Future direct and indirect costs of obesity and the influence of gaining weight: Results from the MONICA/KORA cohort studies, 1995-2005

Over the last two decades, the prevalence of obesity has risen worldwide. As obesity is a confirmed risk factor for a number of diseases, its increasing prevalence nurtures the supposition that obesity may present a growing and significant economic burden to society.The objective of this study is to analyse the correlation between body mass index (BMI) and future direct and indirect costs, as well as the correlation between changing BMI and future in(direct) costs. Health care utilisation and productivity losses were based on data from 2581 participants aged 25-65 years (1994/95) from two cross-sectional, population-representative health surveys (MONICA/KORA-survey-S3 1994/95 and follow-up KORA-survey-F3 2004/05) in Augsburg, Germany.The predicted average adjusted total direct costs per year and per user were estimated to be €1029-(healthy weight), €1093-(overweight) and €1040-(obesity). There are significantly greater future costs in the utilisation of general practitioners per user and per year at higher obesity levels (€72; €75; €96).The average total direct costs per person for those who stay in the same BMI class are €982, €1000 and €973. An overweight participant who becomes obese incurs significant costs of internists of €160 compared with those who remain overweight (€124). An overweight user incurs indirect costs of €2474, compared with €2136 for those who remain a healthy weight.There is a trend for higher predicted (in)direct costs when people are overweight or obese compared with healthy weight persons 10 years earlier. Potential cost savings could be attained if preventive programs effectively targeted these individuals.     

Associations between parental and child overweight and obesity

Results of the analysis showed that parents and children overweight/obesity were significantly correlated. The sample includes 318 pairs of mothers and children, and 336 pairs of fathers and children at the age 11.3 +/- 0.4 years in Trogir, Croatia. Child overweight and obesity were defined according to body mass index (BMI) 25 and 30 equivalents (kg/m2). The prevalence of total overweight in girls was 25.6% and among boys was 20.5%. Mother's weight (p = 0.003) and BMI (p = 0.006) were greater in obese than in other groups of children. Overweight/obese children were more often found among overweight/obese mothers (p = 0.009) and fathers (p = 0.039). Correlation between overweight/obese children and their father (odds ratio 3.2, 95% CI 1.5-6.8) was stronger than between overweight/obese children and their mothers (odds ratio 2.2, 95% CI 1.2-3.9). Associations with mothers' and daughters' overweight/obesity were stronger (p = 0.017) than mothers' and sons'(p = 0.12). Correlations between children's BMI and fathers' BMI (r = 0.265, p < 0.0001) and between children's BMI and mothers' BMI (r = 0.173, p = 0.002) were significant. Children whose parents are overweight/obese look for greater attention in future preventive programme.     

The effect of obesity on overall,circulatory disease- and diabetes-specific mortality

This paper explores the relationship between body mass and risk of death among US adults. The National Health Interview Survey-Multiple Cause of Death linked data set is used for the years 1987-1997, and Cox proportional hazard models are employed to estimate the association between obesity, as measured by the body mass index (BMI), and overall, circulatory disease-specific and diabetes-specific mortality. A U-shaped relationship is found between BMI and overall mortality. Compared with normal weight individuals, mortality during the follow-up period is 34% higher among obese class II individuals and 77% higher among obese class III individuals, controlling for age and sex. A J-shaped relationship exists between circulatory disease mortality and obesity, with a slightly higher risk of death for all categories of BMI. The relationship between BMI and diabetes mortality is striking. Compared with normal weight individuals, obese class I individuals are 2.8 times as likely to die, obese class II individuals are 4.7 times as likely to die, and obese class III individuals are 9.0 times as likely to die of diabetes during the follow-up period, controlling for age and sex. These results demonstrate that obesity heightens the risk of overall and circulatory disease mortality, and even more substantially increases the risk of diabetes mortality. These mortality findings, together with the substantial recent increases in obesity, lend urgency to public health programmes aimed at reducing the prevalence and consequences of obesity.     

BMI,Physical Activity,and Health Care Utilization/Costs among Medicare Retirees

Objective: To examine the influence of physical activity (PA) and BMI on health care utilization and costs among Medicare retirees. Research Methods and Procedures: This cross‐sectional study was based on 42, 520 Medicare retirees in a U.S.‐wide manufacturing corporation who participated in indemnity/perferred provider and one health risk appraisal during the years 2001 and 2002. Participants were assigned into one of the three weight groups: normal weight, overweight, and obese. PA behavior was classified into three levels: sedentary (0 time/wk), moderately active (1 to 3 times/wk), and very active (4+ times/wk). Results: Generalized linear models revealed that the moderately active retirees had $1456, $1731, and $1177 lower total health care charges than their sedentary counterparts in the normal‐weight, overweight, and obese groups, respectively (p < 0.01). The very active retirees had $1823, $581, and $1379 lower costs than the moderately active retirees. Health care utilization and specific costs showed similar trends with PA levels for all BMI groups. The total health care charges were lower with higher PA level for all age groups (p < 0.01). Discussion: Regular PA has strong dose‐response effects on both health care utilization and costs for overweight/obese as well as normal‐weight people. Promoting active lifestyle in this Medicare population, especially overweight and obese groups, could potentially improve their well‐being and save a substantial amount of health care expenditures. Because those Medicare retirees are hard to reach in general, more creative approaches should be launched to address their needs and interests as well as help reduce the usage of health care system.     

Study of insulin-like growth factor I in human obesity.

In obesity there is a decrease in basal and stimulated GH secretion. IGF-I, which has negative feedback effects on GH secretion, could be the initial mediator of such alterations. We studied IGF-I levels in obese subjects and their relationship to the obesity level and GH secretion. We determined plasma IGF-I, basal and stimulated GH in 30 normal and 30 obese women and related these variables to obesity indices (body mass index, BMI, and % overweight). Baseline plasma GH values were 1.2 +/- 0.3 and 2.3 +/- 0.6 micrograms/l in obese subjects and controls, respectively (NS). Mean peak GH secretion after stimuli were 11.2 +/- 1.4 and 34.4 +/- 5.6 micrograms/l in obese subjects and controls, respectively (p less than 0.001). Plasma IGF-I were 1.0 +/- 0.1 U/ml and 0.7 +/- 0.1 U/l in obese subjects and controls, respectively (NS). There was a significant negative correlation between plasma IGF-I and age (r = -0.55, p less than 0.001) and a significant negative correlation between mean peak GH secretion and weight (r = -0.60, p less than 0.001), BMI (r = -0.64, p less than 0.001) and percentage of ideal body weight (r = -0.67, p less than 0.001). We did not find any correlation between IGF-I and indices of overweight. These data suggest that the reduced GH secretion found in obesity is not related to a negative feedback inhibition by elevated levels of IGF-I and that adiposity is not associated with a decline in IGF-I levels. We confirm the existence of a negative correlation between GH secretion and obesity indices.     

Effect of obesity on inpatient rehabilitation outcomes after total hip arthroplasty

Objective: This study examined whether obesity affected inpatient rehabilitation outcomes after total hip arthroplasty (THA). Research Methods and Procedures: This was a retrospective, comparative study conducted using a computerized medical database derived from THA patients at a university‐affiliated rehabilitation hospital (data from 2002 to 2005). Patients were divided into four brackets based on BMI: non‐obese (<25 kg/m²), overweight (25 to 29.9 kg/m²), moderate obesity (30 to 39.9 kg/m²), and severe obesity (≥40 kg/m²). All patients completed an interdisciplinary inpatient rehabilitation program after THA. Functional independence measure (FIM) scores, length of stay (LOS), FIM efficiency scores (FIM/LOS), hospital charges, and discharge disposition location were collected. Results: FIM scores improved from admission to discharge similarly in all groups (25 to 29.5 points). However, FIM efficiency, LOS, and total charges were curvilinearly related with BMI (all p < 0.05). Total hospital charges were highest in the severely obese group compared with the overweight group (p < 0.05). Non‐homebound discharge disposition rates were lower in non‐obese (13.1%) and severely obese groups (10.5%). Discussion: Elevated BMI does not prevent FIM gains in THA patients during inpatient rehabilitation. However, BMI is related with FIM efficiency, LOS, and hospital charges in a curvilinear fashion. Severely obese patients can achieve physical improvements but at a lower efficiency and greater cost.     

Effect of obesity on repeat revascularization in patients undergoing percutaneous coronary intervention with drug-eluting stents

Obesity is a major risk factor for developing coronary artery disease. The impact of obesity on prognosis among those with established coronary disease is less clear. The objective of this study was to evaluate the effect of obesity on repeat revascularization in patients undergoing percutaneous coronary intervention (PCI) with drug-eluting stents (DES). We examined 6,083 patients who were divided into three groups according to BMI: normal (BMI 18.5-24.9 kg/m(2), n = 1,592); overweight (BMI 25-29.9 kg/m(2), n = 3,026) and obese (BMI >30 kg/m(2), n = 1,465). The follow-up focused on clinical-driven repeat revascularization, including target lesion revascularization (TLR) and nonTLR. Median follow-up was 26 months (interquartile range 20-32). There was no significant difference in the incidence of TLR among normal, overweight, and obese patients (6.3% vs. 6.1% vs. 7.1%; P = 0.423). In contrast, the incidence of nonTLR was significantly higher in obese patients compared with normal and overweight (8.4% vs. 6.0% vs. 5.8%, P = 0.003). Multivariate analysis showed that obesity was an independent predictor of nonTLR during follow-up (hazard ratio = 1.39; 95% confidence interval = 1.06-1.83; P = 0.019), along with diabetes and hypercholesterolemia. Concomitant use of statins was independently associated with decreased risk of nonTLR (hazard ratio = 0.75; 95% confidence interval = 0.62-0.92; P = 0.005). In conclusion, among patients undergoing PCI with DES, obesity was not associated with TLR, but was associated with a higher risk of nonTLR.     

HLA associations with obesity

A subgroup of 351 subjects with human leukocyte antigen (HLA) typing were available from the Framingham Heart Study for analyses to identify associations with obesity. The subjects consisted of 143 males and 208 females aged 58-88 years at the 15th biennial examination in 1978. The obese classification was based on maximum body mass index (BMI) over the 16 available biennial examinations of the Framingham Heart Study. The subjects were classified as obese if they exceeded the 95th percentile of BMI for 20- to 29-year-old subjects as described in the NHANES II study; males were obese if BMI greater than 31.1 and females were obese if BMI greater than 32.3. There were 27 obese males (18.9%) and 44 obese females (21.2%) in the sample. Gene frequencies were compared between the nonobese and obese groups for the pooled sample as well as by sex. Among alleles previously shown to be related to obesity, HLA Bw35 appeared to be more frequent in obese females but these data did not confirm a difference for the B18 or Cw4 alleles. More importantly, HLA Aw30 was found to be significantly higher among the obese subjects in both males and females. Further analyses adjusting for potential confounding variables reduced the estimated relative risk for obesity for subjects with the Bw35 allele to approximately 1.30 and no longer significant for this sample size. In contrast, the relative risk for Aw30, while reduced, remained significant after adjustment for confounding variables. Based on these data, individuals with the Aw30 allele have a relative risk of 2.61 for obesity.(ABSTRACT TRUNCATED AT 250 WORDS)     

Skeletal muscle lipid metabolism with obesity

The objectives of this study were to 1). examine skeletal muscle fatty acid oxidation in individuals with varying degrees of adiposity and 2). determine the relationship between skeletal muscle fatty acid oxidation and the accumulation of long-chain fatty acyl-CoAs. Muscle was obtained from normal-weight [n = 8; body mass index (BMI) 23.8 +/- 0.58 kg/m(2)], overweight/obese (n = 8; BMI 30.2 +/- 0.81 kg/m(2)), and extremely obese (n = 8; BMI 53.8 +/- 3.5 kg/m(2)) females undergoing abdominal surgery. Skeletal muscle fatty acid oxidation was assessed in intact muscle strips. Long-chain fatty acyl-CoA concentrations were measured in a separate portion of the same muscle tissue in which fatty acid oxidation was determined. Palmitate oxidation was 58 and 83% lower in skeletal muscle from extremely obese (44.9 +/- 5.2 nmol x g(-1) x h(-1)) patients compared with normal-weight (71.0 +/- 5.0 nmol x g(-1) x h(-1)) and overweight/obese (82.2 +/- 8.7 nmol x g(-1) x h(-1)) patients, respectively. Palmitate oxidation was negatively (R = -0.44, P = 0.003) associated with BMI. Long-chain fatty acyl-CoA content was higher in both the overweight/obese and extremely obese patients compared with normal-weight patients, despite significantly lower fatty acid oxidation only in the extremely obese. No associations were observed between long-chain fatty acyl-CoA content and palmitate oxidation. These data suggest that there is a defect in skeletal muscle fatty acid oxidation with extreme obesity but not overweight/obesity and that the accumulation of intramyocellular long-chain fatty acyl-CoAs is not solely a result of reduced fatty acid oxidation.     

Central obesity as a risk factor for prostatic hyperplasia

Objective: Obesity‐related metabolic diseases may influence prostatic hyperplasia. This study examined the impact of obesity on prostate volume in men without overt obesity‐related metabolic diseases. Research Methods and Procedures: We recruited 146 men over the age of 40 years who did not have overt obesity‐related diseases, such as diabetes, impaired fasting glucose, hypertension, or dyslipidemia. Transrectal ultrasonography was performed on all subjects. The subjects were divided into three groups according to their BMI: normal (18.5 to 22.9 kg/m²), overweight (23 to 24.9 kg/m²), and obese (≥25 kg/m²), and two groups according to their waist circumference: normal waist (≤90 cm) and central obesity (>90 cm). The classification of the subgroups was based on the Asia‐Pacific criteria of obesity. We compared the prostate volume among subgroups and assessed factors related to prostatic hyperplasia. Results: Mean prostate volume was 18.8 ± 5.0, 21.8 ± 7.2, and 21.8 ± 5.6 mL in the normal, overweight, and obese groups, respectively, and was 20.0 ± 5.9 and 23.7 ± 5.3 mL in the normal waist and central obesity group, respectively. Prostate volume was significantly greater in the obese group than in the normal group (P = 0.03) and in the central obesity group compared with the normal waist group (P = 0.002). Prostate volume was positively correlated with BMI and waist circumference after adjustment for age. After adjusting for confounding factors, central obesity was an independent factor affecting prostatic hyperplasia, which was defined as a prostate volume >20 mL (odds ratio = 3.37, p = 0.037). Relative to men with both low BMI (18.5 to 22.9 kg/m²) and normal waist circumference, those with high BMI (≥25 kg/m²) and central obesity were at significantly increased risk of prostatic hyperplasia (odds ratio = 4.88, p = 0.008). However, those with high BMI (≥25 kg/m²) and normal waist circumference were not at significantly increased risk. Discussion: Prostate volume was greater in the obese and central obesity groups than in the normal group after patients with overt obesity‐related metabolic diseases were excluded. Although both BMI and waist circumference were positively correlated with prostate volume, central obesity was the only independent factor affecting prostate hyperplasia. We suggest that central obesity is an important risk factor for prostatic hyperplasia.     

State- and payer-specific estimates of annual medical expenditures attributable to obesity

The goal of this study is to expand prior analyses by presenting current state-level estimates of the costs of obesity in total and separately for Medicare and Medicaid. Quantifying current Medicare and Medicaid expenditures attributable to obesity is important because high public sector costs of obesity have been a primary motivation for publicly funded obesity prevention efforts at the state level. We also present estimates of the obesity-attributable fraction (OAF) of total, Medicare, and Medicaid expenditures and the percentage of total obesity costs within each state that is funded by the public sector. We used the 2006 Medical Expenditure Panel Survey, nationally representative data that include information on obesity and medical expenditures, to generate an equation that predicts annual medical expenditures as a function of obesity status. We used the 2006 Behavioral Risk Factor Surveillance System, state representative data, and the equation generated from the national model to predict state (and payer within state) expenditures and the fraction of expenditures attributable to obesity for each state. Across states, annual medical expenditures would be between 6.7 and 10.7% lower in the absence of obesity. Between 22% (Virginia) and 55% (Rhode Island) of the state-level costs of obesity are financed by the public sector via Medicare and Medicaid. The high costs of obesity at the state level emphasize the need to prevent and control obesity as a way to manage state medical costs.     

Further evidence for the role of ENPP1 in obesity: association with morbid obesity in Finns

The aim of this study was to investigate a series of single-nucleotide polymorphisms (SNPs) in the genes MC2R, MC3R, MC4R, MC5R, POMC, and ENPP1 for association with obesity. Twenty-five SNPs (2-7 SNPs/gene) were genotyped in 246 Finns with extreme obesity (BMI > or = 40 kg/m2) and in 481 lean subjects (BMI 20-25 kg/m2). Of the obese subjects, 23% had concomitant type 2 diabetes. SNPs and SNP haplotypes were tested for association with obesity and type 2 diabetes. Allele frequencies differed between obese and lean subjects for two SNPs in the ENPP1 gene, rs1800949 (P = 0.006) and rs943003 (P = 0.0009). These SNPs are part of a haplotype (rs1800949 C-rs943003 A), which was observed more frequently in lean subjects compared to obese subjects (P = 0.0007). Weaker associations were detected between the SNPs rs1541276 in the MC5R, rs1926065 in the MC3R genes and obesity (P = 0.04 and P = 0.03, respectively), and between SNPs rs2236700 in the MC5R, rs2118404 in the POMC, rs943003 in the ENPP1 genes and type 2 diabetes (P = 0.03, P = 0.02 and P = 0.02, respectively); these associations did not, however, remain significant after correction for multiple testing. In conclusion, a previously unexplored ENPP1 haplotype composed of SNPs rs1800949 and rs943003 showed suggestive evidence for association with adult-onset morbid obesity in Finns. In this study, we did not find association between the frequently studied ENPP1 K121Q variant, nor SNPs in the MCR or POMC genes and obesity or type 2 diabetes.     

Effect of obesity on the reliability of age-at-death indicators of the pelvis

During medicolegal investigations, forensic anthropologists commonly use morphological changes in the auricular surface of the ilium and the symphyseal face of the pubis to estimate age. However, obesity may impact the reliability of age estimations based on pelvic joints. Over the past several decades, the prevalence of obesity has dramatically increased in the United States (US). Since the rate of progression through age-related stages of weight-bearing joints may be influenced by excessive body mass, it is important that anthropologists understand how obesity affects age-related morphological changes in the skeleton. This study investigates the effects of obesity on the validity of the estimated age-at-death based on the Buckberry–Chamberlin and Suchey–Brooks methods by comparing US adults considered normal BMI (BMI 18.5–24.9) and obese (BMI ≥ 30). The obese group exhibits overall greater bias (overestimation of age) and inaccuracy, less precision, and lower correlations between estimated and known age than the normal BMI group using both methods, although differences in the pubic symphysis are not statistically significant. For the auricular surface the age of transition from one phase to the next is lower and the standard deviations are greater for the obese as compared to normal weight individuals. This study helps to elucidate how obesity affects the rate of age-related skeletal change of the human pelvis, and shows that the pubic symphysis may be a more reliable indicator of age in obese individuals and that greater standard deviations are needed for obese individuals when estimating age-at-death from the pelvis. Am J Phys Anthropol 156:595–605, 2015. © 2014 Wiley Periodicals, Inc.     

Acute insulin infusion decreases plasma ghrelin levels in uncomplicated obesity

BACKGROUND: Plasma ghrelin levels have been shown to decrease after insulin infusion in lean subjects. Nevertheless, the mechanism of the suggested inhibitory effect of insulin on ghrelin is still unclear and no data about the effect of acute insulin infusion on plasma ghrelin concentration in obese subjects are available. OBJECTIVE: We sight to evaluate plasma ghrelin concentration during an hyperinsulinemic euglycemic clamp in uncomplicated obese subjects. METHODS: 35 uncomplicated obese subjects, body mass index (BMI) 43.3+/-10.1 kg/m(2), 33 women and 2 men, mean age 34.9+/-10, with a history of excess fat of at least 10 years underwent euglycemic hyperinsulinemic clamp. Blood samples for ghrelin were performed at baseline and steady state of euglycemic insulin clamp. RESULTS: Ghrelin concentrations decreased over time to 10.6+/-15% (range 2-39%) of baseline, from a mean of 205.53+/-93.79 pg/ml to 179.03+/-70.43 pg/ml during the clamp (95% CI, 10.69 to 36.44, P<0.01). In a univariate linear regression analysis baseline plasma ghrelin levels were inversely correlated to BMI (r=-0.564, P=0.04). A linear positive trend between whole body glucose utilization (M(FFMkg) index) and ghrelin reduction during the clamp was found (chi(2) 3.05, p=0.05). CONCLUSIONS: Our data seem to suggest that hyperinsulinemia during a euglycemic clamp is able to suppress plasma ghrelin concentrations in uncomplicated obesity. This effect appears to be positively related to insulin sensitivity.     

Parent predictors of child weight change in family based behavioral obesity treatment

Family based behavioral treatment for overweight and obese children includes parenting skills targeting the modification of child eating and activity change. The purpose of this study was to examine parenting skills and parent weight change as predictors of child weight change in a sample of 80 parent/child dyads who were enrolled in a family based behavioral weight loss program for childhood obesity. Eighty overweight and obese children and their parents who enrolled in treatment in two sites were included in the study. Variables included those related to parent modeling (parent BMI), home food environment, parenting (parent and child report), and demographics. Results suggested that parent BMI change was a significant predictor of child weight, in that a reduction of 1 BMI unit in the parent was associated with a 0.255 reduction in child BMI. None of the other variables were significant in the final model. This study is consistent with other research showing that parent weight change is a key contributor to child weight change in behavioral treatment for childhood obesity. Researchers and clinicians should focus on encouraging parents to lose weight to assist their overweight and obese child in weight management.     

Circulating progesterone and obesity in men.

Progesterone can be detected in male plasma and has been considered to originate mainly from the adrenals. We have examined the association between circulating progesterone and obesity in a sample of thirty-eight lean to morbidly obese men aged 44.5 +/- 9.9 years (BMI: 44.3 +/- 12.8 kg/m (2)). Plasma concentrations of progesterone, 17-OH-progesterone as well as androstenedione, testosterone, DHT and DHEA-S were determined. Negative correlations were observed between plasma progesterone levels and body weight (r = - 0.47, p < 0.05), BMI (r = - 0.56, p < 0.001), waist circumference (r = - 0.58, p < 0.001), as well as subcutaneous adipocyte diameter (r = - 0.50, p < 0.05). Plasma levels of 17-OH-progesterone, DHEA-S, androstenedione, testosterone and DHT were also negatively associated with body weight, BMI and waist circumference. However, the ratio of 17-OH-progesterone-to-progesterone and androstenedione-to-17-OH-progesterone were not related to these variables. A positive correlation was found between circulating progesterone and DHEA-S levels (r = 0.50, p < 0.002 after adjustment for age). Accordingly, using multivariate regression analyses, the best steroid predictor of progesterone level was plasma DHEA-S. Waist circumference was the best predictor of progesterone levels in a multivariate model including steroid concentrations as well as waist circumference, BMI and subcutaneous adipocyte diameter. In conclusion, plasma progesterone was negatively associated with markers of obesity such as BMI, waist circumference and subcutaneous adipocyte diameter in this sample of men. Circulating DHEA-S level was the best steroid correlate of plasma progesterone. We suggest that the low progesterone levels observed in obese men may reflect decreased adrenal C(19) steroid production in the adrenal cortex. Further research is needed to confirm this hypothesis.     

Maternal obesity is associated with younger age at obesity onset in U.S. adolescent offspring followed into adulthood

Objective: The objective was to test the hypothesis that maternal obesity is associated with younger age of offspring's obesity onset. Research Methods and Procedures: We used prospective, nationally representative, longitudinal data collected across Waves I (1995; 12 to 20 years), II (1996; 13 to 20 years), and III (2001; 18 to 28 years) of the National Longitudinal Study of Adolescent Health (N = 14,654; 49% female). Interval regression analysis was used to assess the association between maternal obesity and age at offspring's obesity onset (International Obesity Task Force BMI ≥30 equivalent age‐ and sex‐specific cut‐off points for adolescents and BMI ≥30 for young adults) using self‐reported heights and weights, adjusting for race/ethnicity, sex, parental education, and family income, accounting for complex sampling design. Results: The net effect of having an obese mother varied by race/ethnicity and was associated with a significantly earlier age at obesity onset (p = 0.0001) for whites [β= ?8.1 year, 95% confidence interval (CI), ?9.3; ?6.9)], blacks (β = ?10.8 years, 95% CI, ?12.4; ?9.2), Hispanics (β = ?7.0 years, 95% CI, ?9.2; ?4.8), and Asians (β = ?8.6 years, 95% CI, ?13.3; ?3.9). Earlier obesity onset (<18 years) was associated with increased severity at young adulthood (mean BMI, 36.0 ± 0.3 kg/m²) vs. onset after age 18 (mean BMI, 34.4 ± 0.2 kg/m²; p = 0.0001). There were no sex differences in the association of maternal obesity to age at obesity onset. Conclusions: Having an obese mother was associated with earlier age at obesity onset across all race/ethnic groups, particularly non‐Hispanic blacks. Early obesity onset has important health consequences because of its association with more severe adult obesity.     

Will All Americans Become Overweight or Obese? Estimating the Progression and Cost of the US Obesity Epidemic

We projected future prevalence and BMI distribution based on national survey data (National Health and Nutrition Examination Study) collected between 1970s and 2004. Future obesity-related health-care costs for adults were estimated using projected prevalence, Census population projections, and published national estimates of per capita excess health-care costs of obesity/overweight. The objective was to illustrate potential burden of obesity prevalence and health-care costs of obesity and overweight in the United States that would occur if current trends continue. Overweight and obesity prevalence have increased steadily among all US population groups, but with notable differences between groups in annual increase rates. The increase (percentage points) in obesity and overweight in adults was faster than in children (0.77 vs. 0.46-0.49), and in women than in men (0.91 vs. 0.65). If these trends continue, by 2030, 86.3% adults will be overweight or obese; and 51.1%, obese. Black women (96.9%) and Mexican-American men (91.1%) would be the most affected. By 2048, all American adults would become overweight or obese, while black women will reach that state by 2034. In children, the prevalence of overweight (BMI >/= 95th percentile, 30%) will nearly double by 2030. Total health-care costs attributable to obesity/overweight would double every decade to 860.7-956.9 billion US dollars by 2030, accounting for 16-18% of total US health-care costs. We continue to move away from the Healthy People 2010 objectives. Timely, dramatic, and effective development and implementation of corrective programs/policies are needed to avoid the otherwise inevitable health and societal consequences implied by our projections .