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.
Decreased acetyl-L-carnitine levels associated with depression
July 30 2018. The August 21, 2018 issue of the Proceedings of the National Academy of Sciences reported a link between low levels of acetyl-L-carnitine and a greater risk of depression.
“As a clinical psychiatrist, I have treated many people with this disorder in my practice," commented co-senior author Natalie Rasgon, MD, PhD, who is a professor of psychiatry and behavioral sciences at Stanford University. "It's the No. 1 reason for absenteeism at work, and one of the leading causes of suicide. Worse, current pharmacological treatments are effective for only about 50 percent of the people for whom they're prescribed. And they have numerous side effects, often decreasing long term compliance."
Acting on the findings of animal research conducted by lead author Carla Nasca, PhD, the researchers recruited men and women between the ages of 20 and 70 years who had been admitted to Weill Cornell Medicine or Mount Sinai School of Medicine for treatment of acute depression. Clinical assessments were conducted upon enrollment and blood samples were analyzed for levels of acetyl-L-carnitine.
In comparison with levels measured in blood samples provided by 45 demographically matched healthy men and women, acetyl-L-carnitine blood levels in depressed subjects were substantially lower. Acetyl-L-carnitine levels were lowest among depressed patients who had severe symptoms, a history of treatment resistance, or early onset disease. Having a history of childhood abuse was also associated with low acetyl-L-carnitine levels.
"We've identified an important new biomarker of major depression disorder,” Dr Rasgon stated. “We didn't test whether supplementing with that substance could actually improve patients' symptoms. What's the appropriate dose, frequency, duration? We need to answer many questions before proceeding with recommendations, yet. This is the first step toward developing that knowledge, which will require large-scale, carefully controlled clinical trials."
—D Dye
Omega-3 supplementation by children could improve children’s and parents’ behavior
July 27 2018. A randomized, double-blind trial reported on May 20, 2018 in the journal Aggressive Behavior revealed that supplementing children with omega-3 fatty acids improved their behavior and that of their parents toward each other.
The study included children who were given a fruit drink that contained a gram of omega-3 fatty acids or an unsupplemented fruit drink for 6 months. The children’s adult caregivers provided information concerning inter-partner and child-directed physical and psychological aggression at the beginning of the study, at 6 months, and 6 months after the study’s conclusion.
Among parents of children who received omega-3, a long term decrease in psychological aggression (characterized as arguing and verbal abuse) was reported, which correlated with improvement in child externalizing behavior (problem behaviors directed toward the external environment, including physical aggression and disobeying rules). “This study is the first to show that omega‐3 supplementation in children can reduce inter‐partner psychological aggression among adult caregivers not receiving supplements.,” authors Jill Portnoy, PhD, and colleagues announce.
"This is a promising line of research because omega-3 fatty acids are thought to improve brain health in children and adults,” noted Dr Portnoy, who is an assistant professor at the University of Massachusetts Lowell’s School of Criminology and Justice Studies. “There is more to be learned about the benefits, but if we can improve people's brain health and behavior in the process, that's a really big plus."
"Biology and social environment interact in complex ways that we're just beginning to figure out,” she added. “Before we can design effective interventions, we need to do research to understand what's happening."
—D Dye
High glucose spikes after a meal not uncommon in nondiabetics
July 25 2018. A study reported on July 24, 2018 in the journal PLOS Biology reveals surprisingly high levels of post-meal glucose among healthy individuals. "There are lots of folks running around with their glucose levels spiking, and they don't even know it," commented senior author Michael Snyder, PhD, who is a professor and chair of genetics at Stanford University. "We saw that some folks who think they're healthy actually are misregulating glucose--sometimes at the same severity of people with diabetes--and they have no idea."
The current study evaluated the findings of continuous glucose monitoring in 57 nondiabetic participants. Use of a continuous glucose-monitoring device provides a better picture of an individuals’ glucose behavior throughout the day, as opposed to blood tests that evaluate fasting glucose or hemoglobin A1c. "We think that these continuous glucose monitors will be important in providing the right information earlier on so that people can make changes to their diet should they need to," Dr Snyder noted.
After consuming three different standardized breakfasts (corn flakes with milk, bread with peanut butter, or a nutrition bar), it was observed that the intensity of individual responses to the meals characterized the subjects as one of three “glucotypes”: low moderate or severe. "We were very surprised to see blood sugar in the prediabetic and diabetic range in these people so frequently" Dr Snyder remarked. "The idea is to try to find out what makes someone a ‘spiker’ and be able to give them actionable advice to shift them into the low glucotype."
"Our next study will delve into the physiological causes of glucose dysregulation" Dr Snyder continued. "These include not only genetic variation, but also microbiome composition, and pancreas, liver, and digestive organ functions."
—D Dye
Restoration of mitochondrial DNA improves hair, skin in mice
July 23 2018. An article that appeared on July 20, 2018 in Cell Death & Disease reports findings of research conducted at the University of Alabama Birmingham of a reversal of hair loss and wrinkled skin in mice who underwent restoration of mitochondrial function through deactivation of a gene that is turned on by the antibiotic doxycycline. Mitochondria are organs within a cell that act as the cells’ power plants.
“A general decline in mitochondrial function has been extensively reported during aging,” Keshav Singh, PhD, and colleagues observe. “Furthermore, mitochondrial dysfunction is known to be a driving force underlying age-related human diseases. A mouse that carries elevated mitochondrial DNA mutation is also shown to present signs of premature aging.”
The researchers observed wrinkled skin, dysfunctional hair follicles and hair loss four weeks after inducing the gene mutation to deplete mitochondrial DNA in mice. However, by turning off the gene, the effects were reversed. "To our knowledge, this observation is unprecedented," announced Dr Singh, who is a professor of genetics at the University of Alabama School of Medicine. "This mouse model should provide an unprecedented opportunity for the development of preventive and therapeutic drug development strategies to augment the mitochondrial functions for the treatment of aging-associated skin and hair pathology and other human diseases in which mitochondrial dysfunction plays a significant role."
The findings indicate that mitochondria are reversible regulators of skin aging and hair loss. "It suggests that epigenetic mechanisms underlying mitochondria-to-nucleus cross-talk must play an important role in the restoration of normal skin and hair phenotype," remarked Dr Singh, who is also a professor of pathology at the University of Alabama. "Further experiments are required to determine whether phenotypic changes in other organs can also be reversed to wildtype level by restoration of mitochondrial DNA."
—D Dye
Risk of dying prematurely is lower among coffee drinkers
July 20 2018. A study involving close to half a million men and women found an association between increased coffee intake and a decline in mortality during a decade of follow-up regardless of the presence of genetic variations that impact caffeine metabolism. The findings were published on July 2, 2018 in JAMA Internal Medicine.
The current investigation included 498,134 participants in the UK BioBank population-based study. Questionnaires completed between 2006 and 2010 provided data concerning diet, including coffee consumption. Biologic samples were analyzed for genetic variations that indicate slow or fast caffeine metabolism. Subjects were followed for an average of 10 years, during which 14,225 deaths occurred.
Compared to the risk of death during follow-up experienced by subjects who did not drink coffee, drinking less than a cup of coffee daily was associated with a 6% reduction in premature mortality, 1 cup was associated with an 8% lower risk, 2-5 cups were associated with a 12% reduction, 6 to 7 cups with a 16% decrease and drinking 8 cups or more was associated with a 14% lower risk. The presence of genetic variations that indicate slow or fast caffeine metabolism did not appear to affect mortality risk and the associations were valid for both regular and decaffeinated coffee, which suggests that compounds other than caffeine may be protective factors.
Mechanisms suggested by the authors to help explain the benefit observed in the current study in association with coffee include improvements in inflammation, liver enzyme levels, insulin sensitivity, and endothelial function.
“These results provide further evidence that coffee drinking can be part of a healthy diet and may provide reassurance to those who drink coffee and enjoy it,” authors Erikka Loftfield, PhD, of the U.S. National Cancer Institute and colleagues conclude.
—D Dye
Omega-3 metabolites show anticancer effects
July 18 2018. The July 12, 2018 issue of the Journal of Medicinal Chemistry reported an anticancer property for recently identified omega-3 fatty acid metabolites known as endocannabinoid epoxides (EDP-EAs).
Endocannabinoids are made in the body and have properties similar to cannabinoids that occur in cannabis, without mind-altering effects. "We have a built-in endocannabinoid system which is anti-inflammatory and pain-reducing,” explained lead researcher Aditi Das. “Now we see it is also anticancer, stopping the cells from proliferating or migrating. These molecules could address multiple problems: cancer, inflammation and pain."
In mice with osteosarcoma (a common type of bone cancer), levels of a naturally occurring endocannabinoid epoxide formed from the omega-3 fatty acid DHA were observed to be 80% higher in lung metastases compared to the lung tissue of healthy mice. "The dramatic increase indicated that these molecules were doing something to the cancer - but we didn't know if it was harmful or good," Dr Das noted. "We asked, are they trying to stop the cancer, or facilitating it? So we studied the individual properties and saw that they are working against the cancer in several ways."
The team discovered that high concentrations of the molecules killed cancer cells, slowed tumor and tumor blood vessel growth, and inhibited cancer cell migration. The researchers plan to develop derivatives that can more effectively bind to the endocannabinoid receptor. "Dietary consumption of omega-3 fatty acids can lead to the formation of these substances in the body and may have some beneficial effects,” Dr Das observed. “However, if you have cancer, you want something concentrated and fast acting. That's where the endocannabinoid epoxide derivatives come into play - you could make a concentrated dose of the exact compound that's most effective against the cancer. You could also mix this with other drugs such as chemotherapies."
—D Dye
Flavonoids may help protect against macular degeneration
July 16 2018. An article that appeared on July 9, 2018 in the American Journal of Clinical Nutrition reported findings from the Westmead Institute for Medical Research in Australia of a lower risk of macular degeneration among men and women who consumed higher amounts flavonoids that occur in oranges.
"Our research aims to understand why eye diseases occur, as well as the genetic and environmental conditions that may threaten vision," commented lead researcher Bamini Gopinath.
The study included 2,856 subjects who were at least 49 years old upon enrollment in the Blue Mountains Eye Study in 1992. The Blue Mountains Eye Study is an investigation of the associations between diet and lifestyle factors with health outcomes and chronic diseases. Responses to food frequency questionnaires completed at the beginning of the study were evaluated for flavonoid content. Subjects in the current investigation were followed for 15 years.
The researchers found a higher intake of flavonoids among subjects who did not develop macular degeneration during follow-up in comparison with those diagnosed with the disease. "The data shows that flavonoids found in oranges appear to help protect against the disease," Dr Gopinath observed.
Consuming one or more servings of oranges daily was associated with a 61% lower risk of developing late macular degeneration by the end of follow-up. "Essentially we found that people who eat at least one serving of orange every day have a reduced risk of developing macular degeneration compared with people who never eat oranges," Dr Gopinath stated. "Even eating an orange once a week seems to offer significant benefits.”
"Our research is different because we focused on the relationship between flavonoids and macular degeneration,” she noted. "Flavonoids are powerful antioxidants found in almost all fruits and vegetables, and they have important anti-inflammatory benefits for the immune system.”
—D Dye
Is sleep an antioxidant?
July 13 2018. A study reported on July 12, 2018 in the journal PLOS Biology adds evidence to a controversial hypothesis concerning the purpose of sleep. Although sleep occurs among nearly all animals, its functions are still somewhat of a mystery.
In their introduction to the article, Vanessa M. Hill and colleagues at Columbia University observe that, despite the resulting vulnerability to predators and other dangers, sleep is an evolutionarily conserved behavior throughout the animal kingdom. Acute sleep deprivation can result in cognitive impairment, metabolic abnormalities, and even death, although it is not known whether these are caused by loss of sleep or associated stress.
"A controversial hypothesis for the function of sleep is the free radical flux theory of sleep, proposed in a theoretical paper by Reimund in 1994," Dr Hill and associates write. "Reimund proposed that reactive oxygen species (ROS) accumulate in neurons during the wake state and that sleep allows for the clearance of ROS in the brain . . . Thus, the free radical flux hypothesis proposed that the core function of sleep is to act as an antioxidant for the brain."
The researchers observed that short-sleeping mutant fruit flies (Drosophila) shared the defect of sensitivity to acute oxidative stress, which occurs when there is an imbalance between excess free radicals and antioxidant responses. These flies had shorter lives than normal flies without the mutation. The team found that increasing sleep in normal flies improved survival after an oxidative challenge. Furthermore, lowering oxidative stress in their neurons by the overexpression of antioxidant genes reduced sleep.
"Taken together, our results support an intriguing hypothesis for a bidirectional relationship between sleep and oxidative stress: oxidative stress triggers sleep, which then acts as an antioxidant for both the body and the brain," the authors conclude.
—D Dye
Researchers gain insight regarding curcumin's anticancer property
July 11 2018. On July 9, 2018, the Proceedings of the National Academy of Sciences reported the discovery of a mechanism of action for curcumin, a compound occurring in the spice turmeric, against cancer.
“Curcumin, the active ingredient in Curcuma longa, has been in medicinal use since ancient times,” write Sourav Banerjee of the University of California San Diego and colleagues. “However, the therapeutic targets and signaling cascades modulated by curcumin have been enigmatic despite extensive research.”
Using x-ray crystallography, it was determined that curcumin binds to and inhibits DYRK2, an enzyme that regulates the 26S proteasome. By perturbing 26S proteasome activity in cancer cells, curcumin impairs cancer cell proliferation.
"Although curcumin has been studied for more than 250 years and its anticancer properties have been previously reported, no other group has reported a co-crystal structure of curcumin bound to a protein kinase target until now," Dr Banerjee commented. "Because of their work on the crystallography, our collaborators at Peking University, Chenggong Ji and Junyu Xiao, helped us to visualize the interaction between curcumin and DYRK2."
"The enzyme kinases IKK and GSK3 were thought to be the prime curcumin-targets that lead to anticancer effect but the co-crystal structure of curcumin with DYRK2 along with a 140-panel kinase inhibitor profiling reveal that curcumin binds strongly to the active site of DYRK2, inhibiting it at a level that is 500 times more potent than IKK or GSK3," he explained.
"Our results reveal an unexpected role of curcumin in DYRK2-proteasome inhibition and provide a proof-of-concept that pharmacological manipulation of proteasome regulators may offer new opportunities for hard-to-treat triple-negative breast cancer and multiple myeloma treatment," added co-senior author Jack E. Dixon. "Our primary focus is to develop a chemical compound that can target DYRK2 in patients with these cancers."
—D Dye
Quercetin, dasatinib extend life span of mice
July 9 2018. An article appearing on July 9, 2018 in Nature Medicine reports the finding of Mayo Clinic researchers that the senolytic compounds quercetin and dasatinib delayed physical dysfunction in mice that received senescent cells and extended life span when given to aging mice.
"We can say with certainty that senescent cells can cause health problems in young mice, including causing physical dysfunction and lowering survival rates, and that the use of senolytics can significantly improve both health span and life span in much older naturally aged animals," stated senior author and geriatrics researcher James Kirkland, MD, PhD, who heads the Mayo Clinic’s Kogod Center on Aging.
The researcher team found that injecting a small number of senescent cells into young, healthy mice led to a decrease in health and physical function. Transplantation of senescent cells was associated with a similar effect in older mice, in addition to lower survival. However, giving the quercetin and the drug dasatinib to young mice that received transplanted senescent cells alleviated physical dysfunction. In naturally aged mice, the combination given for 4 months increased post-treatment survival by 36%.
"This study provides compelling evidence that targeting a fundamental aging process--in this case, cell senescence in mice--can delay age-related conditions, resulting in better health and longer life," commented National Institute on Aging Director Richard J. Hodes, MD. "This study also shows the value of investigating biological mechanisms which may lead to better understanding of the aging process."
"This is exciting research," added Felipe Sierra, PhD, who is the director of NIA's Division of Aging Biology. "This study clearly demonstrates that senolytics can relieve physical dysfunction in mice. Additional research will be necessary to determine if compounds, like the one used in this study, are safe and effective in clinical trials with people."
—D Dye
Low dose aspirin could help treat Alzheimer's disease
July 6 2018. On July 2, 2018, The Journal of Neuroscience reported the discovery of an ability of aspirin to decrease amyloid beta plaque in a mouse model of Alzheimer’s disease. The presence in the brain of amyloid beta plaques, along with neurofibrillary tangles made up of hyperphosphorylated tau protein, are among the characteristics of Alzheimer’s disease in humans.
Dr Pahan and colleagues determined that aspirin upregulates transcription factor EB (TFEB), a regulator of lysosome formation. “Lysosomes play a central role in cellular homeostasis by regulating the cellular degradative machinery,” lead researcher Kalipada Pahan, PhD, and colleagues explain. “Since aberrant lysosomal function has been associated with multiple lysosomal storage and neurodegenerative disorders, enhancement of lysosomal clearance has emerged as an attractive therapeutic strategy.”
“Aspirin, one of the most widely-used medications in the world, activates peroxisome proliferator-activated receptor alpha (PPAR alpha) to upregulate TFEB and increase lysosomal biogenesis in brain cells,” they write.
In the brains of male and female Alzheimer’s mice, orally administered aspirin reduced amyloid plaque pathology. "Understanding how plaques are cleared is important to developing effective drugs that stop the progression of Alzheimer's disease," noted Dr Pahan, who is the Floyd A. Davis, MD, Endowed Chair of Neurology and professor of neurological sciences, biochemistry and pharmacology at Rush Medical College. "The results of our study identifies a possible new role for one of the most widely used, common, over-the-counter medications in the world.”
"This research study adds another potential benefit to aspirin's already established uses for pain relief and for the treatment of cardiovascular diseases," Dr Pahan added. "More research needs to be completed, but the findings of our study have major potential implications for the therapeutic use of aspirin in Alzheimer’s disease and other dementia-related illnesses."
—D Dye
Science article suggests limitless longevity
July 2 2018. The July 29, 2018 issue of Science reports the conclusion of researchers from the University of California, Berkeley and Sapienza University of Rome that the risk of death, which increases exponentially up to an approximate age of 80 years, appears to level off after the age of 105. The findings contradict recent speculation by some biologists and demographers that there’s a fixed natural limit to human life.
“Theories about biological limits to life span and evolutionary shaping of human longevity depend on facts about mortality at extreme ages, but these facts have remained a matter of debate,” write authors Elisabetta Barbi and colleagues.
Among 3,836 residents of Italy between the ages of 105 and 109 years there was a 50/50 chance of dying within a year and an anticipated additional life span of 1.5 years. These projections were the same for supercentenarians aged 110 and older, indicating a plateau effect. In contrast, among women aged 90, the chance of dying within a year was found to be 15% and further life expectancy was 6 years, and for 95-year-old women, one-year risk of mortality increased to 24% while life expectancy declined to 3.7 years.
"These are the best data for extreme-age longevity yet assembled," announced senior author Kenneth Wachter, who is a UC Berkeley professor emeritus of demography and statistics. "Our data tell us that there is no fixed limit to the human lifespan yet in sight. Not only do we see mortality rates that stop getting worse with age, we see them getting slightly better over time."
He noted that similar patterns have been observed in other species, including worms and flies. "What do we have in common with flies and worms?" he asked. "One thing at least: We are all products of evolution."
—D Dye
