These results are relevant because they highlight the pitfalls of using SNPs or GRS, derived from the above mentioned GWAS [37], as proxies for plasma leptin concentrations for setting individual-level metrics of genetic risk in Mendelian randomization studies [75], in this, and other populations (i.e., the SNPs obtained in the GWAS undertaken by Kilpeläin et al. [37], have been used in Mendelian randomization studies for the association between leptin and Alzheimer’s disease [40] or bone mineral density [41]). Here, LEP is linked to Alzheimer disease.