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Want to live longer? Try being happy
October 31, 2011. While enduring hunger pangs and engaging in grueling exercise regimens have their adherents among those seeking a longer life span, a study described in an article published online this week in the Proceedings of the National Academy of Sciences reveals a possible survival benefit for simply being happy.
For their research, Andrew Steptoe and Jane Wardle of University College London analyzed data from 3,853 participants aged 52 to 79 years in the English Longitudinal Study of Aging, a cohort of older men and women living in England. Positive affect was assessed by having the subjects rate their feelings of happiness or anxiety four times during the course of a day, a method that avoids reliance on the ability to recall past emotions. The participants were followed for five years, during which any deaths were ascertained.
Positive affect among the participants was categorized as high, medium or low. Among those who rated themselves happiest, 3.6 died over follow-up, compared with 4.6 percent of the medium-rated group and 7.3 percent of those who rated themselves least happy. Those in the highest group had a 35 percent adjusted lower risk of dying compared with those who reported feeling least happy. Anxiety appeared to have little impact on survival. Although those with a higher positive affect reported better self-rated health and less depression, there were no significant differences in the incidence of serious diseases, alcohol intake, ethnicity, employment or education compared with those in the other groups.
"Momentary positive affect may be causally related to survival, or may be a marker of underlying biological, behavioral, or temperamental factors, although reverse causality cannot be conclusively ruled out," the authors write. "The results endorse the value of assessing experienced affect, and the importance of evaluating interventions that promote happiness in older populations."
Vitamin B6 derivative shows promise in reducing the progression of less advanced kidney disease
October 27 2011. An article appearing in the Journal of the American Society Nephrology reveals the finding of researchers from the Collaborative Study Group of a protective effect for a vitamin B6 derivative called Pyridorin (pyridoxamine dihydrochloride) against the progression of mild kidney disease in patients with diabetic nephropathy. Diabetes is a common cause of kidney failure, and the incidence of kidney disease in the U.S. is increasing due to the growing number of diabetics.
In a double-blinded trial, Edmund J. Lewis, MD of Rush University Medical Center and his associates assigned 317 diabetics with protein in their urine to receive 150 milligrams or 300 milligrams Pyridorin, or a placebo twice daily for one year. Serum creatinine, a marker of kidney function, was measured before and at the end of the treatment period. Although the change in creatinine did not differ significantly by the end of the study between those that received Pyridorin and those that received a placebo, when the participants were analyzed according to their renal function at the beginning of the study, a different picture emerged. Among those whose initial serum creatinine levels were among the lowest third (indicating less advanced kidney dysfunction), treatment with the higher dose of Pyridorin was associated with a 50 percent lower rise over the course of the study compared to the placebo.
The authors note that Pyridorin alters the ability of glucose to form advanced glycation end products that have been implicated in the development of diabetic kidney lesions. Additionally, Pyridorin has the ability to trap malondialdehyde, a compound involved in lipid peroxidation.
"It appears the drug may be beneficial in a sub-group of patients with only mild kidney disease but does not appear to be beneficial for patients with more advanced kidney disease," Dr Lewis observed. "The results warrant further trials in patients with mild diabetic kidney disease."
Seven could give you ten
October 27 2011. A presentation on October 23, 2011 at the Canadian Cardiovascular Congress held in Vancouver recommends the adoption of seven simple measures that could add ten years or more to the average life span.
Dr Clyde Yancy of Northwestern University's Feinberg School of Medicine predicts that "Achieving these seven simple lifestyle factors gives people a 90 per cent chance of living to the age of 90 or 100, free of not only heart disease and stroke but from a number of other chronic illnesses including cancer. By following these steps, we can compress life-threatening disease into the final stages of life and maintain quality of life for the longest possible time."
The steps recommended for Canadians and others include increasing physical activity, knowing and controlling cholesterol levels, following a healthy diet, knowing and controlling blood pressure, achieving and maintaining a healthy weight, managing diabetes and not smoking. These factors, while well known to help reduce the risk of heart attack and stroke, are practiced regularly by only less than 10 percent of the population. "We know how to prevent heart disease and stroke – we now need to build the tools to empower our citizens to manage their risk and prevent heart disease," Dr Yancy noted.
Heart and Stroke Foundation of Canada president Bobbe Wood agreed that "Healthy living is key to preventing heart disease and stroke. The Foundation is committed to raising awareness about heart health and to promoting public policies that facilitate healthy lifestyles and communities."
"The opportunity for prevention is not an unrealistic expectation," Dr Yancy affirmed. "Over the past 40 years the rates of heart disease and stroke have steadily declined."
However, given the rising incidence of obesity and diabetes, he emphasized that "We need to act now."
Broccoli compound improves steroid response in COPD patients
October 24 2011. An article published online on October 17, 2011 in the Journal of Clinical Investigation revealed that sulforaphane, a compound that occurs in broccoli and other cruciferous vegetables, improves sensitivity to corticosteroid drugs used to treat chronic obstructive pulmonary disease (COPD), a disease that is mainly result of smoking, characterized by chronic bronchitis and emphysema. The disease is currently treated with corticosteroids, however, the drugs only reduce symptoms by approximately 20 percent.
Individuals diagnosed with COPD experience a reduction in their lungs of histone deacetylase 2 (HDAC2), a substance that is essential to the anti-inflammatory pathway initiated by steroid drugs. In the current research, a team from Johns Hopkins University discovered that S-nitrosylation of HCAC2 due to cigarette smoke exposure resulted in HDAC2 dysfunction in lung macrophages derived from individuals with COPD. "This study provides the mechanism of exaggerated inflammation observed in COPD patients during exacerbations, which has been a barrier to developing effective therapy," stated coauthor Rajesh Thimmulappa, PhD, who is an assistant scientist at Johns Hopkins Bloomberg School of Public Health's Department of Environmental Health Sciences.
It was further discovered that sulforaphane denitrosylates HDAC2, which restored corticosteroid sensitivity. In previous research, the team demonstrated that sulforaphane activates a pathway known as Nrf2. "Restoring corticosteroid sensitivity in patients with COPD by targeting the Nrf2 pathway holds promise for effectively treating exacerbations," noted senior author Shyam Biswal, PhD, who is a professor at the Bloomberg School's Department of Environmental Health Sciences and Division of Pulmonary and Critical Care Medicine.
"Nrf2 activators such as sulforaphane can counteract oxidative and nitrosative stress and mediate glutathione-dependent denitrosylation, thereby restoring HDAC2 activity," the authors write. "The small-molecule Nrf2 activator sulforaphane may be useful as an adjuvant therapy to augment the antiinflammatory effects of glucocorticosteroids in COPD and other inflammatory diseases."
Large analysis links exercise with reduced mortality over a decade
October 21 2011. A meta-study described online on September 5, 2011 in the International Journal of Epidemiology confirms the benefit of regular exercise in contributing to a reduction in deaths from all causes in men and women over an eleven year period.
For their review, Guenther Samitz of the University of Vienna and his associates evaluated data from 80 studies that included 1,338,143 participants who were free of cardiovascular disease, cancer and other chronic conditions upon enrollment. Over a median of eleven years, 118,121 deaths occurred.
When subjects with the highest total activity levels were compared with those whose levels were lowest, a 35 percent reduction in mortality from all causes was observed. Reductions were also observed for those whose leisure activity, activities of daily living and occupational activity levels were higher. The benefit of exercise was more pronounced among women—a finding that may be the result of modifications of female hormone levels, estrogen metabolism and body fat distribution.
Every hour per week increase in vigorous exercise was associated with a 9 percent lower risk of dying over follow up. Those engaging in 5 hours per week of vigorous activity or athletics experienced a 39 percent reduction in mortality risk compared to the remainder of the subjects, while engaging in moderate-intensity activities of daily living was associated with a 19 percent reduction in risk. "Any physical activity is better than none and even activities of daily life are associated with a survival benefit, but more and vigorous-intensity physical activity are associated with a larger reduction in all-cause mortality." Dr Samitz explained. "Nonetheless, sedentary adults should start with moderate-intensity physical activities and slowly increase weekly dose and intensity, because in sedentary adults vigorous-intensity physical activity is associated with increased risk of musculoskeletal injuries and adverse cardiac events."
Acetyl-L-carnitine reduces Alzheimer-like changes associated with elevated homocysteine
October 14 2011. An article published online on October 6, 2011 in the journal Rejuvenation Research describes a role for supplementation with acetyl-L-carnitine (ALC) in reducing the effects of high levels of homocysteine that are associated with some of the features of Alzheimer's disease.
In their introduction to the article, Peng Zhou and colleagues at Huazhong University of Science and Technology in China remark that Alzheimer's disease-like changes including cognitive dysfunction, disrupted blood-brain barrier integrity, increased amyloid-beta levels and tau hyperphosphorylation have observed in mice in which elevated homocysteine levels were induced. Studies have shown that acetyl-L-carnitine reduces some of the cognitive impairment and functional degeneration found in humans with Alzheimer's disease. While in vitro experiments have suggested that acetyl-L-carnitine can reduce amyloid beta neurotoxicity, it had not previously been known whether the amino acid would have a beneficial effect in an animal model.
For the current experiment, 40 rats received water maze training prior to injection with homocysteine or saline for 14 days. Half of the animals in each group were given drinking water supplemented with acetyl-L-carnitine for the two week treatment period. Water maze tests were conducted before and after treatment to assess cognitive function.
Among homocysteine-treated rats that received acetyl-L-carnitine, memory deficits, tau hyperphosphorylation and amyloid beta accumulation were reduced in comparison with animals that did not receive the amino acid. The team additionally found that supplementing with ALC suppressed amyloid beta precursor protein phosphorylation, which is a possible mechanism for the reduction of amyloid beta observed in the study.
"We found that supplement of ALC by drinking water for two weeks could effectively reverse the homocysteine-induced tau protein hyperphosphorylation, amyloid beta accumulation, and memory deficits in rats," the authors conclude. "Our data suggest that ALC may serve as a promising candidate for Alzheimer's disease therapy."
Vitamin D essential to combat TB
October 12 2011. In an article published online on October 12, 2011 in Science Translational Medicine Dr Robert Modlin and his colleagues at the University of California, Los Angeles report an essential role for vitamin D in the body's ability to fight tuberculosis (TB).
The rate of infection for tuberculosis is highest in certain areas of Africa–a fact that may be due to a reduced ability to manufacture vitamin D among individuals with darker skin. In previous research conducted by the team, the vitamin was found to be involved in the production of cathelicidin, which aids the innate immune system's response to tuberculosis infection. In the current study, Dr Modlin and his colleagues discovered that it is necessary to have a sufficient amount of vitamin D in the body in order for white blood cells known as T-cells to release interferon-gamma, which directs infected immune cells to attack the tuberculosis bacteria. When the team subsequently tested the immune responses of blood samples obtained from humans with and without sufficient vitamin D levels, serum from those with vitamin D insufficiency failed to stimulate an immune response; however, the response was restored upon the addition of vitamin D.
"The role of interferon has been speculated for years in numerous studies, but previous research didn't take into account that sufficient vitamin D was needed to help interferon-gamma trigger an effective immune response," stated study coauthor Dr John Adams. "Now we understand better how this chain reaction works."
"Over the centuries, vitamin D has intrinsically been used to treat tuberculosis," noted first author Mario Fabri. "Sanatoriums dedicated to tuberculosis patients were traditionally placed in sunny locations that seemed to help patients -- but no one knew why this worked."
"Our findings suggest that increasing vitamin D levels through supplementation may improve the immune response to infections such as tuberculosis," he concluded.
Free radicals implicated in cancer immunotherapy failures
October 10, 2011. An article published in the October 3, 2011 issue of The Journal of Clinical Investigation reports the finding of researchers at Tampa's H. Lee Moffitt Cancer Center of a mechanism involving the production of the free radical peroxynitrite in tumor cell resistance to a type of cancer immunotherapy.
In an earlier investigation in mice, the research team found that myeloid-derived suppressor cells are a source of peroxynitrite. For the current study, Moffitt Department of Immunology senior member Dmitry Gabrilovich, MD, PhD and his colleagues pretreated mouse and human cells with myeloid-derived suppressor cells or peroxynitrite prior to immunotherapy that involves cytotoxic T-cell responses. This resulted in resistance of the tumor cells to antigen-specific cytotoxic T-cells, an effect that was prevented by treatment of myeloid-derived suppressor cells with a peroxynitrite inhibitor. "We set out to investigate one possible explanation for the failure of cytotoxic T-cells to eliminate tumors," Dr Gabrilovich stated. "We found that therapeutic failure was the result of the presence of the free radical peroyxnitrite, or PNT."
"The results suggest that PNT might be affecting the binding of specific peptides," he remarked. "The data suggests that PNT affects the formation of certain peptide complexes, preventing the cytotoxic T-cells' killing of tumor cells."
Dr Gabrilovich's team sought to confirm the location of PNT in human lung, breast and pancreatic tumor myeloid cells by staining the tissues with nitrotyrosine, a marker of PNT activity. "In each type of tumor, nitrotyrosine staining was significantly higher in myeloid cells than in tumor cells or epithelial cells," Dr Gabrilovich explained. "The data suggests that these cells are the major source of PNT and tumor cell resistance to cytotoxic T-cells."
As to how to prevent the escape of tumors from immune control, he concluded that "This research also suggests that this escape can be diminished by blocking PNT production by using pharmacological inhibitors."
More vitamin D means less pain
October 7, 2011. Older men and women suffering from moderate to extreme chronic pain are likelier than others to have decreased vitamin D levels, according to the results of a report published online on September 29, 2011 in the British Journal of Nutrition.
Vasant Hirani of University College London Medical School reported the outcome of an analysis of serum 25-hydroxyvitamin D levels and pain in 2,070 men and women aged 65 years and older who took part in the 2005 annual Health Survey for England, which assessed health and health-related behaviors in children and adults. Demographic information, medication and supplement use, illnesses, pain symptoms and other data were obtained from interview responses.
Fifty-three percent of the respondents reported experiencing moderate or extreme pain or discomfort. Of these subjects, 80 percent had long-standing illnesses and 60 percent had been diagnosed with musculoskeletal conditions.
The odds of experiencing moderate to severe pain decreased with rising levels of serum 25-hydroxyvitamin D. For those who reported moderate to extreme pain, the odds of having deficient vitamin D levels of less than 25 nanomoles per liter were double that of subjects who did not report pain. While adjustment for general health status weakened the association, it did not significantly weaken after adjustment for age or vitamin D supplementation.
Dr Hirani notes noted that previous studies have found a reduction in pain among individuals who supplemented with vitamin D, and that the active form of the vitamin may play a role in reducing inflammation. "The clinical implications of these findings are that health professionals should be alerted to complaints presented to them by older people, such as pain, muscle and bone pain, so that appropriate interventions can be provided, as both conditions are common in older people and both have adverse health consequences," he concluded.
Vitamin D deficiency associated with advanced cancer
October 5, 2011. The 53rd Annual Meeting of the American Society for Radiation Oncology (ASTRO) was the site of a presentation on October 2, 2011 of the finding of a high prevalence of vitamin D deficiency among cancer patients. The lowest vitamin D levels were uncovered in those with advanced disease.
Thomas Churilla and his associates measured serum 25-hydroxyvitamin D in 160 men and women with a median age of 64 who scheduled a consultation at Northeast Radiation Oncology Center in Dunmore, Pennsylvania. The most common types of cancer diagnosed were those of the breast, colon/rectum, lung, thyroid and prostate.
Seventy-seven percent of the participants had suboptimal or deficient levels of vitamin D, defined as less than 20 nanograms per milliliter or between 20 and 30 nanograms per milliliter, respectively. Levels below the median of 23.5 nanograms per milliliter predicted advanced disease. Supplementation with vitamin D was effective in remedying deficiency, however, it is too soon to know what effect the treatment will have on the subjects' long-term outcomes.
"Until recently, studies have not investigated whether vitamin D has an impact on the prognosis or course of cancer," stated Churilla, who is a medical student at Commonwealth Medical College in Scranton, Pennsylvania. "Researchers are just starting to examine how vitamin D may impact specific features of cancer, such as the stage or extent of tumor spread, prognosis, recurrence or relapse of disease, and even subtypes of cancer."
"The benefits of vitamin D outside of improving bone health are controversial, yet there are various levels of evidence to support that vitamin D has a role in either the prevention or the prediction of outcome of cancer," he added. "Further study is needed to continue to understand the relationship between vitamin D and cancer."
N-acetylglucosamine may help combat MS
October 3, 2011. In an article published online on September 29, 2011, in The Journal of Biological Chemistry, researchers at the University of California, Irvine report that N-acetylglucosamine, a form of glucosamine (commonly used for arthritis), could be helpful in the treatment of multiple sclerosis, an autoimmune disease that affects an estimated 2.5 million men and women worldwide.
In their introduction to the article, Dr Michael Demetriou and colleagues remark that “Current treatments and emerging oral therapies for multiple sclerosis (MS) are limited by effectiveness, cost and/or toxicity.” In previous research, the team found that inherited and environmental risk factors converge to influence the manner in which specific sugars are added to proteins that regulate the disease.
The current study utilized a mouse model of MS-like autoimmune disease. Dr Demetriou’s team found that orally administered N-acetylglucosamine suppressed T-cell hyperactivity and autoimmune response when given after the onset of the disease via greater sugar modifications to T cell proteins. “This sugar-based supplement corrects a genetic defect that induces cells to attack the body in MS making metabolic therapy a rational approach that differs significantly from currently available treatments,” explained Dr Demetriou, who is an associate professor of neurology and microbiology & molecular genetics at UC Irvine.An earlier study conducted by Dr Demetriou found that supplementation with N-acetylglucosamine was associated with a reduction in the growth and function of T-cells responsible for autoimmune attack in a mouse model of diabetes. Other research found improvements in autoimmune inflammatory bowel disease after two years of treatment with the compound. “Together, these findings identify metabolic therapy using dietary supplements such as N-acetylglucosamine as a possible treatment for autoimmune diseases,” Dr Demetriou stated. “Excitement about this strategy stems from the novel mechanism for affecting T-cell function and autoimmunity — the targeting of a molecular defect promoting disease — and its availability and simplicity.”
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