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The world is in the grip of the COVID-19 pandemic. Public health measures that can reduce the risk of infection and death in addition to quarantines are desperately needed. This article reviews the roles of vitamin D in reducing the risk of respiratory tract infections, knowledge about the epidemiology of influenza and COVID-19, and how vitamin D supplementation might be a useful measure to reduce risk. Through several mechanisms, vitamin D can reduce risk of infections. Those mechanisms include inducing cathelicidins and defensins that can lower viral replication rates and reducing concentrations of pro-inflammatory cytokines that produce the inflammation that injures the lining of the lungs, leading to pneumonia, as well as increasing concentrations of anti-inflammatory cytokines. Several observational studies and clinical trials reported that vitamin D supplementation reduced the risk of influenza, whereas others did not. Evidence supporting the role of vitamin D in reducing risk of COVID-19 includes that the outbreak occurred in winter, a time when 25-hydroxyvitamin D (25(OH)D) concentrations are lowest; that the number of cases in the Southern Hemisphere near the end of summer are low; that vitamin D deficiency has been found to contribute to acute respiratory distress syndrome; and that case-fatality rates increase with age and with chronic disease comorbidity, both of which are associated with lower 25(OH)D concentration. To reduce the risk of infection, it is recommended that people at risk of influenza and/or COVID-19 consider taking 10,000 IU/d of vitamin D3 for a few weeks to rapidly raise 25(OH)D concentrations, followed by 5000 IU/d. The goal should be to raise 25(OH)D concentrations above 40-60 ng/mL (100-150 nmol/L). For treatment of people who become infected with COVID-19, higher vitamin D3 doses might be useful. Randomized controlled trials and large population studies should be conducted to evaluate these recommendations.

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Studies have linked an Omega-3 Index (O3I), which measures eicosapentaenoic acid (EPA) + docosahexaenoic acid (DHA) in red blood cell membranes, of ≥8% with improved health. Previous studies found that the American Heart Association (AHA) recommendation of 1-2 seafood meals per week does not achieve an O3I ≥8% even with an EPA + DHA supplement; however, these studies did not assess the frequency or amount of supplemental intake. Among participants in a predominantly US and Canadian cohort with high nutrient supplement use, we hypothesized that those adhering to the AHA guidelines would not have an average O3I ≥8% but that those taking a daily supplement would. Fish consumption and EPA + DHA supplement use were reported by 1795 participants; 985 also completed a blood spot test for O3I. A majority (71%) consumed <2 servings per week of fatty fish, and 61% took an EPA + DHA supplement. The amount of EPA + DHA for 1 serving (based on the product label) significantly differed among the >400 supplement products (50-3570 mg). O3I was ≥8.0% in 19% of participants. Among non-supplement takers, 3% of those consuming 1 fish serving per week and 17% consuming ≥2 achieved an O3I ≥8.0%. Among those consuming ≥2 fish servings per week, only those also taking an average of 1100 mg/d of supplemental EPA + DHA had a median O3I ≥8.0%. Based on the relationship between supplemental EPA + DHA intake and O3I for non-fish eaters (R2 = 0.40, P < .0001), an average of ~1300 mg/d of EPA + DHA achieved an O3I of 8.0%. This study suggests that following the AHA guidelines does not produce an O3I ≥8% nor does taking 1 serving per day of most omega-3 supplements.

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BACKGROUND: Vitamin D nutrition research requires accurate measures of circulating 25-hydroxyvitamin D. Our objectives were to test whether a diurnal fluctuation in blood-spot concentrations of 25-hydroxyvitamin D can be demonstrated statistically in a single individual, and whether such fluctuation is affected by the pre-dose versus post-dose timing of the blood draw. CASE PRESENTATION: The participant in this case study was a generally healthy Caucasian woman in her 40s who has taken 5000 IU vitamin D3 supplement at midday for over 1 year. Each blood sample was drawn individually from a finger prick onto filter paper at morning, midday, or night, on 4 days (three groups of five individual blood samples per collection day). On days 1 and 2, the midday samples were collected approximately 1 hour after the supplement was taken; on days 3 and 4, the midday samples were collected within an hour prior to supplementation (the classical, daily "trough" value for a drug). There was a significant daily pattern of variation in 25-hydroxyvitamin D concentrations (analysis of variance p ≤ 0.02 for 3 of the 4 days): peak midday mean 25-hydroxyvitamin D was approximately 20% higher than in the morning, and approximately 13% higher than in the evening. Trough sampling produced no significant difference in 25-hydroxyvitamin D compared to sampling an hour after the dose. An incidental finding was that acute illness during the study was related to acutely lower 25-hydroxyvitamin D at every sampling time in the day (p < 0.00001). CONCLUSIONS: There was a consistent diurnal variation in 25-hydroxyvitamin D, with the peak at midday. There was no difference between trough versus post-dose blood draws. Acute illness may acutely lower serum 25-hydroxyvitamin D levels. Because within-person, within-day variability in 25-hydroxyvitamin D is approximately 20%, sampling time introduces systematic error in vitamin D nutritional assessment that is bigger than random analytical error or choice of assay method.

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[This corrects the article DOI: 10.1371/journal.pone.0152441.].

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BACKGROUND: While numerous epidemiologic studies have found an association between higher serum 25-hydroxyvitamin D [25(OH)D] concentrations and lower breast cancer risk, few have assessed this association for concentrations >40 ng/ml. OBJECTIVE: To investigate the relationship between 25(OH)D concentration and breast cancer risk across a broad range of 25(OH)D concentrations among women aged 55 years and older. METHODS: Analyses used pooled data from two randomized clinical trials (N = 1129, N = 2196) and a prospective cohort (N = 1713) to examine a broad range of 25(OH)D concentrations. The outcome was diagnosis of breast cancer during the observation periods (median: 4.0 years). Three analyses were conducted: 1) Incidence rates were compared according to 25(OH)D concentration from <20 to ≥60 ng/ml (<50 to ≥150 nmol/L), 2) Kaplan-Meier plots were developed and 3) multivariate Cox regression was used to examine the association between 25(OH)D and breast cancer risk using multiple 25(OH)D measurements. RESULTS: Within the pooled cohort (N = 5038), 77 women were diagnosed with breast cancer (age-adjusted incidence: 512 cases per 100,000 person-years). Results were similar for the three analyses. First, comparing incidence rates, there was an 82% lower incidence rate of breast cancer for women with 25(OH)D concentrations ≥60 vs <20 ng/ml (Rate Ratio = 0.18, P = 0.006). Second, Kaplan-Meier curves for concentrations of <20, 20-39, 40-59 and ≥60 ng/ml were significantly different (P = 0.02), with the highest proportion breast cancer-free in the ≥60 ng/ml group (99.3%) and the lowest proportion breast cancer-free in the <20 ng/ml group (96.8%). The proportion with breast cancer was 78% lower for ≥60 vs <20 ng/ml (P = 0.02). Third, multivariate Cox regression revealed that women with 25(OH)D concentrations ≥60 ng/ml had an 80% lower risk of breast cancer than women with concentrations <20 ng/ml (HR = 0.20, P = 0.03), adjusting for age, BMI, smoking status, calcium supplement intake, and study of origin. CONCLUSIONS: Higher 25(OH)D concentrations were associated with a dose-response decrease in breast cancer risk with concentrations ≥60 ng/ml being most protective.

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BACKGROUND: Given the high rate of preterm birth (PTB) nationwide and data from RCTs demonstrating risk reduction with vitamin D supplementation, the Medical University of South Carolina (MUSC) implemented a new standard of care for pregnant women to receive vitamin D testing and supplementation. OBJECTIVES: To determine if the reported inverse relationship between maternal 25(OH)D and PTB risk could be replicated at MUSC, an urban medical center treating a large, diverse population. METHODS: Medical record data were obtained for pregnant patients aged 18-45 years between September 2015 and December 2016. During this time, a protocol that included 25(OH)D testing at first prenatal visit with recommended follow-up testing was initiated. Free vitamin D supplements were offered and the treatment goal was ≥40 ng/mL. PTB rates (<37 weeks) were calculated, and logistic regression and locally weighted regression (LOESS) were used to explore the association between 25(OH)D and PTB. Subgroup analyses were also conducted. RESULTS: Among women with a live, singleton birth and at least one 25(OH)D test during pregnancy (N = 1,064), the overall PTB rate was 13%. The LOESS curve showed gestational age rising with increasing 25(OH)D. Women with 25(OH)D ≥40 ng/mL had a 62% lower risk of PTB compared to those <20 ng/mL (p<0.0001). After adjusting for socioeconomic variables, this lower risk remained (OR = 0.41, p = 0.002). Similar decreases in PTB risk were observed for PTB subtypes (spontaneous: 58%, p = 0.02; indicated: 61%, p = 0.006), by race/ethnicity (white: 65%, p = 0.03; non-white: 68%, p = 0.008), and among women with a prior PTB (80%, p = 0.02). Among women with initial 25(OH)D <40 ng/mL, PTB rates were 60% lower for those with ≥40 vs. <40 ng/mL on a follow-up test (p = 0.006); 38% for whites (p = 0.33) and 78% for non-whites (p = 0.01). CONCLUSIONS: Maternal 25(OH)D concentrations ≥40 ng/mL were associated with substantial reduction in PTB risk in a large, diverse population of women.

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BACKGROUND: Higher serum 25-hydroxyvitamin D [25(OH)D] concentrations have been associated with a lower risk of multiple cancer types across a range of 25(OH)D concentrations. OBJECTIVES: To investigate whether the previously reported inverse association between 25(OH)D and cancer risk could be replicated, and if a 25(OH)D response region could be identified among women aged 55 years and older across a broad range of 25(OH)D concentrations. METHODS: Data from two cohorts representing different median 25(OH)D concentrations were pooled to afford a broader range of 25(OH)D concentrations than either cohort alone: the Lappe cohort (N = 1,169), a randomized clinical trial cohort (median 25(OH)D = 30 ng/ml) and the GrassrootsHealth cohort (N = 1,135), a prospective cohort (median 25(OH)D = 48 ng/ml). Cancer incidence over a multi-year period (median: 3.9 years) was compared according to 25(OH)D concentration. Kaplan-Meier plots were developed and the association between 25(OH)D and cancer risk was examined with multivariate Cox regression using multiple 25(OH)D measurements and spline functions. The study included all invasive cancers excluding skin cancer. RESULTS: Age-adjusted cancer incidence across the combined cohort (N = 2,304) was 840 cases per 100,000 person-years (1,020 per 100,000 person-years in the Lappe cohort and 722 per 100,000 person-years in the GrassrootsHealth cohort). Incidence was lower at higher concentrations of 25(OH)D. Women with 25(OH)D concentrations ≥40 ng/ml had a 67% lower risk of cancer than women with concentrations <20 ng/ml (HR = 0.33, 95% CI = 0.12-0.90). CONCLUSIONS: 25(OH)D concentrations ≥40 ng/ml were associated with substantial reduction in risk of all invasive cancers combined.

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Unsupplemented vitamin D status is determined by cutaneous synthesis and food inputs; however, their relative magnitudes are largely unknown. In a cohort of 780 non-supplement-taking adults with a mean serum 25-hydroxyvitamin D [25(OH)D] of 33 (±14)ng/ml we assessed the relationship between serum 25(OH)D and non-food environmental variables. Serum 25(OH)D concentration was adjusted for seasonal influence (which removed 2% of the total variance) and these adjusted values were regressed against factors involved in cutaneous synthesis. Indoor tanning use, sun exposure, and percent of work performed outdoors were significantly positively associated and body mass index (BMI) was significantly negatively associated with 25(OH)D values (P<0.03 for each). Latitude, gender, and age were not significantly correlated (P>0.10). Season and non-food predictors together explained 13% of the total variance in serum 25(OH)D concentration. Non-traditional food sources need to be investigated as possible vitamin D inputs. This article is part of a Special Issue entitled 'Vitamin D Workshop'.

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Cutaneous synthesis and traditional food sources do not fully account for unsupplemented vitamin D status. Non-traditional food sources may be an undiscovered input. In a cohort of 780 non-supplement-taking adults with a mean serum 25-hydroxyvitamin D [25(OH)D] of 33 (±14)ng/ml we assessed the relationship between vitamin D status and selected food sources. Serum 25(OH)D concentration was adjusted for season, UVB exposures, and body size. These adjusted values were then regressed against multiple food items and combinations. Whole milk cottage cheese, eggs, red meat, and total protein were positively associated with total 25(OH)D and/or 25(OH)D3 (P<0.05 for each), whereas fish and milk intake were not. The slope of the relationship was such that for every intake of 1serving/day, serum 25(OH)D rose by about 2ng/ml for eggs and 1ng/ml for meat and total protein. For every weekly serving of whole milk cottage cheese, serum 25(OH)D rose by about 1ng/ml. While some food sources were significant predictors of vitamin D status, their ability to explain inter-individual variability was limited. Supplementation will likely remain essential to improving vitamin D status on a population level. This article is part of a Special Issue entitled '16th Vitamin D Workshop'.

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Vitamin D status has been implicated in insulin resistance, type 2 diabetes mellitus, and hypertension, but the range of vitamin D status values over which the association can be found is unknown. Our objective was to define this range in a cohort of nondiabetic adult Canadians. We used a regression modeling strategy, first adjusting insulin-response variables and systolic and diastolic blood pressure for BMI, waist circumference, weight, age, and sex. The resulting residuals were regressed against serum 25-hydroxyvitamin D [25(OH)D] concentration using successive 40% data blocks ranging from the 0th to the 60th percentile of 25(OH)D values. All of the predictor variables were significantly associated with each of the dependent variables, with BMI and waist circumference accounting for >98% of the explained variance. The vitamin D association was localized to the serum 25(OH)D range extending from ∼40 to ∼90 nmol/L (16-36 µg/L). We conclude that vitamin D status is inversely associated with insulin responsiveness and blood pressure. Consistent with the threshold response characteristic typical of nutrients, the association was strongest in a circumscribed region of the range of 25(OH)D values. There was no association at 25(OH)D values >80-90 nmol/L (32-36 µg/L), indicating that the vitamin D association applied principally to values below that level. The differences observed, if they can be further confirmed in prospective studies, are of a magnitude that would be clinically important.

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BACKGROUND: Studies indicate that intake of vitamin D in the range from 1,100 to 4,000 IU/d and a serum 25-hydroxyvitamin D concentration [25(OH)D] from 60-80 ng/ml may be needed to reduce cancer risk. Few community-based studies allow estimation of the dose-response relationship between oral intake of vitamin D and corresponding serum 25(OH)D in the range above 1,000 IU/d. MATERIALS AND METHODS: A descriptive study of serum 25(OH)D concentration and self-reported vitamin D intake in a community-based cohort (n = 3,667, mean age 51.3 ± 13.4 y). RESULTS: Serum 25(OH)D rose as a function of self-reported vitamin D supplement ingestion in a curvilinear fashion, with no intakes of 10,000 IU/d or lower producing 25(OH)D values above the lower-bound of the zone of potential toxicity (200 ng/ml). Unsupplemented all-source input was estimated at 3,300 IU/d. The supplemental dose ensuring that 97.5% of this population achieved a serum 25(OH)D of at least 40 ng/ml was 9,600 IU/d. CONCLUSION: Universal intake of up to 40,000 IU vitamin D per day is unlikely to result in vitamin D toxicity.

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