At 5:15 p.m., I walk in the door after a day of work. I feel hungry, and it will be at least an hour, maybe more, until supper. My stomach tells me to have a big glass of water, an apple or a banana, but my brain is craving some kind of salty, fatty food. I have in my arsenal all of the knowledge acquired during nearly 30 years of schooling and career in health and nutrition, so I should know which of the above options I should pick. Stomach versus brain; who wins? 10 minutes later, after eating a bowl of cheddar cheese popcorn, my willpower defeated, I sheepishly conceded to my brain, “You won.”
What happened? I eat a nutritionally sound diet 90% of the time, but what exactly happens when I bow to high fat, salty, or sweet foods? Why does it seem like my body seems to be fighting against my own good health?
We all know what we should do-eat less and exercise more-but we don’t. Why? New research is beginning to unravel that question, with the latest studies showing there are multiple pathways in the brain that encourage eating. Try a single approach to cutting calories is only an approach to failure; the brain has too many backup systems geared toward maximizing caloric intake and holding onto fat, that no single approach will ever work. As journalist Dan Hurley puts it in a well-written article titled “The Hungry Brain,” in the June 2011 issue of Discover magazine, “The brain’s prime directive to eat and defend against the loss of fat.”
The list of failed, single-approach diets is staggering. Atkins’, Pritikin, portion size, willpower, grapefruit, no-fat, high-fat, blood type, cabbage soup, fasting, single fruit,to name a few. All have shown some degree of weight-loss in the short-term, but the vast majority of dieters gain it back, plus more. The obesity epidemic has really kicked off the race for countermeasures. The latest statistics show nearly two-thirds of Americans are obese or overweight, including 13% of children between the ages of two and five! Something clearly has to be done.
How do we tackle this problem? Over the past 15 years, there has been a big push on finding hormonal pathways to either shut off the hunger signal to blocking the storage of fat. Fat cells release a hormone called leptin, which signals the hypothalamus in the brain to reduce the sense of hunger to stop eating. Although this hormone showed promise in the mid-90’s, clinical trials have been disappointing, to say the least. Low levels of leptin did indeed signal the brain to eat more, but the opposite didn’t ring true-high levels of leptin were totally ignored by the brain. Leptin works well for maintaining weight but doesn’t do much of anything for taking it off.
Although leptin proved disappointing, it ushered in research into other molecules that could turn off the eating drive and/or increase satiety. In 1999, researchers in Japan announced the discovery of ghrelin, which works on a different pathway than leptin. Ghrelin is released by the gut rather than fat cells, and signals hunger rather than satiety to the hypothalamus. In 2002, scientist’s from the University of Washington found that ghrelin levels increase before a meal and fall immediately after. Ghrelin increases hunger while slowing metabolism to promote fat storage.
Current research is now focussing on turning ghrelin off rather than turning leptin on. Thus far, work has been done using animal models; human studies are still years down the road.
Another relatively new finding is that blood sugar, hunger, and weight-gained per calorie consumed increase when our sleep is disrupted and our 24-hour body clocks, responding to light and dark (known as circadian rhythms) are thrown into disarray. Add to it the problem of high stress, which lowers metabolic rate while increasing the desire for high-fat foods, and you have the perfect storm for weight gain. A 2009 study by Harvard University showed that in just 10 days, three of eight healthy volunteers developed pre-diabetic blood-sugar levels when their sleep-wake schedule was gradually shifted out of alignment; weight gain is just around the corner.
Today’s society, in which we are encouraged to burn the midnight oil and keep abreast of all things happening around the globe 24/7, could well be contributing to the exponential increases in metabolic diseases we are seeing today.
Our brains are really smart, and it has no shortage of ways to goad us into eating. Recent research shows that the brains of overweight people are wired to feel more pleasure in response to food. Sleep deprived or not, they just enjoy eating more. And, with that desire, over time,the obese develop a DNA polymorphism, a routine genetic variation in a dopamine receptor gene, causing reduced signaling in the striatum (brain). This defect causes them to eat more food to get the ‘high’, akin to a drug addict needing more of the drug dose to get ‘high’.
The effects of stress on eating has a neurobiological basis, according to University of Pennsylvania neurobiologist Tracy Bale. She showed that neural pathways associated with stress link directly to areas of the brain associated with seeking rewards. “Few things are more rewarding evolutionary that calorie-laden foods (comfort foods); Under stress people don’t crave a salad; they crave something high-calorie. It’s because those stress pathways in the limbic system feed into the reward centers, and they drive reward-seeking behaviors. What that tells us is that in addition to drug companies’ trying to target appetite, they need to look at reward centers. We’re not necessarily fat because we’re hungry but because we’re looking for something to deal with stress.”
Thinking back to my bowl of cheddar cheese popcorn, I didn’t necessarily feel stressful, but maybe stress has become the norm in society today, and we rarely notice it.
How do we fix it? Some scientists insist that the day will come when the correct combination of drugs will work simultaneously on the multiple triggers of eating and metabolism. Others call for a more radical approach. Since the triggers for obesity lie in the brain, neurosurgeons at West Virginia University are attempting to rewire those triggers using deep brain stimulation (DBS). Since 2009 they have performed surgery on three obese patients to insert electrodes into the hypothalamus. All three had failed other medical therapies for obesity. Initially, all three reported less hunger with the stimulus turned on, and increased hunger when turned off. Unfortunately, very little weight loss occurred-the brain just slowed metabolic rate to lower caloric expenditure. Dr. Donald Whiting, one of the neurosurgeons leading the study says “The brain is really pretty smart-it tends to want to reboot to factory sessions whenever it can. We find that we can reset things for a week or two, but then the brain gets back to where it wants.” Despite the challenges, Dr. Whiting remains convinced that finding a safe and effective medical treatment for weight control will be essential to turn the obesity epidemic around-and that “No amount of preaching from Oprah or eating models by Jenny Craig or Weight Watchers will suffice.”
Stay well, John R Blilie, M.S.