Association between dietary acrylamide intake and the risk of multiple myeloma, diffuse large cell lymphoma, and chronic lymphocytic leukemia according to sex and smoking status; the Netherlands Cohort Study on diet and cancer, 1986–2002.¹

1<p>HR  =  hazard ratio; CI  =  Confidence Interval; py  =  person years; Q  =  quintile; T  =  tertile. The number of cases and person-years are the numbers that resulted after listwise deletion of observations with missing values for the selected confounders. HRs were calculated by using Cox proportional hazards analysis.</p>2<p>Adjusted for age and sex.</p>3<p>Adjusted for age (years), sex, height (per 10 cm), education level, fiber (g/d), total fatty acids (g/d), trans unsaturated fatty acid (g/d), mono unsaturated fat (g/d), poly unsaturated fat (g/d), carbohydrates (g/d) and niacin (mg/d).</p>4<p>Insufficient number of cases for analyses with tertiles (N>60 required) or with acrylamide as a continuous variable (N>20 required).</p>5<p>Proportional hazards assumption not met; therefore results not presented.</p

Flow diagram of subcohort members and cases used in the analysis.

<p>NCR  =  Netherlands Cancer Registry, PALGA  =  Netherlands Pathology Registry, LM  =  lymphatic malignancies, MM  =  multiple myeloma, DLCL  =  diffuse large cell lymphoma, CLL  =  chronic lymphocytic leukaemia, FL  =  follicular lymphoma, WMI  =  Waldenstrom macroglobulinemia and immunocytoma, MCL  =  mantle cell lymphoma, T-cell  =  T-cell lymphoma.</p

Acrylamide hazard ratios (and 95% CI) of multiple myeloma, diffuse large cell lymphoma and chronic lymphatic leukemia in <b>women</b> in strata of several covariables and <i>p</i> values for interaction: the Netherlands Cohort Study on diet and cancer, 1986–2002.

<p>Abbreviations: HR  =  hazard ratio; CI  =  confidence interval; AA/d  =  acrylamide per day, MM  =  multiple myeloma; CLL  =  chronic lymphatic leukemia; DLCL  =  diffuse large cell lymphoma.</p>1<p>Adjusted for age, sex, height (per 10 cm), education level, fiber (g/d), total fatty acids (g/d), trans unsaturated fatty acid (g/d), mono unsaturated fat (g/d), poly unsaturated fat (g/d), carbohydrates (g/d) and niacin (mg/d).</p>2<p>Insufficient number of cases.</p

Number of lymphatic malignancies in the Netherlands Cohort Study on diet and cancer (follow up: 16.3 years) according to the WHO classification.

<p>Abbreviations: ICD-O-3, International Classification of Diseases for Oncology, 3^rd edition; MALT, mucosa-associated lymphoid tissue; NOS, not otherwise specified.</p>1<p>N after exclusion of prevalent cases at baseline.</p>2<p>N cases available for analyses, after exclusion of missing and inconsistent data. Only case numbers for subtypes with sufficient number of cases are given (so subgroups do not add up to 1,233).</p

Characteristics of cases and subcohort members according to sex in the Netherlands Cohort Study on diet and cancer, 1986–2002.

<p>MM  =  multiple myeloma; DLCL  =  diffuse large cell lymphoma; CLL  =  chronic lymphocytic leukemia; FL  =  follicular lymphoma; WMI  =  Waldenström macroglobulinemia and immunocytoma; MCL  =  mantle cell lymphoma; T-cell  =  T-cell lymphomas; BW  =  bodyweight; HM  =  hematological malignancies.</p>1<p>Mean (standard deviation) or percentage.</p>2<p>Among former or current smokers.</p

Association between continuously modeled dietary acrylamide intake (per 10 µg/d) and the risk of follicular lymphoma and Waldenstrom macroglobulinemia and immunocytoma (WMI); the Netherlands Cohort Study on diet and cancer, 1986–2002.¹

<p>HR  =  hazard ratio; CI  =  confidence interval; py  =  person years. The number of cases and person-years are the numbers that resulted after listwise deletion of observations with missing values for the selected confounders. HRs were calculated by using Cox proportional hazards analysis.</p>1<p>Adjusted for age and sex.</p>2<p>Adjusted for age (years), sex, height (per 10 cm), education level, fiber (g/d), total fatty acids (g/d), trans unsaturated fatty acid (g/d), mono unsaturated fat (g/d), poly unsaturated fat (g/d), carbohydrates (g/d) and niacin (mg/d).</p>3<p>Insufficient number of cases for analyses with acrylamide as a continuous variable (N>20 requiered).</p

Multivariable adjusted^* hazard rates for exposure, stratified by 5-year age groups based on year of birth, Netherlands Cohort Study on Diet and Cancer, 1986–2002.

<p>*Multivariable adjusted for age, number of children (continuous) and use of oral contraceptives (never, ever).</p>†<p>HR =  Hazard rate; CI =  Confidence Interval.</p

Descriptive data for cases and subcohort members, according to exposure variables and other potential risk factors for ovarian cancer, Netherlands Cohort Study on Diet and Cancer, 1986–2002.

†<p>Only for women who ever used oral contraceptives.</p

Age-adjusted and multivariable adjusted hazard rates for exposure factors for energy restriction, Netherlands Cohort Study on Diet and Cancer, 1986–2002.

<p>*HR =  Hazard Rate; CI =  Confidence Interval.</p>#<p>Multivariable adjusted for age, number of children (continuous) and use of oral contraceptives (never, ever).</p>†<p>Multivariable adjusted for age, number of children (continuous), use of oral contraceptives (never, ever), for hysterectomy (no, possible/probable) and mutually adjusted for the other exposure factors in the table.</p

A Systematic Literature Review and Meta-Regression Analysis on Early-Life Energy Restriction and Cancer Risk in Humans

<div><p>Background</p><p>In animal models, long-term moderate energy restriction (ER) is reported to decelerate carcinogenesis, whereas the effect of severe ER is inconsistent. The impact of early-life ER on cancer risk has never been reviewed systematically and quantitatively based on observational studies in humans.</p><p>Objective</p><p>We conducted a systematic review of observational studies and a meta-(regression) analysis on cohort studies to clarify the association between early-life ER and organ site-specific cancer risk.</p><p>Methods</p><p>PubMed and EMBASE (1982 –August 2015) were searched for observational studies. Summary relative risks (RRs) were estimated using a random effects model when available ≥3 studies.</p><p>Results</p><p>Twenty-four studies were included. Eleven publications, emanating from seven prospective cohort studies and some reporting on multiple cancer endpoints, met the inclusion criteria for quantitative analysis. Women exposed to early-life ER (ranging from 220–1660 kcal/day) had a higher breast cancer risk than those not exposed (RR_{RE all ages} = 1.28, 95% CI: 1.05–1.56; RR_{RE for 10–20 years of age} = 1.21, 95% CI: 1.09–1.34). Men exposed to early-life ER (ranging from 220–800kcal/day) had a higher prostate cancer risk than those not exposed (RR_RE = 1.16, 95% CI: 1.03–1.30). Summary relative risks were not computed for colorectal cancer, because of heterogeneity, and for stomach-, pancreas-, ovarian-, and respiratory cancer because there were <3 available studies. Longer duration of exposure to ER, after adjustment for severity, was positively associated with overall cancer risk in women (<i>p</i> = 0.02). Ecological studies suggest that less severe ER is generally associated with a reduced risk of cancer.</p><p>Conclusions</p><p>Early-life transient severe ER seems to be associated with increased cancer risk in the breast (particularly ER exposure at adolescent age) and prostate. The duration, rather than severity of exposure to ER, seems to positively influence relative risk estimates. This result should be interpreted with caution due to the limited number of studies and difficulty in disentangling duration, severity, and geographical setting of exposure.</p></div