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Wednesday, May 27, 2015




Here’s more sobering news about depression: People who are over 50 and depressed may be twice as likely to have a stroke as someone who isn’t depressed, according to a new study. And even people whose depressive symptoms subside have a higher risk than people who have never been depressed, at least in the short term, the researchers found.


Paola Gilsanz, ScD, Yerby Postdoctoral Research Fellow at the Harvard T.H. Chan School of Public Health, and Maria Glymour, ScD, MS, an associate professor of epidemiology and biostatistics at the University of California, San Francisco, and colleagues looked at data from 16,178 men and women aged 50 and older with no history of stroke enrolled in the Health and Retirement Study between 1998 and 2010. Every two years, researchers asked them about several health factors, including symptoms of depression and history of stroke. During the 12-year study period, participants reported 1,192 cases of stroke.


Study Reveals Depression-Stroke Connection

Gilsanz, Glymour, and colleagues found that people who reported at least three depressive symptoms—such as poor sleep, lack of appetite, and persistent feelings of loneliness or hopelessness—at two consecutive visits (meaning at least four years) had a 114 percent increased risk of experiencing a stroke within the next two years compared with people who reported no symptoms of depression.


The risk remained 66 percent higher for participants who reported that their depressive symptoms had subsided between interviews. Women who reported that their symptoms had abated still had an 86 percent higher stroke risk than non-depressed women. However, recent-onset depression—occurring between interviews—did not have an impact on stroke risk within the next two years.


Possible Links between Depression and Stroke

Researchers aren’t sure why depression increases a person’s risk for stroke, but they have some theories. First, depression may encourage people to adopt unhealthy behaviors, such as smoking or not exercising, that are known to increase stroke risk, the researchers wrote. But depression may also cause or contribute to long- or short-term changes in the brain and body that may, in turn, increase stroke risk, such as high blood pressure, atrial fibrillation (irregular heartbeat), atherosclerosis (buildup of fat and cholesterol that blocks the arteries), or inflammation.


“Our findings suggest that effects [of depression] occur over the longer term through accumulated damage,” since short-term increases or decreases in depressive symptoms did not appear to have an impact on stroke risk, the researchers wrote.


Treat Depression Early to Lower Stroke Risk

Since the findings have not been reported before, other research groups will need to replicate and confirm the results, the authors of the current study said. But “if replicated, these findings suggest that [doctors] should seek to identify and treat depressive symptoms as close to onset as possible, before harmful effects start to accumulate,” said Gilsanz in a news release.


For more coverage of the link between depression and stroke, browse our archives here. To learn more about depression and how to treat it, see the resources at the National Institute of Mental Health.


Image via IntelFreePress on Flickr.

Tuesday, May 26, 2015




Depression is more common in people with Parkinson’s disease (PD) than in the general population, and research suggests it may be a risk factor for the condition, or even an early feature of the disease. Now, a new study published in Neurology strengthens that link.


Gathering data from a national register of health records for the Swedish population, study author Peter Nordström PhD, a professor and chief physician in the Department of Community Medicine and Rehabilitation at Umeå University in Sweden, and his colleagues looked at a sample 140,688 people who were aged 50 or older at the end of 2005 who were diagnosed with depression between 1987 and 2012. They matched each person with depression with three “control” participants of the same age and sex who did not have depression; in total, the study population included 562,631 people. They then followed these patients for up to 26 years.


During that time, 1,485 people with depression (or 1.1 percent of the depressed group) and 1,775 people without depression (or 0.4 percent of the non-depressed group) developed PD. Compared with those without depression, people who were depressed were 3.2 times more likely to develop PD within the year after they were diagnosed—a more than 200 percent increased risk. And 15 to 25 years after the depression diagnosis, they were still 50 percent more likely to develop PD than non-depressed people.


More Severe Depression Increases PD Risk

Researchers found that people who had been hospitalized at least once for depression were 3.5 times more likely to be diagnosed with PD than people who received treatment for depression but were never hospitalized. And people who had been hospitalized for depression five or more times were 40 percent more likely to be diagnosed with PD than people who had been hospitalized for depression only once.


Looking for a Genetic Link

To see whether there might also be genetic or environmental factors contributing to the link between the two conditions, the researchers then looked at the incidence of depression and PD in 540,811 pairs of siblings. Although Parkinson’s was more common among people had a sibling with PD, depression in one sibling did not increase the risk of the other sibling developing PD.


This finding suggests that PD and depression are linked because “if the diseases were independent of each other but caused by the same genetic or early environmental factors, then we would expect to see the two diseases group together in siblings, but that didn’t happen,” Dr. Nordström said in a news release.


Is Depression a Risk Factor or a Symptom?

Dr. Nordström and his colleagues put forward three theories that might explain the link between Parkinson’s and depression. First, they said, depression and/or drugs used to treat depression could increase the risk for PD. Second, depression may be an early symptom of Parkinson’s disease, appearing well before motor symptoms and other manifestations of the disease occur.


Lastly, they said, it’s possible that genetic or environmental factors that cause depression may also cause PD—although the results of their study in siblings make this theory less likely.


Treating Depression Can Help

Even if depression turns out to be an early symptom of Parkinson’s, and therefore a result of neurodegeneration, treating the condition with antidepressant medication and therapy can be beneficial, experts say. 


“How people think about their illness—the coping skills they use, how they respond to symptoms, and how they perceive themselves—can have a big impact,” Roseanne D. Dobkin, PhD, a clinical psychologist at the Robert Wood Johnson Medical School in Piscataway, NJ, told Neurology Now in 2013. “Addressing negative thoughts and maladaptive behavior patterns can relieve some of the depression and related non-motor symptoms of PD, including sleep problems and anxiety.”


For more stories about the link between depression and Parkinson’s, browse our archives here. To learn more about depression and how to treat it, see the resources at the National Institute of Mental Health.


Image via Lloyd Morgan on Flickr.

Friday, May 22, 2015




The nationwide scrutiny of the NFL and sports concussions is unlikely to disappear any time soon. In the latest study of former NFL players, researchers found that those who experienced at least one concussion that caused a loss of consciousness are at a higher risk of brain atrophy, memory problems, and mild cognitive impairment (MCI) later in life.


For the small study, published in JAMA Neurology, researchers at the University of Texas Southwestern Medical Center administered memory tests and magnetic resonance imaging (MRI) scans to 28 former NFL players, 17 of whom reported they had experienced a grade 3 (G3) concussion causing a loss of consciousness, and eight of whom had been diagnosed with mild cognitive impairment and reported a history of concussion, as well as 21 cognitively normal people with no history of concussion and six people with MCI but no history of concussion. The former players’ ages ranged from 36 to 79.

Severe Concussion Linked to Brain Changes

The researchers found that the players with a reported history of concussion but without MCI had lower scores on verbal memory tests than the cognitively normal participants, although their scores still fell within what is considered the “normal” range for verbal memory. Former players with MCI performed worse on these tests than both the retired players without MCI and the healthy control group. The retired players with MCI and the six control subjects with MCI performed about the same on the memory tests.


MRI scans showed that the footballers who had not experienced a G3 concussion had a similar size hippocampus—a brain region linked to memory formation, which is one of the first to be damaged in Alzheimer’s disease—to the healthy controls. The hippocampus is expected to shrink a little over the course of normal aging, but too much shrinkage, or atrophy, could indicate brain disease or memory problems, the researchers explained. The athletes who had experienced at least one G3 concussion had a smaller hippocampus than the control subjects, and a smaller right-side hippocampus than the athletes who had not had a G3 concussion. And those with both MCI and a history of G3 concussion had a smaller left-side hippocampus than the control subjects with MCI.


Taken together, the researchers said, these results suggest that a history of severe concussion (those involving a loss of consciousness) increases the risk of hippocampal atrophy later in life.


Concussion May Be Risk Factor for MCI

As people age, they are more at risk of developing MCI, which may or may not progress into Alzheimer’s disease. But a history of concussion may also be a risk factor for developing MCI, the researchers said.


In this study, seven of the eight retired football players with MCI were over the age of 63, and all seven of those athletes had had a G3 concussion during their playing days. Only one of the former NFL players with no history of G3 concussion had MCI. This suggested to the researchers that after a certain age, having a history of G3 concussion increases the risk of developing MCI. The link between age and concussion history and developing MCI should be explored in future studies, they said.


More Study Needed on Concussion and Cognition

The results of this study should be interpreted with caution. Because the researchers asked this group of former NFL players to report on their concussion history years or even decades after the fact, their responses are subject to what researchers call “recall bias.” The players may not be remembering their experiences with concussion accurately, which could lead to under- or over-reporting of the number and type of head impacts they experienced during their playing days. In addition, they may have had other health problems that would affect their memory, which the researchers did not account for when collecting their data.


Still, the findings do emphasize the need for more research, recognition, and treatment of concussion, not just in professional sports. And future studies can hopefully be designed that take a more rigorous approach with a larger number of patients. “This is a preliminary study, and there is much more to be learned in the area of concussion and cognitive aging,” said study author Munro Cullum, PhD, a professor of psychiatry and neurology and neurotherapeutics at UT Southwestern, in a news release.


The silver lining, Dr. Cullum said, is that these findings apply only to concussions that cause a loss of consciousness, which are fortunately still fairly rare.


For more coverage of the latest sports concussion research, browse our archives here. To learn more about concussion, see Traumatic Brain Injury: The Basics.


Image via COD Newsroom on Flickr.

Wednesday, May 20, 2015




Want to reduce age-related damage to your brain? Get off the couch and onto the treadmill, says a new study that looked at the effects of exercise on the brains of adults between the ages of 55 and 82. Those who were physically fit had less damage to the brain’s white matter—which, along with gray matter, is found throughout the brain and spinal cord and helps transmit information from one part of the brain to another—than less fit adults. In fact, certain parts of the white matter still looked like that of a younger adult.


And it doesn’t take much to reap the neural benefits of exercise, said study author Scott Hayes, PhD, an assistant professor of psychiatry at Boston University School of Medicine and the associate director of the Neuroimaging Research for Veterans Center at the VA Boston Healthcare System, in a news release. Something as simple as regular walking “could potentially improve quality of life by delaying cognitive decline and prolonging independent function,” he said.


Establishing Fitness and White Matter Integrity

As people age, a certain amount of white matter damage is normal, but too much can put you at risk for problems with memory and executive functions such as planning, reasoning, and problem-solving later in life, the study authors explained. Past research has suggested that these effects might be influenced by exercise, and more physically fit people show less evidence of white matter damage on brain scans.


For their small study, Dr. Hayes and his colleagues administered magnetic resonance imaging (MRI) scans and cardiorespiratory fitness tests to 32 younger adults aged 18 to 31 and 27 older adults aged 55 to 82. They classified the older adults as more or less fit based on their performance on the cardiorespiratory tests, which included measurements of oxygen consumption, heart rate, and blood pressure while they exercised on a treadmill.


Better Fitness Equals Less White Matter Damage

As expected, the researchers found that all the older adults had signs of age-related white matter damage on their MRI scans compared with those of the younger adults. But the scans also showed that the fitter 55 to 82-year-olds had less damage to certain areas of the white matter compared with the less fit adults.


Physical fitness didn’t appear to have an impact on white matter in the brains of the 18 to 32-year-olds. This was not surprising, the researchers said, since neural function is believed to be at its peak during young adulthood, so exercise wouldn’t show much of an impact.


Exercise Protects Only Some Parts of the Brain

The researchers then compared MRI scans from the older adults with those of the younger adults. They found that in the more fit adults, certain parts of the brain were nearly identical to those of the younger adults, including the splenium, sagittal stratum, posterior corona radiata, and superior parietal white matter—areas that usually decline with age. This suggests that physical fitness offers protection against white matter damage in these regions, making them appear younger, the researchers said.


However, some areas of the physically fit older adults’ brains still showed signs of white matter damage, suggesting that exercise does not protect against age-related damage universally throughout the brain. It’s unclear why physical fitness would protect certain parts of the brain more than others, the researchers said.


Studies Needed to Determine the Right “Dose”

“We hope this study provides additional motivation for older adults to increase their levels of physical activity, which positively impacts health, mood, cognition, and the brain,” the researchers wrote. They added that more research is needed, in particular to determine how specific exercise programs (for example, weight training or running) or a certain “dose” of exercise (frequency, intensity, and duration) might change white matter in the aging brain.


But in the meantime, you can add this study to the list of reasons to get off the couch and go for a brisk walk now and then.


For more coverage of the link between exercise and brain health, browse our archives here.


Image via Peter Mooney on Flickr.

Tuesday, May 19, 2015



Many people with pre-diabetes—blood sugar that’s higher than normal, but not high enough to be considered diabetes—also have sleep apnea, a condition in which the airway becomes blocked during sleep, causing irregular or interrupted breathing. Now, a new study published in the American Journal of Respiratory and Critical Care Medicine suggests that treating sleep apnea with a continuous positive airway pressure (CPAP) machine may help lower blood sugar levels, too.


CPAP vs Placebo

Sushmita Pamidi, MD, an assistant professor of medicine in the Respiratory Division at McGill University in Montreal, Quebec, and her colleagues studied 26 obese or overweight adults with sleep apnea. They spent 14 nights in a sleep lab and used a CPAP machine, which helps keep the air passage open by blowing air into the mouth or nose, nightly from 11 pm until 7 am. The 26 adults were compared against 13 sleep apnea patients who were given a placebo pill.


The researchers administered blood tests to measure the patients’ glucose metabolism—how well the body is able to turn carbohydrates into glucose (sugar) for energy—before and after the study period. They also measured blood pressure and levels of the “stress hormone” norepinephrine, which can increase heart rate and blood glucose.


CPAP’s Effect on Blood Glucose

After two weeks, the participants who used a CPAP machine had lower fasting glucose and insulin levels than those in the placebo group, as well as lower blood pressure and lower levels of norepinephrine. Taken together, the results suggest that pre-diabetic patients who used a CPAP machine were processing glucose more efficiently than they were at the beginning of the study, which could lower their risk of progressing to type 2 diabetes, the researchers said.


Lab vs. Real Life

Outside the lab and in their own homes, many patients do not use the CPAP machine for a full eight hours every night, the study authors noted. And because of the study design, they could not determine how many hours a night a person would have to use the machine to see the beneficial drop in blood sugar. Future clinical trials should test the effects of CPAP use on blood sugar levels in a real-life setting, the researchers said.


Still, the results should provide a “strong incentive” for sticking with CPAP, Dr. Pamidi said in a news release—and should underscore the importance of getting screened for pre-diabetes if you already have sleep apnea.


To learn more about treating sleep apnea and avoiding its associated health risks, see “Sleep Wise” in the April/May 2015 issue and browse our archives here. For more ways to reduce your risk for diabetes, check out the resources from the American Diabetes Association.