Summary
Genetic variations can affect how nutrients are metabolized, while nutrient deficiencies can have an effect on genetic variation. This article discusses the future challenges and present ethical considerations in the use of personalized nutrition based on genetic polymorphisms that increase an individual's risk for developing, or susceptibility to, marginal nutritional deficiency.
- Deficiency Disorders
- Nutrigenomics
- Deficiency Disorders
- Nutrigenomics
- Nutrition
Genetic variations can affect how nutrients are metabolized, while nutrient deficiencies can have an effect on genetic variation. Carl L. Keen, PhD, University of California, Davis, Davis, California, USA, discussed the future challenges and present ethical considerations in the use of personalized nutrition based on genetic polymorphisms that increase an individual's risk for developing, or susceptibility to, marginal nutritional deficiency.
Over time the benefits expected from a healthy diet have evolved from prevention of illness due to deficiencies in essential nutrients (eg, rickets, scurvy), to the reduction in the onset/progression of select cancers and age-related diseases, to concepts such as the Barker Hypothesis, which proposes an association between maternal diet generational health, and most recently to the belief that healthy diets promote “optimal health”. Although the exact definition of optimal health remains elusive, it has been variously characterized as a sense of well-being, achievement of one's genetic potential, the absence of disease, and the ability to retain excellent visual acuity, reaction time, and fine motor control well into old age. The success of nutritional genomics will be defined by the targets that are set.
Single-nucleotide polymorphisms (SNP) can determine how nutrients are processed in the body and may be useful in determining which foods to consume and in what quantities. The enzyme 5, 10-methylenetetrahydrofolate reductase (MTHFR) is involved in folate metabolism. Polymorphisms of the MTHFR gene are associated with higher rates of neural tube defects [Kirke PN et al. BMJ 2004], which can result in a higher risk of infants born with spina bifida in women who have these genetic defects [De Wals P et al. N Engl J Med 2007]. Food fortification with folic acid has been shown to significantly reduce the rate of neural-tube defects in newborns.
Other nutrient-gene interactions that reduce manganese and copper have been identified that lead to ataxia prolonged bleeding, lysosomal dysfunction, cardiomyopathy, and lung failure in mice and sheep, scoliosis in chickens [Voglis S et al. Am J Respir Crit Care Med 2009; Yoshida M et al. Lab Invest 2009; Huang L et al. Nat Genet 1999; Opsahl W et al. Science 1984], and conditions such as Menkes disease, occipital horn syndrome, and Wilson's disease, in humans [Kodama H et al. Brain Dev 2011].
Low levels of vitamin C are linked to increased risk of heart disease, type 2 diabetes, and cancer. The utilization of vitamin C can be affected by variations in the glutathione S-transferases (GSTs) T1 gene that protects against serum ascorbic acid deficiency. Individuals with the GSTT1 deletion gene variant have an increased risk of ascorbic acid deficiency if they do not meet the Recommended Dietary Allowance for vitamin C (Figure 1) [Cahill LE et al. Am J Clin Nutr 2009].
GSTT1 Genotype, Vitamin C Adequacy and Ascorbic Acid Deficiency
*Relative risk of deficiency for those with the “deletion” variant who do not meet the RDA for vitamin C compared with those who do meet the RDA.
Del=deletion; INS=insertion; RDA=recommended daily allowance.
Reproduced from Cahill LE et al. Intake of carbohydrates compared with intake of saturated fatty acids and risk of myocardial infarction: importance of the glycemic index. Am J Clin Nutr 2009;90(5)1411–1417. With permission from the American Society for Nutrition.
It is generally accepted that sodium intake is associated with hypertension; however, the impact is not the same for everyone. Blood pressure response to high salt intake is greater in individuals with ACE I/D and 11βHSD2 G534A polymorphisms (Figure 2) [Poch E et al. Hypertension 2001].
Salt-Sensitive Hypertension by ACE Genotype
*Relative risk of salt-sensitive hypertension with the GA or AA genotype compared with the GG genotype.
Reproduced from Poch & et al. Hypertension 2001. With permission from the American Society for Nutrition.
The Costa Rica Heart Study [Cornelis MC et al. JAMA 2006] looked at the association between coffee intake and the risk of myocardial infarction (MI), and whether the polymorphic cytochrome P450 1A2 (CYP1A2) enzyme modifies this association. Caffeine intake was associated with an increased risk of nonfatal MI, but only in individuals with AC or CC CYP1A2 genotype (slow caffeine metabolizers; Figure 3).
Coffee Intake, MI, and CYP1A2 Genotype
*p<0.05.
Reproduced with permission from Cornelius MC et al. JAMA 2006. With permission from the American Society for Nutrition.
Adding to the complexity of gene-nutrient interactions is the human microbiome, which contains 100 times as many genes as the human genome. The microbiome produces vitamins, maintains intestinal structure, protects from pathogens, helps maintain immune function, and affects host metabolism and secretion of hormones from the gut. It is significantly impacted by mode of infant feeding (formula vs breast feeding), host genotype, diet, and gut biotics.
Major issues for the future will be the identification of more genetic polymorphisms that increase an individual's risk for developing, or susceptibility to, marginal nutritional deficiency, as well as toxicity, states. Once this information is obtained, attention will need to be paid to the determination of the epigenetic, or persistent, consequences associated with mild micronutrient deficiencies during early development and how these persistent effects contribute to the risk of age-related chronic diseases.
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