Gainesville, Fla. -- Nearly 6 percent of morbidly obese children and adults have a genetic defect that keeps them feeling like their stomach is running on empty, no matter how much they have eaten.
The press release refers to genetic defects. The term "defect" implies an error or mistake. But a type of mutation that occurs in 6% of the population (correction: oops, 6% of the morbidly obese - gotta read more carefully) surely occurs at too high a frequency to be a mistake. The ancestors of the carriers of these mutations gained selective advantage and left more surviving offspring due to the mutations that made them more hungry.
The problem humans face today is that in industrialized countries mutations which increase the desire for food are now more a burden than a benefit. But the mutations are only defects if you use modern conditions as a reference to come up with standards for how humans should function.
Once you cross the bridge of defining modern civilization as the standard by which to decide which genetic variations are defects you've crossed a much larger bridge than most people appreciate. Consider the fight-or-flight reflex where someone feels adrenaline flowing and feels the urge to either run or attack. Since this reflex gets triggered totally inappropriately in arguments in office building meetings (few will start beating up co-workers or running for their lives down aisles of cubicles) it is hard to see the fight-or-flight reflex as adaptive at this point. If anything, the stress from adrenaline rush probably accelerates your aging.
If the fight-or-flight response and other counter-productive responses we have in modern situations are defects because they are counter-productive in modern conditions then all humans are full of defects and humanity is in need of a genetic redesign. I happen to think that, yes, we are in need of a massive redesign to adapt us to the technological and urban environments which we live in and to make it easier for us to live longer. But that will not become the majority view until we develop a far more detailed understanding of many genetic variations and how they govern the way we function.
These University of Florida scientists identified 11 mutations that make a receptor involved in hunger regulation to behave in ways that they consider to be abnormal.
Mutations of the melanocortin-4 receptor, a gene found in brain cells that play a role in regulating hunger, are the most common cause of genetic obesity. Now University of Florida researchers have determined how some of these mutations cause the receptor to miss signals from molecules that tell the body when to eat and when to put down the fork, placing scientists one step closer to finding a way to correct these defects.
In a side-by-side comparison of 40 genetic mutations, UF medicinal chemists found that 11 caused the receptor to behave abnormally, according to findings recently published in the online edition of the journal Biochemistry.
The goal is to discover the molecular glitch that causes the receptor to malfunction so chemists can make drugs to treat it, said Carrie Haskell-Luevano, Ph.D., a UF associate professor of medicinal chemistry and the study's lead author. UF researchers have already found a molecule that seems to correct one of the mutations, keeping the hunger-signaling pathway running smoothly, Haskell-Luevano said.
The collection of melanocortin-4 receptor gene mutations for obesity has been building up for years. See these papers from 1999 and 2004 for examples of earlier work on obesity and the melanocortin-4 receptor.
The discovery of more genetic variations that influence some behavior or metabolic processs opens up targets for drug development and also makes it easy to study the causes of differences in behaviors and metabolic processes.
|Share |||Randall Parker, 2006 August 02 05:51 PM Brain Appetite|