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This study addressed whether remission of overweight before early adulthood reduced the risk of type 2 diabetes in adulthood. Men who had been overweight at 7 years of age had an increased risk of adult type 2 diabetes only if overweight continued until puberty or later.

BackgroundMost identified risk factors for cancer primarily occur in adulthood. As cancers generally have long latency periods, it is possible that risk factors acting earlier in life and accumulation of risks across the life course are important. Thus, focusing only on adult overweight as a modifiable risk factor may overlook childhood as an important aetiologic time window when body size is relevant for future cancer risks. The objective of this study was to review the evidence for associations between birthweight, body mass index (BMI), height and growth from 7–13 years and adult cancer risks based on studies using the Copenhagen School Health Records Register.MethodsThe register contains measured anthropometric information on 372,636 children born in 1930–1989. All studies examining associations between early life body size and risks of adult cancer (until 85 years, diagnosed in 1968–2015) were included, comprising 31 studies on 16 different cancer sites. Cancer diagnoses were retrieved via individual-level linkages to the Danish Cancer Registry.ResultsBirthweight was differentially associated with bladder, breast, colon, glioma, Hodgkin’s disease, liver, kidney (renal cell), melanoma, ovarian, rectal, testicular and thyroid cancer. BMI in childhood was positively associated with risks of bladder (only late childhood), colon, endometrial, kidney, liver, oesophageal (only late childhood), ovarian, pancreatic (<70 years), prostate (only before childhood height adjustment) and thyroid cancer, whereas it was inversely associated with breast cancer. Child height was positively associated with breast, colon, endometrial, glioma, Hodgkin’s disease, kidney, melanoma, oesophageal (only women), ovarian, prostate, testicular and thyroid cancer and inversely associated with bladder cancer. Greater than average increases in childhood BMI or linear growth at ages 7–13 increased risks of several cancers.ConclusionsEarly life body size and growth are associated with many, but not all adult cancers, suggesting that the aetiology of several cancers may lie earlier in life than previously thought.

The early life factors of birthweight, child weight, height, body mass index (BMI) and pubertal timing are associated with risks of breast cancer. However, the predictive value of these factors in relation to breast cancer is largely unknown. Therefore, using a machine learning approach, we examined whether birthweight, childhood weights, heights, BMIs, and pubertal timing individually and in combination were predictive of breast cancer. We used information on birthweight, childhood height and weight, and pubertal timing assessed by the onset of the growth spurt (OGS) from 164,216 girls born 1930-1996 from the Copenhagen School Health Records Register. Of these, 10,002 women were diagnosed with breast cancer during 1977-2019 according to a nationwide breast cancer database. We developed a feed-forward neural network, which was trained and tested on early life body size measures individually and in various combinations. Evaluation metrics were examined to identify the best performing model. The highest area under the receiver operating curve (AUC) was achieved in a model that included birthweight, childhood heights, weights and age at OGS (AUC = 0.600). A model based on childhood heights and weights had a comparable AUC value (AUC = 0.598), whereas a model including only childhood heights had the lowest AUC value (AUC = 0.572). The sensitivity of the models ranged from 0.698 to 0.760 while the precision ranged from 0.071 to 0.076. We found that the best performing network was based on birthweight, childhood weights, heights and age at OGS as the input features. Nonetheless, this performance was only slightly better than the model including childhood heights and weights. Further, although the performance of our networks was relatively low, it was similar to those from previous studies including well-established risk factors. As such, our results suggest that childhood body size may add additional value to breast cancer prediction models.

Background Associations of birthweight, childhood body size and pubertal timing with breast cancer risks by menopausal status and tumor receptor subtypes are inconclusive. Thus, we investigated these associations in a population-based cohort of Danish women. Methods We studied 162,419 women born between 1930 and 1996 from the Copenhagen School Health Records Register. The register includes information on birthweight, measured childhood weights and heights at the age of 7–13 years, and computed ages at the onset of the growth spurt (OGS) and at peak height velocity (PHV). The Danish Breast Cancer Cooperative Group database provided information on breast cancer ( n  = 7510), including estrogen receptor (ER), human epidermal growth factor receptor 2 (HER2) and menopausal status. Hormone replacement therapy use came from the Danish National Prescription Registry. Hazard ratios (HR) and 95% confidence intervals (CI) were estimated by Cox regression. Results We found that birthweight was not associated with any breast cancer subtypes. While childhood BMI was not statistically significantly associated with ER+ tumors nor consistently with ER− tumors among pre-menopausal women, consistent inverse associations were found among postmenopausal women. At the age of 7 years, the HRs for postmenopausal ER+ and ER− tumors were 0.90 (95% CI 0.87–0.93) and 0.84 (95% CI 0.79–0.91) per BMI z -score, respectively. Similarly, childhood BMI was inversely associated with pre- and postmenopausal HER2− tumors, but not with HER2+ tumors. Childhood height was positively associated with both pre- and postmenopausal ER+ tumors, but not with ER− tumors. At the age of 7 years, the HRs for postmenopausal ER+ and ER− tumors were 1.09 (95% CI 1.06–1.12) and 1.02 (95% CI 0.96–1.09) per height z -score, respectively. In general, childhood height was positively associated with HER2+ and HER2− tumors among pre- and postmenopausal women. Ages at OGS and PHV were not associated with any breast cancer subtypes. Conclusions We showed that a high BMI and short stature in childhood are associated with reduced risks of certain breast cancer subtypes. Thus, childhood body composition may play a role in the development of breast cancer.

Introduction: Adult obesity is linked with polycystic ovary syndrome (PCOS), but the importance of body size at ages before PCOS is diagnosed is unknown. Objective: To investigate associations between a woman’s own birthweight, childhood body mass index (BMI), height and growth patterns in relation to her risk of PCOS. Methods: We included 65,665 girls from the Copenhagen School Health Records Register, born in the period 1960–1996, with information on birthweight and measured weight and height at the ages of 7–13 years. Overweight was defined using International Obesity Task Force (IOTF) criteria. From the Danish National Patient Register, 606 women aged 15–50 years were identified. Hazard ratios (HRs) and 95% confidence intervals (CIs) were estimated by Cox regression analysis. Results: Birthweight was not associated with PCOS. At the age of 7–13 years, girls with overweight had a higher risk of developing PCOS than girls without overweight; HR 2.83 (95% CI 2.34–3.42) at age 7 years and 2.99 (95% CI 2.38–3.76) at age 13 years. Furthermore, girls with overweight at both 7 and 13 years had a higher risk of developing PCOS than girls without overweight or overweight at only one age. Height was positively associated with PCOS risk at all ages. Girls who were persistently tall or changed from tall to average height had a higher risk of developing PCOS than girls with average height growth. Conclusion: Overweight and tall stature in childhood are positively associated with PCOS risk, but birthweight is not.

Worldwide, far too many children and adolescents are living with the disease of obesity. Despite decades of public health initiatives, rates are still rising in many countries. This raises the question of whether precision public health may be a more successful approach to preventing obesity in youth. In this review, the objective was to review the literature on precision public health in the context of childhood obesity prevention and to discuss how precision public health may advance the field of childhood obesity prevention. As precision public health is a concept that is still evolving and not fully identifiable in the literature, a lack of published studies precluded a formal review. Therefore, the approach of using a broad interpretation of precision public health was used and recent advances in childhood obesity research in the areas of surveillance and risk factor identification as well as intervention, evaluation and implementation using selected studies were summarized. Encouragingly, big data from a multitude of designed and organic sources are being used in new and innovative ways to provide more granular surveillance and risk factor identification in obesity in children. Challenges were identified in terms of data access, completeness, and integration, ensuring inclusion of all members of society, ethics, and translation to policy. As precision public health advances, it may yield novel insights that can contribute to strong policies acting in concert that ultimately lead to the prevention of obesity in children.

It is increasingly recognized that early life factors play a role in the rising prevalence of cancer in young adult life. Acute childhood infections may protect against development of cancer, but evidence is limited. We investigated whether infection-related hospital contacts during the first 24 months of life were associated with the risk of cancer in early-mid adult life in a large population-based Danish cohort. We included 68,538 individuals (33,569; 49.0 % women) born 1977–1996 from the Copenhagen School Health Records Register. Using individual-level linkage to national registries, we obtained information on infection-related hospital contacts between birth and 24 months and early-onset cancer (diagnosed 15–45 years). Hazard ratios (HR) and 95 % confidence intervals (CI) were estimated using Cox regressions adjusted for maternal education. From birth to 24 months of life, 14,718 individuals (21.5 %) had at least one infection-related hospital contact. During follow-up, 788 individuals were diagnosed with cancer. Compared to individuals who did not have an infection-related hospital contact, those who had a least one had a lower risk of early-mid adulthood cancer (HR=0.82, 95 % CI: 0.68–0.98). We found limited evidence of a dose-response inverse effect of infection-related hospital contacts on cancer risk. Infection-related hospital contacts during the first 24 months of life was associated with a reduced risk of cancer in early-mid adult life. Replication in other populations is warranted and mechanistic studies are needed to understand the biological mechanisms underlying these epidemiological observations. •Novel insights into risk factors for young adult cancers are needed.•Previous limited evidence links acute infections with reduced cancer risk.•Severe infections in the first 24 months of life decreased adult cancer risk.•Studies into the biological mechanisms underlying these associations are warranted.

BackgroundAlthough short adult height is generally associated with increased risks of type 2 diabetes mellitus (T2DM), there are large inconsistencies across studies. The aims of this study were to describe and quantify currently available evidence on the association between adult height and T2DM, to examine whether the reported associations differ by sex, and to examine the shapes of the height and T2DM associations.MethodsRelevant literature was identified using PubMed (1966–May 2018), EMBASE (1947–May 2018) and Google Scholar (May 2018). We identified cross-sectional and cohort studies with original publications on human subjects, which were included in a random-effects meta-analysis.ResultsFrom 15 971 identified sources, 25 studies met the inclusion criteria for the systematic review (N=401 562 individuals). From these 25 studies, 16 (9 cross-sectional studies and 7 cohort studies) were included in the meta-analysis (n=261 496 individuals). The overall random-effects meta-analysis indicated an inverse association between adult height and T2DM (effect estimate=0.88, 95% CI 0.81 to 0.95). No sex differences in the associations between adult height and T2DM were found (effect estimate for men: 0.86, 95% CI 0.75 to 0.99; effect estimate for women: 0.90; 95% CI 0.80 to 1.01; p value for sex interaction=0.80). Due to lack of data, results on the shape of the association between height and T2DM were inconclusive.ConclusionsShorter height is associated with an increased risk of T2DM and the association does not significantly differ by sex. The currently available data are insufficient to support conclusions regarding the shape of the association between height and T2DM.Trial registration number CRD42017062446.

Abstract A high childhood body mass index (BMI) may be protective against benign breast disease (BBD), but little is known about the effects of other early life body size measures. Thus, we examined associations between birthweight, childhood BMI, height, and pubertal timing and BBD risks. We included 171,272 girls, born from 1930 to 1996, from the Copenhagen School Health Records Register, which contains information on birthweight, childhood anthropometry (7–13 years), age at onset of the growth spurt (OGS), and peak height velocity (PHV). During follow-up, 9361 BBD cases (15–50 years) were registered in the Danish National Patient Register. Hazard ratios (HR) and 95% confidence intervals (CI) were estimated by Cox regressions. At all childhood ages, BMI was inversely but non-linearly associated with BBD. The association was slightly stronger in magnitude for BMI z-scores above 0 (HRage 7 = 0.86; 95%CI: 0.83–0.90 per z-score) than below 0 (HRage 7 = 0.95; 95%CI 0.91–0.99 per z-score). Associations between childhood height and BBD differed by age; at 7 years the association was an inverted U-shape, whereas at 13 years height was not associated with BBD. Ages at OGS and PHV were positively associated with BBD. Low and high birthweights were associated with lower BBD risks. Conclusion: A high childhood BMI, a short or tall stature at young childhood ages, an early pubertal onset, and low or high birthweights are associated with reduced risks of BBD. These complex associations suggest that the role of these factors in breast tissue development during early life warrants further investigation in relation to BBD etiology.What is Known:• Benign breast disease (BBD) is common and may be an intermediary marker of breast cancer risks.• Early life body size may relate to the development of BBD, but currently little is known.What is New:• Girls with a high body mass index at school ages or with an early pubertal timing have decreased risks of BBD.• Short and tall heights at young childhood ages and low and high birthweights are associated with lower BBD risks.

BackgroundAlthough weight gain in mid- to late adult life is associated with an increased risk of colon cancer, it is unclear if increases or losses in weight from childhood to early adulthood are differentially associated with risks of adult colon cancer.MethodsWeight and height were measured at 7 or 13 years and in early adulthood (17–26 years) in 64,675 boys in the Copenhagen School Health Records Register and the Danish Conscription Database. Cases of colon cancer (n = 751) were identified in the Danish Cancer Registry. Boys and young men were categorized as normal weight or overweight. Associations between changes in weight and colon cancer were examined using Cox proportional hazards regression to estimate hazard ratios (HRs) and 95% confidence intervals (CIs).ResultsCompared with men with a normal weight at 7 years and in early adulthood, men with overweight at both ages had an increased risk of adult colon cancer (HR: 2.73, 95% CI 1.80–4.15). In contrast, men with overweight at 7 years, but not in early adulthood did not have an increased risk of colon cancer (HR: 0.73, 95% CI 0.35–1.54), nor did men with a normal weight at 7 years and overweight in early adulthood (HR: 1.28, 95% CI 0.96–1.70). Similar results were observed for weight status at age 13 years combined with early adulthood.ConclusionsChildhood overweight that persists into early adulthood is associated with an increased risk of colon cancer, whereas overweight that disappears before early adulthood or developed after childhood is not.