NEWS BRIEFS – October 2014

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A new study has reported that vitamin D deficiency is associated with a substantially increased risk of dementia and Alzheimer’s disease in older people. The researchers found that those who were moderately deficient in vitamin D had a 53% increased risk of developing dementia of any kind; and those who were severely deficient in vitamin D had a 125% increased risk increased of dementia. Similar results were recorded for Alzheimer’s disease (AD), with the moderately deficient group being 69% more likely to develop AD, and the severely deficient subjects having a 122% higher risk of AD.

Dementia is one of the greatest challenges of our time, with 44 million cases worldwide, a number expected to triple by 2050 as a result of rapid population aging. A billion people worldwide are thought to have low vitamin D levels and many older adults may experience poorer health as a result.

The study focused on subjects aged 65 and over who were free of dementia, cardiovascular disease, and stroke. The study was partly funded by the Alzheimer’s Association, and subjects were tracked for six years after their vitamin D status was recorded to see who developed signs of dementia or AD. Diagnosis was made using a wide range of information, including neuroimaging. This is the most robust study of its kind ever conducted. The latest results do not demonstrate that low vitamin D levels cause dementia, only that there seems to be a strong correlation. Clinical trials are now needed to establish whether eating foods such as oily fish or taking vitamin D supplements or increasing sun exposure can delay or even prevent the onset of AD and dementia.

This study was posted on the website of the journal Neurology on August 6, 2014. An abstract of the study can be read online at, and by clicking on the Full Text (PDF) button, you can access or download the entire study without cost.


A not-yet-published study has found that frequent marijuana use can have a significant negative effect on the brains of teenagers and young adults, including cognitive decline, attention and memory deficits, and measurably decreased IQ. The researchers reported that even once weekly cannabis use may result in neurocognitive damage, as well as addiction.

Previous results found that teens who persistently use marijuana can lose a significant average of six IQ points by adulthood. Abnormalities in the gray matter of the brain, which are associated with reduced intelligence, have been found in 16- to 19-year-olds who increased their marijuana use in the past year. These findings remained constant even after researchers controlled for medical conditions, prenatal drug exposure, developmental delays, and learning disabilities. (Marijuana use is increasing, with 2012 figures showing that 6.5% of high school seniors smoke marijuana daily, up from 2.4% in 1993. Additionally, 31% of those aged 18 to 25 used marijuana in the last month. Some legalized forms of marijuana have higher levels of THC than other strains, and some research has shown that frequent use of high potency THC can increase risk of acute and future problems with depression, anxiety and psychosis.)

This report was presented August 9, 2014 in Washington, DC, at the 122nd annual convention of the American Psychological Association. It has not yet been published.


Scientists have found, in a study which is the largest of its kind, that being overweight increases the risk of 10 common cancers, and called for tougher anti-obesity measures. Every BMI increase of 5 was clearly associated with a 62% increased risk of uterus cancer, a 31% higher risk of gallbladder cancer, a 25% greater risk of kidney cancer, a 10% higher risk of cervix cancer, a 9% higher risk of thyroid cancer, and a 9% increased risk of leukemia. (A body-mass index or BMI of 25 to 29.9 is considered overweight, and 30 and over as obese.) With the higher BMI, the risk was 19% higher for liver cancer, 10% higher for colon cancer, and 5% higher for breast cancer.

Remarkably, even among people with normal BMI, the risk for cancer was higher as BMI increased within the normal range. The team said excess body weight may account for 41% of all uterine cancers. Conversely, those with high BMI seemed to be at a slightly lower risk of developing prostate or premenopausal breast cancer. (Being overweight also puts people at a higher risk of heart disease, stroke, and Type 2 diabetes. A recent global analysis found that a third of adults and a quarter of children today are overweight.)

This research was released online on August 14, 2014 before being published in The Lancet. The full-text study can be accessed online now at


A remarkable review of past, published scientific studies reports that bacteria within us affect both our cravings and our moods to influence our eating behaviour and dietary choices to favour consumption of the particular nutrients they grow best on, rather than simply passively living off, whatever nutrients we choose to send their way. And what they manipulate us to eat often drives us towards obesity. (Microbes living within our bodies outnumber our own cells about 100 to one. Bacterial species vary in the nutrients they need. Some prefer fat, and others sugar, for instance. They vie with each other for food and to retain a niche within their ecosystem, which is our digestive tract. The varying interests of the bacteria inside us may or may not align with our own dietary goals. Some bacteria support body health; others produce cancers.)

While it is unclear exactly how this occurs, the authors believe this diverse community of microbes, collectively known as the gut microbiome, may influence our decisions by releasing signaling molecules into our gut. Because the gut is linked to the immune system, the endocrine system and the nervous system, those signals could influence our physiologic and behavioural responses. Fortunately, it is a two-way street, report the scientists. We can influence the compatibility of these microbes by deliberating altering what we ingest, with measurable changes in the microbiome within 24 hours of diet change or even within minutes.

Gut bacteria may be affecting our eating decisions in part by acting through the vagus nerve, which connects 100 million nerve cells from the digestive tract to the base of the brain; in this way, they can change taste receptors, produce toxins to make us feel bad, and release chemical rewards to make us feel good when we eat certain foods. Research in this area is in its infancy, but eventually, beneficially altering specific microbial populations might be accomplished through particular food and supplement choices, by ingesting specific bacterial species, or when required, by killing targeted virulent species with antibiotics. This study was released in advance of publication in an issue of the journal BioEssays. The full text is now available online at for a fee.


A study has found that the presence of a common class of intestinal bacteria called Clostridia protects against food allergies, has the capacity to reverse existing food allergies, and may prevent sensitization to foods. By inducing immune responses that prevent food allergens from entering the bloodstream, Clostridia minimize allergen exposure and prevent the sensitization to these food-based allergens, which is a key step in the development of these allergies. The discovery points toward probiotic therapies for this so-far untreatable condition.

Environmental stimuli such as antibiotic overuse, high fat diets, caesarean birth, excessive modern hygiene, and even formula feeding have affected the internal microbiota with which humans co-evolved. This may be behind the vast increase in food allergies, some of which can prove fatal. Food allergies among children jumped 50% between 1997 and 2011. Food allergies now affect over 16 million North Americans, including one in 13 children.

Researchers exposed a group of mice raised in sterile conditions with no resident microorganisms, and a group of mice treated with antibiotics as newborns (which significantly reduced their gut bacteria) to peanut allergens. Both groups of mice displayed a strong reaction, producing much higher levels of antibodies against peanut allergens than mice with normal gut bacteria. This sensitization was reversed, however, by reintroducing Clostridia bacteria back into the germ-free mice.

Reintroduction of another major group of intestinal bacteria, Bacteroides, failed to alleviate sensitization, indicating that Clostridia have a unique, protective role against food allergens. Analysis found that Clostridia caused the immune system to produce a signaling molecule that decreases permeability of the intestinal lining, preventing peanut allergens from entering.

This study was released online on August 25, 2014 ahead of publication in Proceedings of the National Academy of Sciences. The full-text version of this report can be accessed online at for a US$10 access fee.


Scientists have reported that children born to women who took antidepressants during pregnancy are statistically more at risk to develop the mental disorder called attention-deficit hyperactivity disorder or ADHD. (ADHD is a condition blamed for severe and frequent bouts of inattention, hyperactivity, or impulsivity, often leading to problems in socializing and education. Children and young adolescents are most frequently diagnosed with it. According to a 2013 report by the US Centers for Disease Control and Prevention, 6.8% of American children and teenagers have ADHD.

Doctors often prescribe powerful psychostimulants such as Ritalin, sales of which have boomed in recent years. There is still a long-running debate about the mix of genetic and environmental causes for ADHD.)

Surveying a large group of women, the team found that taking antidepressants during pregnancy was associated with the risk of ADHD in their offspring. The long-term history and severity of maternal depression was excluded as a factor. However, this precaution still does not mean the link is causal, meaning it may be a statistical quirk; previous research found that maternal depression, treated or untreated, is itself a major risk factor for both mother-to-be and her baby. The risk of a depressive relapse is multiplied fivefold if medication for it is discontinued during pregnancy.

This study will be published in the journal Molecular Psychiatry. It was posted online August 26, 2014 at in its full-text version.


A study of 131,000 people who had a low risk of cardiovascular disease and ranged in age from 18 to 95 has demonstrated a link between those who drink greater amounts of tea and a 24% reduced risk of death from non-cardiovascular causes. Participants were divided into three groups according to their normal daily tea-drinking and coffee-drinking levels: none, one to four cups, and more than four cups. Coffee drinkers were more likely to be smokers. Smokers made up 17% of the one-to-four-cup group of coffee drinkers, compared to 24% of tea drinkers at the same consumption level. Coffee drinkers were also less physically active than tea drinkers (41% compared to 45% respectively). Compared to light coffee drinkers, heavier drinkers of coffee had a slightly lower systolic reading, the upper number in the blood pressure ratio.

Among tea drinkers, those with heaviest consumption showed greater decrease in both blood pressure numbers, systolic and diastolic, compared to light tea drinkers. There was no significant change in the risk of death from non-cardiovascular causes, based on the greater the amount of coffee consumed daily. However, there was a significant reduction in the risk of death from non-cardiovascular causes, based on the greater the amount of tea consumed daily. Overall, heavy tea intake reduced this risk by 24%. The study found big differences between genders, although men tended to drink coffee much more than women, while women tended to drink more tea than men. Interestingly, most of the effect of tea on non-cardiovascular mortality was found in current or ex-smokers; there were no such benefits of tea intake among non-smokers. This study is epidemiological and shows associations only; cause-and-effect cannot be proven. This report was presented September 1, 2014 at the ESC Congress in Barcelona. It has not been posted or published yet.


Men who are physically active are at lower risk of nocturia, which is waking up at night to urinate, according to a 2014 study published in the journal Medicine and Science in Sports and Exercise.


Scientists have found a significant link between obesity and a heightened risk of dementia in later life. Furtermore, the age at which a person is obese seems to be a key factor, with an apparent tripling in dementia risk for people who were obese during their 30s. (Estimates suggest that almost 66 million people around the globe will have dementia by 2030, with the numbers predicted to top 115 million by 2050. There is growing evidence that obesity is linked to dementia, but this research indicates that risk may be heightened or lowered, depending on age.)

Researchers assessed data from hospital records for the whole of England for the period 1999-2011. Data in which obesity had been recorded were then searched for any subsequent care for, or death from, dementia. This revealed a greater decrease in overall risk of dementia, the older a person was when a diagnosis of obesity was first recorded, irrespective of gender. For obese persons aged 30-39, the relative risk of developing dementia was 3.5 times higher than those of the same age who were not obese. For obese persons in their 40s, the risk of developing dementia was 70% more; for obese persons in their 50s, the risk of later dementia dropped to 50% more; and for obese persons in their 60s, only 40% more. However, obese people in their 80s were 22% less likely to develop dementia.

The scientists ventured a theory that the higher risk of dementia from early obesity may stem from obesity-triggered diabetes and cardiovascular problems, which are themselves linked to a heightened risk of dementia. This study was posted online August 20, 2014 by Postgraduate Medical Journal. The full report can be read online at with access fee.


An international group of researchers and health charity workers has reported its findings that men all over the world die younger than women and do worse on a host of health indicators, but policy makers rarely focus on this so-called male health gap or adopt programs aimed at addressing it. Public policies should be instituted to change this by addressing the health and longevity of men more directly, the group writes in a perspective in the Bulletin of the World Health Organization.

The team concluded that the international health community has been slow to recognize the benefits to women and children of improving the health and mortality of men. For example, studies have shown that male alcohol dependence is linked to emotional and behavioural problems in their children; the physical illnesses of men can impair the psychological health of their female partners; women often become long-term caretakers when male partners fall ill or become disabled; and when men are sick, injured or die, households and female partners may suffer a loss of income. In the United States alone, it is estimated that premature death and disease among men add up to $479 billion a year in medical payments, lost productivity, and decreased quality of life.

The gender health disparity has persisted in the face of significant health gains around the world over the last 40 years. Since 1970, female life expectancy has gone up 12 years to 73.3, while male life expectancy went up only 11 years to 67.5. The largest difference in life expectancy is in the Russian Federation, where men live on average 11.6 years less than women. So far, only Australia, Brazil and Ireland have adopted national strategies aimed at improving male health.

Prominent among the reasons cited by the researchers for the persistent gender disparity are male gender norms, which include reluctance among men in many areas of the world to seek medical care or follow medical advice. Men are also more likely than women to adopt risky behaviours that are hazardous to health, such as excessive alcohol use, and they are at greater risk of occupational hazards, including physical injury and chemical exposures. The report was published in the August 1, 2014 issue of the Bulletin of the World Health Organization. The full report can be read on the WHO website at without charge.


Scientists have reported that high dietary salt intake may worsen multiple sclerosis symptoms and boost the risk of further neurological deterioration. (Previous research indicated that salt may alter the autoimmune response, which is implicated in the development of multiple sclerosis or MS, but it has not been clear whether it has any direct effect on the course of the disease itself.) The researchers assessed the urine samples of 70 people with the relapsing-remitting form of MS on three separate occasions over a period of nine months to check for levels of salt. Their neurological health was then tracked for two years. After taking account other factors, such as smoking, age, gender, length of time after diagnosis, weight, treatment, and circulating vitamin D, the analysis indicated a link between levels of dietary salt and worsening symptoms. Compared with those consuming the least salt every day, those on moderate to high intake had around three more episodes of worsening symptoms, and were almost four times as likely to have these episodes.

The researchers then looked at x-rays and scans to find out if the disease had progressed further, and once again found a link between dietary salt intake and radiological evidence of further deterioration. Those whose dietary salt intake was high were almost 3.5 times as likely to have radiological signs of further progression. This is an observational study, so no definitive conclusions about cause and effect can be drawn. Salt intakes ranged from 2 grams to 4 grams.

This study was posted online on August 28, 2014. It will be published in a future issue of the Journal of Neurology, Neurosurgery and Psychiatry. The full study is posted at with fee.

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