In some people, obesity appears to be a genetically programmed trait.
These individuals typically become progressively and severely overweight
even before adolescence, and have a family history of extreme obesity.
The pathophysiology in these patients, and the role that genetic factors
play in more common and milder forms of obesity that develop later in
life, are readily inferred but still poorly understood. When both parents
are obese, a child has a 90% chance of being overweight; when one parent
is obese, a 40% chance; and when neither parent is obese, only a 10%
chance. A few syndromes of congenital hypothalamic hyperphagia have
been described, e.g., the Prader Willi syndrome, in which young children
develop severe obesity, hypogonadism, and some degree of mental retardation.
Most often, mild to moderate obesity is acquired later in life. In
addition to a genetic predisposition, this common form of overweight
is attributable principally to a "good life" of ample, dense calories,
with infrequent exercise and poor stress management.
The essential first step in treating patients with routine mild to
moderate adult-onset obesity is to approach it nonjudgmentally, appreciate
its multifaceted pathogenesis, and consider critically whether the patient
really needs to lose any weight, or more likely to exercise more and
consume fewer fats. Unless the extra weight is causing or exacerbating
diabetes mellitus, hyperlipidemia, or hypertension, it is not clear
that mildly to moderately obese people need to lose weight. Some authorities
have demonstrated that repeated cycles of weight loss and gain may promote
cardiovascular illness as much as or even more than simply remaining
at a mildly elevated but stable weight.
The only ways proven to treat mild to moderate obesity effectively
and safely over the long term are those in which patients change their
eating habits by lowering the caloric density of their food, and get
more exercise. Courses of virtually all appetite-suppressing drugs,
whether prescribed or over-the-counter (most of the latter contain phenylpropanolamine
or caffeine), are followed by a weight rebound. Furthermore, many of
these compounds can cause significant medical or psychiatric complications.
Similarly, thyroid hormone preparations have no demonstrated long-term
efficacy but substantial risks, especially for patients with heart disease.
Particularly when a patient is motivated, e.g., by a diagnosis of hypertension
or by early disease or death in obese relatives, the physician may be
able to institute effective and sustainable diet and exercise changes.
Patients with morbid obesity (more than twice desirable weight) can suffer
life-threatening consequences such as cardiopulmonary failure. For these
patients, more aggressive approaches can sometimes be justified. Unfortunately,
behavioral techniques alone seldom work. Gastric surgery with stapling
to reduce stomach size has supplanted previous intestinal bypass procedures,
which led to frequent complications in as many as 50% of patients. Gastric
stapling is often successful for morbid obesity - a serious procedure
but with fewer complications.
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