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Over the last several decades, obesity has rapidly grown to affect more than 2 billion people, making it one of the biggest contributors to poor health globally. Many individuals still have trouble losing weight despite decades of study on diet and exercise regimens. Researchers from Baylor College of Medicine and affiliated institutions now believe they understand why, and they argue that the emphasis should be shifted from treating obesity to preventing it.

The research team reports in the journal Science Advances that early-life molecular processes of brain development are likely a major determinant of obesity risk. Previous large human studies have shown that the genes most strongly associated with obesity are expressed in the developing brain. This most recent study in mice focused on epigenetic development. Epigenetics is a molecular bookmarking system that regulates whether genes are utilized or not in certain cell types.

“Decades of research in humans and animal models have shown that environmental influences during critical periods of development have a major long-term impact on health and disease,” said corresponding author Dr. Robert Waterland, professor of pediatrics-nutrition and a member of the USDA Children’s Nutrition Research Center at Baylor. “Body weight regulation is very sensitive to such ‘developmental programming,’ but exactly how this works remains unknown.”

Strange libraries of supplementary genes nicknamed “Borg” DNA appear to supercharge the microbes that possess them, giving them an uncanny ability to metabolize materials in their environment faster than their competitors.

By learning more about the way organisms use these unusual extrachromosomal packets of information, researchers are hoping to find new ways of engineering life to take a big bite out of methane emissions.

In the wake of a study publicized last year (and now published in Nature), researchers have continued to analyze the diversity of sequences methane-munching microbes store in these unusual genetic depositaries in an effort to learn more about the evolution of life.

A drug has been identified by researchers at Tokyo Medical and Dental University (TMDU) that replicates the benefits of exercise on mice’s bones and muscles.

You can look and feel better by keeping up a regular exercise schedule, but did you know that exercise also supports bone and muscle health? Locomotor fragility, which affects people who are unable to exercise, causes the muscles and bones to deteriorate. Recently, Japanese researchers discovered a new drug that, by producing effects comparable to those of exercise, may help treat locomotor frailty.

Physical inactivity can result in a weakening of the muscles (known as sarcopenia) and bones (known as osteoporosis). Exercise dispels this frailty by boosting muscular strength and suppressing bone resorption while simultaneously promoting bone formation. Exercise therapy, however, cannot be used in every clinical situation. When patients have dementia, cerebrovascular disease, or are already bedridden, drug therapy may be very helpful for treating sarcopenia and osteoporosis. However, there is no one drug that targets both tissues at the same time.

A new discovery could be a game-changer for patients with type 2 diabetes. Researchers at the Diabetes, Obesity, and Metabolism Institute (DOMI) at the Icahn School of Medicine at Mount Sinai have discovered a therapeutic target for the preservation and regeneration of beta cells (β cells), the cells in the pancreas that produce and distribute insulin. The finding could also help millions of individuals throughout the globe by preventing insulin resistance. The study was recently published in the journal Nature Communications.

Nature Communications is a peer-reviewed, open access, multidisciplinary, scientific journal published by Nature Research. It covers the natural sciences, including physics, biology, chemistry, medicine, and earth sciences. It began publishing in 2010 and has editorial offices in London, Berlin, New York City, and Shanghai.

Most scientists believe that the structure of the adult brain is generally rigid and incapable of rapid changes. However, new research has now revealed that this is not true. In a new study, German scientists have shown that in-patient treatment for depression can lead to an increase in brain connectivity. Moreover, those individuals who respond well to this treatment show a greater increase in connectivity than those who don’t.

Presenting the work at the European College for Neuropsychopharmacology Congress in Vienna, lead researcher, Professor Jonathan Repple said:

“This means that the brain structure of patients with serious clinical depression is not as fixed as we thought, and we can improve brain structure within a short time frame, around 6 weeks. We found that if this treatment leads to an increase in brain connectivity, it is also effective in tackling depression symptoms. This gives hope to patients who believe nothing can change and they have to live with a disease forever, because it is “set in stone” in their brain.”