FULL MOON Eclipses Good Night’s Sleep
Ever blamed the full moon for certain behavioral quirks? A new study finds that lunar phases affect sleep patterns, just as folklore has always told.
Christian Cajochen, PhD, at the University of Basel, Switzerland, and his team of researchers studied 33 sleep lab participants for three years starting in 2000, taking electroencephalograms (EEGs) during non–rapid eye movement sleep, measuring nocturnal melatonin and cortisol secretion, and getting subjective feedback on how well rested the participants felt the next day, initially to determine whether age and gender affected sleep patterns. In a surprise twist 10 years later, the team decided to re-analyze their data in relation to lunar phase, largely because as much as 40% of the population anecdotally blames bad sleep on the full moon. In their paper, published in Current Biology, the researchers report that both the objective and subjective measures of human sleep varied with lunar phase— EEGs showed 30% less deep sleep and 20 minutes less total sleep, late evening melatonin levels decreased, and time to fall asleep increased five minutes. Interestingly, “because this study was ‘double blind,’ such that neither the volunteers nor the investigators were ever aware of the purpose of this retrospective analysis, we can exclude potential placebo and nocebo effects,” says Cajochen.
The researchers posit that their findings show human circalunar rhythmicity is not an old wives’ tale after all and that clinicians should consider patients’ periodic sleep complaints carefully. Next steps should focus on “finding out the cause of why we might sleep differently when there is a full moon,” they add.
Using Social Media TO FIGHT OBESITY
In a study published in PLOS ONE, scientists, led by Rumi Chunara, PhD, of Boston’s Children’s Hospital’s Informatics Program (CHIP), looked at data on the proportion of obese and/or overweight populations in metropolitan areas across the U.S. and in New York City neighborhoods, and then cross-referenced those statistics with Facebook aggregate information drawn from what people “like,” as well as other information on their profile and their activity. At the time of the study, about half of the population of the U.S. had a Facebook account.
Nationally, the areas that showed the most activity-related Facebook likes had obesity rates 12% lower than the rest of the country. In NYC, the neighborhood where exercise was most popular — Coney Island — showed a 7.2% lower obesity rate than the neighborhood with the least interest in exercise, southwest Queens. Across the country, obesity rates were only 3.9% higher in areas where Facebook users liked things such as watching television. However, rates were 27.5% higher in northeast Bronx — the NYC neighborhood with the most interest in TV — than they were in Greenpoint, which had the least interest in TV.
The authors concluded that based on these results, social media outlets should be considered as vehicles for collecting data on where obesity rates are most widespread, because information can be obtained unobtrusively, inexpensively, and in real time. These platforms could also be used to intelligently aim health interventions, as the data could inform location-specific campaigns through the same social media platforms.
RECOMBINANT HUMAN GROWTH HORMONE, Body Composition and Muscle Strength in Children
Children suffering from a chronic disease can develop serious conditions due to chronic inflammation, long-term steroid therapy, and decreased physical activity. A team of researchers, led by Dominique Simon, MD, of Hôpital Robert Debré, set out to evaluate rhGH effects on muscle strength in children receiving long-term glucocorticoid therapy. They also wanted to assess the hormone’s effects on height and body composition.
Detailed further in a paper recently published in the Journal of Clinical Endocrinology and Metabolism, the scientists studied 30 children (25 boys and 5 girls) with varying chronic diseases in a randomized, controlled, delayed-start study of rhGH for 12 months, started after randomization (baseline) or six months later (M6).
After six months, high-doses rhGH therapy (0.065mg/kg/d) did not significantly affect composite index of muscle strength. However, the rhGH-treated group showed increases in height, lean mass, and thigh muscle area, compared with the untreated group. After one year of rhGH therapy, height, lean mass, and thigh muscle area increased significantly, but muscle strength was not profoundly changed, while height-related muscle strength remained in the normal range.
While rhGH therapy did not change muscle strength all that much, it was well tolerated and did lead to improvements in height and helped maintain heightrelated strength. The authors wrote, “These data provide a useful basis for future research aimed at optimizing physical fitness in chronically ill children.”
FIRST MOUSE MODEL
Made of Graves’ Orbitopathy
In a study recently published in the journal Endocrinology, researchers led by J. Paul Banga, PhD, King’s College London School of Medicine in the United Kingdom, considered the TSH receptor (TSHR) and IGF-1 receptor (IGF-1R) to be relevant antigens. They then showed that when female mice were immunized with human TSHR (hTSHR) A-subunit plasmid, the mice developed orbital pathology, characterized by interstitial inflammation of extraocular muscles, with the inflammation caused by CD3+T cells, F4/80 macrophages, and mast cells, accompanied by glycosaminoglycan deposition with resultant separation of individual muscle fibers.
The scientists wrote that in vivo MRI scans of the mouse orbital region provided “clear and quantifiable evidence” of orbital muscle hypertrophy with protrusion (proptosis) of the eye, lending even further credence to this new model.
All 22 female BALB/c mice immunized with hTSHR A-subunit plasma showed bilateral orbital pathology, with two of those mice developing apparent unilateral protrusion of the eyes. None of the 12 mice immunized with control plasmids showed any orbital pathology or disease, they wrote.
“Overall,” the authors concluded, “these findings support TSHR as the pathogenic antigen in Graves’ orbitopathy (GO). Development of a new preclinical model will facilitate molecular investigations on GO and evaluation of new therapeutic interventions.”
LOW INFLAMMATION AND
METABOLIC HEALTH in Obese People
Obese people are often at a greater risk for health concerns, but they don’t always develop metabolic issues, a phenomenon that could be explained by reduced levels of inflammation.
In a recent study published in the Journal of Clinical Endocrinology and Metabolism, scientists led by Catherine Phillips, BSc, PhD, of the University College Cork in Ireland, analyzed 2,047 participants aged 50 to 69, classified as obese (BMI >30) and non-obese (BMI <30), between 2010 and 2011. Patients completed lifestyle questionnaires, were assessed physically and clinically, and underwent blood testing to determine inflammatory markers and metabolic profiles. The researchers defined metabolic health status using five existing metabolic health definitions based on a range of cardiometabolic abnormalities. Serum acute-phase reactants, adipocytokines, pro-inflammatory cytokines, and white blood cell counts were determined. Metabolically healthy obese (MHO) people in the cohort exhibited reduced levels of inflammatory markers, such as white blood cells and acutephase response proteins, as well as increased levels of adiponectin — which has an anti-inflammatory effect — compared to their metabolically unhealthy counterparts. This same favorable inflammatory profile is positively associated with metabolic health in both obese and nonobese people, the researchers noted. These findings are of public health and clinical signifi- cance, the authors concluded. Obesity diagnosis, particularly of those at greatest cardiometabolic risk, requires improvement. Better understanding of the association between MHO and inflammation may have implications for predicting those at greatest risk of developing the most serious obesity-related complications.
Vitamin D Receptor Inhibits Expression of BROWN FAT
The Vitamin D Receptor (VDR) may play a role in blocking the process that turns adipocytes into brown fat, according to recent findings published in the journal Molecular Endocrinology.
The study, by Peter J. Malloy, PhD, and Brian J. Feldman, MD, PhD, both of Stanford University, says that obesity reflects an “imbalance between energy storage and energy expenditure” and often results in far more serious complications like metabolic and cardiovascular diseases. Therefore, the scientists wanted to take a closer look at what affects the energy expenditure process.
Using dermal fibroblasts from patients with Hereditary Vitamin D Resistant Rickets (HVDRR), the researchers found that the VDR directly inhibits the expression of uncoupling protein-1 (UCP-1), “the critical protein for uncoupling fatty acid oxidation in brown fat and burning energy.” They also found that when the VDR is removed, UCP-1 expression increases, resulting in “browning” of adipocytes.
Malloy and Feldman noted that this process occurs cell-autonomously and independent of the physiologic VDR hormone ligand, 1,25-dihydroxyvitamn D.
“Importantly,” they concluded, “our data suggest a paradigm where VDR modulates beige versus white adipocyte identity as opposed to a toggle in the recruitment of distinct progenitor cell populations. We believe these results will have important implications for human health.”
OBESE MOTHERS Produce Offspring with Increased Mortality, Cardiovascular Problems
Mothers who were obese during pregnancy produced offspring with greater risk of health problems and shorter life spans, according to a study recently published in the journal BMJ. The increased mortality results especially from cardiovascular problems when the offspring reach adulthood.
Researchers led by Rebecca M. Reynolds, MD, PhD, at the University of Edinburgh, Scotland studied 37,709 people with birth records from 1950 to 1976, gathered from the Aberdeen Maternity and Neonatal databank, and then followed them until the present day through the General Register of Deaths, Scotland, and the Scottish Morbidity Record systems.
All women who had a live singleton birth at term from 1950 to 1976 and who had their weight taken at their first antenatal visit were identified from the databank, and then grouped according to BMI. Their offsprings’ birth records were then linked to the death and morbidity registries to determine outcomes of mortality and cardiovascular events (angina, myocardial infarction, stroke, and others).
The scientists found that among the 37,709 offspring, there were 6,551 deaths from any cause, up until Jan. 1, 2012. The leading cause was cardiovascular disease (24% of deaths in men and 13% of deaths in women) and cancer (26% of deaths in men and 42% of deaths in women). They wrote that there was a significant increase in all-cause mortality in the offspring of mothers who were overweight or obese (BMIs of 25 – 29.9 and >30, respectively).
They also found that overall, 7.6% of the offspring cohort had been admitted to the hospital with some sort of cardiovascular event, with a significant association between the mothers who were overweight or obese and increased cardiovascular events in their offspring.
Only 4% of the mothers in the cohort of 28,540 women were obese, a number that is far smaller than today’s current levels. The authors concluded that their findings “highlight the urgent need for strategies to prevent obesity in women of childbearing age and the need to assess the offspring of obese mothers for their cardiovascular risk.”
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