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.
Meta-analysis concludes testosterone improves women’s sexual well-being
July 31, 2019. A review and meta-analysis reported in The Lancet Diabetes & Endocrinology on July 25, 2019concluded that testosterone hormone replacement for women improves sexual function and well-being. The review is the most comprehensive on the subject to date.
Testosterone is a hormone produced by men and, in lower amounts, women. Like men, testosterone declines in women during aging, which can contribute to diminished libido and sexual response.
Researchers at Monash University selected 46 reports regarding 36 randomized trials that provided a total of 8,480 women (the majority of whom were postmenopausal) for their review. Trials compared the effects of testosterone to a placebo or other hormone replacement on female sexual function.
In comparison with the control subjects, women who received testosterone experienced improvement in sexual desire, arousal, responsiveness to stimuli, self-image, orgasm and pleasure, and less concern and distress about sex. "The beneficial effects for postmenopausal women shown in our study extend beyond simply increasing the number of times a month they have sex," commented senior author Susan Davis. "Some women who have regular sexual encounters report dissatisfaction with their sexual function, so increasing their frequency of a positive sexual experience from never, or occasionally, to once or twice a month can improve self-image and reduce sexual concerns and may improve overall wellbeing."
"Our results suggest it is time to develop testosterone treatment tailored to postmenopausal women rather than treating them with higher concentrations formulated for men," she added. "Nearly a third of women experience low sexual desire at midlife, with associated distress, but no approved testosterone formulation or product exists for them in any country and there are no internationally-agreed guidelines for testosterone use by women. Considering the benefits we found for women's sex lives and personal wellbeing, new guidelines and new formulations are urgently needed."
High dose vitamin D could slow diabetes progression
July 29, 2019. An article published on July 25, 2019 in the European Journal of Endocrinology documents an association between vitamin D supplementation among newly diagnosed type 2 diabetics or those at risk of diabetes and a reduction in the progression of the disease.
“Our study has notable strengths including the randomized, double-blind design and the use of the gold-standard hyperinsulinemic-euglycemic clamp to evaluate insulin sensitivity,” note authors Patricia Lemieux and colleagues. “Furthermore, we selected participants at high risk for type 2 diabetes or with newly type 2 diabetes, a group that had not been specifically studied using the clamp.”
The trial included 96 men and women with serum 25-hydroxyvitamin D levels of less than 22 nanograms per milliliter who were prediabetic or recently diagnosed with type 2 diabetes. Vitamin D levels and markers of glucose metabolism and insulin sensitivity and secretion were measured before and after the six-month treatment period, during which the participants received 5,000 international units of vitamin D or a placebo.
After six months, average serum vitamin D levels were higher among those who received vitamin D supplements in comparison with the placebo group and pretreatment values. Peripheral insulin sensitivity and pancreatic beta-cell function also improved among those who received the vitamin, which suggests that it may slow the progression of metabolic function decline. "The reason we saw improvements in glucose metabolism following vitamin D supplementation in those at high risk of diabetes, or with newly diagnosed diabetes, while other studies failed to demonstrate an effect in people with long-standing type 2 diabetes is unclear,” commented senior author Claudia Gagnon. “This could be due to the fact that improvements in metabolic function are harder to detect in those with longer-term disease or that a longer treatment time is needed to see the benefits."
Slower metabolism associated with reduction in manifestation of harmful effects of mutations
July 26, 2019. Research described on July 25, 2019 in Cell found an association between a slower metabolic rate and a reduction of potentially damaging effects of genetic mutations. The finding could help explain the link between calorie restriction, which slows metabolism, and longer life.
By halving the metabolic rate of fruit flies, Northwestern University researchers observed that the anticipated harmful effects of many mutations failed to manifest. "When the flies developed at a normal rate, developmental problems occurred," stated lead researcher Richard Carthew. "When we slowed the rate, developmental problems disappeared. They develop slower and grow slower, but, otherwise, they are normal animals."
"This upends the paradigm of everything we know about development," added coauthor Luís Amaral. "We have always thought that if you 'break' some genes, there will be serious developmental consequences. It turns out that's not true for some genes -- as long as you also slow the metabolism of the growing organism.”
While it had been believed that microRNAs were necessary for survival, the researchers discovered that fruit flies that lacked microRNAs survive to normal adulthood when their metabolic rate is reduced. "Our result concludes that this entire family of gene regulators is not essential," Dr Carthew observed.
Drs Carthew and Amaral suggest that slower metabolism gives the body more time to correct errors. "When you look at all the different proteins and genes that interact within a cell, you can get overwhelmed by all the components and the interactions among them," Dr Amaral stated. "If you are growing fast and something goes wrong, it can be catastrophic. You need these complex networks because they increase redundancy to prevent catastrophe. But if you are growing slowly, you might not need such a complex system. You have more time to adjust to mistakes and react to changes."
Higher vitamin E levels linked with lower risk of dying among nondiabetics with NAFLD
July 24, 2019. An article published on July 19, 2019 in the Journal of Clinical Medicine reveals the results of a study which found a lower risk of mortality among nondiabetic adults with nonalcoholic fatty liver disease (NAFLD) who had higher levels of vitamin E compared to those who had lower levels.
Nonalcoholic fatty liver disease is characterized by the accumulation of fat in the cells of the liver in the absence of such factors as excessive alcohol intake and viral hepatitis. The condition can include nonalcoholic steatohepatitis (NASH), a progressive form of NAFLD that can lead to cirrhosis of the liver or liver cancer.
The study included 662 diabetic, 836 prediabetic and 906 nondiabetic adults with NAFLD who were enrolled in the National Health and Nutrition Examination Survey (NHANES) III. Participants were followed for a median of 18.8 years, during which 748 deaths occurred.
In comparison with lower levels, a higher serum vitamin E level was associated with a decreased risk of dying from any cause in nondiabetics but not among prediabetics or diabetics. A higher vitamin E to total cholesterol ratio was also associated with a lower risk of all-cause mortality.
“Although the pathogenesis of NAFLD and its progression to fibrosis needs to be fully clarified, oxidative stress and inflammation are believed to play critical roles in the transition from steatosis to NASH,” write authors Peiling Tsou and Chang-Jiun Wu. “Vitamin E is a lipid-soluble, chain-breaking antioxidant that prevents the propagation of free radicals. Moreover, vitamin E interacts with other cellular components and may help promote the antioxidative environment.”
“Further investigations are warranted to elucidate the underlying mechanism of this inverse association of serum vitamin E concentration with all-cause mortality in nondiabetic but not prediabetic or diabetic subjects,” they conclude.
When traveling to Mars, don’t forget to pack resveratrol
July 22, 2019. A study reported on July 18, 2019 in Frontiers in Physiology suggests that resveratrol, a compound occurring in grapes that’s a popular nutritional supplement, could be useful during missions to Mars to help preserve muscle mass.
"After just three weeks in space, the human soleus muscle shrinks by a third," explained lead author Marie Mortreux, of the laboratory of Dr Seward Rutkove of Beth Israel Deaconess Medical Center. "This is accompanied by a loss of slow-twitch muscle fibers, which are needed for endurance."
"Resveratrol has been shown to preserve bone and muscle mass in rats during complete unloading, analogous to microgravity during spaceflight,” she noted. “So, we hypothesized that a moderate daily dose would help mitigate muscle deconditioning in a Mars gravity analogue, too."
During a two-week study, rats were exposed to conditions designed to simulate the lower gravity of Mars or that of earth. Half of each group received drinking water to which resveratrol was added while the remainder received unenhanced water. The researchers measured the animals’ calf circumferences and assessed front and rear paw grip force each week. Calf muscle tissue was analyzed after two weeks.
While the simulated environment of Mars was associated with a reduction in calf circumference, paw grip, muscle weight and slow-twitch fiber content, rats that received resveratrol had nearly the same paw grip as those exposed to Earth conditions, as well as decreased reduction of slow-twitch muscle fibers and no loss of muscle mass.
"Resveratrol treatment promotes muscle growth in diabetic or unloaded animals, by increasing insulin sensitivity and glucose uptake in the muscle fibers," Dr Mortreux commented. "Dietary strategies could be key, especially since astronauts travelling to Mars won't have access to the type of exercise machines deployed on the International Space Station."
Meta-analysis finds lower risk of cardiovascular mortality in association with higher levels of beta-carotene, vitamins C and E
July 19, 2019. The July 2019 issue of Public Health Nutrition published the results of a meta-analysis that revealed an association between higher serum or plasma levels of the antioxidants beta-carotene, vitamin C and vitamin E and a lower risk of dying from cardiovascular disease.
“To our knowledge, no systematic review and meta-analysis has assessed the association of dietary vitamin E, vitamin C and beta-carotene with the risk of cardiovascular disease mortality,” announce authors Ahmad Jayedi and colleagues.
The meta-analysis included 18 observational studies that included a total of 320,548 participants. Follow-up periods ranged from four to 22 years, during which there were 16,974 cardiovascular deaths. Among those whose circulating levels of beta-carotene, vitamin C and vitamin E were among the top categories, the respective risks of dying from cardiovascular disease were 32%, 40% and 18% lower than the risks experienced by those whose levels were among the lowest.
When dietary intake was examined, consuming more vitamin C was associated with a 21% lower risk of cardiovascular mortality, while beta-carotene and vitamin E were associated with smaller reductions. For each 50 milligram per day increase in vitamin C intake there was an 8% lower risk of dying from cardiovascular disease. “The study suggests that the circulating biomarkers of antioxidants may have better predictive value in relation to the risk of total cardiovascular disease mortality,” the authors remark.
“Oxidative stress, vascular inflammation and low-grade systemic inflammation are some of the mediatory pathways through which a possible link has been proposed between dietary antioxidants and cardiovascular disease risk,” they write. “The present meta-analysis demonstrates that higher vitamin C intake and higher circulating concentrations of vitamin C, vitamin E and beta-carotene are associated with a lower risk of cardiovascular disease mortality.”
N-acetylcysteine could help Parkinson's disease patients
July 17, 2019. Findings from a randomized trial reported on June 17, 2019 in Clinical Pharmacology & Therapeuticsadds evidence to earlier research that found an association between supplementation with the amino acid N-acetylcysteine (NAC) and improvements in patients Parkinson’s disease, a disorder characterized by a loss of function of the brain’s dopamine-producing neurons.
N-acetylcysteine acts as a precursor to the amino acid L-cysteine which in turn, is a precursor to the antioxidant glutathione. "This is an exciting study that suggests a natural molecule such as NAC can help improve dopamine function and symptoms in Parkinson's patients," remarked corresponding author Andrew Newberg, MD, who is a Professor and Director of Research at Thomas Jefferson University’s Department of Integrative Medicine and Nutritional Sciences.
The three month trial included 42 Parkinson’s disease patients who received standard care or standard care plus 500 milligrams orally administered NAC twice daily in addition to weekly intravenous NAC infusions. At the beginning and end of the trial, the participants received brain scans that assessed dopamine transporter binding (which decreases in Parkinson’s disease) and were evaluated for cognitive and motor function.
Among those who received N-acetylcysteine, dopamine transporter binding significantly increased in two areas of the brain’s basal ganglia (a region that is most affected by Parkinson’s disease) by the end of the treatment period. The treated group also experienced improvements in physical and mental function. "This study is an important step in understanding how NAC might work as a potentially new avenue for managing Parkinson's patients,” commented first author Daniel Monti, MD, who is Chairman of the Department of Integrative Medicine and Nutritional Sciences and Director of the Marcus Institute of Integrative Health at Thomas Jefferson University. “The NAC appears to enable dopamine neurons to recover some of their function."
Lifestyle could help override genetic factors that increase dementia risk
July 15, 2019. A study published on July 14, 2019 in the Journal of the American Medical Association found that having a healthy lifestyle was associated with a lower risk of dementia among men and women at high risk of the condition in comparison with those who did not engage in favorable practices.
The study included 196,383 participants aged 60 and older who enrolled in the UK Biobank Study between 2006 and 2010 and were followed until 2016 or 2017. Twenty percent of the participants had genetic factors that put them at high risk of dementia, 60% were at intermediate risk and 20% were at low risk. Lifestyle scores reflected whether the subject was a nonsmoker, engaged in regular activity, consumed a healthy diet and had moderate alcohol intake, all of which are believed to be neuroprotective.
Over the follow-up period, 0.82% of those with a favorable lifestyle developed dementia in comparison with 1.16% of those who had an unfavorable lifestyle. “A favorable lifestyle was associated with a lower risk of dementia regardless of genetic risk,” noted Ilianna Lourida, PhD, and colleagues.
Dementia developed among 0.63% at low genetic risk compared to 1.23% of those at high risk. People at high risk of dementia who had unhealthy lifestyle factors had 2.83 times the risk of developing the condition compared to those at low risk who practiced a healthy lifestyle. However, among the high risk group, having a healthy lifestyle was associated with a 32% lower risk of developing dementia than an unhealthy lifestyle.
“Among older adults without cognitive impairment or dementia, both an unfavorable lifestyle and high genetic risk were significantly associated with higher dementia risk,” the authors conclude. “A favorable lifestyle was associated with a lower dementia risk among participants with high genetic risk.”
Curcumin supplementation associated with increase in brain-derived neurotrophic factor
July 12, 2019. The results of a meta-analysis published on May 9, 2019 in Nutrition Research favor an association between short term supplementation with curcumin and an increase in serum brain-derived neurotrophic factor (BDNF), a protein that facilitates the formation of neurons and synapses in the brain and memory in the frontal cortex and hippocampus.
It has been suggested that neuropsychiatric disorders alter BDNF levels by increasing inflammation and oxidative stress. Therefore, agents such as curcumin, which has antioxidant and anti-inflammatory properties, could help restore low BDNF levels.
“To the best of our knowledge, this is the first dose-response meta-analysis of published trials to evaluate the effectiveness of curcumin supplementation on serum BDNF levels,” authors Payam Sarraf and colleagues announce.
Dr Sarraf and associates selected four randomized controlled trials that included a total of 139 men and women. Curcumin doses ranged from 200 mg to 1,820 mg per day given for 8 to 12 weeks. Serum BDNF levels were measured before and after the treatment periods.
The meta-analysis showed a significant increase in serum BDNF among participants who received curcumin compared to the control group. Subsequent analysis found significant increases in women and people over the age of 40 who received curcumin, and among participants in trials that used higher doses of curcumin or lasted longer than 8 weeks.
“There is some evidence to support the use of pharmacological treatments in the management of neurodegenerative and psychiatric diseases; however, a few safe complementary effective prophylactic approaches have been suggested,” the authors conclude. “There is a significant positive impact of curcumin supplementation on BDNF levels, indicating its potential use for neurological disorders that have been correlated with low BDNF levels. Further randomized control trials with higher sample sizes and different doses of curcumin are needed for more comprehensive and precise conclusions.”
Centenarian gene variant associated with healthier blood vessels
July 10, 2019. Research findings reported on July 10, 2019 in the European Heart Journal reveal a cardiovascular benefit for a genetic variant that frequently occurs among long lived humans.
Centenarians have been found to have a greater incidence of a variant in the gene that encodes the protein known as BPIFB4. Known as the longevity associated variant, or LAV, the gene appears to have a rejuvenating effect on the cardiovascular system. By inserting the gene into the genome of laboratory animals that were susceptible to atherosclerosis, endothelial function was improved, and arterial plaque reduced.
"The results were extremely encouraging,” stated first author Annibale Puca, who is a research team coordinator at the University of Salerno and at I.R.C.C. MultiMedica. “We observed an improvement in the functionality of the endothelium (the inner surface of blood vessels), a reduction of atherosclerotic plaques in the arteries and a decrease in the inflammatory state.”
When the LAV-BPIFB4 protein was administered to human blood vessels in the lab, similar benefits were observed. By studying humans, the researchers found that having more of the BPIFB4 protein was associated with healthier blood vessels and that those with the LAV variant had higher levels of this protein.
"This study paves the way to the possibility of therapeutic solutions based on the LAV-BPIFB4 protein,” commented senior author Carmine Vecchione, who is the dean of the Faculty of Medicine of the University of Salerno and director of the Cardiology Unit at Ruggi D'Aragona Hospital. “Of course, much research will still be needed, but we think it is possible, by administering the protein to patients, to slow down cardiovascular damage due to age. In other words, even if a person does not possess those particular genetic characteristics, we could be able to offer the same level of protection."
Pine bark extract could help antidepressant-induced sexual dysfunction
July 08, 2019. A study reported in the March 2019 issue of Physiology International found that Pycnogenol, an antioxidant compound occurring in maritime pine bark, could help lower the incidence of sexual dysfunction as a side effect of antidepressant therapy. While some antidepressant drugs may be helpful for depressed individuals, adverse effects, including sexual dysfunction, can sometimes lead to their discontinuance.
The investigation included 20 men and 47 women diagnosed with a depressive episode or recurrent depressive disorder who had responded to treatment with escitalopram, a selective serotonin reuptake inhibitor (SSRI) antidepressant. Participants were randomized to receive 50 milligrams Pycnogenol daily in combination with escitalopram or escitalopram only for four months. At the first visit and during subsequent monthly examinations, the subjects were evaluated for depressive episode severity, sexual function, blood pressure and other factors.
Depression significantly declined among both groups during the course of the study. After a month of treatment, those who received Pycnogenol experienced a significant improvement in scores of sexual function while scores remained unchanged among the group that received escitalopram only.
In their discussion, authors A. Smetanka of the Comenius University in Bratislava, Slovakia and colleagues propose that the effects associated with Pycnogenol in this study are based on its ability to improve endothelial function via its antioxidant, vasodilatory, anticoagulant and anti-inflammatory actions. They note that the compound had previously been shown to improve erectile function in a pilot study reported in 2003 and has been observed to have a synergistic effect with the amino acid L-arginine, which also benefits endothelial function.
“This study found a beneficial effect of Pycnogenol treatment on antidepressant-induced sexual dysfunction in both genders,” they conclude. “It seems that Pycnogenol supplementation could be useful in reducing the antidepressant-mediated adverse effect on sexual function.”
AI helps identify biologic age markers
July 05, 2019. Artificial intelligence (AI) has been utilized to identify “deep aging clocks” that assess biologic age, as reviewed on July 3, 2019 in the Cell journal Trends in Pharmacological Sciences. Biologic age, which is shaped by genetics, lifestyle and the environment, has been proposed as a more accurate reflection of true age than chronologic age (which only quantifies years lived) and could be a more reliable predictor of health and premature mortality risk.
Predictors of biologic and chronologic age using deep learning, a branch of machine learning based on artificial neural networks, were reported in 2016 and have been gaining acceptance among aging researchers. "Humans are very good at guessing each other's age using images, videos, voice, and even smell,” commented Alex Zhavoronkov, PhD, of Insilico Medicine, who coauthored the current article. “Deep neural networks can do it better and we can now interpret what factors are most important. Very often when someone looks older than their chronological age, they are sick. A trained doctor can guess the health status of a patient just by looking at him or her. At Insilico we developed a broad range of deep biomarkers of aging that can be used by the pharmaceutical and insurance companies, as well as by the longevity biotechnology community. In this paper we describe the recent progress in this emerging field and outline a range of non-obvious applications."
"Deep biomarkers of aging developed utilizing a variety of data types of aging are rapidly advancing the longevity biotechnology industry,” added coauthor Polina Mamoshina. “Using biomarkers of aging to improve human health, prevent age-associated diseases and extend healthy life span is now facilitated by the fast-growing capacity of data acquisition, and recent advances in AI. They hold a great potential for changing not only aging research, but healthcare in general."
Gene variant linked to niacin metabolism associated with risk of schizophrenia
July 03, 2019. Research reported on July 3, 2019 in JAMA Psychiatry reveals a significant prevalence of a genetic variant among Indian men and women with schizophrenia. The variant affects the metabolic pathway of niacin (nicotinic acid) to nicotinamide adenine dinucleotide (NAD+), a coenzyme involved in several metabolic pathways.
Sathish Periyasamy, PhD, and colleagues conducted a genome-wide association study of 1,321 schizophrenic patients, along with 885 family members and 886 unrelated control subjects recruited in Chennai, India. Among subjects with schizophrenia, there was a 27% greater risk a of a single-nucleotide polymorphism (rs10866912) that modifies the gene that encodes NAPRT1. NAPRT1 catalyzes the conversion of niacin to nicotinic acid mononucleotide (NAMN), a precursor of NAD+ which, in the authors’ words, is “a ubiquitous coenzyme fundamental to all living cells and vital for cellular biochemistry, energy metabolism, and DNA synthesis.”
"This study identified a gene called NAPRT1 that encodes an enzyme involved in vitamin B3 metabolism--we were also able to find this gene in a large genomic dataset of schizophrenia patients with European ancestry,” commented senior author Bryan J. Mowry, MD of the University of Queensland.
The findings recall research conducted by Abram Hoffman and Humphrey Osmond regarding the role of niacin deficiency in one type of schizophrenia. While the duo authored numerous articles concerning the potential benefit of niacin in the treatment of the disease, their work, like much that involves nutritional therapies, was dismissed by mainstream medicine.
“Given this gene’s role in niacin metabolism and the evidence for niacin deficiency provoking schizophrenia-like symptoms in neuropsychiatric diseases such as pellagra and Hartnup disease, these results suggest that the rs10866912 genotype and niacin status may have implications for schizophrenia susceptibility and treatment,” the authors conclude.
Infants deficient in vitamin D risk high blood pressure later
July 01, 2019. A study reported on July 1, 2019 in Hypertension revealed a greater risk of high blood pressure in children and adolescents who experienced vitamin D deficiency during infancy and/or early childhood.
The study included 775 infants enrolled in the Children’s Health Study who were followed for up to 18 years of age. Plasma 25-hydroxyvitamin D levels were measured at birth in cord blood and during early childhood. Low vitamin D at birth was defined as plasma values of less than 11 nanograms per milliliter (ng/mL) and low early childhood values were defined as less than 25 ng/mL.
Among subjects between the ages of 3 to 18 years of age, low vitamin D at birth was associated with a 38% increase in the risk of having systolic blood pressure that was greater than or equal to the 75th percentile according to 2017 American Academy of Pediatrics Guidelines in comparison with children who had higher vitamin D levels. Low vitamin D levels during early childhood was associated with a 59% greater risk of elevated systolic blood pressure between the ages of 6 and 18. Those who had low vitamin D levels at birth as well as during early childhood had twice the risk of high systolic blood pressure than children whose vitamin D levels were higher.
"Currently, there are no recommendations from the American Academy of Pediatrics to screen all pregnant women and young children for vitamin D levels,” remarked lead author Guoying Wang, MD, PhD, who is an assistant scientist at Johns Hopkins University Bloomberg School of Public Health. “Our findings raise the possibility that screening and treatment of vitamin D deficiency with supplementation during pregnancy and early childhood might be an effective approach to reduce high blood pressure later in life.”