More than 16 million people in the United States are affected by brain disorders annually. These disorders include stroke, Alzheimer’s disease, traumatic brain injury, epilepsy, Parkinson’s disease, and multiple sclerosis. The global economic burden of brain disorders, including cost of treatment and lost productivity of patients and caregivers, is expected to exceed $6 trillion by 2030 (National Alliance on Mental Illness of Greater Chicago, 2013). Recent economic data indicate the U.S. spends more than $150 billion on direct costs and another $43 billion on indirect costs associated with mental illness.
While there is considerable interest in the elderly brain, let us not forget the developing dynamics of the young brain during gestation and in the first years after birth. Many dietary, genetic, gender, and environmental factors, and perhaps postnatal gut microbial profile, can cause brain development disorders among infants, children, and adolescents.
A recent statement from the American Academy of Pediatrics noted the importance of iodine in brain development, yet many pregnant women present margin iodine deficiency. Evidence from studies among sheep and rodents indicate gestational iodine deficiency leads to significant structural changes, such as reduced nerve tissue formation and growth, relative to normal brain development (de Escobar et al., 2007). It is well established that insufficiencies of nutrients such as folic acid, copper, and vitamin A within 22 days post-conception and during at least the first seven weeks of pregnancy can alter normal formation of the neural tube, which subsequently differentiates into brain and spinal cord (Couperus and Nelson, 2008). Other nutrients, such as iron, zinc, choline, protein, and long-chain polyunsaturated fatty acids, as well as sufficient caloric intake, are also critical in brain development (Georgieff and Rao, 2001).
When nutrient deficiencies or inadequacies occur during critical periods of neurodevelopment, such as cell development, differentiation, and maturation, significant developmental consequences that present throughout gestation and at least one year postnatal may result. For example, the omega-3 fatty acid DHA is critical for myelination (Georgieff, 2007). At some threshold of inadequate myelination, impairment of the central nervous system is likely. Then the question becomes whether there is a potential period of recovery (Kolb and Gibb, 2011).
It is noteworthy that the Y chromosome has a significant impact on gestational testosterone production, especially during weeks 8 and 24. Testosterone exposure influences male-typical behavior development and differences in brain structures during critical periods of neurodevelopment (McCarthy et al., 2009). The XX and XY chromosomal differences may influence an array of cellular signaling mechanisms, which affect cell function and regional differences in size that contribute to gender bias relative to neurologic disorders such as male-dominant autism, attention deficit disorder, and early onset of schizophrenia, whereas conditions such as depression and anxiety typically affect more females (McCarthy, 2010).
Our understanding of genetic influences on brain structure and function has escalated with contemporary imaging technologies (Toga and Thompson, 2005). However, differences in regional activation and cognitive functions remain unclear. Brain mapping techniques that examine cortical patterns and gray matter maturation over the cortical surface indicate heritable aspects of brain structure and function as well as aspects associated with genetic risk for Alzheimer’s disease. For example, about 38% of Alzheimer’s patients present the apolipoprotein E4 allele (ApoE4) whereas only 15% of the normal population is positive for this allele (Roses, 1996). It appears that healthy ApoE4 individuals may present alterations in specific brain structures that may be observed before overt symptoms of the neurological deficits of Alzheimer’s disease are detected. On the other hand, there are some frontal regions that are protected in the ApoE4 positive patient. These observations have stimulated considerable research into these patterns among those at genetic risk of Alzheimer’s disease and subsequent drug development or nutrition intervention to modulate these patterns in efforts to reduce the risk of disease manifestations, including early dementia (Small et al., 2000).
An overview of age-related neurodegenerative diseases indicates several common structural and biochemical alterations, including the deposition of an array of aggregated, filamentous proteins, such as amyloid-β, tau, and α-synuclein. Some therapeutic interventions target inhibiting synthesis of these proteins and increasing their breakdown as well as other steps involved in the misfolding and fibrillization of these proteins (Skovronsky et al., 2006).
While many medical and nutrition interventions can be effective in improving brain health and reducing the risk of neurodegenerative disease development, additional research is paramount in order to reduce the economic burden of these diseases and to improve the quality of brain development and function at all stages of life.
Roger Clemens, Dr.P.H., CFS,
Contributing Editor
Chief Scientific Officer,
Horn Company, La Mirada, Calif.
[email protected]