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Benign Prostatic Hyperplasia - NED Infobite
BANT's scientific NED InfoBites are designed to provide key elements of the latest research using plain language. They provide quick overviews on particular health issues and nutrition topics for a speedy introduction to the science. Visually attractive and easily shareable with clients and social media followers.
2024
Abstract
Benign prostatic hyperplasia (BPH) is a common benign disease in middle-aged and elderly men which causes lower urinary tract symptoms. Age, sex hormones, diet, diabetes, obesity and genetic factors are closely related to BPH occurence. This NED Infobite presents science on obesity and lifestyle factors on the risk of BPH, the impacts of diabetes mellitus on lower urinary tract symptoms in BPH, the impact of testosterone on lower urinary tract symptoms and gene associations.
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Causal relationship between obesity, lifestyle factors and risk of benign prostatic hyperplasia: a univariable and multivariable Mendelian randomization study.
Wang, YB, Yang, L, Deng, YQ, Yan, SY, Luo, LS, Chen, P, Zeng, XT
Journal of translational medicine. 2022;20(1):495
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Benign prostatic hyperplasia (BPH) is a common benign disease in middle-aged and elderly men which is often underestimated and underdiagnosed. If patients are not treated in time, it may lead to serious complications, such as urinary retention, renal insufficiency and renal failure. The aim of this study was to evaluate the possible causal associations of abdominal obesity (measured as waist circumference), overall obesity (measured as body mass index), lifestyle factors (dietary habits, smoking, alcohol drinking, and sedentary behaviour) with risk of BPH. This study is a univariable and multivariable mendelian randomised study. Results show that genetic predisposition to higher waist circumference and sedentary behaviour are independently and causally associated with the risk of BPH. However, there isn’t conclusive evidence that genetic predisposition to relative carbohydrate, fat, protein, and sugar intake, smoking and alcohol drinking are causally associated with the risk of BPH. Authors conclude that further studies are needed to identify comprehensive risk factors on BPH and develop freely accessible prediction models for the BPH. These will help to identify individuals at particular risk and provide decision-making supports for individualised intervention.
Abstract
BACKGROUND Obesity (waist circumference, body mass index (BMI)) and lifestyle factors (dietary habits, smoking, alcohol drinking, Sedentary behavior) have been associated with risk of benign prostatic hyperplasia (BPH) in observational studies, but whether these associations are causal is unclear. METHODS We performed a univariable and multivariable Mendelian randomization study to evaluate these associations. Genetic instruments associated with exposures at the genome-wide significance level (P < 5 × 10-8) were selected from corresponding genome-wide associations studies (n = 216,590 to 1,232,091 individuals). Summary-level data for BPH were obtained from the UK Biobank (14,126 cases and 169,762 non-cases) and FinnGen consortium (13,118 cases and 72,799 non-cases). Results from UK Biobank and FinnGen consortium were combined using fixed-effect meta-analysis. RESULTS The combined odds ratios (ORs) of BPH were 1.24 (95% confidence interval (CI), 1.07-1.43, P = 0.0045), 1.08 (95% CI 1.01-1.17, P = 0.0175), 0.94 (95% CI 0.67-1.30, P = 0.6891), 1.29 (95% CI 0.88-1.89, P = 0.1922), 1.23 (95% CI 0.85-1.78, P = 0.2623), and 1.04 (95% CI 0.76-1.42, P = 0.8165) for one standard deviation (SD) increase in waist circumference, BMI, and relative carbohydrate, fat, protein and sugar intake, 1.05 (95% CI 0.92-1.20, P = 0.4581) for one SD increase in prevalence of smoking initiation, 1.10 (95% CI 0.96-1.26, P = 0.1725) and 0.84 (95% CI 0.69-1.02, P = 0.0741) for one SD increase of log-transformed smoking per day and drinks per week, and 1.31 (95% CI 1.08-1.58, P = 0.0051) for one SD increase in sedentary behavior. Genetically predicted waist circumference (OR = 1.26, 95% CI 1.11-1.43, P = 0.0004) and sedentary behavior (OR = 1.14, 95% CI 1.05-1.23, P = 0.0021) were associated with BPH after the adjustment of BMI. CONCLUSION This study supports independent causal roles of high waist circumference, BMI and sedentary behavior in BPH.
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Organic Food in the Diet of Residents of the Visegrad Group (V4) Countries-Reasons for and Barriers to Its Purchasing.
Soroka, A, Mazurek-Kusiak, AK, Trafialek, J
Nutrients. 2021;13(12)
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The food market is changing dynamically. New food production technologies are emerging, especially those with high and enriched nutritional value and functional food. The aim of this study was to determine the differences in the frequency, reasons, and barriers against buying organic food by residents of the Visegrád Group member states. Results indicate that: - the Poles and Hungarians buy organic food very often, whereas the largest percentages of Slovaks and Czechs do so rarely. - the most important reasons for choosing organic food in all V4 countries were the absence of genetically modified organisms, chemicals and preservatives. - high prices is the main barrier limiting the purchase of organic food. - the differences in the consumption of organic products in individual V4 countries may result from the actual differentiation or different interpretations of the definition of organic products and confusion with home and locally produced food. Authors conclude that to fully utilize the potential of the organic farming sector and organic aquaculture and to ensure their sustainable development, it is necessary to define the goals and activities to be implemented by the Minister of Agriculture in individual countries to produce organic food together with its promotion.
Abstract
This study aimed to determine the differences in the frequency of, reasons for, and barriers to purchasing organic food among the inhabitants of the Visegrád Group member states. The selection of the countries for the study was dictated by the fact that the countries of Central and Eastern Europe play the role of a niche market in the European organic food market. This research employed the method of a diagnostic survey and the discriminant function. A chi-squared test, ANOVA, and Fisher's Post Hoc LSD test were also used to present differences in individual groups. This research shows that respondents from Poland, the Czech Republic, Hungary and Slovakia were guided by similar behaviors regarding the purchase of organic food. However, the attitudes of the respondents slightly differed between countries. In the case of the reasons for choosing organic food, the most important thing was that it is non-genetically modified food, especially for Polish consumers. The following were also mentioned: lack of chemical compounds (Slovaks and Czechs), high health value of such food (Czechs and Slovaks), and excellent taste (Hungarians). The most critical barriers against purchasing are the price (Poles and Hungarians), difficult access (Poles and Hungarians), and the short expiry time of such products (Slovaks).
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Assessment of causal association between thyroid function and lipid metabolism: a Mendelian randomization study.
Wang, JJ, Zhuang, ZH, Shao, CL, Yu, CQ, Wang, WY, Zhang, K, Meng, XB, Gao, J, Tian, J, Zheng, JL, et al
Chinese medical journal. 2021;134(9):1064-1069
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Obesity, dyslipidaemia, and metabolic syndrome are major risk factors for cardiovascular disease, however, effect of thyroid dysfunction on dyslipidaemia and cardiovascular disease is largely unknown. This study used mendelian randomisation (MR), where a genetic variant is used as an instrumental variable to detect the causal effects of exposure to disease. This study used two sample MR analyses to find out whether clinical thyroid function measures show a causal relationship with the changes in lipid levels. The results showed a significant association between the elevated thyrotropin (TSH) level and increased total cholesterol. Also, there was a significant correlation between the free triiodothyronine (FT3): free thyroxine (FT4) ratio and total cholesterol and low-density lipoprotein (LDL). Further robust studies are required to confirm the results and investigate the causal effect of thyroid hormone dysregulation and cardiometabolic diseases due to the limitations of this study. However, healthcare professionals can use the results of this study to understand the importance of the pituitary-thyroid-cardiac axis in lipid metabolism and its impact on cardiometabolic health.
Abstract
BACKGROUND Thyroid dysfunction is associated with cardiovascular diseases. However, the role of thyroid function in lipid metabolism remains partly unknown. The present study aimed to investigate the causal association between thyroid function and serum lipid metabolism via a genetic analysis termed Mendelian randomization (MR). METHODS The MR approach uses a genetic variant as the instrumental variable in epidemiological studies to mimic a randomized controlled trial. A two-sample MR was performed to assess the causal association, using summary statistics from the Atrial Fibrillation Genetics Consortium (n = 537,409) and the Global Lipids Genetics Consortium (n = 188,577). The clinical measures of thyroid function include thyrotropin (TSH), free triiodothyronine (FT3) and free thyroxine (FT4) levels, FT3:FT4 ratio and concentration of thyroid peroxidase antibodies (TPOAb). The serum lipid metabolism traits include total cholesterol (TC) and triglycerides, high-density lipoprotein, and low-density lipoprotein (LDL) levels. The MR estimate and MR inverse variance-weighted method were used to assess the association between thyroid function and serum lipid metabolism. RESULTS The results demonstrated that increased TSH levels were significantly associated with higher TC (β = 0.052, P = 0.002) and LDL (β = 0.041, P = 0.018) levels. In addition, the FT3:FT4 ratio was significantly associated with TC (β = 0.240, P = 0.033) and LDL (β = 0.025, P = 0.027) levels. However, no significant differences were observed between genetically predicted FT4 and TPOAb and serum lipids. CONCLUSION Taken together, the results of the present study suggest an association between thyroid function and serum lipid metabolism, highlighting the importance of the pituitary-thyroid-cardiac axis in dyslipidemia susceptibility.
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Gut and Reproductive Tract Microbiota Adaptation during Pregnancy: New Insights for Pregnancy-Related Complications and Therapy.
Siena, M, Laterza, L, Matteo, MV, Mignini, I, Schepis, T, Rizzatti, G, Ianiro, G, Rinninella, E, Cintoni, M, Gasbarrini, A
Microorganisms. 2021;9(3)
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During pregnancy, several adaptations occur in the female organism. In fact, from fertilization until delivery, the maternal body changes and activates a series of physiological transformations to welcome the new life. The microbiota as a component of human bodies is subject to these modifications. This study is a review that focused on gut and reproductive tract microbiota variations during physiologic pregnancy and in case of pregnancy complications, particularly gestational diabetes mellitus (GDM), pre-eclampsia (PE), and preterm birth (PTB). Results show that: - during pregnancy, major changes have been seen in mothers’ gut microbiota. Between the first and third trimester of pregnancy, to support the foetus growth, there is a shift towards communities of microbes implicated in energy production and storage. - in nonpregnant women, vaginal microbiota could be classified into five major types, representing the community state types. - meconium’s microbes seems to be dominated by the Enterobacteriaceae family, suggesting prenatally stepwise colonization. - gut microbiota may contribute to enhanced insulin resistance in early pregnancy (1st and 2nd trimester). - microbiota imbalances in PE women are related not only with blood pressure levels but also with markers of kidney dysfunction. Thus, it is of key importance to understand the role of microbiota and other factors involved in the etiopathogenesis of PE - dysbiosis is related to PTB (however, further studies are necessary to better understand the correlation between this pregnancy complication and the specific microbiota alteration). Authors conclude that microbiota modulation could be a novel strategy to reduce the morbidity and mortality related to pregnancy complications in the future.
Abstract
Pregnancy is characterized by maternal adaptations that are necessary to create a welcoming and hospitable environment for the fetus. Studies have highlighted how the microbiota modulates several networks in humans through complex molecular interactions and how dysbiosis (defined as quantitative and qualitative alterations of the microbiota communities) is related to human pathologies including gynecological diseases. This review analyzed how maternal uterine, vaginal, and gut microbiomes could impact on fetus health during the gestational period. We evaluated the role of a dysbiotic microbiota in preterm birth, chorioamnionitis, gestational diabetes mellitus and pre-eclampsia. For many years it has been hypothesized that newborns were sterile organisms but in the past few years this paradigm has been questioned through the demonstration of the presence of microbes in the placenta and meconium. In the future, we should go deeper into the concept of in utero colonization to better understand the role of microbiota through the phases of pregnancy. Numerous studies in the literature have already showed interesting results regarding the role of microbiota in pregnancy. This evidence gives us the hope that microbiota modulation could be a novel strategy to reduce the morbidity and mortality related to pregnancy complications in the future.
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Do These Microbes Make Me Look Fat?
Metagenics Institute is a trusted, peer-to-peer, evidence-based educational resource for nutrition and personalized medicine. Its mission is to transform healthcare by inspiring and educating practitioners, and their patients, about personalized lifestyle medicine.
2021
Abstract
This article reflects upon the epidemic of obesity, analysing the role that socioeconomic factors, dietary patterns, lifestyle, environmental toxins, and genetics are playing in metabolic disorders development. Moreover, it presents us with some compelling food for thought regarding the impact that a healthy/unhealthy gut can play in obesity and cardiovascular disease development, and how microbiome research is showing promising results in the field.
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Genetic risk-factors for anxiety in healthy individuals: polymorphisms in genes important for the HPA axis.
Lindholm, H, Morrison, I, Krettek, A, Malm, D, Novembre, G, Handlin, L
BMC medical genetics. 2020;21(1):184
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Anxiety is a complex disorder that involves alterations in hormones secreted from glands in the brain. Genetic variations in these hormones can mean that some individuals are more susceptible to anxiety disorders. The aim of this observational study was to investigate possible relationships between genetic changes in brain hormones and anxiety in 72 individuals. The results showed that women were more likely than men to report feelings of anxiety and there were several relationships between genetic variations in brain hormones and self-reported measures of anxiety. It was concluded that genetic variations in brain hormones are associated with anxiety disorders in healthy individuals. This study could be used by healthcare professionals to understand how genetics could play a role in anxiety and that certain genes could be used to identify individuals at risk of anxiety disorders.
Abstract
BACKGROUND Two important aspects for the development of anxiety disorders are genetic predisposition and alterations in the hypothalamic-pituitary-adrenal (HPA) axis. In order to identify genetic risk-factors for anxiety, the aim of this exploratory study was to investigate possible relationships between genetic polymorphisms in genes important for the regulation and activity of the HPA axis and self-assessed anxiety in healthy individuals. METHODS DNA from 72 healthy participants, 37 women and 35 men, were included in the analyses. Their DNA was extracted and analysed for the following Single Nucleotide Polymorphisms (SNP)s: rs41423247 in the NR3C1 gene, rs1360780 in the FKBP5 gene, rs53576 in the OXTR gene, 5-HTTLPR in SLC6A4 gene and rs6295 in the HTR1A gene. Self-assessed anxiety was measured by the State and Trait Anxiety Inventory (STAI) questionnaire. RESULTS Self-assessed measure of both STAI-S and STAI-T were significantly higher in female than in male participants (p = 0.030 and p = 0.036, respectively). For SNP rs41423247 in the NR3C1 gene, there was a significant difference in females in the score for STAI-S, where carriers of the G allele had higher scores compared to the females that were homozygous for the C allele (p < 0.01). For the SNP rs53576 in the OXTR gene, there was a significant difference in males, where carriers of the A allele had higher scores in STAI-T compared to the males that were homozygous for the G allele (p < 0.01). CONCLUSION This study shows that SNP rs41423247 in the NR3C1 gene and SNP rs53576 in the OXTR gene are associated with self-assessed anxiety in healthy individuals in a gender-specific manner. This suggests that these SNP candidates are possible genetic risk-factors for anxiety.
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Randomized trial of weight loss in primary breast cancer: Impact on body composition, circulating biomarkers and tumor characteristics.
Demark-Wahnefried, W, Rogers, LQ, Gibson, JT, Harada, S, Frugé, AD, Oster, RA, Grizzle, WE, Norian, LA, Yang, ES, Della Manna, D, et al
International journal of cancer. 2020;146(10):2784-2796
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Obesity directly impacts survival in individuals with breast cancer. Previous studies in animals and at the cellular level have shown that calorie restriction and increased physical activity to achieve a negative energy balance may inhibit cancer progression, however effects in patients are unknown. This randomised control trial aimed to determine the impact of a pre surgery weight loss programme in 32 women with breast cancer on tumour biology and other markers of disease. The results were mixed and showed that proteins which bind to hormones involved in breast cancer were increased, which could decrease severity of disease. However, tumour biology was negatively affected; specific genes involved in breast cancer progression were increased and those involved in tumour suppression were decreased. Although this did result in no net effect on the rate at which new tumours were formed. It was concluded that although the study showed mixed results, ultimately the rate at which new tumours were formed remained unaffected. This trial could be used by healthcare professionals to understand that the role of negative energy intake in breast cancer development is complicated and warrants further research.
Abstract
Obesity adversely impacts overall and cancer-specific survival among breast cancer patients. Preclinical studies demonstrate negative energy balance inhibits cancer progression; however, feasibility and effects in patients are unknown. A two-arm, single-blinded, randomized controlled weight-loss trial was undertaken presurgery among 32 overweight/obese, Stage 0-II breast cancer patients. The attention control arm (AC) received basic nutritional counseling and upper-body progressive resistance training whereas the weight loss intervention (WLI) arm received identical guidance, plus counseling on caloric restriction and aerobic exercise to promote 0.68-0.92 kg/week weight loss. Anthropometrics, body composition, blood and survey data were collected at baseline and presurgery ∼30 days later. Tumor markers (e.g., Ki67) and gene expression were assessed on biopsy and surgical specimens; sera were analyzed for cytokines, growth and metabolic factors. Significant WLI vs. AC differences were seen in baseline-to-follow-up changes in weight (-3.62 vs. -0.52 kg), %body fat (-1.3 vs. 0%), moderate-to-vigorous physical activity (+224 vs. +115 min/week), caloric density (-0.3 vs. 0 kcal/g), serum leptin (-12.3 vs. -4.0 ng/dl) and upregulation of tumor PI3Kinase signaling and cell cycle-apoptosis related genes (CC-ARG; all p-values <0.05). Cytolytic CD56dim NK cell expression was positively associated with weight loss; CC-ARG increased with physical activity. Increased tumor (nuclear) TNFα and IL-1β, CX3CL1 and CXCL1 gene expression was observed in the WLI. Tumor Ki67 did not differ between arms. Feasibility benchmarks included 80% accrual, 100% retention, no adverse effects and excellent adherence. Short-term weight loss interventions are feasible; however, mixed effects on tumor biology suggest unclear benefit to presurgical caloric restriction, but possible benefits of physical activity.
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Maternal dysglycaemia, changes in the infant's epigenome modified with a diet and physical activity intervention in pregnancy: Secondary analysis of a randomised control trial.
Antoun, E, Kitaba, NT, Titcombe, P, Dalrymple, KV, Garratt, ES, Barton, SJ, Murray, R, Seed, PT, Holbrook, JD, Kobor, MS, et al
PLoS medicine. 2020;17(11):e1003229
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Diabetes and raised blood sugar levels that develop during pregnancy are associated with poor health outcomes in the offspring, increasing their future risk for disorders such as obesity. It is believed that this is due to the mothers raised blood sugar levels modifying genes during gestation, however previous evidence is mainly observational, highlighting a need for substantial trials. This secondary analysis of a randomised control trial of 557 women with obesity aimed to identify genetic modifications in infants and assess whether lifestyle interventions targeted at levelling blood sugars in the mother would change these. The results showed that diabetes and raised blood sugar during pregnancy was associated with genetic modifications in offspring and these were reduced with diet and physical activity during the second trimester. It was concluded that diabetes and raised blood sugar during pregnancy alters the genes of the offspring and lifestyle interventions in the second trimester could improve the health outcomes of future generations. This study could be used by health professionals to understand the importance of introducing diet and exercise in the second trimester to improve the health of mothers and their unborn children.
Abstract
BACKGROUND Higher maternal plasma glucose (PG) concentrations, even below gestational diabetes mellitus (GDM) thresholds, are associated with adverse offspring outcomes, with DNA methylation proposed as a mediating mechanism. Here, we examined the relationships between maternal dysglycaemia at 24 to 28 weeks' gestation and DNA methylation in neonates and whether a dietary and physical activity intervention in pregnant women with obesity modified the methylation signatures associated with maternal dysglycaemia. METHODS AND FINDINGS We investigated 557 women, recruited between 2009 and 2014 from the UK Pregnancies Better Eating and Activity Trial (UPBEAT), a randomised controlled trial (RCT), of a lifestyle intervention (low glycaemic index (GI) diet plus physical activity) in pregnant women with obesity (294 contol, 263 intervention). Between 27 and 28 weeks of pregnancy, participants had an oral glucose (75 g) tolerance test (OGTT), and GDM diagnosis was based on diagnostic criteria recommended by the International Association of Diabetes and Pregnancy Study Groups (IADPSG), with 159 women having a diagnosis of GDM. Cord blood DNA samples from the infants were interrogated for genome-wide DNA methylation levels using the Infinium Human MethylationEPIC BeadChip array. Robust regression was carried out, adjusting for maternal age, smoking, parity, ethnicity, neonate sex, and predicted cell-type composition. Maternal GDM, fasting glucose, 1-h, and 2-h glucose concentrations following an OGTT were associated with 242, 1, 592, and 17 differentially methylated cytosine-phosphate-guanine (dmCpG) sites (false discovery rate (FDR) ≤ 0.05), respectively, in the infant's cord blood DNA. The most significantly GDM-associated CpG was cg03566881 located within the leucine-rich repeat-containing G-protein coupled receptor 6 (LGR6) (FDR = 0.0002). Moreover, we show that the GDM and 1-h glucose-associated methylation signatures in the cord blood of the infant appeared to be attenuated by the dietary and physical activity intervention during pregnancy; in the intervention arm, there were no GDM and two 1-h glucose-associated dmCpGs, whereas in the standard care arm, there were 41 GDM and 160 1-h glucose-associated dmCpGs. A total of 87% of the GDM and 77% of the 1-h glucose-associated dmCpGs had smaller effect sizes in the intervention compared to the standard care arm; the adjusted r2 for the association of LGR6 cg03566881 with GDM was 0.317 (95% confidence interval (CI) 0.012, 0.022) in the standard care and 0.240 (95% CI 0.001, 0.015) in the intervention arm. Limitations included measurement of DNA methylation in cord blood, where the functional significance of such changes are unclear, and because of the strong collinearity between treatment modality and severity of hyperglycaemia, we cannot exclude that treatment-related differences are potential confounders. CONCLUSIONS Maternal dysglycaemia was associated with significant changes in the epigenome of the infants. Moreover, we found that the epigenetic impact of a dysglycaemic prenatal maternal environment appeared to be modified by a lifestyle intervention in pregnancy. Further research will be needed to investigate possible medical implications of the findings. TRIAL REGISTRATION ISRCTN89971375.
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Genomics in Personalized Nutrition: Can You "Eat for Your Genes"?
Mullins, VA, Bresette, W, Johnstone, L, Hallmark, B, Chilton, FH
Nutrients. 2020;12(10)
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Genetics may have a huge influence on how nutrients are processed within the body, challenging the one-size-fits-all dietary approach and highlighting the possible need for personalised nutrition based on genetics. There are a growing number of companies that offer genetic nutritional testing, however the science behind this is still in its infancy. This review of 130 papers aimed to discuss the role of genetics in nutrition and the possibility for precision nutrition. The paper stated that dietary components, especially those found in the modern Western diet (WD), may detrimentally interact with genetics. Overconsumption of certain nutrients, changes in nutrient exposure throughout history and the ability of certain nutrients to make small genetic changes are all ways that genetics and diet can interact. Therefore, understanding how an individual’s genetics have been and continue to be affected by diet may ensure effective nutrition recommendations. Ethical implications should be considered prior to testing and whether results will motivate or dissuade an individual to make dietary changes assessed. It was concluded that personalised nutrition recommendations in the future will rely upon understanding an individual’s genetics, however current research has a limited understanding of the numerous diet-genetic interactions. This paper could be used by healthcare professionals to evaluate the need for genetic testing to make personalised recommendations.
Abstract
Genome-wide single nucleotide polymorphism (SNP) data are now quickly and inexpensively acquired, raising the prospect of creating personalized dietary recommendations based on an individual's genetic variability at multiple SNPs. However, relatively little is known about most specific gene-diet interactions, and many molecular and clinical phenotypes of interest (e.g., body mass index [BMI]) involve multiple genes. In this review, we discuss direct to consumer genetic testing (DTC-GT) and the current potential for precision nutrition based on an individual's genetic data. We review important issues such as dietary exposure and genetic architecture addressing the concepts of penetrance, pleiotropy, epistasis, polygenicity, and epigenetics. More specifically, we discuss how they complicate using genotypic data to predict phenotypes as well as response to dietary interventions. Then, several examples (including caffeine sensitivity, alcohol dependence, non-alcoholic fatty liver disease, obesity/appetite, cardiovascular, Alzheimer's disease, folate metabolism, long-chain fatty acid biosynthesis, and vitamin D metabolism) are provided illustrating how genotypic information could be used to inform nutritional recommendations. We conclude by examining ethical considerations and practical applications for using genetic information to inform dietary choices and the future role genetics may play in adopting changes beyond population-wide healthy eating guidelines.