Can a Diet High in Sugar and Processed Foods Affect Spine Health and Cause Accelerated Bone Aging?
Back pain is one of the most common reasons for a doctor’s visit, and a leading cause of disability worldwide. The etiologies of back pain can range from vertebral fractures and spinal deformities, to degenerative disc disease and lumbar muscle strains, all resulting in significant declines in quality of life and functional ability. There are a myriad of predisposing factors for low back pain, however scientists have recently started to research the relationship between diet and spinal diseases. An intriguing group of dietary compounds in question are advanced glycation end-products.Advanced glycation end-products (AGEs) are compounds produced by chemical reactions between sugars and other components of fats, proteins and nucleic acids. AGEs can be formed within the body as a result of high blood sugar and can also be consumed through processed foods. Previous research has associated AGEs with possible increased bone fracture risk and has also highlighted diabetes to cause spinal damage (theorized to be due to high AGE content in spinal tissues)
Hence, a group of researchers from Mount Sinai and Rensselaer Polytechnic Institute collaborated to investigate whether high amounts of dietary AGEs would degenerate vertebral structure and function in the absence of diabetes. This animal model study included male and female mice that were fed low-AGE diets or high-AGE diets for six or eighteen months. Although fed different diets, both groups were given the same number of calories. At the end of the experiment, researchers measured bone structure and function in the mice in addition to bone and blood AGE levels.
The results of the study revealed increased AGE levels in the blood and in the outer vertebrae surface of only the six-month-old female mice that were fed the high-AGE diet. Blood glucose and weight remained normal for all animals in the study. While on the high-AGE diet, the six-month-old female mice had more frail vertebrae and decreased bone mineral density. Biomechanical testing and analysis further validated functional decline in the six-month-old female mice. At eighteen-months-old, both male and female mice fed the high-AGE diet had notable, yet small decreases in bone density with no functional changes that could be differentiated from other aging effects. Thus, the study concluded that a high-AGE diet caused degenerated vertebral structure, functional decline, and lowered fracture resistance in young female mice in a way that suggested accelerated bone aging.
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