New recommendation and coverage of low-dose computed tomography for lung cancer screening: uptake has increased but is still low.

BACKGROUND: In 2013, the US Preventive Services Task Force (USPSTF) issued recommendations for low-dose computed tomography for lung cancer screening (LDCT-LCS), but there continues to be a dearth of information on the adoption of LDCT-LCS in healthcare systems. Using a multilevel perspective, our study aims to assess referrals for LDCT-LCS and identify facilitators and barriers to adoption following recent policy changes. METHODS: A retrospective analysis of electronic medical record data from patients aged 55-80 years with no history of lung cancer who visited a primary care provider in a large healthcare system in California during 2010-2016 (1,572,538 patient years). Trends in documentation of smoking history, number of eligible patients, and lung cancer screening orders were assessed. Using Hierarchical Generalized Linear Models, we also evaluated provider-level and patient-level factors associated with lung cancer screening orders among 970 primary care providers and 12,801 eligible patients according to USPSTF guidelines between January 1st, 2014 and December 31st, 2016. RESULTS: Documentation of smoking history to determine eligibility (59.2% in 2010 to 77.8% in 2016) and LDCT-LCS orders (0% in 2010 to 7.3% in 2016) have increased since USPSTF guidelines. Patient factors associated with increased likelihood of lung cancer screening orders include: younger patient age (78-80 vs. 55-64 years old: OR, 0.4; 95% CI, 0.3-0.7), Asian race (vs. Non-Hispanic White: OR, 1.6; 95% CI, 1.1-2.4), reported current smoking (vs. former smoker: OR, 1.7; 95% CI, 1.4-2.0), no severe comorbidity (severe vs. no major comorbidity: OR = 0.2, 95% CI = 0.1-0.3; moderate vs. no major comorbidity: OR = 0.5; 95% CI = 0.4-0.7), and making a visit to own primary care provider (vs. other primary care providers: OR, 2.4; 95% CI, 1.7-3.4). Appropriate referral for lung cancer screening varies considerably across primary care providers. Provider factors include being a female physician (vs. male: OR, 1.6; 95% CI, 1.1-2.3) and receiving medical training in the US (foreign vs. US medical school graduates: OR = 0.4, 95% CI = 0.3-0.7). CONCLUSIONS: Future interventions to improve lung cancer screening may be more effective if they focus on accurate documentation of smoking history and target former smokers who do not regularly see their own primary care providers.

A Comprehensive Model of Colorectal Cancer by Risk Factor Status and Subsite Using Data From the Nurses' Health Study.

We expanded and updated our colon cancer risk model to evaluate colorectal cancer (CRC) and whether subsite-specific risk models are warranted. Using data from 1980-2010 for 90,286 women enrolled in the Nurses' Health Study, we performed competing-risks regression and tests for subsite heterogeneity (proximal colon: n = 821; distal colon: n = 521; rectum: n = 376). Risk factors for CRC were consistent with those in our colon cancer model. Processed meat consumption was associated with a higher risk of distal (hazard ratio (HR) = 1.45; P = 0.02) but not proximal (HR = 0.95; P = 0.72) colon cancer. Smoking was associated with both colon (HR = 1.21) and rectal (HR = 1.27) cancer and was more strongly associated with proximal (HR = 1.31) than with distal (HR = 1.04) colon cancer (P = 0.029). We observed a significant trend of cancer risk for smoking in subsites from the cecum (HR = 1.41) to the proximal colon (excluding the cecum; HR = 1.27) to the distal colon (HR = 1.04; P for trend = 0.040). The C statistics for colorectal (C = 0.607), colon (C = 0.603), and rectal (C = 0.639) cancer were similar, although C was slightly higher for rectal cancer. Despite evidence for site-specific differences for several risk factors, overall our findings support the application of risk prediction models for colon cancer to CRC.

Rotating night shift work, sleep, and colorectal adenoma in women.

PURPOSE: This study aims to investigate the associations of rotating night shift work history and sleep duration with risk of colorectal adenoma. METHODS: We evaluated 56,275 cancer-free participants of the Nurses' Health Study II, who had their first colonoscopy or sigmoidoscopy between 1991 and 2011; rotating night shift work and sleep duration were reported by mailed questionnaire. Multivariable-adjusted logistic regression was used to estimate relative risks (RR) of colorectal adenoma, with 95% confidence intervals (CI), across categories of rotating night shift work history (none, 1-4, 5-9, and ≥10 years) and sleep duration (≤5, 6, 7, 8, and ≥9 h/day). RESULTS: We found no association between duration of rotating night shift work and occurrence of colorectal adenoma (p-trend across shift work categories = 0.5). Women with the longest durations of rotating night shift work (≥10 years) had a similar risk of adenoma compared to women without a history of rotating night shift work (multivariable-adjusted RR = 0.96, 95% CI = 0.83-1.11). Similarly, there were no associations of shorter or longer sleep durations with adenoma risk (p-trend = 0.2 across sleep durations of ≤5 through 7 h/day and p-trend = 0.5 across sleep durations of 7 through ≥9 h/day). Results were similar when we examined associations according to adenoma location and subtype. CONCLUSIONS: Our results do not support an association between rotating night shift work or sleep duration and risk of colorectal adenoma in women.

Chronic inflammation and risk of colorectal and other obesity-related cancers: The health, aging and body composition study.

Evidence of the association between chronic inflammation and the risk of colorectal cancer (CRC) and other obesity-related cancers (OBRC) remains inconsistent, possibly due to a paucity of studies examining repeated measures of inflammation. In the Health ABC prospective study of 2,490 adults aged 70-79 years at baseline, we assessed whether circulating levels of three markers of systemic inflammation, IL-6, CRP and TNF-α, were associated with the risk of CRC and OBRC, a cluster including cancers of pancreas, prostate, breast and endometrium. Inflammatory markers were measured in stored fasting blood samples. While only baseline measures of TNF-α were available, IL-6 and CRP were additionally measured at Years 2, 4, 6 and 8. Multivariable Cox models were fit to determine whether tertiles and log-transformed baseline, updated and averaged measures of CRP and IL-6 and baseline measures of TNF-α were associated with the risk of incident cancer(s). During a median follow-up of 11.9 years, we observed 55 and 172 cases of CRC and OBRC, respectively. The hazard of CRC in the highest tertile of updated CRP was more than double that in the lowest tertile (HR = 2.29; 95% CI: 1.08-4.86). No significant associations were seen between colorectal cancer and IL-6 or TNF-α. Additionally, no significant associations were found between obesity-related cancers and the three inflammatory markers overall, but we observed a suggestion of effect modification by BMI and NSAID use. In summary, in this population, higher CRP levels were associated with increased risk of CRC, but not of OBRC. The findings provide new evidence that chronically elevated levels of CRP, as reflected by repeated measures of this marker, may play a role in colorectal carcinogenesis in older adults.

Application of the Rosner-Wei risk-prediction model to estimate sexual orientation patterns in colon cancer risk in a prospective cohort of US women.

PURPOSE: We examined whether lesbian and bisexual women may be at greater risk of colon cancer (CC) than heterosexual women. METHODS: Working with a large cohort of US women ages 25-64 years, we analyzed 20 years of prospective data to estimate CC incidence, based on known risk factors by applying the Rosner-Wei CC risk-prediction model. Comparing to heterosexual women, we calculated for lesbian and bisexual women the predicted 1-year incidence rate (IR) per 100,000 person-years and estimated incidence rate ratios (IRR) and 95 % confidence intervals (CI), based on each woman's comprehensive risk factor profile. RESULTS: Analyses included 1,373,817 person-years of data from 66,257 women. For each sexual orientation group, mean predicted 1-year CC IR per 100,000 person-years was slightly over 12 cases for each of the sexual orientation groups. After controlling for confounders in fully adjusted models and compared with heterosexuals, no significant differences in IRR were observed for lesbians (IRR 1.01; 95 % CI 0.99, 1.04) or bisexuals (IRR 1.01; 95 % CI 0.98, 1.04). CONCLUSIONS: CC risk is similar across all sexual orientation subgroups, with all groups comparably affected. Health professionals must ensure that prevention, screening, and treatment programs are adequately reaching each of these communities.

An examination of sexual orientation group patterns in mammographic and colorectal screening in a cohort of U.S. women.

PURPOSE: Underutilization of cancer screening has been found especially to affect socially marginalized groups. We investigated sexual orientation group patterns in breast and colorectal cancer screening adherence. METHODS: Data on breast and colorectal cancer screening, sexual orientation, and sociodemographics were gathered prospectively from 1989 through 2005 from 85,759 U.S. women in the Nurses' Health Study II. Publicly available data on state-level healthcare quality and sexual-orientation-related legal protections were also gathered. Multivariable models were used to estimate sexual orientation group differences in breast and colorectal cancer screening, controlling for sociodemographics and state-level healthcare quality and legal protections for sexual minorities. RESULTS: Receipt of a mammogram in the past 2 years was common though not universal and differed only slightly by sexual orientation: heterosexual 84 %, bisexual 79 %, and lesbian 82 %. Fewer than half of eligible women had ever received a colonoscopy or sigmoidoscopy, and rates did not differ by sexual orientation: heterosexual 39 %, bisexual 39 %, and lesbian 42 %. In fully adjusted models, state-level healthcare quality score, though not state-level legal protections for sexual minorities, was positively associated with likelihood of being screened for all women regardless of sexual orientation. CONCLUSIONS: Concerns have been raised that unequal healthcare access for sexual orientation minorities may adversely affect cancer screening. We found small disparities in mammography and none in colorectal screening, though adherence to colorectal screening recommendations was uniformly very low. Interventions are needed to increase screening in women of all sexual orientation groups, particularly in areas with poor healthcare policies.

Preventability of cancer: the relative contributions of biologic and social and physical environmental determinants of cancer mortality.

Whereas models of cancer disparities and variation in cancer burden within population groups now specify multiple levels of action from biologic processes to individual risk factors and social and physical contextual factors, approaches to estimating the preventable proportion of cancer use more traditional direct models often from single exposures to cancer at specific organ sites. These approaches are reviewed, and the strengths and limitations are presented. The need for additional multilevel data and approaches to estimation of preventability are identified. International or regional variation in cancer may offer the most integrated exposure assessment over the life course. For the four leading cancers, which account for 50% of incidence and mortality, biologic, social, and physical environments play differing roles in etiology and potential prevention. Better understanding of the interactions and contributions across these levels will help refine prevention strategies.

Plasma folate, methylenetetrahydrofolate reductase (MTHFR), and colorectal cancer risk in three large nested case-control studies.

Few prospective studies have examined the associations between blood levels of folate, in conjunction with methylenetetrahydrofolate reductase (MTHFR) polymorphisms, and colorectal cancer. We evaluated the associations between plasma folate, MTHFR C677T, and A1298C, and colorectal cancer in three large prospective studies: the Nurses' Health Study, the Health Professionals Follow-up Study, and the Physicians' Health Study. A total of 602 incident cases were identified and individually matched to controls who provided blood specimens. We used conditional logistic regression to calculate the relative risk (RR) and 95% confidence interval (95% CI) and then pooled the estimates using a random effects model. We found a lower risk of colorectal cancer among participants with low plasma folate levels: compared with the lowest quartile, RRs (95% CIs) for each successively higher quartile of plasma folate levels were 1.55 (1.14-2.11), 1.37 (1.00-1.88), and 1.47 (1.07-2.01; P for trend = 0.10). For the MTHFR polymorphisms, RRs (95% CIs) were 0.62 (0.44-0.90) for 677TT versus CC/CT and 0.68 (0.31-1.51) for 1298CC versus AC/AA, and these lower-risk genotypes were associated with lower circulating plasma folate levels. When we partitioned the variation in plasma folate levels, variation due to folate intake was not positively associated with colorectal cancer risk. We found that low plasma folate levels were associated with lower risk of colorectal cancer. The reasons underlying a lower risk of colorectal cancer with low plasma folate levels require elucidation because plasma folate levels can reflect dietary intake, genetic influences, and other factors.

Burden of smoking on cause-specific mortality: application to the Nurses' Health Study.

OBJECTIVE: The burden of smoking on six causes of death in women was evaluated using various novel modelling approaches. DESIGN: A prospective US-based nationwide cohort study. PARTICIPANTS: 102 635 women in the Nurses' Health Study followed biennially from 1980 to 2004. METHODS: The relation between cigarette smoking and cause-specific death was compared using baseline versus biennially updated smoking status. The authors used competing risk survival analysis to formally compare associations of smoking-related variables on risk of death as a result of coronary heart disease (CHD), cerebrovascular diseases, lung cancer, other respiratory diseases, other smoking-caused cancers and other causes. RESULTS: The associations of current and former smoking were stronger with most cause-specific mortality when using updated information. The effect of each smoking-related variable differed significantly (p(h) <0.0001) across some causes of death. For example, risks increased by 5% for death due to other causes up to 37% for lung cancer death for a 5-year earlier age at initiation. Compared with continuing to smoke, former smokers with 5-10 years of cessation had a 25% reduction in risk of dying from other causes of death up to a 61% reduction in risk of dying from CHD and cerebrovascular diseases. CONCLUSIONS: The risks of smoking and the benefits from quitting are greater than previously reported, when utilising repeated measures of smoking data collected during follow-up, and vary by cause of death. Focused efforts to communicate the benefits of quitting to smokers and to prevent smoking initiation among children and youths should remain top public health priorities to reduce the worldwide mortality burden caused by smoking.

Cumulative risk of colon cancer up to age 70 years by risk factor status using data from the Nurses' Health Study.

The authors developed a comprehensive model of colon cancer incidence that allows for nonproportional hazards and accounts for the temporal nature of risk factors. They estimated relative risk based on cumulative incidence of colon cancer by age 70 years. Using multivariate, nonlinear Poisson regression, they determined colon cancer risk among 83,767 participants in the Nurses' Health Study. The authors observed 701 cases of colon cancer between 1980 and June 1, 2004. There was increased risk for a positive family history of colon or rectal cancer (55%), 10 or more pack-years of cigarette smoking before age 30 years (16%), and tallness (67 inches (170 cm) vs. 61 inches (155 cm): 19%). Reduced risk was observed for current postmenopausal hormone use (-23%), being physically active (21 metabolic equivalent (MET)-hours/week vs. 2 MET-hours/week: -49%), taking aspirin (7 tablets/week vs. none: -29%), and being screened (-24%). Women who smoked, had a consistently high relative weight, had a low physical activity level, consumed red or processed meat daily, were never screened, and consumed low daily amounts of folate had almost a 4-fold higher cumulative risk of colon cancer by age 70 years. For women with a high risk factor profile, adopting a healthier lifestyle could dramatically reduce colon cancer risk.

Chronic inflammation and risk of lung cancer in older adults in the health, aging and body composition cohort study.

OBJECTIVES: We examined the association between three inflammatory markers (Interleukin (IL)-6, C-reactive protein (CRP), tumor necrosis factor (TNF)-α) and incident lung cancer using baseline, updated, and averaged inflammatory measures in older adults. METHODS: We fitted multivariable Cox models to assess whether circulating levels of inflammation markers were associated with incident lung cancers in the Health Aging, Body and Composition (HealthABC) prospective cohort of 3075 older adults aged 70-79 years at baseline. IL-6 and CRP were measured biennially, whereas TNF-α was measured at baseline. RESULTS: Baseline levels of IL-6 were significantly associated with incident lung cancer risk in a model that adjusted for age, gender, race, and site (Model 1) (Hazard RatioT3 vs. T1: 3.34, 95% Confidence Interval: 1.91, 5.85) and in a model adjusted for health factors linked to chronic inflammation (Model 2) (HR T3 vs. T1: 2.57, 95% CI: 1.41, 4.65). The associations observed in time-updated IL-6 (HR T3 vs. T1: 2.47, 95% CI: 1.43, 4.28), cumulatively averaged IL-6 (HR T3 vs. T1: 2.47, 95% CI: 1.43, 4.35), and baseline CRP levels (HR T3 vs. T1: 1.85, 95% CI: 1.11, 3.08) with incident lung cancer in Model 1 were not statistically significant in Model 2. CONCLUSIONS: Baseline CRP and IL-6 levels were associated with increased risk of lung cancer in Model 1 and both models, respectively. Chronic IL-6 inflammation, as quantified by repeated measures was associated with incident lung cancer in Model 1, but not Model 2. Further research is needed to understand the role of CRP and IL-6 in lung carcinogenesis.

C-peptide, insulin-like growth factor binding protein-1, glycosylated hemoglobin, and the risk of distal colorectal adenoma in women.

BACKGROUND: Determinants of insulin secretion and insulin-like growth factors (IGF) have been directly associated with risk for colorectal cancer. However, few studies have evaluated whether these factors are also associated with risk of colorectal adenoma, the main precursor lesion to colorectal cancer. METHODS: We identified 380 distal colorectal adenoma cases diagnosed between 1989 and 1998 and 380 controls among nondiabetic women from the cohort of 32,826 women, nested in the Nurses' Health Study, who provided blood samples in 1989 to 1990. Cases and controls were individually matched on year of birth, time period of and indication(s) for endoscopy, and date of blood draw. RESULTS: High concentrations of C-peptide, an indicator of insulin secretion, were statistically significantly associated with risk of distal colorectal adenoma [multivariable relative risk (MVRR) top versus bottom quartile, 1.63; 95% confidence interval (95% CI), 1.01-2.66; P = 0.01], even after including body mass index and physical activity in the statistical model. Fasting IGF binding protein-1 (IGFBP-1) concentrations did not show any clear association with risk for adenoma (MVRR top versus bottom quartile, 1.08; 95% CI, 0.56-2.07). These associations did not differ significantly by size/stage of adenoma. Glycosylated hemoglobin (HbA1c) was associated with a nonstatistically significant increased risk of colorectal adenoma (MVRR top versus bottom quartile, 1.47; 95% CI, 0.89-2.44). CONCLUSIONS: High HbA1c and low IGFBP-1 were not clearly associated with increased risk of distal colorectal adenoma. However, our current results and previous associations between C-peptide and colorectal cancer suggest that hyperinsulinemia may play a role throughout the development of colorectal neoplasia.

Improving colorectal cancer screening by targeting office systems in primary care practices: disseminating research results into clinical practice.

BACKGROUND: Randomized trials have shown the efficacy of an office systems approach in improving colorectal cancer (CRC) screening behaviors; its feasibility in real-world primary care practices has not been well studied. METHODS: Between August 1, 2000, and December 1, 2001, we enrolled 185 primary care clinicians identified through purchased database lists. At the end of follow-up (December 31, 2002), 127 clinicians had completed preintervention and postintervention questionnaires. Trained staff from the American Cancer Society visited practices and identified areas for improvement in CRC screening. They provided clinicians with resources, tools, and support to facilitate positive change. We defined 5 clinician behavior areas related to successful CRC screening, including educating patients, identifying patients due for screening, enabling patient compliance, monitoring patient compliance, and notifying patients of their test results. We measured these areas before and after the intervention using questionnaires and data extracted from medical records. RESULTS: We demonstrated improvements in the passive use of posters and brochures about CRC screening (baseline, 20.5% and follow-up, 69.3%; P<.001) and in the monitoring of fecal occult blood tests using manual tracking systems (baseline, 20.6% and follow-up, 37.3%; P<.05). Based on medical records data among 551 patients, we found a statistically significant increase in the number of patients who became up-to-date with CRC screening recommendations and tests (P< .001 for both). CONCLUSION: Methods shown to improve CRC screening processes in protocol-driven randomized trials may be effective in community practice, and wider dissemination of these strategies shows promise to increase CRC screening.

A prospective study of C-peptide, insulin-like growth factor-I, insulin-like growth factor binding protein-1, and the risk of colorectal cancer in women.

Hyperinsulinemia, hyperglycemia, and elevated insulin-like growth factor (IGF)-1 levels have been implicated in the etiology of colorectal cancer. However, the joint effects of insulin and IGF-I have not been considered, and whether hyperinsulinemia or hyperglycemia is more etiologically relevant is unclear. IGF binding protein-1 (IGFBP-1) has been hypothesized to mediate the effects of insulin, but epidemiologic data on IGFBP-1 are sparse. We conducted a nested case-control study among the 32,826 women of the Nurses' Health Study who provided a blood sample in 1989 to 1990. After excluding diabetics, we confirmed 182 incident colorectal cancer cases over 10 years of follow-up and 350 controls. Cases were matched to two controls on year of birth, date of blood draw, and fasting status. C-peptide levels were weakly associated with risk of colon cancer [top quartile (Q4) versus bottom quartile (Q1): multivariable relative risk (MVRR), 1.76; 95% confidence interval (95% CI), 0.85-3.63]. Fasting IGFBP-1 was inversely associated with risk of colon cancer (MVRR, 0.28; 95% CI, 0.11-0.75). We observed no clear association between glycosylated hemoglobin and risk for colorectal cancer. The IGF-I to IGFBP-3 molar ratio was associated with colon cancer risk (MVRR, 2.82; 95% CI, 1.35-5.88), and women with low levels of both IGF-I/IGFBP-3 and C-peptide (or high IGFBP-1) were at low risk, and elevation of either was sufficient to increase risk. Although altering IGF-I levels may not be practical, the growing burden of obesity and consequently hyperinsulinemia, which seems increasingly important for colon cancer, may be a target for effective prevention.

Vitamin D and actigraphic sleep outcomes in older community-dwelling men: the MrOS sleep study.

STUDY OBJECTIVES: Maintaining adequate serum levels of vitamin D may be important for sleep duration and quality; however, these associations are not well understood. We examined whether levels of serum 25(OH)D are associated with objective measures of sleep in older men. SETTING AND PARTICIPANTS: Cross-sectional study within a large cohort of community-dwelling older men, the MrOS study. INTERVENTIONS: Among 3,048 men age 68 years or older, we measured total serum vitamin D. Objective estimates of nightly total sleep time, sleep efficiency, and wake time after sleep onset (WASO) were obtained using wrist actigraphy worn for an average of 5 consecutive 24-h periods. RESULTS: 16.4% of this study population had low levels of vitamin D (< 20.3 ng/mL 25(OH)D). Lower serum vitamin D levels were associated with a higher odds of short (< 5 h) sleep duration, (odds ratio [OR] for the highest (≥ 40.06 ng/mL) versus lowest (< 20.3 ng/mL) quartile of 25(OH)D, 2.15; 95 % confidence interval (CI), 1.21-3.79; Ptrend = 0.004) as well as increased odds of actigraphy-measured sleep efficiency of less than 70% (OR, 1.45; 95% CI, 0.97-2.18; Ptrend = 0.004), after controlling for age, clinic, season, comorbidities, body mass index, and physical and cognitive function. Lower vitamin D levels were also associated with increased WASO in age-adjusted, but not multivariable adjusted models. CONCLUSIONS: Among older men, low levels of total serum 25(OH)D are associated with poorer sleep including short sleep duration and lower sleep efficiency. These findings, if confirmed by others, suggest a potential role for vitamin D in maintaining healthy sleep.

Early life body fatness and risk of colorectal cancer in u.s. Women and men-results from two large cohort studies.

BACKGROUND: The association between body fatness before adulthood and later risk of colorectal cancer remains unclear. We hypothesized that, independent of adult body fatness, early life body fatness would be associated with a higher risk of developing colorectal cancer. METHODS: We assessed body fatness during childhood and adolescence using a validated 9-level somatotype and inquired body weight in young adulthood in the Nurses' Health Study and Health Professionals Follow-up Study. We used the Cox proportional hazard regression modeling to estimate relative risks [RR, 95% confidence intervals (CI)] adjusting for adult body mass index (BMI) and other known colorectal cancer risk factors. RESULTS: We identified 2,100 incident colorectal cancer cases (1,292 in women and 808 in men) during 22 years of follow-up. Among women, the RR (95% CI) for childhood body fatness of level 5 or higher versus level 1 was 1.28 (1.04-1.58; Ptrend = 0.08) and for adolescent body fatness, it was 1.27 (1.01-1.60; Ptrend = 0.23). The corresponding RRs for men were 1.04 (0.82-1.31; Ptrend = 0.48) and 0.98 (0.75-1.27; Ptrend = 0.20), respectively. Results were generally similar across anatomic subsites within the colorectum. In addition, the RRs comparing BMI categories ≥27.5 to <19 kg/m(2) were 1.44 (1.06-1.95, at age 18; Ptrend = 0.009) for women and 1.18 (0.84-1.65, at age 21; Ptrend = 0.57) for men. CONCLUSION: Increased body fatness in early life, independent of adult obesity, might be a risk factor for colorectal cancer in women, but we observed a weaker association in men. IMPACT: Our findings support the growing evidence that early life body fatness affects the risk of colorectal cancer many decades later.

Low skin carotenoid concentration measured by resonance Raman spectroscopy is associated with metabolic syndrome in adults.

Oxidative stress is increased in patients with metabolic syndrome (MS). Antioxidants, including carotenoids, are decreased in MS. We hypothesized that a low skin carotenoid score (SCS), calculated using resonance Raman spectroscopy, would correlate with the presence of MS. We retrospectively reviewed consecutive patients referred for dietary assessment between 2010 and 2012. For each patient, a nutrition history, medical history, and SCS were recorded. χ(2) and Student t test were used to determine factors associated with MS. Multivariate logistic regression was used to identify factors associated with MS. One hundred fifty-five patients were included. The mean age was 54.1 ± 13.1 years, and the mean body mass index was 28.3 ± 6.1 kg/m(2). Metabolic syndrome was present in 43.9% of patients. The mean SCS was 28 084 ± 14 006 Raman counts (RC), including 23 058 ± 9812 RC for patients with MS and 32 011 ± 15 514 RC for patients without MS (P = .0001). In a multivariate analysis, SCS less than 25 000 RC (odds ratio, 3.71; 95% confidence interval, 1.36-10.7; P = .01) was independently associated with MS. A higher number of MS components was associated with a progressively lower SCS (P = .004). In a consecutive sample of patients referred for dietary assessment, a noninvasively measured SCS was lower among patients with MS.

Body fatness during childhood and adolescence, adult height, and risk of colorectal adenoma in women.

The latest report by the World Cancer Research Fund/American Institute of Cancer Research concluded that there is convincing evidence that adult height and obesity are risk factors for colorectal cancer. However, studies relating body fatness during early life to the risk of colorectal cancer or adenoma are scarce. In the Nurses' Health Study II, participants recalled adult attained height and body shape at ages 5, 10, and 20 years (using a 9-level pictogram: 1 = most lean body shape, 9 = most overweight body shape) at baseline. Among 32,707 women who had at least one lower bowel endoscopy between 1991 and 2005, 2,327 colorectal adenomas were documented. Adult height was positively associated with risk of colorectal adenoma (multivariate OR per 2 inch increment 1.05, 95% CI: 1.01-1.09). Comparing women who were overweight (body shape level 6 or higher) to women who were most lean (body shape level 1), ORs (95% CI, P(trend)) of colorectal adenoma for body shapes at ages 5, 10, and 20 years were 1.44 (1.04-1.99, 0.01), 1.21 (0.93-1.56, 0.05), and 1.03 (0.74-1.42, 0.58), respectively. Adjustment for adult body mass index did not change results substantially. The positive associations for body fatness at ages 5 and 10 years as well as adult height were restricted to distal adenoma, while not seen for proximal or rectal adenoma. Higher height and body fatness during childhood was associated with increased risk of distal adenoma later in life, independent of adult body weight.

Time course of risk factors in cancer etiology and progression.

Patients with cancer increasingly ask what they can do to change their lifestyles and improve outcomes. Risk factors for onset of cancer may differ substantially from those that modify survival with implications for counseling. This review focuses on recent data derived from population-based studies of causes of cancer and of patients with cancer to contrast risk factors for etiology with those that impact survival. For different cancer sites, the level of information to inform the timing of lifestyle exposures and risk of disease onset or progression after diagnosis is often limited. For breast cancer, timing of some exposures, such as radiation, is particularly important. For other exposures, such as physical activity, higher levels may prevent onset and also improve survival. For colon cancer, study of precursor polyps has provided additional insight to timing. Extensive data indicate that physical activity reduces risk of colon cancer, and more limited data suggest that exposure after diagnosis improves survival. Dietary factors including folate and calcium may also reduce risk of onset. More limited data on prostate cancer point to obesity increasing risk of aggressive or advanced disease. Timing of change in lifestyle for change in risk of onset and for survival is important but understudied among patients with cancer. Counseling patients with cancer to increase physical activity and avoid weight gain may improve outcomes. Advice to family members on lifestyle may become increasingly important for breast and other cancers where family history is a strong risk factor.