Amazingly, a maximum lifespan of Homo sapiens 15,000 years ago went as high as 94 years, an age more senior than the corresponding figure of 91 years attached to modern humans. Some will disparage the life expectancy figures, disregarding the absence of contemporary disease in primal times, and the gradual advent of agriculture and civilization around the world that caused human life expectancy to drop significantly. This drop came primarily due to infectious diseases, warfare, and inferior nutrition within the hunter-gatherer diet. When we reduce aging to only chronology, we overlook the accurate indicators of the aging process. They commonly recognized chronological seem to tell a distorted, if not incomplete, story.
Perhaps we need to rethink our definition of aging so that we can understand how to decelerate it by removing age-accelerating lifestyle practices. Today, we have a warped sense of longevity because many of us have accepted adverse lifestyle practices as being the norm. Our organs wear out in 120 years, as opposed to 80. We can reframe our current notion of chronological aging more accurately as an accelerated decline in health and fitness resulting from modern lifestyle practices such as poor nutrition, chronic exercise, lack of adequate sleep or play, or overly sedentary daily routines.
Hayflick limit
On a biological level, our natural maximum life span corresponds with the Hayflick limit—the upper limit on the number of times our cells can divide before expiring by programmed cell death or apoptosis, especially in the absence of adverse lifestyle practices and misfortune that accelerate aging.
Also, a short sequence of genes located at the tip of the chromosome called telomeres can reveal the number of times a cell can divide. Each time cells divide, the length of the telomeres on that cell shortens. Biologists use protein cell telomere length as a biomarker for aging because their evidence has emerged that oxidation, free radical damage, glycation, and inflammation from adverse lifestyle accelerate aging and shorten telomere length. Dr. Ron Rosedale, the author of “The Rosedale Diet,” asserts that the shortening of telomeres is merely a symptom of accelerated aging due to other influences, not a cause. Hence, an examination of one’s telomere length could correlate with lifespan and may reveal that we stand much younger or older than we look or that our chronological age tells us.
We drive the aging factors of oxidation, free radical damage, glycation, and inflammation are mainly by poor dietary habits such as excess consumption of sugar, industrial oils, and other processed foods, as well as excessive stress and insufficient sleep. Even when we sit excessively has been shown that when we sit excessively, we contribute to shortening our telomere length.
Ultimately, suppose we view aging as a decline in strength, power, speed, endurance, flexibility, and your organs’ ability to function beyond a baseline level, along with an absence of disease or disease risk factors. In that case, we can see that the conventionally used aging marker of chronology gets overridden and reframed by our lifestyle behaviors that contribute to or undermine our wellness and longevity.
References
Rudolph, K. Lenhard. Telomeres and Telomerase in Aging, Disease, and Cancer : Molecular Mechanisms of Adult Stem Cell Ageing. Berlin: Springer, 2008.
Sisson, Mark. The Primal Blueprint. 4th edition. ed. Oxnard, CA: Primal Blueprint Publishing, 2019.
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