2022 |
Lucock MD, Jones PR, Veysey M, Thota R, Garg M, Furst J, et al., 'Biophysical evidence to support and extend the vitamin D-folate hypothesis as a paradigm for the evolution of human skin pigmentation', American Journal of Human Biology, 34 (2022) [C1]
Objective: To test the ¿vitamin D-folate hypothesis for the evolution of human skin pigmentation.¿. Methods: Total ozone mapping spectrometer (TOMS) satellite data were used to ex... [more]
Objective: To test the ¿vitamin D-folate hypothesis for the evolution of human skin pigmentation.¿. Methods: Total ozone mapping spectrometer (TOMS) satellite data were used to examine surface UV-irradiance in a large (n¿= 649) Australian cross-sectional study population. Genetic analysis was used to score vitamin D- and folate-related gene polymorphisms (n¿= 22), along with two pigmentation gene variants (IRF4-rs12203592/HERC2-rs12913832). Red cell folate and vitamin D3 were measured by immunoassay and HPLC, respectively. Results: Ultraviolet radiation (UVR) and pigmentation genes interact to modify blood vitamin levels; Light skin IRF4-TT genotype has greatest folate loss while light skin HERC2-GG genotype has greatest vitamin D3 synthesis (reflected in both TOMS and seasonal data). UV-wavelength exhibits a dose¿response relationship in folate loss within light skin IRF4-TT genotype (305 > 310 > 324 > 380 nm). Significant vitamin D3 photosynthesis only occurs within light skin HERC2-GG genotype, and is maximal at 305 nm. Three dietary antioxidants (vitamins C, E, and ß-carotene) interact with UVR and pigmentation genes preventing oxidative loss of labile reduced folate vitamers, with greatest benefit in light skin IRF4-TT subjects. The putative photosensitiser, riboflavin, did not sensitize red cell folate to UVR and actually afforded protection. Four genes (5xSNPs) influenced blood vitamin levels when stratified by pigmentation genotype; MTHFR-rs1801133/rs1801131, TS-rs34489327, CYP24A-rs17216707, and VDR-ApaI-rs7975232. Lightest IRF4-TT/darkest HERC2-AA genotype combination (greatest folate loss/lowest vitamin D3 synthesis) has 0% occurrence. The opposing, commonest (39%) compound genotype (darkest IRF4-CC/lightest HERC2-GG) permits least folate loss and greatest synthesis of vitamin D3. Conclusion: New biophysical evidence supports the vitamin D-folate hypothesis for evolution of skin pigmentation.
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Nova |
2020 |
Jones P, Lucock M, Martin C, Thota R, Garg M, Yates Z, et al., 'Independent and interactive influences of environmental UVR, vitamin D levels, and folate variant MTHFD1-RS2236225 on homocysteine levels', Nutrients, 12 (2020) [C1]
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Nova |
2019 |
Lucock M, Thota R, Garg M, Martin C, Jones P, Furst J, et al., 'Early lifecycle UV-exposure calibrates adult vitamin D metabolism: Evidence for a developmentally originated vitamin D homeostat that may alter related adult phenotypes', American Journal of Human Biology, 31 (2019) [C1]
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Nova |
2018 |
Lucock M, Jones P, Martin C, Yates Z, Veysey M, Furst J, Beckett E, 'Photobiology of vitamins', Nutrition reviews, 76 512-525 (2018) [C1]
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Nova |
2018 |
Lucock M, Thota R, Garg M, Martin C, Jones P, Furst J, et al., 'Vitamin D and folate: A reciprocal environmental association based on seasonality and genetic disposition', AMERICAN JOURNAL OF HUMAN BIOLOGY, 30 (2018) [C1]
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Nova |
2017 |
Lucock M, Beckett E, Martin C, Jones P, Furst J, Yates Z, et al., 'UV-associated decline in systemic folate: implications for human nutrigenetics, health, and evolutionary processes', AMERICAN JOURNAL OF HUMAN BIOLOGY, 29 (2017) [C1]
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Nova |
2017 |
Beckett EL, Jones P, Veysey M, Duesing K, Martin C, Furst J, et al., 'VDR gene methylation as a molecular adaption to light exposure: Historic, recent and genetic influences', AMERICAN JOURNAL OF HUMAN BIOLOGY, 29 (2017) [C1]
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Nova |
2017 |
Beckett EL, Martin C, Boyd L, Porter T, King K, Niblett S, et al., 'Reduced plasma homocysteine levels in elderly Australians following mandatory folic acid fortification A comparison of two cross-sectional cohorts', Journal of Nutrition and Intermediary Metabolism, 8 14-20 (2017) [C1]
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Nova |
2017 |
Beckett EL, Duesing K, Boyd L, Yates Z, Veysey M, Lucock M, 'A potential sex dimorphism in the relationship between bitter taste and alcohol consumption', FOOD & FUNCTION, 8 1116-1123 (2017) [C1]
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Nova |
2016 |
Yates Z, Lucock M, Veysey M, Choi JH, 'Elevated folic acid results in contrasting cancer cell line growth with implications for mandatory folic acid fortification', Journal of Nutrition and Health, 49 72-79 (2016) [C1]
Purpose: The initiation of mandatory folic acid fortification using pteroylmonoglutamic acid (PteGlu) has reduced the rate of congenital malformations. However, it also appears to... [more]
Purpose: The initiation of mandatory folic acid fortification using pteroylmonoglutamic acid (PteGlu) has reduced the rate of congenital malformations. However, it also appears to be responsible for several adverse effects, including increased cancer incidence. This may be related to physicho-chemical characteristics of PteGlu. This study examines the potential effect of high concentrations of PteGlu on a population subjected to mandatory folic acid fortification using an in vitro model. Methods: Caco-2 (colorectal cancer) and MCF7 (breast cancer) cell lines were cultured at 6 different PteGlu concentrations (0, 0.1, 1, 50, 250, and 500µg/ml) for 6 days. Cell growth was determined using thiazolyl blue tetrazolium bromide assay. The genotype of dihydrofolate reductase 19bp deletion/insertion (DHFR 19-del) was also scored in cell lines using a restriction fragment length polymorphism technique to examine whether genetic variations may factor in cell proliferation. Results: PteGlu exhibited differential growth promoting properties between cell lines. Caco-2 cells did not show a significant growth difference at low concentrations compared to control, however, at higher concentrations, the growth showed a contrasting trend in the early experimental period, while MCF7 showed enhanced cell growth at all concentrations. The DHFR 19-del genotype differed in the two cell lines. Conclusions: Altered response to PteGlu by Caco-2 and MCF7 may reflect a tissue specific disease aetiology or genotype specific differential enzyme activity, for example by DHFR, to critical levels of PteGlu. As folic acid fortification is a blanket intervention, and DHFR and other enzyme activities vary between individuals, PteGlu intake may have an as yet undefined effect on health. These findings may be relevant when considering mandatory folic acid fortification for disease prevention.
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Nova |
2016 |
Jones P, Beckett EL, Yates Z, Veysey M, Lucock M, 'Converging Evolutionary, Environmental and Clinical Ideas on
Folate Metabolism', Exploratory Research and Hypothesis in Medicine, 1 34-41 (2016) [C1]
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Nova |
2016 |
Beckett EL, Le Gras K, Martin C, Boyd L, Ng X, Duesing K, et al., 'Vitamin D receptor polymorphisms relate to risk of adenomatous polyps in a sex-specific manner', Nutrition and Cancer, 68 193-200 (2016) [C1]
Vitamin D receptor (VDR) gene polymorphisms may influence risk for adenomatous polyps (AP), a benign precursor to colon cancer, via modulation of vitamin D sensitive pathways, inc... [more]
Vitamin D receptor (VDR) gene polymorphisms may influence risk for adenomatous polyps (AP), a benign precursor to colon cancer, via modulation of vitamin D sensitive pathways, including cell proliferation and differentiation. However, results have been mixed and any association remains contentious. Failure to clinically exclude the presence of (AP in control cohorts may contribute to the lack of consensus. Therefore, we assessed the role of the FokI, BsmI, ApaI, and TaqI VDR polymorphisms in modifying risk for AP, adjusting for a range of dietary and lifestyle variables. Blood was collected from colonoscopy patients (n = 258) and VDR polymorphisms assessed by restriction fragment length polymorphism. Dietary habits were estimated from food frequency questionnaires. Odds ratios for AP were calculated by genotype, stratified by sex, and adjusted for age, lifestyle, and dietary factors. FokI was associated with modified risk for AP in males, whereas the BsmI/ApaI/TaqI haplotype was associated with modified risk in females. No interaction was found between VDR variants and vitamin D intake. This study offers novel insight into the potential for VDR genetics to contribute to risk for AP and is the first to demonstrate a sex-specific relationship between these polymorphisms and risk for AP.
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Nova |
2016 |
Beckett EL, Duesing K, Martin C, Jones P, Furst J, King K, et al., 'Relationship between methylation status of Vitamin D-related genes, Vitamin D levels, and methyl-donor biochemistry', Journal of Nutrition and Intermediary Metabolism, 6 8-15 (2016) [C1]
Vitamin D is known for its role in the regulation of gene expression via the Vitamin D receptor, a nuclear transcription factor. More recently, a role for Vitamin D in regulating ... [more]
Vitamin D is known for its role in the regulation of gene expression via the Vitamin D receptor, a nuclear transcription factor. More recently, a role for Vitamin D in regulating DNA methylation has been identified as an additional mechanism of modulation of gene expression. How methylation status influences Vitamin D metabolism and response pathways is not yet clear. Therefore, we aimed to assess the relationship between plasma 25-hydroxycholecalciferol (25(OH)D) and the methylation status of Vitamin D metabolism enzyme genes (CYP2R1, CYP27B1 and CYP24A1) and the Vitamin D receptor gene (VDR). This analysis was conducted in the context of dietary Vitamin D, and background methyl donor related biochemistry, with adjustment for several dietary and lifestyle variables. Percentage methylation at CpG sites was assessed in peripheral blood cells using methylation sensitive and dependent enzymes and qPCR. Standard analytical techniques were used to determine plasma 25(OH)D and homocysteine, and serum folate and B12, with the relationship to methylation status assessed using multi-variable regression analysis. CYP2R1 and VDR methylation were found to be independent predictors of plasma 25(OH)D, when adjusted for Vitamin D intake and other lifestyle variables. CYP24A1 was related to plasma 25(OH)D directly, but not in the context of Vitamin D intake. Methyl-group donor biochemistry was associated with the methylation status of some genes, but did not alter the relationship between methylation and plasma 25(OH)D. Modulation of methylation status of CYP2R1, CYP24A1 and VDR in response to plasma 25(OH)D may be part of feedback loops involved in maintaining Vitamin D homeostasis, and may explain a portion of the variance in plasma 25(OH)D levels in response to intake and sun exposure. Methyl-group donor biochemistry, while a potential independent modulator, did not alter this effect.
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Nova |
2015 |
Lucock M, Jones P, Martin C, Beckett E, Yates Z, Furst J, Veysey M, 'Vitamin D: Beyond Metabolism', Journal of Evidence-Based Complementary and Alternative Medicine, 20 310-322 (2015) [C1]
Interest in vitamin D and the VDR gene is increasing as putative roles in human health and evolutionary processes are explored. This review looks beyond the classic biochemistry t... [more]
Interest in vitamin D and the VDR gene is increasing as putative roles in human health and evolutionary processes are explored. This review looks beyond the classic biochemistry that links vitamin D to calcium homeostasis; it explores how vitamin D interacts with light in a broader perspective than simple skin photosynthesis. It examines how the vitamin influences circadian rhythm, and how it may have helped drive the evolution of skin pigmentation. To this end, the nutrient¿nutrient relationship with folate is also explored. The VDR gene is additionally examined as a factor in the evolutionary selection of skin depigmentation at higher latitudes to allow vitamin D synthesis. Evidence is given to show that VDR polymorphisms exhibit a latitudinal gradient in allele prevalence consistent with such a paradigm. Overall, the review examines new evo-devo ideas that link light-sensitive vitamins to human health/phenotype, both within and across the lifecycle.
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Nova |
2015 |
Lucock M, Yates Z, Martin C, Choi JH, Beckett E, Boyd L, et al., 'Methylation diet and methyl group genetics in risk for adenomatous polyp occurrence', BBA Clinical, 3 107-112 (2015) [C1]
Purpose: The aim of this study is to explore whether a methylation diet influences risk for adenomatous polyps (AP) either independently, or interactively with one-carbon metaboli... [more]
Purpose: The aim of this study is to explore whether a methylation diet influences risk for adenomatous polyps (AP) either independently, or interactively with one-carbon metabolism-dependent gene variants, and whether such a diet modifies blood homocysteine, a biochemical phenotype closely related to the phenomenon of methylation. Methods: 249 subjects were examined using selective fluorescence, PCR and food frequency questionnaire to determine homocysteine, nine methylation-related gene polymorphisms, dietary methionine, 5-methyltetrahydrofolate, vitamins B6 and B12. Results: 1). Both dietary methionine and 5-methyltetrahydrofolate intake are significantly associated with plasma homocysteine. 2). Dietary methionine is related to AP risk in 2R3R-TS wildtype subjects, while dietary B12 is similarly related to this phenotype in individuals heterozygous for C1420T-SHMT, A2756G-MS and 844ins68-CBS, and in those recessive for 2R3R-TS. 3). Dietary methionine has a marginal influence on plasma homocysteine level in C1420T-SHMT heterozygotes, while B6 exhibits the same effect on homocysteine in C776G-TCN2 homozygote recessive subjects. Natural 5-methyltetrahydrofolate intake is interesting: Wildtype A1298C-MTHFR, heterozygote C677T-MTHFR, wildtype A2756G-MS and recessive A66G-MSR individuals all show a significant reciprocal association with homocysteine. 4). Stepwise regression of all genotypes to predict risk for AP indicated A2756G-MS and A66G-MSR to be most relevant (p= 0.0176 and 0.0408 respectively). Results were corrected for age and gender. Conclusion: A methylation diet influences methyl group synthesis in the regulation of blood homocysteine level, and is modulated by genetic interactions. Methylation-related nutrients also interact with key genes to modify risk of AP, a precursor of colorectal cancer. Independent of diet, two methylation-related genes (A2756G-MS and A66G-MSR) were directly associated with AP occurrence.
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Nova |
2015 |
Choi J-H, Yates Z, Martin C, Boyd L, Ng X, Skinner V, et al., 'Gene-Nutrient Interaction between Folate and Dihydrofolate Reductase in Risk for Adenomatous Polyp Occurrence: A Preliminary Report', JOURNAL OF NUTRITIONAL SCIENCE AND VITAMINOLOGY, 61 455-459 (2015) [C1]
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Nova |
2015 |
Choi JH, Yates Z, Martin C, Boyd L, Ng X, Skinner V, et al., 'Genetic variation in glutamate carboxypeptidase II and interaction with dietary natural vitamin C may predict risk for adenomatous polyp occurrence', Asian Pacific Journal of Cancer Prevention, 16 4383-4386 (2015) [C1]
Background: The C1561T variant of the glutamate carboxypeptidase II (GCPII) gene is critical for natural methylfolylpolyglutamte (methylfolate) absorption, and has been associated... [more]
Background: The C1561T variant of the glutamate carboxypeptidase II (GCPII) gene is critical for natural methylfolylpolyglutamte (methylfolate) absorption, and has been associated with perturbations in folate metabolism and disease susceptibility. However, little is known on C1561T-GCPII as a risk factor for colorectal cancer. Therefore, this study examined whether C1561T-GCPII influences folate metabolism and adenomatous polyp occurrence. Materials and Methods: 164 controls and 38 adenomatous polyp cases were analysed to determine blood folate and plasma homocysteine (Hcy) level, dietary intake of natural methylfolate, synthetic pteroylglutamic acid (PteGlu), vitamin C and C1561T-GCPII genotype. Results: In controls and cases, 7.3 and 18.4 percent of subjects respectively, were found to have the CT genotype, increasing the risk for adenomatous polyp occurrence 2.86 times (95% CI:1.37-8.0, p=0.035). Total dietary folate, methylfolate and PteGlu intake and the level of erythrocyte folate and plasma Hcy did not predict the occurrence of an adenomatous polyp. However, dietary natural vitamin C intake was associated with adenomatous polyp risk within C1561T-GCPII CT genotype subjects (p=0.037). Conclusions: The findings suggest that C1561T-GCPII variation may be associated with risk for adenomatous polyp, and vitamin C may modify risk by interacting with the variant gene, its expression product and/or folate substrates.
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Nova |
2015 |
Beckett EL, Martin C, Duesing K, Jones P, Furst J, Yates Z, et al., 'Vitamin D receptor genotype modulates the correlation between vitamin D and circulating levels of let-7a/b and vitamin D intake in an elderly cohort', Journal of Nutrigenetics and Nutrigenomics, 7 264-273 (2015) [C1]
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Nova |
2015 |
Beckett EL, Martin C, Choi JH, King K, Niblett S, Boyd L, et al., 'Folate status, folate-related genes and serum miR-21 expression: Implications for miR-21 as a biomarker', BBA Clinical, 4 45-51 (2015) [C1]
Background: Free circulating microRNA (miRNA) in serum may be valuable biomarkers for disease diagnosis and prognosis. miR-21, the archetypal oncogenic miRNA, has been proposed as... [more]
Background: Free circulating microRNA (miRNA) in serum may be valuable biomarkers for disease diagnosis and prognosis. miR-21, the archetypal oncogenic miRNA, has been proposed as a biomarker for colorectal cancer and its benign precursor, adenomatous polyps. However, it is now becoming clear that circulating miRNA profiles may be sensitive to lifestyle and environmental influences. Dietary components involved in one-carbon metabolism are particularly well placed to modulate miRNA expression through an influence on DNA methylation pathways. Methods: We investigated the role of methyl group donors (folate, B12, cysteine, homocysteine), polymorphisms of the enzymes of one-carbon metabolism, and serum miR-21 expression in a primary case-control cohort (colonoscopy confirmed adenomatous colon polyps vs controls; n. =. 253) and a secondary cross-sectional cohort (over 65s; n. =. 649). The relationships between these parameters and serum miR-21 levels were assessed, stratified by gender. Conclusions: Serum miR-21 expression was related to occurrence of adenomatous polyps in females, but not males. Folate levels and MTHFR-C677T genotype was associated with miR-21 expression in both genders. Additionally, DHFR-19 del and MSR-A66G were associated with miR-21 expression in females and males, respectively. Stimulation with excess folate increased expression of miR-21 in colon cancer cell lines. General significance: This study demonstrates that serum miR-21 expression correlates with folate status and related genetic status. This may have consequences for the proposed use of miR-21 as a colorectal cancer biomarker.
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Nova |
2015 |
Beckett EL, Le Gras KC, Veysey M, Boyd L, Ng X, Yates Z, et al., 'Vitamin D receptor polymorphism Fok1 alters risk for adenomatous polyps in Australian males', Journal of Nutrigenetics and Nutrigenomics, 8 2-2 (2015)
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2014 |
Choi JH, Yates Z, Veysey M, Heo YR, Lucock M, 'Contemporary issues surrounding folic acid fortification initiatives', Preventive Nutrition and Food Science, 19 247-260 (2014) [C1]
The impact of folate on health and disease, particularly pregnancy complications and congenital malformations, has been extensively studied. Mandatory folic acid fortification the... [more]
The impact of folate on health and disease, particularly pregnancy complications and congenital malformations, has been extensively studied. Mandatory folic acid fortification therefore has been implemented in multiple countries, resulting in a reduction in the occurrence of neural tube defects. However, emerging evidence suggests increased folate intake may also be associated with unexpected adverse effects. This literature review focuses on contemporary issues of concern, and possible underlying mechanisms as well as giving consideration the future direction of mandatory folic acid fortification. Folate fortification has been associated with the presence of unmetabolized folic acid (PteGlu) in blood, masking of vitamin B12 deficiency, increased dosage for anti-cancer medication, photo-catalysis of PteGlu leading to potential genotoxicity, and a role in the pathoaetiology of colorectal cancer. Increased folate intake has also been associated with twin birth and insulin resistance in offspring, and altered epigenetic mechanisms of inheritance. Although limited data exists to elucidate potential mechanisms underlying these issues, elevated blood folate level due to the excess use of PteGlu without consideration of an individual's specific phenotypic traits (e.g. genetic background and undiagnosed disease) may be relevant. Additionally, the accumulation of unmetabolized PteGlu may lead to inhibition of dihydrofolate reductase and other enzymes. Concerns notwithstanding, folic acid fortification has achieved enormous advances in public health. It therefore seems prudent to target and carefully monitor high risk groups, and to conduct well focused further research to better understand and to minimize any risk of mandatory folic acid fortification.
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Nova |
2014 |
Martin C, Yates Z, Veysey M, Lucock MD, 'Vitamin D Receptor Genetics and Calcium Intake in an Elderly Australian Cohort with Osteoporosis', Journal of Nutrigenetics and Nutrigenomics, 7 35-35 (2014)
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2014 |
Yates Z, Lucock MD, Beckett E, Veysey M, 'B-vitamins and cognition - food for thought', NEUROLOGY, (2014)
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2014 |
Beckett E, Martin C, Duesing K, Yates Z, Veysey M, Lucock MD, 'Vitamin D Receptor Genotype Modulates the Correlation Between Circulating Levels of miR-7a/b and Vitamin D Intake in an Elderly Cohort.', Journal of Nutrigenetics and Nutrigenomics, 7 10-10 (2014)
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2014 |
Lucock MD, Martin CE, Yates ZR, Veysey M, 'Diet and Our Genetic Legacy in the Recent Anthropocene: A Darwinian Perspective to Nutritional Health', Journal of Evidence-Based Complementary and Alternative Medicine, 19 68-83 (2014) [C1]
Nutrient-gene research tends to focus on human disease, although such interactions are often a by-product of our evolutionary heritage. This review explores health in this context... [more]
Nutrient-gene research tends to focus on human disease, although such interactions are often a by-product of our evolutionary heritage. This review explores health in this context, reframing genetic variation/epigenetic phenomena linked to diet in the framework of our recent evolutionary past. This "Darwinian/evolutionary medicine" approach examines how diet helped us evolve among primates and to adapt (or fail to adapt) our metabolome to specific environmental conditions leading to major diseases of civilization. This review presents updated evidence from a diet-gene perspective, portraying discord that exists with respect to health and our overall nutritional, cultural, and activity patterns. While Darwinian theory goes beyond nutritional considerations, a significant component within this concept does relate to nutrition and the mismatch between genes, modern diet, obesogenic lifestyle, and health outcomes. The review argues that nutritional sciences should expand knowledge on the evolutionary connection between food and disease, assimilating it into clinical training with greater prominence. © The Author(s) 2013.
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Nova |
2014 |
Lucock M, Yates Z, Martin C, Choi JH, Boyd L, Tang S, et al., 'Vitamin D, folate, and potential early lifecycle environmental origin of significant adult phenotypes.', Evolution, Medicine, and Public Health, 2014 69-91 (2014) [C1]
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Nova |
2014 |
Martin CE, Veysey M, Yates Z, Lucock MD, 'Vitamin D: Genetics, Environment & Health', Food and Nutritional Disorders, 3 1-19 (2014) [C1]
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Nova |
2013 |
Lucock MD, Martin C, Boyd L, Naumovski N, Roach P, Yates Z, Veysey M, 'Response to 'calcium, phosphate and the risk of cardiovascular events and all-cause mortality in a population with stable coronary heart disease'', HEART, 99 349-350 (2013) [C3]
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2013 |
Lucock M, Yates Z, Boyd L, Naylor C, Choi J, Ng X, et al., 'Vitamin C-related nutrient-nutrient and nutrient-gene interactions that modify folate status', European Journal of Nutrition, 52 569-582 (2013) [C1]
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Nova |
2013 |
Lucock M, Yates Z, Martin C, Choi J, Boyd L, Tang S, et al., 'Hydrogen sulphide-related thiol metabolism and nutrigenetics in relation to hypertension in an elderly population', Genes & Nutrition, 8 221-229 (2013) [C1]
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2012 |
Lucock MD, Glanville T, Yates ZR, Walker J, Furst JE, Simpson N, 'Solar cycle predicts folate-sensitive neonatal genotypes at discrete phases of the first trimester of pregnancy: A novel folate-related human embryo loss hypothesis', Medical Hypotheses, 79 210-215 (2012) [C1]
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Nova |
2011 |
Lucock MD, Ng X, Boyd L, Skinner VM, Wai R, Tang S, et al., 'TAS2R38 bitter taste genetics, dietary vitamin C, and both natural and synthetic dietary folic acid predict folate status, a key micronutrient in the pathoaetiology of adenomatous polyps', Food & Function, 2 457-465 (2011) [C1]
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Nova |
2010 |
Lucock MD, Glanville T, Ovadia L, Yates ZR, Walker J, Simpson N, 'Photoperiod at conception predicts C677T-MTHFR genotype: A novel gene-environment interaction', American Journal of Human Biology, 22 484-489 (2010) [C1]
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Nova |
2010 |
Naumovski N, Veysey M, Ng X, Boyd L, Dufficy L, Blades BL, et al., 'The folic acid endophenotype and depression in an elderly population', Journal of Nutrition, Health and Aging, 14 829-833 (2010) [C1]
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2009 |
Ng X, Boyd L, Dufficy L, Naumovski N, Blades BL, Travers C, et al., 'Folate nutritional genetics and risk for hypertension in an elderly population sample', Journal of Nutrigenetics and Nutrigenomics, 2 1-8 (2009) [C1]
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Nova |
2009 |
Yates Z, Tarling E, Langely-Evans S, Salter A, 'Maternal undernutrition programmes atherosclerosis in the APOE3 Leiden mouse', The British Journal of Nutrition: an international journal of nutritional science, 101 1185-1195 (2009) [C1]
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2009 |
Sohn K-J, Jang H, Campan M, Weisenberger DJ, Dickhout J, Wang Y-C, et al., 'The methylenetetrahydrofolate reductase C677T mutation induces cell-specific changes in genomic DNA methylation and uracil misincorporation: A possible molecular basis for the site-specific cancer risk modification', International Journal of Cancer, 124 1999-2005 (2009) [C1]
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Nova |
2009 |
Lucock MD, Yates ZR, 'Folic acid fortification: A double-edged sword', Current Opinion in Clinical Nutrition & Metabolic Care, 12 555-564 (2009) [C1]
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Nova |
2008 |
Palep-Singh M, Picton HM, Yates ZR, Barth J, Balen AH, 'Plasma homocysteine concentrations and the single nucleotide polymorphism in the methionine synthase gene (MTR 2756A\G): Associations with the polycystic ovary syndrome An observational study', European Journal of Obstetrics Gynecology and Reproductive Biology, 138 180-186 (2008) [C1]
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2007 |
Palep-Singh M, Picton H, Yates Z, Barth J, Balen A, 'Polycystic ovary syndrome and the single nucleotide polymorphisms of methylenetetrahydrofolate reductase: a pilot observational study.', Human Fertility: an international multidisciplinary journal dedicated to furthering research and promoting good practice, 10 33-41 (2007) [C1]
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2007 |
Lucock MD, Yates ZR, Ng X, Veysey MJ, Blades BL, Travers C, et al., 'Preliminary evidence for genetic selection of 677T-MTHFR by natural annual cycle of folate abundance', Journal of Nutrigenetics and Nutrigenomics, 1 24-29 (2007) [C1]
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Nova |
2006 |
Dufficy L, Naumovski N, Ng X, Blades BL, Yates ZR, Travers C, et al., 'G80A reduced folate carrier SNP influences the absorption and cellular translocation of dietary folate and its association with blood pressure in an elderly population', Life Sciences, 79 957-966 (2006) [C1]
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2006 |
Glanville T, Yates ZR, Ovadia L, Walker JJ, Lucock MD, Simpson NAB, 'Fetal folate C677T methylenetetrahydrofolate reductase gene polymorphism and low birth weight', Journal of Obstetrics and Gynaecology, 26 11-14 (2006) [C1]
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2006 |
Lucock MD, Yates ZR, 'Synergy between 677 TT MTHFR genotype and related folate SNPs regulates homocysteine level', Nutrition Research, 26 180-185 (2006) [C1]
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2005 |
Lucock MD, Ng X, Veysey MJ, Yates ZR, 'Folic acid: An essential nutrient with added health benefits', Biologist, 52 21-27 (2005) [C1]
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Nova |
2005 |
Lucock MD, Yates Z, 'Folic acid - vitamin and panacea or genetic time bomb?', Nature Reviews Genetics, 6 235-240 (2005) [C1]
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Nova |
2005 |
Yates ZR, Lucock MD, 'G80A reduced folate carrier SNP modulates cellular uptake of folate and affords protection against thrombosis via a non homocysteine related mechanism', Life Sciences, 77 2735-2742 (2005) [C1]
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2005 |
Lucock MD, Yates ZR, 'Human genetic selection by folates', Nature Reviews Genetics, 6 online (2005) [C3]
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2004 |
Sohn K-J, Croxford R, Yates ZR, Lucock MD, Kim Y-I, 'Effect of the methylenetetrahydrofolate reductase C677T polymorphism on chemosensitivity of colon and breast cancer cells to 5-fluorouracil and methotrexate', Journal of the National Cancer Institute, 96 134-144 (2004) [C1]
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Nova |
2004 |
Sohn K-J, Smirnakis F, Moskovitz DN, Novakovic P, Yates ZR, Lucock MD, et al., 'Effects of folylpolyglutamate synthetase modulation on chemosensitivity of colon cancer cells to 5-fluorouracil and methotrexate', GUT, 53 1825-1831 (2004) [C1]
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Nova |
2003 |
Lucock MD, Yates ZR, Glanville T, Leeming R, Simpson N, Daskalakis I, 'A critical role for B-vitamin nutrition in human developmental and evolutionary biology', Nutrition Research, 23 1463-1475 (2003) [C1]
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2003 |
Fenton J, Pratt G, Rawstron A, Sibley K, Rothwell D, Yates Z, et al., 'Genomic characterisation of the chromosomal breakpoints of t(4; 14) of multiple myeloma suggests more than one possible aetiological mechanism', Oncogene, 22 1103-1113 (2003) [C1]
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2003 |
Yates Z, Lucock M, 'Interaction between common folate polymorphisms and B-vitamin nutritional status modulates homocysteine and risk for a thrombotic event', MOLECULAR GENETICS AND METABOLISM, 79 201-213 (2003) [C1]
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2002 |
Lucock M, Yates Z, 'Measurement of red blood cell methylfolate', LANCET, 360 1021-1022 (2002) [C1]
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2002 |
Yates Z, Lucock M, 'Methionine synthase, polymorphism A2756G is associated with susceptibility for thromboembolic events and altered B vitamin/thiol metabolism', HAEMATOLOGICA, 87 751-756 (2002) [C1]
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2002 |
Lucock M, Yates Z, Hall K, Leeming R, Rylance G, MacDonald A, Green A, 'The impact of phenylketonuria on folate metabolism', MOLECULAR GENETICS AND METABOLISM, 76 305-312 (2002) [C1]
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2002 |
Glanville T, Yates Z, Ovadia L, Walker JJ, Lucock MD, Simpson NAB, 'Folate gene Polymorphism and fetal growth restriction.', British Journal of Obstetrics and Gynaecology, 109 481-481 (2002)
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2001 |
Lucock M, Daskalakis I, Yates Z, 'C677T MTHFR genotypes show graded response to vitamin B-12 dependent regeneration of tetrahydrofolate, the main congener of all cellular folates', NUTRITION RESEARCH, 21 1357-1362 (2001) [C1]
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2001 |
Lucock M, Daskalakis I, Hinkins M, Yates Z, 'An examination of polymorphic genes and folate metabolism in mothers affected by a spina bifida pregnancy', MOLECULAR GENETICS AND METABOLISM, 73 322-332 (2001) [C1]
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2001 |
Lucock M, Yates Z, 'Update on folic acid and neural tube defects: 'Comment' article', Clinical Nutrition, 10 25-33 (2001) [C1]
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2001 |
Lucock MD, Yates Z, Cade A, '12 Channel coulometric electrochemical detection for the identification of polyglutamate homology amongst cellular folates.', PTERIDINES, 12 59-59 (2001)
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2001 |
Yates Z, Lucock MD, 'C677T MTHFR genotype is a risk factor for thromboembolism: comparison of T allele frequency and homocysteine level between female thromboembolic and non-thromboembolic vascular patients, NTD mothers and matched NTD controls.', PTERIDINES, 12 92-92 (2001)
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2001 |
Lucock MD, Yates Z, Cade A, 'Gastro-intestinal pH modulates facile interconvertion of native formylfolates during absorption.', PTERIDINES, 12 60-60 (2001)
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2000 |
Lucock M, Daskalakis I, Briggs D, Yates Z, Levene M, 'Altered folate metabolism and disposition in mothers affected by a spina bifida pregnancy: Influence of 677c -\ t methylenetetrahydrofolate reductase and 2756a -\ g methionine synthase genotypes', MOLECULAR GENETICS AND METABOLISM, 70 27-44 (2000) [C1]
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1999 |
Pratt G, Fenton J, Proffitt J, Yates Z, Davies F, Rawstron A, et al., 'Molecular characterisation of chromosome 14q32 translocations in patients with multiple myeloma.', Blood 94, 2435., (1999) [C1] |
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1999 |
Fenton J, Proffitt J, Pratt G, Rawstron A, Yates Z, Davies F, et al., 'Identification of a novel translocation t(14;22)(q32;q12) in multiple myeloma.', British Journal of Cancer, (1999) [C1] |
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1999 |
Pratt G, Fenton J, Proffitt J, Yates Z, Davies F, Rawstron A, et al., 'Rawstron A., Child J., Morgan G. (1999) A novel translocation t(14;22)(q32;q12) in multiple myeloma.', British Journal of Haematology, (1999) [C1] |
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1999 |
Cunningham J, Yates Z, Hamilton J, Mason G, Muller R, Miller D, 'Non-invasive RNA-based determination of fetal Rhesus D type: a prospective study based on 96 pregnancies.', British Journal of Obstetrics and Gynaecology, 1023-1028 (1999) [C1]
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1999 |
Proffitt J, Fenton J, Pratt G, Yates Z, Morgan G, 'Isolation and characterisation of recombination events involving immunoglobulin heavy chain switch regions in multiple myeloma using long distance vectorette PCR (LDV-PCR)', Leukemia, 1100-1107 (1999) [C1]
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1998 |
Pratt G, Fenton J, Proffitt J, Yates Z, Davies F, Rawstron A, et al., 'Rapid characterisation of switch recombination events from patients with multiple myeloma and the characterisation of a novel translocation t(14;22)(q32;q12): Implications for the process of switch recombination and the pathogenesis of myeloma.', Blood 92, 278., (1998) [C1] |
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