It might have been 25 years ago, but Karina Davidson remembers that day like yesterday. She was an intern in clinical psychology, and two concerned parents walked into the hospital with their troubled, seven-year-old son. The boy was severely underweight at just 37 pounds and had been acting out violently toward himself and others. It seemed as though Ritalin, a drug commonly prescribed for Attention Deficit Disorder, might help. But would it?
To find out, the clinical team did something unconventional: they designed for the boy a clinical trial to test the benefit of Ritalin versus a placebo. The boy was randomly assigned to take either the drug or placebo each day for four weeks. As a controlled study, neither clinical staff nor the family knew whether he was taking the drug or placebo at any given time. The result: Ritalin wasn’t the answer. The boy was spared any side effects from long term administration of a medication that wouldn’t help him, and his doctors could turn to other potentially more beneficial approaches to his treatment.
Davidson, now an established clinical psychologist at the Columbia University Irving Medical Center, New York, wants to take the unconventional approach that helped this boy and make it more of the norm in medicine. With support from a 2017 NIH Director’s Transformative Research Award, she and her colleagues will develop three pilot computer applications—or digital platforms—to help doctors conduct one-person studies in their offices.
Tags: 2017 NIH Director’s Transformative Research Award, All of Us, clinical trials, diabetes, digital platform, exercise, high blood pressure, light therapy, melatonin, N-of-1 trials, pain, personalized medicine, precision medicine, standard care, weight loss
When weight loss is the goal, the equation seems simple enough: consume fewer calories and burn more of them exercising. But for some people, losing and keeping off the weight is much more difficult for reasons that can include a genetic component. While there are rare genetic causes of extreme obesity, the strongest common genetic contributor discovered so far is a variant found in an intron of the FTO gene. Variations in this untranslated region of the gene have been tied to differences in body mass and a risk of obesity . For the one in six people of European descent born with two copies of the risk variant, the consequence is carrying around an average of an extra 7 pounds .
Now, NIH-funded researchers reporting in The New England Journal of Medicine  have figured out how this gene influences body weight. The answer is not, as many had suspected, in regions of the brain that control appetite, but in the progenitor cells that produce white and beige fat. The researchers found that the risk variant is part of a larger genetic circuit that determines whether our bodies burn or store fat. This discovery may yield new approaches to intervene in obesity with treatments designed to change the way fat cells handle calories.
Tags: beige fat, CRISPR-Cas, epigenomics, fat, fat cell progenitor, FTO gene, FTO Obesity Risk Variant, FTO obesity variant, genome-wide association studies, GWAS, IRX3, IRX5, obesity, obesity genes, weight loss, white fat
Diet sodas and other treats sweetened with artificial sweeteners are often viewed as guilt-free pleasures. Because such foods are usually lower in calories than those containing natural sugars, many have considered them a good option for people who are trying to lose weight or keep their blood glucose levels in check. But some surprising new research suggests that artificial sweeteners might actually do the opposite, by changing the microbes living in our intestines .
To explore the impact of various kinds of sweeteners on the zillions of microbes living in the human intestine (referred to as the gut microbiome), an Israeli research team first turned to mice. One group of mice was given water that contained one of two natural sugars: glucose or sucrose; the other group received water that contained one of three artificial sweeteners: saccharin (the main ingredient in Sweet’N Low®), sucralose (Splenda®), or aspartame (Equal®, Nutrasweet®). Both groups ate a diet of normal mouse chow.
Tags: antibiotics, artificial sweeteners, aspartame, blood glucose level, calories, DNA sequencing, glucose, glucose intolerance, microbe transplants, microbes, microbiome, nutrition, obesity, saccharin, sucralose, sucrose, sugar, type 2 diabetes, weight loss