Original Content, The Washington Post
Trying to lose weight and stay fit seems daunting at times. The proof of our universal difficulties is evident when you consider that most of us — two-thirds of the U.S. population — tip the scales with numbers higher than medical authorities say is healthful.
When my clients occasionally express hardships, I remind them that in our personal struggles to be slender and healthy, we face two fierce, unforgiving forces: our genetics and our environment. The origin of the frustrations we’re facing today can be traced back 100,000 or more years. By then, our genetic code reflected millions of years of evolution, and it hasn’t changed much since. But our environment has changed dramatically in the last several generations — too quickly for our genetics to adjust.
Our genetics guide us toward certain behaviors that we once needed to survive, according to S. Boyd Eaton, professor of radiology and anthropology at Emory University in Atlanta. But in the relative affluence of modern life, these behaviors now may cause us grief — and girth. “There is a dissonance between ‘stone age’ genes and ‘space age’ circumstances,” says Eaton.
So does the mismatch mean it’s impossible to be slim and fit?
We evolved in an environment where food was scarce; we faced regular famines and our food was obtained with great physical exertion through hunting and gathering. To overcome these obstacles, we developed certain characteristics that enabled us to survive.
For one, we feasted when food was available. Those who demurred when there was food around with, “No thanks, I’m not hungry,” probably didn’t survive.
We also became very efficient at storing body fat, according to Eaton, a trait that kept us alive through lean times. And the most concentrated sources of calories — sugar and fat — were most appealing to us. For millions of years, we survived mainly on fruit, according to Eaton, and that created a natural attraction to sweetness; fat tasted good to us because when food was scarce it was an efficient way of getting calories.
On top of that, our ancestors, in their struggle to survive, burned 3,000 to 3,500 calories a day (compared to the average adult rate today of 2,000).
So take these genetic predispositions that have been in place for millions of years and put them into modern life, particularly into the last half century, during which we have created an environment and culture of abundance without precedent. The U.S. agricultural system produces 3,800 calories per person per day, double what most people need — and we barely have to lift a finger to get any of it. Moreover, the marketing, availability, flavor and abundance of that food — much of it high-calorie, low-nutrient processed foods (which earn the most profit) — make healthful eating a challenge for everyone.
“Because of the deadly combination of the availability of fattening foods and our natural desire to eat it, we live in a toxic environment which is a perfect recipe for creating obesity,” says Kelly Brownell, Director of the Yale Center for Eating and Weight Disorders. “If you were starting a society from scratch to maximize the likelihood of people being overweight, it’s hard to imagine doing it much better.”
Brownell, the author of “Food Fight” (McGraw Hill, 2004) lists factors in the environment that make unhealthful eating more likely. Among them:
• Accessibility Studies show we’re more likely to eat whatever is in our environment. And our environment is chock-full of unhealthy, high-calorie foods. Vending machines and drive-in restaurants are open 24/7, fast foods and snack food are abundant in schools, and even places like gas stations and drugstores have become opportunities to buy food.
• Convenience For people in a hurry (and who isn’t today?), unhealthful foods are easier to acquire, whether from drive-in windows or local convenience stores on every corner.
• Taste It’s easy and cheap to make foods tasty by adding fat, sugar or salt. And most people prefer Haagen-Dazs to Brussels sprouts and Big Macs to broccoli.
“Human beings becoming increasingly obese in a world awash in tasty calories and convenience devices is as easy to understand as polar bears, with their thick white coats, overheating under the Sahara sun,” said David Katz, director of the prevention research center, Yale School of Medicine, at the Time/ABC News Summit on Obesity in May. “While it’s true that we have no native defenses against caloric excess or the lure of the couch, we do have one great asset to fix our weight problem: we’re smarter than the average bear.”
Katz, author of “The Way to Eat” (Sourcebooks, 2002), believes in “skill” power rather than will power. “Overcoming an obstacle begins with identifying it. Then we can apply skills and strategies to all of the obstacles we encounter in our efforts to be thin and healthy,” said Katz. We may not be able to change our genes, but we can change our personal environments. And research confirms the most successful long-term weight losers work at avoiding temptations.
Most of your craving and uncontrolled overeating will be conquered when you feed your body the healthful food it needs regularly during the day and you have the food at your fingertips when you need it.
“With the right dose of skill power, rather than will power, we can navigate safely around the nutritional hazards of the modern landscape,” said Katz.
© 2004 The Washington Post Company
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by Katherine E. Tallmadge
The Washington Post
Okay, it’s not a cure for cancer. But researchers plumbing the human genome have identified genes that play key roles in the killer epidemic of obesity and related diseases.
- Researchers have discovered “healthy” genes which, when activated, clear fat and sugar from the blood stream quickly and efficiently. The genes can be turned on by as little as a single bout of exercise. Conversely, being sedentary for a mere 24 hours turns down the genes’ activity.
A growing body of research is giving scientists a better understanding of why a sedentary lifestyle is correlated with so many chronic diseases. These findings clearly demonstrate that people have the ability, with regular exercise, to effectively turn on genes which will allow them to live healthier lives. The findings help explain why if people don’t exercise, obesity and disease will be the likely results.
“A sedentary lifestyle actually prevents the expression of some healthy genes,” said Frank W. Booth, professor of physiology at the University of Missouri Medical School in Columbia at a recent USDA-sponsored conference in Washington.
- “Keeping these genes activated may help prevent heart disease and insulin resistance or diabetes,” says Booth. “Higher blood levels of fat and sugar increase a person’s risk for these diseases.”
The two genes are referred to as “metabolic” genes. They respond to exercise very rapidly by making proteins which help transfer the food you eat into your muscles for fuel.
The Lipoprotein Lipase gene is one example. It makes the enzyme lipoprotein lipase (LPL). LPL breaks down the fat in your blood after a meal — called triglycerides — into fatty acids. The fatty acids are then taken up by the muscle and burned as fuel. But if you haven’t exercised during the preceding 24 hours, and LPL is not present or is present in lower quantities, the triglycerides stay in the blood at higher levels and for longer periods. This could possibly lead to atherosclerosis — clogging and hardening of the arteries — and obesity, because the excess triglycerides get stored in fat cells instead of going into the muscles to be burned as fuel.
In a study reported in the American Journal of Physiology last year, researchers had men use a bicycle with one leg, the sedentary second leg served as the “control” in the experiment. They found LPL increased, and fat uptake doubled in the exercised leg as compared to the unexercised leg.
Similar results were found in other studies reported in the American Journal of Clinical Nutrition and The American Journal of Physiology last year. When men and women ate high fat meals 16 or 17 hours after exercising, clearance of blood triglyceride and very low density lipoprotein, VLDL (a form of “bad” cholesterol) was significantly faster.
High levels of LPL has several benefits. Scientists suspect LPL lowers triglycerides. LPL also lowers VLDL and increases blood levels of “good” cholesterol, called high density lipoprotein (HDL).
In another one-leg cycling study, the blood coming out of the exercised leg’s vein had more HDL than the unexercised leg. Researchers suspect the LPL in the muscle actually produces HDL.
But the positive effects of LPL are fleeting. After a mere 24 hours of being sedentary, fat -clearing slows. After a week without exercise, even in highly trained athletes, fat – clearing rates return to the levels of a chronically sedentary person.
Another example of a “healthy” metabolic gene is GLUT4. After a single bout of exercise, this gene makes the protein, GLUT4. GLUT4 transfers blood sugar to the muscle so it is burned as fuel.
In a study reported in the Journal of Applied Physiology last year, researchers showed that glucose uptake into the skeletal muscle is directly related to GLUT4 protein concentration in exercising human muscle. As GLUT4 levels increase, more blood glucose is taken into the muscle. GLUT4 causes a smaller rise of glucose and insulin after a meal thereby lowering insulin resistance, and probably the likelihood of diabetes.
“Any time you have a rapid removal of glucose and insulin from the blood, you are lowering insulin resistance,” said Booth.
- Researchers have known for years that exercise lowers blood glucose and insulin levels, but the underlying biological reasons weren’t understood. Scientists are getting closer to understanding why exercise makes such a positive difference.
Testing aerobically trained athletes revealed significantly lower blood glucose and insulin levels after a meal and exercise. No surprise there. But when these athletes weren’t allowed to exercise for just 10 days, their blood glucose and insulin levels increased dramatically after meals. They became more insulin resistant, more diabetic – like. Remarkably, after the sedentary period, all it took was just one exercise bout to return them back to the healthier, exercise levels of blood glucose and insulin.
Researchers see the same effect in obese people. Although obesity increases the risk for insulin resistance and type II diabetes, a study reported in the Annals of Internal Medicine in 1999 showed that cardiovascularly fit obese people with a BMI above 27 cut their diabetes rate in half. The study showed even obese people received an independent effect from exercise.
Experts today believe part of the reason for this improvement is the activation of the GLUT4 gene. The gene responds to exercise very rapidly. An active skeletal muscle needs greater glucose removal from the blood to the muscle for energy or storage to prepare for the next exercise bout.
The activation of the LPL and GLUT4 genes, the researchers surmise, may help explain why people who exercise at least 30 minutes per day experience 30% to 40% less diabetes, heart disease, and stroke.
Of course, the implication of all of this isn’t much comfort to those who hope the genetic revolution will liberate us from the annoying realities of weight control and personal health. The bottom line remains this:
- To control your weight and reduce risk for obesity-related diseases, you need to exercise regularly. And if you don’t, you’re increasing that risk.
But now we have proof that it’s true.