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News flashes are posted here frequently to keep you up-to-date with the latest advances in health and longevity. We have an unparalleled track record of breaking stories about life extension advances.

 

  • Some vitamin studies flawed
  • Vitamin D “sufficiency” is disease-dependent
  • Meta-analysis links higher fiber intake with lower cardiovascular risk
  • Researchers take on age-old advice
  • Mutations synergize to extend worm lifespan
  • Heartburn drugs linked to B12 deficiency
  • How vitamin D works against MS
  • Grape seed compound demonstrates anticancer effect in prostate cancer cells
  • Deficiency = damage
  • “Healthy obesity” questioned
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    Some vitamin studies flawed

    Some vitamin studies flawedDecember 30 2013. The December, 2013 issue of the journal Nutrients published a review article by Alexander J. Michels and Balz Frei of Oregon State University’s Linus Pauling Institute which points out some of the flaws in the design of studies intended to evaluate vitamin supplementation, particularly vitamin C.

    “One of the obvious problems is that most large, clinical studies of vitamins have been done with groups such as doctors and nurses who are educated, informed, able to afford healthy food and routinely have better dietary standards than the public as a whole,” commented Dr Frei, who is an international expert on vitamin C and antioxidants.

    The duo observed that men and women with nutritional inadequacies are the population most likely to exhibit benefits from dietary improvements or supplementation. “More than 90 percent of U.S. adults don’t get the required amounts of vitamins D and E for basic health,” Dr Frei noted. “More than 40 percent don’t get enough vitamin C, and half aren’t getting enough vitamin A, calcium and magnesium. Smokers, the elderly, people who are obese, ill or injured often have elevated needs for vitamins and minerals. It’s fine to tell people to eat better, but it’s foolish to suggest that a multivitamin which costs a nickel a day is a bad idea.”

    He added that the largest trial of multinutrient supplements uncovered a significant reduction in the risk of cataract and cancer among men over the age of 50. “The cancer reduction would be in addition to providing good basic health by supporting normal function of the body, metabolism and growth,” he stated. “If there’s any drug out there that can do all this, it would be considered unethical to withhold it from the general public. But that’s basically the same as recommending against multivitamin/mineral supplements.”

     

     

     

     

    Vitamin D “sufficiency” is disease-dependent

    Vitamin D “sufficiency” is disease-dependentDecember 23 2013. An article published in the December 2013 issue of the journal Nutrients proposes that vitamin D sufficiency is dependent upon the condition targeted for prevention, and that what constitutes a sufficient level to prevent skeletal diseases is significantly lower what is necessary to prevent cardiovascular disease, diabetes and cancer.

    “We hypothesize that just as vitamin D metabolism is tissue dependent, so the levels of 25-hydroxyvitamin D that signify sufficiency are disease dependent,” write Simon Spedding of the University of South Australia and colleagues. “Thus the response to vitamin D supplementation is dependent on the baseline 25-hydroxyvitamin D level, the dose of vitamin D and dose-response characteristics.”

    For their review, the authors evaluated randomized and non-randomized trials, cohort studies, case-control studies and others, that were classified as providing varying levels of evidence concerning vitamin D. While they estimate that the minimum effective level of vitamin D that is sufficient to prevent osteoporosis and fractures is just 20 ng/mL, a reduction in premature mortality, for which there is the highest level of evidence for vitamin D, requires a level of at least 30 ng/mL. For depression, sufficiency also begins at 30 ng/mL, and for diabetes and cardiovascular disease, a minimum sufficient level is 32 ng/mL. To prevent falls and respiratory infections requires a concentration of at least 38 ng/mL, and for cancer prevention, the level is 40 ng/mL or more.

    “In the field of research, trials can be designed to minimize limitations of study design that lead to null outcomes knowing the range of serum 25-OHD in which changes in serum levels will lead to responses in specific body systems,” Dr Spedding and his coauthors write. “This will also provide more clarity when assessing the effectiveness of vitamin D in different diseases, greater uniformity in the results of meta-analyses and less confusing guidelines.”

     

     

     

     

    Meta-analysis links higher fiber intake with lower cardiovascular risk

    Meta-analysis links higher fiber intake with lower cardiovascular riskDecember 20 2013. The results of a systematic review and meta-analysis published on December 19, 2013 in the British Medical Journal add evidence to a protective effect for high fiber diets against the risk of cardiovascular disease.

    For their analysis, researchers at England’s University of Leeds selected 22 prospective studies involving the association between fiber intake and cardiovascular or coronary heart disease published between 1990 and August 2013. Fiber intake was reported as total fiber, soluble or insoluble fiber, or by food source, such as fruit, vegetables or grains.

    Results of a pooled analysis of the twelve studies that evaluated coronary event risk and total fiber intake revealed a 9% decrease in risk with each 7 gram per day increase in fiber. A similar reduction was determined by analyzing the ten studies that examined the association between total fiber intake and cardiovascular disease risk. A modestly greater benefit was observed for insoluble fiber, which occurs mainly in whole grains, in comparison with soluble fiber, which is abundant in legumes, nuts and other sources. Fiber from fruit sources also emerged as significantly protective against the risk of cardiovascular disease.

    Authors Diane E. Threapleton and her colleagues remark that, due to the widespread nature of cardiovascular disease, even small reductions in risk could impact thousands of men and women. They note that an additional seven grams of fiber could be provided by just one portion each of grains and beans, or by consuming two to four servings of vegetables and/or fruit.

    In an accompanying editorial, Dr Robert Baron, who is a professor of medicine at the University of California, commented that the study "increases our confidence that benefit, as reflected by reduced cardiovascular disease and coronary heart disease events, will in fact accrue with higher dietary fiber intakes."

     

     

     

     

    Researchers take on age-old advice

    Researchers take on age-old adviceDecember 18 2013. The Christmas issue of The British Medical Journal contains an article by researchers at the University of Oxford which estimates that the number of lives saved by consuming a daily apple could approach the number resulting from the initiation of treatment with statin drugs. While statins have been shown to significantly reduce the risk of cardiovascular events, they frequently cause side effects, including muscle disease, diabetes and hemorrhagic stroke.

    Using mathematical models, Dr Adam D. M. Briggs and his associates  calculated that if 70% of the 22 million men and women over the age of 50 residing in the United Kingdom complied with the recommendation of “an apple a day,” the result would be the prevention or delay of approximately 8,500 cardiovascular deaths, including those attributable to heart attack and stroke. And if statins became a primary prevention measure for those over the age of 50 years, 9,400 citizens could avoid the same fate.  However, increased use of the drugs would also result in 1,000 more cases of muscle disease and at least 12,000 more diabetics. Lowering the recommended age from 50 to 30 years resulted in an even greater reduction in the calculated risk of death, as did estimating increased compliance.

    "The Victorians had it about right when they came up with their brilliantly clear and simple public health advice: ‘An apple a day keeps the doctor away,’” Dr Briggs commented. “It just shows how effective small changes in diet can be, and that both drugs and healthier living can make a real difference in preventing heart disease and stroke. While no one currently prescribed statins should replace them for apples, we could all benefit from simply eating more fruit."

     

     

     

     

    Mutations synergize to extend worm lifespan

    Mutations synergize to extend worm lifespanDecember 13 2013. An article published in Cell Reports describes the discovery of a significant extension of lifespan in worms known as C. elegans that were engineered to have two mutations linked to a longer life. The genetically modified worms lived up to five times longer than worms without the mutations.

    "In the early years, cancer researchers focused on mutations in single genes, but then it became apparent that different mutations in a class of genes were driving the disease process," commented lead researcher Pankaj Kapahi, PhD, of the Buck Institute for Research on Aging. "The same thing is likely happening in aging. It's quite probable that interactions between genes are critical in those fortunate enough to live very long, healthy lives."

    The team combined a mutation in the nutrient signaling pathway known as Target of Rapamycin (TOR) with a mutation in the insulin signaling pathway Daf-2, which have been demonstrated to increase C. elegans’ lifespan by 30% and 100%, respectively. The combination elicited a far greater extension of lifespan than what would have resulted from an additive effect. "Instead, what we have here is a synergistic five-fold increase in lifespan,” Dr Kapahi stated. "The two mutations set off a positive feedback loop in specific tissues that amplified lifespan. Basically these worms lived to the human equivalent of 400 to 500 years."

    "The germline was the key tissue for the synergistic gain in longevity – we think it may be where the interactions between the two mutations are integrated," added lead author Di Chen, PhD. "The finding has implications for similar synergy between the two pathways in more complex organisms."

     

     

     

     

     

    Heartburn drugs linked to B12 deficiency

    Heartburn drugs linked to B12 deficiencyDecember 11 2013. The December 11, 2013 issue of the Journal of the American Medical Association reports an association between the use of drugs that inhibit excess stomach acid and deficient levels of vitamin B12. By suppressing the production of the stomach’s acid, the drugs, which include proton pump inhibitors (PPIs) and histamine 2 receptor blockers used by patients with gastroesophageal reflux disease (GERD), reduce the amount of the vitamin that is absorbed.

    "Vitamin B12 deficiency is relatively common, especially among older adults; it has potentially serious medical complications if undiagnosed,” write Jameson R. Lam, MPH, of Kaiser Permanente and coauthors in their introduction. “Left untreated, vitamin B12 deficiency can lead to dementia, neurologic damage, anemia, and other complications, which may be irreversible."

    The current study compared 25,956 men and women diagnosed with vitamin B12 deficiency over a four and a half year period with 184,199 subjects who were not deficient. Pharmacy records provided information concerning patients who were dispensed two year or greater supplies of PPIs or histamine 2 receptor-blocking drugs.

    Subjects who received PPIs had a 65% greater risk of being diagnosed with a vitamin B12 deficiency and those who received histamine 2 receptor blockers had a 25% greater risk than those who received neither drug. For those who used the highest dose of proton pump inhibitors, the risk of deficiency was nearly double that of those who didn’t use the drugs. The strength of the association decreased after the drugs were discontinued.

    “These findings do not recommend against acid suppression for persons with clear indications for treatment, but clinicians should exercise appropriate vigilance when prescribing these medications and use the lowest possible effective dose,” the authors write. “These findings should inform discussions contrasting the known benefits with the possible risks of using these medications.”

     

     

     

     

    How vitamin D works against MS

    How vitamin D works against MSDecember 9 2013.  A report published on December 9, 2013 in the Proceedings of the National Academy of Sciences explains how vitamin D, long suspected to play a role in the prevention of multiple sclerosis (MS), works to protect against the disease.

    Acting on the finding of previous research of a preventive benefit for vitamin D in a mouse model of MS, Anne R. Gocke, PhD, and her associates at Johns Hopkins University tested the effects of the bioactive form of vitamin D known as 1,25-dihyroxyvitamin D3 [1,25(OH)2D3] and found that administration of the vitamin prevented the animals from showing symptoms. They observed that immune system cells known as T helper cells, which attack myelin (the protective sheath that covers the nerves) in MS, were abundant in the animals’ bloodstreams, but few had migrated to their brains and spinal cords, which make up the central nervous system. Upon cessation of vitamin D treatment, the animals rapidly developed symptoms, showing that vitamin D temporarily halts the disease.

    "With this research, we learned vitamin D might be working not by altering the function of damaging immune cells but by preventing their journey into the brain,” stated Dr Gocke, who is an assistant professor of neurology at the Johns Hopkins University School of Medicine. "If we are right, and we can exploit Mother Nature's natural protective mechanism, an approach like this could be as effective as and safer than existing drugs that treat MS."

    "Vitamin D doesn't seem to cause global immunosuppression," she noted. "What's interesting is that the T cells are primed, but they are being kept away from the places in the body where they can do the most damage."

    Johns Hopkins is currently conducting a trial of vitamin D in MS patients that will help determine whether supplementing with the vitamin is beneficial to humans.

     

     

     

     

    Grape seed compound demonstrates anticancer effect in prostate cancer cells

    Grape seed compound destroys prostate cancer cellsDecember 6 2013.  The journal Nutrition and Cancer published an article on November 5, 2013 in which researchers from the University of Colorado report an anticancer effect for a compound found in grape seed extract known as B2 3,3”-di-O-gallate (B2G2) in prostate cancer cells.

    The research is the result of years of investigating grape seed’s anticancer action. Working in the laboratory of Chapla Agarwal, PhD, of the University of Colorado Cancer Center, Alpna Tyagi, PhD and colleagues found that the administration of B2G2 isolated from grape seed extract as well as synthesized B2G2 resulted in cell growth inhibition, cell cycle arrest and apoptosis (programmed cell death) in several human prostate cancer cell lines. The compound was discovered to inhibit nuclear factor kappa-beta (NF-kB) transcriptional activity and other factors.

    “We’ve shown similar anticancer activity in the past with grape seed extract, but now we know B2G2 is its most biologically active ingredient which can be synthesized in quantities that will allow us to study the detailed death mechanism in cancer cells,” Dr Tyagi remarked. “Our goal all along has been a clinical trial of the biologically active compounds from grape seed extract against human cancer. But it’s difficult to earn FDA approval for a trial in which we don’t know the mechanisms and possible effects of all active components. Therefore, isolating and synthesizing B2G2 is an important step because now we have the ability to conduct more experiments with the pure compound. Ongoing work in the lab further increases our understanding of B2G2′s mechanism of action that will help for the preclinical and clinical studies in the future.”

     

     

     

     

    Deficiency = damage

    Deficiency = damageDecember 4 2013.  Vitamin D’s benefits to the bone are well known, but what is perhaps more important is its more recently recognized role in the brain. In the December, 2013 issue of the journal Free Radical Biology and Medicine researchers at the University of Kentucky report a damaging effect in the brains of rats that consumed vitamin D deficient diets for three to four months.

    "Given that vitamin D deficiency is especially widespread among the elderly, we investigated how during aging from middle-age to old-age how low vitamin D affected the oxidative status of the brain," stated lead author Allan Butterfield, who is a professor in the Department of Chemistry at the University of Kentucky and director of the Free Radical Biology in Cancer Core of the Markey Cancer Center. “Adequate vitamin D serum levels are necessary to prevent free radical damage in brain and subsequent deleterious consequences."

    Dr Butterfield and his colleagues divided 27 one-year-old rats to receive diets that provided the same amount of calories but contained low, normal or high amounts of vitamin D. After four to five months on the diets, the animals’ brains were examined for markers of oxidative and nitrosative stress.

    Rats in the low vitamin D group showed increased nitrosative stress, which damages the cells. They also observed changes in the levels of several brain proteins, three of which are involved in glycolysis (the metabolic breakdown of glucose that releases energy). “These results suggest that dietary vitamin D deficiency contributes to significant nitrosative stress in brain and may promote cognitive decline in middle-aged and elderly adults,” the authors conclude.

    Dr Butterfield suggests that people get their blood tested to determine their vitamin D levels, and that they consume foods that are high in the vitamin and add vitamin D supplements if needed.

     

     

     

     

    “Healthy obesity” questioned

    “Healthy obesity” questioned 

    December 2 2013.  The results of a review and meta-analysis published on December 2, 2013 in the Annals of Internal Medicine suggest that so-called “healthy obesity,” characterized by an obese body mass index (BMI) in the absence of adverse metabolic features such as disordered lipids, elevated blood glucose or hypertension, is not as healthy as was once believed.

    Researchers from Mount Sinai Hospital and the University of Toronto selected twelve observational studies that included a total of 67,127 subjects for their review. Studies included those that evaluated all-cause mortality and/or cardiovascular events, BMI, and metabolic status as defined by the presence of metabolic syndrome components. Researchers from Mount Sinai Hospital and the University of Toronto selected twelve observational studies that included a total of 67,127 subjects for their review. Studies included those that evaluated all-cause mortality and/or cardiovascular events, BMI, and metabolic status as defined by the presence of metabolic syndrome components. Researchers from Mount Sinai Hospital and the University of Toronto selected twelve observational studies that included a total of 67,127 subjects for their review. Studies included those that evaluated all-cause mortality and/or cardiovascular events, BMI, and metabolic status as defined by the presence of metabolic syndrome components. Researchers from Mount Sinai Hospital and the University of Toronto selected twelve observational studies that included a total of 67,127 subjects for their review. Studies included those that evaluated all-cause mortality and/or cardiovascular events, BMI, and metabolic status as defined by the presence of metabolic syndrome components. While normal weight, overweight and obese subjects that were considered metabolically unhealthy had an elevated risk of mortality and/or cardiovascular events in comparison with metabolically healthy subjects over the course of the studies, those who were metabolically healthy but obese had a 24% greater risk of dying from all causes over ten years or more of follow-up compared to metabolically healthy normal-weight individuals.

    “These data suggest a model in which excess weight is associated initially with the development of subclinical metabolic and vascular dysfunction that ultimately leads to an increased incidence of cardiovascular events and mortality over the long term,” Caroline K. Kramer, MD, PhD, and her coauthors write. “In this regard, previous reports that evaluated metabolically healthy obese individuals over short-term follow-up or that compared these individuals to control groups not fully characterized for cardiovascular risk might have contributed to the concept of a ‘benign obesity’ phenotype that is not associated with adverse outcomes. Our results do not support this concept of ‘benign obesity’ and demonstrate that there is no ‘healthy’ pattern of obesity.”

    The authors of an editorial published in the same issue of the journal remark that physicians should focus on treating the obesity in the same manner as any other chronic disease that requires long term treatment.

     

     

     

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