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.
Vitamin D anticancer mechanism revealed
December 31, 2012. The November 13, 2012 issue of the Proceedings of the National Academy of Sciences reported the discovery of researchers at McGill University in Montreal of a mechanism for vitamin D against cancer. Numerous studies have uncovered associations between higher vitamin D intake or serum levels and a lower risk of cancer; however, the protective mechanisms of the vitamin have not been fully explored.
Professors John White and David Goltzman of McGill's Department of Medicine and their colleagues discovered that the active form of the vitamin, known as 1,25‑dihydroxyvitamin D, inhibits the production and function of cMYC, a transcription factor involved in cell division that is active in at least 50 percent of cancers. In an experiment conducted by the McGill team, 1, 25‑dihydroxyvitamin D was found to inhibit the transcription of genes regulated by cMYC. And in a study in which vitamin D was applied to the skin of mice, cMYC was suppressed and an antagonist of the protein known as MXD1 increased.
"For years, my lab has been dedicated to studying the molecular mechanisms of vitamin D in human cancer cells, particularly its role in stopping their proliferation," Dr White remarked. "We discovered that vitamin D controls both the rate of production and the degradation of cMYC. More importantly, we found that vitamin D strongly stimulates the production of a natural antagonist of cMYC called MXD1, essentially shutting down cMYC function".
"Taken together, our results show that vitamin D puts the brakes on cMYC function, suggesting that it may slow the progression of cells from premalignant to malignant states and keep their proliferation in check," he concluded. "We hope that our research will encourage people to maintain adequate vitamin D supplementation and will stimulate the development of large, well‑controlled cancer chemoprevention trials to test the effects of adequate supplementation."
Cerebral white matter lesions linked to reduced tocopherol levels
December 28, 2012. The December, 2012 issue of The Journal of Nutrition, Health & Aging reported the finding of Japanese researchers of an increase in deep white matter lesions, a sign of ischemic damage, in association with decreased levels of gamma-tocopherols in men and delta‑tocopherols in women. Cerebral white matter lesions, which can be visualized via magnetic resonance imaging (MRI), consist of periventricular hyperintensities and deep (subcortical) white matter lesions. The current study used deep white matter lesions as an early marker of intracranial arteriosclerosis, which increases the risk of stroke.
Researchers at Kyoto Prefectural University of Medicine measured serum carotenoid, tocopherol, folic acid, and vitamin B12 and C levels in 20 men and 19 women between the ages of 44 and 80. Magnetic resonance imaging scans of the brain were evaluated for the presence of cerebral white matter lesions.
White matter lesions increased with age and systolic blood pressure, and were more prevalent in smokers. A significant reduction in serum gamma-tocopherol levels was observed in subjects with deep white matter lesions. Further analysis limited the association to men, who also had lower vitamin C levels. Among women with deep white matter lesions, delta-tocopherol levels were reduced.
The authors suggest that the variation in the average diet between Japanese men and women and the higher incidence of smoking among men could account for some of the gender differences observed in this study. They remark that vitamins C and E have antioxidative properties that may help protect against atherosclerosis by inhibiting the production of lipid peroxides. Additionally gamma-tocopherol may preserve the effectiveness of endothelial nitric oxide synthase, an enzyme that generates nitric oxide in the blood vessels which helps inhibit smooth muscle contraction and platelet aggregation. The authors recommend further research to clarify the relationship between deep white matter lesions and nutrient levels.
Melatonin reduced in premenstrual syndrome
December 24, 2012. Women affected by premenstrual dysphoric disorder (PMDD), also known as premenstrual syndrome (PMS), were found to have lower levels of the hormone melatonin in a pilot study reported on December 19, 2012 in the journal PLoS One. The finding could account for some of the sleep disturbances commonly reported by women during the premenstrual phase and the consequent adverse effects of sleep loss, including daytime drowsiness and irritability.
Dr Diane B. Boivin and her associates at the Centre for Study and Treatment of Circadian Rhythms at Douglas Mental Health University Institute matched five women with PMDD with five women who did not have the disorder. The women were evaluated during the follicular and luteal phases of their menstrual cycles (which represent the first and second halves of a woman's cycle) for mood, ovarian hormones and 24-hour plasma melatonin.
Women with PMDD had lower melatonin levels at night in comparison with those who did not have PMDD. They additionally had a reduction in melatonin during the luteal phase, when premenstrual symptoms occur, as well as a worsening of mood during this phase.
"Clearly understanding the mechanisms and specific pathophysiology of PMDD can help improve treatments, including both pharmacologic and nonpharmacologic approaches, for this disorder", commented lead author Dr Ari Shechter.
"Here, we described abnormal circadian melatonin secretion, which may relate to a serotonergic dysfunction in PMDD women," the authors write. "Findings of this pilot study indicate that pharmacological approaches such as exogenous nocturnal melatonin supplements, melatonin receptor agonists, or agomelatine should be further tested as therapeutic approaches for the management of depressive symptoms, and encourage more work on the chronobiological basis of psychiatric disorders including PMDD."
Deficient maternal vitamin D associated with low infant birth weight
December 21, 2012. The January 2013 issue of the Journal of Clinical Endocrinology & Metabolism reports the finding of researchers at the University of Pittsburgh of a relationship between reduced vitamin D levels in pregnant women and a higher risk of delivering a low birth weight infant. Babies who are born with a low birth weight have a greater chance of dying during their first month of life and experience more chronic diseases later, including type 2 diabetes and cardiovascular disease.
Alison Gernand, PhD, MPH, RD of the University of Pittsburgh's School of Public Health and colleagues measured 25-hydroxyvitamin D levels among 2,146 pregnant women who participated in the Collaborative Perinatal Project between 1959 to 1965. Women whose vitamin D levels were 37.5 nanomoles per liter (nmol/L) or greater gave birth to infants whose birth weight averaged 46 grams higher than children born to mothers whose vitamin D levels were lower than 37.5 nmol/L. In addition, infants born to mothers with higher vitamin D levels had larger average head circumferences than those born to women with lower levels.
"A mother's vitamin D level early in pregnancy may impact the growth of her baby later in pregnancy," stated Dr Gernand, who is a post-doctoral associate in the School's Department of Epidemiology. "Also, if the mother was deficient in vitamin D during the first trimester, her baby had twice the risk of suffering from growth restriction in utero."
"This is one of the largest studies to examine a mother's vitamin D levels and their relationship with birth weights," added senior author Lisa M. Bodnar, PhD, MPH, RD. "It shows that clinical trials to determine if you can improve birth weights by giving women of reproductive age vitamin D supplements may be warranted."
Insufficient vitamin D could explain alcoholism-related muscle condition
December 19, 2012. In a review published online on December 14, 2012 in Alcoholism: Clinical & Experimental Research, Jan W. Wijnia of Slingedael Korsakoff Center in the Netherlands and colleagues suggest that insufficient vitamin D levels could account for the high prevalence of myopathy in men and women suffering from chronic alcoholism. Vitamin D deficiency is a known cause of myopathy, and alcoholism has been associated with reduced levels of the vitamin. "Myopathy simply means 'muscle disease,'" Dr Wijnia explained. "Muscle weakness is by far the most frequent symptom of alcoholic myopathy, causing difficulties in rising from a chair or in climbing a staircase. In alcoholic myopathy, improvement of muscle weakness usually occurs six to nine months following alcohol abstinence."
For their review, the researchers selected 93 articles concerning myopathy related to reduced levels of vitamin D and myopathy associated with alcoholism. "Our review links possible interdependent deficiencies of vitamin D, phosphate, and magnesium with muscle weakness in chronic alcoholism," Dr Wijnia stated. "Previous studies had suggested that changes in alcoholic muscle disease were not due to dietary deficiencies, but our review is one of the few to examine the effects of severe vitamin D deficiency in alcoholic myopathy."
"The causes of vitamin D deficiencies in alcoholics may include liver dysfunction, lack of sun exposure, malabsorption, and inadequate dietary intake," he added.
"We recommend future research focusing on possible beneficial effects of vitamin D supplementation and on optimal dosages," he continued. "It is possible that vitamin D supplementation may assist in prevention and treatment of alcohol-related chronic myopathy, thus, assessment of vitamin D status may help clinicians to early diagnose severe vitamin D deficiency and hence offer appropriate treatment. Further research is needed to determine if this can improve muscle function if alcohol consumption ceases, and what dosages of vitamin D may be optimal."
Vitamin D supplementation reduces respiratory infection
December 17, 2012. Researchers from Sweden's Karolinska Institut report on December 13, 2012 in the journal BMJ Open that supplementation with vitamin D significantly reduced respiratory tract infections among men and women at risk of contracting them.
In the current study, 124 men and women with an antibody deficiency or history of more than four bacterial respiratory tract infections per year were given 4,000 international units (IU) vitamin D per day or a placebo. The subjects were asked to keep a daily record of symptoms arising from the respiratory tract, ears and sinuses; antibiotic treatment, and other factors. After a year of treatment, composite infectious scores were calculated for each participant.
Subjects who received vitamin D had approximately 25 percent fewer respiratory tract infections and nearly half the antibiotic use than those who received the placebo. The findings are in contrast with those recently described in the Journal of the American Medical Association (JAMA) in which vitamin D failed to show a protective effect against viral respiratory tract infection incidence or severity in a New Zealand population. However, the JAMA study involved healthy individuals whose vitamin D levels at the beginning of the study were normal, and the vitamin was administered in large doses on fewer occasions, which is believed to be less effective than daily administration. "The most important difference is probably due to the fact that our participants had much lower initial levels of vitamin D than those in the New Zealand study," commented study coauthor Dr Anna-Carin Norlin of the Karolinska Institutet's Department of Laboratory Medicine.
Lead author Peter Bergman noted that "Our research can have important implications for patients with recurrent infections or a compromised immune defense, such as a lack of antibodies, and can also help to prevent the emerging resistance to antibiotics that come from overuse."
Broccoli compound shows potential against leukemia
December 13, 2012. A compound known as sulforaphane, found in cruciferous vegetables including broccoli, was found to combat acute lymphoblastic leukemia (ALL) cells in a study published on December 12, 2012 in PLoS One. Sulforaphane is an isothiocyanate that had previously been found to have preventive effects against solid tumors in addition to therapeutic benefits.
"Acute lymphoblastic leukemia is a type of cancer of the white blood cells common in children," explained coauthor Dr Daniel Lacorazza, who is an assistant professor of pathology and immunology at Baylor College of Medicine in Houston. "There is about an 80 percent cure rate, but some children don't respond to treatment. For those cases, we are in need of alternative treatments."
"There have not been definitive studies showing how this compound interacts with blood cancers," he observed.
In research led by Dr Koramit Suppipat, human ALL cell lines and primary lymphoblasts derived from children with precursor B-cell lineage ALL and T-cell ALL were cultured for up to 48 hours with varying concentrations of sulforaphane, after which cell viability was assessed. "The treatment of ALL leukemic cells with sulforaphane resulted in dose-dependent apoptosis and G2/M cell cycle arrest, which was associated with the activation of caspases, inactivation of PARP, p53-independent upregulation of p21, and inhibition of the Cdc2/Cyclin B1 complex," the authors report.
Sulforaphane also reduced tumor burden in a mouse model of ALL. While animals that received the a control substance experienced up to a six-fold increase in tumor burden in comparison with pretreatment levels, mice that received sulforaphane showed a significant reduction in tumor growth after four days.
"Sulforaphane is a natural product," Dr Lacorazza remarked. "However, what we used in this study is a concentrated purified form. So while eating cruciferous vegetables is good for you, it will not have the same effect as what we saw in the lab."
Study defines osteocalcin's role in preventing fracture
December 12, 2012. Research described online on November 5, 2012 in the Proceedings of the National Academy of Sciences reveals a significant role for the protein osteocalcin in strengthening bone and reducing fracture risk.
By studying bone on a microscopic scale, Deepak Vashishth of Rensselaer Polytechnic Institute in Troy, New York and his associates found that fractures begin with the formation of dilatational bands measuring approximately 100 nanometers in size. The holes, which function as a defense mechanism by helping to prevent further damage to surrounding bone following an impact, can lead to fracture if the bone is deficient in osteocalcin and/or another bone protein known as osteopontin. "This study is important because it implicates, for the first time, the role of osteocalcin in giving bone the ability to resist fracture," stated Dr Vashishth, who is the head of Rensselaer's Department of Biomedical Engineering. "Since osteocalcin is always the point of fracture, we believe that strengthening it could lead to a strengthening of the overall bone."
For osteocalcin to be absorbed, it needs to be carboxylated by vitamin K. Increasing osteocalcin by boosting vitamin K intake could therefore be a useful strategy to help prevent osteoporosis. "Currently, all of the advice for treating osteoporosis is related to calcium," Dr Vashishth observed. "We believe there's more to the story than just calcium, and the results of this new study raise an important question about vitamin K. Leafy green vegetables are the best source of vitamin K—wouldn't it be great if eating spinach and broccoli was not only healthy, but also good for your bones? We plan to investigate this link in future."
Calorie restriction mechanism identified
December 10, 2012. In an article published online on December 6, 2012 in the journal Science, Eric Verdin of the University of California, San Francisco and his associates report their finding of a mechanism via which a low carbohydrate, calorie restricted diet delays the effects of aging. This pattern of eating results in the production of ketone bodies that include beta-hydroxybutyrate (βOHB) which, when present in low levels, may help protect the body from the effects of damaging oxidative stress.
In experiments in human and animal cells, calorie restriction stimulated βOHB production, which blocked the activity of enzymes known as histone deacetylases (HDACs). These enzymes prevent the activation of two genes that boost cellular oxidative stress resistance. "Over the years, studies have found that restricting calories slows aging and increases longevity—however the mechanism of this effect has remained elusive" Dr Verdin stated. "Here, we find that βOHB—the body's major source of energy during exercise or fasting—blocks a class of enzymes that would otherwise promote oxidative stress, thus protecting cells from aging."
"This breakthrough also greatly advances our understanding of the underlying mechanism behind HDACs, which had already been known to be involved in aging and neurological disease," noted coauthor Katerina Akassoglou, PhD. "The findings could be relevant for a wide range of neurological conditions, such as Alzheimer's, Parkinson's, autism and traumatic brain injury—diseases that afflict millions and for which there are few treatment options."
"Identifying βOHB as a link between caloric restriction and protection from oxidative stress opens up a variety of new avenues to researchers for combating disease," added lead author Tadahiro Shimazu. "In the future, we will continue to explore the role of βOHB—especially how it affects the body's other organs, such as the heart or brain—to confirm whether the compound's protective effects can be applied throughout the body."
Vitamin D needed by women to maintain cognitive health
December 3, 2012. The October, 2012 issue of the Journals of Gerontology Series A: Biological Sciences and Medical Sciences published the outcome of a study conducted by Yelena Slinin, MD, MS, of Minneapolis' Veterans Administration Medical Center which uncovered a protective effect for higher vitamin D levels against the development of cognitive decline in women.
The study included 6,257 women enrolled in the Study of Osteoporotic Fractures. Serum 25-hydroxyvitamin D was measured upon enrollment and tests of cognitive function were administered at the beginning of the study and at follow-up after four years. Women with low vitamin D levels of less than 10 nanograms per milliliter (ng/mL) had a 60 percent greater risk of cognitive impairment at the beginning of the study and a 58 percent greater risk of becoming cognitively impaired over follow-up in comparison with those whose levels were at least 30 ng/mL.
In another study published in the November, 2012 issue of the same journal, Cedric Annweiler, MD, PhD, of Angers University Hospital in France and his associates report an association between reduced vitamin D intake and a greater risk of developing Alzheimer's disease. The study included 498 older women enrolled in the EPIDemiology of OSteoporosis Toulouse cohort study. Dietary questionnaires administered at the beginning of the study were analyzed for the intake of vitamin D from food sources. Over a seven year period, 70 participants developed Alzheimer's disease. In comparison with those who did not develop dementia or developed other types of dementia, women who developed Alzheimer's disease consumed less vitamin D. When participants were grouped according to vitamin D intake, those in the top one-fifth were found to have a 77 percent lower risk of Alzheimer's compared to the lowest fifth.
These studies, and others, reinforce the importance of vitamin D in the maintenance of cognitive health over the course of a lifetime.
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