All calories do not seem to be created equal, and the way the body processes the same calories may vary dramatically from one person to the next.
This is the intriguing suggestion from the latest research into metabolic syndrome, the nasty clique that includes high blood pressure, high blood sugar, unbalanced cholesterol and, of course, obesity. This uniquely modern scourge has swept across America, where obesity rates are notoriously high. But it is also doing damage from Mexico to South Africa and India, raising levels of disease and pushing up health costs.
A study published in Nature Communications by Richard Johnson, of the University of Colorado, explains that glucose may do its harm, in part, through its conversion to fructose.
Dr. Johnson and his colleagues administered a diet of water and glucose to three types of mice. One group acted as a control and two others lacked enzymes that help the body process fructose. The normal mice developed a fatty liver and became resistant to insulin. The others were protected. The body’s conversion of glucose to fructose, therefore, seems to help spur metabolic woes.
Jeffrey Gordon, of Washington University in St Louis, found four pairs of human twins, with one twin obese and the other lean. He collected their stool, then transferred the twins’ bacteria to sets of mice. Fed an identical diet, the mice with bacteria from an obese twin became obese, whereas mice with bacteria from a thin twin remained lean.
Dr. Gordon then tested what would happen when mice with different bacteria were housed together—mouse droppings help to transfer bacteria. Bacteria from the lean mice made their way to the mice with the obese twin’s bacteria, preventing those mice from gaining weight and developing other metabolic abnormalities. But the phenomenon did not work in reverse, probably due to Dr. Gordon’s theory on the microbiota’s job vacancies. Interestingly, the invasion did not occur, and obesity was not prevented, when the mice ate a diet high in fat and low in fruits and vegetables. The transfer of helpful bacteria therefore seems to depend on diet.
Read the full article on The Economist.