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.
Study suggests melatonin could be used to treat polycystic kidney disease
January 29 2021. A report published on November 23, 2020 in the journal Molecules suggests a role for the hormone melatonin against the formation of cysts in a fruit fly model of autosomal dominant polycystic kidney disease (ADPKD).
Polycystic kidney disease, which is one of the most common genetic disorders, is characterized by cyst growth in the kidneys’ nephrons, which filter the blood. It is a progressive disease that can result in the need for a kidney transplant among affected individuals.
For the current investigation, researchers at Montreal’s Concordia University used a fly (Drosophila melanogaster) model of polycystic kidney disease. "Drosophila conserves many of the renal pathway components found in vertebrates and have anatomically isolated renal tubes," explained senior author Chiara Gamberi.
Melatonin was administered during an 18-day period to 50 flies, while a control group received ethanol. Among flies that received melatonin, cysts were fewer and smaller. It was also discovered that the fly tubules (known as nephrons in humans) had sections with unique functions that were differently affected by various compounds, which suggests that different treatments might be developed depending upon the location of cysts in the nephrons.
Because polycystic kidney disease is chronic, toxic compounds cannot be used, as in the case of cancer patients. "We know from oncology that melatonin has two effects when it is administered with chemotherapy," Dr Gamberi remarked. "First, it acts as a drug adjuvant to the chemotherapy, making it work more effectively against cancer cells. Second, it appears to protect healthy cells from the toxicity of the chemotherapy. Basically, melatonin increases the specificity of the chemotherapy. We hope that it can have a similar positive effect when used with an anti-ADPKD drug like tolvaptan, which can damage the liver."
—D Dye
Meta-analysis finds dietary supplements improve sleep quality
January 27 2021. A systematic review and meta-analysis published on January 13, 2021 in Postgraduate Medical Journal found benefits for supplemental vitamin D, melatonin and amino acids in improving the quality of sleep among men and women.
The meta-analysis included 15 randomized, controlled trials that examined the association between subjective sleep quality [as assessed by the Pittsburgh Sleep Quality Index (PSQI)] and supplementation with amino acids, the hormone melatonin, omega 3 fatty acids and vitamin D. Pooled data for the two studies involving amino acid supplements, seven studies involving melatonin, and four studies involving vitamin D each showed significant differences between supplemented and control groups, with more favorable PSQI scores occurring among those who received the supplements. The two studies that evaluated omega 3 did not reveal significant differences between the treatment and control groups.
Two reviewed trials that were not eligible for inclusion in the meta-analysis added evidence to the benefit of melatonin in sleep quality. Other non-included trials found a benefit for nitrate-containing beetroot juice, resveratrol and zinc supplements. Co-supplementation with melatonin, magnesium and zinc was also associated with a significant benefit in comparison with a placebo.
“Although we found a significant improvement in sleep quality by dietary supplementation, randomized, controlled trials with longer duration and larger sample size should be conducted to verify our findings,” noted authors Vicky Chan and Kenneth Lo of The Hong Kong Polytechnic University. “Furthermore, dose–response effect of different supplements on sleep quality has not yet been evaluated.”
“Amino acids, vitamin D and melatonin supplements were significantly beneficial to improve sleep quality,” they concluded. “Further research on the effect of magnesium, zinc, resveratrol and nitrate supplementation on improving sleep quality is required.”
—D Dye
Coffee improves sleep-loss-associated attention deficit
January 25 2021. Reaching for a cup of coffee when you’ve had less than a good night’s sleep really can help make up for some of the effects of sleep loss on brain function according to a study published in the December 26, 2020 issue of Progress in Neuro-Psychopharmacology and Biological Psychiatry.
Diego M. Baur and colleagues investigated whether drinking coffee during a simulated work week would help improve some of the effects of chronic sleep restriction. The study included 26 men and women who were carriers of a genetic variant that renders them sensitive to the effects of caffeine. Participants were restricted to five hours of sleep for five nights after which 12 participants were given regular coffee and 14 were given decaffeinated coffee each day at breakfast and after lunch. Subjects rated their sleepiness and participated in psychomotor vigilance tests and other tasks at four time points during each day of the study.
While both groups reported increasing sleepiness as the study progressed, those who received caffeine had better executive control and sustained and selective attention than those who received decaffeinated coffee. These differences were no longer significant after a sleep recovery night following the sleep restricted period.
"Previous research suggests that acute consumption of caffeinated coffee can reduce the impact of sleep deprivation on deficits of attention and cognitive function in a short-term setting,” commented coauthor Denise Lange. “This study is among the first to examine whether this effect can be translated into a real-world situation, where caffeinated drinks are commonly consumed every day by people who experience chronic sleep restriction. Our study indicates that moderate coffee intake can mitigate some repercussions of reduced sleep over a few days, however, this is not a substitute for a good night's sleep in the long term."
—D Dye
Regular aspirin use needs start early to protect against cancer
January 22 2021. A report published on January 21, 2021 in JAMA Oncology concluded that initiating the use of low-dose aspirin before the age of 70 helps protect against the development of colorectal cancer, while starting aspirin after this age may not be effective.
“Aspirin is considered the most established agent for chemoprevention of colorectal cancer and is currently recommended by the US Preventive Services Task Force for individuals aged 50 to 59 years with specific cardiovascular risk profiles,” Chuan-Guo Guo and colleagues wrote. “However, the US Preventive Services Task Force cited insufficient evidence to issue a recommendation for adults aged 70 years or older.”
The current investigation pooled data from 94,540 participants in the Nurses’ Health Study and the Health Professionals Follow-Up Study who were over the age of 69. The use of aspirin and other factors were documented beginning in 1980 and 1986, and regular low-dose aspirin use was reported starting in 2000. Compared with nonregular use, regular use of aspirin was associated with a 20% lower risk of colorectal cancer at age 70 or older. The association occurred only among those who had started using aspirin prior to 70 years of age. Starting aspirin later was associated with a nonsignificant 8% reduction in risk.
"There is considerable evidence that aspirin can prevent colorectal cancer in adults between 50 and 70 years old," commented lead researcher Andrew T. Chan MD, MPH, who is a gastroenterologist and chief of the Clinical and Translational Epidemiology Unit at Massachusetts General Hospital. "But it has not been clear whether the effect is similar in older adults."
"As people get older, if they are not already taking aspirin, a discussion is warranted about whether to start aspirin after weighing the benefits against the risks," he added.
—D Dye
Boosting NAD+ could help prevent aging-associated muscle decline
January 20 2021. Research published on January 19, 2021 in Cell Reports suggests a role for supplementing with compounds that increase levels of the metabolic cofactor nicotinamide adenine dinucleotide (NAD+) to help protect against the loss of muscle tissue that occurs during aging.
The research is the first to show that aggregated amyloid-like proteins contribute to muscle aging and damage mitochondria, the cell’s energy-producing organelles. “Here, we report that, during natural aging, muscle tissues accumulate amyloid-like deposits,” Mario Romano and colleagues wrote. “Moreover, we also discovered the reversible nature of these deposits, which can be reduced by interventions aimed at restoring mitochondrial homeostasis, such as by enhancing nicotinamide adenine dinucleotide (NAD+) metabolism, even at the onset of aging.”
"During age-associated muscle diseases, such as inclusion body myositis (IBM), our cells struggle to maintain correct protein folding, leading these misfolded proteins to precipitate and forming toxic protein aggregates within the muscles," corresponding author Johan Auwerx explained. "The most prominent component of these protein aggregates is beta-amyloid, just like in the amyloid plaques in the brains of patients with Alzheimer's disease."
Giving adult roundworms known as Caenorhabditis elegans the NAD+ precursor nicotinamide riboside or the cancer drug Olaparib (which also increases NAD+) activated mitochondrial defense systems, reduced amyloid aggregates and increased lifespan. In aged mice, the compounds reduced amyloid aggregates in muscles. In muscle tissue derived from aged humans, amyloid-like deposits were also decreased, and mitochondrial function improved.
“Our results in C. elegans, mice, and humans support the notion that natural aging is typified by muscle amyloidosis and, very importantly, that late-life treatments aimed at restoring metabolic and mitochondrial homeostasis also increase cellular and organismal proteostasis, therefore beneficially impacting on health- and life-span in a more pleiotropic fashion than that reported so far,” the authors concluded.
—D Dye
Taurine aids the body’s defenses
January 18 2021. Research reported on January 15, 2021 in the journal Cell revealed a role for the amino acid taurine in maintaining the body’s defenses against harmful bacteria.
The research was the result of a collaboration of scientists from the National Institute of Health’s National Institute of Allergy and Infectious Diseases, National Institute of General Medical Sciences, National Cancer Institute, National Institute of Diabetes and Digestive and Kidney Diseases, and the National Human Genome Research Institute. They observed that a class of gut microbiota (beneficial micro-organisms that normally reside in the intestinal tract) known as Deltaproteobacteria retain a memory of previous infections with pathogens, thereby helping to protect against future infection. Transferring Deltaproteobacteria to mice that lacked micro-organisms improved protection against Klebsiella pneumonia infection.
“The microbiota shields the host against infections in a process known as colonization resistance,” the authors of the report explained. “Here, we show that gut microbiota from previously infected hosts display enhanced resistance to infection. This long-term functional remodeling is associated with altered bile acid metabolism leading to the expansion of taxa that utilize the sulfonic acid taurine.”
The microbiota inhibited the pathogens’ respiration by converting taurine to a toxic gas known as hydrogen sulfide. However, although taurine is made in the body, its production may not always be optimal. By supplying supplemental taurine to mice, the anticipated change in microbiota function was induced and pathogen resistance was enhanced. Giving the animals the drug bismuth subsalicylate, which inhibits the production of hydrogen sulfide, impaired this resistance.
“This work reveals a process by which the host, triggered by infection, can deploy taurine as a nutrient to nourish and train the microbiota, promoting its resistance to subsequent infection,” authors Apollo Stacy and colleagues concluded.
—D Dye
Human migration patterns contributed to vitamin D deficiencies
January 11 2021. Research reported on January 7, 2021 in the Oxford Economic Papers concluded that migration patterns from regions of high sunlight to areas of low sunlight that occurred during the past 500 years significantly impacted the current era’s health outcomes by leading to decreased vitamin D levels.
“The theory behind our analysis builds on three physiological facts,” authors Thomas Barnebeck Andersen and his associates wrote. “First, vitamin D deficiency is directly associated with higher risk of all-cause mortality. Second, the ability of humans to synthesize vitamin D from sunlight (UV-R) declines with skin pigmentation. Third, skin pigmentation is the result of an evolutionary compromise between higher risk of vitamin D deficiency and lower risk of skin cancer.”
The researchers examined groups of people who currently reside in areas that receive low amounts of sunlight who originated from regions that receive a high amount of sunlight. By utilizing the difference in sunlight intensity between original and current locations as a measure of the risk of vitamin D deficiency, the team observed an association between deficiency and lower average life expectancy. This increased risk of premature mortality is due a variety of illnesses, including cardiovascular disease, diabetes, hypertension and some cancers.
They concluded that the imbalance between skin pigment and ambient sunlight intensity induced by migration of darker-skinned people to regions that received less intense sunlight exposure than their former habitations can explain many health differences.
"This research is important because it is the first research to document a link between an increased risk of vitamin D deficiency and differences in life expectancy across countries and regions,” Dr Anderson announced. “It thus serves to highlight the potentially huge benefit in terms of additional life years of taking vitamin D supplements, particularly during the autumn and winter."
—D Dye
Oxidative stress links gum and kidney diseases
January 8 2021. Research reported on December 27, 2020 in the Journal of Clinical Periodontology indicates that the damaging imbalance between reactive oxygen species and antioxidant capacity known as oxidative stress plays a significant role in the association between gum disease and chronic kidney disease. “Patients with chronic kidney disease are also susceptible to periodontitis,” noted Praveen Sharma of the University of Birmingham and colleagues. “This cross‐sectional study aimed to explore the causal relationship between periodontal inflammation and renal function.”
The investigation included data from 770 participants in the Renal Impairment In Secondary Care study, which recruited chronic kidney disease patients between October 2010 and December 2015. Subjects received periodontal assessments that were used to quantify periodontal inflamed surface areas. Blood samples were analyzed for C-reactive protein (CRP, a marker of inflammation) and markers of oxidative stress.
The researchers uncovered a bidirectional causal relationship between periodontal inflammation and renal function. A 10% increase in periodontal inflamed surface areas was associated with a 3% decrease in estimated glomerular filtration rate (eGFR, a measure of kidney function). Furthermore, a 10% decrease in eGFR was associated with a 25% increase in periodontal inflamed surface areas. It was determined that oxidative stress was the basis of this relationship rather than inflammation.
"This is the first paper to quantify the casual effect of periodontitis on kidney function and vice-versa as well as the first to elucidate the pathways involved,” Dr Sharma announced. "It showed that even a modest reduction in gum inflammation can benefit renal function. Given the relative ease of achieving a 10% reduction in gum inflammation, through simple measures like correct brushing techniques and cleaning between the teeth, these results are very interesting".
"We hope that this research paves the way for further studies,” Dr Sharma added.
—D Dye
Moderate calcium intake, supplementation associated with reduced mortality risk during up to two decades of follow-up
January 6 2021. A study and meta-analysis reported on December 31, 2020 in the European Journal of Epidemiology found a lower risk of premature mortality from any cause among men and women who consumed moderate amounts of calcium. Supplementing with calcium was associated with a lower risk of mortality from all causes among women.
Tiberiu A. Pana and colleagues conducted a study that examined the effects of calcium among 17,968 participants in the European Prospective Investigation of Cancer, Norfolk (EPIC-Norfolk). The results were then included in a meta-analysis of 26 studies with a total of 1,828,149 subjects that evaluated the association between calcium intake and all-cause mortality, cardiovascular mortality, and incident cardiovascular disease, aortic stenosis, heart failure, myocardial infarction, peripheral vascular disease and stroke.
When divided into fifths according to amount of their calcium intake, EPIC-Norfolk participants whose intake of calcium was between 771 mg and 926 mg per day had a 9% lower risk of dying from any cause and participants whose intake was 1074 mg to 1254 mg had a 15% lower risk in comparison with subjects whose intake was among the lowest fifth at less than 770 mg. Cardiovascular disease mortality was also reduced in these groups. A moderate intake of calcium was associated with a significantly lower risk of stroke, while the reduction in risk associated with an intake of more than 1255 mg per day failed to reach significance.
The meta-analysis found a lower risk of all-cause mortality in association with higher calcium intake compared to lower intake. Calcium supplementation was associated with lower all-cause mortality among women, while no significant association was observed among men.
“Moderate dietary calcium intake may protect against cardiovascular and all-cause mortality and incident stroke,” the authors concluded.
—D Dye
Omega 3 fatty acid DHA improves stroke therapy
January 4 2021. An article published on December 29, 2020 in Brain Circulation provides evidence for adding the omega 3 fatty acid DHA or its derivatives to a treatment for ischemic stroke.
Researchers at Louisiana State University hypothesized that the addition of DHA and docosanoids derived from DHA to a drug known as LAU-0901 that blocks the pro-inflammatory platelet-activating receptor could better protect brain cells and improve post-stroke recovery than the administration of a single compound. Using a rat model of stroke, Nicolas G. Bazan, MD, PhD, and colleagues administered one of two doses of LAU-0901 with or without DHA or the DHA derivatives neuroprotectin D1 (NPD1, whose production is stimulated by DHA and which protects brain cells and supports their survival), or aspirin-triggered NPD1 (AT-NPD1), during a period of three hours after stroke onset. Behavior was analyzed the day the treatments were administered and on various days after each combination. Magnetic resonance imaging (MRI) of the brain was conducted following the experiments that involved NPD1 and AT-NPD1.
Receiving LAU-0901 combined with DHA or its derivatives resulted in improved post-stroke behavior in comparison to DHA, NPD1 or AT-NPD1 alone. Rats that received NPD1 had brain lesion volumes that were smaller by 62% and those that received AT-NPD1 experienced reductions of 90% in comparison with animals that received a control substance. "The biological activity of LAU-0901 and AT-NPD1 is due to specific activation or modulation of signaling pathways associated with the immune system, inflammation, cell survival, and cell-cell interactions," Dr Bazan explained. "These findings provide a major conceptual advance of broad therapeutic relevance for cell survival, brain function and, particularly, stroke and neurodegenerative diseases."
"We discovered that these novel molecules promote neuronal cell survival with important anti-inflammatory activity," added first author Ludmilla Belayev. "This combinatorial therapy may hold promise for future therapeutic development against ischemic stroke."
—D Dye
