Background

Youth spend more time with screens than any activity except sleeping. Screen time is a risk factor for obesity, possibly because of the influence of food and beverage advertising on diet.

Objective

We sought to assess longitudinal relations of screen time [ie, television, electronic games, digital versatile discs (DVDs)/videos, and total screen time] with the 2-y changes in consumption of foods of low nutritional quality (FLNQ) that are commonly advertised on screens [ie, sugar-sweetened beverages, fast food, sweets, salty snacks, and the sum of these foods (total FLNQ)] and fruit and vegetables.

Design

With the use of 2004, 2006, and 2008 waves of the Growing Up Today Study II, which consisted of a cohort of 6002 female and 4917 male adolescents aged 9-16 y in 2004, we assessed screen time (change and baseline) in relation to the 2-y dietary changes. Regression models included 4604 girls and 3668 boys with complete screen time and diet data on ≥2 consecutive questionnaires.

Results

Each hour-per-day increase in television, electronic games, and DVDs/videos was associated with increased intake of total FLNQ (range: 0.10-0.28 servings/d; P < 0.05). Each hour-per-day increase in total screen time predicted increased intakes of sugar-sweetened beverages, fast food, sweets, and salty snacks (range: 0.02-0.06 servings/d; P < 0.001) and decreased intakes of fruit and vegetables (range: -0.05 to -0.02 servings/d; P < 0.05). Greater screen time at baseline (except electronic games in boys) was associated with subsequent increased intake of total FLNQ, and greater screen time at baseline (except DVDs/videos) was associated with decreased intake of fruit and vegetables (P < 0.05). Across sex and food groups and in sensitivity analyses, television was most consistently associated with dietary changes.

Conclusions

Increases in screen time were associated with increased consumption of foods and beverages of low nutritional quality and decreased consumption of fruit and vegetables. Our results caution against excessive use of screen media, especially television, in youth.

Objective

Examine the association of prepregnancy habitual consumption of fruits and fruit juices and gestational diabetes mellitus (GDM) risk.

Research design and methods

A prospective study among women with at least one singleton pregnancy in the Nurses' Health Study II from 1991 to 2001.

Results

Among 13,475 women, 860 reported a first diagnosis of GDM. The adjusted relative risks (RRs) for GDM from the lowest to highest quintile of whole fruit consumption were 1.00 (referent), 0.80 (95% CI 0.65-0.98), 0.90 (0.73-1.10), 0.80 (0.64-1.00), and 0.93 (0.76-1.16), respectively. The corresponding RRs for fruit juice were 1.00, 0.82 (0.66-1.01), 0.78 (0.63-0.96), 0.84 (0.68-1.04), and 1.00 (0.81-1.23).

Conclusions

These data suggest that prepregnancy higher consumption of whole fruits is not associated with an increased GDM risk. The association between fruit juices and GDM risk appears to be nonlinear.

Objective

Few prospective studies have examined separate forms of screen time in relation to adiposity. Our objective was to assess independent relations of television, electronic games (video/computer), and digital versatile disc (DVD)/videos and total screen time with change in adolescent BMI.

Methods

Using data from the 2004, 2006, and 2008 waves of the ongoing Growing up Today Study II, we assessed baseline and 2-year change in reported screen time in relation to concurrent change in BMI among 4287 girls and 3505 boys aged 9 to 16 years in 2004. Gender-specific models adjusted for previous BMI, age, race/ethnicity, growth/development, months between questionnaires, and physical activity.

Results

Among girls and boys, each hour per day increase in reported television viewing was associated with a 0.09 increase in BMI (Ps < .001), and each hour per day increase in total screen time was associated with a 0.07 increase among girls and 0.05 increase among boys (Ps < .001). Among girls only, greater baseline television, games, and total screen time and change in DVDs/videos were associated with gains in BMI (Ps < .05). BMI gains associated with change in television and total screen time were stronger among overweight girls than lean girls (Ps-heterogeneity < .001).

Conclusions

Television, which remains the steadiest source of food advertising, was most consistently associated with BMI gains. Among girls, electronic games and DVDs/videos were also related to increased BMI, possibly due to influences of product placements and advergames on diet and/or distracted eating. Adolescents, especially overweight adolescents, may benefit from reduced time with multiple types of media.

Adolescence is a highly susceptible period for mammary carcinogenesis, but few prospective studies have examined the role of adolescent diet in breast cancer risk. Reduced rank regression has previously been used to identify a dietary pattern associated with markers of inflammation (C-reactive protein, IL6, and TNFα receptor 2). We investigated whether an adolescent and early adulthood inflammatory dietary pattern was associated with breast cancer among 45,204 women in the Nurses' Health Study II using reduced rank regression. Participants completed a food frequency questionnaire in 1998 about their high school diet (HS-FFQ) and a FFQ in 1991 when they were ages 27-44 years. Among women who completed the HS-FFQ, 1,477 cases of breast cancer were diagnosed during 22 years of follow-up. An adolescent and early adulthood dietary pattern characterized by inflammation was associated with an increased incidence of premenopausal but not postmenopausal breast cancer. Women in the fifth quintile of the inflammatory pattern score had multivariable adjusted HRs for premenopausal breast cancer of 1.35 for adolescent diet [95% confidence interval (95% CI), 1.06-1.73; P_trend = 0.002] and 1.41 for early adulthood diet (95% CI, 1.11-1.78; P_trend = 0.006) compared with women in the first quintile. The corresponding RRs for postmenopausal breast cancer were 0.84 (95% CI, 0.60-1.17) for adolescent and 0.76 (95% CI, 0.54-1.06) for adult intake. Overall, our findings support the notion that an adolescent and early adulthood diet characterized by high intake of sugar-sweetened and diet soft drinks, refined grains, red and processed meat, and margarine, and low intake of green leafy vegetables, cruciferous vegetables, and coffee may increase the incidence of premenopausal breast cancer. Cancer Res; 77(5); 1179-87. ©2017 AACR.

Obesity is well established as a cause of postmenopausal breast cancer incidence and mortality. In contrast, adiposity in early life reduces breast cancer incidence. However, whether short-term weight change influences breast cancer risk is not well known. We followed a cohort of 77,232 women from 1980 to 2006 (1,445,578 person-years), with routinely updated risk factor information, documenting 4196 incident cases of invasive breast cancer. ER and PR status were obtained from pathology reports and medical records yielding a total of 2033 ER+/PR+ tumors, 595 ER-/PR- tumors, 512 ER+/PR- tumors. The log incidence breast cancer model was used to assess the association of short-term weight gain (over past 4 years) while controlling for average BMI before and after menopause. Short-term weight change was significantly associated with breast cancer risk (RR 1.20; 95 % CI 1.09-1.33) for a 4-year weight gain of ≥15 lbs versus no change (≤5 lbs) (P_trend < 0.001). The association was stronger for premenopausal women (RR 1.38; 95 % CI 1.13-1.69) (P_trend = 0.004) than for postmenopausal women (RR 1.10; 95 % CI 0.97-1.25) (P_trend = 0.063). Short-term weight gain during premenopause had a stronger association for ER+/PR- (RR per 25 lb weight gain = 2.19; 95 % CI 1.33-3.61, P = 0.002) and ER-/PR- breast cancer (RR per 25 lb weight gain = 1.61; 95 % CI 1.09-2.38, P = 0.016) than for ER+/PR+ breast cancer (RR per 25 lb weight gain = 1.13; 95 % CI 0.89-1.43, P = 0.32). There are deleterious effects of short-term weight gain, particularly during pre-menopause, even after controlling for average BMI before and after menopause. The association was stronger for ER+/PR- and ER-/PR- than for ER+/PR+ breast cancer.

Background

Meat, milk, and eggs have been inconsistently associated with the risk of advanced prostate cancer. These foods are sources of choline-a nutrient that may affect prostate cancer progression through cell membrane function and one-carbon metabolism. No study has examined dietary choline and the risk of lethal prostate cancer.

Objective

Our objective was to examine whether dietary choline, choline-containing compounds, and betaine (a choline metabolite) increase the risk of lethal prostate cancer.

Design

We prospectively examined the intake of these nutrients and the risk of lethal prostate cancer among 47,896 men in the Health Professionals Follow-Up Study. In a case-only survival analysis, we examined the postdiagnostic intake of these nutrients and the risk of lethal prostate cancer among 4282 men with an initial diagnosis of nonmetastatic disease during follow-up. Diet was assessed with a validated questionnaire 6 times during 22 y of follow-up.

Results

In the incidence analysis, we observed 695 lethal prostate cancers during 879,627 person-years. Men in the highest quintile of choline intake had a 70% increased risk of lethal prostate cancer (HR: 1.70; 95% CI: 1.18, 2.45; P-trend = 0.005). In the case-only survival analysis, we observed 271 lethal cases during 33,679 person-years. Postdiagnostic choline intake was not statistically significantly associated with the risk of lethal prostate cancer (HR for quintile 5 compared with quintile 1: 1.69; 95% CI: 0.93, 3.09; P-trend = 0.20).

Conclusion

Of the 47,896 men in our study population, choline intake was associated with an increased risk of lethal prostate cancer.

Importance

Nearly 2.5 million men currently live with prostate cancer in the United States, yet little is known about the association between diet after diagnosis and prostate cancer progression and overall mortality.

Objective

To examine postdiagnostic fat intake in relation to lethal prostate cancer and all-cause mortality.

Design, setting, and participants

Prospective study of 4577 men with nonmetastatic prostate cancer in the Health Professionals Follow-up Study (1986-2010).

Exposures

Postdiagnostic intake of saturated, monounsaturated, polyunsaturated, trans, animal, and vegetable fat.

Main outcomes and measures

Lethal prostate cancer (distant metastases or prostate cancer-specific death) and all-cause mortality.

Results

We observed 315 events of lethal prostate cancer and 1064 deaths (median follow-up, 8.4 years). Crude rates per 1000 person-years for lethal prostate cancer were as follows (highest vs lowest quintile of fat intake): 7.6 vs 7.3 for saturated, 6.4 vs 7.2 for monounsaturated, 5.8 vs 8.2 for polyunsaturated, 8.7 vs 6.1 for trans, 8.3 vs 5.7 for animal, and 4.7 vs 8.7 for vegetable fat. For all-cause mortality, the rates were 28.4 vs 21.4 for saturated, 20.0 vs 23.7 for monounsaturated, 17.1 vs 29.4 for polyunsaturated, 32.4 vs 17.1 for trans, 32.0 vs 17.2 for animal, and 15.4 vs 32.7 for vegetable fat. Replacing 10% of energy intake from carbohydrate with vegetable fat was associated with a lower risk of lethal prostate cancer (hazard ratio [HR], 0.71; 95% CI, 0.51-0.98; P = .04) and all-cause mortality (HR, 0.74; 95% CI, 0.61-0.88; P = .001). No other fats were associated with lethal prostate cancer. Saturated and trans fats after diagnosis (replacing 5% and 1% of energy from carbohydrate, respectively) were associated with higher all-cause mortality (HR, 1.30 [95% CI, 1.05-1.60; P = .02] and 1.25 [95% CI, 1.05-1.49; P = .01], respectively).

Conclusions and relevance

Among men with nonmetastatic prostate cancer, replacing carbohydrates and animal fat with vegetable fat may reduce the risk of all-cause mortality. The potential benefit of vegetable fat for prostate cancer-specific outcomes merits further research.

Purpose

It is unknown whether alcohol intake is associated with the risk of lethal (metastatic or fatal) prostate cancer. We examine (1) whether alcohol intake among men at risk of prostate cancer is associated with diagnosis of lethal prostate cancer and (2) whether intake among men with nonmetastatic prostate cancer is associated with metastasis or death.

Methods

This prospective cohort study uses the Health Professionals Follow-Up Study (1986 to 2012). Our analysis of alcohol intake among men at risk of prostate cancer included 47,568 cancer-free men. Our analysis of alcohol intake among men with prostate cancer was restricted to 5,182 men diagnosed with nonmetastatic prostate cancer during follow-up. We examine the association of total alcohol, red and white wine, beer, and liquor with lethal prostate cancer and death. Multivariate Cox proportional hazards regression estimated hazard ratios (HRs) and 95% CIs.

Results

Alcohol drinkers had a lower risk of lethal prostate cancer (any v none: HR, 0.84 [95% CI, 0.71 to 0.99]) without a dose-response relationship. Total alcohol intake among patients with prostate cancer was not associated with progression to lethal prostate cancer (any v none: HR, 0.99 [95% CI, 0.57 to 1.72]), whereas moderate red wine intake was associated with a lower risk (any v none: HR, 0.50 [95% CI, 0.29 to 0.86]; P trend = .05). Compared with none, 15 to 30 g/d of total alcohol after prostate cancer diagnosis was associated with a lower risk of death (HR, 0.71 [95% CI, 0.50 to 1.00]), as was red wine (any v none: HR, 0.74 [95% CI, 0.57 to 0.97]; P trend = .007).

Conclusion

Cancer-free men who consumed alcohol had a slightly lower risk of lethal prostate cancer compared with abstainers. Among men with prostate cancer, red wine was associated with a lower risk of progression to lethal disease. These observed associations merit additional study but provide assurance that moderate alcohol consumption is safe for patients with prostate cancer.

The obesity pandemic continues unabated despite a persistent public health campaign to decrease energy intake ("eat less") and increase energy expenditure ("move more"). One explanation for this failure is that the current approach, based on the notion of energy balance, has not been adequately embraced by the public. Another possibility is that this approach rests on an erroneous paradigm. A new formulation of the energy balance model (EBM), like prior versions, considers overeating (energy intake > expenditure) the primary cause of obesity, incorporating an emphasis on "complex endocrine, metabolic, and nervous system signals" that control food intake below conscious level. This model attributes rising obesity prevalence to inexpensive, convenient, energy-dense, "ultra-processed" foods high in fat and sugar. An alternative view, the carbohydrate-insulin model (CIM), proposes that hormonal responses to highly processed carbohydrates shift energy partitioning toward deposition in adipose tissue, leaving fewer calories available for the body's metabolic needs. Thus, increasing adiposity causes overeating to compensate for the sequestered calories. Here, we highlight robust contrasts in how the EBM and CIM view obesity pathophysiology and consider deficiencies in the EBM that impede paradigm testing and refinement. Rectifying these deficiencies should assume priority, as a constructive paradigm clash is needed to resolve long-standing scientific controversies and inform the design of new models to guide prevention and treatment. Nevertheless, public health action need not await resolution of this debate, as both models target processed carbohydrates as major drivers of obesity.