Source: Long Life Family Study
In 2015 “Old people” are still being clumped together as one group, with an arbitrary cutoff of age 65.
This causes several problems, for example the diseases of young elderly, less than 75-years-old, are often lifestyle-related. Diseases of young-old are primarily cancers, atherosclerotic heart diseases and diabetes. While it is laudable to spend resources ameliorating these conditions, we must face up to facts about aging research.
Researching and treating diseases in the young-old constitutes a low-hanging fruit for medicine and pharmaceutical companies. This is in stark contrast to the complicated web of damages accumulated systemically, perpetuating the declining health of people aged over 80. The 85+ group have been historically ignored due to lack of research on aging itself. I refer to “aging itself” to mean the metabolic waste accumulation ultimately causing the systemic frailty syndrome seen in the old old.
A major problem is that aging has not historically been defined as a disease, warranting detailed scrutiny in order to constitute a target for medicine. The world is paying the price for it. It is still not known exactly what diversifies people aged 100+ on a molecular and cellular level, versus people dying of age-related diseases in their 80s. This is due to a significant lack of autopsies, quantifying the aging damage of the centenarians. Therefore it is not understood exactly how this age category succeed in avoiding lethal pathology for so long, and how their accumulated pathology might differ.
To obtain a broad spectrum of interventions, interventions impacting the fundamental problem of aging, understanding age-related damage on a pathological and histological level is crucial. For example, do centenarians have better protein regulation? Or do they just have better defense mechanistics against dysregulation and protective mechanistics delaying it from turning pathogenic, causing a longevity advantage? Do these people repair DNA damage better? The list of factors to investigate is long.
It is a well known observation that people reaching ages of 110+ have been described by relatives as having been in unusually good shape earlier during their “old age”. Photographic evidence shows that these people often have an unusual physical status for someone their age.
However this is just “anecdotal evidence” of them “aging slower”.
Due to lack of research exactly why “the aging process” occurs differently in centenarians and supercentenarians remains unknown. Having met supercentenarians myself I acknowledge the difficulty in spotting any difference in their agedness compared to other aged frail people in their 90s.
We need the umbrella term “aging research” to be focused on the very aged.
The “very aged” emphasizes the 85+ group, with centenarians as an important subcategory. This is in order to attack for example the accumulation of different harmful tissue accumulations of proteins (amyloidosis) prevalent in the elderly, such as apolipoprotein A and TTR amyloidosis. For example different forms of senile systemic amyloidosis are generally neglected, still no cures exist and little research is ongoing.
This despite them being a major “tipping point”, causing cardiac arrest and death in a very aged body.
Changes like fibrosis (scarring of connective tissue) of especially lungs and heart also contribute to clinical impairment of functionality and frailty. While these changes are common in the 85+ group, here research is also lacking. A 100-year-old person dying of pneumonia might have severely fibrotic lungs with amyloid accumulations, a deteriorated immune system, malnutrition due to nutrient dysregulation in the gut and a low leukocyte count due to loss of stem cells. These comorbidities cause a fatal event that would not have occurred in a young person exposed to the same pathogen.
It’s likely there are also many new molecular pathologies to unravel in the nearby future; ones constituting advanced senescence. These need to be properly quantified, and we must determine the significance of them in order to be able to successfully treat aging itself, namely the often undetermined forms of advanced senility in our older seniors.
This is ultimately the only way forward to successfully get aging under control and truly change the late 80s mortality peak and prolong maximum human lifespan beyond 100. Currently the most common age of death in Sweden is 86 for men and 88 for women, for comparison the life expectancy is 80 and 83.5. From what we can deduce, risk avoidance, as well as avoidance of well known health issues like smoking and obesity, won’t give much. These modifiable factors will only shift the life expectancy towards the most common age of death.
A well known problem in studying the oldest old is the fact that 98% of all people turning 110 fail to reach 115. Furthermore out of over 1600 verified people over 110, only 2 people have lived beyond 117. The oldest person in the world is almost always 114-116 years old with little change. If an individual would in the next few years again “skirt the cliff” and reach 118+, this would warrant urgent attention from the gerontological community. This would provide a nearly unique opportunity for science, to investigate histopathological and genetic data behind the aberrations yielding this “life extension”.
In conclusion aging research is often focused on disease management of common diseases in the “younger old”. I strongly argue that research on the systemically aged people over 80s, and especially centenarians, must be the prioritized target of aging research.
The geriatric costs are staggering, we cannot afford more short-term thinking chasing low hanging fruits labelled diseases in the young-old.
Quantifying the precise systemic tissue damages in the very old is paramount for developing concrete medical targets, targets composing the panel of upcoming therapies bringing aging under medical control.
Guest contributor Victor Bjoerk