Alice G. Walton , CONTRIBUTORI cover health, medicine, psychology and neuroscience.

If you didn’t quite believe that sitting is one of the worst things we can do for our health, a new study should clear any lingering doubt. It finds that sitting isn’t just a physical health risk—it’s a neurological risk as well. The UCLA study reports that people who are more sedentary have thinning in brain regions linked to memory—and even high-levels of exercise don’t seem to undo the effects of sitting too much.

The team looked at the connections between sitting, exercise, and the thickness of his or her medial temporal lobe, which is involved in memory formation, as well as its subregions. Participants, aged 45 to 75, answered questions about how much they’d sat on average over the past week and how much exercise they got at low, medium, and high intensities. Some physical measures were taken, and they were all tested for the “Alzheimer’s gene” variants (APOE). Finally, their brains were scanned with MRI to measure the thickness of regions in the medial temporal lobe.

As mentioned, time spent sitting was significantly correlated with less thickness in the medial temporal lobe, and certain areas within it, including the entorhinal cortex, the parahippocampal cortex, and the subiculum. Interestingly, exercise was not correlated with thickness in these regions, suggesting that exercise can’t undo the damage that excessive sitting brings. The authors write in their paper, “it is possible that sedentary behavior is a more significant predictor of brain structure, specifically [medial temporal lobe] thickness, and that physical activity, even at higher levels, is not sufficient to offset the harmful effects of sitting for extended periods of time.” There wasn’t a link between APOE status and thickness in the regions of interest.

The study is important for a couple of reasons. One is that sedentary behavior is known to be a predictor of Alzheimer’s risk. In fact, the team points out that earlier studies have calculated that about 13% of Alzheimer’s cases may be due to inactivity, and that even a 25% reduction in sedentary behavior would reduce Alzheimer’s prevalence by about one million cases across the globe. Earlier studies have also hinted that more time spent sitting may be linked to worse cognitive performance, which could be a symptom of existing changes to the brain itself. So the new study nicely lays out the neurological changes that may explain these connections.

It also suggests that reducing the amount of sitting that people do may be a more effective intervention than adding exercise alone. This has been said for physical health, and the same may be true for brain health.

Why does sitting affect brain health in this way? There’s a number of potential mechanisms, including a reduction in the birth of new neurons, reduced plasticity, and increased inflammation. All of these variables are known to be enhanced with exercise, so it’s interesting that even exercise, at least in this study, didn’t reverse the effects of sitting.

Finally, numerous studies have found that being sedentary is linked to a slew of physical maladies, from heart disease to cancer to early death. The American Heart Association, in its own advisory on the dangers of sitting too much, has suggested the tagline, “Sit less, move more.” The same may well be true for brain health.

Abstract Physical activity, and specifically exercise, has been suggested as a potential treatment for drug addiction. In this review, we discuss clinical and preclinical evidence for the efficacy of exercise at different phases of the addiction process. Potential neurobiological mechanisms are also discussed focusing on interactions with dopaminergic and glutamatergic signaling and chromatin remodeling in the reward pathway. While exercise generally produces an efficacious response, certain exercise conditions may be either ineffective or lead to detrimental effects depending on the level/type/timing of exercise exposure, the stage of addiction, the drug involved, and the subject population. During drug use initiation and withdrawal, its efficacy may be related to its ability to facilitate dopaminergic transmission, and once addiction develops, its efficacy may be related to its ability to normalize glutamatergic and dopaminergic signaling and reverse druginduced changes in chromatin via epigenetic interactions with BDNF in the reward pathway. We conclude with future directions, including the development of exercise-based interventions alone or as an adjunct to other strategies for treating drug addiction.

Full Article:  Wendy Lynch, Ph.D.

In the U.S., DRUG & ALCOHOL ABUSE IS RAMPANT.

Is this the breakthrough we’ve been searching for?    

I first got drunk at 12 years old.

Young perhaps, but it was Soviet Moscow, where my dad was stationed as an American journalist in the 1980s. I wasn’t very good at drinking, though I tried. When I was 15, I was arrested three times for public drunkenness, twice in one day. Back in the States, while I was still in high school, a litany of drug and alcohol violations got me kicked out of boarding school—with the final incident just hours before my graduation ceremony, my father the keynote speaker (nope, no daddy issues there). In college, the morning I was scheduled to clock in for a new job, I woke up behind the wheel, on a highway in another state, facing the wrong way. Several years later, a DWI and drug charges landed me in the crime log of the newspaper where I worked as a reporter. And so it went.

Fast-forward 17 years and I’m catching my breath near the 14,115-foot summit of Colorado’s Pikes Peak, my race bib fluttering in the wind. Bracing myself at the halfway mark of the grueling mountain marathon, taking in the countless jagged switchbacks I’d just picked across, I couldn’t help but think about the distance I’d put between Then and Now. And the irony: that after nine marathons and thousands of miles, this is how I get high. Standing on a vast rooftop shingled with mountain peaks, the thin air fizzing my brain, I was feeling pretty buzzed. And grateful. I largely have running to thank for my transformation. After years of face-plants (literal and figurative) and a self-image curdled by guilt and self-loathing, a simple pair of running shoes had returned momentum, even joy, to my life and allowed me to evolve into a capable person—a genuine human being…   And I wasn’t alone.

About five years into my running life—mostly solitary back-country road work—I started to come across stories about other troubled souls who had traded in chaos for running shoes: a meth-head-turned-Ironman-competitor; a recovering crack addict who once ran 350 miles in a week; an ex-convict alcoholic who would tackle the equivalent of almost six back-to-back marathons across the Gobi Desert. Later, I’d read about a treatment center in East Harlem that trains rock-bottom people suffering from addiction to finish the New York City Marathon (http://www.runnersworld.com/nyc-marathon) and another in Canada that mandates running, complete with a natural track area on the premises and an annual race named the “Redemption Run.” I wrote a recovery memoir in that time, and when it was released, my in-box swelled with messages from around the country: from other drunks-turned-runners, sober marathoners, freshly quit opioid addicts, the imprisoned, psychiatrists, and drug counselors. Other than some skeptical 12-steppers arguing I’d substituted one addiction for another (I didn’t go the Alcoholics Anonymous route), all were firm believers in the healing power of the run. In something as simple as hitting the road, they, too, had felt a loosening of addictive thoughts and a sparking of positive changes in the brain, and in the heart. But was there much to it beyond our personal stories and a would-be “swapping of vices”?

Full Article:  Special Report_ The Runner’s High _ Runner’s World (1)