Skip to main content
The Journal of Clinical Endocrinology and Metabolism logoLink to The Journal of Clinical Endocrinology and Metabolism
. 2024 Jun 3;109(8):1955–1960. doi: 10.1210/clinem/dgae314

Navigating Complexities: Vitamin D, Skin Pigmentation, and Race

Naykky Singh Ospina 1, Alicia Diaz-Thomas 2, Marie E McDonnell 3, Marie B Demay 4, Anastassios G Pittas 5, Elizabeth York 6, Maureen D Corrigan 7, Robert W Lash 8, Juan P Brito 9, M Hassan Murad 10, Christopher R McCartney 11,
PMCID: PMC11244154  PMID: 38828960

Abstract

Vitamin D plays a critical role in many physiological functions, including calcium metabolism and musculoskeletal health. This commentary aims to explore the intricate relationships among skin complexion, race, and 25-hydroxyvitamin D (25[OH]D) levels, focusing on challenges the Endocrine Society encountered during clinical practice guideline development. Given that increased melanin content reduces 25(OH)D production in the skin in response to UV light, the guideline development panel addressed the potential role for 25(OH)D screening in individuals with dark skin complexion. The panel discovered that no randomized clinical trials have directly assessed vitamin D related patient-important outcomes based on participants' skin pigmentation, although race and ethnicity often served as presumed proxies for skin pigmentation in the literature. In their deliberations, guideline panel members and selected Endocrine Society leaders underscored the critical need to distinguish between skin pigmentation as a biological variable and race and ethnicity as socially determined constructs. This differentiation is vital to maximize scientific rigor and, thus, the validity of resulting recommendations. Lessons learned from the guideline development process emphasize the necessity of clarity when incorporating race and ethnicity into clinical guidelines. Such clarity is an essential step toward improving health outcomes and ensuring equitable healthcare practices.

Keywords: vitamin D, vitamin D deficiency, skin pigmentation, race, ethnicity, GRADE approach


Vitamin D, a fat-soluble vitamin, plays a pivotal role in numerous physiological processes, including calcium and bone metabolism as well as maintenance of musculoskeletal health (1-4). Vitamin D deficiency can cause rickets and osteomalacia, and replenishing vitamin D stores is beneficial in such situations. In longitudinal observational studies, lower vitamin D stores—marked by lower circulating 25-hydroxyvitamin D (25[OH]D) concentrations—have been associated with several undesirable outcomes, including fractures, falls, diabetes, cardiovascular disease, cancer, and overall mortality (5). However, it remains unclear whether vitamin D supplementation lowers the risk of such outcomes. Similarly, the value of vitamin D supplementation for people with already adequate levels—however “adequate” is defined—is unknown (3-5).

There are several risk factors associated with low 25(OH)D levels, including geographic location (eg, latitudes far from equator), older age, higher body mass index (BMI), lower UV exposure (independent of geographic location), and darker skin pigmentation, among others (1, 6). Furthermore, studies have highlighted differences in the prevalence of low 25(OH)D levels among different populations (7-9). An analysis of the National Health and Nutrition Examination Surveys (NHANES) in the United States, spanning from 2001 to 2018, revealed that 2.8% of participants had 25(OH)D levels below 10 ng/mL (25 nmol/L). Considering race and ethnicity categories, this proportion rose to 11.9% among non-Hispanic Black individuals, while it was 3.9% for those in “Other” racial groups, 3.2% for Mexican American participants, and 0.9% for non-Hispanic White participants (7). Moreover, in addition to race and ethnicity, factors such as older age, female sex, winter season, higher BMI, lower socioeconomic status, alcohol consumption, and reduced milk intake were also associated with 25(OH)D levels below 10 ng/mL (25 nmol/L) among all NHANES participants, suggesting multifactorial determinants of low vitamin D status (7).

In this issue of the Journal of Clinical Endocrinology and Metabolism, the Endocrine Society publishes a new clinical practice guideline that includes recommendations regarding screening with blood 25(OH)D tests in generally healthy populations without well-established indications for 25(OH)D testing (5). During guideline development, the panel addressed an important question: Should screening with a 25(OH)D test (with vitamin D supplementation/treatment only if 25(OH)D is below a threshold) be preferred over no screening with a 25(OH)D test for adults with dark complexion?

The panel addressed this question because dark skin complexion can limit the body's ability to produce vitamin D when exposed to sunlight, due to higher concentrations of melanin (10, 11). However, in the absence of studies that addressed outcomes specifically in individuals with dark skin complexion, determining whether race or ethnicity should be used as a proxy for skin complexion—as is common in the field—required careful consideration. This commentary aims to summarize our methodological deliberations in this regard.

Understanding the Relationship Between Skin Complexion and Vitamin D Levels

Vitamin D can be obtained through 2 main mechanisms: (i) UV light exposure and (ii) intake either via food consumption or supplementation (12, 13). UV light converts 7-dehydrocholesterol to vitamin D3 in the skin, mostly in the upper layers. Once formed, vitamin D3 is transported to the liver, where it undergoes 25-hydroxylation, forming 25(OH)D. This is the major circulating form of vitamin D in the bloodstream, and it is commonly used in clinical practice to indicate vitamin D status (12, 13).

Dark skin complexion has been considered a risk factor for lower 25(OH)D levels, as melanin (an important determinant of skin complexion) decreases UV light permeation and thus lowers cutaneous vitamin D3 production, potentially contributing to lower 25(OH)D levels (14). However, more complex biological processes might be at play, including variations in genes encoding proteins responsible for transport, metabolism, and signaling of vitamin D (11, 15). For example, in a study conducted in Denmark during the winter, a period of limited environmental UV light exposure, 40 participants received standardized experimental UV light exposure over a 9-week period. The study revealed significant variability in resulting 25(OH)D increments, and the authors assessed how skin pigmentation, demographic factors, and genetic factors contributed to such variability. Pigment Protection Factor (PPF) was used as an objective measure of skin pigmentation (higher PPF numbers indicate that greater UV light exposure is needed to induce skin erythema). While skin pigmentation predicted some of the variation in 25(OH)D levels in response to UV light, this relationship was not statistically significant when other variables were simultaneously considered: factors such as sex, height, age, and 7 single nucleotide polymorphisms better explained observed changes in 25(OH)D concentrations in response to UV light. The conclusions that can be drawn from this study are somewhat limited, however, as this group of participants had relatively light skin complexion. Nonetheless, the study highlights that factors beyond skin pigmentation alone may be important in determining 25(OH)D increments following UV exposure (15).

Studies addressing how skin complexion modulates 25(OH)D increments following UV light exposure have yielded variable results. This variability can be partly attributed to differences in methods used to measure skin complexion, as well as other methodological considerations that warrant additional rigorous evaluation (14, 16). For example, in a systematic review that included 12 studies relating skin pigmentation to UV radiation-induced changes in circulating 25(OH)D concentrations, 4 studies employed quantitative measurements of skin pigmentation, 4 employed assessments of sun sensitivity using the Fitzpatrick classification, and the rest categorized participants according to their race and ethnicity (14).

Understanding the Relationship Between Race, Ethnicity, and 25(OH)D Levels

Multiple studies have assessed 25(OH)D levels in individuals from diverse racial and ethnic backgrounds (6, 8, 9, 17, 18). However, it is important to recognize that race and ethnicity are social constructs and do not signify biological differences (19-22). Racial groups are arbitrary categories, typically based on common origin and physical features, while ethnicity refers to a person's cultural identity and expression (19, 20). Definitions of race and ethnicity have changed over time, and such designations can have different meanings in different contexts (eg, in different countries).

Importantly, race and ethnicity directly influence healthcare experiences which often lead to differences in measured clinical outcomes (20-23). As highlighted in the National Academy of Medicine Report “Unequal Treatment,” a substantial body of evidence indicates that persons from racially and ethnically underrepresented groups are more likely to receive lower-quality healthcare, even when controlling for factors like insurance, income, and age (24, 25). When disparities in health outcomes across race or ethnicity are observed, it is imperative to scrutinize social, structural, cultural, and demographic factors—including the distribution of social determinants of health (eg, education, income, housing, access to care)—that may underpin these differences (19, 21-24, 26-28).

Cross-sectional population studies, utilizing data from the Canadian Health Measures Survey, shed light on the complexities involved in assessing the associations between skin complexion, social demographic factors such as ethnicity and immigration status, behavioral factors such as sunscreen use, and 25(OH)D levels (17, 18). Thirteen major ethnic categories were included in these studies, and melanin content (measured through noninvasive methods) was used to indicate skin pigmentation (17, 18). In one of these studies, a multivariate model found strong correlations between lower 25(OH)D levels and ethnicity, immigration from other countries, and higher BMI (17). Conversely, factors such as travel to sunny climates, consumption of dairy products, and sunscreen use were associated with higher 25(OH)D levels (17). In this model, investigators determined that skin pigmentation contributed less to 25(OH)D levels than the other listed factors (17). Overall, these observational, hypothesis-generating studies highlight the intricate interplay between biological, socio-demographic, and behavioral factors influencing 25(OH)D levels, necessitating rigorous scientific evaluation to draw accurate inferences that can support appropriate action (17, 18).

Challenges and Concerns When Evaluating Skin Pigmentation, Race, Ethnicity, and 25(OH)D Levels

Addressing the clinical question regarding 25(OH)D screening in individuals with dark skin complexion, in both research and practice settings, presents multiple challenges and concerns.

  • 1. Lack of standard methods to measure skin pigmentation. Skin color, determined by melanin, melanosomes, melanocytes, and other skin cells, refers to visible pigmentation that affects light absorption (29). There is significant debate regarding the optimal method to measure skin pigmentation/complexion (29, 30). A review of 17 tools for assessing skin color revealed that various parameters are commonly assessed, including UV light reactivity and degree of pigmentation (29). Tools to assess skin color commonly follow a questionnaire-based format, rely on color palettes for identification, or involve noninvasive objective color measurements. A widely used tool, the Fitzpatrick Skin Phototype Classification, determines UV tolerance through a questionnaire (eg, physical traits, reaction to sunburn, tanning habits) and can assess an individual's susceptibly to sunburn. Color-based scales seem to outperform those based on survey questions, especially when spectrophotometry is used as the gold standard. However, objective measurements may not always be feasible or cost-effective to implement (29).

  • 2. Race, ethnicity, or both were commonly used as proxies for skin pigmentation despite scientific concerns. Despite being socially constructed, race and ethnicity are commonly used as proxies for skin color. However, race and ethnicity correlate poorly with skin color. This is in part due to the wide variability of skin color among members of the same racial or ethnic group (29, 31, 32-34). For example, a study examining the impact of skin color on potential discrimination in labor markets in the United States sheds light on the significant variation in skin tone among individuals identifying as Black or Hispanic. Skin tone was assessed by the research team using a 10-point visual palette, with 1 representing the lightest color and 10 the darkest. Among 3873 individuals identifying as Black (n = 2155) or Latino (n = 1718), mean (SD) skin tone rating was 4.7 ± 2.5. There was considerable variability in skin tone, with Black participants distributed across all skin tone categories, while those identifying as Latino were predominantly in the lower skin tone categories (31).

    • Viewed through a social lens, skin tone, race, and ethnicity are recognized as distinct variables that significantly influence individuals' life experiences (21, 22). The National Social Life, Health, and Aging Project is a nationally representative, population-based longitudinal study that includes older Americans residing in communities across the United States. In addition to self-identifying race and ethnicity, participants were asked to compare their skin tone to others within their racial and ethnic group. Among the 3976 participants surveyed in 2015 (comprising 2810 White, 590 Black, 428 Latino, and 148 from other racial and ethnic backgrounds), significant variations were noted in self-reported skin tone. For instance, among White participants, 59% reported a light skin tone, 39% reported a medium skin tone, and 2% reported dark skin tone. Among Black participants, 14%, 59%, and 26% reported light, medium, and dark skin tones, respectively, while corresponding percentages among Latino participants were 46%, 48%, and 6%, respectively. Self-reported darker skin tone was associated with increased perceptions of discrimination and stress among Black participants, but not among Latino participants (34).

    • A survey study involving 3386 participants gathered data on various demographic and phenotypic characteristics, including age, sex, self-reported Fitzpatrick skin phototype (FSPT), eye color, hair color, skin color assessed via a color palate (ranging from A for lighter to D for darker), and race and ethnicity. Participants were from diverse racial and ethnic backgrounds and had varying skin colors, and all classifications of the FSPT were represented in the overall cohort. A multivariable logistic regression model was built, aiming to predict individual FSPT, incorporating age, sex, pigmentary phenotypes (skin color), and race and ethnicity as predictor variables. The model's performance, as assessed by a weighted kappa statistic of 0.52, indicated only moderate predictive capability. Additionally, a multivariate logistic regression analysis identified brown or black hair and medium or dark skin color as the strongest patient-reported predictors of higher FSPT (odds ratio [OR] > 6) (32). In this analysis, individuals identifying as Black, Native American, Multiracial, and Asian were statistically more likely to have higher FSPT compared to those identifying as White (OR ranging from 1.56 to 3.56), while those identifying as Latino were not (OR 0.96 [95% CI, 0.75-1.22]) (32).

    • Another study, which involved 558 individuals participating in a free skin cancer screening program, showed a poor correlation between race and objective measures of skin complexion (33). In this study, authors objectively measured skin color using colorimetric methods, clinicians subjectively assessed FSPT, and participants self-reported their race, ethnicity, and skin phototype. Self-reported race correlated very poorly with colorimetric measures of skin color (r values ranging from 0.2 to 0.4). Race exhibited a moderate correlation with physician-assigned FSPT (r = 0.55), but a weak correlation with self-reported skin phototype (r = 0.28). The authors reflected that these findings were not surprising, given the heterogeneity in skin pigmentation within self-identified racial groups (33).

    • These studies indicate that using race and ethnicity as a proxy for skin pigmentation can result in misclassification and thus a lack of rigor in addressing research questions. Moreover, this approach is subject to an ecological fallacy whereby individual characteristics, such as skin pigmentation, are attributed to individuals based on population averages, including perceptions of typical skin pigmentation types in various racial and ethnic groups: this can contribute to misclassification bias (35). To provide another example: if an investigator aimed to assess how standing height predicts high-jump ability, using self-identified gender as a proxy for standing height would be highly inaccurate, even if, on average, men tend to be taller than women.

  • 3. Clinical implications of research findings differ among studies evaluating skin pigmentation vs those evaluating race and ethnicity as primary factors. Studies seeking to address the impact of skin pigmentation on 25(OH)D levels should use rigorous methods to understand the role that skin melanin content has on biological pathways and clinical outcomes (15). The scientific validity of classifying patients’ skin pigmentation based on shared cultural backgrounds and social experiences appears to be low. In addition, using race and/or ethnicity as proxies for skin complexion in relation to vitamin D status while not considering the contributions of race- and ethnicity-based health disparities (eg, differences in social determinants of health) can lead to oversimplified and potentially misleading conclusions. When we are imprecise in defining variables of interest—eg, when conflating race and ethnicity (social constructs) with skin pigmentation (a biological characteristic)—we limit our scientific understanding of the health problems at hand (Table 1).

  • 4. Guideline development methodological considerations. The Endocrine Society has recently adopted a more rigorous implementation of the Grading of Recommendations, Assessment, Development, and Evaluation (GRADE) approach for developing clinical guidelines (36). An essential aspect of this process is evaluating the certainty of the evidence, informed by assessments of study limitations, imprecision, publication bias, inconsistency, and indirectness (37). Using race as a surrogate for skin complexion relates to 2 GRADE domains: indirectness and risk of bias. In some cases, evidence is not available in the specific population of interest, but is available in other populations, such as when a question relates to children but data are only available in adults, or when a question relates to patients with type 1 diabetes but data are only available in patients with type 2 diabetes. Regarding population-related indirect evidence, an important consideration relates to the extent to which the underlying biology differs between the comparison populations, and the degree to which such differences would render the evaluated effects unreliable, this is called indirectness and lowers certainty of evidence (37). Another reason to consider lowering certainty when using race as a surrogate for skin complexion relates to potential confounding, as additional factors (e.g. social determinants of health) may be associated with self-identified race in addition to treatment exposure and/or efficacy. Such concerns clearly pertain to observational studies, but they may also pertain to randomized clinical trials, especially when study groups are small; in such cases, randomization may not fully balance relevant confounders between treatment groups.

Table 1.

Important considerations in clinical research assessing the relationship between skin pigmentation, race, and vitamin D

Research question Main objective and scientific premise Variable of interest and measurement Interpretation
Should screening with a 25(OH)D test be preferred over no screening with a 25(OH)D test for adults with dark skin complexion? Address how the benefits and harms of 25(OH)D screening may be impacted by decreased vitamin D production in response to UV light (a biological concern) Dark complexion determined using objective methods Biological variations in skin pigmentation that impact endogenous vitamin D production among individuals with diverse skin tones
Should screening with a 25(OH)D test be preferred over no screening with a 25(OH)D test for adults that self-identify as Black? Address how the benefits and harms of 25(OH)D screening in adults that self-identify as Black may be impacted by social factors (eg, social determinants of health) that can lead to lower vitamin D levels Race (eg, Black), usually self-reported Upstream and downstream social factors that may contribute to variable 25(OH)D levels among members of distinct racial groups

The conceptual, biological, and practical aspects of using race as a means to identify a population with dark complexion led to discussions about how to evaluate and integrate data from clinical trials reporting subgroup analyses according to race as a proxy for dark skin complexion (indirect evidence), instead of skin complexion per se.

Screening With 25(OH)D in Adults With Dark Skin Complexion

The panel found no randomized clinical trials that addressed this question in adults with dark skin complexion (5). However, there are clinical trials that reported vitamin D–related outcomes on the basis of self-identified race, and the panel evaluated these studies as a secondary analysis. The panel's initial rationale paralleled a common rationale in the field: average skin tone would vary according to self-identified race, and such analyses might indirectly inform the panel's deliberations. Evidence gathered in the secondary analysis did not indicate a clear impact of vitamin D supplementation on fractures, mortality, cardiovascular events, cancer, or adverse events among self-identified Black participants. However, overall evidence was judged to be inadequate in this regard. The panel did not identify clinical trial evidence relevant to other groups in which dark complexion might be common (5).

The panel ultimately suggested against routine 25(OH)D screening in adults with dark complexion (conditional recommendation, very low-quality evidence) (5). The absence of clinical trial data specific to those with dark complexion was a key consideration in the panel's suggestion against 25(OH)D screening in this group. Moreover, the panel judged that the race-based evidence—if stipulated to be reliable—also did not support 25(OH)D screening. The certainty of evidence underpinning this recommendation was judged to be very low, primarily because no available trials evaluated the specific intervention of interest (screening vs no screening) in the specific population of interest (those with dark skin complexion). The panel also fully recognized that self-identified race is an inaccurate proxy for identifying skin complexion.

Given the scientific problems associated with using race as a proxy for skin complexion, in addition to broader uncertainties expressed by Society guideline leaders and internal reviewers, panel leadership considered whether the secondary, race-based analysis should be included in the final manuscript. It was ultimately concluded that doing so would be important, for 3 primary reasons. Most importantly, the panel concluded that full transparency regarding the guideline-development decision-making process was critical. Second, given published differences in circulating 25(OH)D levels according to racial categories in the United States, the panel judged that many readers would value inclusion of the secondary analysis in the guideline manuscript. Third, the panel was cognizant that the Society's 2011 vitamin D–related guideline indicated that African American individuals (children and adults) were candidates for 25(OH)D screening. Such individuals represent a substantial proportion of various populations across the globe, including in the United States, so the panel understood the issue to have broad and profound implications. The secondary analysis, based on clinical trial data published since publication of the Society's 2011 guideline, imply that a crucial criterion for 25(OH)D screening—treatment benefit on the basis of screening results—has not been fully substantiated in those who self-identify as Black, or in generally healthy populations more broadly. Even though the current guideline did not specifically address whether 25(OH)D screening is justified in persons who self-identify as Black, the panel believed that results of the secondary analysis will be helpful for readers to understand.

Importantly, the panel advocated that future clinical trials should assess whether the net benefits of 25(OH)D screening (with vitamin D treatment as indicated) vary according to direct measures of skin pigmentation, rather than using race and ethnicity as proxies for skin complexion. The panel also advocated for research to address whether the net benefits of vitamin D vary according to race/ethnicity, including attempts to disentangle the relative roles of skin complexion, social determinants of health, and other factors that influence clinical outcomes.

Conclusion

This commentary highlights the crucial role of clear definitions in the guideline development process, particularly concerning the target populations. The guideline panel addressed 25(OH)D screening with vitamin D treatment only for those with low 25(OH)D in individuals with darker skin tones, given concerns about their reduced response to UV light and the corresponding impact on 25(OH)D levels. While race is frequently referenced in the literature, guideline leadership contemplated the scientific validity of using race as a marker of skin tone when evaluating the evidence. Endocrine Society guideline leadership has concluded that such deliberations were critically important, have strengthened the Endocrine Society's clinical practice guideline program, and can support appropriate assessments of race and ethnicity as clinical variables in the future.

Abbreviations

25(OH)D

25-hydroxyvitamin D

BMI

body mass index

FSPT

Fitzpatrick skin phototype

OR

odds ratio

Contributor Information

Naykky Singh Ospina, Division of Endocrinology, University of Florida, Gainesville, FL 32610, USA.

Alicia Diaz-Thomas, Division of Pediatric Endocrinology, Department of Pediatrics, The University of Tennessee Health Science Center, Memphis, TN 38163, USA.

Marie E McDonnell, Division of Endocrinology, Diabetes and Hypertension, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA.

Marie B Demay, Endocrine Unit, Department of Medicine, Massachusetts General Hospital and Harvard Medical School, Boston, MA 02114, USA.

Anastassios G Pittas, Division of Endocrinology, Diabetes and Metabolism, Department of Medicine, Tufts Medical Center, Boston, MA 02111, USA.

Elizabeth York, Endocrine Society, Washington, DC 20036, USA.

Maureen D Corrigan, Endocrine Society, Washington, DC 20036, USA.

Robert W Lash, Endocrine Society, Washington, DC 20036, USA.

Juan P Brito, Division of Diabetes, Endocrinology, Metabolism, and Nutrition, Department of Medicine, Mayo Clinic, Rochester, MN 55905, USA.

M Hassan Murad, Mayo Clinic, Evidence-Based Practice Center, Rochester, MN 55905, USA.

Christopher R McCartney, Division of Endocrinology and Metabolism, Department of Medicine, West Virginia University, Morgantown, WV 26506, USA.

Funding

N.S.O. was supported by the National Cancer Institute of the National Institutes of Health under Award Number K08CA248972. The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health.

Author Contributions

N.S.O. and C.M. conceptualized and wrote the first draft of the manuscript. All authors were substantively involved in at least some of the deliberations described in this manuscript; all authors provided critical feedback on the manuscript; and all authors approved the final version.

Disclosures

Authors report no conflicts of interest.

Data availability

No new data were generated or analyzed in support of this research.

References

  • 1. Kahwati  LC, LeBlanc  E, Weber  RP, et al.  Screening for Vitamin D deficiency in adults: updated evidence report and systematic review for the US Preventive Services Task Force. JAMA. 2021;325(14):1443‐1463. [DOI] [PubMed] [Google Scholar]
  • 2. Bischoff-Ferrari  HA, Dawson-Hughes  B, Willett  WC, et al.  Effect of vitamin D on FallsA meta-analysis. JAMA. 2004;291(16):1999‐2006. [DOI] [PubMed] [Google Scholar]
  • 3. Bouillon  R, Manousaki  D, Rosen  C, Trajanoska  K, Rivadeneira  F, Richards  JB. The health effects of vitamin D supplementation: evidence from human studies. Nat Rev Endocrinol. 2022;18(2):96‐110. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 4. US Preventive Services Task Force . Screening for vitamin D deficiency in adults: US preventive services task force recommendation statement. JAMA. 2021;325(14):1436‐1442. [DOI] [PubMed] [Google Scholar]
  • 5. PLACE HOLDER FOR THE ENDOCRINE SOCIETY VITAMIN D 2024 GUIDELINES.
  • 6. Cui  A, Zhang  T, Xiao  P, Fan  Z, Wang  H, Zhuang  Y. Global and regional prevalence of vitamin D deficiency in population-based studies from 2000 to 2022: a pooled analysis of 7.9 million participants. Front Nutr. 2023;10:1070808. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 7. Cui  A, Xiao  P, Ma  Y, et al.  Prevalence, trend, and predictor analyses of vitamin D deficiency in the US population, 2001-2018. Front Nutr. 2022;9:965376. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 8. Weiler  HA, Sarafin  K, Martineau  C, et al.  Vitamin D status of people 3 to 79 years of age from the Canadian health measures survey 2012–2019. J Nutr. 2023;153(4):1150‐1161. [DOI] [PubMed] [Google Scholar]
  • 9. Herrick  KA, Storandt  RJ, Afful  J, et al.  Vitamin D status in the United States, 2011-2014. Am J Clin Nutr. 2019;110(1):150‐157. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 10. Shoenfeld  N, Amital  H, Shoenfeld  Y. The effect of melanism and vitamin D synthesis on the incidence of autoimmune disease. Nat Clin Pract Rheumatol. 2009;5(2):99‐105. [DOI] [PubMed] [Google Scholar]
  • 11. Hanel  A, Carlberg  C. Skin colour and vitamin D: an update. Exp Dermatol. 2020;29(9):864‐875. [DOI] [PubMed] [Google Scholar]
  • 12. Jukic  AMZ, Hoofnagle  AN, Lutsey  PL. Measurement of vitamin D for epidemiologic and clinical research: shining light on a complex decision. Am J Epidemiol. 2018;187(4):879‐890. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 13. Holick  MF. Vitamin D deficiency. N Engl J Med. 2007;357(3):266‐281. [DOI] [PubMed] [Google Scholar]
  • 14. Xiang  F, Lucas  R, de Gruijl  F, Norval  M. A systematic review of the influence of skin pigmentation on changes in the concentrations of vitamin D and 25-hydroxyvitamin D in plasma/serum following experimental UV irradiation. Photochem Photobiol Sci. 2015;14(12):2138‐2146. [DOI] [PubMed] [Google Scholar]
  • 15. Datta  P, Philipsen  PA, Olsen  P, et al.  Pigment genes not skin pigmentation affect UVB-induced vitamin D. Photochem Photobiol Sci. 2019;18(2):448‐458. [DOI] [PubMed] [Google Scholar]
  • 16. Libon  F, Cavalier  E, Nikkels  AF. Skin color is relevant to vitamin D synthesis. Dermatology. 2013;227(3):250‐254. [DOI] [PubMed] [Google Scholar]
  • 17. Yousef  S, Manuel  D, Colman  I, et al.  Vitamin D status among first-generation immigrants from different ethnic groups and origins: an observational study using the Canadian health measures survey. Nutrients. 2021;13(8):2702. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 18. Yousef  S, Papadimitropoulos  M, Faris  M, et al.  Melanin levels in relation to vitamin D among first-generation immigrants from different ethnic groups and origins: a comparative national Canadian cross-sectional study. Front Med (Lausanne). 2023;9:992554. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 19. Flanagin  A, Frey  T, Christiansen  SL, Committee AMoS . Updated guidance on the reporting of race and ethnicity in medical and science journals. JAMA. 2021; 326(7):621‐627. [DOI] [PubMed] [Google Scholar]
  • 20. Ford  ME, Kelly  PA. Conceptualizing and categorizing race and ethnicity in health services research. Health Serv Res. 2005;40(5p2):1658‐1675. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 21. Siddique  SM, Tipton  K, Leas  B, et al.  The impact of health care algorithms on racial and ethnic disparities. Ann Intern Med. 2024;177(4):484‐496. [DOI] [PubMed] [Google Scholar]
  • 22. Davidson  KW, Mangione  CM, Barry  MJ, et al.  Actions to transform US preventive services task force methods to mitigate systemic racism in clinical preventive services. Jama. 2021;326(23):2405‐2411. [DOI] [PubMed] [Google Scholar]
  • 23. Agarwal  S, Wade  AN, Mbanya  JC, et al.  The role of structural racism and geographical inequity in diabetes outcomes. Lancet. 2023;402(10397):235‐249. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 24. Fiscella  K, Franks  P, Gold  MR, Clancy  CM. Inequality in QualityAddressing socioeconomic, racial, and ethnic disparities in health care. JAMA. 2000;283(19):2579‐2584. [DOI] [PubMed] [Google Scholar]
  • 25. Institute of Medicine (US) Committee on Understanding and Eliminating Racial and Ethnic Disparities in Health Care . Unequal treatment: confronting racial and ethnic disparities in health care. In: Smedley  BD, Stith  AY, Nelson  AR, eds. National Academies Press; 2003. [PubMed] [Google Scholar]
  • 26. Chen  DW, Ospina  NS, Haymart  MR. Social determinants of health and disparities in thyroid care. J Clin Endocrinol Metabol. 2024;109(3):e1309‐e1313. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 27. Golden  SH, Brown  A, Cauley  JA, et al.  Health disparities in endocrine disorders: biological, clinical, and nonclinical factors—an endocrine society scientific statement. J Clin Endocrinol Metab. 2012;97(9):E1579‐E1639. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 28. Diaz-Thomas  AM, Golden  SH, Dabelea  DM, et al.  Endocrine health and health care disparities in the pediatric and sexual and gender minority populations: an endocrine society scientific statement. J Clin Endocrinol Metabol. 2023;108(7):1533‐1584. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 29. Harvey  VM, Alexis  A, Okeke  CAV, et al.  Integrating skin color assessments into clinical practice and research: a review of current approaches. J Am Acad Dermatol. 2024. doi: 10.1016/j.jaad.2024.01.067 [DOI] [PubMed] [Google Scholar]
  • 30. Coleman  W, Mariwalla  K, Grimes  P. Updating the Fitzpatrick classification: the skin color and ethnicity scale. Dermatol Surg. 2023;49(8):725‐731. [DOI] [PubMed] [Google Scholar]
  • 31. Abascal  M, Garcia  D. Pathways to skin color stratification: the role of inherited (dis)advantage and skin color discrimination in labor markets. Sociol Sci. 2022;9(9):346‐373. [Google Scholar]
  • 32. He  SY, McCulloch  CE, Boscardin  WJ, Chren  MM, Linos  E, Arron  ST. Self-reported pigmentary phenotypes and race are significant but incomplete predictors of Fitzpatrick skin phototype in an ethnically diverse population. J Am Acad Dermatol. 2014;71(4):731‐737. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 33. Chan  JL, Ehrlich  A, Lawrence  RC, Moshell  AN, Turner  ML, Kimball  AB. Assessing the role of race in quantitative measures of skin pigmentation and clinical assessments of photosensitivity. J Am Acad Dermatol. 2005;52(4):609‐615. [DOI] [PubMed] [Google Scholar]
  • 34. Monk EP  J, Kaufman  J, Montoya  Y. Skin tone and perceived discrimination: health and aging beyond the binary in NSHAP 2015. J Gerontol Ser B. 2021;76(Supplement_3):S313‐S321. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 35. Shih  YT, Bradley  C, Yabroff  KR. Ecological and individualistic fallacies in health disparities research. J Natl Cancer Inst. 2023;115(5):488‐491. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 36. McCartney  CR, Corrigan  MD, Drake  MT, et al.  Enhancing the trustworthiness of the Endocrine Society's clinical practice guidelines. J Clin Endocrinol Metabol. 2022;107(8):2129‐2138. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 37. Guyatt  GH, Oxman  AD, Kunz  R, et al.  Grade guidelines: 8. Rating the quality of evidence—indirectness. J Clin Epidemiol. 2011;64(12):1303‐1310. [DOI] [PubMed] [Google Scholar]

Associated Data

This section collects any data citations, data availability statements, or supplementary materials included in this article.

Data Availability Statement

No new data were generated or analyzed in support of this research.


Articles from The Journal of Clinical Endocrinology and Metabolism are provided here courtesy of The Endocrine Society

RESOURCES