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I am on a diet again, so I take my coffee black today to avoid the terrible caloric burden of a tablespoon of milk. I drink it with my breakfast: two doughnuts — one of which is slathered in dark chocolate — eaten hastily from a paper bag.
If you can’t swallow the incongruity of these choices, then count yourself lucky (and probably thin). Because, to me, this morning is a perfect microcosm of a life spent gaining and losing weight, forcing down kale for lunch, only to have french fries find their way inexorably into my face-hole hours later. And if I contradict myself? Well, I am large.
I have lived this life of undereating and overeating, starvation diets and bloated bingeing, in the broad genetic shadow of my extra-large father. Now that same shadow cascades onto the tiny, ravenous 1-year-old who has taken up residence in my heart and my kitchen. How do you feed a daughter in a healthy way when you’ve spent 40 years failing to properly feed yourself? And, as science increasingly confirms that our relationship to food is largely governed by the DNA that took up residence in our ancestors’ genes hundreds of thousands of years ago, does it even matter?
“The most important reason why some people are overweight and obese and others are not is because of our genes,” says Clare Llewellyn, an obesity researcher in Britain who has spent years studying the genetic and environmental underpinnings of weight gain by tracking 2,400 sets of identical and fraternal twins from birth. The subjects of the Gemini study, as it’s called, are now turning 10 years old. As they continue to age, they may shed even more light on the respective roles played by genetics and environment — by nature and nurture — and how these affect what we see when we step on the scale.
Different-sized twins who aren’t genetically identical but grow up together are ideal subjects for minimizing the home environment as the cause of obesity, Llewellyn says. Studies in recent decades, Llewellyn says, have already shown that around 70 percent of the differences in people’s weights can be explained by differences in their genes. But how? Can the decision to wolf down two doughnuts — and then shake out the decorative curls of chocolate that collect in the bottom of the bag and eat those, too — really be foretold by something deep in my family’s DNA?
Or, in Llewellyn’s words: “What on earth is going on?”
Our genes, it now seems clear, exert a powerful influence on our weight. Some of us react much more strongly to the allure of tasty food; some simply require more food to begin to feel full. Recent research at Harvard and MIT has shown that certain genetic variations in how we metabolize food — an advantage as recently as a century ago, when food shortages were fairly common, even in the developed world — are now pretty good at making us fat. Those researchers, who detailed their findings in a 2015 publication, discovered what they called a genetic master switch that lives inside our developing fat cells and effectively decides whether we burn the calories we’ve just eaten or stash them in our beer bellies.
But while one key genetic component of obesity, an enzyme called FTO, was discovered in 2007 and quickly became known as the obesity gene, it’s only part of the picture. A recent far-reaching study of genetic samples from some 300,000 people found more than 140 locations across the human genome that play some part in obesity, according to the Broad Institute, a research community affiliated with Harvard and MIT. Scientists say the research may one day be key in treating or even curing obesity.
Back at home, my toddler will devour a Mason jar full of oatmeal for breakfast or guzzle 6 ounces of whole milk and immediately demand another cupful. She’ll eat a whole banana by splitting it in two and shoving the pieces into her mouth, like Joey Chestnut at a hot dog eating contest. This is good. Toddlers are supposed to eat, and her growth is right on track.
“Genes set your potential,” Llewellyn says. “But the way that you are fed and your early feeding environment probably acts as a volume control.” My daughter is comfortably in the average range on the height/weight growth charts that her doctor unveils to us every few months. But how am I supposed to know how far to turn the volume knob? When she mashes the last of a banana into her little mouth and demands more before it’s chewed and swallowed, do I peel another?
Half of her genes, and a lot more than half of her meals, come from her mother. But I can’t help wonder though whether this is already evidence of what may be my — and now my child’s — birthright: an appetite without borders.
All over Kendall Square, people are carrying bright yellow bags from the popular local sandwich chain Al’s. They cradle them in the crook of their elbows like footballs or clutch them like loaves of bread — which they sort of are. For less than $10, Al’s will pile a long, soft 16-inch sub roll with shaved steak, cheese, peppers, onions, and any number of other toppings, wrap it tight, and slide it into one of their trademark yellow paper sheaths.
And if I keel over now, cradling a sandwich the size of my forearm, then I will have done the golden thing that every obituary writer searches for in the sad detritus of sudden death: “He died,” friends and family will say, only half-jokingly, “doing what he loved.” At least I will not have squandered the passion for eating that was my inheritance.
My father has always been large. Bearded and barrel-chested, strong from years loading trucks, he used to keep boxes of sugary cereal in a cabinet outside the back door of our three-decker apartment. His kids weren’t allowed to have it, but when he arrived home from work, he’d dump half a box of Count Chocula or Crunch Berries into a vast bowl and fill it with whole milk.
My parents split while I was still in grade school, and Sunday mornings with dad involved vast piles of food at IHOP or stacks of pancakes at a diner. In his small apartment, we’d feast on steak and cheese sandwiches with bacon from a corner store called the Food Connection. And I remember childhood trips to the Big & Tall store — “Big & Fat,” he called it — for belts that seemed impossibly long. By high school, I was heading that way, too, but making use of my 6-foot-2-inch, 260-pound body on the defensive line.
After my dad injured his back at work, requiring spinal surgery, the long battle with his weight ended in unconditional surrender. He is now hundreds of pounds overweight. Routine trips to the doctor require an ambulance and a crew. Walking is a struggle, so he rarely leaves home; when his teeth hurt, he pulls them out himself, with a pair of pliers.
I text him about this article — about the genetic burden he and his only son appear saddled with. “I’m an expert on eating,” he writes back. “For me to stop eating is a 24/7 job and I’m really bad at it.”
To some extent, his genetics almost certainly explain that. “All my mother’s family were and are heavy,” he says. In Puerto Rico, where he grew up, “we were country people. It was never a shortage on food.”
Genetics, obesity expert Clare Llewellyn says, can effectively explain things like our very different fullness gauges — that thing controlled by the hypothalamus that tells you when you’ve had enough and it’s time to stop eating. That doesn’t even depend on the food actually being tasty, and the difference — even between fraternal twins — is observable very early in life.
“If you fasted a roomful of people overnight, they would all eat quite a different amount of porridge before they felt that they had enough,” says Llewellyn (she’s British, hence the porridge). I haven’t tried this experiment, but I imagine I would eat several bowls; my father would eat all the porridge on site and then order delivery.
And that doesn’t even really account for the psychological drivers. Dive deep into the research on eating and obesity and it becomes possible to see your hulking reflection everywhere. One study, published by the Journal of Consumer Research in 2012, suggests that people order (and eat) ever larger meals to “signal to others their relative rank in a social hierarchy.” Those who lack social status, the study found, can eat more in an apparent effort to elevate themselves. So even our insecurity can make us overeat.
In their 2008 book Nudge, Richard Thaler, a University of Chicago economist who won the 2017 Nobel Prize, and Cass Sunstein, a Harvard Law School professor, describe the unconscious social forces that drive our eating habits. Eating with others, it turns out, can be hazardous. Eating with just one other person leads you to eat 35 percent more, while eating in a group of four ups that to 75 percent, they write, citing Cornell scholar Brian Wansink and earlier research. And women tend to eat less than usual on dates, while men — perhaps in a wrongheaded attempt to impress — gorge themselves.
“Obesity,” Thaler and Sunstein write, “is contagious.”
It would be easy to blame Rino’s Place, the East Boston hole-in-the-wall known for vast portions of perfect checkered-tablecloth Italian. Or Branch Line’s remarkable rotisserie chicken. And Benedetto and The Smoke Shop and Flank and others I’ve reviewed in recent years as a restaurant critic for the Globe. There were massive marrow bones and house-made pastas and prime-grade brisket and lobster ravioli served on a plate the size of a Toyota’s tire. An overactive appetite is a job requirement, right? Even if I were more than a sporadic exerciser, running and lifting my way out of these meals while maintaining a job and a family is simply beyond my capabilities.
But no less an authority than Melissa Hartwig, co-creator of the wildly popular Whole30 diet, saw through that. The Whole30, a month of intense restrictions that forbids any and all cheating, is one of countless eating plans I’ve tried over the years.
I explain to Hartwig that my professional eating responsibilities sometimes tended toward ornate gluttony. “Are you really obligated to crush a huge plate of pasta?” Hartwig asks me. Well, no. But if you put one in front of someone like me, that’s probably what’s going to happen.
I think I lost about 20 pounds on the Whole30, even though, as Hartwig points out, the plan’s goal is not weight loss. Whole30 forbids body measurements during the month, including stepping on the scale. “That little number holds your self-confidence hostage,” Hartwig says. “It’s almost like we’re opening you up to this whole new world of eating healthier.”
Manolis Kellis came to that new world a different way.
“I’m the kind of guy who used to eat like two pizzas in a sitting with my brother. He’d have two pizzas, I’d have two pizzas,” says Kellis, an MIT professor who in 2009 lost about 50 pounds on what he calls the MIT Professor Diet (it involves apples, water, and vast amounts of salad). He got down to about 140 pounds and appears to have kept almost all of the weight off.
In 2015, Kellis was part of a team of researchers from MIT and Harvard that published a groundbreaking paper in the New England Journal of Medicine. Their research focused on the role of the FTO gene region and its effect on metabolism. Research has shown that this single region was responsible for a 7-pound difference in body weight between those at genetically high risk and those at low risk.
As it happens, that difference is evident in Kellis’s own home.
“My wife is homozygous non-risk, for the FTO obesity region. And then I’m homozygous risk — opposite ends of the spectrum. “I’ll bring back some nice pizza and she won’t even touch it. She’ll just like sit next to me and cook something healthy.”
But the paper Kellis coauthored had less to do with scarfing down slices and more to do with what happens next. FTO, researchers found, primarily acted independently of the brain, controlling metabolism rather than appetite. Critically, this meant that the same lifestyle could lead to dramatically different results.
It’s fairly easy to see why a genetic predisposition to hoard calories would have been advantageous not so long ago, when food scarcity was a serious, if occasional, problem even in the developed world. And, indeed, only since World War II has the FTO gene region appeared to be related to obesity, Kellis says. That’s when we were suddenly flooded with readily available, highly caloric food and work began to involve sitting at a desk all day. The gene that saved that extra bite of mastodon for a lean week of hunting was suddenly working against us.
“We blame obese people for eating too much and for the choices they make,” Kellis says. “Instead, we should be focusing on how everybody’s metabolism is different and how we adapt nutrition and lifestyle recommendations to those differences.”
Getting to a healthy weight and staying there will likely never be easy for me. I can’t help but think that I’m battling my biology, and I hope that what my wife and I can teach our daughter outweighs whatever genetic burden I’ve saddled her with.
My dad is obsessed with his granddaughter, waiting eagerly for every new picture of her we share. And he seems concerned by the notion that whatever genetic factors led to his weight problem, and then to mine, might also make life a little harder for the tiny girl we both worship.
She is “a real happy girl, and I hate to see anything lowering that happiness level,” he says. “She’s a beautiful girl, but it don’t hurt to watch her weight.”
In a way, she’s watching mine for me: Motivated in large part by my desire to spend as much of her life with her as I can — and despite these dalliances with doughnuts and trysts with cheesesteaks — I lost about 45 pounds last year by reining in my diet and forcing myself to work out. I gained some of that back over the holidays, and I still have about 40 pounds to go. But it helps to know that DNA isn’t destiny.Nestor Ramos is a Boston Globe staff writer. Send comments to firstname.lastname@example.org. Follow him on Twitter @nestoraramos.