Turn Off the Fat Genes: The Revolutionary Guide to Losing Weightby Neal Barnard
Breakthrough genetic research indicates that genes are not just onoff switches for characteristics we can't control (like gender or eye color). Some genes, including those that shape our bodies, actually adapt to outside influences. In Turn Off the Fat Genes, Dr. Neal Barnard draws on this cutting-edge research to create a revolutionary new program for activating thin genes and suppressing fat genes, a dramatic tool for sculpting away excess pounds to reveal the healthy, vital body that nature intended.
In Turn Off the Fat Genes, Dr. Barnard begins by explaining the dynamics of nutrition and its impact on genetics. Once you understand how the genes that control your shape can be influenced, the next step is positive intervention. The heart of Dr. Barnard's book is a three-week gene-control program (complete with menus and recipes) specifically designed to influence the five key genes that determine: (1) which foods you prefer, (2) the strength of your appetite, (3) whether your calories are burned or stored as fat, (4) how fast you burn calories, and (5) your muscular type and ability to exercise. Dr. Barnard's program enables all of us to enjoy the same virtually effortless weight control as the naturally thin people we have always admired.
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The Gene Search Pays Off
Genetics deals each of us a different hand, giving us our individual strengths and weaknesses. You don't necessarily have to accept what you're given. Let me make an analogy.
Casino Square in Monaco is as beautiful a place as exists on earth. As you look up from the café veranda at the swallows soaring in the light that dapples the Mediterranean waters, the place goes to your head even before the waiter arrives with a cool drink. The old casino is as stately as ever, standing shoulder to shoulder with the Hotel de Paris, one of the world's most luxurious addresses.
Beautiful as it is, I was oblivious to all of it. I was inside the casino, staring at a jack of clubs and a six of diamonds. The blackjack dealer had a ten up, and I was in trouble.
I grew up in Fargo, North Dakota, where low-stakes blackjack is common in restaurants and hotels. I played at a hotel whose tables benefited the local community theater and wagered as ruthlessly as I could, knowing that I might be all that stood in the way of another production of Oklahoma! Card-counting is not particularly difficult to learn, and a good run at the right casino can pay for a ticket to France, a rental car to Monaco, and dry cleaning for a polyester tuxedo.
This had been a good game. My bets had gradually escalated before the inevitable happened. The cards started to sour. One seemingly unbeatable hand after another crumpled as the dealer collected from a table of increasingly disgruntled players.
Sitting at "third base," I was the last to play before the dealer prepared to garrote us all. Seeing my hand and that I was considering taking another card, the other players glared and muttered in six different languages that if I was to take a hit in the vain hope of getting a four or a five, I would undoubtedly fail. Not only would I likely go over twenty-one; I might also take the critical cards that would make the dealer bust.
But with a ten up, all the dealer needed was another ten, which means any ten card or any face card at all, and his twenty would instantly wipe us all out. Drawing to a sixteen is risky, but standing was an almost certain loss.
"Carte, s'il vous plait," I said, closing my ears to the cursing from a table full of bets ten times larger than mine.
The dealer paused to see if I was serious, then dealt a card and turned it over: a four of hearts, for twenty. I breathed a sigh of relief. The table was not appeased, however, for many gamblers believe that dangerous play casts a spell on the cards.
The dealer took his next card. A five, giving him fifteen. The players cheered in anticipation of what was to follow. He pulled a ten and busted.
The truth is, my decision was not actually the gutsy play it appeared to be. By keeping track of the cards, I knew that many small cards were left in the deck, and that the odds of my getting one were far greater than usual. The hand was untenable as it stood, and it made sense to improve it.
Some of us have healthy bodies from birth, others have bigger challenges. You cannot control the initial deal of the cards. But you don't have to settle for the hand you've got. To a degree, you can improve it. No system is perfect, and even the best players don't succeed every time. But we can take the genetic hand we have been dealt and play it to win. Working toward a healthy body is much less risky than blackjack and is far more rewarding.
THE SEARCH FOR FAT AND THIN GENES
Scientists have long searched for genes that promote thinness and others that cause weight gain. In some families, almost everyone is thin. They can eat virtually anything without it showing up on the bathroom scale. In others, just thinking about food seems to bring on the pounds. A slight frame or a stocky build in Mom and Dad is reflected in their children and sometimes their grandchildren.
It's not just size. Shape runs in families, too. If your parents carried extra weight in their hips and thighs, you are likely to find it there, too. If they carried weight around their waistlines, you may well have inherited that trait.
However, a trait that runs in a family is not necessarily genetic, hardwired forever into your chromosomes. The fact is, we give our children a lot more than DNA. We also give them recipes. We pass on our tastes for foods, ideas about the role of food in the family, and innumerable mealtime traditions. So what looks like a genetic pattern may really be habits passed from generation to generation.
The question, then, is: Are weight problems caused by our genes or by too many heavy meals? Researchers have separated the effects of genes from family habits by looking at twins. Identical twins have exactly the same genes. They started as a single fertilized egg that split in two, producing two babies. Fraternal twins, on the other hand, start out as two separate eggs. Their genes are no more alike than for any other pair of brothers or sisters.
When researchers ask sets of twins to stand on a scale, or use a tape measure to measure around their waists and hips, or check how much of their bodies are made of fat or muscle, they find that identical twins are more alike than fraternal twins. The most likely reason, of course, is that they have exactly the same genes. If they overeat, identical twins put on a similar amount of weight, and it adds to their bodies in much the same places. If they go on a diet, they lose weight similarly, much more so than fraternal twins.
Claude Bouchard and his team of researchers at Quebec's Laval University set out to deliberately overfeed a group of young men-twelve pairs of identical twins-adding an extra thousand calories to their daily diet six days a week for one hundred days. For one man, this resulted in a weight gain of only nine pounds, despite continuous overfeeding. Another, however, gained fully twenty-nine pounds. Normally, when you overeat, your body gives off heat for several hours, eliminating some of the extra calories you took in. But this man was not able to do this to any appreciable degree. The energy he took in was stored as fat, not burned as heat.1
The main finding of the study, however, was that each man's weight gain was fairly similar to that of his twin. If overfeeding caused a small weight change or a massive one in one man, his twin had a similar response, showing that genes play a role not only in our everyday weight, but also in how we respond to marked changes in eating habits.
Even when identical twins are separated and reared in different homes, their similarity persists. Researchers at the University of Pennsylvania and in Stockholm, Sweden, compared twins who had been separated in infancy.2 Despite being raised apart, the identical twins had a similar body size and shape, more so than fraternal twins.
The most remarkable finding, however, was that even though the identical twins were similar, they were by no means identical in either body size or shape. Their eyes were exactly the same color, their hair color was the same, and their heights were virtually identical, but their weights were not precisely the same. Genes had an influence, but they were clearly not the last word. Even with identical genes, weight can change, sometimes dramatically.
The researchers found that it did not make any difference at all in which family the twins were raised. What determined their weight was their genes and their current environment, which is to say, their current eating habits. In other words, despite genetic influences, the key factor in your weight is the type of food you are eating now.
This is vitally important. Genes do not cut out a single predetermined body size like so many paper dolls. As we will see, your weight is affected by many different genes, and the foods you eat allow the fat genes, slim genes, or a combination to reveal their effects. Your genes permit many different body sizes, and foods let you choose which one is you at any moment in time.
THE SEARCH PAYS OFF, A LITTLE TOO WELL
The search for fat genes has not been easy or direct. Some researchers looked for genes causing weight gain in livestock or in rodents, then looked for similar genes in humans. While several human genes do resemble those that cause obesity in animals, most have turned out to have little or nothing to do with human weight problems.3
A more comprehensive method, called genome scanning, carefully examines each individual chromosome for gene patterns that can be linked to weight problems running in families.3 In the Human Genome Project, scientists use special enzymes to slice DNA samples into tiny pieces, which are then passed through an electrical field that sorts them according to size. These pieces are reproduced and analyzed in detail using miniaturized and highly automated machinery. The end result is a detailed map of the molecules that make up each chromosome and the actions in the body to which they correspond. With these and other techniques, researchers are nailing down the genes that make us thin or heavy.
One genetic culprit was hiding on chromosome 15. A slight alteration on this chromosome causes an enormous appetite that kicks in between ages twelve and eighteen. Most teenagers are big eaters, of course, but children with this condition, called the Prader-Willi syndrome, have an appetite so far beyond normal that most end up with severe heart disease or diabetes, and few survive past age thirty.
This syndrome is rare. It occurs only once in every 25,000 people, and if you were to check earlier in an affected child's life, you would see signs that not all was well: reduced fetal movements, then sluggishness at birth, followed by slow growth and unusually small hands and feet.1 Oddly enough, the syndrome only results when the abnormal chromosome is inherited from Dad. If it comes from Mom, the child has other problems-abnormal movements and intellectual problems-but not obesity.1
Another gene linked to overweight turned up on chromosome 2. This one causes not just increasing weight, but also visual and hearing problems and diabetes. Doctors call this combination the Alstrom syndrome. The gene is recessive, meaning that you have to inherit the gene from both parents to see its effects.4
Another fat gene was found on chromosome 3. And yet another on chromosome 4. And 5. In all, of the twenty-three pairs of human chromosomes (twenty-two autosomes, plus two X chromosomes for women and an X and a Y chromosome for men), genes linked to specific human weight problems turned up on chromosomes 2, 3, 4, 5, 7, 8, 11, 12, 15, 16, 20, and the X chromosome.5
A "thin gene" was identified on chromosome 7. It makes leptin, a hormone that curbs your appetite and makes your body burn calories faster. (Its name comes from the Greek leptos, which means thin.) Leptin is made in fat cells, and when you have enough body fat, leptin travels in your bloodstream to your brain, where it signals a slowdown in your appetite.
In 1997, English researchers reported the case of two cousins who had developed massive obesity early in life. They demanded food continuously and ate much more than their siblings. At age eight, one weighed 189 pounds, and fat tissue made up 57 percent of her body weight. She had so much trouble walking that she had to have liposuction of her legs. Her cousin was only two years old, but already weighed 64 pounds. It turned out that they shared a rare mutation blocking the leptin gene. With no leptin to curb hunger, their appetites were voracious.6
You are not likely to have this same gene abnormality; most of us have a working leptin signal to turn down our appetites. However, certain kinds of diets can disrupt leptin's effect. In chapter 3, we will look at ways to keep leptin working normally.
These rare abnormalities are just the tip of the iceberg of genetic influences. Most common weight problems are caused not by a single gene but by several different genes conspiring together. One might affect your appetite, another slows your metabolism, and still another influences how your body responds to exercise. Their effects may be pronounced in some people and more subtle in others. In some cases, scientists have spotted a gene's effects, but have not yet pinpointed its exact location-that is, which chromosome it is on. Nonetheless, we know what these genes are doing and we can use them wherever they may be.
From the Hardcover edition.
Meet the Author
NEAL BARNARD, M.D., is president of the Physicians Committee for Responsible Medicine and a leading advocate for the critical role of diet in health. The author of six books and hundreds of articles, Dr. Barnard travels and lectures widely. He lives in Washington, D.C.
From the Hardcover edition.
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