Taking probiotics during pregnancy could reduce the risk of gestational diabetes for two thirds of women, according to a New Zealand study published in the British Journal of Nutrition.
Researchers from the University of Otago in Wellington studied the impact of a probiotic, lactobacillus rhamnosus HN001, which is used to produce fermented milk products such as yogurt, on the risk of gestational diabetes.
Characterized by an intolerance of carbohydrates, gestational diabetes disturbs the regulation of glucose levels and results in an excess of blood sugar. Generally affecting between 1 and 4 percent of pregnancies globally and up to as much as 10 percent in some populations, the illness is not only dangerous to expectant mothers, it also exposes their babies to certain risks (excessive growth and weight gain).
For the purposes of the study, 194 women took the probiotic early in their pregnancy while another 200 women were administered a placebo. Gestational diabetes was evaluated between the 24th and 30th week of pregnancy.
The study found that 6.5 percent of women who were administered a placebo contracted gestational diabetes, as opposed to 2.1 percent of expectant mothers who were given the probiotic, which amounts to a 68 percent reduction in risk.
“We found that the protective effects were stronger amongst older women and amongst women who had previously had gestational diabetes,” explains study leader Dr. Julian Crane.
The researchers discovered that the probiotic interacted with microbiota and significantly lowered blood glucose levels among pregnant women.
Lactobacillus rhamnosus HN001 may reduce diabetes and slow the progression of prediabetes among adults at risk. More extensive studies will be required to test its effectiveness in these fields.
Probiotics, dietary supplements composed of micro-organisms, often referred to as “good bacteria,” are naturally present in yogurt and fermented milk, and also in kefir (a drink produced from fermented milk or fruit juice), sauerkraut and olives.
These findings were published in the British Nutrition Journal.
Women with breast cancer who sleep at least nine hours a night may be more likely to die from their tumors than patients who get just eight hours of rest, a recent study suggests.
Compared to women sleeping eight hours a night, women who slept at least nine hours were 46 percent more likely to die of breast cancer, the study found. After up to 30 years of follow-up, the women who got more sleep were also 34 percent more likely to die of other causes.
“Sleep duration, but also changes in sleep duration before versus after diagnosis, as well as regular difficulties to fall or to stay asleep, may also be associated with mortality among women with breast cancer,” said lead study author Claudia Trudel-Fitzgerald of the Harvard T.H. Chan School of Public Health in Boston.
“Given that long sleep duration has been associated with mortality among cancer-free individuals, as well as among breast cancer patients in recent studies including ours, it is possible that the relationship of sleep duration with survival also exists for other types of cancer,” Trudel-Fitzgerald said by email. “However, further research is warranted.”
For the study, researchers examined data on post-diagnosis sleep duration for 3,682 women with breast cancer. They also examined pre-diagnosis sleep duration in a subset of 1,949 women and post-diagnosis sleep difficulties in a subset of 1,353 women.
At diagnosis, women were 65 years old on average and most had what’s known as stage one or two tumors, meaning malignancies hadn’t spread beyond the breast or nearby lymph nodes.
At least half the women in the study were still alive 11 years after their diagnosis.
During the study, there were 976 deaths, including 412 caused by breast cancer, researchers report in the British Journal of Cancer.
Among the subset of women who had data on pre-diagnosis sleep duration, sleeping longer after their diagnosis was associated with 35 percent higher odds of death from all causes and 29 percent greater likelihood of death from breast cancer.
For the group of patients who had data on sleep difficulties, researchers found women who regularly struggled to fall or stay asleep were 49 percent more likely to die from all causes than women who rarely or never had these issues.
The study wasn’t a controlled experiment designed to prove that time spent sleeping directly influences survival after a breast cancer diagnosis.
Other limitations of the study include its reliance on women to accurately recall and report on their own sleep duration and quality, the authors note. It’s also possible that breast cancer contributes to sleep problems rather than sleep difficulties increasing the odds of mortality after a cancer diagnosis, researchers point out.
“People who are sicker are more likely to be fatigued from their illness, be it breast cancer or other cause, and thus sleep more,” said Cheryl Thompson, a researcher at Case Western Reserve University in Cleveland, Ohio, who wasn’t involved in the study.
In the current study, patients who reported getting more than nine hours of sleep were also more likely to be obese and have more advanced cancer, Thompson said by email.
Some patients might sleep more because they get less physical activity, spend more time in bed, or experience more social isolation or depression, said Kristen Knutson, a researcher at the Center for Circadian and Sleep Medicine at Northwestern University’s Feinberg School of Medicine in Chicago.
When patients do notice changes in how long or how well they sleep, it is worth discussing with their doctor, Knutson, who wasn’t involved in the study, said by email.
“Sleep should be considered a vital sign,” Knutson said. “Changes in sleep and excessive sleepiness are important signs that physicians can use to help care for their patients.”
Researchers at the Stanford University School of Medicine have identified a handful of nerve cells in the brainstem that connect breathing to states of mind.
The finding, published in the journal Science, explains how slow breathing induces tranquility.
Medical practitioners sometimes prescribe breathing-control exercises for people with stress disorders. Similarly, the practice of pranayama, controlling breath in order to shift one’s consciousness from an aroused or even frantic state to a more meditative one, is a core component of virtually all varieties of yoga.
The tiny cluster of neurons linking respiration to relaxation, attention, excitement and anxiety is located deep in the brainstem. This cluster, located in an area Mark Krasnow, professor of biochemistry at Stanford, calls the pacemaker for breathing, was discovered in mice by study co-author Jack Feldman, a professor of neurobiology at University of California, Los Angeles, who published his findings in 1991. An equivalent structure has since been identified in humans.
The lead author of the new study is former Stanford graduate student Kevin Yackle, now a faculty fellow at the University of California, San Francisco.
“The respiratory pacemaker has, in some respects, a tougher job than its counterpart in the heart,” Krasnow was quoted as saying in a news release. “Unlike the heart’s one-dimensional, slow-to-fast continuum, there are many distinct types of breaths: regular, excited, sighing, yawning, gasping, sleeping, laughing, sobbing. We wondered if different subtypes of neurons within the respiratory control center might be in charge of generating these different types of breath.”
On that hunch, Yackle searched through public databases to assemble a list of genes that are preferentially activated in the part of the mouse brainstem where the breathing-control center resides. The center’s technical term is the pre-Bötzinger complex, or preBötC. He pinpointed a number of such genes, allowing the investigators to identify more than 60 separate neuronal subtypes, physically differentiated from one another by their gene-activation signatures but comingling in the preBötC like well-stirred spaghetti strands.
The researchers used these genes, and the protein products for which they are recipes, as markers allowing them to zero in on the different neuronal subtypes.
They were able to systematically assess the role of each neuronal subpopulation in laboratory mice, selectively destroy any one of these neuronal subtypes and only that subtype based on its unique signature of active genes, and observe how this particular subtype’s loss affected the animals’ breathing. In 2016, they reported in the journal Nature that they succeeded in isolating a subpopulation of neurons in the preBötC that explicitly controls one type of breathing: sighing. Knocking out these neurons eliminated sighing but left other modes of breathing unaffected.
Krasnow and Yackle then set out to discover the respiratory role of another subpopulation of about 175 preBötC neurons distinguished by their shared expression of two genetic markers called Cdh9 and Dbx1, and bioengineered mice in which they could wipe out, at will, the neurons bearing both of these markers. But once these rodents had their Cdh9/Dbx1 neurons eliminated, they seemed to take the loss in stride. Unlike their sigh-deprived brethren, there was no lacuna in these mice’s portfolio of breathing variations.
“I was initially disappointed,” said Yackle. However, a few days afterward, he noticed something: for mice, the animals were extraordinarily calm. “If you put them in a novel environment, which normally stimulates lots of sniffing and exploration,” he said, “they would just sit around grooming themselves.” Further analysis showed that while these mice still displayed the full palette of breathing varieties from sighs to sniffs, the relative proportions of those varieties had changed. There were fewer fast “active” and faster “sniffing” breaths, and more slow breaths associated with chilling out.
Surmising that rather than regulating breathing, these neurons were spying on it instead and reporting their finding to another structure, the locus coeruleus, in the brainstem, which in turn sends projections to practically every part of the brain and drives arousal, the researchers proved that the preBötC neurons that express Cadh9 and Dbx1 not only project to the locus coeruleus but activate its long-distance-projections, promoting brainwide arousal.
Neurons in the locus coeruleus are known to exhibit rhythmic behavior whose timing is correlated with that of breathing.
“The preBötC now appears to play a key role in the effects of breathing on arousal and emotion, such as seen during meditation,” said Feldman. “We’re hopeful that understanding this center’s function will lead to therapies for stress, depression and other negative emotions.”
Depression affects 86 million people in South-East Asia region, the WHO said today while lauding India for passing the Mental Healthcare Bill recently and asked nations to scale up mental health services quality.
Noting that depression can lead to suicide, which is the second highest cause of death among people of age group 15-29 years in the region, WHO’s South-East Asia Regional Director, Poonam Khetrapal Singh, said depression-related health services must be made more accessible and of higher quality.
On the eve of World Health Day, Singh said if untreated, the most severe form of depression can lead to suicide and asked communities to openly talk about the syndrome to prevent hardships and precious lives being cut short by it.
The World Health Day this year focuses on depression, a condition involving persistent sadness or loss of interest or pleasure in things normally enjoyed.
Singh complimented India for its recent legislation that decriminalizes suicide and seeks to provide healthcare and services for persons with mental health conditions.
“Mental health has been among the top 10 health priorities in Bangladesh, Bhutan, Indonesia, Maldives and Sri Lanka in recent years. Eight of the 11 member countries have mental health policies or plans,” she said.
“By talking about depression more openly and by better understanding of signs and symptoms of the condition, we are in a stronger position to help ourselves if we experience depression-like symptoms,” Singh said.
“We are also better placed to support colleagues, friends or loved ones who may have depression,” she said.
Though depression affects all demographic groups, it is more common among adolescents and youths, women of childbearing age (particularly following childbirth), and those above the age of 60.
Signs and symptoms of depression include disturbed sleep, loss of appetite, guilty feeling, low self-worth, feelings tired and lethargy. It may also manifest as agitation or physical restlessness, substance abuse, reduced concentration and suicidal thoughts or acts, Singh said.
“People experiencing depression often find a range of evidence-based coping mechanisms useful, from talking to someone they trust to exercising regularly or staying connected with loved ones.
“Avoiding or restricting alcohol intake and refraining from using illicit drugs help keep depression at bay. But many people also find professional help an important part of managing the condition,” she said.
Emphasizing on how support for persons experiencing depression is vitally important, Singh said, “Health services across the region, related to depression, must be made more accessible and of higher quality. This is possible even in low and middle-income settings.”
“At present less than 1 per cent of governments’ health expenditure in low and middle-income countries is allocated for mental health,” she said.
Healthcare workers at all levels can be better trained to detect the signs and symptoms of depression, community health facilities can be better integrated with national mental health networks, Singh said.
World Health Day is celebrated on April 7 every year to mark the anniversary of the founding of the World Health Organization and each year a theme is selected that highlights a priority area of public health.
Scientists said Wednesday they have identified a gene that keeps us humans sleeping soundly.
In a study published in the U.S. journal Science Advances, Jason Gerstner of the Washington State University and colleagues colleagues demonstrated that the gene, called FABP7, plays a role in controlling the sleep quality of mice and fruit flies as well.
“It’s the first time we’ve really gained insight into a particular … molecular pathway’s role in complex behavior across such diverse species,” Gerstner said in a statement.
Gerstner first noticed the gene FABP7 when he was a doctoral student at the University of Wisconsin studying genes that change expression over the sleep-wake cycle.
He found that expression of FABP7 changed over the day throughout the brain of mice.
During the current study, Gerstner and his colleagues saw that mice with a knocked out FABP7 gene slept more fitfully compared to normal mice with the gene intact, suggesting the gene is required for normal sleep in mammals.
To see if FABP7 is indeed required for normal sleep in humans, Gerstner and colleagues in Japan looked at data from nearly 300 Japanese men who underwent a seven-day sleep study that included an analysis of their DNA.
It turned out that 29 of them had a variant of the gene responsible for the production of FABP7, and like the mice, they tended to sleep more fitfully.
While these people would get the same amount of sleep as other people, they would wake up more often during the night.
Next, the researchers made transgenic fruit flies by inserting mutated and normal human FABP7 genes into star-shaped glial cells called astrocytes that were previously known to perform many different support roles in the brain, including nutrient delivery and injury repair.
They found flies with the mutated FABP7 gene also woke up more often, similar to what was observed in mice and humans.
“This suggests that there’s some underlying mechanism in astrocytes throughout all these species that regulates consolidated sleep,” said Gerstner.
While the researchers were excited about finding a gene with an apparently strong influence on sleep, they stressed that other genes are almost certainly involved in the process.