What's Hot
What's Hot
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.
Medicare patients at risk of premature mortality due to high cost of medications
December 30 2020. A report released by the nonprofit West Health Policy Center on November 19, 2020 concluded that over 1.1 million Medicare recipients are at risk of dying during the next decade due to an inability to afford their prescribed medications.
Medicare beneficiaries currently pay 25% of their prescription drug costs.
“One of the biggest contributors to poor health, hospital admissions, higher healthcare costs and preventable death is patients failing to take their medications as prescribed,” explained West Health Policy Center president Timothy Lash. “Cost-related nonadherence is a significant and growing issue that is direct result of runaway drug prices and a failure to implement policies and regulations that make drugs more affordable.”
The cost of branded pharmaceutical drugs increased by 159% between 2007 and 2018 and continues to rise. The Centers for Medicare & Medicaid Services predicts that prescription drug spending will grow more rapidly than that of any major medical service or good during the next few years. If this increase continues, an estimated 112,000 premature deaths per year could occur among Medicare beneficiaries—more than the number attributable to diabetes, kidney disease or influenza. However, if Medicare were permitted to negotiate prices directly with drug companies, the result could be approximately 94,000 fewer lives lost and a savings to Medicare of $475.9 billion during the upcoming decade.
Sean Dickson, who is the Director of Health Policy at West Health Policy Center and Chair of the Council for Informed Drug Spending Analysis (a group of experts from leading academic institutions) asserted that “The costs of doing nothing about high drug prices are too high especially when policy changes such as allowing Medicare to negotiate drug prices would result in saving millions of lives and billions of dollars.”
—D Dye
High homocysteine, vitamin deficiencies more common in cognitively impaired adults
December 28 2020. The October 2020 issue of MEDICC Review published the finding of Cuban researchers of a greater incidence of high homocysteine levels and low levels of several vitamins among older men and women with mild cognitive impairment or Alzheimer disease.
The study included 43 Alzheimer disease patients, 131 individuals with mild cognitive impairment and 250 subjects without cognitive impairment who participated in Cuba’s Aging and Alzheimer Study. Blood samples were analyzed for levels of vitamins A, B1, B2, B12, C and folate, and homocysteine.
Compared to the cognitively healthy group, Alzheimer disease patients had over five times the prevalence of vitamin A deficiency, nearly two times the rate of being deficient in vitamin B1, nearly three times the rate of B2 deficiency, more than double the rate of vitamin B12 deficiency, nearly four times the rate of vitamin C deficiency, three times the rate of folate deficiency, and more than three times the rate of elevated homocysteine levels. Subjects with mild cognitive impairment also had a greater risk of having high homocysteine and deficiencies in vitamins A and B2.
“This is the first study in Cuba to examine vitamin and homocysteine levels in older adults with Alzheimer disease or mild cognitive impairment, and results show a relationship between these nutritional indicators and the cognitive disorders,” authors Yeneisy Lanyau-Domínguez, MS, PhD, and colleagues announced.
They remarked that the availability of antioxidant vitamins is decreased in cognitive disorders due to oxidative stress, which increases the body’s antioxidant requirement. Furthermore, deficient B vitamin levels due to insufficient intake is a cause of high homocysteine in older adults, which can contribute to cognitive impairment and Alzheimer disease through several mechanisms.
“Longitudinal studies are needed to further understand the relationship between different nutritional biomarkers and dementia,” they recommended.
—D Dye
Remnant cholesterol more strongly associated with cardiovascular events than LDL in study
December 18 2020. The December 8, 2020 issue of the Journal of the American College of Cardiology published the results of a study that examined the association of the occurrence of major cardiovascular events with triglyceride levels and cholesterol fractions in older men and women at risk of cardiovascular disease. The investigation uncovered a greater association of these events with remnant cholesterol [which is composed of very low-density lipoprotein (VLDL) and intermediate-density lipoprotein (IDL)] than with low-density lipoprotein (LDL) cholesterol, which is believed to be the primary driver of cardiovascular disease. Triglyceride levels were also found to have a significant association with the development of major cardiovascular events.
The investigation included 6,901 participants in the PREDIMED (Prevención con Dieta Mediterránea) trial, which compared the effects of a Mediterranean diet enhanced with extra-virgin olive oil or nuts to a control diet for the prevention of cardiovascular disease among at-risk individuals. Blood samples collected upon enrollment beginning in 2003 were analyzed for total, high-density lipoprotein (HDL) and LDL cholesterol, triglycerides and other factors. Remnant cholesterol was calculated by subtracting LDL and HDL cholesterol from total cholesterol levels.
Major adverse cardiovascular events occurred among 263 participants during the follow-up period, which concluded at the end of 2010. While LDL and HDL cholesterol were not significantly associated with major adverse cardiovascular events, each 10 milligram per deciliter increase in triglycerides, non-HDL cholesterol and remnant cholesterol was associated with 4%, 5% and 21% respective increases in risk.
In an accompanying editorial, John Burnett, Amanda Hooper and Robert Hegele predicted that “One could envision a future where in addition to the routine lipid profile, newer analytes such as remnant cholesterol as well as lipoprotein(a) and apo B are reported to improve prognostication and help guide preventive treatments.”
—D Dye
Healthy heart rate recovery supported by omega 3s
December 16 2020. The December 1, 2020 issue of Prostaglandins, Leukotrienes & Essential Fatty Acids published the finding of researchers at the Cooper Institute and the Fatty Acid Research Institute of an association between higher red blood cell levels of omega 3 fatty acids and more rapid heart rate recovery after exercise. Slow heart rate recovery is associated with a greater risk of sudden cardiac death, as have lower levels of omega 3.
"These new findings from the Cooper Center Longitudinal Study harmonize with the known benefits of omega 3 fatty acids on resting heart rate and provide new clues to how these important fatty acids can preserve cardiac health," commented coauthor William Harris, co-inventor of the Omega-3 Index.
The study included 13,912 healthy men and women who received comprehensive medical examinations at the Cooper Clinic. Exams included treadmill exercise testing and determination of the Omega-3 Index, which measures levels of the omega 3 fatty acids EPA and DHA in red blood cells. Heart rate measured one, three and five minutes after maximal exercise tests were used to calculate heart rate recovery.
An association was observed between higher Omega-3 Index values and better heart rate recovery, particularly among women. After adjustment for age and other factors, each 2% increase in the Omega-3 Index was associated with a 0.35 beat per minute greater heart rate recovery in men and a 0.69 beat per minute increase in women.
"These benefits on cardiac autonomic tone join other cardioprotective effects of omega 3 fatty acids, including the reduction in blood pressure, chronic inflammation and platelet aggregation, to at least partially explain why omega-3s are good for the heart,” Dr Harris commented. “Future treatment studies should define the omega 3 intake (and Omega-3 Index) that optimizes this aspect of cardiac function."
—D Dye
Mothers’ vitamin D deficiency may help explain boys’ greater risk of autism
December 14 2020. Research reported on December 10, 2020 in Molecular Autism suggests deficient maternal levels of vitamin D could be responsible for the higher risk of autism spectrum disorder (ASD) that occurs among male children.
“The ‘prenatal sex steroid’ hypothesis links excessive sex-steroid exposure during fetal life with the behavioral differences observed in ASD,” explained Asad Amanat Ali and colleagues at the University of Queensland in Australia. “However, the reason why sex steroid exposure may be excessive remains unclear.”
"Vitamin D is involved in pathways controlling many sex hormones," Dr Ali observed.
In previous research, corresponding author Darryl Eyles demonstrated that vitamin D is critical for brain development and that supplementing mice with the vitamin prevented ASD traits in their offspring. In the current study, it was discovered that vitamin D deficiency during pregnancy resulted in an increase in testosterone in the brains of male rat fetuses.
"The biological cause of autism spectrum disorder (ASD) is unknown, but we have shown that one of the many risk factors—low vitamin D in mothers—causes an increase in testosterone in the brain of the male fetuses, as well as the maternal blood and amniotic fluid," Dr Eyles stated. "In addition to its role in calcium absorption, vitamin D is crucial to many developmental processes.”
"Our research also showed that in vitamin D-deficient male fetuses, an enzyme which breaks down testosterone was silenced and could be contributing to the presence of high testosterone levels," he added. "We have only studied one risk factor for ASD -- vitamin D deficiency during development -- our next step is to look at other possible risk factors, such as maternal stress and hypoxia - lack of oxygen - and see if they have the same effect."
—D Dye
Melatonin enhances long-term memory
December 11 2020. Research reported on October 30, 2020 in the Journal of Pineal Research found evidence for improved long-term memory in association with the administration of the hormone melatonin and two of its metabolic byproducts.
"We know that melatonin is converted into N1-acetyl-N2-formyl-5-methoxykynuramine (AFMK) and N1-acetyl-5-methoxykynuramine (AMK) in the brain and we suspected that they might promote cognition," corresponding author Atsuhiko Hattori of Tokyo Medical and Dental University explained.
The study tested the effects of melatonin and its metabolites in mice given novel object recognition tasks to evaluate memory. This method of memory assessment is based on the observation that young mice indicate recognition of an object by spending less time with it after having been previously exposed to it than when exposed to it for the first time. Older mice are more likely to act as if both new and previously encountered objects are unfamiliar, which suggests the presence of cognitive decline.
Higher doses of melatonin, AMK or AFMK given an hour after mice were familiarized with objects resulted in better memory the following day compared to results associated with chance performance, with AMK showing the greatest benefit. In one experiment, old mice that received AMK 15 minutes after exposure to a new object remembered the object up to four days later. All compounds were found to have accumulated in the brain’s hippocampus, an area that is important for memory formation.
"We have shown that melatonin's metabolite AMK can facilitate memory formation in all ages of mice," Dr Hattori stated. "Its effect on older mice is particularly encouraging and we are hopeful that future studies will show similar effects in older people. If this happens, AMK therapy could eventually be used to reduce the severity of mild cognitive impairment and its potential conversion to Alzheimer's disease."
—D Dye
Melatonin’s anticancer effect explored
December 9 2020. A review and meta-analysis of microRNA networks identified genes potentially regulated by melatonin in some cancers.
MicroRNAs are small RNA molecules that have a role in post-transcriptional regulation of gene expression rather than encoding proteins.
“It’s essential to understand how the hormone influences molecular signaling at the genetic level as a guideline for personalized therapies based on melatonin,” commented first author Luiz Gustavo Chuffa, of São Paulo State University. “Most tumor cells have low levels of melatonin, but laboratory trials have shown that treatment with the hormone increases tumor cell death and reduces tumor cell proliferation, both of which are important to avoid progression of the cancer and metastasis.”
The meta-analysis, published in the November 2020 issue of the Journal of Pineal Research, was conducted to determine how melatonin regulates the expression of microRNAs and their target genes in a variety of cancers. “In this first stage, we found 14 quite recent studies that associated melatonin with altered microRNA expression,” Dr Chuffa reported. “For the seven cancers on which we focused, we found 46 microRNAs with altered expression.”
“When we cross-referenced the information with The Cancer Genome Atlas, a public database, we identified the target genes for these 46 microRNAs with altered expression,” he added. “These genes targeted by melatonin relate to important biological processes in cancer, such as cell cycle regulation, cell death, and cell migration and senescence. Melatonin appears to act more strongly on breast, oral, and stomach cancer.”
When the genes were compared to those of mice with breast cancer that were treated with melatonin, genes associated with immune response and programmed cell death were found to be upregulated and those related to metastasis and tumor aggressiveness were downregulated.
“Melatonin is a multitasking molecule and acts on various cellular substrates, so we’re now taking the study deeper to find out how the hormone influences microRNA expression and hence the regulation of the cellular mechanisms identified,” Dr Chuffa concluded.
—D Dye
Omega 3 fatty acids have different immune effects
December 7 2020. An article appearing on December 7, 2020 in Atherosclerosis reported the outcome of a randomized, double-blind study conducted by researchers at the Jean Mayer USDA Human Nutrition Research Center on Aging at Tufts University which found varying effects for the omega-3 fatty acids EPA and DHA in modulating the inflammatory response.
The crossover study included nine men and 12 women between the ages of 50 and 75 years with chronic inflammation. Participants received EPA or DHA twice daily for 10 weeks followed by a 10-week period during which both groups receive no supplements. Supplement regimens were then switched for another 10 weeks.
While EPA lowered the genetic expression of one type of proinflammatory protein, DHA lowered four types. Similarly, EPA lowered white blood cell secretion of one type of proinflammatory protein while DHA decreased three types. EPA, however, improved the balance between anti-inflammatory and proinflammatory proteins and produced byproducts associated with immune regulation. "In our bodies, there is always this balance between proinflammatory and anti-inflammatory proteins, and we found EPA was better than DHA at enhancing that balance,” first author Jisun So explained. “For the prevention of cardiovascular disease, previous research tells us that balance is very important."
"The jury has been out, so to speak, on how the two major components of fish oil work - and whether one might be better than the other,” added corresponding author Stefania Lamon-Fava. “These results suggest that DHA is the more powerful of the two on markers of inflammation in the body, but that's not the end of the story."
"Our study gives us a snapshot of how EPA and DHA may work to reduce chronic inflammation, and how each has distinct effects,” she added. “Our results provide insight for future research to explore why."
—D Dye
Glycine supplementation could help improve NAFLD
December 4 2020. The December 2, 2020 issue of Science Translational Medicine published the finding of researchers at the University of Michigan, Wayne State University and Technion-Israel Institute of Technology of a potential benefit for the amino acid glycine in people with nonalcoholic fatty liver disease (NAFLD).
"Lower circulating glycine is consistently reported in patients with NAFLD and related comorbidities including diabetes, obesity and cardiovascular diseases," first author Oren Rom, PhD, RD, noted. "Our studies not only offer a metabolic explanation for defective glycine metabolism in NAFLD, but also uncover a potential glycine-based treatment."
To verify whether alterations in glycine metabolism contribute to the development of NAFLD, the team induced fatty livers in mice by feeding them a Western diet characterized by high amounts of fat, cholesterol and fructose for 12 weeks. Among all amino acids, plasma glycine was reduced to the greatest extent while its precursor amino acids were increased, suggesting impairment of the animals’ ability to synthesize glycine. Giving mice a Western Diet without glycine exacerbated elevations in lipids, glucose and fatty liver.In livers from mice and humans with NAFLD, genes that synthesize glycine, particularly alanine-glyoxylate aminotransferase 1 (AGXT1), were suppressed.
In light of these and other findings that have associated low glycine levels with unhealthy lipids and diabetes, the researchers examined the effects of treatment with glycine-based compounds, including the tripeptide DT-109, which contains glycine and the amino acid leucine. They found that DT-109 was the only compound that reduced glucose in mice more efficiently than glycine. Mice that received a Western diet supplemented with DT-109 had lower glucose, total cholesterol and LDL cholesterol than animals that received glycine, leucine or water.
"Glycine-based treatment attenuates experimental NAFLD by stimulating hepatic fatty acid oxidation and glutathione synthesis, thus warranting clinical evaluation," the authors wrote.
—D Dye
Age-related vision loss reversed in mice
December 2 2020. An article that appeared on December 2, 2020 in Nature documented the use of epigenetic reprogramming to reverse vision loss in mice due to glaucoma and aging.
"Our study demonstrates that it's possible to safely reverse the age of complex tissues such as the retina and restore its youthful biological function," stated senior author David Sinclair, who is a professor of genetics at the Blavatnik Institute of Harvard Medical School. "If affirmed through further studies, these findings could be transformative for the care of age-related vision diseases like glaucoma and to the fields of biology and medical therapeutics for disease at large."
Dr Sinclair’s approach is based on a hypothesis of aging which proposes that changes to the epigenome (the body’s system that activates and deactivates genes in specific patterns without changing DNA) causes the cells to read the wrong genes, leading diseases associated with aging.
The research team utilized a virus to deliver three of four youth-restoring genes known as Yamanaka Factors into the retinas of mice. The genes were previously found to eliminate epigenetic markers on cells and return cells to their embryonic state from which they can develop into other types of cells.
After receiving the genes, mice with damaged optic nerves experienced nerve regeneration and vision loss was restored in a mouse model of glaucoma. Vision was also restored in 12-month-old mice who had aging-related impairment. In these mice, gene expression patterns and optic nerve cell electric signals became similar to young mice. The study is the first to successfully reset an aging clock to reverse glaucoma.
"What this tells us is the clock doesn't just represent time--it is time," Dr Sinclair remarked. "If you wind the hands of the clock back, time also goes backward."
—D Dye
