf War illness symptoms like headaches, fatigue with exertion, irritability, recall problems and muscle pain also improved.
"The statistical significance of these benefits, despite the small sample size, underscores the large magnitude of the effects," Golomb said. "Mounting evidence suggests findings in Gulf War illness are relevant to toxin-induced health problems in the civilian sector, so what we learn by studying health challenges of these veterans, will likely benefit others."
Golomb and colleagues are seeking additional funding to test a more complete "mitochondrial cocktail," which combines CoQ10 with additional nutrients that support cell energy and reduce oxidative damage to cells.
Co-Q10 deficiency may relate to statin drugs, diabetes risk
A laboratory study has shown for the first time that coenzyme Q10 offsets cellular changes that may be linked to a side-effect of some statin drugs - an increased risk of adult-onset diabetes.
Statins are some of the most widely prescribed drugs in the world, able to reduce LDL, or “bad” cholesterol levels, and the risk of heart attacks or other cardiovascular events. However, their role in raising the risk of diabetes has only been observed and studied in recent years.
The possibility of thousands of statin-induced diabetics is a growing concern, and led last year to new labeling and warnings by the Food and Drug Administration about the drugs, especially when taken at higher dosage levels.
The findings of the new research were published as a rapid communication in Metabolic Syndrome and Related Disorders, and offer another clue to a possible causative mechanism of this problem.
Pharmacy researchers at Oregon State University who authored the study said the findings were made only in laboratory analysis of cells, and more work needs to be done with animal and ultimately human studies before recommending the use of coenzyme Q10 to help address this concern.
“A number of large, randomized clinical trials have now shown that use of statins can increase the risk of developing type-2 diabetes by about 9 percent,” said Matthew K. Ito, an OSU professor of pharmacy and president-elect of the National Lipid Association.
“This is fairly serious, especially if you are in the large group of patients who have not yet had a cardiovascular event, but just take statin drugs to lower your risks of heart disease,” Ito said.
A suspect in this issue has been altered levels of a protein called GLUT4, which is part of the cellular response mechanism, along with insulin, that helps to control blood sugar levels. A reduced expression of GLUT4 contributes to insulin resistance and the onset of type-2 diabetes, and can be caused by the use of some statin drugs.
The statins that reduce cholesterol production also reduce levels of coenzyme Q10, research has shown. Coenzyme Q10 is needed in cells to help create energy and perform other important functions. And this study showed in laboratory analysis that if coenzyme Q10 is supplemented to cells, it prevents the reduction in GLUT4 induced by the statins.
Not all statin drugs, however, appear to cause a reduction in GLUT4.
The problems were found with one statin, simvastatin, that is “lipophilic,” which means it can more easily move through the cell membrane. Some of the most commonly used statins are lipophilic, including simvastatin, atorvastatin, and lovastatin. All of these statins are now available as generic drugs, and high dosage levels have been most often linked with the increase in diabetes.
Coenzyme Q10 and Breast Cancer
Aa reportes in the journal Molecular Aspects of Medicine an open-label (nonblinded), uncontrolled clinical study in Denmark followed 32 breast cancer patients for 18 months. The disease in these patients had spread to the axillary lymph nodes, and an unreported number had distant metastases. The patients received antioxidant supplementation (vitamin C, vitamin E, and beta carotene), other vitamins and trace minerals, essential fatty acids, and coenzyme Q10 (at a dose of 90 mg/day), in addition to standard therapy (surgery, radiation therapy, and chemotherapy, with or without tamoxifen).
The patients were seen every 3 months to monitor disease status (progressive disease or recurrence), and, if there was a suspicion of recurrence, mammography, bone scan, x-ray, or biopsy was performed. The survival rate for the study period was 100% (4 deaths were expected). Six patients were reported to show some evidence of remission; however, incomplete clinical data were provided, and information suggestive of remission was presented for only 3 of the 6 patients. None of the 6 patients had evidence of further metastases. For all 32 patients, decreased use of painkillers, improved quality of life, and an absence of weight loss were reported. Whether painkiller use and quality of life were measured objectively (e.g., from pharmacy records and validated questionnaires, respectively) or subjectively (from patient self-reports) was not specified.
In a follow-up of the above study reported in Biochemical and Biophysical Research Communications, 1 of the 6 patients with a reported remission and a new patient were treated for several months with higher doses of coenzyme Q10 (390 and 300 mg/day, respectively). Surgical removal of the primary breast tumor in both patients had been incomplete. After 3 to 4 months of high-level coenzyme Q10 supplementation, both patients appeared to experience complete regression of their residual breast tumors (assessed by clinical examination and mammography).. In the follow-up study report, the researchers noted that all 32 patients from the original study remained alive at 24 months of observation, whereas 6 deaths had been expected.
In another report in Biochemical and Biophysical Research Communications, of by the same investigators, 3 breast cancer patients were followed for a total of 3 to 5 years on high-dose coenzyme Q10 (390 mg/day). One patient had complete remission of liver metastases (determined by clinical examination and ultrasonography), another had remission of a tumor that had spread to the chest wall (determined by clinical examination and chest x-ray), and the third patient had no microscopic evidence of remaining tumor after a mastectomy (determined by biopsy of the tumor bed).
Thursday, June 25, 2015
For the first time, researchers at Fred Hutchinson Cancer Research Center have found that weight loss, in combination with vitamin D supplementation, has a greater effect on reducing chronic inflammation than weight loss alone. Chronic inflammation is known to contribute to the development and progression of several diseases, including some cancers.
Results of the randomized, controlled clinical trial -- which involved more than 200 overweight, postmenopausal women who had insufficient levels of vitamin D at the beginning of the study -- are published online ahead of the July print issue of Cancer Prevention Research, a journal of the American Association for Cancer Research.
"We know from our previous studies that by losing weight, people can reduce their overall levels of inflammation, and there is some evidence suggesting that taking vitamin D supplements can have a similar effect if one has insufficient levels of the nutrient," said lead and corresponding author Catherine Duggan, Ph.D., a principal staff scientist in the Public Health Sciences Division at Fred Hutch. However, it has not been known whether combining the two -- weight loss and vitamin D -- would further boost this effect. "It's the first study to test whether adding vitamin D augments the considerable effect of weight loss on inflammatory biomarkers," she said.
To explore this question, Duggan and colleagues recruited 218 healthy, overweight older women who had lower-than-recommended levels of vitamin D (less than 32 ng/mL). The women then took part in a 12-month diet and exercise program (including 45 minutes of moderate-to-vigorous exercise five days a week). Half of the study participants were randomly selected to receive 2,000 IU of vitamin D daily for the duration of the year-long trial, and the other half received an identical-appearing placebo, or dummy vitamin. Biomarkers of inflammation were measured at the beginning and end of the study. The researchers then compared changes in these levels between the two groups.
At the end of the study, all of the participants had reduced levels of inflammation, regardless of whether they took vitamin D, "which highlights the importance of weight loss in reducing inflammation," Duggan said. However, those who saw the most significant decline in markers of inflammation were those who took vitamin D and lost 5 to 10 percent of their baseline weight. These study participants had a 37 percent reduction in a pro-inflammatory cytokine called interleukin-6, or IL-6, as compared to those in the placebo group, who saw a 17.2 percent reduction in IL-6. The researchers found similar results among women in the vitamin D group who lost more than 10 percent of their starting weight. While IL-6 has normal functions in the body, elevated levels are associated with an increased risk of developing certain cancers and diabetes and may be implicated as a cause of depression, Duggan said.
"We were quite surprised to see that vitamin D had an effect on an inflammation biomarker only among women who lost at least 5 percent of their baseline weight," Duggan said. "That suggests vitamin D can augment the effect of weight loss on inflammation."
Vitamin D is a steroid hormone that has multiple functions beyond its widely recognized role in regulating calcium levels and bone metabolism. Vitamin D receptors are found in more than 30 cell types and the research focus around this nutrient recently has shifted from bone health to vitamin D's effect on cancer, cardiovascular health and weight loss, among other health issues.
Inflammation occurs when the body is exposed to pathogens, such as bacteria or viruses, which puts the immune system in overdrive until the "attack" ceases and the inflammatory response abates. Overweight or obese people, however, exist in a state of chronic inflammation. This sustained upregulation of the inflammatory response occurs because fat tissue continually produces cytokines, molecules that are usually only present for a short time, while the body is fighting infection, for example.
"It is thought that this state of chronic inflammation is pro-tumorigenic, that is, it encourages the growth of cancer cells," she said. There is also some evidence that increased body mass "dilutes" vitamin D, possibly by sequestering it in fat tissue.
"Weight loss reduces inflammation, and thus represents another mechanism for reducing cancer risk," Duggan said. "If ensuring that vitamin D levels are replete, or at an optimum level, can decrease inflammation over and above that of weight loss alone, that can be an important addition to the tools people can use to reduce their cancer risk."
Duggan encourages women to speak to their health care providers about measuring their levels of vitamin D to determine the most appropriate dosage.
Fructose not only results in a lower level of satiety, it also stimulates the reward system in the brain to a lesser degree than glucose. This may cause excessive consumption accompanied by effects that are a risk to health, report researchers from the University of Basel in a study published in the scientific journal PLOS ONE. Various diseases have been attributed to industrial fructose in sugary drinks and ready meals.
Fruit sugar, or fructose, is a carbohydrate that occurs naturally in fruits and vegetables and is generally harmless in this form. Despite their similar structures, fructose and glucose - that is, pure grape sugar - affect the body very differently: an intake of glucose causes a sharp increase in blood insulin within minutes, whereas fructose stimulates insulin secretion to a limited degree only.
Teams of researchers led by Professor Christoph Beglinger from the University Hospital and Professor Stefan Borgwardt from the Psychiatric University Clinics (UPK Basel) have now taken a more in-depth look at how these two types of sugar affect interactions between the gastrointestinal tract and the brain. Their work was funded by the Swiss National Science Foundation. In their study, the researchers used combined pharmacological and imaging methods such as functional magnetic resonance imaging (MRI).
Brain activity examined
In the placebo-controlled, double-blind study, twelve healthy young men were given either fructose, glucose or a placebo by way of a feeding tube. Blood samples were then taken from the subjects to measure satiety hormones. The subjects were also asked about how satiated they felt, and their brain activity was monitored by MRI while at rest.
The findings of the pilot study were as follows. Unlike glucose, fructose is less effective at creating feelings of satiety and stimulating the reward system in the brain. An analysis of the MRIs in fact showed that the two types of sugar differed greatly in terms of network activation within the hippocampus and amygdala areas of the limbic system, i.e. the regions of the brain that regulate emotions and impulses. Furthermore, in contrast to glucose (which stimulated a strong signal) the levels of satiety hormones in the blood barely or only minimally increased following fructose consumption. The subjective feeling of satiety also tended to be less affected by the consumption of fructose.
The problem of fructose
"The study may provide the first key findings about the lack of satiety and rewarding effects triggered by fructose," state lead authors Dr Bettina Wölnerhanssen and Dr Anne Christin Meyer-Gerspach. The role of the differing insulin levels and other effects will have to be demonstrated in further studies with more test subjects. Research is increasingly finding indications that isolated, industrially manufactured fructose - which is increasingly used in sugary drinks, sweets and ready meals - is problematic for the human body. It is suspected that fructose promotes the development of various disorders such as obesity, diabetes, fatty liver disease and gout.
The 2008 Physical Activity Guidelines for Americans recommended a minimum of 75 vigorous-intensity or 150 moderate-intensity minutes per week of aerobic activity for substantial health benefit and suggested additional benefits by doing more than double this amount. However, the upper limit of longevity benefit or possible harm with more physical activity is unclear. A total of 661 137 men and women (median age, 62 years; range, 21-98 years) and 116 686 deaths were included in this study. Median follow-up time was 14.2 years.
Compared with individuals reporting no leisure time physical activity, the authors observed a 20% lower mortality risk among those performing some but less than the recommended minimum recommended hours per week, a 31% lower risk at 1 to 2 times the recommended minimum, and a 37% lower risk at 2 to 3 times the minimum. An upper threshold for mortality benefit occurred at 3 to 5 times the physical activity recommendation; however, compared with the recommended minimum, the additional benefit was modest (31% vs 39%). There was no evidence of harm at 10 or more times the recommended minimum
Wednesday, June 24, 2015
Vitamin B12 tweaks how genes behave in the facial bacteria of some people who normally enjoy clear skin. The activity changes of the facial bacteria promote inflammation and lead to pimples.
By shedding light on one mechanism behind B12's role in acne, the UCLA finding may identify drug targets that lead to new treatments for acne.
Huiying Li, an assistant professor of molecular and medical pharmacology at the David Geffen School of Medicine at UCLA, and Dr. Noah Craft, a dermatologist at LA BioMed at Harbor-UCLA Medical Center, are available for interviews.
Science Translational Medicine publishes the findings in its June 24 edition.
Tuesday, June 23, 2015
In a Viewpoint published today in the Journal of the Medical Association (JAMA), researchers from the Friedman School of Nutrition Science and Policy at Tufts University and Boston Children's Hospital call on the federal government to drop restrictions on total fat consumption in the forthcoming 2015 Dietary Guidelines for Americans.
Co-authors Dariush Mozaffarian, M.D., Dr.P.H., dean of the Friedman School, and David Ludwig, M.D., Ph.D., director of the New Balance Foundation Obesity Prevention Center at Boston Children's Hospital, highlight a key, but overlooked, focus of the 2015 Dietary Guidelines for Americans Committee (DGAC), a group of independent scientists convened by the federal government to review current scientific and medical literature on nutrition. For the first time since 1980, the DGAC did not propose restricting total fat consumption in its technical report, released in February. According to the current dietary guidelines, only up to 35 percent of daily calories should come from fat.
By the end of this year, the U.S. Department of Agriculture (USDA) and the U.S. Department of Health and Human Services (HHS) will write the final Dietary Guidelines for Americans, referring to the DGAC report for guidance. The 2015 Dietary Guidelines for Americans are scheduled to be published later this year.
'Placing limits on total fat intake has no basis in science and leads to all sorts of wrong industry and consumer decisions,' Mozaffarian said. 'Modern evidence clearly shows that eating more foods rich in healthful fats like nuts, vegetable oils, and fish have protective effects, particularly for cardiovascular disease. Other fat-rich foods, like whole milk and cheese, appear pretty neutral; while many low-fat foods, like low-fat deli meats, fat-free salad dressing, and baked potato chips, are no better and often even worse than full-fat alternatives. It's the food that matters, not its fat content.'
For obesity prevention, the DGAC recommends shifting the focus from total fat intake to adoption of a healthier food-based dietary pattern with more vegetables, fruits, whole grains, nuts, seafood and beans; and fewer meats, sugars, and refined grains.
'When U.S. guidelines began recommending low-fat diets in 1980, people responded by turning to low-fat or non-fat products, away from healthy high-fat foods and toward refined grains and added sugars,' Ludwig said. 'A growing body of research shows that refined carbohydrates increase metabolic dysfunction and obesity. Yet, foods rich in added sugars, starches and refined grains like white bread, white rice, chips, crackers and bakery desserts still account for most of the calories people eat. Lifting the restriction on total fat would clear the way for restaurants and industry to reformulate products containing more healthful fats and fewer refined grains and added sugars.'
To maximize success, Mozaffarian and Ludwig call on a wide range of other government agencies and programs to also lift the limit on total fat. This includes the National School Lunch program, which recently banned whole milk while keeping sugar-sweetened non-fat milk on cafeteria menus; the FDA, which regulates health claims and food package labeling and remains strongly low-fat focused; and the National Institutes of Health, whose guidelines on healthy diets for families and children classify fat-free creamy salad dressing and trimmed beef and pork as foods to 'eat almost any time' while being cautious about eating vegetables cooked with added fat, nuts, vegetable oil and olive oil.
'From agriculture to food producers to school cafeterias to restaurants, the Dietary Guidelines for Americans serve as a beacon for countless dietary choices in the public and private sector,' Mozaffarian said. 'With obesity and chronic disease impacting public health so deeply, we can't miss this critical opportunity to improve the food supply. The USDA and HHS must use the 2015 guidelines to send the message that limiting total fat provides no benefits and actually leads to confusion and bad dietary choices.'
Friday, June 19, 2015
Increased prostate cancer risk from vitamin E supplements
Men who took 400 international units (I.U.) of vitamin E daily had more prostate cancers compared to men who took a placebo, according to an updated review of data from the Selenium and Vitamin E Cancer Prevention Trial (SELECT). The findings showed that, per 1,000 men, there were 76 prostate cancers in men who took only vitamin E supplements, vs. 65 in men on placebo over a seven-year period, or 11 more cases of prostate cancer per 1,000 men. This represents a 17 percent increase in prostate cancers relative to those who took a placebo. This difference was statistically significant and therefore is not likely due to chance. The results of this update appeared Oct. 12, 2011, in the Journal of the American Medical Association.
SWOG, an international network of research institutions, carried out SELECT at more than 400 clinical sites in the United States, Puerto Rico, and Canada. SELECT was funded by the National Cancer Institute (NCI) and other institutes that comprise the National Institutes of Health.
The crystalline structure of Vitamin E“Based on these results and the results of large cardiovascular studies using vitamin E, there is no reason for men in the general population to take the dose of vitamin E used in SELECT as the supplements have shown no benefit and some very real risks,” said Eric Klein, M.D., a study co-chair for SELECT, and a physician at the Cleveland Clinic. “For now, men who were part of SELECT should continue to see their primary care physician or urologist and bring these results to their attention for further consideration.”
The SELECT study began in 2001 and included over 35,000 men. It was started because earlier research had suggested that selenium or vitamin E might reduce the risk of developing prostate cancer. However, based on an independent safety monitoring review in autumn 2008, participants were told to stop taking their study supplements because it had become clear that the trial would never produce the 25 percent reduction in prostate cancer the study was designed to show with the use of these supplements. In 2010, the study sites were closed and over half of the participants consented to have their health monitored via mail questionnaires. Now, because of this latest finding, researchers are encouraging all participants to consider taking part in long-term study follow-up so investigators can continue to track outcomes.
SELECT was undertaken to substantiate earlier, separate findings from studies in which prostate cancer risk was not the primary outcome. A 1998 study of male smokers in Finland who took 50 I.U. of vitamin E daily to prevent lung cancer, showed 32 percent fewer prostate cancers in men who took the supplement. A 1996 study of men and women with a history of skin cancer who took selenium for prevention of disease recurrence showed that men who took the supplement had 52 percent fewer prostate cancers than men who did not take the supplement.
Based on these and other findings, men were recruited to participate in SELECT. They were randomly assigned to take one of four sets of supplements or placebos, with more than 8,000 men in each group. One group took both selenium and vitamin E; one took selenium and a placebo that looked similar to vitamin E; one took vitamin E and a placebo that looked similar to selenium; and the final group received placebos of both supplements. Men who took selenium alone or vitamin E and selenium together were also more likely to develop prostate cancer than men who took a placebo, but those increases were small and possibly due to chance.
“SELECT has definitively shown a lack of benefit from vitamin E and selenium supplements in the prevention of prostate cancer and has shown there is the potential for harm,” said Lori Minasian, M.D., study co-author and acting director of NCI’s Division of Cancer Prevention. “Nevertheless, this type of research has been critically important to understanding the potential benefits and risks from supplements.”
SELECT researchers are now measuring the amount of vitamin E, selenium, and other nutrients in the blood of participants when they joined the trial, to see if the effect of the supplements depended upon this baseline level of micronutrient. Other researchers are looking at single nucleotide polymorphisms, which are DNA changes known as SNPs, to see if a change in one or more genes could affect cancer risk or perhaps increase a man’s risk of developing prostate cancer while taking vitamin E.
The participant samples come from the study biorepository of blood and toe nail clippings which, when coupled with the extensive clinical information on participants, is a vital resource for further study. “SWOG is soliciting proposals from researchers nationwide to use the SELECT biorepository to help answer the biological question of why vitamin E increased risk instead of decreasing it,” said Laurence Baker, D.O., study co-author and chairman of SWOG. “There are many more questions raised by these study results than we have answers for, and thus the need for further investigation.”
Except for skin cancer, prostate cancer is the most common type of cancer in men in the United States. The current lifetime risk of prostate cancer for American men is 16 percent. In 2011, there will be an estimated 240,890 new cases of prostate cancer and 33,720 deaths from this disease in the United States.
Vitamin E supplements hamper endurance training
Vitamin C and E supplements may blunt the improvement of muscular endurance – by disrupting cellular adaptions in exercised muscles – suggests a new study published February 2014 in The Journal of Physiology.
As vitamin C and E supplements are widely used, understanding if they interfere with cellular and physiological adaptations to exercise is of interest to people exercising for health purposes as well as to athletes.
Dr Gøran Paulsen, who led the study at the Norwegian School of Sport Sciences, explains:
"Our results show that vitamin C and E supplements blunted the endurance training-induced increase of mitochondrial proteins, which are needed to improve muscular endurance."
In the 11-week trial, 54 young, healthy men and women were randomly allocated to receive either 1000mg vitamin C and 235mg vitamin E (consistent with amounts found in shop supplements), or a placebo (a pill containing no active ingredients). Neither the subjects nor the investigators knew which participant received the vitamins or placebos.
The participants completed an endurance training programme, consisting of three to four sessions per week, of primarily running. Fitness tests, blood samples and muscle biopsies were taken before and after the intervention.
Whilst the supplements did not affect maximal oxygen uptake or the results of a 20 metre shuttle test, the results showed that markers for the production of new muscle mitochondria – the power supply for cells – increased only in the group without supplements.
The National Health Service (NHS) says taking less than 540mg vitamin E and 1000mg vitamin C supplements per day is unlikely to cause any harm.
Dr Paulsen says:
"Our results indicate that high dosages of vitamin C and E – as commonly found in supplements – should be used with caution, especially if you are undertaking endurance training."
A significant trend has been identified, but the molecular processes requires further research. Dr Paulsen says:
"Future studies are needed to determine the underlying mechanisms of these results, but we assume that the vitamins interfered with cellular signalling and blunted expression of certain genes."
Previous studies show that exercising increases muscle oxidant production, which participates in the signalling processes leading to muscle adaption. It is possible that high doses of vitamins C and E act as antioxidants and take away some of this oxidative stress, hence blocking muscular endurance development.
Vitamin E may decrease and increase mortality of male smokers
Six-year vitamin E supplementation decreased mortality by 41% in elderly male smokers who had high dietary vitamin C intake, but increased mortality by 19% in middle-aged smokers who had high vitamin C intake, according to a study published in the American Journal of Epidemiology.
Large-scale controlled trials have not found any overall effects of vitamin E supplementation on the mortality of participants. Nevertheless, the effect of vitamin E on respiratory infections has significantly diverged between different population groups suggesting that the effects of vitamin E may not be uniform over all the population.
Dr. Harri Hemila, and Professor Jaakko Kaprio, of the University of Helsinki, Finland, studied whether the effect of vitamin E supplementation on mortality might diverge between different population groups. They analyzed the data of the large randomized trial (Alpha-Tocopherol Beta-Carotene Cancer Prevention Study) which was conducted in Finland between 1985-1993 and included male smokers aged 50-69 years. There were 3571 deaths in 29,133 participants during the 6-year supplementation of 50 mg/day of vitamin E.
Although vitamin E had no overall effect on mortality, its effect was modified by age and dietary vitamin C intake. Vitamin E had no effect on participants who had low dietary vitamin C intake, less than 90 mg/day. However, in those who had high vitamin C intake, over 90 mg/day, the effect of vitamin E diverged so that it increased mortality in young participants (50-62 years), but decreased mortality in old participants (66-69 years).
The US nutritional recommendations, issued by the prestigious Institute of Medicine, consider that vitamin E is safe in doses up to 1000 mg/day. This new study gives further evidence indicating that in some population groups vitamin E may be harmful in a substantially lower dose, 50 mg/day.
The researchers concluded that "in people younger than 65 years, taking vitamin E supplements should be strongly discouraged, until clear evidence emerges that some population groups of younger or middle-aged people benefit". They also concluded that the effect of vitamin E on elderly people should be further investigated.
Vitamin E may increase the life expectancy of older men
Depending on the level of smoking and dietary vitamin C intake, vitamin E supplementation may extend the life-span of restricted groups of men, according to a study published in the Age and Ageing.
Several large randomized trials of humans found that vitamin E supplementation does not reduce mortality. However, the average effect on mortality in a group of people with a wide age range may mask an effect of vitamin E on the life-span.
Dr. Harri Hemila, and Professor Jaakko Kaprio, of the University of Helsinki, Finland, studied the age-dependency of vitamin E effect on mortality in the large randomized trial (Alpha-Tocopherol Beta-Carotene Cancer Prevention Study) which was conducted in Finland between 1985-1993. Their study was restricted to follow-up period over 65 years and 10,837 participants contributed to the analysis.
Among all analyzed participants, vitamin E had no effect on mortality when participants were 65 to 70 years old, but reduced mortality by 24% when participants were 71 or older.
Among 2,284 men with dietary vitamin C intake above the median who smoked less than a pack of cigarettes per day, vitamin E extended life-span by two years at the upper limit of the follow-up age span. In the other participants, consisting of 80% of the cohort, vitamin E did not affect mortality, which shows that vitamin E is no panacea for extending life expectancy.
The researchers concluded that "if vitamin E influences the life-span, it is possible that a benefit on the oldest participants might be camouflaged by the large middle-aged majority of study participants". Therefore, they propose that it might be useful to analyze the effect of vitamin E supplementation in large controlled trials by the age of the participant at the follow-up and not just by the time after randomization that has been customary.