Some people have better genes than others, at least when it comes to living a longer, healthier life. They are perhaps more resistant to some forms of biological damage, perhaps have better repair mechanisms, perhaps can respond more effectively at a cellular level to good diet and lifestyle choices. The reasons why natural longevity has an inherited component are largely unknown and will be a subject for research for the next few decades - indeed, I expect the first generation of meaningful rejuvenation therapies to arrive in advance of a full understanding of the natural differences in human longevity. That full understanding simply isn't necessary for researchers to make progress in repairing and reversing the known biochemical differences between an old person and a young person.
One noteworthy study of human longevity is the Long Life Family Study - the link there goes to a secure site with a self-signed certificate, so your browser will require you to click through a warning message in order to view it.
The goal of the Long Life Family Study (LLFS) is to answer an important question: Why do some people and their families live very long lives? LLFS is a unique international project that is studying families who have several members reaching a very old age. Families from the United States and Denmark will help us learn why some people live until a very old age and why some families maintain their health far longer than the average family.
A recent open access paper crunches some the numbers from the Long Life Family Study and presents graphs and tables that illustrate the degree to which long-lived folk have better measures of health throughout their old age when compared with the rest of us. It is an interesting read on a number of levels, not least as an introduction to how these studies work under the hood, and what the researchers are looking at.
This paper compares the prevalence of disease as well as physical and cognitive functioning in LLFS probands and offspring to two community based cohorts that were not selected for longevity. These comparison cohorts include the Cardiovascular Health Study (CHS), the [Framingham Heart Study (FHS)] original and FHS offspring cohorts.
Probands and offspring of the LLFS cohort were less likely to have diabetes, chronic pulmonary disease and peripheral artery disease than the CHS and FHS cohort members. Measures of physical function and cardiovascular risk factors were more optimal in LLFS compared to the other groups. High density lipids were higher and triglycerides were lower in LLFS probands and offspring. This is consistent with previous reports of the children of centenarians having better lipid profiles than controls. These findings suggest that the strategy of recruiting families with a history of longevity yielded rates of healthy aging not unlike that seen when recruiting offspring of centenarians.
One of the goals of the mainstream aging research establishment is to try and replicate the factors that lead to the upper end of natural human longevity: adding a decade or so to healthy life through genetic manipulation and drugs aimed at altering metabolism. As a goal considered in isolation this is laudable - but in the broader context of what is possible, this is a slow, poor way forward in comparison to damage repair strategies.