The results of a large study suggest that high lean muscle levels could help protect against Alzheimer’s. But according to the researchers, additional studies are necessary to determine the underlying biological pathways, in addition to the health implications.
Obesity has been linked to an increased risk of Alzheimer’s in countless studies, probably explained by the accompanied insulin resistance, increased inflammation, and higher fat tissue levels of amyloid ß, the protein that’s harmful to the health of the brain.
Lower lean muscle levels have also been linked to an increased risk of Alzheimer’s, but it isn’t clear if this might happen before or after a diagnosis.
In an attempt to determine this, the researchers made use of Mendelian randomization, a method that makes use of genetic variants as proxies for a specific risk factor, which in this instance was lean muscle, for obtaining genetic evidence supporting a specific result, which in this study was Alzheimer’s risk.
Data were used from 450,243 participants in the UK Biobank study; an independent sample of 21,982 individuals with Alzheimer’s, and 41,944 individuals without Alzheimer’s; an additional sample of 7329 individuals with Alzheimer’s, and 252,879 individuals without Alzheimer’s to confirm the results; and 269,867 individuals participating in an intelligence and genes study.
An electric current flowing at varied rates throughout the body determined by its composition known as bioimpedance was made use of for estimating fat tissue and lean muscle in the legs and arms, after adjusting for sex, age, and genetic ancestry.
About 584 genetic variants were linked to lean muscle mass of which none were located in the APOE gene area that’s linked to Alzheimer’s vulnerability. These combined genetic variants accounted for 10% of the lean muscle mass difference in the legs and arms of the individuals.
Increased lean muscle mass was related to a small, but statistically significant, Alzheimer’s risk reduction on average.
This result was replicated in the additional sample of 7329 individuals with Alzheimer’s, and 252,879 individuals without Alzheimer’s, making use of different lean muscle mass measures as well as whole body and trunk measures.
Lean mass was also linked to improved cognitive task performance, but this connection didn’t account for the protective effect that lean mass had on the risk of Alzheimer’s.
Nor was body fat linked to Alzheimer’s risk, but it was linked to poorer performance on cognitive tasks.
These analyses provide evidence that supports a cause-and-effect connection between lean mass and Alzheimer’s risk.
The results also largely refute the effect of fat mass on Alzheimer’s risk and highlight the significance of distinguishing between fat mass and lean mass when examining the effect of measures of adiposity on health outcomes.
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