Why do some people live and stay healthier much longer than others?
Individuals who have reached an exceptional age have been recorded throughout history; Jeanne Calment, an exceptionally long-lived Frenchwoman born in 1875, became the world’s oldest person in 1997, aged 122.
This longevity can be attributed in part to environmental and behavioral factors such as better nutrition, medical care, hygiene and luck. But as average life expectancy continues to increase around the world due to general improvements in these and other factors, it is clear that exceptional longevity and healthy aging tend to run in families.
This suggests that genetic differences play a role in ensuring longer life expectancy and lifelong good health.
A recent study showed that children of exceptionally long-lived parents have a similarly reduced risk of developing type II diabetes compared to the general population. Surprisingly, this benefit also extends to their spouses.
Among children and their spouses, 3.7% and 3.8% developed type II diabetes over the course of the study, respectively. This corresponds to a rate of 4.6 to 4.7 new cases of type II diabetes per 1,000 person-years, which is about 53% lower than the rate of 9.9 among people aged 45 to 64 in the population. general of the USA.
“While this latest finding may not be intuitive, previous studies have also reported marked survival and health advantages among spouses of children from long-lived families,” says first author Iva Miljkovic, professor at the University of Pittsburgh School of Public Health, US.
The study was part of the Long Life Family Study (LLFS), which focuses on families in the US and Denmark with several exceptionally long-lived members. The objective was to identify over two generations which biological processes are associated with long life and healthy aging.
It monitored the health of 4,559 long-lived focal women and men (over 90 years of age at enrollment), 1,445 of their siblings (they are over 80 years of age), 2,329 children (between 32 and 88 years of age) of the focal person or their brother, and 785 of the spouses of these children, from 2006 to 2017.
By taking blood samples, the researchers studied the levels of biomarkers that affect the risk of type II diabetes among children and their spouses and found that there appear to be different underlying factors that promote this lower risk of type II diabetes.
“We found that pro-inflammatory biomarkers and growth factor signals appear to have stronger positive and negative effects on diabetes risk in the spouses of children of exceptional survivors than in the children themselves,” says Miljkovic.
“This suggests that different biological risk factors affect this risk in the two groups.”
Does this mean that spouses resemble each other in their blood levels of biomarkers simply by sharing a home and lifestyle, regardless of their genetic origin in early life?
“It is possible that people unconsciously tend to choose their mates through so-called ‘selective mating’ – that is, tending to match their phenotypes and the underlying genotypes, including those that affect diabetes risk and longevity,” she explains.
“Further LLFS studies to identify the mechanisms and pathways—genetic, epigenetic, molecular, health trajectories and behaviors, and lifestyle patterns—are needed to understand why being married to a long-lived family member also brings metabolic and health care. survival. advantage, similar to that of the spouse”, he adds.
The research was published in the journal Borders in Clinical Diabetes and Health.
Cellular aging and senescence
The short film of the International Scientific Film Festival SCINEMA 2021 Cell Senescence explores the biological phenomenon of cellular senescence, a hallmark of aging.
This is a process in which cells irreversibly stop dividing through mitosis and their growth is stopped permanently, without undergoing cell death.
The process was discovered in 1961 by Leonard Hayflick and Paul Moorhead, when they discovered that human fetal fibroblast cells in culture could only reach a maximum of 40-60 cell population doublings (through mitotic cell division) before becoming senescent.
Called the Hayflick limit, this is the number of times a normal somatic cell can undergo cell division before senescence is triggered.
Each time a cell undergoes mitosis, the telomeres at the ends of each chromosome – which work to protect the DNA from degradation – shorten slightly, and once they shorten to a critical length, cell division ceases.
This fundamental process is a double-edged sword for the body: it is beneficial as an antitumor mechanism because it can also be triggered by other cellular stress signals and prevent the proliferation of cancer cells, but it also promotes aging.
As we age, more and more cells go into senescence, and the accumulation of these cells can compromise tissue repair and regeneration and is ultimately harmful.
You can watch the movie here.