Can We Really Extend Lifespan and Healthspan? Better Aging Series Part 1

We age every moment we are alive. But the process of aging appears different depending on where one sits on the curve of life. When we are young, aging develops us. When we are old, aging diminishes our abilities. But aging begins before its effects are apparent. It’s just that we’re more likely to care about it when it’s evident. The desire within humans to avoid the perils of biological aging is as old as time itself, but now aging is a field of scientific inquiry, and the promise of extraordinary solutions is imminent. One big aim of this field is to find ways to extend lifespan. Just as interesting, if not more so, is to find strategies that preserve abilities throughout the duration of life. This article is the first in a series to address both.

In the last 100 years, several factors have contributed to a significant extension of lifespan. This includes advances that help fight infectious disease (hygiene to antibiotics), drugs and medical techniques that decrease mortality risk for the sick, and even some improvements in nutrition (mostly addressing calorie and nutrient adequacy). This is an incredible feat. However, it has not been accompanied by an equally large increase in the length of time a person spends living with full health (i.e., healthspan). Old age is still the most important risk factor for a host of chronic diseases – such as atherosclerosis, diabetes, most cancers, and dementias – because as we age there is an increasing amount of time to accumulate damage. Eventually, the cumulative damage induced by living overwhelms the body’s ability to fully repair itself. It is at this point where we start to recognize signs of aging more reliably.

Diseases that occur with a greater incidence as we age account for the majority of health care expenditures in developed nations. We now see chronic disease happening earlier in life. When you combine this with modern medicine’s ability to extend life in the unhealthy, we have an unsustainable and undesirable condition for humanity, especially when considering that the world’s elderly population has been growing more rapidly than ever. Thus, extending lifespan without extending healthspan actually presents major problems for the individual and his or her family and support team. It may also threaten social and economic stability in a manner never seen before.

Modern medicine treats symptoms of conditions that occur when biological damage occurs. This at least partly explains the paradigm of preventing and managing each age-related disease individually. While this approach certainly has its merits, having already prolonged and improved countless lives, it rarely attacks the root cause of these conditions. But even if we were to eliminate diseases that cause premature mortality, which is a primary focus of modern medicine, medicine still does not intend to address biological aging directly. Estimates based on mortality data in the United States predict that if cancer was eliminated as a cause of death, average human life span would increase only 3-4%. The same is true if ischemic heart disease were to be cured. That means if you eliminate these two major causes of premature mortality, median life expectancy in the US would go from 76 to 83 years old. While we do want to cure diseases that cause us to die early, additional enhancements to the aging process can occur beyond the treatment of disease, especially when the focus of our health treatment moves beyond symptom management. Either medicine needs to change or we need to find other credible sources that care for our health in ways modern medicine does not in order to attain a complete approach to life-long health.

There is now hard evidence (but incomplete) that suggests with certain dietary, lifestyle, and pharmacological interventions, it is possible to make age a modifiable risk factor. In other words, with the right multipronged stack of strategies, more humans can realistically delay the loss of function and perform youthfully well into 6th, 7th, 8th, maybe even the 9th decade of life. Soon, however, this preservation of function may be shifted even further into the lifespan, and lifespan itself may be elongated to heretofore unprecedented levels.

Therefore, for those seeking to maximize “years of life and life in years” (borrowing a quote from David Katz, MD), high-level aims are to minimize the risk of premature mortality and to optimize techniques that preserve functioning and elongate lifespan. Admittedly, there is overlap in what to do to achieve these aims, but importantly, there are aspects that are mutually exclusive.

Studies on invertebrates and rodents noted by Fontana et al., 2010 have shown that some forms of dietary restriction can extend lifespan by up to 50%. These regimens act on biochemical pathways that are evolutionarily well-conserved, meaning that they remain relatively unchanged across a large segment of the tree of living organisms. This makes it scientifically conceivable that the lifespan-elongating effects demonstrated in numerous model organisms – ranging from yeast, worms, flies, rodents, and primates – may also be seen in humans.

Unfortunately, studies directly measuring the effects of an intervention on human lifespan are difficult to design and carry out. These types of research protocols require long study periods, which are often highly impractical and raise complex ethical issues. Therefore, in humans, most of the evidence to date has relied upon surrogate measures to inform us of the potential of a therapy to extend life and to extend health. A surrogate measure is a measure that can be assessed today – for example, blood pressure and waist circumference – that is thought to have value in predicting the future outcome of a therapy or even a health condition. A specific example could be measuring an inflammatory marker in response to dietary fasting to then estimate the potential of fasting as a therapy to extend health and life, given that chronic inflammation is associated with reductions in health and lifespan.

Preliminary studies on the effects of these dietary restrictions have been carried out in humans and have shown benefits in surrogate measures of aging. Some benefits demonstrated include delayed deterioration of the functioning of our autonomic nervous system, delays in age-related stiffening of cardiac tissue, and the slowing of disease progression in those with existing diabetes and dementia.

This is exciting because it suggests that we can modify the way we eat – a lifestyle factor that is well within our control – to produce real results towards the outcome we seek. The next blog post in this series will take a closer look at various forms of dietary restriction, its effects on aging, and possible mechanisms by which the desirable effects of a specific intervention occur.