Body Fat In Adulthood Research Articles

Association between birth conditions and bone mineral density in adults from the 1982 and 1993 birth cohorts in Pelotas, Rio Grande do Sul State, Brazil

This study assessed the association of birth weight, gestational age, and intrauterine growth with bone mineral density (BMD) at 22 and 30 years of age in the 1982 and 1993 birth cohorts in Pelotas, Rio Grande do Sul State, Brazil. BMD was measured by dual-energy X-ray absorptiometry (DXA) and the association was assessed using analysis of variance. Multiple linear regression was used to control for confounding factors: sex; household income at birth; maternal smoking during pregnancy; maternal schooling; maternal ethnicity/skin color; and pre-pregnancy body mass index. The study tested whether body fat in adulthood was a mediator of the association analyzed, using the G-computation Formula. A total of 6,803 participants from the 1982 and 1993 cohorts were evaluated at 30 and 22 years of age, respectively. Birth weight was associated with BMD at all sites, with a greater difference at the femoral neck. Individuals born weighing less than 2,000g had on average -0.036g/cm2 (95%CI: -0.064; -0.008) of BMD in the femoral neck than individuals weighing more than 3,500g. Individuals with an intrauterine growth z-score at least 1.28 standard deviation below the mean had an average of -0.013g/cm2 (95%CI: -0.024; -0.002) of BMD in the lumbar spine compared with individuals with an above-average z-score. The mediation analysis showed that body fat in adulthood did not mediate the association. Birth conditions have been associated with BMD in adulthood and the identification of early factors related to bone loss is essential due to the demographic inversion that has been taking place in low- and middle-income countries.

Historical Obesity and Early-Onset Cancers: A Propensity-Weighted Analysis of the National Health and Nutrition Examination Survey.

The incidence of early-onset obesity-related cancers (diagnosed < 50years) is increasing in the U.S. We examined the reported historical body mass index (BMI) of adults with early and later-onset cancers to explore relation to obesity. We queried the 1999-2018 NHANES database for adults diagnosed with obesity-related cancers (colorectal, non-colorectal gastrointestinal, uterine, breast). We classified early and late-onset cancer based on a diagnosis age of < 50 and ≥ 50years, respectively. Propensity-weighted analysis was used to compare prior historical BMIs between the matched groups. After weighing, we included 2,966,528 patients with obesity-related cancers, 846,211 (28%) of which were < 50years. In the matched analysis, 69.1% of early-onset CRC cases were diagnosed as obese (BMI ≥ 30kg/m2) before cancer diagnosis, compared to 47.2% of late-onset cases (p < 0.03). Similarly, a higher percentage of adults with other early-onset gastrointestinal cancers had prior obesity as compared to the late-onset cohort (70.3% vs. 40.5%, p = 0.0002). BMI showed a trend toward higher values at ages 20-24 for early-onset CRC and 30-34 for other gastrointestinal cancers. In contrast, later-onset CRC and other gastrointestinal cancers exhibited higher BMI values at later ages (30-34 and 35-39, respectively). Early-onset uterine cancer was linked to a higher BMI compared to later-onset cancer (34.0 vs. 31.1kg/m2, p < 0.0001), with a trend towards a higher BMI before 19years old. Our nationally representative data reveal that higher and earlier body fatness in adulthood associates with early-onset gastrointestinal and uterine cancers. These findings underscore the importance of intensifying efforts to combat early-life obesity.

Trajectories of body mass index in adulthood and risk of subtypes of postmenopausal breast cancer

BackgroundBody fatness is a dynamic exposure throughout life. To provide more insight into the association between body mass index (BMI) and postmenopausal breast cancer, we aimed to examine the age at onset, duration, intensity, and trajectories of body fatness in adulthood in relation to risk of breast cancer subtypes.MethodsBased on self-reported anthropometry in the prospective Norwegian Women and Cancer Study, we calculated the age at onset, duration, and intensity of overweight and obesity using linear mixed-effects models. BMI trajectories in adulthood were modeled using group-based trajectory modeling. We used Cox proportional hazards models to calculate hazard ratios (HRs) with 95% confidence intervals (CIs) for the associations between BMI exposures and breast cancer subtypes in 148,866 postmenopausal women.ResultsA total of 7223 incident invasive postmenopausal breast cancer cases occurred during follow-up. Increased overweight duration and age at the onset of overweight or obesity were associated with luminal A-like breast cancer. Significant heterogeneity was observed in the association between age at overweight and overweight duration and the intrinsic-like subtypes (pheterogeneity 0.03). Compared with women who remained at normal weight throughout adulthood, women with a descending BMI trajectory had a reduced risk of luminal A-like breast cancer (HR 0.54, 95% CI 0.33–0.90), whereas women with ascending BMI trajectories were at increased risk (HR 1.09; 95% CI 1.01–1.17 for “Normal-overweight”; HR 1.20; 95% CI 1.07–1.33 for “Normal-obesity”). Overweight duration and weighted cumulative years of overweight and obesity were inversely associated with luminal B-like breast cancer.ConclusionsIn this exploratory analysis, decreasing body fatness from obesity in adulthood was inversely associated with overall, hormone receptor-positive and luminal A-like breast cancer in postmenopausal women. This study highlights the potential health benefits of reducing weight in adulthood and the health risks associated with increasing weight throughout adult life. Moreover, our data provide evidence of intrinsic-like tumor heterogeneity with regard to age at onset and duration of overweight.

The impact of early sports participation on body fatness in adulthood is not mediated by current physical activity.

The aim was to analyze the relationship between early sports participation (ESP) and body fatness (BF) in adults, as well as to identify whether this possible relationship is directly influenced by the current physical activity (PA) level. This cross-sectional study combined baseline data of two cohort. The BF estimated by DXA. The ESP, the subjects reported the engagement in sports during childhood (7-10 years) and adolescence (11-17 years) through two yes/no questions and current PA (described as steps) was device-measured using pedometers. Were identified as potential covariates and therefore adjusted the multivariate models: age, ethnicity, alcohol consumption, smoking, and sleep quality. Statistical analysis consisted of the chi-square test, analysis of variance/covariance, and structural equation modeling (software BioEstat version 5.0; p-value < .05). Adults engaged in ESP had lower BF; among women, the variance in BF explained by ESP was 25.5%; among men, it was 9.2%. Sports participation in early life (r = -.436 [95% CI: -0.527 to -0.346]) and current PA (r = -.431 [95% CI: -0.522 to -0.340]) were inversely related to BF, as well as positively related to each other (r = .328 [95% CI: 0.226 to 0.430]). In the mediation model, current PA partially mediated (18.5%) the impact of ESP on BF, while current PA and ESP remained relevant determinants of BF. Early sports participation and current PA have a significant impact on BF in adulthood, which is of similar magnitude and independent of each other.

Long-term excess body fat in adulthood and the risk of pre- and postmenopausal breast cancer in Chinese women.

This study aimed to investigate the association between long-term excess body fat and breast cancer risk by studying adult weight gain together with the subsequent weight fluctuations. Weight gain measure in three different time periods in adulthood of 1500 participants was collected in a case-control study of Western China. Logistic regression models were used to estimate odds ratios and 95% CIs. The increased risk of postmenopausal BC was associated with adult weight gain at 5years and at 10years before enrollment (OR 1.24, 95% CI 1.03-1.49 per 5kg increase; OR 1.40, 95% CI 1.14-1.70 per 5kg increase) but was not associated with adult weight gain at enrollment (OR 0.97, 95% CI 0.81-1.16 per 5kg increase). Only a positive association was observed in premenopausal women who had gained > 5.0kg at 10years before enrollment (OR 1.61, 95% CI 1.10-2.35). Women who had gained > 5.0kg at 10years before enrollment and continued to gain during the subsequent 5years had the highest postmenopausal BC risk (OR 3.34, 95% CI 1.58-7.08). Adult weight gain at 5years and 10years before enrollment are more closely associated with postmenopausal BC risk than adult weight gain at enrollment in Western China. Controlling body weight as early as possible throughout adulthood to keep weight gain not more than 5.0kg is particularly necessary for Chinese women.

Body fatness at a young age, body fatness gain and risk of breast cancer: systematic review and meta-analysis of cohort studies.

Higher body fatness in adulthood has been consistently associated with an increased risk of postmenopausal breast cancer, as well as a tendency towards a lower risk of premenopausal breast cancer. However, the association between body fatness at a young age (≤30years), body fatness gain and the risk of breast cancer is less defined. PubMed and Web of Science databases were searched to identify relevant publications. Risk estimates with 95% confidence intervals from each study were transformed into a continuous variable for each 5kgm-2 increase in body mass index (BMI) and were pooled under a random-effects model. Each 5kgm-2 increase in BMI was significantly associated with a 14%, 12% and 17% lower risk of breast cancer later in life among all women, premenopausal women and postmenopausal women, respectively. Significant heterogeneity and publication bias were observed. The results remained unchanged after the trim and fill method was applied to correct the bias. Each 5kgm-2 increase in BMI from a young age until cohort entry was significantly associated with a 13% and 14% higher risk of breast cancer in all women and postmenopausal women, respectively. In summary, higher body fatness at a young age may have a protective role in the later development of breast cancer in both premenopausal and postmenopausal women. However, this potential benefit should not be overemphasized, as our findings suggest that increased body fatness gain from a young age is positively associated with postmenopausal breast cancer risk. These findings further justify the need to maintain a steady weight throughout life.

Body fatness at an early age and risk of colorectal cancer.

While there is convincing evidence that excess body fatness in adulthood is positively associated with colorectal cancer risk, the association between body fatness at an early age (≤30 years) and the risk of colorectal cancer has been equivocal. The present meta-analysis was performed to clarify this association. PubMed and Web of Science databases were searched for relevant studies that investigated this association. The risk estimates from each study were transformed into a continuous variable for each 5 kg/m2 increase in body mass index (BMI). A random effects model was used to calculate the summary relative risks (RRs) with 95% confidence intervals (CIs). A total of 15 observational studies (13 cohort studies and two case-control studies) were included in this meta-analysis. Each 5 kg/m2 increase in BMI was significantly associated with a 13% (RR 1.13, 95% CI 1.08, 1.19), 17% (RR 1.17, 95% CI 1.09, 1.25) and 8% (RR 1.08, 95% CI 1.04, 1.11) higher risk of colorectal cancer overall, in men, and in women, respectively. Substantial heterogeneity was observed across studies. Based on the anatomic subsite, each 5 kg/m2 increase in BMI was significantly associated with a 14% (RR 1.14, 95% CI 1.07, 1.22) higher risk of colon cancer, whereas no association (RR 1.03, 95% CI 0.95, 1.13) was observed with rectal cancer. In summary, body fatness at an early age may affect colon cancer risk later in life. Prevention of overweight and obesity in young individuals should be emphasized to prevent early-onset colon cancer attributed to excess body fatness.

Early Diet and Later Cancer Risk: Prospective Associations of Dietary Patterns During Critical Periods of Childhood with the GH-IGF Axis, Insulin Resistance and Body Fatness in Younger Adulthood

Early life, adiposity rebound, and puberty represent critical growth periods when food choices could have long-term relevance for cancer risk. We aimed to relate dietary patterns during these periods to the growth hormone-insulin-like-growth-factor (GH-IGF) axis, insulin resistance, and body fatness in adulthood. Data from the Dortmund Nutritional and Anthropometric Longitudinally Designed (DONALD) Study participants with outcome data at 18–37 years, and ≥2 dietary records during early life (1–2 yr; n = 128), adiposity rebound (4–6 years, n = 179), or puberty (girls 9–14, boys 10–15 yr; n = 213) were used. Dietary patterns at these ages were derived by 1) reduced rank regression (RRR) to explain variation in adult IGF-I, IGF-binding protein-3 (IGFBP-3), homoeostasis model assessment for insulin resistance (HOMA-IR) and fat-mass index; 2) principal component analysis (PCA). Regarding RRR, the patterns “cake/canned fruit/cheese & eggs” (early life), “sweets & dairy” (adiposity rebound) and “high-fat foods” (pubertal boys) were independently associated with higher adult HOMA-IR. Furthermore, the patterns “favorable carbohydrate sources” (early life), “snack & convenience foods” (adiposity rebound), and “traditional & convenience carbohydrates” (pubertal boys) were related to adult IGFBP-3 (P trend < 0.01). PCA identified “healthy” patterns for all periods, but none was associated with the outcomes (P trend > 0.1). In conclusion, dietary patterns during sensitive growth periods may be of long-term relevance for adult insulin resistance and IGFBP-3.

A cis-eQTL in PFKFB2 is associated with diabetic nephropathy, adiposity and insulin secretion in American Indians

A prior genome-wide association study (GWAS) in Pima Indians identified a variant within PFKFB2 (rs17258746) associated with body mass index (BMI). PFKFB2 encodes 6-phosphofructo-2-kinase/fructose 2,6-bisphosphatase isoform 2, which plays a role in glucose metabolism. To follow-up on the GWAS, tag SNPs across PFKFB2 were genotyped in American Indians (AI) who had longitudinal data on BMI (n = 6839), type 2 diabetes (T2D; n = 7710), diabetic nephropathy (DN; n = 2452), % body fat (n = 555) and insulin secretion (n = 298). Two SNPs were further genotyped in urban AI to assess replication for DN (n = 864). PFKFB2 expression was measured in 201 adipose biopsies using real-time RT-PCR and 61 kidney biopsies using the Affymetrix U133 array. Two SNPs (rs17258746 and rs11120137), which capture the same signal, were associated with maximum BMI in adulthood (β = 1.02 per risk allele, P = 7.3 × 10(-4)), maximum BMI z-score in childhood (β = 0.079, P = 0.03) and % body fat in adulthood (β = 3.4%, P = 3 × 10(-7)). The adiposity-increasing allele correlated with lower PFKFB2 adipose expression (β = 0.81, P = 9.4 × 10(-4)). Lower expression of PFKFB2 further correlated with higher % body fat (r = -0.16, P = 0.02) and BMI (r = -0.17, P = 0.02). This allele was also associated with increased risk for DN in both cohorts of AI [odds ratio = 1.64 (1.32-2.02), P = 5.8 × 10(-6)], and similarly correlated with lower PFKFB2 expression in kidney glomeruli (β = 0.87, P = 0.03). The same allele was also associated with lower insulin secretion assessed by acute insulin response (β = 0.78, P = 0.03) and 30-min plasma insulin concentrations (β = 0.78, P = 1.1 × 10(-4)). Variation in PFKFB2 appears to reduce PFKFB2 expression in adipose and kidney tissues, and thereby increase risk for adiposity and DN.

Liver-specific GH receptor gene-disrupted (LiGHRKO) mice have decreased endocrine IGF-I, increased local IGF-I, and altered body size, body composition, and adipokine profiles.

GH is an important regulator of body growth and composition as well as numerous other metabolic processes. In particular, liver plays a key role in the GH/IGF-I axis, because the majority of circulating "endocrine" IGF-I results from GH-stimulated liver IGF-I production. To develop a better understanding of the role of liver in the overall function of GH, we generated a strain of mice with liver-specific GH receptor (GHR) gene knockout (LiGHRKO mice). LiGHRKO mice had a 90% decrease in circulating IGF-I levels, a 300% increase in circulating GH, and significant changes in IGF binding protein (IGFBP)-1, IGFBP-2, IGFBP-3, IGFBP-5, and IGFBP-7. LiGHRKO mice were smaller than controls, with body length and body weight being significantly decreased in both sexes. Analysis of body composition over time revealed a pattern similar to those found in GH transgenic mice; that is, LiGHRKO mice had a higher percentage of body fat at early ages followed by lower percentage of body fat in adulthood. Local IGF-I mRNA levels were significantly increased in skeletal muscle and select adipose tissue depots. Grip strength was increased in LiGHRKO mice. Finally, circulating levels of leptin, resistin, and adiponectin were increased in LiGHRKO mice. In conclusion, LiGHRKO mice are smaller despite increased local mRNA expression of IGF-I in several tissues, suggesting that liver-derived IGF-I is indeed important for normal body growth. Furthermore, our data suggest that novel GH-dependent cross talk between liver and adipose is important for regulation of adipokines in vivo.

Childhood Overweight and Maturational Timing in the Development of Adult Overweight and Fatness: The Newton Girls Study and Its Follow-up

Although several studies have suggested that early menarche is associated with the development of adult overweight, few have accounted for childhood overweight before menarche. A 30-year follow-up of the original participants in the Newton Girls Study, a prospective study of development in a cohort of girls followed through menarche, provided data on premenarcheal relative weight and overweight (BMI >85th percentile), prospectively obtained age at menarche, self-reported adult BMI, overweight (BMI > 25), obesity (BMI > 30) and, for a subset of participants, percentage body fat by dual-energy x-ray absorptiometry. Of the 448 women who participated in the adult follow-up at a mean age of 42.1 years (SD: 0.76 years), 307 had childhood data with which to characterize premenarcheal and menarcheal weight status and age at menarche. After a follow-up of 30.1 years (SD: 1.4 years), reported BMI was 23.4 (4.8), 28% were overweight, and 9% were obese. In multivariate linear and logistic-regression analyses, almost all of the influence on adult weight status was a result of premenarcheal weight status (model R2 = 0.199). Inclusion of a variable to reflect menarcheal timing provided very little additional information (model R2 = 0.208). Girls who were overweight before menarche were 7.7 times more likely to be overweight as adults (95% confidence interval: 2.3, 25.8), whereas early menarche (at < or = 12 years of age) did not elevate risk (odds ratio: 1.3, 95% confidence interval: 0.66, 2.43). A similar pattern of results was observed when percentage body fat in adulthood was evaluated. The apparent influence of early maturation on adult female overweight is largely a result of the influence of elevated relative weight on early maturation. Interventions to prevent and treat overweight should focus on girls before they begin puberty.

Nutrition and cancer.

Evidence from both animal and epidemiologic studies indicate that throughout life excessive energy intake in relation to requirements increases risk of human cancer. Rapid growth rates in childhood lead to earlier age at menarche, which in turn increases risk of breast cancer, and accumulation of body fat in adulthood in related to cancers of the colon, kidney, and endometrium as well as postmenopausal breast cancer. Higher intake of vegetables and fruits has been associated with lower risks of many cancers. The constituents responsible for these apparent protective effects remain uncertain, although evidence supports a contribution of folic acid. Recent evidence suggests that the percentage of energy from fat in the diet is not a major cause of cancers of the breast or colon. Higher intake of meat and dairy products has been associated with greater risk of prostate cancer, which may be related to their saturated fat content. Also, red meat consumption has been associated with risk of colon cancer in numerous studies, but this appears to be unrelated to its fat content. Excessive consumption of alcohol increases risks of upper gastrointestinal tract and even moderate intake appears to increase cancers of the breast and large bowel. Although many details remain to be learned, evidence is strong that remaining physically active and lean throughout life, consuming an abundance of fruits and vegetables, and avoiding high intakes of red meat, foods high in animal fat, and excessive alcohol will substantially reduce risk of human cancer.