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.
Metformin could delay heart disease in type 1 diabetics
August 31 2016. Research reported on August 26, 2016 in Cardiovascular Diabetology suggests a use for metformin, commonly used to treat type 2 diabetes, to delay the development of heart disease in type 1 diabetics.
Twenty-three type 1 diabetics with no evidence of heart disease were given metformin in addition to standard therapy for eight weeks while nine type 1 diabetics received standard insulin therapy. Twenty-three healthy nondiabetics served as a control group. Circulating endothelial progenitor cells, proangiogenic cells, endothelial cells and other factors were assessed before and after the treatment period.
"For the first time, this study has shown metformin has additional benefit beyond improving diabetes control when given to patients with relatively well controlled type 1 diabetes," reported lead researcher Jolanta Weaver. "We have established the drug increases patients own vascular stem cells, which will help delay or slowdown heart disease. Our findings also show that the cells associated with damaged blood vessels were reduced, confirming that the repair of blood vessels was taking place in our patients."
"Metformin could routinely be used by patients with Type 1 diabetes to help lower their chances of developing heart disease, by increasing a repair mechanism created by vascular stem cells released from the bone marrow," she predicted.
"As the outcomes of heart disease are worse in diabetic versus nondiabetic patients, there is a need to identify additional treatment options," Dr Weaver continued. "We have shown that all our patients in the study had their insulin doses reduced after taking metformin and have not suffered any serious adverse effect."
—D Dye
Omega 3 supplementation protects against intracranial atherosclerosis
August 29 2016. Research reported on August 16, 2016 in Neuroscience found a protective effect for supplementation with the omega 3 fatty acid alpha-linolenic acid, a precursor of the omega 3 EPA, against the risk of intracranial atherosclerosis, a leading cause of recurrent ischemic stroke.
Researchers gave rats a diet that contained high or normal amounts of cholesterol for up to six weeks. Animals that received the high cholesterol diet were treated for the first two weeks with a compound that rendered them susceptible to atherosclerosis, and half of the group was given omega 3 daily for six weeks. Blood levels of triglycerides, and HDL, LDL and total cholesterol were measured at three and six weeks.
The high cholesterol diet induced increases in triglycerides and total and LDL cholesterol at both time points in comparison with levels measured in the animals given normal diets, however, animals that received omega 3 had significantly lower levels of these lipids than the unsupplemented group. While protective HDL cholesterol levels had declined after six weeks in the untreated high cholesterol-fed animals compared to the animals fed normal diets, they increased in the group that received omega 3.
Middle cerebral artery lumen stenosis (narrowing) and increased intima media thickness (an assessment of the width of one of the innermost layers of the arterial wall) was observed after six weeks in animals given high cholesterol diets, however, lumen diameter was significantly greater and media thickness was decreased in animals that received omega 3. Omega 3 supplementation was also associated with reductions of CD68 (an inflammatory marker) in the middle cerebral artery, and with lower blood levels of other factors that were higher in the unsupplemented high cholesterol diet group.
"Thus, the inexpensive, widely available omega 3 fatty acid could be a promising prevention strategy for intracranial atherosclerotic stenosis," the authors conclude.
—D Dye
More positive evidence for melatonin in breast cancer battle
August 26 2016. An article published in the May 2016 issue of Genes and Cancer describes how melatonin, a hormone that facilitates sleep, suppresses breast cancer growth.
"Cancer stem cells pose a challenge in cancer treatment, as these cells can drive tumor growth and are resistant to chemotherapy," write Juliana Lopes and colleagues in their introduction. "Melatonin exerts its oncostatic effects through the estrogen receptor (ER) pathway in cancer cells, however its action in cancer stem cells is unclear."
"From studies of cancer stem cells, the transcription factor OCT4, encoded by the POU5F1 gene, was found to be a critical factor for self-renewal and maintenance of pluripotency of stem cells," they note. "Based on the idea that breast cancer treatment is particularly complicated by cancer stem cells, and that the control of the disease requires the inhibition of these cells, the objective of this study was to evaluate the effect of melatonin on regulation of the OCT4/POU5F1 by the ER-alpha in breast cancer stem cells after induction with tumor initiation chemical BPA and with estrogen."
The team created three dimensional tumors known as mammospheres from breast cancer stem cells for their research. The growth of these tumors was enhanced by the administration of estrogen or Bisphenol A (BPA), a chemical used in food packaging. Following administration of melatonin, mammospheres significantly decreased in size and number in comparison with controls that did not receive the hormone. The researchers also observed a decrease in ER-alpha binding to OCT4 and a reduction of OCT4 and ER-alpha expression.
"This work establishes the principal by which cancer stem cell growth may be regulated by natural hormones, and provides an important new technique to screen chemicals for cancer-promoting effects, as well as identify potential new drugs for use in the clinic," coauthor James E. Trosko concluded.
—D Dye
Omega-3 shows promise as stroke treatment
August 24 2016. Findings from experimental research appearing on August 11, 2016 in PLOS ONE reveal a potential use for the omega 3 fatty acid docosahexaenoic acid (DHA) as a protective therapy against damage caused by ischemic stroke.
Vadim S. Ten, MD, PhD, and colleagues at Columbia University Medical Center induced a stroke-like condition in ten-day-old mice followed by treatment with saline or an emulsion that contained EPA or DHA. A second dose was administered an hour later. Neurologic function was evaluated 24 hours and eight to nine weeks post-stroke.
After 24 hours, animals that received DHA had experienced a reduction in brain injury, as indicated by a decrease in cerebral infarct volume and improved reflex assessment compared to saline-treated animals. At eight to nine weeks, animals treated with EPA or DHA showed mildly improved spatial learning in comparison with the control group, however, navigational memory was significantly improved in DHA-treated mice. Animals that received DHA also exhibited increased mitochondrial DHA content. "Our findings suggest that injecting the omega 3 fatty acid DHA after a stroke-like event has the ability to protect brain mitochondria against the damaging effects of free radicals," stated Dr Ten, who is an associate professor of pediatrics at Columbia University Medical Center.
"Clinical trials are needed to determine if administering lipid emulsions containing DHA shortly after a stroke-like brain injury offers the same neuroprotective effects in babies and adults, as seen in mice,” noted senior co-author Richard J. Deckelbaum, MD, CM, who is the Robert R. Williams Professor of Nutrition and Professor of Epidemiology and director of the Institute of Nutrition at CUMC. “If successful, such trials could lead to the development of a novel therapy for stroke in newborns, children, and adults, addressing a major medical need.”
—D Dye
Study suggests protective effect for omega-3 against diabetic retinopathy
August 22 2016. An article published on August 18, 2016 in JAMA Ophthalmology reports an association between higher omega-3 polyunsaturated fatty acid (PUFA) intake and a lower risk of diabetic retinopathy, a major cause of vision loss worldwide.
The study included 3,482 diabetic men and women who participated in the Prevencion con Dieta Mediterranea (PREDIMED) randomized trial, which compared the cardioprotective effects of Mediterranean diets supplemented with extra virgin olive oil or nuts to a low fat control diet. Food frequency questionnaires administered at enrollment and yearly during follow-up provided information concerning omega-3 fatty acid intake.
Over a median six year follow-up period, diabetic retinopathy was diagnosed in 69 participants. Those who met the target baseline intake of at least 500 milligrams of the omega 3 fatty acids EPA and DHA for cardiovascular disease prevention were found to have a 48% lower adjusted risk of developing diabetic neuropathy than those who failed to consume this amount.
As potential mechanisms, authors Aleix Sala-Vila, DPharm, PhD, of the Lipid Clinic in Barcelona and colleagues note that experimental studies have shown that anti-inflammatory compounds derived from supplemental omega 3 fatty acids delay the progression of neovascularization, which is a hallmark of proliferative diabetic neuropathy.
"To the best of our knowledge, this is the first study in humans on long chain omega 3 PUFA and diabetic retinopathy, and the results reinforce a notion heretofore only explored in experimental models," the authors announce. "Our findings support the view that regular consumption of oily fish might be beneficial to delay the onset or progression of vascular diseases in arterial beds other than the coronary and cerebrovascular ones."
They conclude that the findings "add to the notion of fish-derived long chain omega 3 polyunsaturated fatty acids as a healthy fat."
—D Dye
Mediterranean diet, exercise associated with less Alzheimer's-related brain changes
August 19 2016. The September 2016 issue of the American Journal of Geriatric Psychiatry reports the finding in individuals with mild memory loss of an association between healthy lifestyle factors and a lower amount of amyloid beta deposits and tau protein tangles characteristic of Alzheimer's disease.
The study included 44 adults between the ages of 40 to 85 years with mild memory complaints. Participants provided information concerning diet, physical activity levels and other lifestyle factors.
Positron emission tomography (PET) scans quantified the presence of amyloid beta plaque and neurofibrillary tangles that are increased in the brains of Alzheimer's disease patients. The researchers observed less of these changes on average in those who adhered to a Mediterranean diet, maintained healthy physical activity levels and had a healthy body mass index. (A Mediterranean diet is characterized by a high intake of fruit, vegetables, legumes, grains and fish, low amounts of meat and dairy, and a high ratio of monounsaturated to saturated fat.)
The study is the first to link lifestyle factors with abnormal brain proteins in individuals with mild memory loss, according to lead author Dr David Merrill of UCLA's Semel Institute for Neuroscience and Human Behavior. "The fact that we could detect this influence of lifestyle at a molecular level before the beginning of serious memory problems surprised us," he stated. "The study reinforces the importance of living a healthy life to prevent Alzheimer's, even before the development of clinically significant dementia. This work lends key insight not only into the ability of patients to prevent Alzheimer's disease, but also physicians' ability to detect and image these changes."
—D Dye
Japanese green tea consumers have reduced risk of dementia
August 17 2016. The October 2016 issue of the American Journal of Geriatric Psychiatry reported the finding of researchers at Tohoku University of a lower incidence of dementia among green tea drinkers in Japan.
"Because of the high rates of tea consumption by the global population, even small effects of this daily habit on an individual could have a large impact on public health," observe authors Yasutake Tomata and colleagues.
The study included 13,645 participants in the Ohsaki cohort 2006 study that enrolled men and women aged 65 years and older residing in Ohsaki City. Surveys completed upon enrollment included questions regarding average consumption of tea in addition to various food items. Subjects were also queried concerning current psychological distress, motor function, subjective memory complaints and other factors. The group was followed from April 2007 until the end of November 2012, during which 8.7% developed dementia.
Subjects who consumed high amounts of green tea were likelier to be women and to be nonsmokers. Compared with those who consumed less than one cup per day, those who consumed three to four cups had a 16% lower adjusted risk of dementia and subjects who consumed more than five cups had a 24% lower risk. Limiting the analysis to those who did not report memory complaints upon enrollment failed to substantially affect the results.
While nonsignificant protective effects for oolong and black tea were observed, the stronger effects found for green tea suggest that its high epigallocatechin gallate (ECGC) content could be responsible for the neuroprotective benefit uncovered in this study.
"This study has shown that green tea consumption is associated with a decreased risk of incident dementia in Japanese elderly individuals," the authors conclude. "This suggests that green tea consumption may have a preventive effect against dementia."
—D Dye
Increased calcium intake associated with lower colorectal cancer risk in large analysis
August 15 2016. A study of participants in the Nurses' Health Study and the Health Professionals Follow-Up Study reported an association between a relatively high intake of calcium and a reduced risk of colorectal cancer. The findings were reported on July 28, 2016 in the International Journal of Cancer.
Boston researchers evaluated data from 88,509 women who participated in the Nurses' Health Study between 1980 and 2012 and 47,740 men enrolled in the Health Professionals Follow-Up study from 1986 to 2012. Calcium intake was assessed every four years.
Over the studies' follow-up periods, 3,078 cases of colorectal cancer were diagnosed. Subjects whose total calcium intake from food and supplements was greater than 1,400 mg per day had a 22% lower risk of colorectal cancer than those whose intake was less than 600 mg. Further analysis found a stronger protective effect for calcium against distal colon cancer than against proximal malignancies.
Calcium's protective benefit appeared to be strongest 12 to 16 years before diagnosis. "This finding suggested that the latency for colorectal cancer associated with calcium intake is about 10 years, which is similar to the progression time of adenomas that develop into cancers," the authors write. "Because most sporadic colorectal cancer develops from the adenoma-carcinoma sequence, our findings not only add another line of evidence to support the notion that calcium is a promising chemopreventive agent for colorectal cancer but also suggest that higher calcium intake may reduce early development of carcinogenesis."
"Given that calcium is a simple, modifiable, inexpensive agent and the benefit of calcium intake on colorectal cancer is expected to continue beyond 1,000 mg/day, both calcium supplement users and nonusers may further reduce their colorectal cancer risk through additional calcium intake," they suggest.
—D Dye
NHANES analysis adds evidence to vitamin deficiency-ED link
August 12 2016. The results of an analysis of participants in the National Health and Nutrition Examination Survey (NHANES) 2001-2004 provides more evidence for an association between vitamin D deficiency and an increased risk in vascular erectile dysfunction. The findings were published in the September 2016 issue of the journal Atherosclerosis.
The study included 3,390 men participants in NHANES 2001-2004 who were free of atherosclerotic cardiovascular disease. Results of blood tests for serum 25-hydroxyvitamin D were categorized as deficient, intermediate or optimal.
Seven hundred seventy-five men reported having ED. In all statistical models, the incidence of ED rose in association with decreasing levels of vitamin D. In the model adjusted for demographics, lifestyle factors, cardiovascular disease risk factors and medication use, men with deficient vitamin D levels of less than 20 nanograms per milliliter (ng/mL) had a 30% greater risk of ED than those with levels of at least 30 ng/mL, defined as optimal. When severe ED was examined, the adjusted risk was 80% higher among those with vitamin D deficiency.
As potential mechanisms for vitamin D deficiency in ED, authors Yousef M. K. Farag and colleagues list improved glucose metabolism and endothelial function, and decreased inflammation and arterial calcification.
"25(OH)D is an easy biomarker to screen for through simple commercially-available laboratory tests, and deficiencies can be treated with supplementation and/or modest sunlight exposure," they note. "Thus, if a causal relationship is confirmed in other studies (such as in randomized placebo controlled interventional trials), treatment of vitamin D deficiency has the potential to improve erectile function through improvement of endothelial function, decreased atherosclerosis risk, and anti-inflammatory properties."
—D Dye
Vitamin D deficiency could explain gout effect in men
August 10 2016. The authors of a letter published in the August 2016 issue of The Journal of Rheumatology suggest that vitamin D deficiency could explain the association between gout and an increased risk of erectile dysfunction (ED). "To our knowledge, no interventional studies have assessed the beneficial effect of vitamin D supplementation in male subjects with ED and/or gout," note Zheng-Tao Lv, MD, and An-Min Chen, PhD, of Huazhong University of Science and Technology in China.
Recent research has concluded that vitamin D deficiency contributes to erectile dysfunction because reduced levels of the vitamin are associated with cardiovascular disease, which has many of the same risk factors as ED. Indeed, ED is now considered to be an early indicator of atherosclerosis.
Drs Lv and Chen note that studies have found a higher incidence of ED in gout patients compared to those without the disease. Mechanisms underlying the occurrence of ED in gout patients include endothelial dysfunction, oxidative stress and inflammation caused by elevated serum levels of uric acid that characterize gout.
An association has been observed between higher serum uric acid levels and lower serum calcitriol, the active form of vitamin D. In kidney failure patients with increased uric acid levels, it was found that uric acid could suppress the synthesis of calcitriol. Another study found that male gout patients had significantly lower serum calcitriol levels than healthy men. "We emphasize the pivotal role of vitamin D deficiency in the pathogenesis of gout and ED," Drs Lv and Chen conclude. "If proven by future studies that vitamin D deficiency is a risk factor for ED and gout, then men with gout and/or ED should be routinely screened for vitamin D deficiency. For the patients with low levels of vitamin D, replacement therapy to raise it to above 30 ng/ml is suggested."
—D Dye
Pomegranate improves synaptic function in experimental model of Alzheimer's disease
August 8 2016. An article published on July 28, 2016 in the journal Oncotarget reports improvement in the loss of synaptic proteins that occurs with aging in association with pomegranate intake in a mouse model of Alzheimer's disease. Synapses are the connections that enable the transmission of messages between neurons. Impairment of synaptic plasticity—the ability of synapses to strengthen or weaken over time in response to variation in their activity—is one of several neurologic changes observed in Alzheimer's disease that contributes to cognitive impairment.
"Synaptic dysfunction represents another pathological presentation of Alzheimer's disease," explain authors Nady Braidy of the University of New South Wales and colleagues. "Since impairments in synaptic plasticity precede synaptic loss, changes to synaptic regulatory protein may represent an important biomarker for disease progression and cognitive impairments."
The current study investigated the effects of the addition of pomegranate to the diets of Alzheimer's disease transgenic mice that develop amyloid beta brain deposits characteristic of the disease. The mice were provided with a standard diet or a standard diet enhanced with 4% pomegranate fruit for 15 months, while normal mice served as controls.
"The present study demonstrated for the first time that pomegranate diet administered for 15 months enhanced synaptic plasticity by increasing the expression of synaptic proteins," the authors report.
"Together with other mechanisms, such as inhibition of neuroinflammation, and increased autophagy, pomegranates may represent alternative treatment to lower Alzheimer's disease pathology," they conclude.
—D Dye
Soy isoflavones could help lower insulin in women with PCOS
August 5 2016. An article appearing on August 4, 2016 in the Journal of Clinical Endocrinology & Metabolism reveals a potential benefit for soy isoflavones for women with polycystic ovary syndrome (PCOS)--a disorder characterized by mildly elevated male hormones and insulin which is associated with weight gain, infertility, and a greater risk of diabetes and coronary heart disease. The condition is estimated to affect 5 to 6 million U.S. women.
In a randomized trial, 70 women aged 18 to 40 years with PCOS were assigned to consume 50 milligrams per day of a soy isoflavone supplement or a placebo for 12 weeks. Blood samples collected at the beginning and end of the study were analyzed for levels of hormones, lipids, and biomarkers of inflammation and insulin resistance.
At the end of the trial, participants who received soy isoflavones had lower insulin and markers of insulin resistance, free androgens, and serum triglycerides in comparison with those who received a placebo. They also experienced an increase in plasma glutathione and a decrease in malondialdehyde, a marker of oxidative stress.
"Our research found that women who have PCOS may benefit from incorporating soy isoflavones in their diets," remarked first author, Zatollah Asemi, PhD, of Kashan University of Medical Sciences in Iran. "In the first study to examine the connection, we found women who consumed soy isoflavones regularly saw improvement in biological markers that reflect how effectively the body utilizes insulin to process sugars and had reduced levels of harmful cholesterol."
"There is growing interest in how adding soy to the diet can help address metabolic syndrome and related health conditions," Dr Asemi added. "Our findings indicate consuming soy isoflavone regularly may help women with PCOS improve their metabolic and cardiovascular health."
—D Dye
Omega 3 heals the heart
August 3 2016. Results from the OMEGA-REMODEL randomized clinical trial reported on August 1, 2016 in the American Heart Association journal Circulation reveal improved heart function and less scarring in patients given omega 3 fatty acids from fish oil for six months following a heart attack. The findings suggest a role for omega 3 in the prevention of cardiac remodeling, a condition characterized by alterations in heart shape and function that can occur after a heart attack, which is associated with heart failure.
The trial included 360 heart attack survivors who received 4 grams omega 3 fatty acids or a placebo within a month of the attack. At the beginning and end of the treatment period, blood samples were analyzed for omega 3 levels, inflammation biomarkers and other factors, and magnetic resonance imaging (MRI) evaluated cardiac structure and tissue characteristics.
At the end of the study, participants whose red blood cell omega 3 index rose to the top 25% of subjects had a 13% reduction in left ventricular systolic volume index (a marker of heart remodeling) compared to those whose levels were among the lowest 25%. Participants who received omega 3 experienced significant reductions in markers of inflammation and heart muscle fibrosis, without adverse effects.
"Heart failure is still a major problem after a heart attack despite all the therapy we have and the advances in interventional care," noted senior author Raymond Y. Kwong, MD, MPH, who is the director of Cardiac Magnetic Resonance Imaging at Brigham and Women's Hospital and an associate professor of medicine at Harvard Medical School. "Our findings show that omega-3 fatty acids are a safe and effective treatment in improving cardiac remodeling, so it may be promising in reducing the incidence of heart failure or death, which are still major healthcare burdens to patients who suffer a heart attack."
—D Dye
Low cysteine levels implicated in Huntington's disease
August 1 2016.An article published on July 26, 2016 in the Proceedings of the National Academy of Sciences suggests that oxidative stress caused by low cysteine levels may play a role in Huntington's disease.
"We show here that the master regulator of amino acid homeostasis, activating transcription factor 4 (ATF4), is dysfunctional in Huntington's disease because of oxidative stress contributed by aberrant cysteine biosynthesis and transport," write authors Juan I. Sbodio, PhD, and colleagues at The Johns Hopkins University School of Medicine. "Consistent with these observations, antioxidant supplementation reverses the disordered ATF4 response to nutrient stress."
The team cultured brain cells derived from mice with Huntington's disease as well as healthy brain cells in a low cysteine environment. While healthy cells increased ATF4 activity, ATF4 in cells from the Huntington's disease mice was undetectable. Repeating the experiment in medium that was deficient in other amino acids resulted in normal ATF4 levels in both types of cells. "That intrigued us, and we wondered if elevated oxidative stress would affect the response of ATF4 because of cysteine's role in cellular defense," commented coauthor Bindu Paul, PhD.
The question was answered by inducing oxidative stress in healthy cells by exposing them to hydrogen peroxide and depleting them of cysteine, which resulted in a significant decrease of ATF4. Furthermore, Huntington's cells grown in cysteine-depleted conditions to which vitamin C, an antioxidant, was administered enabled the cells to produce ATF4 and their own cysteine. "These findings implicate a vicious cycle where low levels of cysteine cause oxidative stress, which leads to decreased cysteine levels, therefore creating more oxidative stress, further slowing cysteine production," Dr Sbodio explained.
"We identify a molecular link between amino acid disposition and oxidative stress that underlies multiple degenerative processes in Huntington's disease," Dr Sbodio and colleagues conclude. "Agents that restore cysteine balance may provide therapeutic benefit."
—D Dye
