INTRODUCTION:

The human genome, which is diploid and ready for replication, is encased in a single cell embryo at the beginning of life. The biggest molecules in a cell, called chromosomes, contain the same genetic material in almost all cells of multicellular organisms¹.

There are hundreds of genes on these chromosomes, as well as extensive sections of intergenic DNA². In order to replace cells that die or are lost, the genome must be precisely copied millions of times throughout development, both during fetal and adult phases, and continuously thereafter³. Mistakes in DNA proofreading may lead to defective replication, which depends on a number of substrates and cofactors. Accumulating such mistakes may cause base sequence or chromosomal level alterations and programmed cell death (apoptosis)⁴. The role of these mutations, which can be caused by both internal and external genotoxic factors, in developmental abnormalities, premature aging, and increased vulnerability to degenerative diseases such as cancer, infertility, immune dysfunction, cardiovascular disease, and neurodegenerative disorders is being more acknowledged⁵.

Nutritional genomics, which emerged with the sequencing of the human genome, has replaced the older idea of nutrient-gene interactions⁶. There are two primary branches of this science: nutrigenomics, which studies the effects of food on genes and protein metabolism and function, and nutrigenetics, which studies how different people's genes react to different foods. Studies have shown that nutrients play a crucial role as cofactors in DNA metabolism and repair, and that dietary variables have a substantial influence on these processes⁷. The impact of nutritional deficits or excesses on the accuracy of DNA replication is, however, poorly known. Another possible molecular way to investigate nutrition's function in health is via single nucleotide polymorphisms (SNPs), which are common genetic variants that might affect metabolic reactions to food⁸. A balanced diet is essential for reducing health risks, even if life expectancy has been steadily rising, which is a result of advances in longevity⁹. The prevention of non-communicable diseases (NCDs) is a top priority for health authorities, who are tackling the dual problems of undernutrition and overnutrition by promoting dietary control that ensures people get the nutrients they need¹⁰.

Figure 1: Trends in Growth and Forecasts of Size and Share Analysis of the Nutrigenomics Market for the Years 2024–2033.¹¹

The purpose of this study is to take a close look at the complex web of relationships between genes and nutrition, with a focus on how nutrigenomics and nutrigenetics help us understand how different people's diets affect their health and how to avoid certain diseases. We want to shed light on the impact of genetic differences on food metabolism and dietary requirements by combining current research from many scientific sources. This will be especially helpful in understanding non-communicable diseases (NCDs) including cancer, heart disease, obesity, and diabetes. Personalized nutrition methods may optimize health outcomes and mitigate illness risks. This research aims to emphasize their relevance in shaping future dietary recommendations and health policy. Thorough literature research was carried out using several academic databases, such as PubMed, Karger, Cambridge Press, and IntechOpen, to investigate the function of nutrition in health and wellbeing. So that we could include the most recent findings, we limited our search to articles published between 2010 and 2024. "Nutrition," "nutritional genomics," "nutrigenetics," "non-communicable diseases," "dietary interventions," and "health outcomes" were crucial search keywords used.

Overview of Nutrigenetics and Nutrigenomics:

Dr. R.O. Brennan defined the word "nutrigenetics" in 1975 to describe the study of how a person's genes affect their body's reaction to food¹². Some monogenic and polygenic disorders may have their roots in dietary mismatches, according to this area of study that investigates gene-nutrient relationships. Enzyme activity and, by extension, the metabolism of several nutrients and substances, may be influenced by genetic polymorphisms, which in turn can affect general health. For example, phenylketonuria (PKU) and hemochromatosis are metabolic illnesses that may be controlled by dietary adjustments that are specific to each person's genetic makeup¹³. Mutations in some genes influence nutrition metabolism and the likelihood of developing diseases including cancer and heart problems. Personalized dietary approaches to disease prevention have been emphasized by nutrigenetic research, which also emphasizes the function of single nucleotide polymorphisms (SNPs) in modifying nutrient absorption and metabolism. The intricate relationship between diet and genetics is further shown by several polymorphisms, for example in the glutathione peroxidase, PPAR, and VDR genes, which impact illnesses ranging from cancer to cardiovascular disorders¹⁴.

The field of nutrigenomics aims to decipher the genetic and epigenetic mechanisms by which macronutrients and micronutrients affect human health. It uses functional genomic methods to investigate the metabolic pathways and homeostatic regulation affected by nutrition, as well as the effects of nutrients on gene transcription, expression, and the responses of gene variations¹⁵. While nutrigenetics aids in customizing customized nutrition by determining the ideal diet for an individual, nutrigenomics seeks to establish optimum diets based on changes in nutrition. This study relies heavily on techniques like metabolomics, transcriptomics, and proteomics. Nutritional factors may influence gene expression by modulating chromatin shape, protein function, and gene activity, according to studies¹⁶. Diet has a role in the development of many chronic illnesses, including diabetes, obesity, and cardiovascular disease, which are impacted by a combination of hereditary and environmental variables¹⁷. Lipid metabolism and cancer growth are two examples of the many processes that nutrients may influence via their direct and indirect regulation of transcription factors and signal transduction pathways. As an example, a family of nutrient sensors called PPARs affects genes that are involved in the metabolism of the liver. Deficits in micronutrients, such as vitamins B, E, and D, are associated with a number of disorders, whereas dietary compounds, including polyphenols and polyunsaturated fatty acids (PUFAs), influence gene expression. Nutritional cues, such as carbs and amino acids, may also change metabolic pathways and gene expression. Determinants of illness severity, course, and onset are genes that are modulated by chemicals in the food^18,19.

Research in the fields of nutrigenomics and nutrigenetics aims to better understand the interplay between genes and nutrition by examining the effects of various nutrients on gene expression and the ways in which genetic variants impact dietary responses^29,30. Personalized nutrition strategies for health optimization and illness prevention are the ultimate goal of these areas, which use genetic data and modern 'omic' technology to better understand nutrient-gene interactions³¹. The effect of cultural and geographical variations on food, the impact of genetic variability across people and ethnic groups that affects nutrient metabolism, and the impact of malnutrition on gene expression and genome stability are all variables that highlight their relevance^32,33. Recommended dietary allowances (RDAs), are based on population-level data that may not take into consideration individual variations in nutrient metabolism, highlighting the need of tailored nutrition plans³⁴. Some of the most important ideas in the fields of nutrigenomics and nutrigenetics propose that dietary factors influence gene expression and that changes in genetic makeup influence the processing of nutrients. Genetic vulnerability and gene expression are both significantly impacted by epigenetics, the study of dietary effects on gene regulation³⁵. Personalized nutrition is an exciting new area of study that has the potential to improve health outcomes by shedding details about disease etiology and guiding dietary therapies in accordance with specific genetic profiles^36,37.

Impact of Nutrition on Non-Communicable Diseases:

In the last five decades, life expectancy has increased by 5.5 years on average throughout the world, and in many nations, it is already more than 80 years³⁸. Unfortunately, the burden of age-related noncommunicable diseases (NCDs) such as diabetes, cardiovascular disease, and cancer has grown along with the increase in lifespan, putting a strain on both people and healthcare systems³⁹. Organizations like the World Health Organization place a premium on avoiding noncommunicable diseases (NCDs) because of the substantial correlation between NCDs and modifiable risk factors, such as sedentary lifestyles and poor nutrition⁴⁰. Essential for development and upkeep throughout life, proper nutrition is a key component in health promotion. Thanks to our contemporary lives, we tend to eat a lot of calorie-dense, nutrient-poor foods, which adds to the problem of undernutrition and overnutrition. The yearly economic cost of poor diets and inactivity in the European Union is estimated at €1.3 billion⁴¹. Health officials have emphasized cutting down on sugar, salt, fat, and calories, but encouraging people to eat enough of each component is still crucial for maintaining a healthy diet. The need for country-specific guidelines is underscored by differences in nutrient intake and eating habits across time⁴².

Table 2: Medical Nutrition: Improving Health Status and Clinical Outcomes⁴³.

Clinical Nutrition	Clinical Condition	Clinical Advantages
Malnutrition Management by Nutrition	Short Bowel Syndrome; Stroke	Life-saving moment
	COPD	Enhanced Respiratory Function
	Older Patients	Better health, less illness, and longer life expectancy
	Surgical Patients	Low Complications
Nutritional Disease Management	Crohn’s Disease	Remission Induction
	Cow’s Milk Allergy	Lessened Signs, Accelerated Recovery
	IEMs: PKU, MSUD, FAOD, GSD	Normal Growth and Development
	Intractable Epilepsy	Regular Growth and Development; lower Seizures

The worldwide epidemic of poor dietary and lack of physical exercise can only be reversed by health policies and programs that target the general public's food consumption. Still, high-risk populations, such the elderly, may need individualized strategies to close chronic dietary deficits and forestall health problems⁴⁴. In particular, undernourishment affects 5–10% of persons living in the community who are 70 and older, and 30–65% of those confined to nursing homes. Calcium, vitamin D, and vitamin B₆ and B₁₂ deficiencies are prevalent in the elderly population⁴⁵. Reduced sun exposure and inadequate dietary sources of vitamin D have made it a common health problem affecting people of all ages. When this nutrient is missing, it may lead to a host of musculoskeletal problems, such as weak muscles and bones. Vitamin D and calcium taken together greatly lower the risk of fracture, according to studies. This is especially true for those living in institutions. Vitamin K is vital for bone health and has a synergistic impact with vitamin D, according to study⁴⁶. Vitamin D's effects on health are still up for debate, but current research suggests that tailored supplementation may be helpful, especially for those who are deficient in the vitamin or who are at risk.

Cardiovascular Disease:

The primary cause of morbidity and death, and the main driver of healthcare expenses, is cardiovascular diseases, even though the worldwide mortality rate from these causes has been declining. Conditions including obesity, hypertension, and dyslipidemia are consequences of a sedentary lifestyle, poor nutrition, and cigarette smoking, all of which contribute to cardiovascular ageing. The prevalence of cardiovascular disease is highest among the elderly, affecting 85% of those over the age of 80 and 68% of those between the ages of 60 and 79. There has been a lack of focus on the function of undernutrition in relation to cardiovascular disease, despite the fact that proper nutrition may slow its development⁴⁷. It is well-known that overnutrition may negatively affect cardiovascular health, but less research has looked at how improving dietary shortages might do the same, particularly in older persons. There has been conflicting evidence on the possible advantages of vitamin D and vitamin B nutrients. Taking vitamin D supplements had no impact on cardiovascular outcomes, while taking B vitamins lowered homocysteine levels but only reduced the risk of stroke considerably^48,49. The effectiveness of vitamin supplementation, especially in reducing cardiovascular risks associated with homocysteine, may be further affected by factors including genetic variations. At the same time, research on the cardiovascular preventive benefits of vitamins E and K has shown conflicting findings, especially in some subgroups^50–53.

Eye Disorders:

Visual and auditory impairments rank as the second most common forms of disability. Glaucoma, cataracts, diabetic retinopathy, age-related macular degeneration (AMD), and cataracts are among the most prevalent causes of visual loss in the aged population⁵⁴. Although age is the main factor that increases the likelihood of AMD, other lifestyle and environmental variables, including smoking, oxidative stress, food, and excessive blue light exposure, may also play a role. Carotenoids, especially lutein and zeaxanthin, shield the eyes from potentially damaging blue light and boost retinal antioxidant defences⁵⁵. Individuals with poor macular pigment optical density may benefit from supplements that enhance visual function and decrease the development of AMD. People with low dietary intake of lutein and zeaxanthin had a decreased chance of developing advanced age-related macular degeneration (AMD) in the AREDS2 study, and this supplement may also decrease the risk of undergoing cataract surgery. If the AREDS2 complex were to be extensively used, it might significantly save healthcare expenses by preventing age-related macular degeneration and cataracts in the elderly. To better prevent age-related eye problems, future studies should investigate the best ways to take these carotenoids and how they interact with other nutrients⁵⁶.

Nutrigenomic Biomarkers and the Gene-Diet Relationship in Disease:

Protecting against non-communicable diseases (NCDs) such as malignancies, cardiovascular disease, obesity, diabetes, respiratory illness, metabolic syndrome, and obesity-related disorders is the goal of nutrigenomics research, which examines the relationship between genes, nutrition, and disease⁵⁷. Chronic exposure to certain dietary components, especially those associated with city living and junk food intake, is commonly related with these NCDs. Biomarkers that may lead to the diagnosis of nutritional issues include aberrant lipid profiles, high blood pressure, and insulin sensitivity. These symptoms might be indicators of metabolic syndrome or cardiovascular disease. Proteomics and metabolic changes produced by a person's genotype may be detected with the use of biomarkers, which include proteins, metabolites, and different bodily processes. The presence of DNA adducts, abasic sites, strand breaks, telomere shortening, and mitochondrial DNA damage are some of the ways that molecular DNA damage may be detected⁵⁸. Research establishing a connection between diet and illness has provided credence to the use of these damaged DNA markers. Among nutritional genomics biomarkers, the micronucleus test in cytokinesis-blocked lymphocytes is the gold standard at the moment. Analyzing gene expression by microarray assays enables the evaluation of hundreds of genes concurrently; transcriptomics is another established method in nutrigenomics. Researchers have discovered disease-specific gene-expression patterns in peripheral blood cells; these patterns have been used as biomarkers for the identification of diseases such as leukemia and breast cancer.

Popular genetic markers that contribute to genetic diversity include single nucleotide variants (SNVs) and single nucleotide polymorphisms (SNPs). By analyzing these changes, genotypic variances may be identified, which in turn allows for personalized dietary advice to avoid NCDs such cancer, heart disease, obesity, and diabetes. Examples include the work of Ramos-Lopez et al., who brought attention to the link between taste perception in Mexico and the sweet taste receptor (TAS1R2), and the link between the CD36 gene and dyslipidemia in those who consume a lot of carbs and fats. The risk of breast cancer is higher in those who do not get enough folate, vitamin B₆, or vitamin B₁₂ because of single nucleotide polymorphisms (SNPs) in genes that control homocysteine metabolism, such as MTHFR and MTR⁵⁹. Osteoporosis and other vitamin D-related disorders may develop in postmenopausal women who don't get enough calcium from their diets because of polymorphisms in the vitamin D receptor (VDR) gene⁶⁰.

Insulin resistance, hypertension, and type-2 diabetes are among the metabolic disorders associated with obesity, a chronic inflammatory sickness. When it comes to the complex interplay between heredity and lifestyle variables like food, sleep, and exercise, nutrigenomics is crucial for making sense of the obesity crisis. Along with being susceptible to environmental variables, genetic susceptibility is a major contributor to obesity, according to research⁶³. Research conducted by Nakamura et al., Nettleton et al., and Reddon et al. supports the idea that hereditary variables impact an individual's susceptibility to obesity, meaning that not everyone exposed to an obesogenic environment will acquire obesity. Consequently, metabolic problems associated with obesity may be better managed with a mix of good eating and frequent exercise.

In their explanation of energy balance, Hill et al. state that when caloric intake is more than caloric expenditure, adipose tissue accumulates triacylglycerol, which promotes obesity. When the energy balance is negative, on the other hand, lipolysis and fatty acid mobilization are encouraged⁶⁴. Additionally, epigenetic variables are important in obesity; for example, Goldberg et al. discovered that a person's dietary environment during pregnancy and the first few months after giving birth might affect their risk of being overweight later in life. Epigenetic changes, like DNA methylation, control gene expression without changing the DNA sequence, drawing attention to the fact that heredity and environment interact in the context of obesity. In the context of cardiovascular disease (CVD), nutrigenomics has shown that dietary influences on susceptibility to CVD may be influenced by certain genetic polymorphisms. Apolipoprotein E is one example of a lipid transport protein whose polymorphisms influence both cholesterol levels and the likelihood of atherosclerosis, a key risk factor for cardiovascular disease. Consumption of high-fat meals is associated with elevated levels of low-density lipoprotein (LDL) cholesterol in those who have the APOE4 gene. The significance of individualized nutrition in controlling cardiovascular health is underscored by dietary treatments that focus on the macronutrient composition and sources of fat, such as olive oil instead of animal fats, which may substantially affect CVD risk⁶⁵. Last but not least, nutrigenomics has shown how dietary variables interact with genetic ones to affect cancer risk. Flavonoids, phenols, and omega-3 fatty acids are a few examples of the bioactive substances contained in diet that have been shown to modify carcinogen metabolism and lower cancer risk⁶⁶. One example is the correlation between a high red meat intake and an increased risk of colorectal cancer, especially in those who have fast-acetylating NAT2 polymorphisms. In addition, vitamins, antioxidants, and dietary fibre may influence gene expression and cellular processes associated with carcinogenesis, which in turn can protect against cancer⁶⁷.

Maximizing Health and Performance with Nutrigenetics and Nutrigenomics:

There are obvious gender and age-related variances in dietary requirements, but nutrition studies have often assumed that everyone has the same nutritional requirements. Deficiency illnesses are the primary focus of dietary recommendations, which often take the form of Recommended Dietary Allowances (RDAs) and outline the minimum amounts of nutrients that the majority of people should consume each day to be healthy. Although these recommendations are revised on a regular basis to reflect the most recent scientific findings, there is an increasing need for a more sophisticated comprehension of nutritional needs due to the proliferation of nutrition-related chronic disorders⁶⁸.

Consumers may enter their age, sex, height, weight, and degree of physical activity to get individualized eating plans with the use of the online 'Mypyramid' tool, which is a noteworthy breakthrough in the field of personalized dietary advice. The need for more advanced approaches to dietary personalization is underscored by the fact that this strategy only partly accounts for individual variances. Nutrigenomics and nutrigenetics have recently made strides in understanding how genes and variations impact dietary requirements. Research on these connections in animals and using systems biology methods has yielded some understanding, but there has been little success in applying this information to humans. Still, there's a growing interest in the idea of genetically-based personalized diet⁶⁹.

There is mounting evidence that people respond differently to medical treatments aimed at preventing and treating illness, which lends credence to the need for tailored dietary plans. Although personalized pharmacology was sluggish to gain traction, it is now showing promise in tackling problems like adverse drug responses by adapting medication selection and dose to individual genetic profiles. As an example, it is becoming normal practice to do genetic testing for variations in medication metabolism, which may improve the effectiveness of therapy. With the increasing desire for personalized consumer goods, there are similar potential in nutrigenomics and nutrigenetics. This suggests that personalized nutrition might be useful in managing some health disorders⁷⁰.

The successful use of personalized diet is shown by the case of coeliac disease. A gluten-free diet is essential for controlling inflammatory symptoms and preventing major health consequences with this disorder, which is characterized by an unfavorable response to gluten. There is substantial evidence linking specific genetic variations to an increased risk of developing coeliac disease. Currently, genetic screening for coeliac disease is not often done, but it might help identify those who are at risk and then we can implement dietary therapies specifically for them⁷¹.

Personalized diet plans have the potential to improve obesity prevention efforts. Weight reduction and maintenance results may be greatly enhanced with individualized meal plans that are influenced by genetic data, according to research. Diet and exercise plans based on individuals' specific genetic variations led to more weight loss and better maintenance of weight loss than those who followed more generalized plans. Although our own pilot research in Auckland showed that individualized diets may be effective, it also showed that people have a hard time sticking to their programs, especially when it comes to exercise. It is becoming more and more crucial to comprehend the hereditary components impacting disorders such as Alzheimer's and Parkinson's as the population becomes older. Dietary therapies have shown some success in animal studies, but we still need to do more study to see if they work for humans. Personalized nutrition is gaining popularity among customers, but it's still a problem for the food sector to satisfy their demands while also catering to their everyday habits and tastes⁷¹.

CONCLUSION:

Health outcomes and the prevention of non-communicable diseases (NCDs) may be better understood by examining the complex relationship between genetics and diet. Nutrigenomics and nutrigenetics provide light on how genetic variants impact reactions to food components; this, in turn, reveals that tailored nutrition plans might improve health and reduce the likelihood of illness. The growing number of noncommunicable diseases (NCDs) throughout the world is a clear indication that health officials must act swiftly to advocate for personalized dietary therapies that take genetic variability into consideration. The development of personalized dietary recommendations that suit the specific metabolic demands of people, especially vulnerable groups like the elderly, is made possible by advances in genetic research, which provide a promising foundation. Improved public and individual health outcomes may be achieved by more research into the gene-diet link, the development of more accurate nutritional assessment biomarkers, and the application of genomic findings to real-world dietary recommendations.

ACKNOWLEDGEMENT:

The authors thank to the INTI University, Malaysia and this review work is supported by INTI University.

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Received on 06.11.2024 Revised on 20.03.2025

Accepted on 26.05.2025 Published on 13.01.2026

Available online from January 17, 2026

Research J. Pharmacy and Technology. 2026;19(1):411-419.

DOI: 10.52711/0974-360X.2026.00060

This work is licensed under a Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International License. Creative Commons License.

Micronutrients	Operation in genomic stability	Result of deficiency
Vits C	Prevent lipid, DNA oxidation	Baseline levels of DNA damage, chromosomal breakage, oxidative DNA lesions, and lipid peroxide adducts on DNA are elevated.
Folate and Vits B₂, B₆, B₁₂	Effective recycling of folate, maintenance DNA methylation, and dTMP production from dUMP	DNA hypomethylation, chromosomal breakage, and uracil misincorporation
Vit D	Increase antioxidant activity in normalm cells Induce apoptosis in malignant cells
Vit E	Prevent lipid, DNA oxidation
Niacin, Nicotinic acid	Important for DNA cleavage and recombination, telomere length maintenance, and DNA repair; substrate for poly (ADP-ribose) polymerase.	DNA hypomethylation, chromosomal breakage, and uracil misincorporation
Zn, Mn and Se	Zinc is an essential element for many biochemical reactions, including those involving DNA replication, P53 activity, endonuclease IV, Cu/Zn supperoxid dismutase, and zinc finger proteins like poly (ADP-ribose) polymerase. The mitochondrial Mn superoxide dismutase enzyme requires manganese, which is a mineral. Selenium, an essential component of glutathione peroxidase and other peroxidases.	Enhanced chromosomal damage rate, DNA oxidation and breakage
Iron	Essential for the proper functioning of mitochondrial cytochromes and ribonucleotide reductase.	Decreased ability to repair DNA, heightened susceptibility to oxidative stress on mitochondrial DNA
Mg²⁺, Ca²⁺	Several DNA polymerases rely on magnesium as a cofactor; these enzymes are essential for chromosomal segregation and microtubule polymerisation, among other processes. Ca is essential for cell death and has a significant impact on chromosomal segregation.	Problems with DNA repair, chromosomal segregation, DNA replication fidelity, and the ability of genomically abnormal cells to survive