THE PROBLEMS OF WEIGHT LOSS: YOU MAY BE GENETICALLY PREDISPOSED TO WEIGHT GAIN

Do you have fat in your genes? Are your parents or grandparents heavy? When your family pulls together several generations of aunts, uncles, cousins, grandfolks, and miscellaneous other relatives for a family reunion, is the most striking cross-generational physical resemblance an expansive hip or waist girth? When you say you have a "large family," are you referring more to the physical size of the individual members than the extent of the family unit? Unfortunately, there is a genetic correlation between what Grandma weighed and what you weigh.

While it may be fashionable (and of questionable honesty) to lay the blame for all of life's ills at the feet of Mom and Dad, the genesis of excess fat goes beyond psychological fashion statements and is in a very real sense a genetic gift from your ancestors. Studies show that if your parents were heavy, you may very well be heavy, too.

An article appearing in the peer review journal Metabolism confirms the connection between genetics and weight problems. Predisposition to weight gain starts very early in life and is probably already entrenched from the moment of conception. A study done in 1976 on mice supports the notion that there is a metabolic difference between obese and lean mice, and while we certainly aren't mice, the metabolic similarities of mice and men can't be completely ignored.

These mice were studied between the ages of seventeen days and eight weeks of age. By the age of four weeks, the obese mice already showed signs of altered weight, including elevated blood sugar and systemic insulin, obesity, reduced skeletal growth, and insulin resistance—differences that were unrelated to diet. All the mice in the study belonged to the same species of mice so their capacity to store fat, secrete insulin, and resist the effects of insulin were based on another genetic component. Fat was, literally, in their genes.

Some of these issues of genetic tendency are too complicated to explore adequately in this context but there may be several faulty mechanisms at work here, including low thyroid function (a body-slowing trait that can be passed on generationally), inadequate levels or activity of brown adipose tissue, excessive production of insulin (or its counterpart, excessive sensitivity to carbohydrates), and others. We will deal with these issues in detail in later chapters.

When obese Zucker rats were studied to learn just why they were obese when their brothers, sisters, and cousins were thin, it was found that the tendency toward obesity was already evident within the first week of life. One article stated that "the main characteristics of the [obese Zucker rats] are hyperphagia [overeating], hyperinsulinemia [excessive levels of insulin in the blood stream], impaired thermogenic capacity [body temperatures were too low], high white adipose tissue lipoprotein lipase activity [increased tendency to store fat tissue], and a high rate of hepatic lipogenesis [liver producing too many fats]."

Researchers forgave the little rats for overeating by saying,

total additional energy consumed over the fifteen-week period cannot account for the greater body weight gain of the obese rats . . . the energy absorbed by the gainers was not significantly greater than that absorbed by the resisters or controls . . . that differences exist in the metabolic response to the purified moderately high fat diet… obesity prone individuals are more efficient than their leaner counterparts and thus utilize less energy per unit…

In other words, the obese rats gained weight not because they ate more but because their bodies were more efficient and required fewer calories to maintain core body activities than their lean counterparts. It had nothing to do with diet and everything to do with genetics.

Thankfully, we are not passive victims of our family tree. Although we may have to work a little harder than our lean human counterparts, we can unravel the genetic tangle by utilizing proper nutrition.

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