Healthy living isn’t meaningless, but while all of us can make positive lifestyle modifications, genes play a massive role in longevity – or there would be no species variation. We’re still discovering exactly which genes provide a longevity boost and what they do, but we now know 7 variants could help give you an advantage.
The search for a longevity gene
Previous efforts to search out a ‘longevity gene’ have been largely unsuccessful, so researchers led by Stuart Kim at Stanford decided to focus on ‘bad’ gene variants this time – or more crucially a lack of them. They analysed 800 people over 100 and 5000 people over 90 and found that while many variants are common in the average person, possession of fewer ‘bad’ versions of 5 crucial genes was indeed associated with longevity. Many long-lived individuals are able to avoid chronic disease despite harmful lifestyle choices like smoking, and this could be one of the explanations. These confirmed 5 add to 2 already associated with longer lifespans.
7 known genes linked to longevity in centenarians
This gene codes for Apolipoprotein E, a class of protein that transports cholesterol around the body. Carrying a variant called E4 in this gene is the largest known risk factor for developing Alzheimer’s disease; those with two alleles of E4 have between 10 to 30 times increased risk of developing Alzheimer’s disease by 75 years of age. Positive variations in this gene reduce risk of developing Alzheimer’s, and can also have a beneficial influence on cholesterol levels. Mutations in Apolipoprotein B have also been linked to extreme longevity too.
Controls your blood group. Blood group O appears to be protective against heart disease, cancer and poor cholesterol. Centenarians have a higher proportion of O group individuals than the general population.
Regulates cell life cycles and affects cellular senescence. Positive mutations in this region have been linked to reduced rates of coronary artery disease and diabetes.
Encodes for a signalling protein that affects creation of new blood cells and regulation of cytokines – small signalling molecules with a huge range of roles. Mutations in this region that lead to a loss of function result in life extension in the fruit fly Drosophila, and a protective version of the gene in centenarians protects against a wide range of disease including rheumatoid arthritis, cancer and diabetes.
Involved in histocompatibility – essentially how the immune system recognises your body’s own cells. Harmful mutations in this gene have wide ranging implications and increase likelihood of auto-immune disease. Versions linked to centenarians appear to be protective, and result in lower cholesterol and reduced rates of rheumatoid arthritis.
Involved in the insulin/IGF-1 signaling, we know from animal studies modifying this pathway can lead to longevity and improved stress responses. Carrying a particular allele in this gene has been associated with increased health and probability of reaching post-100.
Shortened telomeres are included in the hallmarks of aging, and longer telomeres are a reasonable biomarker of health as you get older. Mutations in the hTERT gene that result in increased expression of the enzyme telomerase are common in Ashkenazi Jewish centenarians in particular. Although there were initial fears, it’s not yet clear whether increased telomere protection can increase cancer incidence, and maintaining telomere length appears to provide some health benefits.
“It’s the first time someone has shown that particular disease [variants] are depleted in centenarian populations. It points to important processes that are impaired in ageing populations.”
In many ways these are unsurprising gene targets. Lipid transport and neuro-protection, nutrient sensing and stress responses, better immune activity, increased capacity for division…these are all issues we know go downhill in the aging process. While these 7 are not an exhaustive list, it seems like making it over 100 is more to do with a lack of harmful versions of genes, than any ‘special’ longevity gene.
Read more at New Scientist