There’s a predictable narrative to a lot of discoveries in molecular biology. The story begins when a scientist discovers that Molecule X causes Phenomenon Y. Perhaps we’re talking about CREB and long-term memory, or serotonin and depression, or cholesterol and heart disease. At first, the data looks really solid -- when the gene for Molecule X is knocked out of a mouse, Phenomenon Y disappears! And when patients take a drug that increases/reduces Molecule X, you get a change in Phenomenon Y! The causal relationship seems so simple.

And that’s when things start to get complicated. Time and time again, the neat relationship between Molecule X and Phenomenon Y disintegrates into a knot of feedback loops, enzymatic pathways, environmental interactions and regulatory genes. It’s not that Molecule X doesn’t matter -- it’s that it doesn’t exist by itself. Instead, the Molecule exerts its effects by interacting with a byzantine list of other molecules, all of which can also influence the biological outcome.

This leads me to stress. Last month, I had an article in Wired on the dangerous chemistry of chronic stress. Scientists have known for years that glucocorticoids -- the molecules released by the body during the stress response -- trigger a wide range of negative health outcomes. The list of ailments connected to stress is staggeringly diverse and includes everything from the common cold and lower-back pain to Alzheimer’s disease, major depressive disorder, and heart attack. Stress hollows out our bones and atrophies our muscles. It triggers adult-onset diabetes and is a leading cause of male impotence. In fact, numerous studies of human longevity in developed countries have found that psychosocial factors such as stress are the single most important variable in determining the length of a life.


So far, so obvious: Glucocorticoids are Molecule X, and your health is Phenomenon Y. We should all be on beta-blockers, or at least practice Zen meditation. And yet, the situation isn’t quite so straightforward. As I note in the article, there are plenty of things that increase glucocorticoids levels but don’t seem to cause any negative outcomes:

Not every bout of stress is so devastating. As the Whitehall data demonstrates, executives in the corner office report high levels of stress and yet seem to survive just fine. Other experiments show that intense exercise -- like running for hours on a treadmill -- can lead to the release of glucocorticoids. And yet physical exercise is reliably associated with all sorts of positive health effects.

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These anomalies have led some scientists, including Gould, to search for the additional molecules in the brain that might serve as buffers for the stress response. Gould’s short list of candidates focuses on neuromodulators like dopamine and oxytocin that are released when we experience pleasure. She argues that these feelings of enjoyment -- the ability to find meaning in our work, even if it’s stressful work -- may counteract the toxic effects of glucocorticoids. These molecules might also explain why not every janitor dies of heart disease at a young age and why enjoyable forms of exercise are good for us. “There are important individual differences in how people respond to stress,” Gould says. “Soldiers experience lots of stress in war, but most of them won’t get posttraumatic stress disorder. What accounts for those differences? And how can we help the people who are most vulnerable?”

Just look at sex. It turns out that sex often triggers a large stress response, leading to a spike in glucocorticoid levels. The good news, though, is that this stress is good for us. While chronic stress normally leads to a dramatic reduction in neurogenesis, or the birth of new brain cells, the stress produced by sex has the exact opposite effect. That, at least, is the conclusion of a brand new paper by Gould and colleagues in PLoS ONE:

Adult male rats were exposed to a sexually-receptive female once (acute) or once daily for 14 consecutive days (chronic) and levels of circulating glucocorticoids were measured. [SNIP] To evaluate whether sexual experience alters hippocampal function, rats were tested on two tests of anxiety-like behaviour: novelty suppressed feeding and the elevated plus maze. We found that acute sexual experience increased circulating corticosterone levels and the number of new neurons in the hippocampus. Chronic sexual experience no longer produced an increase in corticosterone levels but continued to promote adult neurogenesis and stimulate the growth of dendritic spines and dendritic architecture. Chronic sexual experience also reduced anxiety-like behaviour. These findings suggest that a rewarding experience not only buffers against the deleterious actions of early elevated glucocorticoids but actually promotes neuronal growth and reduces anxiety.

The takeaway lesson is that sex is both stressful and good for the brain. The “hedonic value” of the experience more than outweighs the temporary surge in corticosterone levels, at least in rats. Although sex appears to get less stressful the more we do it -- we pump out fewer stress hormones during the act -- such “chronic sex” still promotes all sorts of helpful neural habits, such as increased plasticity and new dendritic spines. (Of course, these findings probably only apply to pleasurable coitus. If you’re not enjoying the act, then don’t expect lots of neurogenesis in the dentate gyrus.) As I note in the article, these findings have led Gould to search for the additional molecules (let’s called them Molecules Y and Z) that modulate and mitigate the usually destructive chemistry of glucocorticoids, at least when we’re engaged in “naturally rewarding” activities. This data wouldn’t surprise Marvin Gaye, who sang so passionately about the benefits of “Sexual Healing”:


Sexual Healing is good for me

Makes me feel so fine, it’s such a rush

Helps to relieve the mind, and it’s good for us.