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.
Subnormal selenium levels linked with increased mortality over 6.8 year period
June 29 2015. On June 24, 2015 the European Journal of Clinical Nutrition reported an association between decreased serum selenium levels and a greater risk of mortality in an older population over a period of 6.8 years.
"About half of the selenium in whole blood is found in the plasma, of which selenoprotein P (SEPP1) usually constitutes more than 60% and glutathione peroxidase constitutes 25%," U. Alehagen and colleagues write. "SEPP1 contains up to 10 selenocysteine residues and is the means of transporting selenium around the body to tissues that need it. It has an antioxidative role in the blood and, among other biological effects, it is believed to be active in endothelial protection."
The investigation included 449 older men and women who participated in an epidemiologic project in southeast Sweden. Serum selenium levels were measured upon enrollment in the current study and in 98 subjects after 48 months. Selenium levels averaged 67.1 micrograms per liter at the beginning of the study in January 2003.
Through February 2010 there were 122 deaths from all causes, including 85 that were attributable to cardiovascular disease. Among those whose selenium levels were among the lowest 25% of subjects, there was an adjusted 43% increase in the risk of dying from any cause and a 56% risk of cardiovascular mortality in comparison with the remainder of the study population.
"The mean serum selenium concentration in an elderly Swedish population was 67.1 micrograms/liter, which is below the physiological saturation level for several selenoprotein enzymes," the authors conclude. "This result may suggest the value of modest selenium supplementation in order to improve the health of the Swedish population."
Cancer drug increases lifespan in experimental research
June 26 2015. Research conducted at University College London reveals a life extension benefit in fruit flies for the drug trametinib, which inhibits Ras signaling in skin cancer. The finding was described in an article published on June 25, 2015 in the journal Cell.
"Our aim is to understand the mechanisms of aging and alter the processes that lead to loss of function and to disease," commented Nazif Alic of the UCL Institute of Healthy Ageing, who is one of the first authors of the report. "We studied this molecular pathway in flies because they are reasonably complex and yet age more quickly than mammals. We were able to extend their lifespan both genetically and by using a cancer drug to target the Ras pathway, which provides us with the first evidence for the antiaging potential of drugs developed to dampen this pathway."
By adding an amount of trametinib to the flies' diets that was equivalent to the daily dose given to human cancer patients, average life expectancy increased by 8%. Giving the flies a higher dose of the drug resulted in a life span that averaged 12% longer.
"Identifying the importance of the Ras-Erk-ETS pathway in animal aging is a significant step on the way to developing treatments that delay the onset of aging," noted co-first author, Cathy Slack. "The pathway is the same in humans as it is in flies and, because the Ras protein plays a key role in cancer, many small molecule drugs already exist, some of which have been approved for clinical use. With support from pharma, we can refine these molecules over the next 10-20 years to develop anti-aging treatments which don't have the adverse effects of cancer drugs."
Periodic low calorie diet might be all that's necessary to obtain benefits of prolonged fasting
June 24 2015. An article published on June 18, 2015 in Cell Metabolism reports that periodic fasting could provide some of the same benefits as prolonged fasting. Fasting, an intensive form of dietary restriction, has been associated with numerous health benefits and has prolonged life span in experimental models.
"Strict fasting is hard for people to stick to, and it can also be dangerous, so we developed a complex diet that triggers the same effects in the body," stated lead researcher Valter Longo, of the University of Southern California Longevity Institute.
Following positive findings in yeast, mice were administered diets that included bi-monthly cycles of four days of a low calorie regimen or a control diet that provided the same amount of calories per month beginning in middle age. Dr Longo's team observed a decrease in visceral fat, skin lesions and cancer, accompanied by slowed bone mineral density loss, immune system rejuvenation and greater longevity in the periodically fasted group comparison with a control group. The treatment group also had enhanced hippocampal neurogenesis and better cognitive performance compared to the control animals.
In a pilot study involving 19 human participants, three cycles of a similar diet for five days was associated with a reduction in biomarkers for aging, cardiovascular disease, cancer and diabetes. "It's about reprogramming the body so it enters a slower aging mode, but also rejuvenating it through stem cell-based regeneration," Dr Longo explained. "It's not a typical diet because it isn't something you need to stay on."
"If the results remain as positive as the current ones, I believe this fasting mimicking diet will represent the first safe and effective intervention to promote positive changes associated with longevity and health span, which can be recommended by a physician," he added.
Meta-analysis adds evidence to protective effect for vitamin E against nonalcoholic steatohepatitis
June 19 2015. A meta-analysis of randomized trials examining the effects of vitamin E supplementation in individuals with nonalcoholic steatohepatitis (NASH) affirmed a benefit for the vitamin in association with several facets of the disease. The analysis appeared this year in the International Journal of Clinical and Experimental Medicine.
"Non-alcoholic fatty liver disease (NAFLD) is characterized by fat accumulation in hepatocytes in the absence of significant alcohol intake," write Renfan Xu and colleagues at Huazhong University of Science and Technology. "The majority of patients with NAFLD have simple steatosis, which has a benign clinical outcome, whereas approximately 15%-20% of patients will progress to nonalcoholic steatohepatitis (NASH), which includes macrovesicular steatosis, hepatocyte ballooning, lobular inflammation and fibrosis and can develop into cirrhosis or even liver failure."
Dr Xu and associates selected three articles that met the criteria for their analysis, which included a total of 245 men and women with NASH. Trials involved daily supplementation with a placebo or vitamin E alone or in combination with other compounds. In the two studies that compared pretreatment to post-treatment histological factors, including steatosis (abnormal cellular retention of lipids), ballooning (a form of programmed cell death) and lobular inflammation, all were improved to a greater extent among those who received vitamin E by the end of the trials in comparison with the control groups. For all three trials, vitamin E supplementation was associated with improvement in fibrosis compared to controls.
"This meta-analysis revealed that vitamin E supplementation resulted in significant improvements in histological parameters in NASH patients," the authors conclude. "Additional large-scale high-quality studies are needed to investigate the effect of vitamin E supplementation on NASH patients with outcomes (histological parameters, biochemical variables and adverse events) oriented to obtain more comprehensive information on supplementation for clinical use."
Trial finds benefit for ubiquinol in Parkinson's disease
June 17 2015. A pilot trial evaluating the effects of the reduced form of CoQ10 known as ubiquinol in men and women with Parkinson's disease (PD) found improvement among a group of subjects experiencing "wearing off"—a return of symptoms that occurs when treating the disease with levodopa which indicates the need for adjustment of dosage or change in medication. The study, which appeared online on May 29, 2015 in the journal Parkinsonism & Related Disorders, is the first double-blinded, placebo-controlled trial of ubiquinol in Parkinson's disease patients.
"A recent trial of the oxidized form of CoQ10 for PD failed to show benefits; however, the reduced form of CoQ10 (ubiquinol-10) has shown better neuroprotective effects in animal models," write authors Asako Yoritaka of Japan's Juntendo University and associates. "These findings are in agreement with an observation of a higher plasma concentration of CoQ10 after ingestion of the reduced form versus the oxidized form, indicating that the reduced form is absorbed more efficiently."
The trial compared the effects of 300 milligrams ubiquinol to a placebo among a group of Parkinson's disease patients who had exhibited wearing off and another group of subjects with early disease not treated with levodopa. Participants in the first group were treated for 48 weeks, while those with early disease received 96 weeks of treatment. Unified Parkinson's Disease Rating Scale (UPDRS) scores were used to grade the subjects' symptoms before, during and after treatment.
By the end of the trial, the change in total UPDRS scores compared to baseline values indicated improved symptoms among the first group. The study authors concluded that ubiquinol "…is effective in treating PD, perhaps by reversing mitochondrial abnormalities characteristic of Parkinson's disease," and they suggest that "It is important to confirm these effects in a larger clinical study."
Aspirin study indicates protective effect against breast cancer
June 15 2015. In the July 2015 issue of Laboratory Investigation, researchers at the Kansas City Veterans Affairs Medical Center in Missouri report a protective effect for aspirin (acetylsalicylic acid) against the development of breast cancer in cell cultures and in mice that received tumor implants. The current findings also suggest a role for aspirin in preventing breast cancer relapse.
By administering varying doses of aspirin to breast cancer cell cultures, Dr Sushanta K. Banerjee of the VA's Cancer Research Unit and colleagues found an increase in the rate of cell death and a reduction in growth among surviving cells. In mice that received implanted breast cancer tumors, 15 days of low dose aspirin therapy resulted in tumors that were 47% smaller on average than those of animals who did not receive the drug. And in another experiment, mice that were pretreated with aspirin for 10 days prior to cancer cell exposure were found to have less cancerous growth in comparison with those that were not pretreated. "We find that acetylsalicylic acid not only prevents breast tumor cell growth in vitro and tumor growth in nude mice xenograft model through the induction of apoptosis, but also significantly reduces the self-renewal capacity and growth of breast tumor-initiating cells (BTICs)/breast cancer stem cells (BCSCs) and delays the formation of a palpable tumor," the authors report.
"We found aspirin caused these residual cancer cells to lose their self-renewal properties," Dr Banerjee explained. "Basically, they couldn't grow or reproduce. So there are two parts here. We could give aspirin after chemotherapy to prevent relapse and keep the pressure on, which we saw was effective in both the laboratory and the mouse model, and we could use it preventatively."
NAC extends maximum life span in C. elegans
June 8 2015. A report published in the journal Clinics reveals a life-extending effect for the amino acid N-acetylcysteine (NAC) in C. elegans, a roundworm frequently used in gerontological research.
"In this study, we examined the effect of NAC supplementation on resistance to various environmental stressors, including oxidative stress, heat shock, and ultraviolet (UV) irradiation in vivo," Seung-Il Oh and colleagues write. "We also determined whether NAC can extend lifespan and affect fertility, which is closely related to aging."
In the first experiment, 60 worms were given varying concentrations of NAC or no NAC followed by the herbicide paraquat, an inducer of oxidative stress. The researchers observed longer survival among worms that received all but the highest concentration of NAC. In another experiment, worms received three different concentrations of NAC throughout their lives and their lifespan was compared with untreated worms. Both average and maximum lifespan significantly increased in worms treated with the two highest concentrations of NAC.
To test the effect of NAC on heat shock stress resistance, three day old worms treated with NAC were placed in a 35 degree Celsius environment for 10 hours after which they were transferred back to a 20 degree environment. Forty percent of the NAC-treated worms remained alive following 10 hours of heat exposure, in comparison with 29.6% of untreated worms exposed to the same heat environment. In other experiments, NAC improved survival following exposure to ultraviolet radiation, boosted fertility, and increased the expression of genes related to longevity.
"Our results suggest that dietary supplementation with NAC can modulate an organism’s response to environmental stressors and aging, potentially through the induction of stress-responsive transcriptional markers and genes associated with longevity," the authors conclude. "Further studies should identify the cellular signaling pathways involved in NAC-induced longevity and reveal the underlying cellular mechanisms of aging in C. elegans."
Higher carotenoid levels associated with breast cancer protection
June 5 2015. A case-control study reported in the June 2015 issue of the American Journal of Clinical Nutrition found a protective effect for high plasma levels of carotenoids against the risk of developing breast cancer.
The study included 2,188 Nurses' Health Study participants who developed breast cancer over the 20 years following an initial blood sample collection during 1989-1990, and an equal number of matched controls who did not develop the disease. Initial and subsequently collected blood samples were analyzed for plasma alpha carotene, beta carotene, beta cryptoxanthin, lutein and zeaxanthin, and lycopene.
Among women whose total carotenoid levels were among the top 20% of subjects, there was a 23% lower risk of breast cancer in comparison with those whose levels were among the lowest 20%. Among individual carotenoids, alpha carotene, beta carotene, and lycopene were significantly protective. High levels of carotenoids were more protective against recurrent or lethal breast cancer than nonrecurrent and nonlethal disease, with whose total carotenoid levels were among the top fifth experiencing half the risk of recurrent or lethal disease than those whose levels were lowest.
"These results suggest carotenoids may inhibit tumor initiation, which is compatible with hypothesized mechanisms, including the conversion of provitamin A carotenoids to retinol, which regulates cell growth, differentiation, and apoptosis, and the antioxidant capacity to scavenge reactive oxygen species and prevent DNA damage," write A. Heather Eliassen of Harvard University and colleagues.
"Because intake of fruit and vegetables is beneficial for many reasons, the association of higher plasma carotenoid concentrations with lower risk of aggressive and lethal breast cancer may encourage women to increase their consumption of carotenoid-rich fruit and vegetables," they conclude.
AMPK slows age-related muscle loss
June 3 2015. In an article appearing on June 3, 2015 in Cell Metabolism, scientists from McMaster University describe the role of AMPK, an enzyme that activates autophagy, in maintaining muscle mass. Previous research by the team revealed that the enzyme is activated by exercise as well as the drug metformin.
The current research utilized mice that were modified to lack skeletal muscle AMPK. Fasting animals that were deficient in the enzyme exhibited low blood sugar due to insufficient levels of an amino acid needed for gluconeogenesis that was caused by a reduction in the breakdown of muscle protein. The animals also exhibited reduced muscle and mitochondrial function.
"We found that the body's fuel gauge, AMP-activated protein kinase (AMPK), is vital to slow muscle wasting with aging," reported lead researcher Gregory Steinberg, who is a professor of medicine at McMaster's Michael G. DeGroote School of Medicine and codirector of the Metabolism and Childhood Obesity Research Program. "Mice lacking AMPK in their muscle developed much greater muscle weakness than we would have expected to see in a middle-aged mouse. Instead these mice, which were the equivalent of being just 50 years old, had muscles like that of an inactive 100-year-old."
"It is known that AMPK activity in muscle is 'dialed down' with aging in humans, so this may be an important cause of muscle loss during aging," he added. "We know we can turn on the AMPK pathway with intense exercise and commonly-used Type 2 diabetes medications. By knowing that AMPK is vital for maintaining muscle mass with aging, we can now try to adapt exercise regimes and existing drugs to switch on AMPK in muscle more effectively. The development of new selective activators of the AMPK pathway in muscle may also be effective to prevent muscle loss with aging."
Metformin use associated with reduced glaucoma risk
June 1 2015. The results of research published in the August 2015 issue of JAMA Ophthalmology reveal a protective effect for metformin, a diabetes drug that has shown calorie restriction mimetic properties, against the risk of developing glaucoma in a diabetic population.
Julia E. Richards, PhD, of the University of Michigan and her colleagues examined the medical records of 150,016 diabetics aged 40 and older with no history of open-angle glaucoma (OAG) prior to January 1, 2001. Glaucoma was diagnosed in 5,893 subjects during the subsequent decade. Metformin hydrochloride use was documented among 40.1% of the subjects, sulfonylureas were used by 31%, thiazolidinediones were used by 23.8%, meglitinide by 2.4%, and insulin by 22.6% of the group.
For those whose metformin use was among the highest quarter of subjects, a 25% lower risk of developing glaucoma was observed in comparison with those who did not use the drug. Dr Richards and her associates predicted that a standard dose 2 gram per day dose of metformin taken for two years would result in a 20.8% reduction in open angle glaucoma risk compared to the risk experienced by nonusers.
"Metformin use is associated with reduction in risk of developing open angle glaucoma, and risk is reduced even when accounting for glycemic control in the form of glycated hemoglobin level," the authors conclude. "Other diabetes medications did not confer a similar OAG risk reduction. This study suggests that metformin may be affecting OAG risk on multiple levels, some involving improved glycemic control and some involving mechanisms outside glycemic control such as neurogenesis, inflammatory systems, or longevity pathways targeted by caloric restriction mimetic drugs. If confirmed by prospective clinical trials, these findings could lead to novel treatments for this sight-threatening disease."