Back in 2008, I reported on a small study that found that daily doses of Pycnogenol® for three months improved working memory in older adults, and noted research indicating that the extract from the bark of the French maritime pine tree had reduced symptoms in children with ADHD. Now another study, involving 53 Italian university students, has found that cognitive performance improved in those taking 100 mg of Pycnogenol every day for eight weeks.

Students taking the supplement had higher scores on university exams than the control group, and they were apparently happier, less anxious, and more alert. It seems plausible that the improvement in academic performance results from working memory benefits.

The plant extract is an antioxidant, and benefits may have something to do with improved vascular function and blood flow in the brain.

However, the control group was apparently not given a placebo (I’m relying on the abstract and press release here, as this journal is not one to which I have access), they were simply “a group of equivalent students”. I cannot fathom why a double-blind, placebo procedure wasn’t followed, and it greatly lessens the conclusions of this study. Indeed, I wouldn’t ordinarily report on it, except that I have previously reported on this dietary supplement, and I am in hopes that a better study will come along. In the meantime, this is another small step, to which I wouldn’t give undue weight.

The study involved 104 healthy older adults (average age 87) participating in the Oregon Brain Aging Study. Analysis of the nutrient biomarkers in their blood revealed that those with diets high in omega 3 fatty acids and in vitamins C, D, E and the B vitamins had higher scores on cognitive tests than people with diets low in those nutrients, while those with diets high in trans fats were more likely to score more poorly on cognitive tests.

These were dose-dependent, with each standard deviation increase in the vitamin BCDE score ssociated with a 0.28 SD increase in global cognitive score, and each SD increase in the trans fat score associated with a 0.30 SD decrease in global cognitive score.

Trans fats are primarily found in packaged, fast, fried and frozen food, baked goods and margarine spreads.

Brain scans of 42 of the participants found that those with diets high in vitamins BCDE and omega 3 fatty acids were also less likely to have the brain shrinkage associated with Alzheimer's, while those with high trans fats were more likely to show such brain atrophy.

Those with higher omega-3 scores also had fewer white matter hyperintensities. However, this association became weaker once depression and hypertension were taken into account.

Overall, the participants had good nutritional status, but 7% were deficient in vitamin B12 (I’m surprised it’s so low, but bear in mind that these are already a select group, being healthy at such an advanced age) and 25% were deficient in vitamin D.

The nutrient biomarkers accounted for 17% of the variation in cognitive performance, while age, education, APOE genotype (presence or absence of the ‘Alzheimer’s gene’), depression and high blood pressure together accounted for 46%. Diet was more important for brain atrophy: here, the nutrient biomarkers accounted for 37% of the variation, while the other factors accounted for 40% (meaning that diet was nearly as important as all these other factors combined!).

The findings add to the growing evidence that diet has a significant role in determining whether or not, and when, you develop Alzheimer’s disease.

The study involved 1,292 children followed from birth, whose cortisol levels were assessed at 7, 15, and 24 months. Three tests related to executive functions were given at age 3. Measures of parenting quality (maternal sensitivity, detachment, intrusiveness, positive regard, negative regard, and animation, during interaction with the child) and household environment (household crowding, safety and noise levels) were assessed during the home visits.

Earlier studies have indicated that a poor environment in and of itself is stressful to children, and is associated with increased cortisol levels. Interestingly, in one Mexican study, preschool children in poor homes participating in a conditional cash transfer scheme showed reduced cortisol levels.

This study found that children in lower-income homes received less positive parenting and had higher levels of cortisol in their first two years than children in slightly better-off homes. Higher levels of cortisol were associated with lower levels of executive function abilities, and to a lesser extent IQ, at 3 years.

African American children were more affected than White children on every measure. Cortisol levels were significantly higher; executive function and IQ significantly lower; ratings of positive parenting significantly lower and ratings of negative parenting significantly higher. Maternal education was significantly lower, poverty greater, homes more crowded and less safe.

The model derived from this data shows executive function negatively predicted by cortisol, while the effect on IQ is marginal. However, both executive function and IQ are predicted by negative parenting, positive parenting, and household risk (although this last variable has a greater effect on IQ than executive function). Neither executive function nor IQ was directly predicted by maternal education, ethnicity, or poverty level. Cortisol level was inversely related to positive parenting, but was not directly related to negative parenting or household risk.

Indirectly (according to this best-fit model), poverty was related to executive function through negative parenting; maternal education was related to executive function through negative parenting and to a lesser extent positive parenting; both poverty and maternal education were related to IQ through positive parenting, negative parenting, and household risk; African American ethnicity was related to executive function through negative parenting and positive parenting, and to IQ through negative parenting, positive parenting, and household risk. Cortisol levels were higher in African American children and this was unrelated to poverty level or maternal education.

Executive function (which includes working memory, inhibitory control, and attention shifting) is vital for self-regulation and central to early academic achievement. A link between cortisol level and executive function has previously been shown in preschool children, as well as adults. The association partly reflects the fact that stress hormone levels affect synaptic plasticity in the prefrontal cortex, where executive functions are carried out. This is not to say that this is the only brain region so affected, but it is an especially sensitive one. Chronic levels of stress alter the stress response systems in ways that impair flexible regulation.

What is important about this study is this association between stress level and cognitive ability at an early age, that the effect of parenting on cortisol is associated with positive aspects rather than negative ones, and that the association between poverty and cognitive ability is mediated by both cortisol and parenting behavior — both positive and negative aspects.

A final word should be made on the subject of the higher cortisol levels in African Americans. Because of the lack of high-income African Americans in the sample (a reflection of the participating communities), it wasn’t possible to directly test whether the effect is accounted for by poverty. So this remains a possibility. It is also possible that there is some genetic difference. But it also might reflect other sources of stress, such as that relating to prejudice and stereotype threat.

Based on mother’s ethnic status, 58% of the families were Caucasian and 42% African American. Two-thirds of the participants had an income-to-need ratio (estimated total household income divided by the 2005 federal poverty threshold adjusted for number of household members) less than 200% of poverty. Just over half of the mothers weren’t married, and most of them (89%) had never been married. The home visits at 7, 15, and 24 months lasted at least an hour, and include a videotaped free play or puzzle completion interaction between mother and child. Cortisol samples were taken prior to an emotion challenge task, and 20 minutes and 40 minutes after peak emotional arousal.

Long-term genetic effects of childhood environment

The long-term effects of getting off to a poor start are deeper than you might believe. A DNA study of forty 45-year-old males in a long-running UK study has found clear differences in gene methylation between those who experienced either very high or very low standards of living as children or adults (methylation of a gene at a significant point in the DNA reduces the activity of the gene). More than twice as many methylation differences were associated with the combined effect of the wealth, housing conditions and occupation of parents (that is, early upbringing) than were associated with the current socio-economic circumstances in adulthood (1252 differences as opposed to 545).

The findings may explain why the health disadvantages known to be associated with low socio-economic position can remain for life, despite later improvement in living conditions. The methylation profiles associated with childhood family living conditions were clustered together in large stretches of DNA, which suggests that a well-defined epigenetic pattern is linked to early socio-economic environment. Adult diseases known to be associated with early life disadvantage include coronary heart disease, type 2 diabetes and respiratory disorders.

Obesity has been linked to cognitive decline, but a new study involving 300 post-menopausal women has found that higher BMI was associated with higher cognitive scores.

Of the 300 women (average age 60), 158 were classified as obese (waist circumference of at least 88cm, or BMI of over 30). Cognitive performance was assessed in three tests: The Mini-Mental Statement Examination (MMSE), a clock-drawing test, and the Boston Abbreviated Test.

Both BMI and waist circumference were positively correlated with higher scores on both the MMSE and a composite cognitive score from all three tests. It’s suggested that the estrogen produced in a woman’s fat cells help protect cognitive function.

Interestingly, a previous report from the same researchers challenged the link found between metabolic syndrome and poorer cognitive function. This study, using data from a large Argentinean Cardiovascular Prevention Program, found no association between metabolic syndrome and cognitive decline — but the prevalence of metabolic syndrome and cognitive decline was higher in males than females. However, high inflammatory levels were associated with impairment of executive functions, and higher systolic blood pressure was associated with cognitive decline.

It seems clear that any connection between BMI and cognitive decline is a complex one. For example, two years ago I reported that, among older adults, higher BMI was associated with more brain atrophy (replicated below; for more recent articles relating obesity to cognitive impairment, click on the obesity link at the end of this report). Hypertension, inflammation, and diabetes have all been associated with greater risk of impairment and dementia. It seems likely that the connection between BMI and impairment is mediated through these and other factors. If your fat stores are not associated with such health risk factors, then the fat in itself is not likely to be harmful to your brain function — and may (if you’re a women) even help.

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Overweight and obese elderly have smaller brains

Analysis of brain scans from 94 people in their 70s who were still "cognitively normal" five years after the scan has revealed that people with higher body mass indexes had smaller brains on average, with the frontal and temporal lobes particularly affected (specifically, in the frontal lobes, anterior cingulate gyrus, hippocampus, and thalamus, in obese people, and in the basal ganglia and corona radiate of the overweight). The brains of the 51 overweight people were, on average, 6% smaller than those of the normal-weight participants, and those of the 14 obese people were 8% smaller. To put it in more comprehensible, and dramatic terms: "The brains of overweight people looked eight years older than the brains of those who were lean, and 16 years older in obese people." However, overall brain volume did not differ between overweight and obese persons. As yet unpublished research by the same researchers indicates that exercise protects these same brain regions: "The most strenuous kind of exercise can save about the same amount of brain tissue that is lost in the obese."

Research into the effects of cannabis on cognition has produced inconsistent results. Much may depend on extent of usage, timing, and perhaps (this is speculation) genetic differences. But marijuana abuse is common among sufferers of schizophrenia and recent studies have shown that the psychoactive ingredient of marijuana can induce some symptoms of schizophrenia in healthy volunteers.

Now new research helps explain why marijuana is linked to schizophrenia, and why it might have detrimental effects on attention and memory.

In this rat study, a drug that mimics the psychoactive ingredient of marijuana (by activating the cannabinoid receptors) produced significant disruption in brain networks, with brain activity becoming uncoordinated and inaccurate.

In recent years it has become increasingly clear that synchronized brainwaves play a crucial role in information processing — especially that between the hippocampus and prefrontal cortex (see, for example, my reports last month on theta waves improving retrieval and the effect of running on theta and gamma rhythms). Interactions between the hippocampus and prefrontal cortex seem to be involved in working memory functions, and may provide the mechanism for bringing together memory and decision-making during goal-directed behaviors.

Consistent with this, during decision-making on a maze task, hippocampal theta waves and prefrontal gamma waves were impaired, and the theta synchronization between the two was disrupted. These effects correlated with impaired performance on the maze task.

These findings are consistent with earlier findings that drugs that activate the cannabinoid receptors disrupt the theta rhythm in the hippocampus and impair spatial working memory. This experiment extends that result to coordinated brainwaves beyond the hippocampus.

Similar neural activity is observed in schizophrenia patients, as well as in healthy carriers of a genetic risk variant.

The findings add to the evidence that working memory processes involve coordination between the prefrontal cortex and the hippocampus through theta rhythm synchronization. The findings are consistent with the idea that items are encoded and indexed along the phase of the theta wave into episodic representations and transferred from the hippocampus to the neocortex as a theta phase code. By disrupting that code, cannabis makes it more difficult to retain and index the information relevant to the task at hand.