Reference Number: 675
Year: 2023
Link: Link to original paper
Summary
Abstract:
The relationship between nutrition and genes has long been hinted at and sometimes plainly associated with certain diseases. Now, after many years of research and coincidental findings, it is believed that this relationship, termed “Nutrigenomics,” is certainly a factor of major importance in various conditions. In this review article, we discuss nutrigenomics, starting with basics definitions and enzymatic functions and ending with its palpable association with cancer. Now, diet is basically what we eat on a daily basis. Everything that enters through our alimentary tract ends up broken down to minute molecules and amino acids. These molecules interact with our microbiome and genome in discreet ways. For instance, we demonstrate how proper intake of probiotics enhances beneficial bacteria and may alleviate IBS and prevent colorectal cancer on the long term. We also show how a diet rich in folic acid is essential for methylenetetrahydrofolate reductase (MTHFR) function, which lowers risk of colorectal cancer. Also, we discuss how certain diets were associated with development of certain cancers. For example, red and processed meat are highly associated with colorectal and prostate cancer, salty diets with stomach cancer, and obesity with breast cancer. The modification of these diets significantly lowered the risk and improved prognosis of these cancers among many others. We also examined how micronutrients had a role in cancer prevention, as vitamin A and C exert anti-carcinogenic effects through their function as antioxidants. In addition, we show how folic acid prevent DNA mutations by enhancing protein methylation processes. Finally, after a systematic review of myriad articles on the etiology and prevention of cancer, we think that diet should be a crucial feature in cancer prevention and treatment programs. In the future, healthy diets and micronutrients may even be able to successively alter the liability to genetic mutations that result in cancer. It also will play a role in boosting treatment and improving prognosis of diagnosed cancers.
Summary of Findings
This paper explores how the food we eat interacts with our genes and gut microbes to influence health, disease risk, and treatment outcomes. The authors argue that nutrigenomics—the study of how nutrients affect gene activity—is a key component of personalized medicine. They also highlight how the microbiome (the trillions of microbes in our gut) plays a central role in nutrient metabolism, immune function, and disease prevention.
Key Gene–Nutrient Interactions
MTHFR (Methylenetetrahydrofolate Reductase)
- MTHFR is an enzyme involved in folate metabolism and one-carbon cycles, which are essential for DNA methylation and repair.
- A common genetic variant, MTHFR 677C?T, reduces enzyme activity. People with the TT genotype may have higher folate requirements.
- In one study, men with the TT genotype and adequate folate levels had a 55% lower risk of colorectal cancer compared to those with other genotypes. However, this protective effect was lost when folate levels were low.
- The TT variant is also linked to increased risk of neural tube defects (NTDs) in pregnancy if folate intake is insufficient.
- These findings suggest that folate supplementation should be tailored to genetic background to reduce disease risk.
CYP450 (Cytochrome P450 Enzymes)
- CYP450 enzymes help metabolize drugs, toxins, and food compounds. Their activity is influenced by both genetic variants and dietary intake.
- CYP1A2, for example, is activated by compounds in cruciferous vegetables and grilled meats, but inhibited by naringenin found in grapefruit.
- This means that how someone metabolizes carcinogens from cooked meat depends not only on their CYP1A2 genotype but also on their diet.
- Diets low in fat and glycemic load have also been shown to alter gene expression in prostate tissue, suggesting a role for CYP450 pathways in cancer prevention.
GST (Glutathione S-Transferases)
- GST enzymes detoxify harmful compounds by attaching them to glutathione, preventing DNA damage and mutations.
- There are several GST classes (GSTA, GSTP, GSTM, GSTT), each with different tissue distributions. For example, GSTP is dominant in the lungs, while GSTA is most abundant in the liver.
- Impaired GST function—due to genetic variants—can increase susceptibility to cancer and other diseases.
- For instance, people with the GSTM1 null genotype may be more vulnerable to aflatoxin-induced liver cancer, especially if exposed to contaminated foods like peanut butter.
Microbiome and Diet
The paper also emphasizes the microbiome’s role in shaping health. Diet can alter the balance of gut bacteria, which in turn affects nutrient absorption, inflammation, and disease risk. Probiotics, fiber, and fermented foods support beneficial microbes, while poor diets can lead to dysbiosis—an imbalance linked to obesity, diabetes, and cancer.
Significance for the Baker
Integrating nutrigenomics, microbiome analysis, and personalized dietary strategies could revolutionize healthcare. By tailoring nutrition to genetic and microbial profiles, we can better prevent disease, improve treatment outcomes, and promote long-term wellbeing.
