The Disease of Morbid Obesity
The Disease of Morbid Obesity : “Dispelling a Destructive Myth”
J. K. Champion MD FACS
Within our society today there exists a myth that all obesity is related to “weak will power“.
How many times have you heard from a misinformed prejudiced healthcare provider , “all you have to do to lose weight is push away from the table”. This article exposes that myth for the sub-group of individuals who have “clinically severe obesity”, by reviewing the genetic , biochemical , and physiologic factors controlling this complex disease
Obesity has become an epidemic problem in the United States. Obesity is defined as being 20% over ideal body weight , or a body mass index of 28. Currently 55% of the U.S. population meets these criteria. This condition accounts for 75% of all diabetes, 50% of high blood pressure, and 50% of abnormal cholesterol levels. Many people can be managed at this level with supervised low calorie diets and exercise.
Among the overweight population there exists a subgroup having “clinically severe obesity” or morbid obesity that are 100 pounds overweight, or have a body mass index of 40.This subgroup, which comprises 5% of obese patients, was identified by the National Institutes of Health ( NIH )as having an extremely high risk of associated health problems and early death. At a BMI of 40 there is a 6-8 year reduction in life expectancy, and at a BMI of 50 there is a 1200% increase risk of medical problems and a 10-15 year reduction in life.
There is a 95% failure with diets and medical treatment, with the average weight loss being only 6 pounds after 2 years of therapy. Only 5% of morbidly obese patients are overeaters. I hear two comments routinely in my practice :
1) “ I’m never full”
2) “ I eat the same amount as everyone else , yet I weigh 300 pounds “.
Both these observations are true due to the disease of morbid obesity, as we will explain utilizing the accompanying diagram.
Morbid obesity is primarily a disease of fat metabolism ; i.e. how fat is stored and burned to produce energy for our bodies to function. To understand how this is accomplished , we need to back up for a moment and provide you with a crash course in medical science. Within each cell of our body there exist strands of protein material called DNA , which direct all our body’s functions. Each strand of DNA is like a strand of beads , made up of connected segments called genes. Think of each gene as being a light switch (either on or off ) . Genes work by producing chemical messengers ( hormones), which enter our blood stream and tell other cells what to do . The light switch for each gene is called areceptor , so when the receptor comes in contact with a particular hormone in our blood it is either turned on or off. This complicated arrangement and its end results is called “ genetics” , “biochemistry” , and “ physiology “ and it is responsible for regulating all our bodies functions , including metabolism and the predilection for morbid obesity.
As we examine the diagram , let’s begin at the left mid border where it lists food and exercise as the two external factors under our control. The current medical approach to management of obesity focuses on only these two areas. Let’s follow the energy trail inside the body to understand what’s really going on and why the “weak willpower ” concept is a myth.
Our metabolism is controlled by between 8 and 30 genes. If you inherit 30 dysfunctional genes , you’re going to be obese; but if you inherit only 8 , then you may not be obese with regular dieting and exercise. Recently the Beta-3 Andrenergic ( beta-3a) receptor was identified which slows the metabolism by 75 calories per day. This equals 12 pounds per year . Around 25% of Afro-American and Hispanic women have this defect. Other evidence reveals that morbidly obese people are 20% more efficient at burning calories , so they need 20% less than the normal population . This means living on around 1200 calories per day . Many people can do this for a short period on a diet , but invariably revert back to 1600-2000 calories and regain their weight. This is responsible for yo-yo dieting, because there is no control of “hunger”.
Following the energy trail downward , excess calories are converted to fat ( adipocytes) for storage. Insulin plays an active role in this process. Two chemicals produced in the upper small bowel help control the release of insulin (GLIP and GDP), and with the gastric bypass they are bypassed and insulin regulation and diabetes is better controlled. The OB gene has been identified in brown fat cells which tend to concentrate at the waist , and are present in higher numbers in women. This gene produces the hormone Leptin which helps to regulate fat storage by telling the brain to stop eating. We initially thought that obese patients did not produce enough leptin , but we now know that they produce high leptin levels , however the brain is resistant to its intended effect. The SOS-3 gene has been identified as possibly playing a role in blocking leptin’s effect . This results in never feeling full. The stomach itself produces a chemical called Ghrelin which increases hunger and appetite, and is stimulated as food comes in contact with the gastric wall.
The hunger center in the brain contains multiple receptors involved in appetite control. The Melanocortin-4 ( MC-4 ) receptor is activated by leptin normally to signal “stop eating “ . The protein CART ( cocaine and amphetamine transcript ) is one chemical messenger produced in the brain, which acts on the MC-4 receptor to stop eating. In addition , Dopamine receptor-D2 ( DRD2), which is part of the brain’s reward center, is involved in modifying our response to food.
The brain itself produces two chemical messengers ; Orexis and Neuropeptide-Y, which tell the hunger center “ feed me “ . Neuropeptide-Y also acts to slow the body’s metabolism and store fat , further enhancing an individual’s obesity potential.
Finally , other factors play a role peripherally in our body to regulate our metabolism . Uncoupling protein ( UCP ) activates the burning of fat to produce heat , and Peroxide- Proliferator Activated Receptor ( PPA ) cause primitive cells in our blood stream ( fibroblasts ) to turn into new fat cells.
These recent discoveries represent the tip of the iceberg with numerous other genes and receptors awaiting identification. The large numbers of factors, which regulate fat production, make it unlikely that any one drug will address every defect. In the future individuals may undergo DNA testing and a specific medication or replacement gene could be given to treat obesity.
Morbid obesity is not a moral issue or “ weak willpower “, but rather a complex multifactorial disease with genetic , biochemical , and physiologic facets. The next time a misinformed healthcare provider suggests “weak willpower“ , recommend they test it themselves. Ask them to eat an entire package of Ex-lax and then use willpower to not have a bowel movement for the next 24 hours. Then let’s see if willpower has any effect on the body’s physiologic response !
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