Exercise

How physical exercise and fitness improves your brain function

Hippocampal volume and PTSD

April, 2011

A new study supports the association between hippocampal size and recovery from PTSD, pointing to the role of neurogenesis in stress resilience.

Following previous research suggesting that the volume of the hippocampus was reduced in some people with chronic PTSD, a twin study indicated that this may not be simply a sign that stress has shrunk the hippocampus, but that those with a smaller hippocampus are at greater risk of PTSD. Now a new study has found that Gulf War veterans who recovered from PTSD had, on average, larger hippocampi than veterans who still suffer from PTSD. Those who recovered had hippocampi of similar size to control subjects who had never had PTSD.

The study involved 244 Gulf War veterans, of whom 82 had lifetime PTSD, 44 had current PTSD, and 38 had current depression.

Because we don’t know hippocampal size prior to trauma, the findings don’t help us decide whether hippocampal size is a cause or an effect (or perhaps it would be truer to say, don’t help us decide the relative importance of these factors, because it seems most plausible that both are significant).

The really important question, of course, is whether an effective approach to PTSD treatment would be to work on increasing hippocampal volume. Exercise and mental stimulation, for example, are known to increase the creation of new brain cells in the hippocampus. In this case, the main mediator is probably the negative effects of stress (which reduces neurogenesis). There is some evidence that antidepressant treatment might increase hippocampal volume in people with PTSD.

The other conclusion we can derive from these findings is that perhaps we should not simply think of building hippocampal volume / creating new brain cells as a means of building cognitive reserve, thus protecting us from cognitive decline and dementia. We should also think of it as a means of improving our emotional resilience and protecting us from the negative effects of stress and trauma.

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Metabolic syndrome linked to memory loss in older people

March, 2011

Three more studies point to the increased risk of memory loss in older adults with cardiovascular problems.

The new label of ‘metabolic syndrome’ applies to those having three or more of the following risk factors: high blood pressure, excess belly fat, higher than normal triglycerides, high blood sugar and low high-density lipoprotein (HDL) cholesterol (the "good" cholesterol). Metabolic syndrome has been linked to increased risk of heart attack.

A new French study, involving over 7,000 older adults (65+) has found that those with metabolic syndrome were 20% more likely to show cognitive decline on a memory test (MMSE) over a two or four year interval. They were also 13% more likely to show cognitive decline on a visual working memory test. Specifically, higher triglycerides and low HDL cholesterol were linked to poorer memory scores; diabetes (but not higher fasting blood sugar) was linked to poorer visual working memory and word fluency scores.

The findings point to the importance of managing the symptoms of metabolic syndrome.

High cholesterol and blood pressure in middle age tied to early memory problems

Another study, involving some 4800 middle-aged adults (average age 55), has found that those with higher cardiovascular risk were more likely to have lower cognitive function and a faster rate of cognitive decline over a 10-year period. A 10% higher cardiovascular risk was associated not only with increased rate of overall mental decline, but also poorer cognitive test scores in all areas except reasoning for men and fluency for women.

The cardiovascular risk score is based on age, sex, HDL cholesterol, total cholesterol, systolic blood pressure and whether participants smoked or had diabetes.

Memory problems may be sign of stroke risk

A very large study (part of the REGARDS study) tested people age 45 and older (average age 67) who had never had a stroke. Some 14,842 people took a verbal fluency test, and 17,851 people took a word recall memory test. In the next 4.5 years, 123 participants who had taken the verbal fluency test and 129 participants who had taken the memory test experienced a stroke.

Those who had scored in the bottom 20% for verbal fluency were 3.6 times more likely to develop a stroke than those who scored in the top 20%. For the memory test, those who scored in the bottom 20% were 3.5 times more likely to have a stroke than those in the top quintile.

The effect was greatest at the younger ages. At age 50, those who scored in the bottom quintile of the memory test were 9.4 times more likely to later have a stroke than those in the top quintile.

 

Together, these studies, which are consistent with many previous studies, confirm that cardiovascular problems and diabetes add to the risk of greater cognitive decline (and possible dementia) in old age. And point to the importance of treating these problems as soon as they appear.

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[2147] Raffaitin, C., Féart C., Le Goff M., Amieva H., Helmer C., Akbaraly T. N., et al.
(2011).  Metabolic syndrome and cognitive decline in French elders.
Neurology. 76(6), 518 - 525.

The findings of the second and third studies are to be presented at the American Academy of Neurology's 63rd Annual Meeting in Honolulu April 9 to April 16, 2011

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Exercise improves executive function and math in sedentary children

February, 2011
  • A three-month trial comparing the effects of exercise programs on cognitive function in sedentary, overweight children, has found dose-related benefits of regular aerobic exercise.

A study involving 171 sedentary, overweight 7- to 11-year-old children has found that those who participated in an exercise program improved both executive function and math achievement. The children were randomly selected either to a group that got 20 minutes of aerobic exercise in an after-school program, one that got 40 minutes of exercise in a similar program, or a group that had no exercise program. Those who got the greater amount of exercise improved more. Brain scans also revealed increased activity in the prefrontal cortex and reduced activity in the posterior parietal cortex, for those in the exercise group.

The program lasted around 13 weeks. The researchers are now investigating the effects of continuing the program for a full year. Gender, race, socioeconomic factors or parental education did not change the impact of the exercise program.

The effects are consistent with other studies involving older adults. It should be emphasized that these were sedentary, overweight children. These findings are telling us what the lack of exercise is doing to young minds. I note the report just previous, about counteracting what we have regarded as “normal” brain atrophy in older adults by the simple action of walking for 40 minutes three times a week. Children and older adults might be regarded as our canaries in the coal mine, more vulnerable to many factors that can affect the brain. We should take heed.

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Walking counteracts brain atrophy in older adults

February, 2011
  • Walking 40 minutes a day three days a week prevented ‘normal’ atrophy in the brains of older adults.

Another study has come out proclaiming the cognitive benefits of walking for older adults. Previously sedentary adults aged 55-80 who walked around a track for 40 minutes on three days a week for a year increased the size of their hippocampus, as well as their level of BDNF. Those assigned to a stretching routine showed no such growth. There were 120 participants in the study.

The growth of around 2% contrasts with the average loss of 1.4% hippocampal tissue in the stretching group — an amount of atrophy considered “normal” with age. Although both groups improved their performance on a computerized spatial memory test, the walkers improved more.

The findings are consistent with a number of animal studies showing aerobic exercise increases neurogenesis and BDNF in the hippocampus, and human studies pointing to a lower risk of cognitive decline and dementia in those who walk regularly.

Reference: 

[2097] Erickson, K. I., Voss M. W., Prakash R S., Basak C., Szabo A., Chaddock L., et al.
(Submitted).  Exercise training increases size of hippocampus and improves memory.
Proceedings of the National Academy of Sciences.

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Importance of exercise for Alzheimer's gene carriers

January, 2011

A small study suggests that physical activity may be of greater benefit to those carrying the Alzheimer’s gene in protecting against cognitive decline.

A study involving 68 healthy older adults (65-85) has compared brain activity among four groups, determined whether or not they carry the Alzheimer’s gene ApoE4 and whether their physical activity is reported to be high or low. The participants performed a task involving the discrimination of famous people, which engages 15 different functional regions of the brain. Among those carrying the gene, those with higher physical activity showed greater activation in many regions than those who were sedentary. Moreover, physically active people with the gene had greater brain activity than physically active people without the gene.

And adding to the evidence supporting the potential for exercise to lower the risk of dementia, another recent study has found that after ten years exercise (in terms of the number of different types of exercises performed and number of exercise sessions lasting at least 20 minutes) was inversely associated with the onset of cognitive impairment. The study used data from the National Long Term Care Survey.

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Vascular disease underlies cognitive decline in healthy aging

December, 2010
  • New findings add to evidence that the key to not becoming cognitively impaired in old age is vascular health.

More evidence that vascular disease plays a crucial role in age-related cognitive impairment and Alzheimer’s comes from data from participants in the Alzheimer's Disease Neuroimaging Initiative.

The study involved more than 800 older adults (55-90), including around 200 cognitively normal individuals, around 400 people with mild cognitive impairment, and 200 people with Alzheimer's disease. The first two groups were followed for 3 years, and the Alzheimer’s patients for two. The study found that the extent of white matter hyperintensities (areas of damaged brain tissue typically caused by cardiovascular disease) was an important predictor of cognitive decline.

Participants whose white matter hyperintensities were significantly above average at the beginning of the study lost more points each year in cognitive testing than those whose white matter hyperintensities were average at baseline. Those with mild cognitive impairment or Alzheimer's disease at baseline had additional declines on their cognitive testing each year, meaning that the presence of white matter hyperintensities and MCI or Alzheimer's disease together added up to even faster and steeper cognitive decline.

The crucial point is that this was happening in the absence of major cardiovascular events such as heart attacks, indicating that it’s not enough to just reduce your cardiovascular risk factors to a moderate level — every little bit of vascular damage counts.

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Walk for your brain’s sake

November, 2010

Walking helps older adults fight brain shrinkage, which is in turn associated with a reduced risk of cognitive impairment and dementia.

A long-running study involving 299 older adults (average age 78) has found that those who walked at least 72 blocks during a week of recorded activity (around six to nine miles) had greater gray matter volume nine years later. Gray matter does shrink as we get older, so this is not about growth so much as counteracting decline. Walking more than 72 blocks didn’t appear to confer any additional benefit (in terms of gray matter volume). Moreover, when assessed four years after that, those who had shown this increased brain size were only half as likely to have developed dementia (40% of the participants had developed dementia by this point).

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Insulin sensitivity may explain link between obesity, memory problems

November, 2010

A new study suggests that the link between midlife obesity and cognitive impairment and dementia in old age may be explained by poorer insulin sensitivity.

Previous research has indicated that obesity in middle-age is linked to higher risk of cognitive decline and dementia in old age. Now a study of 32 middle-aged adults (40-60) has revealed that although obese, overweight and normal-weight participants all performed equally well on a difficult cognitive task (a working memory task called the 2-Back task), obese individuals displayed significantly lower activation in the right inferior parietal cortex. They also had lower insulin sensitivity than their normal weight and overweight peers (poor insulin sensitivity may ultimately lead to diabetes). Analysis pointed to the impaired insulin sensitivity mediating the relationship between task-related activation in that region and BMI.

This suggests that it is insulin sensitivity that is responsible for the higher risk of cognitive impairment later in life. The good news is that insulin sensitivity is able to be modified through exercise and diet.

A follow-up study to determine if a 12-week exercise intervention can reverse the differences is planned.

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Physical fitness improves memory in children

October, 2010

More evidence for the benefits of physical exercise for cognition, this time involving 9-10 year old children.

Brain imaging of 49 children aged 9-10 has found that those who were physically fit had a hippocampus significantly bigger (around 12%) than those who were not fit. Animal studies and those with older adults have shown that aerobic exercise increases the growth of new brain cells in the hippocampus. Physical fitness was measured by how efficiently the children used oxygen while running on a treadmill. Fitter children also did better on tests of relational (but not item) memory, and this association was directly mediated by hippocampal volume.

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Adolescents with type 2 diabetes have diminished cognitive performance and brain abnormalities

September, 2010

Another study adds to growing evidence that diabetes, or poor glycaemic control, has serious implications for brain function.

A small study comparing 18 obese adolescents with type 2 diabetes and equally obese adolescents without diabetes or pre-diabetes has found that those with diabetes had significantly impaired cognitive performance, as well as clear abnormalities in the integrity of their white matter (specifically, reduced white matter volume, especially in the frontal lobe, as well as impaired integrity in both white and grey matter). Similar abnormalities have previously been found in adults with type 2 diabetes, but the subjects were elderly and, after many years of diabetes, generally had significant vascular disease. One study involving middle-aged diabetics found a reduction in the volume of the hippocampus, which was directly associated with poor glycaemic control.

It remains to be seen whether such changes can be reversed by exercise and diet interventions. While those with diabetes performed worse in all cognitive tasks tested, the differences were only significant for intellectual functioning, verbal memory and psychomotor efficiency.

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