2017/03/27
Keio University School of Medicine
A research group led by Kenji Miyamoto (Project Associate Professor, Endowed Chair for the Treatment of Advanced Musculoskeletal Disorders) from the Department of Orthopedic Surgery, Keio University School of Medicine, has now revealed that individuals with a genetic polymorphism that causes them to flush easily when drinking alcohol are 2.48 times more likely to experience proximal femoral fractures due to osteoporosis compared to those without this polymorphism, based on a comparison of the prevalence of rs671. Furthermore, they also discovered that vitamin E intake may be effective in prevention.
People who tend to flush when drinking alcohol have a genetically weak or deficient enzyme protein called ALDH2, which functions to break down acetaldehyde, a substance produced during alcohol metabolism after drinking. This genetic trait is said to be common among East Asian populations, including the Japanese.
This study reveals that individuals who carry the gene for flushing after drinking are more susceptible to proximal femoral fractures due to osteoporosis, regardless of their usual alcohol consumption.
ALDH2 plays a crucial role in breaking down acetaldehyde. However, the loss of ALDH2 function leads to an accumulation of acetaldehyde, which causes dysfunction in osteoblasts, the cells that form bone.
On the other hand, they found through in vitro culture that adding vitamin E to dysfunctional osteoblasts can prevent this dysfunction.
The number of patients with proximal femoral fractures due to osteoporosis continues to increase. In 2014, there were 190,000 cases of proximal femoral fractures annually in Japan, and this number is expected to rise further. While one's innate genetic polymorphism cannot be changed, this study suggests that vitamin E intake can reduce the effects of this genetic polymorphism and is expected to be effective in preventing fractures.
The results of this research were published in the interdisciplinary general journal *Scientific Reports* on March 27, 2017.
For the full press release, please see below.