Genetic Variants Associated with Risk of Hypertension and Obesity also Correlate with Reduced Life Expectancy
Identification of genetic variants associated with specific conditions has been a going concern for some time, but the creation of large national databases of genetic and biometric data in a number of countries has greatly expanded this area of study. In today's research materials, scientists demonstrate one way in which this can be used, as a confirmation of the importance of hypertension and obesity in present variations in human life expectancy. People with genetic variants that increase the odds of suffering either of these conditions tend to live shorter lives, something that also shows up in standard epidemiological studies.
Why is this the case? Hypertension, chronically increased blood pressure, results from the stiffening of blood vessels due to various low-level processes of cell and tissue damage. Cross-links that reduce elasticity in blood vessel walls, inflammation resulting from senescent cells, and so forth. The resulting increase in blood pressure leads to an acceleration of atherosclerosis, and pressure damage to delicate tissues in the kidneys, brain, and elsewhere. This is very harmful to organ function over the long term, as illustrated by the fact that even forcing a reduction in blood pressure, overriding regulatory mechanisms without addressing the underlying causes of the problem, can reduce mortality in old people.
The excess visceral fat of obesity, on the other hand, can be argued to accelerate the aging process by generating excessive numbers of senescent cells. This and other mechanisms in visceral fat tissue lead to greater levels of chronic inflammation, which in turn accelerates the development and progression of all of the common age-related conditions. Epidemiological studies suggest that any excess weight is harmful, but outright obesity is in the same ballpark as smoking when it comes to negative effects on health and life expectancy.
It's in our genome: Uncovering clues to longevity from human genetics
Part of DNA is composed of genes, of which proteins are produced that participate in virtually every process within our cells and organs. While variations in the genetic code determine biological traits, such as eye color, blood type, and risk for diseases, it is often a group of numerous variations with tiny effects that influence a phenotypic trait. Harnessing a huge amount of genetic and clinical data worldwide and a methodological breakthrough, it is now possible to identify individuals at several-fold increased risk of human diseases using genetic information.
Researchers have discovered that individuals who have a genetic susceptibility to certain traits, such as high blood pressure or obesity, have a shorter lifespan. To achieve their goal, the researchers analyzed genetic and clinical information of 700,000 individuals from biobanks in the UK, Finland and Japan. From these data, the researchers calculated polygenic risk scores, which are an estimate of genetic susceptibility to a biological trait, such as a risk for disease, to find out which risk factor causally influences lifespan.
The researchers found that high blood pressure and obesity were the two strongest risk factors that reduced lifespan of the current generation. Interestingly, while high blood pressure decreased lifespan across all populations the researchers investigated, obesity significantly reduced lifespan in individuals with European ancestry, suggesting that the Japanese population was somehow protected from the detrimental effects obesity has on lifespan.
While polygenic risk scores (PRSs) are poised to be translated into clinical practice through prediction of inborn health risks, a strategy to utilize genetics to prioritize modifiable risk factors driving heath outcome is warranted. To this end, we investigated the association of the genetic susceptibility to complex traits with human lifespan in collaboration with three worldwide biobanks (n = 675,898; BioBank Japan, UK Biobank, and FinnGen). In contrast to observational studies, in which discerning the cause-and-effect can be difficult, PRSs could help to identify the driver biomarkers affecting human lifespan.
A high systolic blood pressure PRS was trans-ethnically associated with a shorter lifespan (hazard ratio = 1.03) and parental lifespan (hazard ratio = 1.06). The obesity PRS showed distinct effects on lifespan in Japanese and European individuals. The causal effect of blood pressure and obesity on lifespan was further supported by Mendelian randomization studies. Beyond genotype-phenotype associations, our trans-biobank study offers a new value of PRSs in prioritization of risk factors that could be potential targets of medical treatment to improve population health.
I came up with an idea. What if pills could be made that caused limited time hypertension or high blood pressure. Maybe it could get some of the plague out. That the plague would not be part of the blood artery walls. Flush it out? Taking it regularly so it don't accumulate? Is this possible?
If you want a really temporarily bump in no hurry to some strain physically. That's the nature's way
Sounds extremely dangerous. A big part of what makes plaques bad is that they can break off and get lodged in places, obstructing blood flow often fatally. You don't want to be making that happen on purpose.
I ment that you can start as young and every month so that microscopic plague fell off.