Low-carb, low-fat, low-cal, Atkins, South Beach, The Zone ?? wouldn't dieting be easier if the human body was equipped with an ON/OFF switch that controlled our appetite?
In fact, neurologists and psychiatrists have identified several ways in which the human brain influences cravings and feeding behaviors. If scientists could harness these functions, doctors could rewire the brain like a biological control panel to battle obesity and other appetite disorders.
Recent research has revealed the role of one such pathway, governed by a specific type of brain cell that sends 'I need food' messages to the rest of the body.
These cells, called NPY/AgRP neurons, are located in the arcuate nucleus, a tiny bundle of about 5,000 cells located directly behind the bridge of the nose that acts as a very simple control tower. It senses the presence of various hormones in the bloodstream, decides if the body needs calories and nutrients and tells the body if it needs to eat or if it can afford to be active.
The arcuate nucleus is strategically positioned within the brain to perform this sensory role effectively, according to Ann Kelley, a UW-Madison neurology professor who studies the brain mechanisms of food intake, obesity and 'food pleasure.'
'Those neurons are in a part of the brain that's really close to the blood-brain barrier, so they're really sensitive to what's circulating in the bloodstream,' Kelley said.
This neuron-driven message delivery system is one of the human brain's simplest processes, called 'low-order' functions. These are primal, hormone-driven systems, according to Kelley.
NPY/AgRP neurons are one of two types that make up the arcuate nucleus. Their counterparts' long-established function is to deactivate hunger behaviors when hormone and nutrient levels indicate the body is well fed. Defects in these neurons can cause obesity.
Researchers at the University of Washington's Howard Hughes Medical Institute suspected the NPY/AgRP neurons performed the opposite role, reactivating hunger behaviors'the ON switch to counter the other neurons' OFF signal.
Led by neurologist Serge Luquet, the HHMI team tested the role of these cells by meticulously eliminating only NPY/AgRP neurons in mice. They made those cells susceptible to a strain of bacteria that is otherwise harmless. By injecting the mice with the bacteria, Luquet deactivated NPY/AgRP neurons but left the rest of the tiny mouse brains intact.
The experimental mice lost their appetite steadily until they stopped eating entirely five days after the injection, proving NPY/AgRP neurons are vital for rebooting the appetite.
Luquet's findings are only the latest piece of an intricate puzzle that scientists have been working to assemble for years. Kelley's research focuses on 'higher-order' appetite-related brain functions that involve complicated thought processes.
'It's really a matter of circuitry and networking,' Kelley said. 'It's sort of like laying out a map.'
She explained that food-related chemicals in the bloodstream are only the simplest signals driving eating habits. Emotions, addictions and logic can also affect appetite.
'You can be hungry and think, 'I'm on a diet and I don't want to eat,' and some people can refrain from eating and others can't,' Kelley said. 'Why does high-calorie food make us feel good? Why do we eat when we're stressed? Which parts of the brain are used when trying to refrain and dieting'?
Although Luquet's findings seem promising for dieters'his research subjects fasted completely without second thought'behaviors are difficult to control when they react to as many motivation systems as eating does.
Kelley also said no diet pills currently on the market are reliable. Drugs designed to target brain functions like the NPY/AgRP messaging system are ineffective because the brain has countless backup systems for regulating hunger. When one appetite regulation system becomes ineffective, other systems take over.
'The obesity epidemic is a huge public health problem. Everyone would love to find something that could help us curb appetite,' Kelley said. 'The problem is these brain functions have been developed over thousands of years, and they're redundant.'
