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Learn MoreGenetic testing is trending in the hair loss industry. The premise? Our genes hold the secrets to better hair growth, and genetic testing can help hair loss sufferers unlock new levels of hair gains with customized treatments. It’s an enticing proposition, and one that holds little-to-no scientific support. In this article, we explore 12 genes often used by genetic testing companies to “customize” hair loss products. The science supporting the recommendations? Data that, in many cases, has nothing to do with hair loss; for instance, studies on newborn umbilical cords, patients with lung cancer, and children with leukemia. But it’s not all bad. This article reveals more.
Imagine if your genes could predict how much hair you’ll regrow from minoxidil… or whether you could get side effects from finasteride. This would be a breakthrough in hair loss treatments… and yet, according to some genetic testing companies, this breakthrough is already here and available (for a price).
Certain telehealth companies now offer to sequence your DNA to help you create a more tailored, personalized treatment plan for your hair loss.[1]TrichoTest. (no date). Personalizing alopecia treatment. Fagron Genomics. Available at: https://gxsciences.com/trichotest/. (Accessed: October 2024) Depending on your genetics, they might recommend substituting finasteride for dutasteride, oral over topical minoxidil, or adding corticosteroids – all based on the latest scientific data.
Who wouldn’t want to do this? It would enable you to create the highest-value and lowest-risk treatment plan for yourself.
However, the quality of the evidence surrounding this approach isn’t so cut and dry. That’s why we conducted a four-month research project in which we identified 12 genes that some companies say are associated with treatment efficacy. We looked at the available literature to determine what the science says, the quality behind it, and whether it is even relevant to hair loss.
SNPs are changes at a single position in a DNA sequence. They can occur within genes or in the regions between genes. SNPs are the most common type of genetic variation in humans, occurring once in every 100-300 nucleotides in the human genome.[2]Nelson, M.R., Marnellos, G., Kammerer, S., Hoyal, C.R., Shi, M.M., Cantor, C.R., Braun, A. (2004). Large-scale validation of single nucleotide polymorphisms in gene regions. Genome Research. … Continue reading
In coding regions of genes, SNPs can be:
SNPs in non-coding regions of genes can affect gene expression, gene splicing, or other regulatory processes.[4]Degtyareva, A.O., Antontseva, E.V., Merkulova, T.I. (2021). Regulatory SNPs: Altered Transcription Factor Binding Sites Implicated in Complex Traits and Diseases. International Journal of Molecular … Continue reading Like genes, SNPs are inherited from parents to their children and contribute to genetic differences between people.
SNPs in certain genes may increase susceptibility to specific diseases. For example, a large-scale genome-wide association study identified 71 significantly associated loci for male pattern baldness, indicating a genetic aspect to the pathogenesis of androgenic alopecia.[5]Pirastu, N., Joshi, P.K., deVries, P.S., Cornerlis, M.C., McKeigue, P.M., Keum, N., Franceschini, N., Colombo, M., Giovannucci, E.L., Spiliopoulou, A., Franke, L., North, K.E., Kraft, Morrison, A.C., … Continue reading
So, now that we’ve discussed genes and SNPs, let’s examine what we found.
We’ve created a table of every gene we analyzed to give you an overview of the articles. Below, we will summarize each gene and its potential for advising treatment efficacy.
Gene | SNP | What the Genetic Testing Companies Say | What the Evidence Says | Treatment Relevance (1-5) |
ACE | rs4341 | People with a deletion variant of this polymorphism (CG or GG) may want to try treatments that improve blood flow to the scalp. | The deletion allele (G) is associated with increased ACE activity, which leads to vasoconstriction and reduced blood flow.
No studies show an association between this polymorphism and the response to hair treatments that may improve blood flow. |
1 |
rs4343 | People with a deletion variant of this polymorphism (AG or GG) may want to try treatments that improve blood flow to the scalp. | The deletion allele (G) is associated with increased ACE activity, which leads to vasoconstriction and reduced blood flow.
No studies show an association between this polymorphism and the response to hair treatments that may improve blood flow. |
||
BTD | rs13078881 | People with the CC or CG variants may be good candidates for biotin supplementation. | The CC and CG genotypes were associated with biotinidase deficiency in a study of 19 children.
Adults with this polymorphism exhibited biotinidase deficiency but presented no symptoms. No studies show an association between this polymorphism and hair loss or the response to biotin supplementation. |
1 |
COL1A1 | rs1800012 | People with the GT variant may benefit from supplementation that supports collagen formation. | People with the GT variant were found to have an increased ratio of α1 to α2 chains, which could lead to instability of the collagen molecules.
No studies show an association between this polymorphism and the response to supplements that support collagen formation. |
1 |
CRABP2 | rs12724719 | People with the AA variant may not benefit from standard retinoic acid supplementation and may require an increased dose or alternative treatment. | Newborn babies with the AA variant were found to have increased retinoic acid levels in their umbilical cord blood. It is not known if the same effect is seen in adults.
No studies show an association between this polymorphism and the response to retinoic acid supplementation. |
1 |
CYP19A1 | rs2470152 | People with the TC variant may benefit from treatment with replacement hormones (e.g., estradiol) or anti-androgens. | People with the TC variant were found to exhibit increased testosterone levels and a reduced ratio of estradiol to testosterone.
No studies show an association between this polymorphism and hair loss or the response to replacement hormones and anti-androgens. |
1 |
rs700519 | People with the CC variant may be a good candidate for the typical or higher dosages of 5α-reductase inhibitors.
People with the CT or TT variants may be good candidates for lower dosages of 5α-reductase inhibitors. |
People with the CT or TT variant were shown to respond better to treatment with dutasteride. However, some people with CT or TT were still classified as being poor responders to dutasteride treatment. | ||
GPR44 | rs533116 | People with the AA variant may be good candidates for treatment with PGD2 inhibitors. | People with the AA variant exhibited increased GPR44 expression in their white blood cells, which may increase sensitivity to PGD2.
No studies show an association between this polymorphism and the response to treatment with PGD2 inhibitors. |
1 |
rs545659 | People with the GG variant may be good candidates for treatment with PGD2 inhibitors. | People with the GG variants exhibited greater GPR44 mRNA stability, which may increase PGD2 activity.
No studies show an association between this polymorphism and the response to treatment with PGD2 inhibitors. |
||
GRα/GRꞵ (NR3C1) | rs6198 | People with the GG variant may not respond as well to glucocorticoid treatment. | People with the GG variant exhibited a form of the glucocorticoid receptor that does not bind as well to glucocorticoids.
No studies show an association between this polymorphism and the response to glucocorticoid treatment for hair loss. |
1 |
IGF1R | rs2229765 | People carrying at least one A allele may be good candidates for IGF-1 supplementation. | People with the AG or AA genotype were found to exhibit lower levels of IGF-1 in their plasma.
No studies show an association between this polymorphism and the response to supplementation with IGF-1. |
1 |
PGTFR | rs10782665 | People carrying at least one T allele have an increased probability of a positive response to treatment with Latanoprost. | The presence of a G allele was found to increase the probability of a positive response to Latanoprost treatment for intraocular pressure in mice.
No studies show an association between this polymorphism and hair loss response to treatment with Latanoprost. |
2 |
rs1328441 | People carrying at least one G allele have an increased probability of a positive response to treatment with Latanoprost. | The presence of a G allele was found to increase the probability of a positive response to Latanoprost treatment for intraocular pressure in mice.
No studies show an association between this polymorphism and hair loss response to treatment with Latanoprost. |
||
rs6686438 | People carrying at least one G allele have an increased probability of a positive response to treatment with Latanoprost. | The presence of a G allele was found to increase the probability of a positive response to Latanoprost treatment for intraocular pressure in mice.
No studies show an association between this polymorphism and hair loss response to treatment with Latanoprost. |
||
PTGES2 | rs13283456 | People with the CT variant have reduced PTGES2 enzymatic activity, which reduces PGE2 levels. This makes them better candidates for treatment with minoxidil, which increases PGE2 levels. | The CT variant is associated with reduced BMI in males. However, no direct evidence exists that it is associated with PTGES2 activity or PGE2 levels.
There are no studies that show an association between this polymorphism and the response to treatment with minoxidil. |
1 |
SRD5A1
& SRD5A2 |
rs248793 | People carrying at least one C allele have increased levels of DHT, which may make them good candidates for treatment with 5α-reductase inhibitors. | The presence of a C allele in adults was found to be associated with an increased DHT/T ratio.
No studies show an association between this polymorphism and the response to treatment with 5α-reductase inhibitors. |
2 |
rs523349 | People with the GG variant have increased 5α-reductase activity, which may make them good candidates for treatment with 5α-reductase inhibitors. | The GG variant is associated with increased 5α-reductase activity, which may increase DHT levels.
No studies show an association between this polymorphism and the response to treatment with 5α-reductase inhibitors. |
||
SULT1A1 | rs9282861 | People carrying at least one A allele have reduced sulfotransferase activity, which may alter their response to minoxidil. | Sulfotransferase activity was reduced in people with the GA variant and further in those with the AA variant.
Sulfotransferase catalyzes the conversion of minoxidil to its active form, minoxidil sulfate. Small-scale human studies have shown that people with the GG variant may respond better to minoxidil treatment for hair loss. |
3 |
ACE is a key enzyme in blood pressure regulation. It converts angiotensin I to angiotensin II, causing vasoconstriction. The ACE gene has an insertion/deletion (I/D) polymorphism that affects enzyme activity, with the deletion (D) allele associated with higher ACE levels and increased vasoconstrictions.[6]Wong, M. K. S. (2016). Angiotensin Converting Enzymes. In Handbook of Hormones. pp. 263-e29D-4. Elsevier. Available at: https://doi.org/10.1016/B978-0-12-801028-0.00254-3
Some research suggests a link between ACE gene polymorphisms and androgenic alopecia (AGA). Certain genetic testing companies propose that individuals with specific ACE polymorphisms may benefit from treatments that improve scalp blood flow. The theory is that higher ACE activity leads to increased vasoconstriction, potentially reducing blood flow to hair follicles. Therefore, treatments like minoxidil or caffeine, which may work partly through vasodilation, could be more effective for individuals with these genetic variants.
However, while this hypothesis is intriguing, no direct evidence demonstrates that people with particular ACE polymorphisms respond differently to hair loss treatments that improve blood flow.
Read our ACE gene article here.
The BTD gene encodes biotinidase, an enzyme crucial for recycling and utilizing biotin (Vitamin B7) in the body. Biotin is vital in various biological functions, including hair health, through its involvement in protein synthesis and keratin production.[8]Leon‐Del‐Rio, A. (2019). Biotin in metabolism, gene expression, and human disease. Journal of Inherited Metabolic Disease, 42(4), 647-654. Available at: https://doi.org/10.1002/jimd.12073
Mutations in BTD can lead to biotinidase deficiency, which can cause biotin deficiency or dependency. This condition can result in various symptoms, including hair abnormalities and alopecia.
According to some, certain BTD polymorphisms might predict the efficacy of biotin treatment for hair loss. However, the evidence supporting this claim is limited and inconclusive.[9]Bhattarai, D., Banday, A. Z., Sadanand, R., Arora, K., Kaur, G., Sharma, S., & Rawat, A. (2021). Hair microscopy: an easy adjunct to diagnosis of systemic diseases in children. Applied … Continue reading Studies have shown conflicting results regarding the impact of this polymorphism on biotinidase activity in adults and children, and none specifically address hair loss.
Read our BTD gene article here.
COL1A1 encodes one of the chains of type I collagen, the most abundant collagen in the body. Type I collagen is crucial in supporting tissue structure throughout the body.[10]Ricard-Blum, S. (2011). The collagen family. Cold Spring Harbor perspectives in biology, 3(1), a004978. Available at: https://doi.org/10.1101/cshperspect.a004978
COL1A1 gene expression is upregulated in people with AGA.[11]Michel, L., Reygagne, P., Benech, P., Jean‐Louis, F., Scalvino, S., Ly Ka So, S., Hamidou, Z., Bianovici, S., Pouch, J., Ducos, B. and Bonnet, M., 2017. Study of gene expression alteration in male … Continue reading Furthermore, studies have shown the SNPs in the COL1A1 gene can affect collagen stability.[12]Mann, V., Hobson, E.E., Li, B., Stewart, T.L., Grant, S.F., Robins, S.P., Aspden, R.M. and Ralston, S.H. (2001). A COL1A1 Sp1 binding site polymorphism predisposes to osteoporotic fracture by … Continue reading
While these findings suggest a potential role for COL1A1 in hair growth and loss, the exact mechanisms are not fully understood. More research is needed to clarify how variations in COL1A1 might influence hair loss and treatment responses. Currently, limited evidence supports targeting COL1A1 specifically for hair loss treatments.
Read our COL1A1 gene article here.
CRABP2 is one of two genes in the cellular retinoic acid-binding protein family and is crucial for regulating retinoic acid by transporting it within cells and aiding its metabolism. Retinoic acid is important for hair health, but its deficiency and excess can lead to hair loss, indicating a dose-dependent relationship.[14]Wei, L. N. (2016). Cellular retinoic acid binding proteins: Genomic and non-genomic functions and their regulation. The Biochemistry of Retinoid Signaling II: The Physiology of Vitamin A-Uptake, … Continue reading
This gene is highly expressed in dermal papilla cells, which are vital for hair follicle growth and development.[15]He, M., Lv, X., Cao, X., Yuan, Z., Quan, K., Getachew, T., Mwacharo, J.M., Haile, A., Li, Y., Wang, S. and Sun, W. (2023). CRABP2 Promotes the Proliferation of Dermal Papilla Cells via the … Continue reading Overexpression of CRABP2 promotes cell growth, suggesting a positive role in hair maintenance. However, increased CRABP2 expression and elevated retinoic acid levels have also been associated with hair loss conditions like alopecia areata and AGA.[16]Duncan, F.J., Silva, K.A., Johnson, C.J., King, B.L., Szatkiewicz, J.P., Kamdar, S.P., Ong, D.E., Napoli, J.L., Wang, J., King Jr, L.E. and Whiting, D.A. (2013). Endogenous retinoids in the … Continue reading
Despite this paradox, treatments using tretinoin have shown promise, stimulating hair regrowth in over half of patients, with further improvements observed after combination with minoxidil.[17]Bazzano, G. S., Terezakis, N., & Galen, W. (1986). Topical tretinoin for hair growth promotion. Journal of the American Academy of Dermatology, 15(4), 880-893. Available at: … Continue reading
One large study involving over 25,000 AGA patients found an association between this polymorphism and AGA, suggesting that genetic differences in CRABP2 could impact hair health and treatment efficacy.[19]Francès, M. P., Vila-Vecilla, L., Russo, V., Caetano Polonini, H., & de Souza, G. T. (2024). Utilising SNP Association Analysis as a Prospective Approach for Personalising Androgenetic Alopecia … Continue reading Ultimately, further research is needed to show exactly how it might affect treatment efficacy.
Read our CRABP2 gene article here.
CYP19A1 encodes the enzyme aromatase, which converts androgens like testosterone into estrogens like estradiol. Reduced expression of CYP19A1 and lower enzyme activity have been associated with female pattern hair loss (FPHL) and AGA. Aromatase levels are higher in non-balding scalp regions and significantly higher in women than men, possibly explaining gender differences in hair loss patterns.[20]Nebert, D. W., Wikvall, K., & Miller, W. L. (2013). Human cytochromes P450 in health and disease. Philosophical Transactions of the Royal Society B: Biological Sciences, 368(1612), 20120431. … Continue reading
Aromatase helps decrease levels of DHT, and aromatase inhibitors have been linked to hair thinning, indicating a role for the enzyme in hair health. Treatments like minoxidil may increase aromatase activity, which can improve hair growth by increasing estradiol and reducing DHT levels.[21]Gallicchio, L., Calhoun, C., & Helzlsouer, K. J. (2013). Aromatase inhibitor therapy and hair loss among breast cancer survivors. Breast cancer research and treatment, 142, 435-443. Available at: … Continue reading
While certain genetic variations have been associated with better response to treatments like dutasteride, the study also showed that some people with this SNP can be poor responders, indicating that it is probably a combination of SNPs that affects treatment response.
So, while there is evidence that CYP19A1 SNPs can affect treatment efficacy, studies have not been done to determine the relationship between these and hair growth.
Read our CYP19A1 gene article here.
The GPR44 gene encodes G-protein-coupled receptor 44 (the prostaglandin D2 receptor or DP2). GPR44 is significant because it mediates the effects of prostaglandin D2, a lipid compound involved in inflammation and the immune response.[23]National Library of Medicine. (2024). PTGDR2 Prostaglandin D2 Receptor 2 [Homo sapiens (human)]. NIH. Available at: https://www.ncbi.nlm.nih.gov/gene/11251 (Accessed: 12 July 2024.)
PGD2 levels are elevated in balding scalps compared to haired scalps. Additionally, PGD2 inhibits hair growth in isolated human hair follicles and mouse models. Overexpression of PGD2 has been shown to lead to premature hair follicle regression and alopecia in mice. Furthermore, mice lacking the GPR44 receptor did not exhibit hair loss when exposed to PGD2, indicating that GPR44 is important for PGD2’s hair growth inhibition.[24]Nieves, A., Garza, L.A. (2014). Does Prostaglandin D2 Hold the Cure to Male Pattern Baldness? Experimental Dermatology. 23(4). 224-227. Available at: https://doi.org/10.1111/exd.12348,[25]Garza, L.A., Liu, Y., Alagesan, B., Lawson, J.A., Norberg, S.M., Loy, D.R., Zhao, T., Blatt, H.B., Stanton, D.C., Carrasco, L., Ahluwalia, G., Fischer, S.M., Fitzgerald, G.A., Cotsarelis, G. (2012). … Continue reading
However, one clinical trial using setipiprant, a GPR44 antagonist, showed no significant improvement in hair growth compared to a placebo in men with AGA, indicating that PGD2 signaling through GPR44 alone might not be sufficient for treating hair loss.[27]DuBois, J., Bruce, S., Stewart, D., Kempers, S., Harutunian, C., Boodhoo, T., Weitzenfeld, A, Chang-Lin, J.E. (2021). Setipiprant for Androgenetic Alopecia in Males: Results from a Randomized, … Continue reading
SNPs in GPR44 have been associated with increased receptor expression and asthma severity, hinting that similar mechanisms might affect hair loss.[28]Campos Alberto, E., Maclean, E., Davidson, C., Palikhe, N.S., Storie, J., Tse, C., Brenner, D., Mayers, I., Vliagoftis, H., El-Sohemy, A., Cameron, L. (2012). The Single Nucleotide Polymorphism CRTh2 … Continue reading,[29]Huang, J.L., Gao, P.S., Mathias, R.A., Yao, T.C., Chen, L.C., Kuo, M.L., Hsu, S.C., Plunkett, B., Togias, A., Barnes, K.C., Stellato, C., Beaty, T.H., Huang, S.K. Sequence Variants of the Gene … Continue reading
Nonetheless, conflicting study results and poorly controlled variables make it unclear whether targeting GPR44 is effective for treating hair loss.
Read our GPR44 gene article here.
IGF1R encodes the insulin-like growth factor-1 receptor, which mediates the effects of IGF-1, a protein crucial for hair follicle development and the hair growth cycle. IGF-1 promotes cell growth, division, and survival in hair follicles and regulates the transition between the growth (anagen) and red (catagen) phases.[30]Ahn, S. Y., Pi, L. Q., Hwang, S. T., & Lee, W. S. (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 … Continue reading
Studies have linked low levels of IGF-1 to AGA and hair loss. For instance, individuals with Laron syndromes, characterized by deficient IGF-1 production, often experience thinner hair and alopecia in adulthood.[31]Lurie, R., Ben-Amitai, D., & Laron, Z. (2004). Laron syndrome (primary growth hormone insensitivity): a unique model to explore the effect of insulin-like growth factor 1 deficiency on human … Continue reading IGF-1 is also significantly reduced in balding compared to non-balding scalps.[32]Panchaprateep, R., & Asawanonda, P. (2014). Insulin‐like growth factor‐1: roles in androgenetic alopecia. Experimental dermatology, 23(3), 216-218. Available at: … Continue reading Additionally, middle-aged women with lower circulating IGF-1 levels have a higher risk of developing hair loss.[33]Noordam, R., Gunn, D. A., Drielen, K. V., Westgate, G., Slagboom, P. E., Craen, A. D., & Heemst, D. V. (2016). Both low circulating insulin‐like growth factor‐1 and high‐density lipoprotein … Continue reading
Genetic variation in IGF1R influences plasma IGF-1 levels, with some maintaining normal levels and some exhibiting reduced levels. This suggests a potential role of IGF-1 supplementation in those with lower IGF-1 levels.[34]Bonafè, M., Barbieri, M., Marchegiani, F., Olivieri, F., Ragno, E., Giampieri, C., Mugianesi, E., Centurelli, M., Franceschi, C. and Paolisso, G. (2003). Polymorphic variants of insulin-like growth … Continue reading
However, no direct link has been established between the rs2229765 SNP and specific hair loss disorders.
Read the full IGF1R gene article here.
NR3C1 encodes the glucocorticoid receptor (GR), which mediates the action of glucocorticoids, impacting metabolism, immune response, and stress response. There are two main isoforms: GRɑ, which binds glucocorticoids, and GRβ, which can inhibit GRɑs activity.[36]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. … Continue reading
GRs regulate the transitions between different phases of the hair cycle. They can influence the transition from anagen (active growth) to catagen (regression) phases. Furthermore, GRs are expressed in various components of the hair follicle, including dermal papilla cells, outer root sheath keratinocytes, and hair matrix cells.[37]Kwack, M.H., Hamida, O.B., Moon, K.K., Kim, J.C., Sung, Y.K. (2022). Dexamethasone, a Synthetic Glucocorticoid, Induces the Activity of Androgen Receptor in Human Dermal Papilla Cells. Skin … Continue reading
Certain genetic variants in NR3C1 have been linked to glucocorticoid resistance due to altered mRNA stability, affecting GR function. While these variations do impact glucocorticoid activity, there is no evidence to connect these effects to responsiveness to corticosteroids in hair loss, as the study was conducted in children with acute lymphoblastic leukemia.[38]Gasic, V., Zukic, B., Stankovic, B., Janic, D., Dokmanovic, L., Lazic, J., Krstovski, N., Dolzan, V., Jazbec, J., Pavlovic, S., Kotur, N. (2018). Pharmacogenomic Markers of Glucocorticoid Response in … Continue reading
Read more about the NR3C1 gene here.
The PGTFR gene encodes the prostaglandin F2 alpha receptor and plays a key role in hair follicle health and pigmentation. This receptor also involves broader physiological processes, including reproduction, inflammation, and cancer. Still, its influence on hair growth has made it a target in hair loss research.[40]Ricciotti, E., FitzGerald, G.A. (2011). Prostaglandins and Inflammation. Arteriosclerosis, Thrombosis, and Vascular Biology. 31(5). 986-1000. Available at: … Continue reading Studies in animal models have shown that PGF2ɑ and its analogs, such as latanoprost, stimulate the hair follicle and melanocyte growth, hinting at potential therapeutic benefits for hair loss treatments.
Genetic variants within PGTFR have been linked to varied responses to latanoprost in glaucoma treatment. Those with one genotype have been associated with greater response to latanoprost, while others were associated with reduced effectiveness.[41]Sakurai, M., Higashide, T., Takahashi, M., Sugiyama, K. (2007). Association between Genetic Polymorphisms of the Prostaglandin F2ɑ Receptor Gene and Response to Latanoprost. Ophthalmology. 114(6). … Continue reading Similarly, other SNPs have corresponded with lower receptor activity, indicating decreased response to PGF2ɑ analogs.
In the context of hair loss, we know that some evidence exists to show that latanoprost might benefit hair regrowth.[43]Blume-Peytavi, U., Lonngors, S., Hillmann, K., Bartels, N.G. (2012). A Randomized, Double-Blind, Placebo-Controlled Pilot Study to Assess the Efficacy of a 24-Week Topical Treatment by Latanoprost … Continue reading However, no studies have linked any SNPs to treatment efficacy in the hair follicle.
Read the PGTFR gene article here.
The PTGES2 gene encodes prostaglandin E synthase 2, an enzyme that converts prostaglandin H2 (PGH2) to prostaglandin E2 (PGE2). This enzyme is critical in the prostaglandin synthesis pathway and plays a role in inflammation and hair growth. PGE2 levels are higher in non-balding scalp regions than in balding ones, suggesting that PTGES2 and its product PGE2 might contribute to hair preservation and growth.[44]Garza, L.A., Liu, Y., Alagesan, B., Lawson, J.A., Norberg, S.M., Loy, D.R., Zhao, T., Blatt, H.B., Stanton, D.C., Carrasco, L., Ahluwalia, G., Fischer, S.M., Fitzgerald, G.A., Cotsarelis, G. (2012). … Continue reading
Studies on AGA patients have found that PTGES2 expression increases in balding areas, likely as a compensatory response.[45]Villareal-Villareal, C.D., Sinclair, R.D., Martinez-Jacobo, L., Garza-Rodriguez, V., Rodriguez-Leon, S.A., Lamadrid-Zertuche, A.C., Rodriguez-Gutierrez, R., Ortiz-Lopez, R., Rojas-Martinez, A., … Continue reading Genetic association studies have also linked a PTGES2 SNP to AGA. However, this does not appear to correlate with the severity of hair loss.[46]Frances, M.P., Vila-Vecilla, L., Russo, V., Polonini, H.C., de Souza, G.T. (2024). Utilizing SNP Association Analysis as a Prospective Approach for Personalising Androgenetic Alopecia Treatment. … Continue reading
Interestingly, some research suggests PTGES2 could influence responses to minoxidil as it has been shown to increase PGE2 production in hair follicle cells.[48]Michelet, J.F., Commo, S., Billoni, N., Mahe, Y.F., Bernard, B.A. (1997). Activation of cytoprotective prostaglandin synthase-1 by minoxidil as a possible explanation for its hair growth-stimulating … Continue reading This indicates that individuals with PTGES2 variants possibly associated with lower enzyme activity might benefit more from minoxidil, as the treatment could help elevate PGE2 levels. However, general genetic findings should be interpreted carefully, as gene expression patterns in hair follicles may differ significantly from those in other tissues.
Read the PTGES2 gene article here.
The SRD5A1 and SRD5A2 genes encode type I and type II 5ɑ-reductase enzymes, which are crucial for converting testosterone into dihydrotestosterone (DHT).[49]Scaglione, A., Montemiglio, L.C., Parisi, G., Asteriti, I.A., Bruni, R., Cerutti, G., Testi, C., Savino, C., Mancia, F., Lavia, P. and Vallone, B. (2017). Subcellular localization of the five members … Continue reading Inhibitors targeting these enzymes, particularly finasteride, and dutasteride, are central to AGA treatment. Genetic variations in SRD5A1 and SRD5A2 have shown potential in influencing the effectiveness of these treatments.
In a study of AGA patients treated with dutasteride, certain SNPs in SRD5A1 were positively associated with treatment response, meaning individuals with these variants responded better. However, even patients with these SNPs displayed varied responses, suggesting that the overall genetic profile, rather than individual SNPs alone, likely plays a role in treatment efficacy.[50]Rhie, A., Son, H.Y., Kwak, S.J., Lee, S., Kim, D.Y., Lew, B.L., Sim, W.Y., Seo, J.S., Kwon, O., Kim, J.I. and Jo, S.J. (2019). Genetic variations associated with response to dutasteride in the … Continue reading Interestingly, no SRD5A2 SNPs were found to significantly impact dutasteride response in this study, although variations in SRD5A2 may still affect DHT production and, consequently, treatment outcomes.
Additional research hints that SRD5A gene variants influence enzyme activity. In particular, individuals with higher DHT levels due to SRD5A1 or SRD5A2 variants might require higher doses or longer treatment durations for 5ɑ-reductase inhibitors to show efficacy. Lab studies have further suggested that specific variants of SRD5A2 might respond differently to finasteride versus dutasteride, emphasizing that personalized treatment approaches could optimize hair loss management.[51]Makridakis, N.M., di Salle, E., and Reichardt, J.K. (2000). Biochemical and pharmacogenetic dissection of human steroid 5α-reductase type II. Pharmacogenetics and Genomics, 10(5), 407-413. Available … Continue reading
While further clinical studies are needed to confirm these findings, early data suggest that SRD5A1 and SRD5A2 genotyping could improve the efficacy of 5ɑ-reductase inhibitor treatments.
Read the full SRD5A1 and SRD5A2 gene article here.
The SULT1A1 gene encodes the enzyme sulfotransferase 1A1, part of the sulfotransferase family. This enzyme plays a critical role in the metabolism and detoxification of various compounds. In hair loss treatment, SULT1A1 is especially important because it activates minoxidil through sulfonation, converting it into minoxidil sulfate, the active form needed to stimulate hair growth.[52]Goren, A., Castano, J.A., McCoy, J., Bermudez, F., Lotti, T. (2014). Novel enzymatic assay predicts minoxidil response in the treatment of androgenetic alopecia. Dermatologic Therapy. 27. 171-173. … Continue reading
Evidence suggests that specific SULT1A1 gene variants correlate with varying levels of enzyme activity and minoxidil responsiveness. Some genetic variations have been shown to lead to higher sulfotransferase activity and greater hair growth response after minoxidil treatment, whereas those with other genotypes exhibited lower enzyme activity and may have a weaker response to the drug.[53]Raghad, N.A., Al-Gazally, M.E., Ewahd, W.A. (2017). Assessment the effect of different genotypes of sulfotransferase 1A1 gene on the response to minoxidil in patients with androgenic alopecia. … Continue reading
Recent studies have begun using SULT1A1 genotyping as a tool to optimize minoxidil treatment, especially in female-pattern hair loss. However, some people with the “favorable” gene variations still fail to respond, while others with “less favorable” gene variations show substantial hair regrowth. This highlights the need for larger validation studies..[55]Ramos, P.M., Gohad, P., McCoy, J., Wambier, C., Goren, A. (2021). Minoxidil Sulfotransferase Enzyme (SULT1A1) genetic variants predict response to oral minoxidil treatment for female pattern hair … Continue reading
Read more about these studies in the SULT1A1 gene article here.
Based on the evidence in the articles, SULT1A1 currently has the most evidential support. This is especially true as it is one of (if not the only) gene that we have examined that actually examined these SNPs in the hair follicles of people with hair loss.
Aside from this, we don’t see the utility in using our genes to predict hair loss treatment efficacy. That is not to say that we won’t eventually see a use for this, however. As the research evolves, new information might come to light, which we will keep you updated on.
References[+]
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↑21 | Gallicchio, L., Calhoun, C., & Helzlsouer, K. J. (2013). Aromatase inhibitor therapy and hair loss among breast cancer survivors. Breast cancer research and treatment, 142, 435-443. Available at: https://doi.org/10.1007/s10549-013-2744-2 |
↑22 | Rhie, A., Son, H.Y., Kwak, S.J., Lee, S., Kim, D.Y., Lew, B.L., Sim, W.Y., Seo, J.S., Kwon, O., Kim, J.I. and Jo, S.J. (2019). Genetic variations associated with response to dutasteride in the treatment of male subjects with androgenetic alopecia. Plos one, 14(9), e0222533. Available at: https://doi.org/10.1371/journal.pone.0222533 |
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↑25 | Garza, L.A., Liu, Y., Alagesan, B., Lawson, J.A., Norberg, S.M., Loy, D.R., Zhao, T., Blatt, H.B., Stanton, D.C., Carrasco, L., Ahluwalia, G., Fischer, S.M., Fitzgerald, G.A., Cotsarelis, G. (2012). Prostaglandin D2 Inhibits Hair Growth and is Elevated in Bald Scalp of Men with Androgenetic Alopecia. Science Translational Medicine. 4(126). 1-21. Available at: https://doi.org/10.1126/scitranslmed.3003122 |
↑26 | Stanton, D.C., Carrasco, L., Ahluwalia, G., Fischer, S.M., Fitzgerald, G.A., Cotsarelis, G. (2012). Prostaglandin D2 Inhibits Hair Growth and is Elevated in Bald Scalp of Men with Androgenetic Alopecia. Science Translational Medicine. 4(126). 1-21. Available at: https://doi.org/10.1126/scitranslmed.3003122 |
↑27 | DuBois, J., Bruce, S., Stewart, D., Kempers, S., Harutunian, C., Boodhoo, T., Weitzenfeld, A, Chang-Lin, J.E. (2021). Setipiprant for Androgenetic Alopecia in Males: Results from a Randomized, Double-Blind, Placebo-Controlled Phase 2a Trial. Clinical Cosmetic and Investigative Dermatology. 14. 1507-1517. Available at: https://doi.org/10.2147/CCID.S319676 |
↑28 | Campos Alberto, E., Maclean, E., Davidson, C., Palikhe, N.S., Storie, J., Tse, C., Brenner, D., Mayers, I., Vliagoftis, H., El-Sohemy, A., Cameron, L. (2012). The Single Nucleotide Polymorphism CRTh2 rs533116 is Associated with Allergic Asthma and Increased Expression of CRTh2. Allergy. 67(11). 1357-1364. Available at: https://doi.org/10.1111/all.12003 |
↑29 | Huang, J.L., Gao, P.S., Mathias, R.A., Yao, T.C., Chen, L.C., Kuo, M.L., Hsu, S.C., Plunkett, B., Togias, A., Barnes, K.C., Stellato, C., Beaty, T.H., Huang, S.K. Sequence Variants of the Gene Encoding Chemoattractant Receptor Expressed on Th2 Cells (CRTH2) are Associated with Asthma and Differentially Influence mRNA Stability. Human Molecular Genetics. 13(21). 2691-2697. Available at: https://doi.org/10.1093/hmg/ddh279 |
↑30 | Ahn, S. Y., Pi, L. Q., Hwang, S. T., & Lee, W. S. (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. Available at: https://doi.org/10.5021/ad.2012.24.1.26 |
↑31 | Lurie, R., Ben-Amitai, D., & Laron, Z. (2004). Laron syndrome (primary growth hormone insensitivity): a unique model to explore the effect of insulin-like growth factor 1 deficiency on human hair. Dermatology, 208(4), 314-318. Available at: https://doi.org/10.1159/000077839 |
↑32 | Panchaprateep, R., & Asawanonda, P. (2014). Insulin‐like growth factor‐1: roles in androgenetic alopecia. Experimental dermatology, 23(3), 216-218. Available at: https://doi.org/10.1111/exd.12339 |
↑33 | Noordam, R., Gunn, D. A., Drielen, K. V., Westgate, G., Slagboom, P. E., Craen, A. D., & Heemst, D. V. (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. Available at: https://doi.org/ 10.1111/bjd.14529 |
↑34, ↑35 | Bonafè, M., Barbieri, M., Marchegiani, F., Olivieri, F., Ragno, E., Giampieri, C., Mugianesi, E., Centurelli, M., Franceschi, C. and Paolisso, G. (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. The Journal of Clinical Endocrinology & Metabolism, 88(7), 3299-3304. Available at: https://doi.org/10.1210/jc.2002-021810 |
↑36 | 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. Available at: https://doi.org/10.1016/j.jaci.2013.09.007 |
↑37 | Kwack, M.H., Hamida, O.B., Moon, K.K., Kim, J.C., Sung, Y.K. (2022). Dexamethasone, a Synthetic Glucocorticoid, Induces the Activity of Androgen Receptor in Human Dermal Papilla Cells. Skin Pharmacology and Physiology. 35(5). 299-304. Available at: https://doi.org/10.1159/000525067 |
↑38 | Gasic, V., Zukic, B., Stankovic, B., Janic, D., Dokmanovic, L., Lazic, J., Krstovski, N., Dolzan, V., Jazbec, J., Pavlovic, S., Kotur, N. (2018). Pharmacogenomic Markers of Glucocorticoid Response in The Initial Phase of Remission Induction Therapy in Childhood Acute Lymphoblastic Leukemia. Radiology and Oncology. 52(3). 296-306. Available at: https://doi.org/10.2478/raon-2018-0034 |
↑39 | Gasic, V., Zukic, B., Stankovic, B., Janic, D., Dokmanovic, L., Lazic, J., Krstovski, N., Dolzan, V., Jazbec, J., Pavlovic, S., Kotur, N. (2018). Pharmacogenomic Markers of Glucocorticoid Response in The Initial Phase of Remission Induction Therapy in Childhood Acute Lymphoblastic Leukemia. Radiology and Oncology. 52(3). 296-306. Available at: https://doi.org/10.2478/raon-2018-0034 |
↑40 | Ricciotti, E., FitzGerald, G.A. (2011). Prostaglandins and Inflammation. Arteriosclerosis, Thrombosis, and Vascular Biology. 31(5). 986-1000. Available at: https://doi.org/10.1161/ATVBAHA.110.207449. |
↑41 | Sakurai, M., Higashide, T., Takahashi, M., Sugiyama, K. (2007). Association between Genetic Polymorphisms of the Prostaglandin F2ɑ Receptor Gene and Response to Latanoprost. Ophthalmology. 114(6). 1039-1045. Available at: https://doi.org/10.1016/j.ophtha.2007.03.025. |
↑42 | ↑4 Sakurai, M., Higashide, T., Takahashi, M., Sugiyama, K. (2007). Association between Genetic Polymorphisms of the Prostaglandin F2ɑ Receptor Gene and Response to Latanoprost. Ophthalmology. 114(6). 1039-1045. Available at: https://doi.org/10.1016/j.ophtha.2007.03.025. |
↑43 | Blume-Peytavi, U., Lonngors, S., Hillmann, K., Bartels, N.G. (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). 797-800. Available at: https://doi.org/10.1016/j.jaad.2011.05.026. |
↑44 | Garza, L.A., Liu, Y., Alagesan, B., Lawson, J.A., Norberg, S.M., Loy, D.R., Zhao, T., Blatt, H.B., Stanton, D.C., Carrasco, L., Ahluwalia, G., Fischer, S.M., Fitzgerald, G.A., Cotsarelis, G. (2012). Prostaglandin D2 Inhibits Hair Growth and is Elevated in Bald Scalp of Men with Androgenetic Alopecia. Science Translational Medicine. 4(126). 1-21. Available at: https://doi.org/10.1126/scitranslmed.3003122 |
↑45 | Villareal-Villareal, C.D., Sinclair, R.D., Martinez-Jacobo, L., Garza-Rodriguez, V., Rodriguez-Leon, S.A., Lamadrid-Zertuche, A.C., Rodriguez-Gutierrez, R., Ortiz-Lopez, R., Rojas-Martinez, A., Ocampo-Candiani, J. (2019). Prostaglandins in androgenetic alopecia in 12 men and four female. Journal of the European Academy of Dermatology and Venereology. 33(5). E214-e215. Available at: https://doi.org/10.1111/jdv.15479 |
↑46 | Frances, M.P., Vila-Vecilla, L., Russo, V., Polonini, H.C., de Souza, G.T. (2024). Utilizing SNP Association Analysis as a Prospective Approach for Personalising Androgenetic Alopecia Treatment. Dermatology and Therapy (Heidelb). 14(4). 971-981. Available at: https://doi.org/10.1007/s13555-024-01145-y |
↑47 | Chovarda, E., Sotiriou, E., Lazaridoi, E., Vakirlis, E., Ioannides, D. (2021). The Role of Prostaglandins in Androgenetic Alopecia. International Journal of Dermatology. 60. 730-735. Available at: https://doi.org/10.1111/ijd.15378 |
↑48 | Michelet, J.F., Commo, S., Billoni, N., Mahe, Y.F., Bernard, B.A. (1997). Activation of cytoprotective prostaglandin synthase-1 by minoxidil as a possible explanation for its hair growth-stimulating effect. Journal of Investigative Dermatology. 108(2). 205-209. Available at: https://doi.org/10.1111/1523-1747.ep12334249 |
↑49 | Scaglione, A., Montemiglio, L.C., Parisi, G., Asteriti, I.A., Bruni, R., Cerutti, G., Testi, C., Savino, C., Mancia, F., Lavia, P. and Vallone, B. (2017). Subcellular localization of the five members of the human steroid 5α-reductase family. Biochimie open, 4, 99-106. Available at: https://doi.org/10.1016/j.biopen.2017.03.003 |
↑50 | Rhie, A., Son, H.Y., Kwak, S.J., Lee, S., Kim, D.Y., Lew, B.L., Sim, W.Y., Seo, J.S., Kwon, O., Kim, J.I. and Jo, S.J. (2019). Genetic variations associated with response to dutasteride in the treatment of male subjects with androgenetic alopecia. Plos one, 14(9), e0222533. Available at: https://doi.org/10.1371/journal.pone.0222533 |
↑51 | Makridakis, N.M., di Salle, E., and Reichardt, J.K. (2000). Biochemical and pharmacogenetic dissection of human steroid 5α-reductase type II. Pharmacogenetics and Genomics, 10(5), 407-413. Available at: https://doi.org/10.1097/00008571-200007000-00004 |
↑52 | Goren, A., Castano, J.A., McCoy, J., Bermudez, F., Lotti, T. (2014). Novel enzymatic assay predicts minoxidil response in the treatment of androgenetic alopecia. Dermatologic Therapy. 27. 171-173. Available at: https://doi.org/10.1111/dth.12111 |
↑53 | Raghad, N.A., Al-Gazally, M.E., Ewahd, W.A. (2017). Assessment the effect of different genotypes of sulfotransferase 1A1 gene on the response to minoxidil in patients with androgenic alopecia. Journal of Global Pharma Technology. 10(9). 144-149 |
↑54 | Raghad, N.A., Al-Gazally, M.E., Ewahd, W.A. (2017). Assessment the effect of different genotypes of sulfotransferase 1A1 gene on the response to minoxidil in patients with androgenic alopecia. Journal of Global Pharma Technology. 10(9). 144-149 |
↑55 | Ramos, P.M., Gohad, P., McCoy, J., Wambier, C., Goren, A. (2021). Minoxidil Sulfotransferase Enzyme (SULT1A1) genetic variants predict response to oral minoxidil treatment for female pattern hair loss. Journal of the European Academy of Dermatology and Venererology. 35(1). E24-e26. Available at: https://doi.org/10.1111/jdv.16765 |
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