Environmental variables and group mean cognitive differences, part I
While obviously genetic differences exist between groups, they may not fully explain cognitive differences which are observed. Using recent research, I hope to illustrate some associated ‘environmental’ causes of cognitive differences between groups.
Learning and memory are fundamental brain functions affected by dietary and environmental factors. Here, we show that increasing brain magnesium using a newly developed magnesium compound (magnesium-L-threonate, MgT) leads to the enhancement of learning abilities, working memory, and short- and long-term memory in rats. The pattern completion ability was also improved in aged rats. MgT-treated rats had higher density of synaptophysin-/synaptobrevin-positive puncta in DG and CA1 subregions of hippocampus that were correlated with memory improvement. Functionally, magnesium increased the number of functional presynaptic release sites, while it reduced their release probability. The resultant synaptic reconfiguration enabled selective enhancement of synaptic transmission for burst inputs. Coupled with concurrent upregulation of NR2B-containing NMDA receptors and its downstream signaling, synaptic plasticity induced by correlated inputs was enhanced. Our findings suggest that an increase in brain magnesium enhances both short-term synaptic facilitation and long-term potentiation and improves learning and memory functions.
[Slutsky I, Abumaria N, Wu LJ, et al. Enhancement of learning and memory by elevating brain magnesium. Neuron. 2010; 65(2):165-77.]
I eagerly await easily available MgT supplements. Currently, the “Magnesium” you see in stores is actually Magnesium Oxide or some other crap that has difficulty crossing the blood-brain barrier.
How much Magnesium do different groups consume in their diet?
Despite the role of magnesium in maintaining health, much of the U.S. population has historically not consumed adequate amounts of magnesium. Furthermore, significant racial or ethnic disparities in magnesium intake exist. Our objective was to provide more recent data about magnesium intake in the U.S. population. We analyzed the 24-h dietary recall data from 4257 participants aged >or=20 y from the National Health and Nutrition Examination Survey 1999-2000. The median intake of magnesium was 326 mg/d (mean 352 mg/d) among Caucasian men, 237 mg/d (mean 278 mg/d) among African American men, 297 mg/d (330 mg/d) among Mexican American men, 237 mg/d (mean 256 mg/d) among Caucasian women, 177 mg/d (mean 202 mg/d) among African American women, and 221 mg/d (mean 242 mg/d) among Mexican American women. Among men and women, Caucasians had significantly higher mean intakes of dietary magnesium than African Americans but not Mexican Americans. Magnesium intake decreased with increasing age (P for linear trend = 0.035 for Caucasians; P for linear trend <0.001 for African Americans and Mexican Americans). Men had higher intakes of magnesium than women for each of the three race or ethnic groups (P < 0.001 in each group). Caucasian men, African American men and Caucasian women who used vitamin, mineral or dietary supplements consumed significantly more magnesium in their diets than did those who did not. Substantial numbers of U.S. adults fail to consume adequate magnesium in their diets. Furthermore, racial or ethnic differences in magnesium persist and may contribute to some health disparities.
[Ford ES, Mokdad AH. Dietary magnesium intake in a national sample of US adults. J Nutr. 2003; 133(9):2879-82.]
Environmental contaminates like Lead have been shown to be associated with poor cognitive performance. Do disparities in blood lead levels exist between races?
The geometric mean blood lead level declined 41% from 2.76 microg/dL (0.13 micromol/L) in 1988-1994 to 1.64 microg/dL (0.08 micromol/L) in 1999-2002. The percentage of adults with blood lead levels of 10 microg/dL (0.48 micromol/L) or higher declined from 3.3% in 1988-1994 to 0.7% in 1999-2002 (P<.001). In 1999-2002, the multivariable-adjusted odds ratio of having a blood lead level of 10 microg/dL (0.48 micromol/L) or higher was 2.91 (95% confidence interval [CI], 1.74-4.84) and 3.26 (1.83-5.81) for non-Hispanic blacks and Mexican Americans, respectively, compared with non-Hispanic whites. After multivariable adjustment, persons in the highest quartile (>or=2.47 microg/dL [>or=0.12 micromol/L]) compared with those in the lowest quartile (<1.06 microg/dL [<0.05 micromol/L]) of blood lead levels were 2.72 (95% CI, 1.47-5.04) and 1.92 (95% CI, 1.02-3.61) times more likely to have chronic kidney disease and peripheral arterial disease, respectively. In addition, higher blood lead levels were associated with a higher multivariable-adjusted odds ratio of hypertension among non-Hispanic blacks and Mexican Americans.
[Muntner P, Menke A, DeSalvo KB, et al. Continued decline in blood lead levels among adults in the United States: the National Health and Nutrition Examination Surveys. Arch Intern Med. 2005;165(18):2155-61]
What about pregnant women and blood lead levels?
Our results show that calories are positively related to lead level. Insofar as diet serves as amajor vehicle for the ingestion of lead in the United States, our finding is consistent withcalories’ being an indicator of dietary quantity. This finding also agrees with several otherstudies with multivariable analyses that take other nutrients into account (Hammad et al.1996; Lucas et al. 1996) although it does not agree with all (Mahaffey et al. 1986; Mootyet al. 1975).
[Lawrence M Schell, Melinda Denham, Alice D Stark, et al. Blood lead concentration, diet during pregnancy, and anthropometry predict neonatal blood lead in a socioeconomically disadvantaged population. Environ Health Perspect. 2003; 111(2): 195–200.]
How does fetal nutrition further affect offspring?
It is increasingly accepted that alterations of the intrauterine and early postnatal nutritional, metabolic, and hormonal environment may cause predispositions for the development of diseases in later life. Studies in the offspring of diabetic mothers have decisively contributed to this perception. Alterations of the fetal and neonatal environment which offspring of diabetic mothers ‘experience’ seem to program a disposition to develop obesity, diabetes mellitus and Syndrome X-like alterations throughout later life. Underweight at birth is also suggested to lead to an increased risk of Syndrome X in later life (‘Barker hypothesis’). Pathophysiological mechanisms are unclear. Hormones are important environment-dependent organizers of the developing neuro–endocrine–immune network, which finally regulates all fundamental processes of life. When present in non-physiological concentrations during ‘critical periods’ of perinatal life, induced by alterations in the intrauterine or neonatal environment, hormones can act as ‘endogenous functional teratogens’. Perinatal hyperinsulinism is pathognomonic in the offspring of diabetic mothers. Early hyperinsulinism also occurs as a result of early postnatal overfeeding. In rats, endogenous hyperinsulinism, as well as peripheral or only intrahypothalamic insulin treatment during perinatal development, may lead to ‘malprogramming’ of neuroendocrine systems regulating body weight, food intake and metabolism. This results in an increased disposition to become obese and to develop diabetes throughout life. In conclusion, a complex malprogramming of the central regulation of body weight and metabolism may provide a general etiopathogenetic concept, explaining perinatally acquired dispositions, thereby opening a wide field of primary prevention.
[Plagemann A. Perinatal programming and functional teratogenesis: Impact on body weight regulation and obesity. Physiol Behav. 2005;86(5):661-8.]
So-called “metabolic programming” may explain the high rate of obesity and coronary heart disease amongst blacks and Hispanics.
In addition to perinatal diet, maternal stress also plays a role in the state-of-mind of her offspring:
….However, considering that these newborns are brought up by mothers that are themselves stressed, it is more appropriate to define the stress as perinatal rather than simply prenatal, and to take into account postnatal maternal factors as well. It has been suggested that maternal glucocorticoids, one of the most important actors of the HPA axis, underlie the correlation between low birthweight and stress-related cardiovascular, metabolic and neuroendocrine disorders such as hypertension, type 2 diabetes, ischemic heart disease and different types of cognitive and behavioral disorders in adulthood
[Darnaudéry M, Maccari S. Epigenetic programming of the stress response in male and female rats by prenatal restraint stress. Brain Res Rev. 2008;57(2):571-85.]
So, looks like that whole pregnancy thing is kind of important. At least ethnic minorities in the United States take advantage of prenatal care – right?
In 2005, 78% of Hispanic pregnant women and 76% of black non-Hispanic (NH) women, compared with 89% of white NH women in the United States, began PNC in the first trimester
[Kuo TM, Gavin NI, Adams EK, et al. Racial disparities in Medicaid enrollment and prenatal care initiation among pregnant teens in Florida: comparisons between 1995 and 2001. Med Care. 2008;46(10):1079-85.]
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