Biophysical evidence to support and extend the vitamin D‐folate hypothesis as a paradigm for the evolution of human skin pigmentation

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 s...

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Published inAmerican journal of human biology Vol. 34; no. 4; pp. e23667 - n/a
Main Authors Lucock, Mark D., Jones, Patrice R., Veysey, Martin, Thota, Rohith, Garg, Manohar, Furst, John, Martin, Charlotte, Yates, Zoe, Scarlett, Christopher J., Jablonski, Nina G., Chaplin, George, Beckett, Emma L.
Format Journal Article
LanguageEnglish
Published Hoboken, USA John Wiley & Sons, Inc 01.04.2022
Wiley Subscription Services, Inc
Subjects
Antioxidants
Australia
Blood
Calciferol
Carotene
Cross-Sectional Studies
Evolution
Folic Acid
Gene mapping
Gene polymorphism
Genes
Genetic analysis
Genotype
Genotype & phenotype
High-performance liquid chromatography
Humans
Hypotheses
Immunoassay
Interferon regulatory factor 4
Irradiance
Light levels
Liquid chromatography
Methylenetetrahydrofolate reductase
Photosynthesis
Pigmentation
Population genetics
Population studies
Riboflavin
Skin pigmentation
Skin Pigmentation - genetics
Skin tests
Total Ozone Mapping Spectrometer
Ultraviolet radiation
Ultraviolet Rays - adverse effects
Vitamin B
Vitamin D
Vitamin D receptors
Vitamin D3
Vitamins
β-Carotene
Australia
Online AccessGet full text
ISSN1042-0533
1520-6300
1520-6300
DOI10.1002/ajhb.23667

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Abstract 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 β‐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.
AbstractList 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 β‐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.
To test the "vitamin D-folate hypothesis for the evolution of human skin pigmentation." 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 D were measured by immunoassay and HPLC, respectively. 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 D 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 D photosynthesis only occurs within light skin HERC2-GG genotype, and is maximal at 305 nm. Three dietary antioxidants (vitamins C, E, and β-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 D 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 D . New biophysical evidence supports the vitamin D-folate hypothesis for evolution of skin pigmentation.
ObjectiveTo test the “vitamin D‐folate hypothesis for the evolution of human skin pigmentation.”MethodsTotal 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.ResultsUltraviolet 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 β‐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.ConclusionNew biophysical evidence supports the vitamin D‐folate hypothesis for evolution of skin pigmentation.
To test the "vitamin D-folate hypothesis for the evolution of human skin pigmentation."OBJECTIVETo test the "vitamin D-folate hypothesis for the evolution of human skin pigmentation."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.METHODSTotal 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.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 β-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 .RESULTSUltraviolet 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 β-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 .New biophysical evidence supports the vitamin D-folate hypothesis for evolution of skin pigmentation.CONCLUSIONNew biophysical evidence supports the vitamin D-folate hypothesis for evolution of skin pigmentation.
Author Lucock, Mark D.
Jones, Patrice R.
Martin, Charlotte
Thota, Rohith
Jablonski, Nina G.
Veysey, Martin
Garg, Manohar
Scarlett, Christopher J.
Furst, John
Chaplin, George
Beckett, Emma L.
Yates, Zoe
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  organization: University of Newcastle
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  givenname: Patrice R.
  surname: Jones
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  organization: Hull York Medical School
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  organization: University of Newcastle
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  organization: The Pennsylvania State University
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  surname: Beckett
  fullname: Beckett, Emma L.
  organization: University of Newcastle
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Notes Funding information
National Health and Medical Research Council (NHMRC) Early Career Fellowship; Australian Government Research Training Program scholarship and a Hunter Medical Research Institute (HMRI) Greaves Family Scholarship; Australian Research Council, Grant/Award Number: G0188386
Mark D. Lucock and Patrice R. Jones are joint first authors.
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Snippet Objective To test the “vitamin D‐folate hypothesis for the evolution of human skin pigmentation.” Methods Total ozone mapping spectrometer (TOMS) satellite...
To test the "vitamin D-folate hypothesis for the evolution of human skin pigmentation." Total ozone mapping spectrometer (TOMS) satellite data were used to...
ObjectiveTo test the “vitamin D‐folate hypothesis for the evolution of human skin pigmentation.”MethodsTotal ozone mapping spectrometer (TOMS) satellite data...
To test the "vitamin D-folate hypothesis for the evolution of human skin pigmentation."OBJECTIVETo test the "vitamin D-folate hypothesis for the evolution of...
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StartPage e23667
SubjectTerms Antioxidants
Australia
Blood
Calciferol
Carotene
Cross-Sectional Studies
Evolution
Folic Acid
Gene mapping
Gene polymorphism
Genes
Genetic analysis
Genotype
Genotype & phenotype
High-performance liquid chromatography
Humans
Hypotheses
Immunoassay
Interferon regulatory factor 4
Irradiance
Light levels
Liquid chromatography
Methylenetetrahydrofolate reductase
Photosynthesis
Pigmentation
Population genetics
Population studies
Riboflavin
Skin pigmentation
Skin Pigmentation - genetics
Skin tests
Total Ozone Mapping Spectrometer
Ultraviolet radiation
Ultraviolet Rays - adverse effects
Vitamin B
Vitamin D
Vitamin D receptors
Vitamin D3
Vitamins
β-Carotene
Title Biophysical evidence to support and extend the vitamin D‐folate hypothesis as a paradigm for the evolution of human skin pigmentation
URI https://onlinelibrary.wiley.com/doi/abs/10.1002%2Fajhb.23667
https://www.ncbi.nlm.nih.gov/pubmed/34418235
https://www.proquest.com/docview/2645822696
https://www.proquest.com/docview/2563422302
Volume 34
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