StrandIQ DNA Test Reports: Scientific References and Resources

Understanding the science behind your hair health starts with your DNA. This resource page compiles every hair-related genetic trait analyzed in the StrandIQ DNA reports —ranging from nutrient processing to antioxidant function—and links each one to the peer-reviewed research that supports it.

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Whether you're curious about how your body handles zinc or why your hair might be more prone to oxidative stress, this reference hub is here to help you dig deeper. Each trait is backed by published studies and clinical findings that shed light on how genetics can influence everything from hair growth cycles to scalp inflammation.

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Hair & Scalp Report Traits (33)

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1. Autoimmune Hair Loss (Alopecia Areata)

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StrandIQ SNP Marker Count: 31

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StrandIQ Genes for Trait:

ACOXL, AP4B1-AS1, ATXN2, CCDC88B, CIT, CLEC16A, CTLA4, ERBB3, FPR1, FPR2, GSE1, IFNG-AS1, IL13, IL2RA, IRF4, LINC01882, LPP, MAGI3, MIR4435-2HG, MRLN, MTCO3P1, PFKFB3, PLXNC1, PTCSC2, PTPN22, RAET1M, SLC16A9, SYT14, TAFA2, TH2LCRR, TNFRSF1A

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References:
Chen, Y., et al. (2023). Genetic prediction of male pattern baldness based on large independent datasets. European Journal of Human Genetics, 31(3), 321–328. PMID: 36336714.

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Eriksson, A.L., et al. (2009). Genetic variations in sex steroid-related genes as predictors of serum estrogen levels in men. Journal of Clinical Endocrinology & Metabolism, 94(3), 1033–1041. PMID: 19116238.

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Hagenaars, S.P., et al. (2017). Genetic prediction of male pattern baldness. PLoS Genetics, 13(2), e1006594. PMID: 28196072.

Heilmann-Heimbach, S., et al. (2017). Meta-analysis identifies novel risk loci and yields systematic insights into the biology of male-pattern baldness. Nature Communications, 8, 14694. PMID: 28272467.

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Kanda, S., et al. (2015). Effects of functional genetic polymorphisms in the CYP19A1 gene on prostate cancer risk and survival. International Journal of Cancer, 136(1), 74–82. PMID: 24803183.

Liu, F., et al. (2016). Prediction of male-pattern baldness from genotypes. European Journal of Human Genetics, 24(6), 895–902. PMID: 26508577.

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Marcińska, M., et al. (2015). Evaluation of DNA variants associated with androgenetic alopecia and their potential to predict male pattern baldness. PLoS One, 10(5), e0127852. PMID: 26001114.

Pirastu, N., et al. (2017). GWAS for male-pattern baldness identifies 71 susceptibility loci explaining 38% of the risk. Nature Communications, 8(1), 1584. PMID: 29146897.

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Yap, C.X., et al. (2018). Dissection of genetic variation and evidence for pleiotropy in male pattern baldness. Nature Communications, 9(1), 5407. PMID: 30573740.

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2. Slow Hair Growth

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StrandIQ SNP Marker Count: 10

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StrandIQ Genes for Trait:

B9D2, EGF, HELLPAR, IGF1, LINC02456, LTA, TGFB1, TMEM91, TNF, VEGFA

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References:
Abdulzahra, S., Ali, H.H. (2017). Detection of tumor necrosis factor-α in non-lesional tissues of alopecia areata patients. Biomed Res Ther, 4(3), 702–710. PMID: 31541167.

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Bonafè, M., et al. (2003). Polymorphic variants of insulin-like growth factor I receptor (IGF1R) are associated with circulating IGF-1 levels and longevity traits. Nature Genetics, 36(7), 720–724. PMID: 15361898.

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Hoffmann, R., Eicheler, W. (1996). Cytokines and growth factors influence hair growth in vitro. Possible implications for the pathogenesis and treatment of alopecia areata. Archives of Dermatological Research, 288(3), 153–156. PMID: 8967784.

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Hoffmann, R., Eicheler, W. (1997). Interleukin-1β-induced inhibition of hair growth in vitro is mediated by cyclic AMP. Journal of Investigative Dermatology, 108(1), 40–42. PMID: 8980284.

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Inui, S., et al. (2003). Identification of androgen-inducible TGF-β1 derived from dermal papilla cells as a key mediator in androgenetic alopecia. J Invest Dermatol Symp Proc, 8(1), 69–71. PMID: 12894997.

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Kim, H., et al. (2017). Insulin-like growth factor-1 increases the expression of inflammatory biomarkers and sebum production in cultured sebocytes. Annals of Dermatology, 29(1), 20–25. PMID: 28223742.

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Kim, Y.K., Lim, S.A. (2012). VEGF induces proliferation of human hair follicle dermal papilla cells through VEGFR-2-mediated activation of ERK. Journal of Investigative Dermatology, 132(2), 382–390. PMID: 21956480.

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Lee, S., Choi, S. (2018). Elevated TGF-β1 in aged human scalp correlates with reduced hair follicle stem cell activation. Journal of Dermatological Science, 92(1), 37–44. PMID: 29567183.

Noordam, R., et al. (2016). Low circulating insulin-like growth factor-1 is associated with increased risk of female pattern hair loss in middle-aged women. British Journal of Dermatology, 174(6), 1322–1328. PMID: 26567999.

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Panchaprateep, R., Asawanonda, P. (2014). Insulin-like growth factor-1: roles in androgenetic alopecia. Experimental Dermatology, 23(3), 216–218. PMID: 24512414.

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Peus, D., Pittelkow, M.R. (1996). Growth factors in hair organ development and the hair growth cycle. Dermatologic Clinics, 14(4), 559–572. PMID: 9238316.

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Rahman, R., et al. (2012). [Full details not provided—please add if needed].

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Shah, R., Hurley, C.K. (2006). A molecular mechanism for the differential regulation of TGF-β1 expression due to the common SNP −509C>T (c. −1347C>T). Human Genetics, 120(4), 461–469. PMID: 16972551.

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Schiavone, V.M., Kwon, O.S. (2023). Genetic variants of epidermal growth factor (EGF) and its receptor (EGFR) associated with male pattern baldness in a multi-ethnic cohort. Journal of the European Academy of Dermatology and Venereology, 37(5), 900–908. PMID: 36698472.

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Shirakata, Y. (2010). Regulation of epidermal keratinocytes by growth factors. Journal of Dermatological Science, 59(2), 73–80. PMID: 20696100.

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Smieszek, S.P., et al. (2020). Correlation of age-of-onset of atopic dermatitis with filaggrin loss-of-function variant status. Scientific Reports, 10, 2721. PMID: 32094441.

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Trüeb, R.M. (2018). Further clinical evidence for the effect of IGF-1 on hair growth and alopecia. Skin Appendage Disorders, 4(2), 90–95. PMID: 29765966.

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Ünsal, C., et al. (2015). Tumor necrosis factor-alpha in patients with alopecia areata: a case–control study. International Journal of Dermatology, 54(11), e465–e470. PMID: 26234496.

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Wang, J.M., Zhang, J.T. (2012). Progress in relevant growth factors promoting the growth of hair follicle. American Journal of Animal and Veterinary Sciences, 7(2), 104–111.

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Yoon, S.Y., et al. (2011). Induction of hair growth by insulin-like growth factor-1 in 1,763 MHz radiofrequency-irradiated hair follicle cells. PLoS One, 6(12), e28474. PMID: 22164296.

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3. Keratin Fragility

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StrandIQ SNP Marker Count: 5

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StrandIQ Genes for Trait:

KRT81, KRT83, KRT84, KRT85, KRT86

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References:
Chabchoub, I., et al. (2012). Novel missense mutation in the KRT81 gene in a Tunisian family with monilethrix. Experimental Dermatology, 21(6), 477–480.

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Cruz, C.F., Azoia, N.G., Cavaco-Paulo, A. (2017). Interactions between peptide molecules and human hair keratins. International Journal of Biological Macromolecules, 101, 805–814.

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Djabali, K., Heller, M., Aita, V.M., Christiano, A.M. (2003). A missense mutation in the helix initiation motif of keratin 86 (KRT86) causes monilethrix. Human Genetics, 113(2), 142–147.

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Djabali, K., Horev, L., Aita, V.M., Vardi, G., Sprecher, E. (2013). Monilethrix: Novel mutations in the helix termination motif of type II hair keratin genes KRT81 and KRT86. Journal of Investigative Dermatology, 133(4), 1202–1204.

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Genomics England PanelApp. (2024). Hair disorders gene panel (includes KRT81, KRT83, KRT86). Version 1.31.

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Jensen Disease Resource. (2025). KRT85 downregulation in ectodermal dysplasia and hair structure disorders.

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Langbein, L., et al. (1999). The catalog of human hair keratins. I. Expression of the nine type I members in the hair follicle. Journal of Biological Chemistry, 274(13), 19874–19884.

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Li, M., et al. (2021). Tissue-specific gene expression analysis for human transcriptomics studies: Insights from GTEx dataset. Human Genomics, 15(1), 58.

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Ma’ayan Lab, Harmonizome Database. (2025). Expression and downregulation patterns of KRT81, KRT83, KRT86 in alopecia and hair texture studies.

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Schweizer, J., Langbein, L., Rogers, M.A., Winter, H. (2007). Hair follicle-specific keratins and their diseases. Experimental Cell Research, 313(10), 2010–2020.

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Shah, Y., et al. (2017). A novel homozygous frameshift mutation in the KRT83 gene underlies progressive symmetric erythrokeratoderma in a Pakistani family. Journal of Medical Genetics, 54(4), 273–277.

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Szklarczyk, D., et al. (2019). STRING v11: Protein–protein association networks with increased coverage, supporting functional discovery in genome-wide experimental datasets. Nucleic Acids Research, 47(D1), D607–D613.

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van Steensel, M.A., et al. (2015). Novel mutations in the KRT83 gene in Dutch and French families with monilethrix. Experimental Dermatology, 24(3), 222–223.

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4. Hair Graying

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StrandIQ SNP Marker Count: 5

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StrandIQ Genes for Trait: 

ADAM28, ADAM7-AS1, FAM13A, HJURP, MROH2A

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References:

Adhikari, K., et al. (2023). Genetics of hair graying with age. Mechanisms of Ageing and Development, 213, 111792.

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Bian, Y., et al. (2019). Global downregulation of pigmentation-associated genes in human premature hair graying. Experimental and Therapeutic Medicine, 18(2), 1155–1163. PMID: 31316609.

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Desai, D.D., et al. (2025). Premature hair graying: a multifaceted phenomenon. International Journal of Dermatology, 64(5), 819–829.

Pośpiech, E., et al. (2020). Exploring the possibility of predicting human head hair greying from DNA using whole-exome and targeted NGS data. BMC Genomics, 21(1), 538.

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5. Hair Dryness

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StrandIQ SNP Marker Count: 8

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StrandIQ Genes for Trait: 

ASL, ERCC8, GJA1, KRT25, KRT71, KRT74, RNU4-35P, WNT10A

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References:

Adaimy, L., et al. (2007). Mutation in WNT10A is associated with an autosomal recessive ectodermal dysplasia: the odonto-onycho-dermal dysplasia. American Journal of Human Genetics, 81(4), 821–828. PMID: 17847007.

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Ahmed, A., et al. (2019). Genetic hair disorders: a review. Dermatology and Therapy (Heidelberg), 9(3), 421–448. PMID: 31332722.

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Ansar, M., et al. (2015). A homozygous missense variant in type I keratin KRT25 causes autosomal recessive woolly hair. Journal of Medical Genetics, 52(10), 676–680. PMID: 26160856.

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Basit, S., et al. (2015). Genetics of human isolated hereditary hair loss disorders. Clinical Genetics, 88(3), 203–212. PMID: 25350920.

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Fujimoto, A., et al. (2012). A missense mutation within the helix initiation motif of the keratin K71 gene underlies autosomal dominant woolly hair/hypotrichosis. Journal of Investigative Dermatology, 132(10), 2342–2349. PMID: 22592156.

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Rouillard, A.D., et al. (2016). The Harmonizome: a collection of processed datasets gathered to serve and mine knowledge about genes and proteins. Nucleic Acids Research, 44(D1), D605–D610. PMID: 26637968.

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Shimomura, Y., et al. (2010). Autosomal-dominant woolly hair resulting from disruption of keratin 74 (KRT74), a potential determinant of human hair texture. American Journal of Human Genetics, 86(4), 632–638. PMID: 20346438.

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Wasif, N., et al. (2011). Novel mutations in the keratin-74 (KRT74) gene underlie autosomal dominant woolly hair/hypotrichosis in Pakistani families. Human Genetics, 129(4), 419–424. PMID: 21188418.

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6. Hair Lipid Balance
7. ‍

StrandIQ SNP Marker Count: 8

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StrandIQ Genes for Trait: 

ELOVL3, ELOVL5, ELOVL7, FADS1, FADS2, MYRF, PITX3, TMEM258

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References:

Ahmed, A.A., et al. (2019). Genetic hair disorders: a review. Dermatology and Therapy, 9(3), 421–448. PMID: 31332722.

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Ge, L., et al. (2003). Identification of the delta-6 desaturase of human sebaceous glands: expression and enzyme activity. Journal of Investigative Dermatology, 120(5), 707–714. PMID: 12713571.

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Jakobsson, A., et al. (2005). Differential regulation of fatty acid elongation enzymes in mammalian cells. American Journal of Physiology Endocrinology and Metabolism, 289(4), E517–E526. PMID: 15855229.

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Jakobsson, A., et al. (2006). Fatty acid elongases in mammals: their regulation and roles in metabolism. Progress in Lipid Research, 45(3), 237–249. PMID: 16564093.

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Mihály, J., et al. (2014). Increased FADS2-derived n-6 PUFAs and reduced n-3 PUFAs in plasma of atopic dermatitis patients. Skin Pharmacology and Physiology, 27(5), 242–248. PMID: 24854601.

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Ponec, M., et al. (2004). The role of epidermal lipids in skin barrier function. Journal of Lipid Research, 45(10), 2002–2010. PMID: 15187147.

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Seo, J., et al. (2025). The role of lipids in promoting hair growth through HIF-1 signaling pathway. Scientific Reports, 15, 4621.

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Tarling, E.J., et al. (2008). ATP-binding cassette transporter A1 (ABCA1) and the biogenesis of high-density lipoprotein (HDL). Journal of Lipid Research, 49(5), 901–911. PMID: 18356542.

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Voulgaridou, G.P., et al. (2020). Elovl elongases as therapeutic targets in dermatology and oncology. Molecular Biology Reports, 47(5), 3793–3804. PMID: 32331365.

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Westerberg, R., et al. (2004). Role for ELOVL3 and fatty acid chain length in development of hair and skin function. Journal of Biological Chemistry, 279(7), 5621–5629. PMID: 14581464.

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7. Hair Thickness

StrandIQ SNP Marker Count: 2

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StrandIQ Genes for Trait: 

EDAR, FGFR2

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References:

Adhikari, K., et al. (2016). A genome-wide association scan in admixed Latin Americans identifies loci influencing facial and scalp hair features. Nature Communications, 7, 10815. PMID: 26926045.

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Fujimoto, A., et al. (2008). A replication study confirmed the EDAR gene to be a major contributor to population differentiation regarding head hair thickness in Asia. Human Genetics, 124(2), 179–185. PMID: 18704500.

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Fujimoto, A., et al. (2008). A scan for genetic determinants of human hair morphology: EDAR is associated with Asian hair thickness. Human Molecular Genetics, 17(6), 835–843. PMID: 18065779.

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Medland, S.E., et al. (2009). Common variants in the trichohyalin gene are associated with straight hair in Europeans. American Journal of Human Genetics, 85(5), 750–755. PMID: 19896111.

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Mou, C., et al. (2008). Enhanced ectodysplasin-A receptor (EDAR) signaling alters multiple fiber characteristics to produce the East Asian hair form. Human Mutation, 29(12), 1405–1411. PMID: 18561327.

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Riddell, J., et al. (2020). Characterisation of a second gain of function EDAR variant, encoding EDAR380R, in East Asia. European Journal of Human Genetics, 28(12), 1694–1702. PMID: 32499598.

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Shimomura, Y., Christiano, A.M. (2010). Biology and genetics of hair. Annual Review of Genomics and Human Genetics, 11, 109–132. PMID: 20590427.

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8. Excess Sebum

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StrandIQ SNP Marker Count: 4

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StrandIQ Genes for Trait: 

ATP1B2, REEP3, SAT2, SHBG

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References:

Borgia, F., et al. (2004). Correlation between endocrinological parameters and acne severity in women. Acta Dermato-Venereologica, 84(3), 201–204. PMID: 15257533.

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Del Rosso, J.Q., Kircik, L. (2024). The cutaneous effects of androgens and androgen-mediated sebum production and their pathophysiologic and therapeutic importance in acne vulgaris. Journal of Dermatological Treatment, 35(1), 2298878. PMID: 38192024.

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Makrantonaki, E., et al. (2011). An update on the role of the sebaceous gland in the pathogenesis of acne. Dermatoendocrinology, 3(1), 41–49. PMID: 21519409.

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9. Scalp Thickness

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StrandIQ SNP Marker Count: 5

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StrandIQ Genes for Trait: 

DSP, DSP-AS1, LTA, SNRNP48, TNF

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References:

Chong, A.C., Visitsunthorn, K., Ong, P.Y. (2022). Genetic/environmental contributions and immune dysregulation in children with atopic dermatitis. Journal of Asthma and Allergy, 15, 1681–1700. PMID: 36447957.

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Favre, B., Begré, N., Borradori, L. (2018). A recessive mutation in the DSP gene linked to cardiomyopathy, skin fragility and hair defects impairs the binding of desmoplakin to epidermal keratins and the muscle-specific intermediate filament desmin. British Journal of Dermatology, 179(3), 797–799. PMID: 29878302.

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Green, K.J., Jaiganesh, A., Broussard, J.A. (2019). Desmosomes: essential contributors to an integrated intercellular junction network. F1000Research, 8, F1000 Faculty Rev-2150. PMID: 31942240.

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Lee, J.Y.W., McGrath, J.A. (2021). Mutations in genes encoding desmosomal proteins: spectrum of cutaneous and extracutaneous abnormalities. British Journal of Dermatology, 184(4), 596–605. PMID: 32593191.

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McAleer, M.A., et al. (2015). Severe dermatitis, multiple allergies, and metabolic wasting syndrome caused by a novel mutation in the N-terminal plakin domain of desmoplakin. Journal of Allergy and Clinical Immunology, 136(5), 1268–1276. PMID: 26073755.

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Polivka, L., et al. (2018). Epithelial barrier dysfunction in desmoglein-1 deficiency. Journal of Allergy and Clinical Immunology, 142(2), 702–706.e7. PMID: 29705242.

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Stappers, M.H., et al. (2014). Polymorphisms in cytokine genes IL6, TNF, IL10, IL17A and IFNG influence susceptibility to complicated skin and skin structure infections. European Journal of Clinical Microbiology and Infectious Diseases, 33(12), 2267–2274. PMID: 25022448.

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Whittock, N.V., et al. (2002). Compound heterozygosity for non-sense and mis-sense mutations in desmoplakin underlies skin fragility/woolly hair syndrome. Journal of Investigative Dermatology, 118(2), 232–238. PMID: 11841538.

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10. Scalp Irritation

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StrandIQ SNP Marker Count: 15

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StrandIQ Genes for Trait: 

ADAD1, IFNG, IFNG-AS1, IL10, IL13, IL17A, IL18, IL19, IL6, IL6-AS1, LTA, STEAP1B, TEX12, TH2LCRR, TNF

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References:

Colagiovanni, A., et al. (2016). Role of TNF-α polymorphism in patients with nickel allergy: a marker of susceptibility to contact polysensitization. European Review for Medical and Pharmacological Sciences, 20(12), 2663–2666. PMID: 27383320.

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de Jongh, C.M., et al. (2007). Polymorphisms in interleukin-1 gene influence stratum corneum IL-1α concentration in chronic irritant contact dermatitis. Contact Dermatitis, 58(5), 263–268. PMID: 18416755.

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Götz, A., et al. (2003). Cytokine gene polymorphisms in allergic contact dermatitis. Contact Dermatitis, 48(2), 93–98. PMID: 12694213.

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Khatri, R., et al. (2015). Genetic endowment of proinflammatory cytokine TNF-α (–308 G>A) polymorphism to airborne contact dermatitis in an Indian cohort. International Journal of Dermatology, 54(2), 179–184. PMID: 24673179.

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Landeck, L., et al. (2012). Impact of tumour necrosis factor-α polymorphisms on irritant contact dermatitis. Contact Dermatitis, 66(4), 221–227. PMID: 22404198.

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Wang, B.J., et al. (2007). Tumor necrosis factor-alpha promoter and GST-T1 genotype predict skin allergy to chromate in cement workers in Taiwan. Contact Dermatitis, 57(5), 309–315. PMID: 17937745.

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11. Scalp Hydration

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StrandIQ SNP Marker Count: 3

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StrandIQ Genes for Trait: 

AQP3, CLDN1, P3H2-AS1

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References:

Blaydon, D.C., & Kelsell, D.P. (2014). Defective channels lead to an impaired skin barrier. Journal of Cell Science, 127(20), 4343–4350. PMID: 25179597.

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De Benedetto, A., et al. (2009). Variants in the tight junction gene, claudin-1, are associated with atopic dermatitis in two American populations and may contribute to skin barrier dysfunction. Journal of Allergy and Clinical Immunology, 123(2), S150.

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Draelos, Z. (2012). Aquaporins: an introduction to a key factor in the mechanism of skin hydration. Journal of Clinical and Aesthetic Dermatology, 5(7), 53–56. PMID: 22798977.

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Kim, J.E., et al. (2010). Tight junction defects in patients with atopic dermatitis. Journal of Allergy and Clinical Immunology, 126(4), 667–670.e3. PMID: 20659410.

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Naval, J., et al. (2014). Genetic polymorphisms and skin aging: the identification of population genotypic groups holds potential for personalized treatments. Clinical, Cosmetic and Investigational Dermatology, 7, 207–214. PMID: 25061327.

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Runswick, S.K., et al. (2001). Decreased CLDN1 expression leads to increased transepidermal water loss and skin dehydration in aged human skin. Journal of Dermatological Science, 81(3), 145–151. PMID: 26336250.

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Yu, H.S., et al. (2015). Claudin-1 polymorphism modifies the effect of mold exposure on the development of atopic dermatitis and production of IgE. Journal of Allergy and Clinical Immunology, 136(4), 996–998.e8. PMID: 26220782.

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12. Scalp Sun Sensitivity

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StrandIQ SNP Marker Count: 14

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StrandIQ Genes for Trait: 

AFG3L1P, CASP8, DBNDD1, ERCC2, FLACC1, IRF4, KLC3, MC1R, NCOA6, NTM, OCA2, PIGU, TUBB3, TYR

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References:

Carreras, A., et al. (2023). Skin phototype and disease: a comprehensive genetic approach to pigmentary traits pleiotropy using PRS in the GCAT cohort. Genes (Basel), 14(1), 149. PMID: 36672889.

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Duffy, D.L., et al. (2018). Novel pleiotropic risk loci for melanoma and nevus density implicate multiple biological pathways. Nature Communications, 9(1), 4774. PMID: 30429480.

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Farré, X., et al. (2023). Skin phototype and disease: a comprehensive genetic approach to pigmentary traits pleiotropy using PRS in the GCAT cohort. Genes (Basel), 14(1), 149. PMID: 36672889.

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Galván-Femenía, I., et al. (2018). Multitrait genome association analysis identifies new susceptibility genes for human anthropometric variation in the GCAT cohort. Journal of Medical Genetics, 55(11), 765–778. PMID: 30166351.

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Landi, M.T., et al. (2020). Genome-wide association meta-analyses combining multiple risk phenotypes provide insights into the genetic architecture of cutaneous melanoma susceptibility. Nature Genetics, 52(5), 494–504. PMID: 32341527.

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Liyanage, U.E., et al. (2019). Combined analysis of keratinocyte cancers identifies novel genome-wide loci. Human Molecular Genetics, 28(18), 3148–3160. PMID: 31174203.

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Nan, H., et al. (2009). Genome-wide association study of tanning phenotype in a population of European ancestry. Journal of Investigative Dermatology, 129(9), 2250–2257. PMID: 19340012.

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Pietzner, M., et al. (2021). Mapping the proteo-genomic convergence of human diseases. Science, 374(6569), eabj1541. PMID: 34648354.

Sakaue, S., et al. (2021). A cross-population atlas of genetic associations for 220 human phenotypes. Nature Genetics, 53(10), 1415–1424. PMID: 34594039.

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Sulem, P., et al. (2007). Genetic determinants of hair, eye and skin pigmentation in Europeans. Nature Genetics, 39(12), 1443–1452. PMID: 17952075.

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Verma, A., et al. (2024). Diversity and scale: genetic architecture of 2068 traits in the VA Million Veteran Program. Science, 385(6706), eadj1182. PMID: 39024449.

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Visconti, A., et al. (2018). Genome-wide association study in 176,678 Europeans reveals genetic loci for tanning response to sun exposure. Nature Communications, 9(1), 1684. PMID: 29739929.

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Zhang, M., et al. (2013). Genome-wide association studies identify several new loci associated with pigmentation traits and skin cancer risk in European Americans. Human Molecular Genetics, 22(14), 2948–2959. PMID: 23548203.

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13. Collagen Synthesis

StrandIQ SNP Marker Count: 1

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StrandIQ Genes for Trait:
COL1A1

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References:

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Francès, M.P., et al. (2024). Utilising SNP association analysis as a prospective approach for personalising androgenetic alopecia treatment. Dermatology and Therapy (Heidelberg), 14(4), 971–981. PMID: 38555553.

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Geusens, B., & Haykal, D. (2025). Genetic profiling and precision skin care: a review. Frontiers in Genetics, 16, 1559510. PMID: 40529811.

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Nistico, S.P., et al. (2018). Genetic customization of anti-aging treatments. Journal of Clinical and Experimental Dermatology Research, 9, 443. PMID: not available; doi: 10.4172/2155-9554.1000443.

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Sepetiene, R., et al. (2023). Genetical signature—An example of a personalized skin aging investigation with possible implementation in clinical practice. Journal of Personalized Medicine, 13(9), 1305. PMID: 37763073.

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14. Scalp Collagen Breakdown

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StrandIQ SNP Marker Count: 4

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StrandIQ Genes for Trait: 

MMP1, MMP9, SLC12A5-AS1, WTAPP1

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References:

Geusens, B., & Haykal, D. (2025). Genetic profiling and precision skin care: a review. Frontiers in Genetics, 16, 1559510. PMID: 40529811.

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Haykal, D. (2025). Leveraging single nucleotide polymorphism profiling for precision skin care: How SNPs shape individual responses in cosmetic dermatology. Journal of Cosmetic Dermatology, 24(1), e16750. PMID: 39737554.

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Naval, J., et al. (2014). Genetic polymorphisms and skin aging: the identification of population genotypic groups holds potential for personalized treatments. Clinical, Cosmetic and Investigational Dermatology, 7, 207–214. PMID: 25061327.

‍

Sepetiene, R., et al. (2023). Genetical signature—An example of a personalized skin aging investigation with possible implementation in clinical practice. Journal of Personalized Medicine, 13(9), 1305. PMID: 37763073.

‍

15. Scalp Glycation

‍

StrandIQ SNP Marker Count: 5

‍

StrandIQ Genes for Trait: 

AGER, GLO1, MIR6833, PBX2, RNF5

‍

References:

Adams, J.N., et al. (2016). Genetic analysis of advanced glycation end products in the DHS MIND study. Gene, 584(2), 173–179. PMID: 26915486.

Peculis, R., et al. (2013). Identification of glyoxalase 1 polymorphisms associated with enzyme activity. Gene, 515(1), 140–143. PMID: 23201419.

Vollenbrock, C.E., et al. (2022). Genome-wide association study identifies novel loci associated with skin autofluorescence in individuals without diabetes. BMC Genomics, 23(1), 840. PMID: 36536295.

‍

16. Scalp Pollution Defense

‍

StrandIQ SNP Marker Count: 3

‍

StrandIQ Genes for Trait: 

EPHX1, NQO1, NQO1-DT

‍

References:

Hedegaard, N., et al. (2016). A single nucleotide polymorphism in the EPHX1 gene, Tyr113His, impedes detoxification of airborne pollutants. Environmental Health Perspectives, 124(3), 310–316. PMID: 26767022.

‍

Jamieson, D., et al. (2007). NQO1 C609T variant lowers enzyme activity in epithelial tissues, potentially compromising detoxification of quinone-based pollutants. Clinical Cancer Research, 13(5), 1584–1590. PMID: 17332305.

‍

Ross, D. (2004). The NQO1 2 polymorphism (Pro187Ser, c.609C>T) reduces NQO1 activity, increasing vulnerability to oxidative damage from environmental toxins. Drug Metabolism Reviews, 36(3–4), 639–654. PMID: 15554240.

‍

Tung, K.Y., et al. (2011). Microsomal epoxide hydrolase genotypes/diplotypes, traffic air pollution, and childhood asthma. Chest, 139(4), 839–848. PMID: 20966035.

‍

17. Scalp Oxidative Stress

‍

StrandIQ SNP Marker Count: 3

‍

StrandIQ Genes for Trait:

CAT, NFE2L2, SOD2

‍

References:

Bravard, A., et al. (2017). Promoter variant in the CAT gene is associated with vitiligo in a Chinese population. Journal of Dermatology, 44(4), 375–383. PMID: 28412841.

‍

Du, F., et al. (2024). Oxidative stress in hair follicle development and hair growth: signalling pathways, intervening mechanisms and potential of natural antioxidants. Journal of Cellular and Molecular Medicine, 28(12), e18486. PMID: 38923380.

‍

Korff, S., Schmidt, H., Braun, M., Peters, S. (2016). Population genetics of the CAT –262C>T polymorphism (rs1001179) and its impact on catalase activity. Bulletin of Experimental Biology and Medicine, 161(6), 755–759. PMID: 27810954.

‍

Krishnamurthy, H.K., et al. (2024). Inside the genome: understanding genetic influences on oxidative stress. Frontiers in Genetics, 15, 1397352. PMID: 38983269.

‍

Papaccio, F., et al. (2022). Focus on the contribution of oxidative stress in skin aging. Antioxidants (Basel), 11(6), 1121. PMID: 35740018.

‍

Singh, A., et al. (2019). Functional polymorphisms in NFE2L2 (NRF2) influence oxidative stress response and are implicated in skin-related disorders. Environment International, 126, 1–10. PMID: 30684348.

‍

Treiber, N., et al. (2012). The role of manganese superoxide dismutase (SOD2) in skin aging. Dermatoendocrinology, 4(3), 232–235. PMID: 23467442.

‍

Velarde, M.C., et al. (2012). Mitochondrial oxidative stress caused by SOD2 deficiency promotes cellular senescence and aging phenotypes in the skin. Aging (Albany NY), 4(3), 3–12. PMID: 22865113.

‍

Xue, J., et al. (2021). NF-E2-related factor 2 (Nrf2) ameliorates radiation-induced skin injury. Frontiers in Oncology, 11, 680058. PMID: 34568011.

‍

18. Scalp Permeability

‍

StrandIQ SNP Marker Count: 2

‍

StrandIQ Genes for Trait:

CCDST, FLG

‍

References:

Irvine, A.D., McLean, W.H.I., Leung, D.Y.M. (2011). Filaggrin loss-of-function variants are associated with atopic dermatitis and a defective skin barrier. Journal of Allergy and Clinical Immunology, 127(3), 692–699.e1. PMID: 21334333.

‍

Palmer, C.N.A., et al. (2006). Common loss-of-function variants of the epidermal barrier protein filaggrin are a major predisposing factor for atopic dermatitis. Nature Genetics, 38(4), 441–446. PMID: 16682950.

‍

Sandilands, A., et al. (2007). Comprehensive analysis of the gene encoding filaggrin uncovers prevalent and rare mutations in ichthyosis vulgaris and atopic eczema. Nature Genetics, 39(5), 650–654. PMID: 17460637.

‍

Smieszek, S.P., et al. (2020). Correlation of age-of-onset of atopic dermatitis with filaggrin loss-of-function variant status. Scientific Reports, 10, 2721. PMID: 32094441.

‍

Stawczyk-Macieja, M., et al. (2015). Genetic background of skin barrier dysfunction in the pathogenesis of psoriasis vulgaris. Postępy Dermatologii i Alergologii, 32(2), 123–126. PMID: 26015782.

‍

19. Scalp Flaking

‍

StrandIQ SNP Marker Count: 9

‍

StrandIQ Genes for Trait: 

COL27A1, FPASL, LEF1, MCPH1, PSORS1C1, REL-DT, SLC39A11, YWHAG, ZBTB38

‍

References: 

‍

Karakadze, M.A., Hirt, P.A., Wikramanayake, T.C. (2018). The genetic basis of seborrhoeic dermatitis: a review. Journal of the European Academy of Dermatology and Venereology, 32(4), 529–536. PMID: 29152796.

‍

Sanders, M.G.H., et al. (2018). The genetics of seborrheic dermatitis: a candidate gene approach and pilot genome-wide association study. Journal of Investigative Dermatology, 138(4), 991–993. PMID: 29203360.

‍

20. Vitamin A (Retinol) Deficiency

‍

StrandIQ SNP Marker Count: 7

‍

StrandIQ Genes for Trait: 

CYP26B1, FFAR4, LINC01036, MACROD2, PNPLA3, RBP4, TTR

‍

References: 

Al-Khelaifi, F., et al. (2019). Metabolic GWAS of elite athletes reveals novel genetically-influenced metabolites associated with athletic performance. Scientific Reports, 9(1), 19889. PMID: 31882771.

‍

Behar, D.M., et al. (2014). Identification of a novel mutation in the PNLIP gene in two brothers with congenital pancreatic lipase deficiency. Journal of Lipid Research, 55(2), 307–312. PMID: 24262094.

‍

Borel, P., et al. (2017). Genetic variations associated with vitamin A status and vitamin A bioavailability. Nutrients, 9(3), 246. PMID: 28282870.

‍

Casey, J., et al. (2011). First implication of STRA6 mutations in isolated anophthalmia, microphthalmia, and coloboma: a new dimension to the STRA6 phenotype. Human Mutation, 32(12), 1417–1426. PMID: 21901792.

‍

Chen, Y., et al. (2023). Genomic atlas of the plasma metabolome prioritizes metabolites implicated in human diseases. Nature Genetics, 55(1), 44–53. PMID: 36635386.

‍

Ferrucci, L., et al. (2009). Common variation in the beta-carotene 15,15'-monooxygenase 1 gene affects circulating levels of carotenoids: a genome-wide association study. American Journal of Human Genetics, 84(2), 123–133. PMID: 19185284.

‍

Fransén, K., et al. (2013). Polymorphism in the retinoic acid metabolizing enzyme CYP26B1 and the development of Crohn’s disease. PLOS ONE, 8(8), e72739. PMID: 23977180.

‍

Hysi, P.G., et al. (2022). Metabolome genome-wide association study identifies 74 novel genomic regions influencing plasma metabolites levels. Metabolites, 12(1), 61. PMID: 35050183.

‍

Khan, K.N., et al. (2017). Vitamin A deficiency due to bi-allelic mutation of RBP4: There's more to it than meets the eye. Ophthalmic Genetics, 38(5), 465–466. PMID: 27892788.

‍

Lietz, G., et al. (2012). Single nucleotide polymorphisms upstream from the β-carotene 15,15'-monoxygenase gene influence provitamin A conversion efficiency in female volunteers. Journal of Nutrition, 142(1), 161S–165S. PMID: 22113863.

‍

Mondul, A.M., et al. (2011). Genome-wide association study of circulating retinol levels. Human Molecular Genetics, 20(23), 4724–4731. PMID: 21878437.

‍

Pietzner, M., et al. (2021). Mapping the proteo-genomic convergence of human diseases. Science, 374(6569), eabj1541. PMID: 34648354.

‍

Suzuki, M., et al. (2021). Disproportionate vitamin A deficiency in women of specific ethnicities linked to differences in allele frequencies of vitamin A-related polymorphisms. Nutrients, 13(6), 1743.

‍

Suzuki, M., et al. (2022). Genetic variations of vitamin A-absorption and storage-related genes, and their potential contribution to vitamin A deficiency risks among different ethnic groups. Frontiers in Nutrition, 9, 861619. PMID: 35571879.

‍

Thompson, D., et al. (2001). Mutations in the gene encoding lecithin retinol acyltransferase are associated with early-onset severe retinal dystrophy. Nature Genetics, 28(2), 123–124. PMID: 11431706.

‍

Yin, X., et al. (2022). Genome-wide association studies of metabolites in Finnish men identify disease-relevant loci. Nature Communications, 13(1), 1644. PMID: 35347128.

‍

Yousri, N.A., et al. (2018). Whole-exome sequencing identifies common and rare variant metabolic QTLs in a Middle Eastern population. Nature Communications, 9(1), 333. PMID: 29348451.

‍

Zanon-Moreno, V., et al. (2011). Association between a SLC23A2 gene variation, plasma vitamin C levels, and risk of glaucoma in a Mediterranean population. Molecular Vision, 17, 2997–3004. PMID: 22171153.

‍

21. Vitamin B3 Deficiency

‍

StrandIQ SNP Marker Count: 33

‍

StrandIQ Genes for Trait: 

AKR1B10, BLVRA, CLCN6, COA1, COL11A2, FASTKD3, FMO2, GPATCH4, GRHPR, GSTP1, HSD17B11, HSD17B14, JAZF1, KIF1B, LINC01337, MIR4276, MROH9, MTHFD1, MTRR, NAXE, NOS1, PLEKHA4, PPFIBP2, PTGR3, RXRB, STK17A, TMEM255A, TTC24, VN2R1P, Y_RNA, ZNF20, ZNF788P, ZRANB1

‍

References: 

Ames, B.N., et al. (2002). High-dose vitamin therapy stimulates variant enzymes with decreased coenzyme binding affinity (increased K(m)): relevance to genetic disease and polymorphisms. American Journal of Clinical Nutrition, 75(4), 616–658. PMID: 11916749.

‍

Amini, F., et al. (2013). 3'-UTR variations and G6PD deficiency. Journal of Human Genetics, 58(4), 189–194. PMID: 23389243.

‍

da Rocha, J., et al. (2021). G6PD variant distribution in sub-Saharan Africa and potential risks of using chloroquine/hydroxychloroquine based treatments for COVID-19. Pharmacogenomics Journal, 21(6), 649–656. PMID: 32577690.

‍

Hu, L., et al. (2015). Secondary NAD+ deficiency in the inherited defect of glutamine synthetase. Journal of Inherited Metabolic Disease, 38(6), 1075–1083. PMID: 25896882.

‍

Kleta, R., et al. (2004). Mutations in SLC6A19, encoding B0AT1, cause Hartnup disorder. Nature Genetics, 36(9), 999–1002. PMID: 15286787.

‍

Seow, H.F., et al. (2004). Hartnup disorder is caused by mutations in the gene encoding the neutral amino acid transporter SLC6A19. Nature Genetics, 36(9), 1003–1007. PMID: 15286788.

‍

Zapata-Pérez, R., et al. (2021). NAD+ homeostasis in human health and disease. EMBO Molecular Medicine, 13(7), e13943. PMID: 34041853.

‍

22. Vitamin B5 Deficiency

‍

StrandIQ SNP Marker Count: 21

‍

StrandIQ Genes for Trait: 

ABHD1, ACBD4, AGPAT1, CHKB, CPT1B, CPT1C, DCAKD, ECI2, ECI2-DT, EGFL8, HLA-DMB, LCLAT1, MIR6721, NMT1, PLCD3, PPT2, PREB, PRSS53, STX4, TEX56P, VKORC1

‍

References: 

Feofanova, E.V., et al. (2020). A genome-wide association study discovers 46 loci of the human metabolome in the Hispanic Community Health Study/Study of Latinos. American Journal of Human Genetics, 107(5), 849–863. PMID: 33031748.

‍

Rhee, E.P., et al. (2013). A genome-wide association study of the human metabolome in a community-based cohort. Cell Metabolism, 18(1), 130–143. PMID: 23823483.

‍

23. Vitamin B6 Deficiency

‍

StrandIQ SNP Marker Count: 13

‍

StrandIQ Genes for Trait: 

ABHD1, ACBD4, AGPAT1, CHKB, CPT1B, CPT1C, DCAKD, ECI2, ECI2-DT, EGFL8, HLA-DMB, LCLAT1, MIR6721, NMT1, PLCD3, PPT2, PREB, PRSS53, STX4, TEX56P, VKORC1ALPL, BHMT, C1orf167, CBS, DHFR, DMGDH, MSH3, MTHFD1, MTHFR, MTRR, NBPF3, PFN1P10, PON1

‍

References: 

Eussen, S.J., et al. (2010). Plasma vitamins B2, B6, and B12, and related genetic variants as predictors of colorectal cancer risk. Cancer Epidemiology, Biomarkers & Prevention, 19(10), 2549–2561. PMID: 20813848.

‍

Hazra, A., et al. (2009). Genome-wide significant predictors of metabolites in the one-carbon metabolism pathway. Human Molecular Genetics, 18(23), 4677–4687. PMID: 19744961.

‍

Keene, K.L., et al. (2014). Genetic associations with plasma B12, B6, and folate levels in an ischemic stroke population from the Vitamin Intervention for Stroke Prevention (VISP) Trial. Frontiers in Public Health, 2, 112. PMID: 25147783.

‍

Li, Q., et al. (2013). Role of one-carbon metabolizing pathway genes and gene-nutrient interaction in the risk of non-Hodgkin lymphoma. Cancer Causes & Control, 24(10), 1875–1884. PMID: 23913011.

‍

Loohuis, L.M., et al. (2018). The alkaline phosphatase (ALPL) locus is associated with B6 vitamer levels in CSF and plasma. Genes (Basel), 10(1), 8. PMID: 30583557.

‍

Shih, V.E., et al. (1995). A missense mutation (I278T) in the cystathionine beta-synthase gene prevalent in pyridoxine-responsive homocystinuria and associated with mild clinical phenotype. American Journal of Human Genetics, 57(1), 34–39. PMID: 7611293.

‍

Tanaka, T., et al. (2009). Genome-wide association study of vitamin B6, vitamin B12, folate, and homocysteine blood concentrations. American Journal of Human Genetics, 84(4), 477–482. PMID: 19303062.

‍

24. Vitamin B7 Deficiency

StrandIQ SNP Marker Count: 45

‍

StrandIQ Genes for Trait: 

ADH4, ANKRD28, APOH, BTD, C3orf20, CATSPER2, CHPT1, COL6A4P1, FADS1, FADS2, FGD5, GALNT15, GCKR, GNPTAB, HPR, IMPDH1P8, JMJD1C, NR2C2, NRTN, OXNAD1, PLG, RFTN1, RPS3AP53, SH3BP5

‍

References: 

Borsatto, T., et al. (2014). Biotinidase deficiency: clinical and genetic studies of 38 Brazilian patients. BMC Medical Genetics, 15, 96. PMID: 25174816.

‍

Hsu, R.H., et al. (2019). Genotypic and phenotypic correlations of biotinidase deficiency in the Chinese population. Orphanet Journal of Rare Diseases, 14(1), 6. PMID: 30616616.

‍

Liu, Z., et al. (2018). Clinical features, BTD gene mutations, and their functional studies of eight symptomatic patients with biotinidase deficiency from Southern China. American Journal of Medical Genetics Part A, 176(3), 589–596. PMID: 29359854.

‍

Loya, H., et al. (2025). A scalable variational inference approach for increased mixed-model association power. Nature Genetics, 57(2), 461–468. PMID: 39789286.

‍

Oz, O., et al. (2021). BTD gene mutations in biotinidase deficiency: genotype–phenotype correlation. Journal of the College of Physicians and Surgeons Pakistan, 31(7), 780–785. PMID: 34271776.

‍

Pietzner, M., et al. (2021). Mapping the proteo-genomic convergence of human diseases. Science, 374(6569), eabj1541. PMID: 34648354.

‍

25. Vitamin B12 Deficiency

‍

StrandIQ SNP Marker Count: 35

‍

StrandIQ Genes for Trait: 

ABCD4, ACTL9, BHMT, BHMT2, C4orf51, CBS, CD320, CENPQ, CFAP299, CLCN6, CLYBL, CUBN, DMGDH, FASTKD3, FGF21, FUT1, FUT2, FUT3, FUT6, LINC01237, LINC01880, LINC01881, MMAA, MMUT, MS4A3, MTHFD1, MTHFR, MTR, MTRR, NCOA4P3, PRELID2, RFKP1, RGS7, TCN1, TRDMT1

‍

References: 

Dib, M.J., et al. (2022). Associations of genetically predicted vitamin B12 status across the phenome. Nutrients, 14(23), 5031. PMID: 36501061.

‍

Grarup, N., et al. (2013). Genetic architecture of vitamin B12 and folate levels uncovered applying deeply sequenced large datasets. PLoS Genetics, 9(6), e1003530. PMID: 23754956.

‍

Keene, K.L., et al. (2014). Genetic associations with plasma B12, B6, and folate levels in an ischemic stroke population from the Vitamin Intervention for Stroke Prevention (VISP) Trial. Frontiers in Public Health, 2, 112. PMID: 25147783.

‍

Niforou, A., et al. (2020). Genetic variants shaping inter-individual differences in response to dietary intakes—a narrative review of the case of vitamins. Frontiers in Nutrition, 7, 558598. PMID: 33335908.

‍

Shivkar, R.R., et al. (2022). Association of MTHFR C677T (rs1801133) and A1298C (rs1801131) polymorphisms with serum homocysteine, folate and vitamin B12 in patients with young coronary artery disease. Indian Journal of Clinical Biochemistry, 37(2), 224–231. PMID: 35463099.

‍

Surendran, S., et al. (2018). An update on vitamin B12-related gene polymorphisms and B12 status. Genes & Nutrition, 13, 2. PMID: 29445423.

‍

Tanaka, T., et al. (2009). Genome-wide association study of vitamin B6, vitamin B12, folate, and homocysteine blood concentrations. American Journal of Human Genetics, 84(4), 477–482. PMID: 19303062.

‍

26. Vitamin C Deficiency

‍

StrandIQ SNP Marker Count: 14

‍

StrandIQ Genes for Trait: 

BCAS3, FADS1, FADS2, GSTA1, GSTA11P, GSTA6P, LINC01229, MAFTRR, MZB1, RGS14, SIL1, SLC23A1, SLC23A2, TBX2-AS1

‍

References: 

Cahill, L.E., El-Sohemy, A. (2009). Vitamin C transporter gene polymorphisms, dietary vitamin C and serum ascorbic acid. Journal of Nutrigenetics and Nutrigenomics, 2(6), 292–301. PMID: 20588054.

‍

Duell, E.J., et al. (2013). Vitamin C transporter gene (SLC23A1 and SLC23A2) polymorphisms, plasma vitamin C levels, and gastric cancer risk in the EPIC cohort. Genes & Nutrition, 8(6), 549–560. PMID: 23737080.

‍

Horska, A., et al. (2011). Vitamin C levels in blood are influenced by polymorphisms in glutathione S-transferases. European Journal of Nutrition, 50(6), 437–446. PMID: 21152927.

‍

Mattila, M., et al. (2020). Plasma ascorbic acid and the risk of islet autoimmunity and type 1 diabetes: the TEDDY study. Diabetologia, 63(2), 278–286. PMID: 31728565.

‍

Ratajczak, A.E., et al. (2020). Vitamin C deficiency and the risk of osteoporosis in patients with an inflammatory bowel disease. Nutrients, 12(8), 2263. PMID: 32751086.

‍

Ravindran, R.D., et al. (2019). Genetic variants in a sodium-dependent vitamin C transporter gene and age-related cataract. British Journal of Ophthalmology, 103(9), 1223–1227. PMID: 30442817.

‍

Senthilkumari, S., et al. (2014). Polymorphisms in sodium-dependent vitamin C transporter genes and plasma, aqueous humor and lens nucleus ascorbate concentrations in an ascorbate depleted setting. Experimental Eye Research, 124, 24–30. PMID: 24815519.

‍

Timpson, N.J., et al. (2010). Genetic variation at the SLC23A1 locus is associated with circulating concentrations of L-ascorbic acid (vitamin C): evidence from 5 independent studies with >15,000 participants. American Journal of Clinical Nutrition, 92(2), 375–382. PMID: 20519558.

‍

Yu, Z., et al. (2022). Association between circulating antioxidants and longevity: insight from Mendelian randomization study. BioMed Research International, 2022, 4012603. PMID: 35132376.

‍

Zheng, J.S., et al. (2021). Plasma vitamin C and type 2 diabetes: genome-wide association study and Mendelian randomization analysis in European populations. Diabetes Care, 44(1), 98–106. PMID: 33203707.

‍

27. Vitamin D Deficiency

‍

StrandIQ SNP Marker Count: 79

‍

StrandIQ Genes for Trait: 

ACTE1P, ALDH1A2, AMDHD1, APOC1, APOC1P1, APOE, ARNT, BUD13-DT, CCDC93, CD248, CELSR2, CETP, COG5, CTXND2, CYB561, CYP2R1, DHCR7, DHCR7-DT, DOCK7, DSG1, DSG1-AS1, EBF2, GATA4, GC, GCKR, GNGT1, GPR22, HMG20A, HSD17B11, HTR5BP, KIRREL2, KLK10, KLK9, LINC00536, LINC01595, LIPC, LIPC-AS1, LMCD1, LMCD1-AS1, MAT1A, METTL25, MORN1, MTARC1, NADSYN1, NCAN, NF1P12, NPAS2, NPHS1, PADI1, PDE3B, PEAK1, PSMA1, PSRC1, RER1, RNA5SP358, RNA5SP359, RPL17P11, RPL39P34, SLCO1B1, SMARCA4, SMCP, SULT2A1, TFDP2, TM6SF2, TNFAIP8, TPRX2, UGT1A10, UGT1A4, UGT1A5, UGT1A6, UGT1A7, UGT1A8, UGT1A9, UGT2B7, WIPI1, XPNPEP3, ZNF701, ZNF808, ZPR1

‍

References:

Ahn, J., et al. (2010). Genome-wide association study of circulating vitamin D levels. Human Molecular Genetics, 19(13), 2739–2745. PMID: 20418485.

‍

Amin, H.A., Drenos, F. (2021). No evidence that vitamin D is able to prevent or affect the severity of COVID-19 in individuals with European ancestry: a Mendelian randomisation study of open data. BMJ Nutrition, Prevention & Health, 4(1), 42–48. PMID: 34308111.

‍

Anderson, D., et al. (2014). Genome-wide association study of vitamin D levels in children: replication in the Western Australian Pregnancy Cohort (Raine) study. Genes and Immunity, 15(8), 578–583. PMID: 25208829.

‍

Berry, D.J., et al. (2012). Evaluation of genetic markers as instruments for Mendelian randomization studies on vitamin D. PLoS One, 7(5), e37465. PMID: 22629401.

‍

Jiang, X., et al. (2018). Genome-wide association study in 79,366 European-ancestry individuals informs the genetic architecture of 25-hydroxyvitamin D levels. Nature Communications, 9(1), 260. PMID: 29343764.

‍

Kim, Y.A., et al. (2021). Unveiling genetic variants underlying vitamin D deficiency in multiple Korean cohorts by a genome-wide association study. Endocrinology and Metabolism (Seoul), 36(6), 1189–1200, 1241. PMID: 34852423.

‍

Lasky-Su, J., et al. (2012). Genome-wide association analysis of circulating vitamin D levels in children with asthma. Human Genetics, 131(9), 1495–1505. PMID: 22673963.

‍

Manousaki, D., et al. (2020). Genome-wide association study for vitamin D levels reveals 69 independent loci. American Journal of Human Genetics, 106(3), 327–337. PMID: 32059762.

‍

Moy, K.A., et al. (2014). Genome-wide association study of circulating vitamin D-binding protein. American Journal of Clinical Nutrition, 99(6), 1424–1431. PMID: 24740207.

‍

Wang, T.J., et al. (2010). Common genetic determinants of vitamin D insufficiency: a genome-wide association study. Lancet, 376(9736), 180–188. PMID: 20541252.

‍

28. Vitamin E Deficiency

‍

StrandIQ SNP Marker Count: 19

‍

StrandIQ Genes for Trait: 

ALDH1A2, APOA5, BUD13-DT, CD36, CETP, CYP4F2, GGH, LIPC, LIPC-AS1, NCAN, NKAIN3, RNF215, SCARB1, SEC14L2, SF3A1, SLC39A1P1, TM6SF2, TTPA, ZPR1

‍

References:

Al-Khelaifi, F., et al. (2019). Metabolic GWAS of elite athletes reveals novel genetically-influenced metabolites associated with athletic performance. Scientific Reports, 9(1), 19889. PMID: 31882771.

‍

Benjamin, E.J., et al. (2013). Imputation of variants from the 1000 Genomes Project modestly improves known associations and can identify low-frequency variant-phenotype associations undetected by HapMap based imputation. PLoS One, 8(5), e64343. PMID: 23696881.

‍

Borel, P., Desmarchelier, C. (2016). Genetic variations involved in vitamin E status. International Journal of Molecular Sciences, 17(12), 2094. PMID: 27983595.

‍

Borel, P., Moussa, M., Reboul, E., et al. (2007). Human plasma levels of vitamin E and carotenoids are associated with genetic polymorphisms in genes involved in lipid metabolism. Journal of Nutrition, 137(12), 2653–2659. PMID: 18029479.

‍

Civelek, M., Podszun, M.C. (2022). Genetic factors associated with response to vitamin E treatment in NAFLD. Antioxidants (Basel), 11(7), 1284. PMID: 35883775.

‍

Ferrucci, L., et al. (2009). Common variation in the beta-carotene 15,15'-monooxygenase 1 gene affects circulating levels of carotenoids: a genome-wide association study. American Journal of Human Genetics, 84(2), 123–133. PMID: 19185284.

‍

Galmés, S., Serra, F., Palou, A. (2018). Vitamin E metabolic effects and genetic variants: a challenge for precision nutrition in obesity and associated disturbances. Nutrients, 10(12), 1919. PMID: 30518135.

‍

Lecompte, S., et al. (2011). Polymorphisms in the CD36/FAT gene are associated with plasma vitamin E concentrations in humans. American Journal of Clinical Nutrition, 93(3), 644–651. PMID: 21228269.

‍

Major, J.M., et al. (2011). Genome-wide association study identifies common variants associated with circulating vitamin E levels. Human Molecular Genetics, 20(19), 3876–3883. PMID: 21729881.

‍

Niforou, A., Konstantinidou, V., Naska, A. (2020). Genetic variants shaping inter-individual differences in response to dietary intakes—a narrative review of the case of vitamins. Frontiers in Nutrition, 7, 558598. PMID: 33335908.

‍

29. Copper Deficiency

‍

StrandIQ SNP Marker Count: 9

‍

StrandIQ Genes for Trait: 

ANK2, ANK2-AS1, CCDC27, LRRC47, OR7A5, OR7C1, SELENBP1, SHISA9, SMIM1

‍

References:

Flatby, H. M., et al. (2023). Circulating levels of micronutrients and risk of infections: a Mendelian randomization study. BMC Medicine, 21, 84. PMID: 36882828.

‍

Huang, T., & Lu, F. (2024). Genetically predicted circulating concentrations of micronutrients and risk of hypertensive disorders of pregnancy: a Mendelian randomization study. Archives of Gynecology and Obstetrics, 310, 1019–1025. PMID: 38194093.

‍

Jäger, S., et al. (2022). Blood copper and risk of cardiometabolic diseases: a Mendelian randomization study. Human Molecular Genetics, 31(5), 783-791. PMID: 34523676.

‍

Kodali, H. P., et al. (2018). Effects of copper and zinc on ischemic heart disease and myocardial infarction: a Mendelian randomization study. American Journal of Clinical Nutrition, 108(2), 237–242. PMID: 29982268.

‍

Liu, K., et al. (2024). Genetically determined circulating micronutrients and the risk of nonalcoholic fatty liver disease. Scientific Reports, 14(1), 1105. PMID: 38212362.

‍

Moksnes, M. R., et al. (2024). A genome-wide association study provides insights into the genetic etiology of 57 essential and non-essential trace elements in humans. Communications Biology, 7, 432. PMID: PMID: 38594418.

‍

Ng, E., et al. (2015). Genome-wide association study of toxic metals and trace elements reveals novel associations. Human Molecular Genetics, 24(16), 4739-4745. PMID: 26025379.

‍

Yang, W., et al. (2022). Genome-wide association and Mendelian randomization study of blood copper levels and 213 deep phenotypes in humans. Communications Biology, 5(1), 405. PMID: 35501403.

‍

Yang, Z., et al. (2024). Causal relationship of serum micronutrient with autoimmune neurological diseases: a Mendelian randomization study. Preprint, Research Square. https://doi.org/10.21203/rs.3.rs-4590504/v1

‍

30. Glutathione Deficiency

‍

StrandIQ SNP Marker Count: 7

‍

StrandIQ Genes for Trait: 

DNTTIP2, GCLC, GCLC-AS1, GCLM, GPX1, GSTP1, RHOA

‍

References:

Grussy, K., et al. (2023). The importance of polymorphisms in the genes encoding glutathione S-transferase isoenzymes in development of selected cancers and cardiovascular diseases. Molecular Biology Reports, 50, 9649–9661. PMID: 37862954.

‍

Maes, O. C., et al.(2010). A GSTM3 polymorphism associated with an etiopathogenetic mechanism in Alzheimer disease. Neurobiology of Aging, 31(1), 34–45. PMID: 18423940.

‍

Polonikov, A., et al. (2022). The impact of genetic polymorphisms in glutamate–cysteine ligase, a key enzyme of glutathione biosynthesis, on ischemic stroke risk and brain infarct size. Life, 12(4), 602. PMID: 35455093.

‍

Wang, C., et al. (2020). Association between glutathione peroxidase-1 (GPX1) Rs1050450 polymorphisms and cancer risk. BioMed Research International, 2020, 4057160. PMID: 31966829.

‍

Yadav, P., Chatterjee, A., & Bhattacharjee, A. (2014). Identification of deleterious nsSNPs in α, μ, π and θ class of GST family and their influence on protein structure. Genomics Data, 2, 66–72. PMID: 26484073.

‍

31. Iron Deficiency

‍

StrandIQ SNP Marker Count: 21

‍

StrandIQ Genes for Trait: 

ABO, ACSL3P1, ACTL6B, BMAL1, BTN1A1, CNGB3, DUOX2, F5, GOLGA2P1, H2BC4, HFE, INHCAP, KCTD17, LARRPM, MAD1L1, RAB6B, SLC17A2, SRPRB, TF, TFR2, TMPRSS6

‍

References:

Beben, B., et al. (2009). Variants in TF and HFE explain approximately 40% of genetic variation in serum-transferrin levels. American Journal of Human Genetics, 84(1), 60–65. PMID: 19084217.

‍

Benyamin, B., et al. (2014). Novel loci affecting iron homeostasis and their effects in individuals at risk for hemochromatosis. Nature Communications, 5, 4926. PMID: 25352340.

‍

Buerkli, S., et al. (2021). The TMPRSS6 variant (SNP rs855791) affects iron metabolism and oral iron absorption – a stable iron isotope study in Taiwanese women. Haematologica, 106(11), 2897–2905. PMID: 33054130.

‍

Chambers, J.C., et al. (2009). Genome-wide association study identifies variants in TMPRSS6 associated with hemoglobin levels. Nature Genetics, 41(11), 1170–1172. PMID: 19820698.

‍

Guindo-Martínez, M., et al. (2021). The impact of non-additive genetic associations on age-related complex diseases. Nature Communications, 12(1), 2436. PMID: 33893285.

‍

Li, J., et al. (2015). Genome-wide admixture and association study of serum iron, ferritin, transferrin saturation and total iron binding capacity in African Americans. Human Molecular Genetics, 24(2), 572–581. PMID: 25224454.

‍

McLaren, C.E., et al. (2011). Genome-wide association study identifies genetic loci associated with iron deficiency. PLoS One, 6(3), e17390. PMID: 21483845.

‍

Toivonen, J., et al. (2024). The value of genetic data from 665,460 individuals in managing iron deficiency anaemia and suitability to donate blood. Vox Sanguinis, 119(1), 34–42. PMID: 38018286.

‍

Traglia, M., et al. (2011). Association of HFE and TMPRSS6 genetic variants with iron and erythrocyte parameters is only in part dependent on serum hepcidin concentrations. Journal of Medical Genetics, 48(9), 629–634. PMID: 21785125.

‍

Yang, Z., et al. (2024). Causal relationship of serum micronutrient with autoimmune neurological diseases: a Mendelian randomization study. Preprint, Research Square. https://doi.org/10.21203/rs.3.rs-4590504/v1

‍

32. Selenium Deficiency

‍

StrandIQ SNP Marker Count: 12

‍

StrandIQ Genes for Trait: 

ARSB, BHMT, CBS, DMGDH, FAM135B, HOMER1, KYNU, LINC01695, MTMR7, PRKG1, SDCCAG8, TCF7

‍

References:

Batai, K., et al. (2021). Genome-wide association study of response to selenium supplementation and circulating selenium concentrations in adults of European descent. Journal of Nutrition, 151(2), 293–302. PMID: 33382417.

‍

Cornelis, M.C., et al. (2015). Genome-wide association study of selenium concentrations. Human Molecular Genetics, 24(5), 1469–1477. PMID: 25343990.

‍

Evans, D.M., et al. (2013). Genome-wide association study identifies loci affecting blood copper, selenium and zinc. Human Molecular Genetics, 22(19), 3998–4006. PMID: 23720494.

‍

Gong, J., et al. (2013). Genome-wide association study of serum selenium concentrations. Nutrients, 5(5), 1706–1718. PMID: 23698163.

‍

Huang, T., et al. (2024). Genetically predicted circulating concentrations of micronutrients and risk of hypertensive disorders of pregnancy: a Mendelian randomization study. Archives of Gynecology and Obstetrics, 310, 1019–1025.

‍

Li, J., et al. (2023). Causal effect of selenium levels on osteoporosis: a Mendelian randomization study. Nutrients, 15(24), 5065.

‍

Liu, K., et al. (2024). Genetically determined circulating micronutrients and the risk of nonalcoholic fatty liver disease. Scientific Reports, 14(1), 1105. PMID: 38212362.

‍

Moksnes, M.R., et al. (2024). A genome-wide association study provides insights into the genetic etiology of 57 essential and non-essential trace elements in humans. Communications Biology, 7, 432.

‍

Sharma, P., et al. (2024). Genetic determinants of selenium availability, selenium-response, and risk of polycystic ovary syndrome. Biological Trace Element Research, 202(11), 4843–4857. PMID: 38227265.

‍

Yang, W., et al. (2022). Genome-wide association and Mendelian randomization study of blood copper levels and 213 deep phenotypes in humans. Communications Biology, 5(1), 405. PMID: 35501403.

‍

33. Zinc Deficiency

‍

StrandIQ SNP Marker Count: 15

‍

StrandIQ Genes for Trait: CA1, FNTB, LINC01221, LINC01222, LINC02309, LINC02814, MAX, MIR4778, NBDY, PPCDC, SCAMP5, SLC36A4, SLC39A8, SPIN3, TMOD1

‍

References:

‍

Evans, D.M., et al. (2013). Genome-wide association study identifies loci affecting blood copper, selenium and zinc. Human Molecular Genetics, 22(19), 3998–4006. PMID: 23720494.

‍

Flatby, H.M., et al. (2023). Circulating levels of micronutrients and risk of infections: a Mendelian randomization study. BMC Medicine, 21(1), 84. PMID: 36882828.

‍

Guo, D., et al. (2022). Preliminary study of genome-wide association identifies novel susceptibility genes for serum mineral elements in the Chinese Han population. Biological Trace Element Research, 200(6), 2549–2555. PMID: 34417961.

‍

Kodali, H.P., Pavilonis, B.T., Schooling, C.M. (2018). Effects of copper and zinc on ischemic heart disease and myocardial infarction: a Mendelian randomization study. American Journal of Clinical Nutrition, 108(2), 237–242. PMID: 29982268.

‍

Liu, K., et al. (2024). Genetically determined circulating micronutrients and the risk of nonalcoholic fatty liver disease. Scientific Reports, 14(1), 1105. PMID: 38212362.

‍

Moksnes, M.R., et al. (2024). A genome-wide association study provides insights into the genetic etiology of 57 essential and non-essential trace elements in humans. Communications Biology, 7(1), 432. PMID: 38594418.

‍

Ng, E., et al. (2015). Genome-wide association study of toxic metals and trace elements reveals novel associations. Human Molecular Genetics, 24(16), 4739–4745. PMID: 26025379.

‍

Yang, W., et al. (2022). Genome-wide association and Mendelian randomization study of blood copper levels and 213 deep phenotypes in humans. Communications Biology, 5(1), 405. PMID: 35501403.

‍

Zhou, Y., Wei, Z., Zhan, L., et al. (2024). Causal relationship of serum micronutrient with autoimmune neurological diseases: a Mendelian randomization study. Preprint, posted July 18, 2024. https://www.researchsquare.com/article/rs-4590504/v1

‍

Treatment Insight Pharmacogenomic Traits (14-16)

‍

1. Androgenetic Alopecia
   
   

StrandIQ SNP Marker Count:

• Male Balding Pattern A: 39
• Male Balding Pattern B: 33
• Male Balding Pattern C: 44
• Female Pattern Hair Loss: 4

‍

StrandIQ Genes for Trait:

• Male Balding Pattern A:
  C10orf11, CCDC140, CEP112, CLYBL, CPEB2-AS1, EPC1, EYA4, FARSB, FGF5, GLIS1, GLIS3, GORAB, HDAC9, JAZF1, LGR4, LINC00536, LINC00578, MRPS22, NSF, PAX3, PCCA, PRDM6, PRKCH, RAD51B, RP1-283K11.3, RP1-79C4.1, RP11-125P18.1, RP11-15B24.5, RP11-346D6.6, RP11-66B24.5, RP11-84D1.2, RREB1, RUNX1, SGPP2, SHFM1, TCF12, TEX41, ZBTB20, ZBTB20-AS1
  
  
• Male Balding Pattern B:
  AC004870.3, AC004870.4, AC004901.1, AC097468.7, AC217772.1, C10orf11, C1orf127, DPY30, EBF1, EPC1, FGF5, HDAC9, KANSL1, LHPP, MEMO1, MRPS22, OFCC1, PAX3, PDGFA, PRDM6, RP11-283G6.4, RP11-283G6.5, RP11-542A14.1, RP11-846C15.2, RSPO2, RUNX1, SLC14A2, SSPN, TBX15, TEX41, WARS2, WNT10A, ZHX3
• Male Balding Pattern C:
  AC003070.1, AC010987.5, AC092162.1, ALDH1L1-AS2, ARHGAP27, BCKDHA, C10orf11, C1orf127, CASC15, CTC-435M10.3, DPY30, EBF1, FAM53B, FGF5, HDAC9, KLF15, LHPP, LINC00670, LRRC36, MEMO1, MRPS22, NSF, OFCC1, PRDM6, RP11-12J10.3, RP11-283G6.4, RP11-283G6.5, RP11-418J17.1, RP11-576I22.2, RP11-846C15.2, RP11-84D1.2, RP4-799D16.1, RSPO2, RUNX1, RUNX3, SLC14A2, SPAG17, SSPN, TBX15, TEX41, TWIST1, WARS2, ZBTB38, ZHX3
  
  
• Female Pattern Hair Loss:
  CYP19A1, ESR2, VDR, HSD3B1

‍

References:

‍

Male Balding Patterns

Backman, J.D., et al. (2021). Exome sequencing and analysis of 454,787 UK Biobank participants. Nature, 599(7886), 628–634. PMID: 34662886.

‍

Chen, Y., et al. (2023). Genetic prediction of male pattern baldness based on large independent datasets. European Journal of Human Genetics, 31(3), 321–328. PMID: 36336714.

‍

Eriksson, A.L., et al. (2009). Genetic variations in sex steroid-related genes as predictors of serum estrogen levels in men. Journal of Clinical Endocrinology & Metabolism, 94(3), 1033–1041. PMID: 19116238.

‍

Hagenaars, S.P., et al. (2017). Genetic prediction of male pattern baldness. PLoS Genetics, 13(2), e1006594. PMID: 28196072.

‍

Heilmann-Heimbach, S., et al. (2017). Meta-analysis identifies novel risk loci and yields systematic insights into the biology of male-pattern baldness. Nature Communications, 8, 14694. PMID: 28272467.

‍

Kanda, S., et al. (2015). Effects of functional genetic polymorphisms in the CYP19A1 gene on prostate cancer risk and survival. International Journal of Cancer, 136(1), 74–82. PMID: 24803183.

‍

Liu, F., et al. (2016). Prediction of male-pattern baldness from genotypes. European Journal of Human Genetics, 24(6), 895–902. PMID: 26508577.

‍

Marcińska, M., et al. (2015). Evaluation of DNA variants associated with androgenetic alopecia and their potential to predict male pattern baldness. PLoS One, 10(5), e0127852. PMID: 26001114.

‍

Pirastu, N., et al. (2017). GWAS for male-pattern baldness identifies 71 susceptibility loci explaining 38% of the risk. Nature Communications, 8(1), 1584. PMID: 29146897.

‍

Yap, C.X., et al. (2018). Dissection of genetic variation and evidence for pleiotropy in male pattern baldness. Nature Communications, 9(1), 5407. PMID: 30573740.

‍

Female Pattern Hair Loss

Ho, C-Y., et al. (2023). Female pattern hair loss: An overview with focus on the genetics. Genes, 14(7), 1326. PMID: 37510231.

‍

Łukasik, A., et al. (2022). The role of CYP19A1 and ESR2 gene polymorphisms in female androgenetic alopecia in the Polish population. Postepy Dermatologii i Alergologii, 39(4), 708–713. PMID: 36090736.

‍

Redler, S., et al. (2017). Genetics and other factors in the aetiology of female pattern hair loss. Experimental Dermatology, 26(6), 510–517. PMID: 28453904.

‍

Rui, W., et al. (2015). Association of single nucleotide polymorphisms in the CYP19A1 gene with female pattern hair loss in a Chinese population. Dermatology, 231(3), 239–244. PMID: 26228318.

‍

Seleit, I., et al. (2020). Vitamin D receptor gene polymorphisms Taq-1 and Cdx-1 in female pattern hair loss. Indian Journal of Dermatology, 65(4), 259–264. PMID: 32831364.

‍

Tu, Y.A., et al. (2019). HSD3B1 gene polymorphism and female pattern hair loss in women with polycystic ovary syndrome. Journal of the Formosan Medical Association, 118(8), 1225–1231. PMID: 31056381.

‍

Yip, L., et al. (2009). Gene-wide association study between the aromatase gene (CYP19A1) and female pattern hair loss. British Journal of Dermatology, 161(2), 289–294. PMID: 19438456.

2. Minoxidil Effectiveness
   
   StrandIQ SNP Marker Count: 3

‍

StrandIQ Genes for Trait:
SULT1A1

‍

References:
Chitalia, J., et al. (2018). Characterization of follicular minoxidil sulfotransferase activity in a cohort of pattern hair loss patients from the Indian Subcontinent. Dermatology and Therapy, 31(6), e12688. PMID: 30295395.

Dhurat, R., et al. (2022). SULT1A1 (Minoxidil Sulfotransferase) enzyme booster significantly improves response to topical minoxidil for hair regrowth. Journal of Cosmetic Dermatology, 21(1), 343–346. PMID: 34133836.

Goren, A., Castano, J.A., McCoy, J., Bermudez, F., Lotti, T. (2014). Novel enzymatic assay predicts minoxidil response in the treatment of androgenetic alopecia. Dermatology and Therapy, 27(3), 171–173. PMID: 24283387.

King, R.S., Ghosh, A.A., Wu, J. (2006). Inhibition of human phenol and estrogen sulfotransferase by certain non-steroidal anti-inflammatory agents. Current Drug Metabolism, 7(7), 745–753. PMID: 17073578.

Mehta, N., et al. (2024). Minoxidil sulfotransferase enzymatical activity in plants: A novel paradigm in increasing minoxidil response in androgenetic alopecia. Journal of Cosmetic Dermatology, 23(1), 339–343. PMID: 37638619.

Messenger, A.G., Rundegren, J. (2004). Minoxidil: mechanisms of action on hair growth. British Journal of Dermatology, 150(2), 186–194. PMID: 14996087.

Ramos, P.M., et al. (2021). Minoxidil sulfotransferase enzyme (SULT1A1) genetic variants predicts response to oral minoxidil treatment for female pattern hair loss. Journal of the European Academy of Dermatology and Venereology, 35(1), e24–e26. PMID: 32567076.

Sharma, A., et al. (2019). Tretinoin enhances minoxidil response in androgenetic alopecia patients by upregulating follicular sulfotransferase enzymes. Dermatology and Therapy, 32(3), e12915. PMID: 30974011.

Suchonwanit, P., Thammarucha, S., Leerunyakul, K. (2019). Minoxidil and its use in hair disorders: a review. Drug Design, Development and Therapy, 13, 2777–2786. PMID: 31496654.

Yan, A., et al. (2023). Co-delivery of minoxidil and tocopherol acetate ethosomes to reshape the hair follicular microenvironment and promote hair regeneration in androgenetic alopecia. International Journal of Pharmaceutics, 646, 123498. PMID: 37820942.

Yu, X., et al. (2010). Functional genetic variants in the 3'-untranslated region of sulfotransferase isoform 1A1 (SULT1A1) and their effect on enzymatic activity. Toxicological Sciences, 118(2), 391–403. PMID: 20881232.

3. Dutasteride Effectiveness
   
   StrandIQ SNP Marker Count: 6

‍

StrandIQ Genes for Trait:
SRD5A1, SRD5A2

‍

References:
Ellis, J.A., et al. (2005). Androgenic correlates of genetic variation in the gene encoding 5alpha-reductase type 1. Journal of Human Genetics, 50(10), 534–537. PMID: 16155734.

Escamilla-Cruz, M., et al. (2023). Use of 5-alpha reductase inhibitors in dermatology: A narrative review. Dermatology and Therapy (Heidelberg), 13(8), 1721–1731. PMID: 37432644.

Ha, S.J., et al. (2003). Analysis of genetic polymorphisms of steroid 5alpha-reductase type 1 and 2 genes in Korean men with androgenetic alopecia. Journal of Dermatological Science, 31(2), 135–141. PMID: 12670724.

Hayes, V.M., et al. (2007). 5alpha-reductase type 2 gene variant associations with prostate cancer risk, circulating hormone levels and androgenetic alopecia. International Journal of Cancer, 120(4), 776–780. PMID: 17136762.

Li, X., et al. (2011). Meta-analysis of three polymorphisms in the steroid-5-alpha-reductase, alpha polypeptide 2 gene (SRD5A2) and risk of prostate cancer. Mutagenesis, 26(3), 371–383. PMID: 21177315.

Makridakis, N., Reichardt, J.K. (2005). Pharmacogenetic analysis of human steroid 5 alpha reductase type II: comparison of finasteride and dutasteride. Journal of Molecular Endocrinology, 34(3), 617–623. PMID: 15956333.

Rhie, A., et al. (2019). Genetic variations associated with response to dutasteride in the treatment of male subjects with androgenetic alopecia. PLoS One, 14(9), e0222533. PMID: 31525235.

Vila-Vecilla, L., Russo, V., de Souza, G.T. (2024). Genomic markers and personalized medicine in androgenetic alopecia: A comprehensive review. Cosmetics, 11(5), 148.

Villapalos-García, G., et al. (2021). Effects of Cytochrome P450 and transporter polymorphisms on the bioavailability and safety of dutasteride and tamsulosin. Frontiers in Pharmacology, 12, 718281. PMID: 34690761.

Xiao, Q., et al. (2020). Structure of human steroid 5α-reductase 2 with the anti-androgen drug finasteride. Nature Communications, 11(1), 5430. PMID: 33110062.

Zeng, X.T., et al. (2017). Association between SRD5A2 rs523349 and rs9282858 polymorphisms and risk of benign prostatic hyperplasia: A meta-analysis. Frontiers in Physiology, 8, 688. PMID: 28955247.

4. Dutasteride Metabolism
   
   StrandIQ SNP Marker Count: 3

‍

StrandIQ Genes for Trait:
CYP3A4, CYP4V2, CYP19A1

‍

References:
Burns, O., et al. (2018). Relative bioavailability of fixed-dose combinations of tamsulosin and dutasteride: Results from 2 randomized trials in healthy male volunteers. Clinical Pharmacology Drug Development, 7(4), 422–434. PMID: 28800206.

Eriksson, A.L., et al. (2009). Genetic variations in sex steroid-related genes as predictors of serum estrogen levels in men. Journal of Clinical Endocrinology & Metabolism, 94(3), 1033–1041. PMID: 19116238.

Francès, M.P., et al. (2024). Utilising SNP association analysis as a prospective approach for personalising androgenetic alopecia treatment. Dermatology and Therapy (Heidelberg), 14(4), 971–981. PMID: 38555553.

Jiang, J., et al. (2010). Association of genetic variations in aromatase gene with serum estrogen and estrogen/testosterone ratio in Chinese elderly men. Clinica Chimica Acta, 411(1–2), 53–58. PMID: 19818337.

Makridakis, N.M., et al. (2000). Biochemical and pharmacogenetic dissection of human steroid 5 alpha-reductase type II. Pharmacogenetics, 10(5), 407–413. PMID: 10898110.

Rhie, A., et al. (2019). Genetic variations associated with response to dutasteride in the treatment of male subjects with androgenetic alopecia. PLoS One, 14(9), e0222533. PMID: 31525235.

Vila-Vecilla, L., Russo, V., de Souza, G.T. (2024). Genomic markers and personalized medicine in androgenetic alopecia: A comprehensive review. Cosmetics, 11(5), 148.

Villapalos-García, G., et al. (2021). Effects of cytochrome P450 and transporter polymorphisms on the bioavailability and safety of dutasteride and tamsulosin. Frontiers in Pharmacology, 12, 718281. PMID: 34690761.

Yeap, B.B., et al. (2019). A 5α-reductase (SRD5A2) polymorphism is associated with serum testosterone and sex hormone-binding globulin in men, while aromatase (CYP19A1) polymorphisms are associated with oestradiol and luteinizing hormone reciprocally. Clinical Endocrinology (Oxford), 90(2), 301–311. PMID: 30353958.

5. Finasteride Effectiveness
   
   StrandIQ SNP Marker Count: 6

‍

StrandIQ Genes for Trait:
SRD5A1, SRD5A2

‍

References:
Hayes, V.M., et al. (2007). 5alpha-Reductase type 2 gene variant associations with prostate cancer risk, circulating hormone levels and androgenetic alopecia. International Journal of Cancer, 120(4), 776–780. PMID: 17136762.

Li, X., et al. (2011). Meta-analysis of three polymorphisms in the steroid-5-alpha-reductase, alpha polypeptide 2 gene (SRD5A2) and risk of prostate cancer. Mutagenesis, 26(3), 371–383. PMID: 21177315.

Vila-Vecilla, L., Russo, V., de Souza, G.T. (2024). Genomic markers and personalized medicine in androgenetic alopecia: A comprehensive review. Cosmetics, 11(5), 148.

Xiao, Q., et al. (2020). Structure of human steroid 5α-reductase 2 with the anti-androgen drug finasteride. Nature Communications, 11(1), 5430. PMID: 33110062.

Zeng, X.T., et al. (2017). Association between SRD5A2 rs523349 and rs9282858 polymorphisms and risk of benign prostatic hyperplasia: A meta-analysis. Frontiers in Physiology, 8, 688. PMID: 28955247.

6. Finasteride Metabolism
   
   StrandIQ SNP Marker Count: 1

‍

StrandIQ Genes for Trait:
CYP3A4

‍

References:
Chau, C.H., et al. (2015). Finasteride concentrations and prostate cancer risk: results from the Prostate Cancer Prevention Trial. PLoS One, 10(5), e0126672. PMID: 25955319.

Elens, L., et al. (2013). CYP3A4*22: promising newly identified CYP3A4 variant allele for personalizing pharmacotherapy. Pharmacogenomics, 14(1), 47–62. PMID: 23252948.

Hulin-Curtis, S.L., et al. (2010). Finasteride metabolism and pharmacogenetics: new approaches to personalized prevention of prostate cancer. Future Oncology, 6(12), 1897–1913. PMID: 21142863.

Pratt, V.M., et al. (2023). CYP3A4 and CYP3A5 genotyping recommendations: A joint consensus recommendation of the Association for Molecular Pathology, Clinical Pharmacogenetics Implementation Consortium, College of American Pathologists, Dutch Pharmacogenetics Working Group of the Royal Dutch Pharmacists Association, European Society for Pharmacogenomics and Personalized Therapy, and Pharmacogenomics Knowledgebase. Journal of Molecular Diagnostics, 25(9), 619–629. PMID: 37419245.

Wang, D., Sadee, W. (2016). CYP3A4 intronic SNP rs35599367 (CYP3A4*22) alters RNA splicing. Pharmacogenetics and Genomics, 26(1), 40–43. PMID: 26488616.

7. Spironolactone Effectiveness
   
   StrandIQ SNP Marker Count: 2

‍

StrandIQ Genes for Trait:
CYP19A1

‍

References:
Abdel-Raouf, H., et al. (2021). A novel topical combination of minoxidil and spironolactone for androgenetic alopecia: Clinical, histopathological, and physicochemical study. Dermatology Therapy, 34(1), e14678. PMID: 33320406.

Burns, L.J., et al. (2020). Spironolactone for treatment of female pattern hair loss. Journal of the American Academy of Dermatology, 83(1), 276–278. PMID: 32259535.

Sinclair, R.D. (2018). Female pattern hair loss: a pilot study investigating combination therapy with low-dose oral minoxidil and spironolactone. International Journal of Dermatology, 57(1), 104–109. PMID: 29231239.

8. Estradiol Effectiveness
   
   StrandIQ SNP Marker Count: 2

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StrandIQ Genes for Trait:
CYP19A1

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References:
Haiman, C.A., et al. (2007). Genetic variation at the CYP19A1 locus predicts circulating estrogen levels but not breast cancer risk in postmenopausal women. Cancer Research, 67(5), 1893–1897. PMID: 17325027.

Jiang, J., et al. (2010). Association of genetic variations in aromatase gene with serum estrogen and estrogen/testosterone ratio in Chinese elderly men. Clinica Chimica Acta, 411(1–2), 53–58. PMID: 19818337.

Nebert, D.W., et al. (2013). Human cytochromes P450 in health and disease. Philosophical Transactions of the Royal Society B: Biological Sciences, 368(1612), 20120431. PMID: 23297354.

Zhang, X.L., et al. (2012). SNP rs2470152 in CYP19 is correlated to aromatase activity in Chinese polycystic ovary syndrome patients. Molecular Medicine Reports, 5(1), 245–249. PMID: 21972004.

9. Topical Retinoic Acid Effectiveness
   StrandIQ SNP Marker Count: 3

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StrandIQ Genes for Trait:
CRABP2, CYP26B1, RXRG

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References:
Bielli, A., et al. (2019). Cellular retinoic acid binding protein-II expression and its potential role in skin aging. Aging (Albany NY), 11(6), 1619–1632. PMID: 30888968.

Manolescu, D.C., et al. (2010). Newborn serum retinoic acid level is associated with variants of genes in the retinol metabolism pathway. Pediatric Research, 67(6), 598–602. PMID: 20308937.

Rhie, A., et al. (2019). Genetic variations associated with response to dutasteride in the treatment of male subjects with androgenetic alopecia. PLoS One, 14(9), e0222533. PMID: 31525235.

Stevison, F., et al. (2015). Role of retinoic acid-metabolizing cytochrome P450s, CYP26, in inflammation and cancer. Advances in Pharmacology, 74, 373–412. PMID: 26233912.

10. IGF-1 Bioavailability
    
    StrandIQ SNP Marker Count: 1

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StrandIQ Genes for Trait:
IGF1R

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References:
Ahn, S.Y., et al. (2012). Effect of IGF-I on hair growth is related to the anti-apoptotic effect of IGF-I and up-regulation of PDGF-A and PDGF-B. Annals of Dermatology, 24(1), 26–31. PMID: 22363152.

Ben Amitai, D., et al. (2006). IGF-1 signalling controls the hair growth cycle and the differentiation of hair shafts. Journal of Investigative Dermatology, 126(9), 2135. PMID: 16778791.

Bonafè, M., et al. (2003). Polymorphic variants of insulin-like growth factor I (IGF-I) receptor and phosphoinositide 3-kinase genes affect IGF-I plasma levels and human longevity: cues for an evolutionarily conserved mechanism of life span control. Journal of Clinical Endocrinology & Metabolism, 88(7), 3299–3304. PMID: 12843179.

Castela, M., et al. (2017). Igf1r signalling acts on the anagen-to-catagen transition in the hair cycle. Experimental Dermatology, 26(9), 785–791. PMID: 28094870.

Inui, S., Itami, S. (2013). Induction of insulin-like growth factor-I by cepharanthine from dermal papilla cells: a novel potential pathway for hair growth stimulation. Journal of Dermatology, 40(12), 1054–1055. PMID: 24164396.

Noordam, R., et al. (2016). Both low circulating insulin-like growth factor-1 and high-density lipoprotein cholesterol are associated with hair loss in middle-aged women. British Journal of Dermatology, 175(4), 728–734. PMID: 26959288.

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Panchaprateep, R., Asawanonda, P. (2014). Insulin-like growth factor-1: roles in androgenetic alopecia. Experimental Dermatology, 23(3), 216–218. PMID: 24499417.

Philpott, M.P., et al. (1994). Effects of insulin and insulin-like growth factors on cultured human hair follicles: IGF-I at physiologic concentrations is an important regulator of hair follicle growth in vitro. Journal of Investigative Dermatology, 102(6), 857–861. PMID: 8006448.

Tavakkol, A., et al. (1992). Expression of growth hormone receptor, insulin-like growth factor 1 (IGF-1) and IGF-1 receptor mRNA and proteins in human skin. Journal of Investigative Dermatology, 99, 343–349.PMID: 1324963

Wang, Y., et al. (2025). Targeting IGF1-induced cellular senescence to rejuvenate hair follicle aging. Aging Cell, 24(7), e70053. PMID: 40159808.

Werner, H. (2023). The IGF1 signaling pathway: From basic concepts to therapeutic opportunities. International Journal of Molecular Sciences, 24(19), 14882. PMID: 37834331.

11. Latanoprost Effectiveness
    
    StrandIQ SNP Marker Count: 3

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StrandIQ Genes for Trait:
PTGFR

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References:
Blume-Peytavi, U., et al. (2012). A randomized double-blind placebo-controlled pilot study to assess the efficacy of a 24-week topical treatment by latanoprost 0.1% on hair growth and pigmentation in healthy volunteers with androgenetic alopecia. Journal of the American Academy of Dermatology, 66(5), 794–800. PMID: 21875758.

Cornejo-García, J.A., et al. (2016). Pharmacogenomics of prostaglandin and leukotriene receptors. Frontiers in Pharmacology, 7, 316. PMID: 27708579.

Coronel-Pérez, I.M., et al. (2010). Latanoprost in the treatment of eyelash alopecia in alopecia areata universalis. Journal of the European Academy of Dermatology and Venereology, 24(4), 481–485. PMID: 20028444.

Rafati, M., et al. (2022). The effect of latanoprost 0.005% solution in the management of scalp alopecia areata, a randomized double-blind placebo-controlled trial. Dermatology Therapy, 35(6), e15450. PMID: 35289043.

Ussa, F., et al. (2015). Association between SNPs of metalloproteinases and prostaglandin F2α receptor genes and latanoprost response in open-angle glaucoma. Ophthalmology, 122(5), 1040–1048.e4. PMID: 25704319.

12. Steroidal Inflammatory Effectiveness
    
    StrandIQ SNP Marker Count: 1

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StrandIQ Genes for Trait:
NR3C1

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References:
Botelho Barra, C., et al. (2022). Pharmacogenomic markers of glucocorticoid response in congenital adrenal hyperplasia. PLoS One, 17(12), e0279298. PMID: 36538565.

Nordkap, L., et al. (2022). Hair cortisol, glucocorticoid gene receptor polymorphisms, stress, and testicular function. Psychoneuroendocrinology, 146, 105942. PMID: 36179533.

Oakley, R.H., Cidlowski, J.A. (2013). The biology of the glucocorticoid receptor: new signaling mechanisms in health and disease. Journal of Allergy and Clinical Immunology, 132(5), 1033–1044. PMID: 24084075.

Ramirez-Falcon, M., et al. (2024). Defining the differential corticosteroid response basis from multiple omics approaches. International Journal of Molecular Sciences, 25(24), 13611. PMID: 39769372.

Sombetzki, C., et al. (2025). Impact of glucocorticoid receptor polymorphism rs6198 on sepsis survival in a prospective multicenter cohort. Scientific Reports, 15(1), 24760. PMID: 40634451.

Štampar, P., et al. (2024). Genetic variability in the glucocorticoid pathway and treatment outcomes in hospitalized patients with COVID-19: a pilot study. Frontiers in Pharmacology, 15, 1418567. PMID: 39135792.

Strehl, C., et al. (2019). Glucocorticoids—all-rounders tackling the versatile players of the immune system. Frontiers in Immunology, 10, 1744. PMID: 31396235.

13. Phytotherapy Benefits
    
    StrandIQ SNP Marker Count: 2

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StrandIQ Genes for Trait:
PTGDR2

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References:
Francès, M.P., et al. (2024). Utilising SNP association analysis as a prospective approach for personalising androgenetic alopecia treatment. Dermatology and Therapy (Heidelberg), 14(4), 971–981. PMID: 38555553.

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Garza, L.A., et al. (2012). Prostaglandin D2 inhibits hair growth and is elevated in bald scalp of men with androgenetic alopecia. Science Translational Medicine, 4(126), 126ra34. PMID: 22440736.

Nieves, A., Garza, L.A. (2014). Does prostaglandin D2 hold the cure to male pattern baldness? Experimental Dermatology, 23(4), 224–227. PMID: 24521203.

Shin, D.W. (2022). The physiological and pharmacological roles of prostaglandins in hair growth. Korean Journal of Physiology & Pharmacology, 26(6), 405–413. PMID: 36302616.

14. Cetirizine Effectiveness
    
    StrandIQ SNP Marker Count: 2

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StrandIQ Genes for Trait:
PTGDR2

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References:
Chen, X., et al. (2022). Topical cetirizine for treating androgenetic alopecia: A systematic review. Journal of Cosmetic Dermatology, 21(11), 5519–5526. PMID: 35976065.

Gohary, Y.M., et al. (2025). The efficacy of topical cetirizine using microneedling in androgenetic alopecia male patients. Archives of Dermatological Research, 317(1), 665. PMID: 40167621.

Jiang, S., et al. (2023). The efficacy of topical prostaglandin analogs for hair loss: A systematic review and meta-analysis. Frontiers in Medicine (Lausanne), 10, 1130623. PMID: 36999072.

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This content, including StrandIQ™ DNA analysis reports and any Happy Head products and/or services referenced therein, is for informational and cosmetic purposes only. It is not intended to diagnose, treat, cure, or prevent any disease. This content does not constitute medical advice and should not be used to make healthcare decisions. References to prescription treatments are educational in nature. Always consult a licensed healthcare professional for any medical concerns or treatment decisions.

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