Abstract
Objective
To evaluate the independent association between alcohol consumption and risk of developing psoriasis and to determine if this risk is associated with different types of alcoholic beverages.
Design
A prospective study of female nurses who were followed up from 1991 to 2005.
Setting
Nurses’ Health Study II, a cohort of 116 671 US women aged 27 to 44 years in 1991.
Participants
The study included 82 869 women who reported amount and type of alcohol intake on biennial questionnaires. We excluded participants with a history of psoriasis prior to 1991.
Main Outcome Measure
The main outcome measure consisted of a self-report of incident physician-diagnosed psoriasis. For a sensitivity analysis, we had a subset of confirmed psoriasis cases.
Results
There were 1,150 cases of incident psoriasis. Compared with women who did not drink alcohol, the multivariate relative risk (RR) of psoriasis was 1.73 (95% confidence interval [CI], 1.16–2.58) for alcohol consumption ≥ 2.3 drinks/week. When examined by type of alcoholic beverage, the association with alcohol intake was due to non-light beer (multivariate RR for ≥5 drinks/wk 1.83; 95% CI, 1.16–2.86); light beer, red wine, white wine, and liquor were not significantly associated with psoriasis risk. The association with non-light beer intake became stronger in a subset of confirmed psoriasis cases (multivariate RR for 2.29; 95% CI, 1.36 – 3.85).
Conclusions
Non-light beer intake is associated with an increased risk of developing psoriasis among women. Other alcoholic beverages did not increase the risk of psoriasis in this study.
INTRODUCTION
Psoriasis is a common immune-mediated skin disease 1, 2. The association between alcohol consumption and increased risk of psoriasis onset and psoriasis worsening has long been suspected. For example, individuals with psoriasis drink more alcohol than individuals without psoriasis 3, and alcohol intake may exacerbate psoriasis severity 4. Case-control studies reported a significant association between alcohol consumption and psoriasis, but these studies retrospectively ascertained alcohol consumption. Furthermore, these associations showed a marked gender difference in men 3, 5, and did not show a significant association between alcohol and psoriasis in women 6. One case-control study of alcohol intake and newly diagnosed psoriasis and showed a dose-response, but the findings were not significant after adjusting for cofactors 7.
Alcohol may induce psoriasis via multiple mechanisms, including immunological changes such as keratinocyte proliferation 8 and up-regulation of pro-inflammatory cytokines 9. Other potential mechanisms include an increased risk of infection and mechanical trauma, which are well known to trigger psoriasis 10.
Risk of psoriasis may vary depending on type of alcoholic beverage (ie, beer, wine, and spirits), as does the risk of other diseases, but no data are available on psoriasis. One prospective study confirmed, for example, that beer confers a larger risk of gout than spirits and wine 11. Risk for psoriasis may vary by type of alcoholic beverage given previous evidence that different types of alcoholic beverages have conferred deleterious effects in other inflammatory diseases. If certain types of alcoholic beverages have different effects on risk of psoriasis, then this fact would have practical implications for psoriasis prevention and management.
We prospectively evaluated the association between total alcohol consumption and risk of incident psoriasis in a cohort of women in the United States with no history of psoriasis. In this study, we also explored the association between type of alcoholic beverage and risk for incident psoriasis.
METHODS
Study population
The Nurses’ Health Study II (NHS II) is an ongoing longitudinal study of 116,430 female registered nurses from 15 states in the United States who were between the ages of 25 and 42 when they completed and returned a baseline questionnaire in 1989 12, 13. The cohort is followed with biennial questionnaires and the follow-up rate exceeds 90%.
Assessment of Psoriasis
In 2005, NHS II participants were asked if they had ever received a physician diagnosis of psoriasis and if so, the date of diagnosis. Of the 82,869 participants who responded to the psoriasis question in 2005, a total of 2,430 women reported being diagnosed with psoriasis; 1,280 of these were prevalent cases at baseline in 1991 and 1,150 incident cases occurred between 1991 and 2005. We started follow-up in 1991 because it is the first year for which we have information regarding alcohol intake. There were 1,069 women with incident psoriasis included in this analysis.
We confirmed a subset of self-reports using the Psoriasis Screening Tool (PST) questionnaire14. The PST is a one page self-administered questionnaire that assigns a diagnosis of psoriasis based on responses to seven questions. The questions on the PST were derived from expert opinion and the National Psoriasis Foundation’s survey on psoriasis. Three questions inquire about being diagnosed with psoriasis by some type of medical provider, such as a dermatologist, a primary care doctor, or a nurse practitioner. Four questions inquire about having morphological skin changes of psoriasis, three of which are accompanied by pictures. Pictures were chosen to represent each of three common psoriasis phenotypes, namely plaques, nail changes, and scalp psoriasis. One non-pictorial question inquires about inverse psoriasis. Scoring algorithms were developed to assign a diagnosis of psoriasis depending on a participant’s response to the questions. These scoring algorithms were based on multiple a priori hypotheses. A pilot study showed that the PST was able to screen for psoriasis with 99% sensitivity and 94% specificity14 in a population of adults attending an outpatient dermatology clinic of a tertiary care referral center. The PST has yet to be tested in a population with an expected low prevalence of psoriasis. However using Bayes’ theorem, the calculated positive predictive value of the PST is 25%. In other words, a positive test result on the PST increases the pre-test probability of having psoriasis from 2% (assumed prevalence of psoriasis in the United States population15, 16) to 25%. We mailed the PST to all NHS II participants who self-reported a physician diagnosis of psoriasis with an overall response rate of 87%.
Assessment of Alcohol Intake
Information on alcohol intake was updated in 1995, 1999, and 2003. The 1991 questionnaire included questions on the average intake of alcoholic beverages (regular beer, light beer, red wine, white wine, and liquor) during the past year. Nurses responded to the following question: “For each food listed, fill in the circle indicating how often on average you have used the amount specified during the past year.” Intake of each beverage was ascertained in nine categories (number of drinks): none or less than once per month, 1 to 3 per month, 1 per week, 2 to 4 per week, 5 to 6 per week, 1 per day, 2 to 3 per day, 4 to 5 per day, and 6 or more per day. Total amount of alcohol consumed was estimated at 12.8 g for a glass, bottle, or can of beer (12 oz), 11 g for a glass of wine (4 oz), and 14 g for a shot of liquor (1.5 oz). Total alcohol intake was computed as the sum of the intake from beer, wine, and liquor. One drink was defined as 12.8g of alcohol (median amount of alcohol in beer, wine, and liquor). Beverage-specific consumption was also calculated and analyzed separately. The reproducibility and validity of this questionnaire for alcohol intake have been previously documented in the NHS I cohort 17.
Assessment of Covariates
Date of birth and height were reported on the 1989 questionnaire. Participants reported their current weight 13, smoking status 12, dietary intake, and physical activity on the biennial mailed questionnaires. Quintiles of dietary folate equivalents (DFE) were calculated from a validated semi-quantitative food frequency questionnaire and quintiles of metabolic equivalents (METS) were calculated from questions about various type of physical activity. Body mass index was calculated by dividing updated weight in kilograms by the square of height in meters. Previously, the accuracy of self-reported anthropometric measures was validated among 140 NHS I participants. Self-reported and measured weights were highly correlated (0.97) 18.
Statistical analysis
We computed person-time of follow-up for each participant from the return date of the 1991 questionnaire to the date of diagnosis of psoriasis or the end of the study period. We used Cox proportional hazards models to estimate the age-adjusted and multivariate relative risk of incident psoriasis in women who reported alcohol intake compared to those who did not. We categorized alcohol intake into six categories-none, 1 to 4 g per week, 5 to 9 g per week, 10 to14 g per week, 15 to 29 g per week, and 30 g or more per week. We categorized type of alcoholic beverage (regular beer, light beer, red wine, white wine, and liquor) into four categories-none, 1 to 3 per month, 1 per week, 2 to 4 per week, and 5 or greater per week. We categorized body mass index at baseline and at each questionnaire cycle into six categories: <21kg/m2, 21–22.9, 23–24.9, 25–27.4, 27.5–29.9, 30–34.9 and ≥35. We categorized DFE as low and high based on the median for DFE. Median DFE was available only in 1999 and 2003. The median DEF was 976 mcg in 1999 and 1000 mcg in 2003. We applied the 1999 median DFE to three time periods: 1991–1994, 1995–1998, and 1999–2002. We applied the 2003 median DFE to the 2003–2006 time period. We explored potential interactions by DFE (high and low according to the period specific median) by testing the significance of interaction terms added to our final multivariate models. For all relative risks, we calculated 95% confidence intervals and all p-values were two-sided. Statistical analyses were performed using SAS software, version 9.1 (SAS Institute Inc, Car, NC). The Partners Health Care System Institutional Review Board approved this study.
RESULTS
Over the 14-year follow-up period, 1069 incident cases of psoriasis occurred. There was no material difference in mean age between alcohol drinkers and abstainers (Table 1). Alcohol abstainers had a higher BMI and were less physically active. Proportion of current and past smokers was higher in alcohol drinkers and dietary folate intake was higher in abstainers.
Table 1.
Baseline characteristics according to alcohol consumption status
| Alcohol Consumption | Alcohol Intake† (drinks/wk) | ||||||
|---|---|---|---|---|---|---|---|
| No | Yes | 0.1 – 0.3 | 0.4 – 0.7 | 0.8 – 1.1 | 1.2 – 2.3 | ≥ 2.3 | |
| Characteristics | n = 35 058 | n = 47 614 | n = 32 030 | n = 8253 | n = 4233 | n = 2221 | n = 877 |
| Age* (years, mean) | 36.3 | 36.1 | 36 | 36 | 36.6 | 37 | 37.6 |
| Body mass index (kg/m2, mean) | 24.8 | 23.4 | 23.7 | 22.8 | 22.7 | 22.8 | 23.1 |
| Smoking (never, %) | 75 | 59 | 64 | 55 | 49 | 42 | 32 |
| Smoking (current, %) | 8 | 14 | 12 | 14 | 19 | 22 | 37 |
| Smoking (past, %) | 16 | 27 | 24 | 31 | 32 | 35 | 31 |
| Dietary folate equivalent (mcg, mean) | 913 | 916 | 921 | 932 | 909 | 883 | 794 |
| Physical activity (metabolic equivalents per week) | 18.3 | 22.4 | 21.5 | 24.1 | 25.1 | 24.6 | 22.8 |
in 1991
breakdown of the 47 614 who reported yes to alcohol consumption
We observed an increased age-adjusted relative risk of psoriasis in women who consumed greater than 2.3 alcoholic beverages per week compared to nondrinkers (Table 2). This risk remained significant after adjusting for age, BMI (both continuous and categorical), smoking, physical activity, and DFE. Although the relative risks did not reach statistical significance in women who consumed less than 2.3 drinks per week, there was a significant trend towards increased risk for psoriasis with greater alcohol intake (p for trend 0.002).
Table 2.
Age-adjusted and multivariate relative risks for incident psoriasis by amount of alcohol intake among women
| Alcohol intake (drinks/wk) |
N* | RR (95% CI) Age-adjusted |
RR (95% CI) Multivariate † |
RR (95% CI) Multivariate ‡ |
|---|---|---|---|---|
| None (referent) | 442 | 1.00 | 1.00 | 1.00 |
| 0.1 – 0.3 | 371 | 0.93 (0.80 – 1.07) | 0.96 (0.83 – 1.10) | 0.97 (0.82 – 1.12) |
| 0.4 – 0.7 | 109 | 0.93 (0.75 – 1.15) | 1.00 (0.80 – 1.23) | 1.02 (0.82 – 1.26) |
| 0.8 – 1.1 | 76 | 1.11 (0.87 – 1.41) | 1.19 (0.93 – 1.53) | 1.21 (0.94 – 1.55) |
| 1.2 – 2.3 | 43 | 1.15 (0.84 – 1.57) | 1.20 (0.87 – 1.65) | 1.18 (0.85 – 1.64) |
| ≥ 2.3 | 28 | 1.89 (1.29 – 2.77) | 1.79 (1.21 – 2.64) | 1.72 (1.15 – 2.57) |
| Total cases | 1069 | |||
| P for trend | 0.004 | 0.002 | 0.003 |
Abbreviations: RR, relative risk; CI, confidence interval, BMI, body mass index (calculated as weight in kilograms divided by height in meters squared); DFE, dietary folate equivalents; METS, metabolic equivalents
Number of incident cases of psoriasis
Adjusted for age, smoking (never, current, past), BMI (21–22.9, 23–24.9, 25–27.4, 27.5–29.9, 30–34.9, ≥35 kg/m2), quintiles of DFE, and physical activity in quintiles of METS per week
Adjusted for age, smoking (never, current, past), BMI (continuous), quintiles of DFE and physical activity in quintiles of METS per week
We also found that the risk of psoriasis varied by type of alcoholic beverage. After adjusting for age, women who drank ≥ 5 beers per week had a greater relative risk of psoriasis (Table 3). The excess risk of psoriasis associated with consumption of at least 5 non-light beers per week for all NHS2 participants was 1.53%. We calculated the excess risk, which was 106 per 100K person-years (PY) − 46 per 100K PY = 60 per 100K PY. This gave a relative risk increase of 1.3. This risk remained significant after simultaneously adjusting for age, BMI, smoking, physical activity, and DFE. Women who drank any amount of light beer, white wine, red wine, or liquor were not at increased risk of incident psoriasis. We performed analyses with a common reference group that excluded any women who drank any type of alcohol and found no difference in the effect estimates. We also evaluated the multivariate effect of beer on psoriasis risk in a model that included all types of alcoholic beverages and there was no material change in the association.
Table 3.
Age-adjusted and multivariate relative risks for incident psoriasis by type of alcohol beverage among women
| Beer (# drinks) | N | RR (95% CI) Age-adjusted |
RR (95% CI) Multivariate * |
|---|---|---|---|
| None (referent) | 817 | 1.00 | 1.00 |
| 1 – 3/mo | 112 | 1.02 (0.83 – 1.24) | 1.02 (0.84 – 1.25) |
| 1/wk | 37 | 0.80 (0.57 – 1.10) | 0.83 (0.60 – 1.16) |
| 2 – 4/wk | 21 | 0.80 (0.50 – 1.18) | 0.80 (0.51 – 1.23) |
| ≥ 5/wk | 22 | 1.81 (1.18 – 2.76) | 1.76 (1.15 – 2.69) |
| Total cases† | 1009 | ||
| P for trend | 0.001 | 0.003 | |
| Light beer (# drinks) | |||
| None (referent) | 787 | 1.00 | 1.00 |
| 1 – 3/mo | 115 | 0.93 (0.76 – 1.13) | 0.92 (0.75 – 1.12) |
| 1/wk | 45 | 0.91 (0.67 – 1.21) | 0.91 (0.67 – 1.23) |
| 2 – 4/wk | 33 | 0.88 (0.62 – 1.24) | 0.87 (0.61 – 1.23) |
| ≥ 5/wk | 22 | 1.07 (0.70 – 1.64) | 0.98 (0.64 – 1.51) |
| Total cases† | 1002 | ||
| P for trend | 0.47 | 0.78 | |
| White wine (# drinks) | |||
| None (referent) | 585 | 1.00 | 1.00 |
| 1 – 3/mo | 238 | 1.01 (0.87 – 1.18) | 1.07 (0.92 – 1.24) |
| 1/wk | 74 | 0.88 (0.69 – 1.12) | 0.98 (0.77 – 1.25) |
| 2 – 4/wk | 74 | 1.11 (0.87 – 1.41) | 1.26 (0.99 – 1.62) |
| ≥ 5/wk | 38 | 1.03 (0.74 – 1.43) | 1.17 (0.84 – 1.63) |
| Total cases† | 1009 | ||
| P for trend | 0.78 | 0.35 | |
| Red wine (# drinks) | |||
| None (referent) | 725 | 1.00 | 1.00 |
| 1 – 3/mo | 167 | 1.03 (0.87 – 1.22) | 1.08 (0.91 – 1.28) |
| 1/wk | 47 | 0.72 (0.53 – 0.97) | 0.78 (0.58 – 1.05) |
| 2 – 4/wk | 47 | 0.83 (0.62 – 1.12) | 0.93 (0.69 – 1.26) |
| ≥ 5/wk | 23 | 0.80 (0.52 – 1.20) | 0.88 (0.58 – 1.34) |
| Total cases† | 1009 | ||
| P for trend | 0.88 | 0.69 | |
| Liquor (# drinks) | |||
| None (referent) | 770 | 1.00 | 1.00 |
| 1 – 3/mo | 155 | 1.11 (0.93 – 1.31) | 1.08 (0.91 – 1.29) |
| 1/wk | 38 | 0.86 (0.62 – 1.19) | 0.85 (0.62 – 1.18) |
| ≥ 2/wk | 49 | 1.13 (0.85 –1.51) | 1.08 (0.81 – 1.45) |
| Total cases† | 1012 | ||
Abbreviations: RR, relative risk; CI, confidence interval, BMI, body mass index (calculated as weight in kilograms divided by height in meters squared); DFE, dietary folate equivalents; METS, metabolic equivalents
Simultaneously adjusted for age, smoking (never, current, past), BMI (21–22.9, 23–24.9, 25–27.4, 27.5–29.9, 30–34.9, ≥35 kg/m2), quintiles of DFE and physical activity in quintiles of METS per week
Number of cases may not total 1150 due to missing data
We also evaluated the influence of DFE intake on the association between beer and risk of psoriasis. Although the risk for psoriasis was higher in the low DFE group (multivariate RR ≥ 5 drinks/wk 2.11; 95% CI 1.15–3.89), the interaction was not statistically significant (p=0.18).
The PST was sent to 2430 who self-reported a physician diagnosis of psoriasis. Of these, 1150 were incident cases and 1280 were prevalent cases. Of the 1150 incident cases, only 1069 were used for analysis. The response rate to the PST among the incident psoriasis cases was 73%, and the response rate among the prevalent psoriasis cases was 82%. Of the incident cases who responded with a completed PST questionnaire, 86% were actually confirmed to have psoriasis as determined by the PST. Among these confirmed cases, we observed a materially elevated and statistically significant relative risk of psoriasis in women who consumed ≥ 2.3 alcoholic beverages per week and in women who drank ≥ 5 non-light beers per week (Table 4).
Table 4.
Age-adjusted and multivariate relative risks for confirmed* incident psoriasis by amount of alcohol intake and amount of beer intake
| Alcohol intake (drinks/wk) |
N | RR (95% CI) Age-adjusted | RR (95% CI) Multivariate † |
|---|---|---|---|
| None (referent) | 213 | 1.00 | 1.00 |
| 0.1 – 0.3 | 198 | 1.03 (0.85 – 1.25) | 1.08 (0.89 – 1.31) |
| 0.4 – 0.7 | 57 | 1.02 (0.76 – 1.36) | 1.12 (0.83 – 1.50) |
| 0.8 – 1.1 | 41 | 1.26 (0.90 – 1.77) | 0.40 (0.99 – 1.97) |
| 1.2 – 2.3 | 22 | 1.24 (0.80 – 1.93) | 1.34 (0.85 – 2.08) |
| ≥ 2.3 | 19 | 2.68 (1.67 – 4.29) | 2.54 (1.57 – 4.10) |
| Total cases‡ | 550 | ||
| P for trend | 0.0005 | 0.0002 | |
| Beer (# drinks) | |||
| None (referent) | 418 | 1.00 | 1.00 |
| 1 – 3/mo | 68 | 1.20 (0.92 – 1.55) | 1.20 (0.93 – 1.56) |
| 1/wk | 18 | 0.76 (0.47 – 1.22) | 0.81 (0.50 – 1.29) |
| 2 – 4/wk | 12 | 0.85 (0.48 – 1.50) | 0.88 (0.49 – 1.57) |
| ≥ 5/wk | 15 | 2.40 (1.40 – 3.96) | 2.29 (1.36 – 3.85) |
| Total cases‡ | 531 | ||
| P for trend | <0.0001 | 0.001 | |
Abbreviations: RR, relative risk; CI, confidence interval, BMI, body mass index (calculated as weight in kilograms divided by height in meters squared); DFE, dietary folate equivalents; METS, metabolic equivalents
Confirmed using the psoriasis screening tool 32
Simultaneously adjusted for age, smoking (never, current, past), BMI (21–22.9, 23–24.9, 25–27.4, 27.5–29.9, 30–34.9, ≥35 kg/m2), and physical activity in quintiles of METS per week
Number of cases may not total 577 due to missing data
DISCUSSION
In this prospective study of US women, we found the risk for psoriasis varied by the amount and type of alcoholic beverage. Although overall women who drank more than 2.3 alcoholic beverages per week were at greater risk for psoriasis, non-light beer was the only alcoholic beverage that conferred an increased risk for psoriasis. The risk for psoriasis was 1.8 times higher among women who consumed ≥ 5 non-light beers per week per day compared to those who abstained from alcohol. When we used a more precise definition for psoriasis, the risk was 2.3 times higher among women who consumed ≥ 5 non-light beers per week. These associations were independent of other potential risk factors for psoriasis such as age, smoking, BMI, physical activity, and DFE. The excess risk of psoriasis associated with consumption of at least 5 non-light beers per week for all NHS2 participants was 1.53%; however this excess risk would likely be more pronounced in the general population where the prevalence of non-light beer consumption is higher than the prevalence of beer consumption in this cohort. For example, this excess risk increases to 15.3% given the prevalence of drinking in the general US population19.
Non-light beer was the only alcoholic beverage that increased the risk for psoriasis, suggesting that certain non-alcoholic components of beer, which are not found in wine or liquor, may play an important role in new onset psoriasis. One of these components may be the starch-source used in making beer. Beer is one of the few non-distilled alcoholic beverages that use a starch-source for fermentation, which is commonly barley. This differs from wine that uses a fruit-source (grapes) for fermentation. Some types of liquors such as vodka may use a starch-source for fermentation; however these starches are physically separated from the liquor during distillation. Starch sources such as barley contain gluten, which has been shown to be associated with psoriasis. For example, individuals with psoriasis have elevated levels of anti-gliadin antibodies (AGA) and may have a so called ‘latent-gluten sensitivity’ compared to individuals without psoriasis 20. Several studies have shown that a gluten-free diet may improve psoriasis severity in patients with gluten sensitivity 20–23. One case report describes a patient with Celiac disease and psoriasis whose skin lesions improved shortly after starting a gluten-free diet 24. Light beer also contains gluten, however, this study did not show an association between light beer intake and incident psoriasis. This may be due possibly to the lower amounts of grain used to make light beer compared to non-light beer (personal communication, W. Kerr (wkerr@arg.org)). Although a gluten free diet helps clear psoriasis 22, 24, it remains unknown whether gluten contributes to new onset psoriasis and whether this only occurs in predisposed individuals, such as those with latent gluten sensitivity.
Limitations of our study deserve comment. The retrospective recall of psoriasis onset may have led to misclassification of psoriasis onset. We were also unable to examine whether the risk for psoriasis was different for early-onset psoriasis versus later-onset psoriasis given the age of the NHS II cohort at baseline (25 to 42 years). This well-educated female cohort provides high quality data with little loss to follow-up but does not represent a random sample of US women. Although the absolute rates of psoriasis and distribution of alcohol intake may not be representative of a random sample of US women, the biological effects of alcohol intake on psoriasis should be similar. Our study was observational; thus, we cannot rule out the possibility that statistical error and unmeasured factors, such as socioeconomic status and stress, might contribute to the observed associations, however we included as many known risk factors (obesity, smoking, dietary intake, and physical activity) that met the definition of possible confounders into our analyses. As in other epidemiological studies on psoriasis 25–29, our diagnosis of psoriasis relied on self-reports of physician-diagnosed psoriasis and we did not require an examination by a dermatologist. Previous validation studies in the Nurses’ Health Study for another skin condition, basal cell carcinoma, found self-reports to be greater than 90% accurate 30, 31. Furthermore, in the subset of confirmed psoriasis cases, we found a stronger association between risk of incident psoriasis and overall alcohol intake as well as non-light beer intake.
In conclusion, our prospective study indicates that non-light beer intake is associated with an increased risk of psoriasis, whereas light beer, wine, and liquor did not increase the risk among women. Specifically, women who drank at least five non-light beers per week were 1.8 times more likely to develop psoriasis compared to women who abstained from alcohol. Lower intake of non-light beer and intake of other types of alcoholic beverages do not appear to influence the risk of developing psoriasis. Women with a high risk of psoriasis may consider avoiding higher intake of non-light beer. We suggest further investigation into the potential mechanisms of non-light beer inducing new-onset psoriasis.
Acknowledgement
We thank Elaine-Coughlan Gifford, MS, Channing Laboratory, Brigham & Women’s Hospital, Boston, MA, for her assistance with data analysis and programming. Ms Gifford did not receive compensation for her contributions. We also thank William Kerr, PhD, Senior Scientist of the Alcohol Research Group, Emeryville, CA for his expertise on the contents of light beer. Dr Kerr did not receive compensation for his contribution.
Funding support: This study was supported by grants K07 CA108978 (Dr Qureshi) and R01 CA050385 from the National Institutes of Health/National Cancer Institute.
Role of the Sponsors: The sponsors had no role in the design and conduct of the study; in the collection, analysis, and interpretation of data; or in the preparation, review, or approval of the manuscript.
Footnotes
Author Contributions: Dr Qureshi had full access to all the data in the study and takes responsibility for the integrity of the data and the accuracy of the data analysis. Study concept and design: Dr. Qureshi, Dr. Dominguez and Dr. Curhan. Acquisition of data: Dr. Qureshi and Dr. Dominguez. Analysis and interpretation of data: Dr. Qureshi, Dr. Dominguez, Dr. Han and Dr. Curhan. Drafting of the manuscript: Dr. Qureshi, Dr. Dominguez, Dr. Choi, and Dr. Curhan. Critical revision of the manuscript for important intellectual content: Dr. Qureshi, Dr. Dominguez, Dr. Choi, Dr. Han, and Dr. Curhan. Statistical analysis: Dr. Qureshi, Dr. Choi, Dr. Han, and Dr. Curhan. Obtained funding: Dr. Qureshi and Dr. Curhan. Administrative, technical, or material support: Dr. Qureshi and Dr. Dominguez. Study supervision: Dr. Qureshi.
Financial disclosure: Relationships relevant to this manuscript: None. All other relationships: Dr. Qureshi has served as a consultant to Amgen and Genentech. Drs. Dominguez, Choi, Han, and Curhan have no conflicts of interest to declare.
Contributor Information
Abrar A. Qureshi, Email: abrar.qureshi@channing.harvard.edu.
Patrick L. Dominguez, Email: pdominguez@partners.org.
Hyon K. Choi, Email: hchoibos@yahoo.com.
Jiali Han, Email: nhhan@channing.harvard.edu.
Gary Curhan, Email: gcurhan@partners.org.
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