I am sure you have heard the catchphrase, 60 is the new 30. This boomer manifesto asserts that we feel and act younger than our chronologic years. Perhaps as the songs goes, we are the generation that’s “gonna live forever and learn how to fly.”
And then along came COVID-19 with a wakeup call.
Suddenly boomers became vulnerable people, and the science of the immune system, inflammation and aging itself became fodder for news stories of survival and demise. We began to acknowledge and be more cognizant of our aches and pains…the slight change of gait…and the worry that one day our annual checkup would end in a “diagnosis.”
The question was finally asked by us 72 million aging boomers…
Why is one Granny on a ventilator and another practicing her golf swing for when she can get back on the links? Another way to put it, “What is OLD?”
Geroscientists know the answer. Birthdays do not count much for how our aging progresses. Our genetics occupies as little as 20% of the puzzle, lessening as science discovers more “geroprotectors” to ward off the aging process. We know that calorie restriction, walks, aerobic exercise, sleep and relaxation all empower our body’s biology for greater longevity—check out my blog on biohacking, the habits you can embrace to make a difference in your aging.
Knowing a bit of geroscience helps you keep an eye on the manner in which you are aging.
Don’t worry. To understand how 60 can be the new 30, you need to know only three scientific concepts…no medical degree required.
The first is how we age…the second is why we age…and the third is the unique rate or pace of our individual aging.
#1. How We Age The answer can be seen in this diagram presented by Dr. Nir Barzilai, director of the Institute for Aging Research at Albert Einstein College of Medicine and one of the world’s leading geroscientists. You can listen to Dr. Nir in a webcast I moderated on “The Coronavirus Meets Metabesity: The Nexus Between Pandemics and Age-Related Diseases,” in which he explains the hallmarks of aging.
Proteostasis failure: Failure of protein homeostasis, or biological balance, in the brain cells associated with conditions such as Alzheimer’s disease.
Shortened telomeres: The ends of chromosomes shorten with age, causing cell dysfunction.
Metabolic syndrome: You know this one—increased blood pressure, high blood sugar, excess body fat around the waist.
Immune dysfunction: Increased vulnerability to the COVID-19 syndrome and other illnesses of all kinds.
Inflammation: Persistent inflammation through the body.
Senescence: Deterioration of cell regeneration with age.
Decrease in quality of mitochondria: Membrane-bound cell case that generates the chemical energy needed to power a cell’s biochemical reactions.
#2. Why We Age
The decline in each of the Hallmarks of Aging is a common cause of the diseases of aging. Until recently, we attacked the product of the decline such as cancer, Alzheimer’s, diabetes and other age-related diseases. More recently, we are targeting metabesity, the common causes of the illnesses, and aging decline itself.
If you are not familiar with the term metabesity, you are not alone. The word was coined by Alexander Fleming, MD. He, with his company Kinexum, produced the first Targeting Metabesity Conference in London in 2017…in Washington, DC in 2019…and with me as moderator in October 2020.
The purpose of the Targeting Metabesity Conference is the delay and prevention of all the common causes of aging, with the ultimate goal of faster-to-the-public pharmacology and medical devices that disrupt aging. In other words, metabesity aims to change how we age by retarding the factors that cause aging.
#3. When We Age
In 2015, Daniel Belsky, PhD, and colleagues from Duke University collaborated on a study of 26-, 32-, and 38-year-olds to measure their rate of aging. The researchers discovered that even in young, healthy people, biological aging is quite different. For example, the status of certain proteins that are markers of aging were at different levels of health in people of the same chronological age.
In May 2020, Dr. Belsky and the team published a new Age-Pace study under the auspices of the Columbia University Mailman School of Public Health. The age-pace researchers found a wide variance in how fast individuals age. On average, there should be one year of biological aging for one year of chronological aging. Yet, the range went from 0.6 for those aging 40% slower…to 1.4 for those aging 40% faster than average.
In response to their findings, the research team developed a new blood test called DunedinPoAm, to determine whether a treatment, drug or lifestyle change is making us biologically younger, older or not effecting change. In the process, the researchers got new insight on what governs the rate of aging.
A great deal of how fast you will age, how long you will live and how healthy you will be is governed by lifestyle and environmental factors from the moment you are born.
The parenting you received (abused kids age faster)…your financial level (poor people age more quickly)…air quality and other environmental factors, including public sanitation and the very water you drink…are in the mix.
You can hear my interview with Dr. Belsky on my podcast at Generation Bold Radio. I asked him what one item he was wanted to pursue in his future research. He answered that it is the impact of poverty on age pacing. Indeed.
On a personal note, the Columbia Age-Pace study was done in conjunction with the Butler Columbia Aging Center, where I was an Age Boom Fellow.
Dr. Butler won a Pulitzer for his book Why Survive? Being Old in America.I find it fitting that the Center should work on delaying and preventing aging itself. Dr. Belsky writes, “Slowing the pace of aging is an emerging frontier in medical research as a novel approach to preventing multiple chronic diseases.”
We have heard the aphorism, Time is money. Now we are clear that Money is time.
The more geroscience learns and translates its discoveries into practice, cure and medical breakthroughs, the more significant potential for longevity inequality. Who will afford treatments, medicines, supplements, health-tech devices, better nutrition and stress relievers that are proven to keep us healthier longer? How will we assure that everyone has equal opportunity for longevity if the very fact of being born in poverty makes us age faster? In the past, society might have been less aware that progress creates haves and have-nots. Today we can do better.
Making 60 the new 30 for everyone should be the next frontier.
With geroscience in the spotlight because of COVID-19 and health-span advances in the news, we can also promote longevity equality as we discover the surprising nongenetic factors of why, how and when we age.