Published 05/28/2024
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Gulsen Meral , Elif S. Aslan , Verda Tunaligil , Neval Burkay , Esma Gökcen Alper Acar , Muhammed Yunus Alp
Published 06/26/2024
Our findings revealed a notable reduction in foxp3 gene methylation levels among HT
patients who adhered to a diet excluding casein and gluten. The control maintained normal dietary guidelines and showed no significant alterations in methylation levels.
Elif S. Aslan , Gulsen Meral , Ece Aydin , Sinan Caglayan , Aytug Altundag , Seyda Demirkol , Gizem Gormus , Mustafa Solak , Furkan Ayaz
Published 08/15/2024
Background: Nutrigenetics explores how genetic variations influence an individual's responses to nutrients, enabling personalized nutrition. As dietary supplements gain popularity, understanding genetic factors in their metabolism and effectiveness is crucial for optimal health outcomes. This study examines the role of genetic differences in the metabolism and effects of nutraceuticals, underscoring the significance of personalized nutrition within precision health. It aims to reveal how individual genetic profiles influence responses to dietary supplements, highlighting the value of nutrigenetics in optimizing health interventions. The study explores how genetic variations affect the absorption and effects of nutraceuticals, focusing on personalized supplement choices based on nutrigenetics.
Gulsen Meral , Elif S. Aslan , Neval Burkay , Esma Gökcen Alper Acar , Mustafa Fevzi Karagöz , Merve Özkaya , Esra Sahin , Muhammed Yunus Alp
Published 15 December 2024
Background/Aim: Loss of smell, also known as anosmia, is a prevalent and often prolonged
symptom following infection with SARS-CoV-2. While many patients regain olfactory function within
weeks, a significant portion experience persistent anosmia lasting over a year post-infection. The
underlying mechanisms responsible for this sensory deficit remain largely uncharacterized. Previous
studies, including genome-wide association studies (GWAS), have identified genetic variants near
the UGT2A1 and UGT2A2 genes that are linked to anosmia in COVID-19 patients. However, the role
of epigenetic changes in the development and persistence of smell loss has not been well explored.
In this study, we aimed to investigate epigenetic alterations in the form of DNA methylation in the
UGT1A1 gene, which is a locus associated with olfactory dysfunction in COVID-19 patients. Methods:
We analysed DNA methylation patterns in blood samples from two carefully matched cohorts of
20 COVID-19 patients each, which are differentiated by their olfactory function—those with normal
smell (normosmia) and those suffering from smell loss (anosmia). The cohorts were matched for
age and sex to minimize potential confounding factors. Results: Using quantitative analysis, we
found significantly lower levels of DNA methylation in the UGT1A1 locus in the anosmia group
compared to the normosmia group, with a 14% decrease in median methylation values in patients
with smell loss (p < 0.0001). These findings highlight potential epigenomic alterations in the UGT1A1
gene that may contribute to the pathogenesis of anosmia following COVID-19 infection. Our results
suggest that the methylation status at this locus could serve as a biomarker for olfactory dysfunction
in affected individuals. Conclusion: This study is among the first to describe epigenetic changes
associated with smell loss in COVID-19, providing a foundation for future research into targeted
interventions and potential therapeutic strategies aimed at reversing persistent anosmia. Further
investigations involving larger cohorts and additional loci may help elucidate the complex interaction
between genetic, epigenetic, and environmental factors influencing long-term sensory impairment
post-COVID-19.
Elif Sibel Aslan, Kenneth White, Savas Gur, Mehmet Dokur, Gulsen Meral, Zeyneb Nur Akcay, Aytug Altundag, Mehmet Akif Baktir and Lutfiye Karcioglu Batur
ABSTRACT The global phenomenon of ageing and the expectation that the number of people aged 65 and over will reach 1.5 billion by 2050 is well recognized. The challenges that an ageing population poses to health systems, social security structures and national economies are evident. In the context of the World Health Organization's “Global Action Plan on Healthy Ageing”, it is important to emphasize the impact of epigenetic mechanisms on biological ageing. Epigenetic changes, especially DNA methylation, are considered as factors that accelerate or slow down the aging process and age-related diseases (such as diabetes, cancer, cardiovascular diseases and dementia). How DNA methylation and epigenetic changes shape biological aging independent of chronological age is examined through molecular processes and single carbon metabolism. In addition, how lifestyle and environmental factors affect the epigenetic structure and the negative effects of physical activity, smoking and alcohol consumption on the epigenetic clock were discussed.In addition, the use of epigenetic clocks in biological age estimation to promote healthy aging and the role of nutrigenetics-based epigenetic approach provided by personalized medicine in this process were discussed.Nutrition, probiotics and vitamin supplements stand out as potential factors that may affect the aging process by modulating DNA methylation.Together with the influence of genetic variations and environmental factors in the aging process, it is concluded that epigenetic treatment approaches may play a role in preventing diseases and promoting healthy aging.Aging is an inevitable biological phenomenon, but this process can be delayed by a healthy lifestyle.
Background: Vitamin D deficiency is a global health concern affecting all age groups, despite the implementation of supplementation strategies. This study aimed to investigate the roles of genetic polymorphisms, epigenetic mechanisms, and microbiota interactions in vitamin D metabolism, as well as their potential contributions to allergies, autoimmune thyroiditis, and autism spectrum disorder. Methods: This retrospective, descriptive study analyzed data from 60 individuals (16 males and 44 females) who underwent nutrigenetic testing between 2022 and 2024 at Epigenetic Coaching, Istanbul, Turkey. Genetic analyses focused on the cytochrome P450 family 2 subfamily R member 1 (CYP2R1) gene, groupspecific component (GC) gene, and vitamin D receptor (VDR) polymorphisms. Inclusion criteria included the presence of allergic symptoms, a diagnosis of autism spectrum disorder, or a diagnosis of Hashimoto’s thyroiditis, along with prior genetic testing for the selected variants. Individuals with any known genetic disorder other than the studied variants were excluded. Results: CYP2R1, GC, and VDR polymorphisms associated with vitamin D insufficiency were found at higher frequencies in patients with autism, Hashimoto’s thyroiditis, and allergic conditions. When examining the associations between genetic variants and diseases, VDR FokI, VDR ApaI, and VDR BsmI variants were more frequently observed in patients with Hashimoto’s thyroiditis, while the VDR TaqI variant was more common in individuals with autism. In the allergy group, BsmI, FokI, ApaI, and TaqI variants were identified at higher frequencies. Conclusion: Genetic variants and epigenetic modifications may disrupt vitamin D metabolism and alter gut microbiota diversity, contributing to the development of various diseases. Evaluating vitamin D deficiency together with its genetic, epigenetic, and microbiota determinants is essential for developing effective prevention and treatment strategies. These findings emphasize the necessity of personalized, nutrigeneticbased approaches to optimize vitamin D function and support overall health.
Early life is a critical period when nutrition and environmental exposures significantly influence development and long-term health. This review examines the interactions among genetic factors, nutrigenetics, epigenetic mechanisms and the gut microbiota in early life, emphasizing maternal effects during prenatal and infancy stages. Maternal nutrition can alter fetal epigenetic marks, shaping gene expression patterns that persist into adulthood. Genetic variations in mother and child affect nutrient metabolism and requirements, influencing developmental outcomes. The infant’s microbiota, seeded by maternal microbes and shaped by diet, is crucial for metabolic and immune system training. The concept of early-life programming, known as the “Developmental Origins of Health and Disease,” is discussed. Evidence from both human and animal studies links early nutrition and microbial exposure to lifelong health outcomes. Immune development relies on early microbial and nutrient signals, affecting tolerance and allergy risks. By integrating epigenetics, nutrigenetics and microbiome research, this article brings the role of maternal diet quality and microbial transmission in infant development to prominence. Understanding these processes may guide strategies, such as optimized maternal nutrition and microbiota-based interventions, to improve health outcomes across generations.
The Diamond Model of Epigenetic Healing is a conceptual framework linking epigenetic adaptation with populationlevel resilience. Drawing on the metaphor of carbon’s transformation into diamond under stress, the model emphasizes that environmental and social stressors leave measurable epigenetic marks, but targeted interventions can modulate or reverse harmful modifications, termed “epigenetic healing.” This research note summarizes the model, synthesizes supporting evidence, and proposes directions for integrating molecular indicators into public health strategies. Interventions such as prenatal care, nutrition, trauma-informed services, pollution remediation, and social equity policies can produce measurable improvements in epigenetic profiles and downstream health outcomes. Identifying epigenetic markers as population-level indicators reframes prevention to include molecular restoration. Key next steps include community intervention trials with pre/post epigenetic measures, longitudinal cohort analyses linking social determinants with molecular change, and policy evaluation incorporating epigenetic outcomes. Recognizing epigenetic healing reorients public health toward active restoration, supporting longer, healthier lives and improved biological resilience across generations.
Cancer is associated with significant psychological burdens, including anxiety, depressive symptoms, and a decline in quality of life. Psycho-oncological outcomes are shaped by the complex interplay of biological, psychological, and social factors, necessitating personalized and multidisciplinary approaches. In recent years, there has been growing interest in whether genetic variations in enzymes such as catechol-O-methyltransferase (COMT) and monoamine oxidase (MAO) may modulate psychological responses in cancer patients. Correspondingly, due to epigenetic effects in cancer patients, nutraceutical compounds such as epigallocatechin-3-gallate (EGCG) and curcumin are noteworthy for their antioxidant and anti-inflammatory effects and are being investigated for their potential interactions with the COMT/MAO pathways. Preclinical and mechanistic studies suggest that these compounds may influence neurotransmitter metabolism, gene expression, and stress responses. However, direct clinical studies assessing their effects on psychological outcomes by COMT/MAO genotype are quite limited. The aim of this review is to evaluate the relationships among COMT and MAO polymorphisms, nutraceutical interventions, and antidepressants (particularly SSRIs and MAO inhibitors) commonly used in psycho-oncological patients. This review positions COMT and MAO based nutrigenetic approaches alongside psychotropic drug use as a promising but still developing field; it emphasizes the need for more robust and direct clinical evidence to safely and effectively translate these approaches into clinical practice. In this context, personalized strategies that go beyond standard approaches, considering genetic variations, individual biochemical responses, and nutraceutical interactions together, may be more rational and effective; therefore, the need for a personalized approach in this field is increasingly recognized
The worldwide prevalence of all cancer types continues to rise. In this context, the psychological burden of cancer—particularly anxiety and depression—has emerged as a critical yet frequently overlooked component of comprehensive oncological care. In addition to clinical and psychosocial factors, growing evidence suggests that epigenetic mechanisms significantly influence both cancer biology and mental health, indicating that gene-environment interactions may affect psychological vulnerability in oncology contexts. Nutrigenetics-based epigenetic approaches enable personalized dietary and nutraceutical interventions based on individual genetic variability. Green tea catechins and curcumin are widely used bioactive compounds due to their epigenetic and anticancer potential. However, by altering the activity of catechol-O-methyltransferase (COMT) and monoamine oxidase (MAO), important enzymes that degrade dopamine, norepinephrine, and serotonin, these substances have an impact on monoaminergic neurotransmission. Functional polymorphisms in the COMT and MAO genes may lead to substantial interindividual differences in mood regulation, stress responsiveness, and anxiety susceptibility. This review addresses molecular, clinical, and psycho-oncological aspects of the effects of green tea and curcumin on COMT and MAO pathways within a nutrigenetics-based epigenetic nutrition framework. The findings emphasize that the potential clinical benefits of epigenetically active nutraceuticals should be evaluated through a genotype-guided, individualized, and balanced approach.
Background: Taste perception–related genetic variants may influence dietary behavior and energy balance; however, their relationship with body mass index (BMI) remains unclear. This study aimed to investigate the association between taste-related genetic variants and BMI using both statistical analysis and an explainable machine learning approach. Methods: This retrospective observational study included 200 individuals aged 5–60 years with available genotype and BMI data. Variants in TAS2R38, TAS1R2, TAS1R3, and FGF21 were analyzed. Associations with BMI categories were evaluated using chi-square tests. A Random Forest classification model was developed, and SHAP (SHapley Additive exPlanations) values were used to quantify the contribution of each variant and explore allele-dose effects. Results: No significant associations were found between genetic variants and BMI categories in adults (p > 0.05). In children, rs35744813 showed a significant inverse association with BMI (p = 0.011). SHAP analysis revealed that TAS2R38 variants (rs10246939 and rs1726866) and FGF21 rs838133 demonstrated the highest relative contributions to BMI classification. Allele-dose patterns suggested differences in model attribution across genotype groups. Conclusion: Taste-related genetic variants did not demonstrate independent associations with BMI classification in the present study. However, explainable machine learning approaches identified heterogeneous model contributions across genetic variants, suggesting potential differences in genotype-related patterns within a multifactorial framework. These findings may contribute to future research exploring gene–phenotype relationships and precision nutrition approaches.