Stewart Lonky, MD
Yes. In fact, evidence suggests that both parents’ diets may play a crucial role in their unborn child’s susceptibility to developing obesity later in life.1
So, having overweight parents may significantly increase one’s obesity risk, but how does this happen, exactly?
As you may know, DNA is often thought of as the “blueprint of life” because it contains all the information that determines our physical appearance and health, although some scientists have complained that the “blueprint for life” metaphor is inadequate for something as “intricate, complex, multilayered and dynamic” as DNA.2 We inherit about 23,000 genes from both our mother and father.
Currently, there’s no reliable way to alter our genes, although scientists tried gene editing inside the body of Brian Madeux, a 44-year-old California man with Hunter syndrome, an incurable metabolic disease. Madeux didn’t benefit in any measurable way from the gene editing treatment he received.3
If we can’t change our genes, what can we do?
Although we can’t yet directly alter our genes, some factors influence their expression. Our environment and experiences leave chemical “signatures” on our genes. Collectively, these signatures are called the epigenome.
The word “epigenetics” means “above” or “on top of” genetics and, simply stated, refers to external DNA modifications that turn gene expression on or off. Both positive experiences, such as exercise and a healthy diet, and negative influences, like environmental toxins exposure, can change the chemistry that encodes genes in our cells. This process, known as epigenetic modification, can be reversible but is heritable.
In one study, researchers demonstrated that differences in gene expression (epigenetics) play a crucial role in determining one’s predisposition to obesity. In genetically identical mice and human twins, epigenetic markers altered the activity of weight-control genes to produce distinct subpopulations of lean and obese individuals.4
These modifications do not change the genetic code but do alter the physical structure of DNA. Moreover, these modifications change the “behavior” or “expression” of that gene. One way our bodies turn genes on or off is with modifications called methyl groups, which attach to DNA and change how it interacts with other molecules. DNA methylation—the addition of a methyl group to part of the DNA molecule, which often prevents specific genes from being expressed—is the most common epigenetic change. Epigenetic changes in a fetus may be introduced from food that the mother consumes, but environmental toxins, such as pesticides, compounds in cigarette smoke, or even the non-stick cookware she uses to prepare meals may influence development as well.
Since epigenetic markers control genetic expression, effectively turning the gene “on” or “off”, early life experiences that change the epigenome—when the specialized cells of internal organs such as the brain, heart or kidneys are first developing—can have a powerful impact on a child’s lifetime physical and mental health.
How do parents epigenetically influence their child’s development?
A growing body of research suggests that parents epigenetically influence embryonic development. How a child responds to stress, her overall health and how she will eventually parent her own children could be influenced by epigenetic changes her parents, and even grandparents, made to her DNA. Writing in the peer-reviewed journal Science, UC Santa Cruz researchers were able to show how “epigenetic memory can be passed across generations and from cell to cell during [embryonic and fetal] development.”5,6
Not surprisingly, these changes may also influence how easy or hard it may be for a child to avoid obesity. Poor nutrition before and at the beginning of pregnancy, and possibly while a baby is nursing7, can be stored as a type of epigenetic memory on a child’s genome, setting the table for metabolic diseases, including obesity or even diabetes.8 The period following conception—the stage in development when the rate of DNA synthesis is extremely high—leaves an embryo vulnerable to epigenetic modifications.
Nutrition’s “epigenetic memory” was also observed by University of Cambridge researchers, who were able to demonstrate the epigenetic transfer of nutrition memory in mouse models.9 While further research is needed, it’s becoming clearer that our life choices and experiences may epigenetically influence the health of future generations.
In another study, researchers at the London School of Hygiene and Tropical Medicine looked at specialized regions of the genome called metastable epialleles, or MEs. These regions are critical because they’re the sites where epigenetic (methylation) markers are “laid down” during the first few days following conception. In the study, the researchers analyzed the DNA methylation patterns of Chinese human embryos conceived via in vitro fertilization throughout the stages of early development.
Specifically, they looked at the establishment and elimination of epigenetic markers and compared the findings with fully-differentiated, 6-to-10-week-old liver cells. They found atypical and variable ME methylation patterns when compared to other regions on the genome, especially in the embryonic liver cells. These findings suggest that methylation patterns may be sensitive to external environmental factors, leading to speculation that these regions could have evolved to sense the mother’s nutritional environment, record the information on DNA and help the baby adapt to its circumstances.10
In a separate experiment, the same team discovered that methylation patterns of MEs could be affected by the mother’s (and possibly the father’s) pre-conceptional nutrition habits, confirming the volatility of the methylation in these genomic regions.11
What this boils down to is that embryos may be keenly aware of their mother’s nutritional environment and adjust accordingly to survive.
These findings also underscore the importance of a healthy maternal environment in the early stages of embryonic development and reinforce the fact that epigenetic modifications stemming from diet and the environment can be passed down to future generations, potentially jeopardizing a child’s health.
So, is there an ideal diet to reduce a child’s obesity risk?
Though I’ve never been a fan of one-size-fits-all diets, there’s good evidence that the Mediterranean Diet, which emphasizes plant-based foods, including vegetables, legumes, fruits, cereals and nuts has some health advantages. Importantly, the diet draws amply on healthy, monounsaturated fat from virgin olive oil. Red meat is eaten in low amounts—
if at all—while wine and fish are consumed moderately. The diet has long been associated with a reduced risk of cardiovascular disease12,13, cancer14, Alzheimer’s disease15, obesity and metabolic syndrome12,13, and might confer some epigenetic benefits on expectant parents. Some research suggests that the Mediterranean Diet might epigenetically protect the fetus from developing diseases later in life by adjusting histone modifications (histones are a family of proteins that associate with DNA in the nucleus and help condense it).16
What is the takeaway message?
For anyone newly pregnant or considering pregnancy, it’s critical that both parents maintain a healthy diet and avoid, as much as possible, exposure to toxic chemicals. Indeed, the fact that certain epigenetic markers are sensitive to and affected by nutrient input at conception focuses attention on how vital it is for both parents to eat a healthy and well-balanced diet before conception and during pregnancy.
The takeaway here is to better understand the epigenetic influences on weight gain and how patterns are established early on. With further research, we can expect to come to a heightened and enlightened understanding of epigenetic nutritional memory so we may better understand how early life experiences set the stage for positive or negative health outcomes throughout our lives.
About the Author: Stewart Lonky, M.D., is a physician, toxicologist, and biomedical engineer. He is board certified in internal medicine, pulmonology and critical care medicine, and a recognized expert in the related fields of preventive medicine and environmental toxicology and its associated diseases. Dr. Lonky is known for his cutting edge research into the causes, treatment and prevention of toxic chemical exposures and heralded for his in-depth knowledge of obesity’s biological, environmental, and social influences, which is the subject of his forthcoming book. Dr. Lonky resides and practices in Los Angeles, California. www.stewartlonky.com
- Huypens P, Sass S, Wu M, et al. Epigenetic germline inheritance of diet-induced obesity and insulin resistance. Nature genetics. 2016;48(5):497-499.
- Ainsworth C. DNA is life’s blueprint? No, there’s far more to it than that. 2015; https://www.newscientist.com/article/mg22630251-000-dna-is-lifes-blueprint-no-theres-far-more-to-it-than-that/, 2019.
- Kaiser J. New gene-editing treatment might help treat a rare disorder, hints first human test. 2018; https://www.sciencemag.org/news/2018/09/new-gene-editing-treatment-might-help-treat-rare-disorder-hints-first-human-test, 2019.
- Dalgaard K, Landgraf K, Heyne S, et al. Trim28 Haploinsufficiency Triggers Bi-stable Epigenetic Obesity. Cell. 2016;164(3):353-364.
- Stephens T. Study shows how epigenetic memory is passed across generations. 2014; https://news.ucsc.edu/2014/09/epigenetics.html, 2019.
- Gaydos LJ, Wang W, Strome S. Gene repression. H3K27me and PRC2 transmit a memory of repression across generations and during development. Science (New York, NY). 2014;345(6203):1515-1518.
- Verduci E, Banderali G, Barberi S, et al. Epigenetic effects of human breast milk. Nutrients. 2014;6(4):1711-1724.
- Lee HS. Impact of Maternal Diet on the Epigenome during In Utero Life and the Developmental Programming of Diseases in Childhood and Adulthood. Nutrients. 2015;7(11):9492-9507.
- Kazachenka A, Bertozzi TM, Sjoberg-Herrera MK, et al. Identification, Characterization, and Heritability of Murine Metastable Epialleles: Implications for Non-genetic Inheritance. Cell. 2018;175(5):1259-1271.e1213.
- Kessler NJ, Waterland RA, Prentice AM, Silver MJ. Establishment of environmentally sensitive DNA methylation states in the very early human embryo. Science advances. 2018;4(7):eaat2624.
- Dominguez-Salas P, Moore SE, Baker MS, et al. Maternal nutrition at conception modulates DNA methylation of human metastable epialleles. Nature communications. 2014;5:3746.
- Kastorini CM, Panagiotakos DB, Chrysohoou C, et al. Metabolic syndrome, adherence to the Mediterranean diet and 10-year cardiovascular disease incidence: The ATTICA study. Atherosclerosis. 2016;246:87-93.
- Godos J, Zappala G, Bernardini S, Giambini I, Bes-Rastrollo M, Martinez-Gonzalez M. Adherence to the Mediterranean diet is inversely associated with metabolic syndrome occurrence: a meta-analysis of observational studies. International journal of food sciences and nutrition. 2017;68(2):138-148.
- Schwingshackl L, Schwedhelm C, Galbete C, Hoffmann G. Adherence to Mediterranean Diet and Risk of Cancer: An Updated Systematic Review and Meta-Analysis. Nutrients. 2017;9(10).
- ingh B, Parsaik AK, Mielke MM, et al. Association of mediterranean diet with mild cognitive impairment and Alzheimer’s disease: a systematic review and meta-analysis. Journal of Alzheimer’s disease : JAD. 2014;39(2):271-282.
- Lorite Mingot D, Gesteiro E, Bastida S, Sanchez-Muniz FJ. Epigenetic effects of the pregnancy Mediterranean diet adherence on the offspring metabolic syndrome markers. Journal of physiology and biochemistry. 2017;73(4):495-510.vvv