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.
Greater magnesium intake associated with lower risk of fatal heart disease, sudden cardiac death in women
December 30, 2019.The January 2020 issue of the Journal of Women's Health revealed the findings of Charles Eaton, MD, of Brown University’s Alpert Medical School and colleagues of a lower risk of fatal coronary heart disease and sudden cardiac death among women who had a higher intake of the mineral magnesium.
The study included 153,569 postmenopausal women who enrolled in the Women’s Health Initiative between 1993 and 1998. Dietary questionnaires completed upon enrollment were evaluated for magnesium intake. Deaths from fatal coronary heart disease and sudden cardiac death were documented during an average 10.5 years of follow-up.
An inverse relationship was observed between increasing magnesium intake and declines in fatal coronary heart disease and sudden cardiac death. Women who were among the lowest 25% of magnesium consumers at a median of 189 milligrams (mg) per day had a 19% greater fully adjusted risk of dying from coronary heart disease and a 24% greater adjusted risk of sudden cardiac death compared to participants whose median intake of 330 mg daily placed them among the top 25%.
The authors note that magnesium has a protective role against inflammation, endothelial dysfunction, thrombosis and vascular smooth muscle calcification, all of which influence coronary heart disease. They add that “Magnesium has antiarrhythmic properties while chronic hypomagnesemia may be proarrhythmic and has been associated with a higher risk of sudden cardiac death.”
Journal of Women’s Health Editor-in-Chief Susan G. Kornstein, MD, who is the Executive Director of the Virginia Commonwealth University Institute for Women's Health commented "If the findings of this study are confirmed, future research should test whether high-risk women would benefit from magnesium supplementation to reduce their risk of fatal coronary heart disease."
—D Dye
Green tea compound shows promise against TB
December 27, 2019. Research reported on November 14, 2019 in Scientific Reports suggests a benefit for epigallocatechin gallate (EGCG) found in green tea leaves (Camellia sinensis) against infection with tuberculosis (TB).
“EGCG has reported activity against TB and was described to impact the integrity of the mycobacterial cell wall,” note authors Wuan-Geok Saw and colleagues.
Mycobacterium tuberculosis cells require the enzyme F-ATP synthase to generate energy for their activity. “During infection, Mycobacterium tuberculosis undergoes a wide range of metabolic changes, which correlate with either replicative growth or nonreplicative persistence,” the authors observe. “Such forms of adaptation include the ability of mycobacteria to respire, regenerate reducing equivalents, and generate the biological energy currency adenosine triphosphate (ATP) via oxidative phosphorylation.”
In addition to other findings, the researchers determined that EGCG inhibits the mycobacterial F-ATP synthase enzyme, thereby limiting the energy available to the bacteria for its growth and stability. The team also identified sites on the enzyme on which it is necessary for EGCG to bind in order to impact Mycobacterium tuberculosis growth.
"Though tuberculosis is curable, the success of current drugs on the market is increasingly being overshadowed by the bacteria's clinical resistance,” remarked senior author Gerhard Grüber of Nanyang Technological University in Singapore. “Our discovery of the EGCG's ability to inhibit the growth of M. tuberculosis will allow us to look at how we can improve the potency of this compound in green tea, and other similar compounds, to develop new drugs to tackle this airborne disease."
—D Dye
Antioxidant supplementation associated with tinnitus symptom improvement
December 23, 2019. A randomized, double-blind trial reported on December 12, 2019 in Nutrients found that antioxidant supplementation benefitted men and women with tinnitus, a condition in which sufferers experience ringing in the ears or other noise in the absence of outside stimuli. Among some individuals, tinnitus can be chronic and causes severe psychological stress.
“Oxidative stress has been proposed to play a critical role in the pathogenesis of tinnitus, since it could lead to cellular changes in hair cells, hair cell apoptosis, cochlear degeneration, changes in supporting structures and stria vascularis, changes in nerve fibers of the acoustic nerve, irregular neural activity in the auditory pathway and dysfunction of the central cortex,” note Anna I. Petridou of the University of Athens and colleagues.
The trial included 70 participants who received an antioxidant supplement or a placebo for three months. Supplemented nutrients included vitamin A, thiamin (B1), riboflavin (B2), niacin (B3), pyridoxine (B6), folic acid, pantothenic acid (B5), biotin, vitamin B12, para-aminobenzoic acid, choline, inositol, vitamin C, vitamin E, calcium, magnesium, iron, copper, manganese, selenium, chromium, molybdenum, iodine, grapeseed extract and alpha-lipoic acid. Participants received baseline assessments prior to treatment, including hearing tests and tinnitus assessment tests. Tinnitus Handicap Inventory questionnaire, Tinnitus Functional Index and Visual Analogue Scale assessments were administered to measure subjective tinnitus-associated discomfort. Blood samples were analyzed for markers of oxidative stress. These assessments were repeated at the end of the study.
Among the group that received antioxidants, tinnitus loudness significantly decreased from levels measured at the beginning of the study. Tinnitus Handicap Inventory questionnaire and Visual Analogue Scale scores also declined in the treated group, indicated improved comfort levels.
“Antioxidant therapy seems to reduce the subjective discomfort and tinnitus intensity in tinnitus patients,” the authors concluded.
—D Dye
Lower glutamine levels associated with increased inflammation in adipose tissue
December 20, 2019. A study reported on December 19, 2019 in Cell Metabolism has found an association between lower levels of the amino acid glutamine and an increase in harmful inflammation in adipose (fatty) tissue.
“While obesity and associated metabolic complications are linked to inflammation of white adipose tissue (WAT), the causal factors remain unclear,” Paul Petrus of Sweden’s Karolinska Institutet and colleagues write. “We hypothesized that the local metabolic environment could be an important determinant.”
The research team compared metabolites released from abdominal white adipose tissue of 52 obese women and 29 women who were not obese. They found the greatest differences in levels of glutamine, which were lower among the obese group. Low glutamine levels were associated with larger fat cells and higher percentage of body fat independent of body mass index.
In adipose tissue cells, decreased glutamine levels stimulated an increase in proinflammatory genes that was reduced after the administration of glutamine. When obese mice were injected with glutamine for two weeks, they experienced less inflammation in their adipose tissue, lower body fat mass and fat cell volume, and decreased glucose levels in comparison with animals that received a control solution.
"Our study shows that glutamine is anti-inflammatory in the fat tissue by changing the gene expression in several different cell types," reported corresponding author Mikael Ryden, who is a professor and senior physician at the Karolinska Institutet’s Department of Medicine. "This means that a lack of glutamine, which may occur during long-term obesity, could lead to epigenetic changes that fuel inflammation in the body."
—D Dye
Increased selenium intake associated with lower osteoporosis risk
December 18, 2019. A study reported in BMC Musculoskeletal Disorders on December 4, 2019 found a reduced risk of osteoporosis among older individuals with a greater intake of the mineral selenium in comparison with those whose selenium intake was lower.
“Selenium (Se), a trace mineral element essential for human beings, can regulate cellular processes by behaving as a component of Se-dependent antioxidant enzymes that eliminate intracellular reactive oxygen species (ROS),” write Yuqing Wang of Central South University in Hunan, China and colleagues. “Therefore, deficiency in Se can lead to an increase in ROS levels, which has been considered as the proximal culprit in the pathogenesis of osteoporosis.”
The cross-sectional study included 6,267 men and women aged 40 years and older who received health screenings at Xiangya Hospital in Hunan, China between 2013 and 2015. Dietary questionnaire responses were analyzed to obtain average selenium intake. Bone mineral density assessment determined the presence of osteopenia or osteoporosis.
A relationship was observed between increasing selenium intake and a decreasing risk of osteoporosis. Among the top 25% of selenium consumers, the adjusted risk of osteoporosis was less than half that of individuals who were among the lowest 25%.
The study is the first to the authors’ knowledge to associate selenium intake “in a general context” with a lower risk of osteoporosis. “The findings of our study may give a hint of the pathogenesis of osteoporosis, and future studies of dietary intake, including selenium supplementary intake, on the risk of osteoporosis are warranted,” they conclude.
—D Dye
Hot new way to live longer
December 16, 2019. Research reported on December 16, 2019 in the Journal of the American College of Cardiology has uncovered a link between regular intake of capsaicin and a lower risk of mortality during an eight year period. Capsaicin is a component of chili peppers whose irritant property provides a “hot” sensation in various cuisines.
"Chili pepper is a fundamental component of our food culture,” observed Licia Iacoviello of the I.R.C.C.S. Neuromed in Pozzilli, Italy. “We see it hanging on Italian balconies, and even depicted in jewels. Over the centuries, beneficial properties of all kinds have been associated with its consumption, mostly on the basis of anecdotes or traditions, if not magic. It is important now that research deals with it in a serious way, providing rigor and scientific evidence. And now, as already observed in China and in the United States, we know that the various plants of the capsicum species, although consumed in different ways throughout the world, can exert a protective action towards our health.”
The investigation included 22,811 participants in the Moli-Sani study, which involves residents of the Molise region of Italy. It was found that people who consumed chili pepper four times per week or more had a 23% lower risk of all-cause mortality, a 40% lower risk of dying from a heart attack and an over 50% lower risk of dying from cerebrovascular disease in comparison with those who did not consume the spice during an eight year period.
"An interesting fact is that protection from mortality risk was independent of the type of diet people followed,” noted first author Marialaura Bonaccio. “In other words, someone can follow the healthy Mediterranean diet, someone else can eat less healthily, but for all of them chili pepper has a protective effect".
—D Dye
Some schizophrenia cases could be undiagnosed vitamin deficiency
December 13, 2019. An investigation reported on December 12, 2019 in Schizophrenia Research suggests that some cases of schizophrenia may be due to deficient levels of the B vitamin niacin.
Severe niacin deficiency known as pellagra, characterized by “the three Ds” (dermatitis, dementia and death) was once prevalent in the United States, particularly in the South between 1906 and 1940. Psychosis resembling schizophrenia occurred in up to 10% of cases. "Treatment with niacin quickly and permanently cures the disease including the psychosis and the dermatitis," noted coauthor Rukshan Mehta. "By 1941, flour was fortified with niacin in the USA and the disease was soon after largely eradicated."
In the 1960s, Drs Abram Hoffer and Humphrey Osmond conducted research and wrote books concerning the effects of niacin against schizophrenia, but their work remained largely ignored.
First author Esme Fuller-Thomson of the University of Toronto revived the deficiency hypothesis after reviewing recent research that uncovered an association between schizophrenia and a gene variant that reduces the ability to utilize niacin. "When I read this study a light bulb went on in my head," she stated. "This seems to be the missing link that explains all these medical mysteries."
The mysteries being referred to include positive findings for niacin supplementation in Canadian trials of schizophrenic patients in the 1950s that failed to be replicated in later trials. However, the earlier trials involved patients born prior to the fortification of flour with niacin, resulting in an increased likeliness of niacin-deficient mothers.
"We acknowledge that this hypothesis is highly speculative, but feel further exploration of these ideas are warranted," Dr Fuller-Thomson remarked. "In cases where the psychosis is due to pellagra, these patients could be inexpensively, quickly, and permanently cured with high dose niacin, allowing them to live a healthy normal life."
—D Dye
Investigational Alzheimer’s disease therapies may also slow aging
December 11, 2019. Research reported on November 19, 2019 in eLife suggests that two promising plant-derived compounds being investigated for their effects against Alzheimer’s disease may also slow some of the aspects of aging.
“Because old age is the greatest risk factor for dementia, a successful therapy will require an understanding of the physiological changes that occur in the brain with aging,” wrote Antonio Currais and colleagues at the Salk Institute for Biological Studies. “Here, two structurally distinct Alzheimer's disease (AD) drug candidates, CMS121 and J147, were used to identify a unique molecular pathway that is shared between the aging brain and AD.”
In a mouse model of rapid aging, CMS121, derived from the flavonol fisetin, and J147, which is a modified version of curcumin, decreased cognitive decline and lowered markers of aging in the brain after four months of treatment. The team found that the compounds preserved mitochondrial homeostasis through the regulation of acetyl-coenzyme A metabolism. "There was already some data from human studies that the function of mitochondria is negatively impacted in aging and that it's worse in the context of Alzheimer's," noted coauthor Pamela Maher, who is a senior staff scientist at Salk. "This helps solidify that link."
"This study further validated these two compounds not only as Alzheimer's drug candidates but also as potentially more widely useful for their antiaging effects," she concluded. "The bottom line was that these two compounds prevent molecular changes that are associated with aging.”
"The contribution of old age-associated detrimental processes to the disease has been largely neglected in Alzheimer's disease drug discovery," Dr Currais observed. "We are now using a variety of animal models to investigate how this neuroprotective pathway regulates specific molecular aspects of mitochondrial biology, and their effects on aging and Alzheimer's."
—D Dye
Chronic inflammation “a substantial public health crisis”
December 9, 2019. An article appearing on December 5, 2019 in the journal Nature Medicine indicts systemic chronic inflammation as the factor behind diseases that represent the world’s leading causes of disability and mortality, including cardiovascular disease, cancer, diabetes, chronic kidney disease, nonalcoholic fatty liver disease, and neurodegenerative and autoimmune disorders.
While short-term, acute inflammation is a natural and necessary response to infection and illness, inflammation that becomes chronic increases the risk of disease. In fact, authors David Furman of the Buck Institute for Research on Aging and colleagues estimate that diseases related to inflammation are behind half of all deaths worldwide. They list several risk factors that promote “this health-damaging phenotype,” which include poor diet, physical inactivity, psychological stress, infections and exposure to industrial and environmental toxins. "Chronic inflammation is influenced by many social, environmental and lifestyle factors," commented senior author George Slavich, who is the director of the UCLA Laboratory for Stress Assessment and a research scientist at the Norman Cousins Center for Psychoneuroimmunology at UCLA. "If we make people aware of these risk factors, our hope is that individuals will reduce the factors that apply to them."
The authors of the article recommend the identification of new biomarkers in the body that improve the ability to screen for, diagnose and treat chronic inflammation. Currently, only a few are known, including C-reactive protein (CRP).
"It's also important to recognize that inflammation is a contributor not just to physical health problems, but also mental health problems such as anxiety disorders, depression, post-traumatic stress disorder, schizophrenia, self-harm and suicide," Dr Slavich added. "This is a substantial public health crisis."
—D Dye
Study suggests benefit for luteolin against prostate cancer
December 6, 2019. The August 2020 issue of journal Carcinogenesis reported a role for the antioxidant flavonoid luteolin against prostate cancer, including castration-resistant disease. While prostate cancer is dependent upon male hormones during its initial stages, castration-resistant prostate cancer (CRPC) refers to disease that no longer responds to androgen-blocking therapy, making it more difficult to treat. Existing therapies for CRPC have demonstrated limited success.
For the current study, Aya Naiki-Ito of Nagoya City University and colleagues investigated the effects of luteolin in a rat model of prostate cancer and found that the flavonoid induced apoptosis (programmed cell death), thereby inhibiting the cancer’s progression. Luteolin also induced apoptosis in rat and human castration-resistant prostate cancer cells and dose-dependently decreased cell proliferation.
In castrated mice that received implanted rat and human prostate cancer tumors, oral administration of luteolin also enhanced apoptosis as well as inhibited angiogenesis, which is the formation of new blood vessels that helps facilitate a tumor’s growth. Luteolin was shown to block the expression of androgen receptor splice variant 7 (AR-V7), which is a contributor to cell proliferation and treatment resistance in castration-resistant disease.
Genetic analysis identified MiR-8080 as a gene that is upregulated by luteolin. In human castration-resistant prostate cancer cells that received the gene, AR-V7 expression level was lowered and apoptosis induced. Conversely, knocking out the gene blocked luteolin’s ability to decrease AR-V7 and cell proliferation in human castration-resistant prostate cancer cells.
When luteolin was added to the chemotherapy enzalutamide in mice that received the human castration-resistant prostate cancer grafts, AR-V7 was downregulated and the drug’s action was enhanced.
“These results indicate luteolin inhibits castration-resistant prostate cancer by AR-V7 suppression through miR-8080, highlighting luteolin and miR-8080 as promising therapeutic agents for this disease,” the authors concluded.
—D Dye
Boosting NAD+ extends lifespan in models of accelerated aging
December 4, 2019. Research reported on November 21, 2019 in Nature Communications revealedthat the metabolic cofactor nicotinamide adenine dinucleotide (NAD+) is depleted in Werner syndrome, a premature aging disease characterized by metabolic dysfunction. It was determined that the disease is caused by faults in a cleanup process known as mitophagy, which breaks down defective mitochondria that produce energy within the cells.
“We are showing for the first time that Werner Syndrome is due to errors in the clean-up process,” announced Vilhelm A. Bohr of the Center for Healthy Aging at the University of Copenhagen and the National Institute on Aging.
Dr Bohr and associates studied mitophagy in blood samples derived from Werner syndrome patients and in fly and worm models of the disease. Boosting NAD+ levels by administering the NAD+ precursors nicotinamide riboside and nicotinamide mononucleotide improved faulty mitophagy and delayed accelerated aging, including stem cell dysfunction. “It strongly reinforces our findings that the clean-up process seems to be important in both human cells and across different animals,” he stated. “And then it is encouraging that in living animals, we can improve lifespan and delay the aging processes which are the key symptoms of Werner Syndrome.”
“Our findings suggest that accelerated aging in Werner syndrome is mediated by impaired mitochondrial function and mitophagy, and that bolstering cellular NAD+ levels counteracts Werner syndrome phenotypes,” the authors conclude.
“Our results are so promising that we have received inquiries from Japan with a view to performing clinical studies of patients with Werner Syndrome,” Dr Bohr added. “We very much hope that the studies will point in the same direction so that patients can live longer and with a higher quality of life.”
—D Dye
Markers of immune status, inflammation associated with premature mortality
December 2, 2019. A study published on December 2, 2019 in JAMA Network Open found an association between a greater risk of premature mortality and markers of inflammation and immune function.
Researchers analyzed information collected upon the enrollment of 31,178 participants in the National Health and Nutrition Examination Survey (NHANES) who were recruited during 1999 to 2010. The team found that having lymphopenia, which is a reduction in white blood cells known as lymphocytes (indicating impaired immune function), was associated with a 30% greater risk of mortality during 12 years of follow-up in comparison with those who did not have the condition. Increases in red blood cell distribution width (a measure of the body's ability to maintain a healthy red blood cell population) and C-reactive protein (CRP), a marker of inflammation, were additionally associated with greater mortality risk. Subjects who had the highest scores of immunohematologic status, indicating severe lymphopenia, high red blood cell distribution width (indicative of bone marrow dysregulation) and high CRP levels, experienced the greatest mortality ten-year mortality risk. Conversely, participants who did not have lymphopenia and whose red blood cell distribution width and CRP levels were among the lowest one-third of the study population had the lowest mortality risk.
"Scientists have gone to great lengths and expense to develop novel biomarkers to identify people at the highest risk for death and disease," commented senior author Jarrod Dalton, PhD. "Here we have taken a more pragmatic approach - investigating the predictive power of components of a patient's white blood cell count, which is collected as part of routine blood work during standard health exams. The complete blood count test is convenient, inexpensive and, as our findings suggest, may be used to help physicians screen for and prevent disease and disease-related mortality."
—D Dye
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