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Has Evolution Trained Our Brains to Gorge on Food and Sex?
Submitted by Gary Wilson and... on Sun, 11/28/2010 - 10:49
Can dopamine receptors reveal clues about binging?
Romeo Guinea Pig Causes Baby Boom
A guinea pig called Sooty enjoyed a night of passion with twenty-four females after fooling his way into their cage in south Wales. Sooty wooed the lady guinea pigs, one by one, and has now become the proud father of forty-two baby guinea pigs. . . . "He was absolutely shattered. We put him back in his cage and he slept for two days."
The Coolidge Effect is biology's gallant resolve to leave no novel mate unfertilized whatever the cost. It's typical in mammals, has also been seen in females, and can be traced all the way back to our distant relatives: rodents. Although we humans are pair bonders, our bonding program still competes with this older have-opportunity-will-get-it-on impulse.
All animal behavior, including the Coolidge Effect, is based on the rise and fall of neurochemicals and changes in receptors. Recent research suggests that some of the mechanics behind Sooty's heroic feat may lurk in the striatum—a complex group of structures that function as the central hub of the brain's reward circuitry. The striatum is associated with reward and aversion, and strongly influences our decisions. Sex, love and bonding run through these structures. If they don't light up, "it ain't happening."
For example, recreational drugs often flood the brain with dopamine. Key neurons in the striatum react by shutting down lots of D2 (dopamine) receptors, bringing the high to an end. This mutes feelings of reward and motivation until the brain recovers. Fewer D2 receptors seems to mean, "I need more dopamine to feel okay." The reward circuit is crying our for stimulation and only the really exciting stuff will do. Sex, drugs and rock 'n' roll...or maybe Häagen Dazs. In fact, heavy drug users with depleted dopamine receptors tend to lose interest in sex and bonding; they need stronger kicks. D2 receptors also help put the brakes on overconsumption. Fewer D2 receptors make cravings harder to resist.
In the research mentioned above, scientists seeking to learn more about binge eating in humans reported some interesting dopamine-receptor findings. Feeding rats super-stimulating food (fatty cheesecake and sausage) swiftly decreases the number of D2 receptors. Where? In the striatum. After the rats had eaten their last morsel of super-yummy food, receptor density remained low for at least two weeks (the duration of the experiment).
As with recreational drug use, the striatum reacted to the over-stimulation, but it did so very differently from the way it reacts to, say, cocaine. In the case of cocaine, D2 receptor density bounces back in two days (although other changes may continue). But with food—a natural reinforcer (buzz)—the D2 depletion continues far longer. It's curious that the depletion lasts longer after food, considering that cocaine causes a bigger blast of dopamine. Is a genetic program kicking in?
Something more sinister was going on, too. As with continued drug use, the brains of the rats registered less pleasure activation. And it showed up in their post-binge behavior: standard rat chow lost all appeal. Consumption remained lower than normal for weeks. "Cheesecake or nothing," the rats seemed to be thinking. (Interestingly, the opioids produced by sugar consumption act as another anti-satiety mechanism by interfering with oxytocin production.)
Obviously, a "binge trigger" (via whatever mechanisms) is an evolutionary advantage in situations where survival is furthered by engaging in a behavior past the point of normal satiety. Think of bear gorging on high fat salmon before hibernating. Or wolves, which need to stow away up to twenty pounds of a single kill at one go. Or our ancestors, who needed to store high-quality calories as a few extra pounds for easy transport to survive hard times. Or yourself when you're jam-packed with turkey and mashed potatoes and your favorite Thanksgiving pie appears.
When our primitive brain perceives something as really valuable, it wants us to exploit the golden opportunity...fully. It can't do that with warm, fuzzy feelings of satisfaction. Nope. It has to create feelings of lack or dissatisfaction (cravings) in order to drive us past our normal limits.
Key changes in receptors make us feel like something is...not right. We want to feel good again, whatever it takes. Not everything will do it for us, either. We won't settle for normal, because our brains want us to focus on the super-goodies...only. Normal levels of dopamine aren't enough. We become demanding. We want something hyperstimulating, something that registers as "high value" (whether or not it is), something that will trigger release of the dopamine (and pleasure response) our brain is now craving. Dopamine is released when something is better than expected, and a spike of dopamine will stimulate the few remaining receptors in the striatum to give us another taste of good feelings...before we feel dissatisfied again.
Keep in mind that the reward circuitry's job is to remain slightly dissatisfied even under the best of circumstances. In this way, we're primed to seize promising opportunities, or look forward enthusiastically to the deferred gratification of achievement, successful courtship or saving to increase future options.
Normally this aspect of our make-up gives us a zest for life and accomplishment. But when we over-stimulate and desensitize our reward circuitry, normal pleasures and ambitious plans for the future don't offer the usual buzz. Worse yet, we may not value the companionship and warm affection we tribal, pair-bonding primates need for a sense of well-being. Instead, we're likely to feel very dissatisfied—even with our loved ones—and quite certain that any fault lies with them for not meeting our exaggerated needs. We want immediate gratification, even if we imperil our future goals. Our genes have successfully hijacked our attention for their goals.
Could a better understanding of how super-stimulation alters receptor density help humans to make sense of the fact that 65% of Americans are overweight and men with computers everywhere find Internet porn riveting? Are we being pushed around by low D2 receptors and other related brain changes caused by, what would have been for our ancestors, truly extraordinary stimulation?
Think of Sooty seizing his chance to court his harem. Or musician John Mayer's confession that he now prefers hours of porn to relationships with real women. (And yes, women binge on "cheesecake" too. See (singer) 'Katy Perry skips work to watch porn!')
A gadfly brain signal becomes a risky liability where highly prized foods or extraordinarily stimulating novel mates are available in inexhaustible supply. When the binge trigger remains activated, satisfaction eludes us no matter how much stimulation we consume or experience. Ironically, when someone finds himself seeking hotter and hotter stimuli, it's not because he is getting more pleasure, but because he is getting less. A breath of air is glorious to a drowning woman because her oxygen is low. Similarly, a numbed brain is seeking what it doesn't have—pleasurable stimulation—because its normal sensitivity is reduced. A feverish urge to seek pleasure can easily be mistaken for pleasure, even if it is technically the elusive promise of pleasure.
The rats in the study quickly became obese when offered unlimited amounts of extravagancies. Unlike normal rats, they didn't lay off the goodies even when threatened with electric shocks. They ate to unhealthy extremes; they were not satisfied. Think drug addicts.
Do porn users struggle against this same binge trigger in the striatum when they can't get enough of the highly stimulating new "mates" who beckon at each click? Sooty got a much-needed rest after mating with the cage full of females, but a porn user's work is never done. There's always another virtual "mate" moaning for attention. Our brains goad us to stay on task when goodies abound. There seems to be something unique about our brain's response to very tempting food and sexual stimulation.
It may also be that when orgasm hasn't offered a full range of soothing bonding behaviors (as in sex without a partner), we are especially vulnerable to feeling dissatisfied soon afterward. After all, from our genes' perspective, our fertilization duty isn't done. If so, is this horniness true libido—or synthetic insatiability caused by brain changes that dampen feelings of satisfaction?
Is it possible that even one orgasm sometimes increases subsequent cravings? No one knows for sure. However, a rat's dopamine receptor density declines sharply with its first heavenly helping of fatty food. There seems to be some overlap in the binge trigger that drives both mating and eating. Recovering porn users find that consuming junk food increases cravings for porn during withdrawal. And perhaps you've heard that popular joke about the ideal girlfriend, who turns into a pizza at midnight.
The neurochemistry of orgasm and eating certainly can't be reduced to D2-receptor changes. However, receptor changes could definitely be part of the puzzle of why sexual desire sometimes escalates without offering lasting satisfaction. (If the concept of a lingering cycle after orgasm is new to you, you might be intrigued to learn that research has already revealed a cycle of at least seven days in men.)
Maybe research will one day furnish a roadmap of brain changes after different sexual activities. Then we won't be left solely to the mercy of our brain's binge trigger in our search for contentment.
Explained researcher Paul Kenny, the brain releases dopamine in response to enjoyable experiences such as eating cheesecake, having sex or snorting cocaine. But, too much pleasure skews the brain's reward pathways by overstimulating the D2 receptor and causing it to shut down. For the rats addicted to junk food, the only way to stimulate their pleasure centers was to eat more high-fat, high-calorie food. "They're not experiencing rewards the way they should," Kenny said.
NEW: Why it's so hard to diet (Tufts research confirms that "overweight and underweight animals both have "exactly the same deficit in the brain—a significant lack of dopamine released in the site that mediates reward."