“Regular gym work-outs could stave off Alzheimer’s,” say scientists.
People with leaner muscles are less likely to develop the disease, according to new research.
“Based on human genetics data, individuals randomized to lifelong higher lean muscle mass had a 12 percent lower risk of Alzheimer’s disease and scored higher for cognitive performance,” said Dr. Iyas Daghlas, Lead Author from the University of California. San Francisco.
The U.S. team analyzed over a million volunteers, including 450,243 from the UK Biobank, which contains information on their DNA.
They used a technique known as “Mendelian randomization” variants linked to specific risk factors.
“Some of us are naturally programmed to have lean muscles. They can also be built by combining a healthy diet with resistance training – such as lifting weights,” said the scientists.
The number of dementia cases worldwide will pass 150 million by 2050. It’s estimated a third are caused by avoidable issues – such as middle-age spread.
With no cure in sight, there’s an increasing focus on protective lifestyles.
“Despite the steady increase in the prevalence, no effective treatments for this devastating disease exist,” said Dr. Daghlas.
“Prevention of Alzheimer’s through identification of modifiable risk factors is thus a key public health aim.”
Piling on the pounds fuels inflammation. It’s also been linked to increasing neuron-destroying rogue proteins called amyloid beta.
Lower levels of lean muscle have also been associated with dementia. The study in BMJ Medicine sheds fresh light on the link.
Those with high amounts had a reduction in Alzheimer’s risk. Results were “statistically robust” after taking into account age, sex, and ancestry.
“These analyses provide new evidence supporting a cause-and-effect relation between lean mass and risk of Alzheimer’s disease,” said Dr. Daghlas.
“They also refute a large effect of fat mass on the risk of Alzheimer’s disease and highlight the importance of distinguishing between lean mass and fat mass when investigating the effect of adiposity measures on health outcomes.”
Identifying biological mechanisms behind the phenomenon would open the door to developing drugs that target them.
“Several Mendelian randomization analyses have identified the effects of cardiometabolic risk factors on the risk of Alzheimer’s disease, which could be further investigated as potential mediators of the effect of lean mass,” said Dr. Daghlas.
The effect could also be mediated by new mechanisms, including circulating myokines – proteins released during strenuous exercise.
“Potentially relevant secreted myokines include irisin, brain-derived neurotrophic factor 5, and cathepsin B,” said Dr. Daghlas
“Identification of the key causal pathways might lead to the development of treatments that harness and potentiate the Neuroprotective effects of lean mass.”
“Our findings need to be replicated with independent lines of complementary evidence before informing public health or clinical practice,” said Dr. Daghlas.
“Also, more work is needed to determine the cut-off values for age and degree of pathology of Alzheimer’s disease after which modifications of lean mass might no longer reduce the risk.”
Nor is it clear whether increasing lean mass could reverse the pathology of Alzheimer’s disease in patients with preclinical disease or mild cognitive impairment.
But if future studies back the findings “Public health efforts to shift the population distribution of lean mass, potentially through campaigns to promote exercise and physical activity, might reduce the population burden of Alzheimer’s disease,” said Dr. Daghlas.
Produced in association with SWNS Talker
