Abstract Objective Systemic inflammation may play an important role in the development of atherosclerosis, type 2 diabetes, and some cancers. Few studies have comprehensively assessed the direct ...relations between dietary fiber and inflammatory cytokines, especially in minority populations. Using baseline data from 1958 postmenopausal women enrolled in the Women's Health Initiative Observational Study, we examined cross-sectional associations between dietary fiber intake and markers of systemic inflammation (including serum high-sensitivity C-reactive protein hs-CRP, interleukin-6 IL-6, and tumor necrosis factor-α receptor-2 TNF-α-R2) in addition to differences in these associations by ethnicity. Methods Multiple linear regression models were used to assess the relation between fiber intake and makers of systemic inflammation. Results After adjustment for covariates, intakes of dietary fiber were inversely associated with IL-6 ( P values for trend were 0.01 for total fiber, 0.004 for soluble fiber, and 0.001 for insoluble fiber) and TNF-α-R2 ( P values for trend were 0.002 for total, 0.02 for soluble, and <0.001 for insoluble fibers). Although the samples were small in minority Americans, results were generally consistent with those found among European Americans. We did not observe any significant association between intake of dietary fiber and hs-CRP. Conclusion These findings lend support to the hypothesis that a high-fiber diet is associated with lower plasma levels of IL-6 and TNF-α-R2. Contrary to previous reports, however, there was no association between fiber and hs-CRP among postmenopausal women. Future studies on the influence of diet on inflammation should include IL-6 and TNF-α-R2 and enroll participants from ethnic minorities.
Purpose: Inflammation is a process central to carcinogenesis and in particular to colorectal cancer (CRC). Previously, we developed a dietary inflammatory index (DII) from extensive literature review ...to assess the inflammatory potential of diet. In the current study, we utilized this novel index in the Women's Health Initiative to prospectively evaluate its association with risk of CRC in postmenopausal women. Methods: The DII was calculated from baseline food frequency questionnaires administered to 152,536 women aged 50–79 years without CRC at baseline between 1993 and 1998 and followed through 30 September 2010. Incident CRC cases were ascertained through a central physician adjudication process. Multiple covariate-adjusted Cox proportional hazards regression models were used to estimate hazard ratios (HR) and 95 % confidence intervals (95 % CI) for colorectal, colon (proximal/distal locations), and rectal cancer risk, by DII quintiles (Q). Results: During an average 11.3 years of follow-up, a total of 1,920 cases of CRC (1,559 colon and 361 rectal) were identified. Higher DII scores (representing a more pro-inflammatory diet) were associated with an increased incidence of CRC (HRQ5-Q1 1.22; 95 % CI 1.05, 1.43; Ptrend = 0.02) and colon cancer, specifically proximal colon cancer (HRQ5-Q1 1.35; 95 % CI 1.05, 1.67; Ptrend 0.01) but not distal colon cancer (HRQ5-Q1 0.84; 95 % CI 0.61, 1.18; Ptrend = 0.63) or rectal cancer (HRQ5-Q1 1.20; 95 % CI 0.84, 1.72; Ptrend = 0.65). Conclusion: Consumption of pro-inflammatory diets is associated with an increased risk of CRC, especially cancers located in the proximal colon. The absence of a significant association for distal colon cancer and rectal cancer may be due to the small number of incident cases for these sites. Interventions that may reduce the inflammatory potential of the diet are warranted to test our findings, thus providing more information for colon cancer prevention.
Smoking and mortality--beyond established causes Carter, Brian D; Abnet, Christian C; Feskanich, Diane ...
The New England journal of medicine,
2015-Feb-12, Letnik:
372, Številka:
7
Journal Article
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Mortality among current smokers is 2 to 3 times as high as that among persons who never smoked. Most of this excess mortality is believed to be explained by 21 common diseases that have been formally ...established as caused by cigarette smoking and are included in official estimates of smoking-attributable mortality in the United States. However, if smoking causes additional diseases, these official estimates may significantly underestimate the number of deaths attributable to smoking.
We pooled data from five contemporary U.S. cohort studies including 421,378 men and 532,651 women 55 years of age or older. Participants were followed from 2000 through 2011, and relative risks and 95% confidence intervals were estimated with the use of Cox proportional-hazards models adjusted for age, race, educational level, daily alcohol consumption, and cohort.
During the follow-up period, there were 181,377 deaths, including 16,475 among current smokers. Overall, approximately 17% of the excess mortality among current smokers was due to associations with causes that are not currently established as attributable to smoking. These included associations between current smoking and deaths from renal failure (relative risk, 2.0; 95% confidence interval CI, 1.7 to 2.3), intestinal ischemia (relative risk, 6.0; 95% CI, 4.5 to 8.1), hypertensive heart disease (relative risk, 2.4; 95% CI, 1.9 to 3.0), infections (relative risk, 2.3; 95% CI, 2.0 to 2.7), various respiratory diseases (relative risk, 2.0; 95% CI, 1.6 to 2.4), breast cancer (relative risk, 1.3; 95% CI, 1.2 to 1.5), and prostate cancer (relative risk, 1.4; 95% CI, 1.2 to 1.7). Among former smokers, the relative risk for each of these outcomes declined as the number of years since quitting increased.
A substantial portion of the excess mortality among current smokers between 2000 and 2011 was due to associations with diseases that have not been formally established as caused by smoking. These associations should be investigated further and, when appropriate, taken into account when the mortality burden of smoking is investigated. (Funded by the American Cancer Society.).
Diet modulates inflammation and inflammatory markers have been associated with cancer outcomes. In the Women's Health Initiative, we investigated associations between a dietary inflammatory index ...(DII) and invasive breast cancer incidence and death.
The DII was calculated from a baseline food frequency questionnaire in 122 788 postmenopausal women, enrolled from 1993 to 1998 with no prior cancer, and followed until 29 August 2014. With median follow-up of 16.02 years, there were 7495 breast cancer cases and 667 breast cancer deaths. We used Cox regression to estimate multivariable-adjusted hazards ratios (HRs) and 95% confidence intervals (95% CIs) by DII quintiles (Q) for incidence of overall breast cancer, breast cancer subtypes, and deaths from breast cancer. The lowest quintile (representing the most anti-inflammatory diet) was the reference.
The DII was not associated with incidence of overall breast cancer (HRQ5vsQ1, 0.99; 95% CI, 0.91-1.07; Ptrend=0.83 for overall breast cancer). In a full cohort analysis, a higher risk of death from breast cancer was associated with consumption of more pro-inflammatory diets at baseline, after controlling for multiple potential confounders (HRQ5vsQ1, 1.33; 95% CI, 1.01-1.76; Ptrend=0.03).
Future studies are needed to examine the inflammatory potential of post-diagnosis diet given the suggestion from the current study that dietary inflammatory potential before diagnosis is related to breast cancer death.
Inflammation is important in chronic disease and can be modulated by dietary exposures. Our aim was to examine whether the inflammatory potential of diet after cancer diagnosis, assessed using the ...dietary inflammatory index (DII), is associated with all-cause and cause-specific mortality among women diagnosed with invasive breast cancer in the Women's Health Initiative (WHI).
Our analytic cohort included 2,150 postmenopausal women, ages 50 to 79 years at baseline, who developed invasive breast cancer during follow-up and completed a food frequency questionnaire (FFQ) on average 1.5 years after diagnosis. Women were followed from breast cancer diagnosis until death or the end of follow-up by October 2014. Energy-adjusted DII (E-DII) scores were calculated from food plus supplements using a nutrient-density approach. Cox proportional hazards models were fit to estimate multivariable-adjusted HRs and 95% confidence intervals (CIs) for all-cause, breast cancer-specific, and cardiovascular disease (CVD) mortality.
After a median 13.3 years of follow-up, 580 deaths from any cause occurred, including 212 breast cancer deaths and 103 CVD deaths. Lower (i.e., more anti-inflammatory) E-DII scores were associated with a lower risk of CVD mortality (HR
= 0.44; 95% CI, 0.24-0.82;
= 0.005), but not with breast cancer-specific mortality (HR
= 0.96; 95% CI, 0.62-1.49;
= 0.96) or all-cause mortality (HR
= 0.82; 95% CI, 0.63-1.05;
= 0.17).
Consuming a more anti-inflammatory diet after breast cancer diagnosis may be a means for reducing risk of death from CVD.
Survival after invasive breast cancer diagnosis may be improved by consumption of an anti-inflammatory diet.
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Behavior Matters Fisher, Edwin B., PhD; Fitzgibbon, Marian L., PhD; Glasgow, Russell E., PhD ...
American journal of preventive medicine,
05/2011, Letnik:
40, Številka:
5
Journal Article
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Abstract Behavior has a broad and central role in health. Behavioral interventions can be effectively used to prevent disease, improve management of existing disease, increase quality of life, and ...reduce healthcare costs. A summary is presented of evidence for these conclusions in cardiovascular disease/diabetes, cancer, and HIV/AIDS as well as with key risk factors: tobacco use, poor diet, physical inactivity, and excessive alcohol consumption. For each, documentation is made of (1) moderation of genetic and other fundamental biological influences by behaviors and social–environmental factors; (2) impacts of behaviors on health; (3) success of behavioral interventions in prevention; (4) disease management; (5) quality of life, and (6) improvements in the health of populations through behavioral health promotion programs. Evidence indicates the cost effectiveness and value of behavioral interventions, especially relative to other common health services as well as the value they add in terms of quality of life. Pertinent to clinicians and their patients as well as to health policy and population health, the benefits of behavioral interventions extend beyond impacts on a particular disease or risk factor. Rather, they include broad effects and benefits on prevention, disease management, and well-being across the life span. Among priorities for dissemination research, the application of behavioral approaches is challenged by diverse barriers, including socioeconomic barriers linked to health disparities. However, behavioral approaches including those emphasizing community and social influences appear to be useful in addressing such challenges. In sum, behavioral approaches should have a central place in prevention and health care of the 21st century.
While observational studies have suggested that vitamin D deficiency increases risk of depression, few clinical trials have tested whether vitamin D supplementation affects the occurrence of ...depression symptoms. The authors evaluated the impact of daily supplementation with 400 IU of vitamin D(3) combined with 1,000 mg of elemental calcium on measures of depression in a randomized, double-blinded US trial comprising 36,282 postmenopausal women. The Burnam scale and current use of antidepressant medication were used to assess depressive symptoms at randomization (1995-2000). Two years later, women again reported on their antidepressant use, and 2,263 completed a second Burnam scale. After 2 years, women randomized to receive vitamin D and calcium had an odds ratio for experiencing depressive symptoms (Burnam score ≥0.06) of 1.16 (95% confidence interval: 0.86, 1.56) compared with women in the placebo group. Supplementation was not associated with antidepressant use (odds ratio = 1.01, 95% confidence interval: 0.92, 1.12) or continuous depressive symptom score. Results stratified by baseline vitamin D and calcium intake, solar irradiance, and other factors were similar. The findings do not support a relation between supplementation with 400 IU/day of vitamin D(3) along with calcium and depression in older women. Additional trials testing higher doses of vitamin D are needed to determine whether this nutrient may help prevent or treat depression.
Summary Background In the post-intervention period of the Women's Health Initiative (WHI) trial, women assigned to treatment with oestrogen plus progestin had a higher risk of cancer than did those ...assigned to placebo. Results also suggested that the combined hormone therapy might increase mortality from lung cancer. To assess whether such an association exists, we undertook a post-hoc analysis of lung cancers diagnosed in the trial over the entire follow-up period. Methods The WHI study was a randomised, double-blind, placebo-controlled trial undertaken in 40 centres in the USA. 16 608 postmenopausal women aged 50–79 years with an intact uterus were randomly assigned by a computerised, stratified, permuted block algorithm to receive a once-daily tablet of 0·625 mg conjugated equine oestrogen plus 2·5 mg medroxyprogesterone acetate (n=8506) or matching placebo (n=8102). We assessed incidence and mortality rates for all lung cancer, small-cell lung cancer, and non-small-cell lung cancer by use of data from treatment and post-intervention follow-up periods. Analysis was by intention to treat. This study is registered with ClinicalTrials.gov , number NCT00000611. Findings After a mean of 5·6 years (SD 1·3) of treatment and 2·4 years (0·4) of additional follow-up, 109 women in the combined hormone therapy group had been diagnosed with lung cancer compared with 85 in the placebo group (incidence per year 0·16% vs 0·13%; hazard ratio HR 1·23, 95% CI 0·92–1·63, p=0·16). 96 women assigned to combined therapy had non-small-cell lung cancer compared with 72 assigned to placebo (0·14% vs 0·11%; HR 1·28, 0·94–1·73, p=0·12). More women died from lung cancer in the combined hormone therapy group than in the placebo group (73 vs 40 deaths; 0·11% vs 0·06%; HR 1·71, 1·16–2·52, p=0·01), mainly as a result of a higher number of deaths from non-small-cell lung cancer in the combined therapy group (62 vs 31 deaths; 0·09% vs 0·05%; HR 1·87, 1·22–2·88, p=0·004). Incidence and mortality rates of small-cell lung cancer were similar between groups. Interpretation Although treatment with oestrogen plus progestin in postmenopausal women did not increase incidence of lung cancer, it increased the number of deaths from lung cancer, in particular deaths from non-small-cell lung cancer. These findings should be incorporated into risk–benefit discussions with women considering combined hormone therapy, especially those with a high risk of lung cancer. Funding National Heart, Lung and Blood Institute, National Institutes of Health.
Self-report of dietary intake could be biased by social desirability or social approval thus affecting risk estimates in epidemiological studies. These constructs produce response set biases, which ...are evident when testing in domains characterized by easily recognizable correct or desirable responses. Given the social and psychological value ascribed to diet, assessment methodologies used most commonly in epidemiological studies are particularly vulnerable to these biases.
Social desirability and social approval biases were tested by comparing nutrient scores derived from multiple 24-hour diet recalls (24HR) on seven randomly assigned days with those from two 7-day diet recalls (7DDR) (similar in some respects to commonly used food frequency questionnaires), one administered at the beginning of the test period (pre) and one at the end (post). Statistical analysis included correlation and multiple linear regression.
Cross-sectionally, no relationships between social approval score and the nutritional variables existed. Social desirability score was negatively correlated with most nutritional variables. In linear regression analysis, social desirability score produced a large downward bias in nutrient estimation in the 7DDR relative to the 24HR. For total energy, this bias equalled about 50 kcal/point on the social desirability scale or about 450 kcal over its interquartile range. The bias was approximately twice as large for women as for men and only about half as large in the post measures. Individuals having the highest 24HR-derived fat and total energy intake scores had the largest downward bias due to social desirability.
We observed a large downward bias in reporting food intake related to social desirability score. These results are consistent with the theoretical constructs on which the hypothesis is based. The effect of social desirability bias is discussed in terms of its influence on epidemiological estimates of effect. Suggestions are made for future work aimed at improving dietary assessment methodologies and adjusting risk estimates for this bias.
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