Protection of the human epigenome through nutritional epigenetics intervention programs

By | July 22, 2024

Dr. Renee J. Dufault, Executive Director of the Food Ingredients and Health Research Institute, explains the importance of nutritional epigenetics in understanding the impact of nutrients and dietary chemicals on patterns of gene expression, as well as their role in the development of conditions such as autism and ADHD.

Rates of autism, attention deficit/hyperactivity disorder, and type 2 diabetes are increasing worldwide and may be explained by changes in the human epigenome. Nutrients and dietary chemicals can alter or modify the expression of genes and affect behavioral patterns across generations. (one) Nutritional epigenetics is a field of research in which scientists study the effects of nutrients and dietary chemicals on gene expression. (2), (3) Heritable and reversible patterns of gene expression result from changes in DNA chromatin structure that occur mostly through methylation mechanisms. (2) Genes can be methylated (silenced) or demethylated (turned on) at specific locations in the human genome, including all genes. Inherited DNA methylation patterns can be reversed depending on prenatal dietary exposure to nutrients and dietary chemicals. (3), (4)

Exposure to dietary chemicals

Dietary chemical exposures can vary depending on food production and farming practices. Dietary chemicals enter the food supply directly as food ingredients and permitted residues or indirectly as contaminants. Food quality depends on food ingredient and pesticide safety regulations, which vary by country and, in some cases, by geographic region. For example, in the United States, the Food and Drug Administration regulates petroleum-based food colorants by certifying each batch to ensure that heavy metal impurities do not exceed permitted levels. (5), (6) For example, batches of yellow #5 (E-102) and yellow #6 (E-110) may each contain up to 10 ppm of lead (Pb), up to 3 ppm of arsenic (As), and up to 1 ppm of mercury (Hg). (6) In the European Union and the United Kingdom, any product containing these two petroleum-based food colouring ingredients must carry the warning: ‘May have adverse effects on activity and attention in children’. (7)

Dietary chemical exposure from consumption of ultra-processed foods influences gene behavior Yellow #5, Yellow #6, and high fructose corn syrup are examples of ingredients in ultra-processed food products that can lead to harmful zinc losses in the body and may contain traces of certain heavy metals. (6), (8), (9), (10) Consumption of any dietary chemical or component known to cause zinc loss or deficiency may affect metallothionein (MT) gene behavior and lead to accumulation of heavy metals in the blood and other tissues. (10), (11), (12) The MT gene provides instructions for making metallothionein proteins, which consist of zinc and copper atoms partially linked to cysteine ​​molecules. (13) MTs function as metal carrier proteins in the body and play an important role in the detoxification and excretion of heavy metals. (13)

Children with autism and ADHD often have zinc deficiency and therefore have difficulty excreting heavy metals from the body due to the defect in the MT gene. (10), (12), (13) As a result, these individuals have a tendency to accumulate Cd, Pb and/or Hg, and the severity of their symptoms is directly related to the levels of heavy metals in their blood. (14), (15), (16)

Epigenome changes induced by concurrent exposure to dietary chemicals

Dietary and concurrent exposure to other chemicals from consumption of ultra-processed foods can affect child development and gene methylation patterns across generations. In a recent study, researchers found that concurrent prenatal exposure to organophosphate (OP) pesticide and Pb residues, combined with an unhealthy ultra-processed food diet, resulted in a significantly increased risk of ADHD in human offspring. (17) In another recent study, researchers found that a family history of unhealthy diets affects DNA methylation patterns in tissues, leading to insulin resistance in offspring and predisposing them to type 2 diabetes. (18) An unhealthy maternal diet consisting of ultra-processed foods results in poor prenatal nutrition and leads to changes in the human epigenome. (18), (19) Therefore, preventing unhealthy diets before and after pregnancy may reduce the prevalence of autism and ADHD in children. Nutritional epigenetics education intervention programs can now be used to protect the human epigenome from further damage and promote recovery.

Nutritional epigenetics educational interventions

Dr. Dufault and his collaborators at the nonprofit Food Ingredients and Health Research Institute were the first in the world to develop nutritional epigenetics models to explain autism and ADHD. (1), (10), (16) They created a curriculum for differentiated nutritional epigenetics education that was successfully used during a clinical trial to significantly reduce parents’ intake of overly processed foods. (20) Parents participating in the clinical trial also significantly increased their consumption of unprocessed, whole foods. (20) When parents understand gene expression behavioral patterns in terms of nutritional epigenetics, they are better equipped to prevent developmental disorders in their children.

References

  1. Dufault, RJ et al. Higher rates of autism and attention-deficit/hyperactivity disorder in American children: Do food quality issues influence epigenetic inheritance? World J Clin Pediatr. 12(2), 25-37 (2023).
  2. Choi, SW., Frisco, S. Epigenetics: a new bridge between nutrition and health. Adv Nutr. 1(1), 8-16 (2010).
  3. Farhud, DD, Yeganeh, MZ, Yeganeh, MZ Nutrigenomics and nutrigenetics. Iran J Public Health. 39(4), 1-14 (2010).
  4. Kaati, G., Bygren, LO, Pembrey, M., Sjostrom, M. Intergenerational response to nutrition, early life conditions and longevity. European Journal of Human Genetics. 15, 784-790 (2007).
  5. United States Food and Drug Administration. Color Additives in Foods. (2023, July 6). Available at URL https://www.fda.gov/food/color-additives-information-consumers/color-additives-foods
  6. United States Code of Federal Regulations. Part 74: List of color additives subject to certification, Subpart A – Foods. (2024, April 25). Available at URL https://www.ecfr.gov/current/title-21/chapter-I/subchapter-A/part-74
  7. United Kingdom. Food Standards Agency. Food additives. (2024, 12 April)
  8. Harder, NHO et al. Effects of dietary glucose and fructose on copper, iron, and zinc metabolism parameters in humans. Nutrients. 12(9), 2581 (2020).
  9. Ward, NI et al. Effect of the chemical additive tartrazine on the zinc status of hyperactive children–a double-blind placebo-controlled study. J Nutr Med. 1, 51-57 (1990).
  10. Dufault, R. et al. Mercury exposure, nutritional deficiencies, and metabolic disorders may affect learning in children. Behavior Brain Function. 5, 44 (2009).
  11. Bakthavachalu, P. et al. Food coloring and autism: a meta-analysis. Adv Neurobiol. 24, 481-504 (2020).
  12. de Oliveira, Z. et al. Synthetic colors in foods: a warning for children’s health. Int J. Environ. Res. Public Health. 21, 682 (2024).
  13. Coyle, P., Philcox, JC, Carey, LC, Rofe, AM Metallothionein: the multipurpose protein. Cell Mol Life Sci. 59, 627-647 (2002).
  14. Awadh et al. The role of environmental trace element toxicants in autism: a medical biochemistry perspective. Ecotoxicol Environ Saf. 251, 114561 (2023).
  15. Baj, J. et al. Autism spectrum disorder: trace element imbalances and the pathogenesis and severity of autistic symptoms. Neurosci Biobehav Rev.129, 117-132 (2021).
  16. Dufault, RJ. et al. Linking blood inorganic mercury and lead measurements to dietary exposures that may affect child development. World J Methodol. 11(4), 144-159 (2021).
  17. Maitre, L. et al. Early life environmental exposure determinants of child behavior in Europe: a longitudinal, population-based study. Environ Int. 153:10652d3 (2021).
  18. Nilsson, E., Ling, C. DNA methylation links genetics, fetal environment, and an unhealthy lifestyle to the development of type 2 diabetes. Clinical Epigenetics. 9, 105 (2017).
  19. Rijlaarsdam, J. et al. Prenatal unhealthy diet, insulin-like growth factor 2 gene (IGF2) methylation, and attention deficit hyperactivity disorder symptoms in youth with early-onset conduct problems. J Child Psychol Psychiatry. 58, 1, 19-27 (2017).
  20. Dufault, RJ. et al. Nutritional epigenetics education improves diet and attitudes of parents of children with autism and attention-deficit/hyperactivity disorder. World Journal of Psychiatry. 14(1):159–178 (2024).

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