“Sarafand?” I asked.
He nodded.
“That’s where I served!”
He had served with the British army, and I had served more than fifty years later with the Israeli army, and we discovered we’d even lived in the same barracks. For Benjamin, having a job as a truck driver at the base and being able to live in the barracks had been a godsend. For me, the time I spent at Sarafand had also been a godsend, though in a very different way. Over the course of the three years I spent with the Israeli Medical Corps in the 1970s, I progressed from a medic to an instructor of medics to a chief medic to the army’s chief medical officer. I went from bunking with fifty other soldiers to having my own office, car, and secretary and doing inspections by helicopter. A lifetime career in three years.
I realized that the man pouring coffee across the kitchen table from me not only had had a life that preceded the state of Israel but had also been born before radio broadcasting, penicillin, and air travel. And because he had endured and continued to thrive, our lives were now intertwined. He was a pharmacist and I a doctor, both of us living outside New York City, both of us far from our original homes. How much we had to say to each other and learn from each other. Nothing separated our stories but time, and as we talked, a century contracted to the size of the kitchen table. This, I thought, this is what it should be like to age. We should all be so lucky!
With that goal in mind, it was time to start testing some hypotheses.
A Perfect Genome?
In light of the disappointing results we got from the very expensive process of human genome sequencing, we decided to focus on the genes that we thought were the best candidates to be involved in aging. To create a list of these “candidate genes,” we measured several blood components in families of centenarians and found out about their biology. With gene sequencing, we could find out if any of the centenarians’ variants we found differed from the variants of members of an unrelated control group.
To test the hypothesis that centenarians had a perfect genome, we conducted the entire genome sequencing in our first forty-four centenarians. After performing the sequencing, which consists of reading the sequence of approximately 3.2 billion nucleotides that make up the genome of each individual, we obtained information from a database called ClinVar, an important library that compiles the background on the twenty-thousand-plus variants that are the probable causes of all disease. The data comes from people who are healthy and those who have diseases, and we use it to try to find the causes of age-related diseases and illnesses. We wanted to know whether centenarians exhibited any of the determinants of diseases, and our theory was that they did not.
We were stunned by what we found. The forty-four centenarians we studied didn’t even come close to having perfect genomes. Between them, they had more than 230 variants that ClinVar identified as most likely to cause age-related illnesses, such as Parkinson’s disease, Alzheimer’s disease, inflammatory diseases (including heart disease), and cancers. They exhibited an average of five to six variants that should have caused disease but didn’t. Most striking, two of the centenarians had variants that are a major risk for Alzheimer’s (APOE4)—the textbooks say they should have been suffering from dementia at age seventy and dead at eighty—but they were alive and mentally well at one hundred plus! As for the million other variants we looked at, on average, the centenarians had as many variants that are genetically associated with age-related diseases as the control group had.
So with our first hypothesis shot down, we turned to another.
Centenarians’ Interactions with Their Environments
A one-hundred-year-old Japanese artist is being interviewed for a newspaper piece about working long after the average retirement age.
“What’s the secret of your longevity?” the reporter asks.
The artist finishes cleaning his paintbrush. “I don’t know, but I really love fish. I eat it twice a day, and so does my father.”
“Your father? How old is he?”
“He’s 125. He eats fish three times a day. Would you like to meet him?”
“Sure. Where is he?”
“He’s helping my grandfather herd the cattle.”
“Your grandfather? I suppose he eats fish four times a day.”
“No, Grandfather hates fish.”
As with most jokes, there’s a lot of truth in this one. Just when you think you’ve isolated the cause of something, new information complicates the picture. While the discussion of nature versus nurture is ongoing, I was starting to see centenarians’ longevity as a cooperative effort between nature and nurture or, more specifically, between genetics and environment. Studies correlating the age at which the parents died and the age at which their children died seemed to suggest that the genetic influence on aging accounts for only about 20 percent of the variations in life span and that environment is responsible for the rest.
But then again, I could see a problem with this low assessment of the genetic contribution in my own family. My grandfather Dov had a heart attack and died at age sixty-eight, while my father, David, had a heart attack at the same age but didn’t die till sixteen years later, thanks to bypass surgery. So the relationship of mortality between parents and children changed not because of a difference in aging (they both had heart attacks at the same age) but because of the change in the environment, which in this case was medical intervention. Meanwhile, studies of identical twins who were separated early in life and had different levels of health and different diseases in midlife suggest that genetics account for about 25 percent of the variations in life span. That means that even if you have genes that increase your risk for type 2 diabetes, if you’re physically active, eat healthy foods, and manage your stress, you may never develop the disease. So the effects of genes and the effects of environment are not easy to isolate, but as we learn more about genetics’ share of the responsibility, we can plan better strategies to protect ourselves from the environment.
All that said, though, all bets are off when it comes to people with exceptional longevity. Other studies suggest that for people with such long life spans, genetics may deserve up to 80 percent of the credit. We still had questions about how much environment might have added to our SuperAgers’ longevity, though, so we began a study to assess their lifestyle factors.
The study included 477 Ashkenazi Jews who had been living independently as of ages 95–109. Our nurse, Bill Grainer, collected data on body measurements and administered study questionnaires to gather information on lifestyle factors. In addition to asking them about their habits, we asked them why they thought they lived so long, and all in all, their responses were not what I was expecting. Here are the top ten reasons they gave us:
#10: HELPING THOSE IN NEED
Many of our 477 SuperAgers volunteered and worked in service of others throughout their lives, even past the century mark. At age ninety-five, Fanny Freund serves as a vital link between the generations as a volunteer for the Dorot Foundation, which creates mutually beneficial relationships between seniors and younger people. During visits facilitated by the foundation, she hosts students at her home for discussions of her family’s experiences during the Holocaust and her time on a kibbutz in Israel. Another SuperAger, 104-year-old Lilly (Brock) Port, wrote Access: The Guide to a Better Life for Disabled Americans (Yonkers, NY: Consumers Union, 1978), one of the first books to empower the disabled with economic information specific to their situation, during her time as director of consumer education at the Department of Consumer Affairs. She also provided education by way of a consumer affairs radio show. And Irving Kahn served as a trustee emeritus for the Jewish Foundation for Education of Women and founded the New York City Job and Career Center, which helped prepare high school students for the workforce.