Optimizing weight gain in pregnancy to prevent obesity in women and children.

Pregnancy is now considered to be an important risk factor for new or persistent obesity among women during the childbearing years. High gestational weight gain is the strongest predictor of maternal overweight or obesity following pregnancy. A growing body of evidence also suggests that both high and low gestational weight gains are independently associated with an increased risk of childhood obesity, suggesting that influences occurring very early in life are contributing to obesity onset. In response to these data, the US Institute of Medicine (IOM) revised gestational weight gain guidelines in 2009 for the first time in nearly two decades. However, less than one third of pregnant women achieve guideline-recommended gains, with the majority gaining above IOM recommended levels. To date, interventions to optimize pregnancy weight gains have had mixed success. In this paper, we summarize the evidence from human and animal studies linking over-nutrition and under-nutrition in pregnancy to maternal and child obesity. In addition, we discuss published trials and ongoing interventions to achieve appropriate gestational weight gain as a strategy for obesity prevention in women and their children.

Changes in Physical Activity and Television Viewing From Pre-pregnancy Through Postpartum Among a Socioeconomically Disadvantaged Perinatal Adolescent Population.

STUDY OBJECTIVE: Adolescent pregnancy contributes to accelerated trajectories of adiposity and cardiometabolic diseases. Two potentially low-cost prevention strategies include promoting physical activity (PA) and limiting television (TV) viewing. Few studies have explored these behavior patterns in perinatal adolescents. This study sought to characterize PA and TV viewing in a socioeconomically disadvantaged perinatal adolescent population. DESIGN, SETTING, PARTICIPANTS, AND INTERVENTIONS: A cross-sectional, retrospective, 10-item survey was used to explore behavior patterns in 79 predominantly Black (86%) postpartum adolescents. MAIN OUTCOME MEASURES: Outcomes included self-reported changes in PA from pre-pregnancy through pregnancy, and 7-day recall of PA and TV viewing in postpartum. RESULTS: The majority of adolescents (66%) reported being active on ≥3 days/week in pre-pregnancy; however, many reported low PA (≤2 days/wk) in their first (59%), second (66%), and third (54%) trimesters. Adolescents who reported being active on ≥5 days/wk in pre-pregnancy (19%) experienced first trimester PA decline, which subsequently plateaued. This group remained the most active throughout pregnancy. In postpartum, over half (54%) of all adolescents reported low PA and irrespective of PA, spent considerable time watching TV (median = 1680.0 minutes, inerquartile range = 2940). CONCLUSION: Interventions promoting PA coupled with reducing TV viewing during pregnancy and in postpartum may benefit perinatal adolescents. The findings from this study suggest that PA history is a predictor of gestational PA, and low PA and high TV viewing in postpartum underscore the need for behavioral intervention. Conducting a brief assessment of PA history in early gestation may offer important insight.

Human prostatic cancer cells, PC3, elaborate mitogenic activity which selectively stimulates human bone cells.

Prostatic cancer typically produces osteoblastic metastases which are not attended by marrow fibrosis (i.e., osteoblast but not stromal fibroblast proliferation). In the present study we sought to test the hypothesis that prostatic cancer cells produce factor(s) which act selectively on human osteoblasts. Such a paracrine mechanism would explain the observed increase in osteoblasts, unaccompanied by an increase in marrow fibroblasts. To test this hypothesis we investigated the mitogenic activity released by the human prostatic tumor cell line, PC3. PC3 cells have been reported previously to produce mitogenic activity for cells that was relatively specific for rat osteoblasts compared to rat fibroblasts. However, the effects of this activity on human cells has not been examined previously. PC3-conditioned medium (CM) (5-50 micrograms CM protein/ml) stimulated human osteoblast proliferation by 200-950% yet did not stimulate human fibroblast proliferation [( 3H]thymidine incorporation). PC3 CM also increased cell numbers in human osteoblast but not fibroblast cell cultures. To determine whether the osteoblast-specific mitogenic activity could be attributed to known bone growth factors, specific assays for these growth factors were performed. PC3 CM contained 10 pg insulin-like growth factor (IGF) I, less than 2 pg IGF II, 54 pg basic fibroblast growth factor, and 16 pg transforming growth factor beta/microgram CM protein. None of these growth factors alone or in combination could account for the observed osteoblast-specific PC3 cell-derived mitogenic activity. Furthermore, when 5 micrograms/ml PC3 CM was tested in combination with maximally effective concentrations of either basic fibroblast growth factor, IGF I, IGF II, or transforming growth factor beta, it produced an additive effect suggesting that PC3 CM stimulates osteoblast proliferation by a mechanism independent of these bone mitogens. Biochemical characterization supported the hypothesis that the PC3 cell growth factor was unique from other growth factors. The PC3 growth factor did not bind to heparin and was resistant to acid as well as the reducing agent, dithiothreitol. Sephadex G-75 and fast protein liquid chromatography Mono S cation-exchange chromatography revealed the PC3-derived mitogen to be an Mr 26,000-30,000 basic protein. Therefore, we conclude that PC3 cells release a mitogen which exhibits higher specificity for human osteoblasts than human fibroblasts and is unique from other growth factors tested. Production of this mitogen by human prostatic carcinoma cells could play an etiological role in the intense osteoblast-specific stimulation that occurs at sites of bone metastases.

Initial weight loss goals: have they changed and do they matter?

OBJECTIVE: Nearly 20 years ago, participants in behavioural weight loss programmes reported goals that greatly exceeded the amount of weight typically produced by these programmes. Whether having unrealistic weight loss goals impacts weight loss or attrition is unclear. The intent of the current study was to revisit current weight loss goals and examine whether goals impact outcomes. METHODS: Adults (N = 308, BMI = 33.7 ± 4.2 kg/m2) participated in a 12-month behavioural weight management programme and completed questionnaires about their goals. RESULTS: Participants' weight loss goal was 19.8 ± 7.9% of their body weight, and 90.4% selected a goal ≥10%. Weight goals were not associated with weight loss at 3 (p = 0.75) or 12 months (p = 0.47), or from 3 to 12 months (p = 0.55). Weight loss goals were not related to attrition at 3 (p = 0.91) or 12 months (p = 0.86). Participants believed that weight reduction would positively impact their health and psychosocial functioning. CONCLUSION: Weight loss goals have decreased, but still greatly exceed what can be expected by most. Unrealistic goals, however, had no impact on weight loss or attrition. These results question the utility of counseling people with obesity to set more realistic weight loss goals, which is typically practiced in behavioural weight management.

Development of valid methods to measure insulin-like growth factors-I and -II in bone cell-conditioned medium.

A variety of human cells and biological fluids have been shown to produce or contain insulin-like growth factor (IGF)-specific binding proteins (BPs). The existence of these BPs in serum and conditioned medium of cell and organ cultures has complicated radioligand assays for measurement of IGFs. Various strategies have been proposed to avoid interference of BPs with these assays, including acid-ethanol precipitation of BPs and acid-gel filtration. Many of these procedures are time consuming, exhibit low recoveries, and do not completely eliminate BP artifacts. In this study we have investigated interference of inhibitory IGF-BP (In-IGF-BP) purified from bone cell-conditioned medium in an IGF-II RRA and IGF-I RIA and developed methods to neutralize In-IGF-BP artifacts in IGF assays. In the IGF-II RRA, purified In-IGF-BP competed for [125I]IGF-II binding to H-35 cells in a dose-dependent manner and, thus, increased the apparent value for IGF-II in the medium. Fifty percent inhibition of [125I]IGF-II binding to H-35 cells was seen at 12.2 and 5.7 ng/ml unlabeled IGF-II and IN-IGF-BP, respectively. In-IGF-BP also competed for [125I]IGF-I in the IGF-I RIA; however, the interference was much less in the IGF-I RIA compared to the IGF-II RRA. Fifty percent displacement of [125I]IGF-I binding was seen at 0.25 and 5 ng/ml unlabeled IGF-I and In-IGF-BP, respectively. Our approach to eliminate BP artifacts was as follows. We knew that In-IGF-BP showed comparatively equal binding affinities with both IGF-I and IGF-II, and binding of these ligands to cell receptors (IGF-II) and antibodies (IGF-I) was very specific (2% and 0.5% cross-reactivity for IGF-I and IGF-II, respectively). Therefore, in the IGF-I RIA we blocked the In-IGF-BP artifacts by adding an excess of IGF-II, and in the IGF-II RRA we blocked the In-IGF-BP artifacts by adding an excess of IGF-I. By incubating purified In-IGF-BP with different amounts of IGF-I, we found that 30-min preincubation of 5 ng In-IGF-BP with 10 ng IGF-I completely blocked BP artifacts in the IGF-II RRA. Similarly, preincubation of In-IGF-BP with IGF-II blocked BP artifacts in the IGF-I RIA.(ABSTRACT TRUNCATED AT 250 WORDS)

A randomized comparison of a commercially available portion-controlled weight-loss intervention with a diabetes self-management education program.

OBJECTIVE: This study examined the efficacy of a commercially available, portion-controlled diet (PCD) on body weight and HbA1c over 6 months in obese patients with type 2 diabetes. RESEARCH DESIGN AND METHODS: One-hundred participants with a mean±s.d. age of 55.6±10.6 year, body weight of 102.9±18.4 kg and HbA1c of 7.7±1.3% were randomly assigned to a 9-session group lifestyle intervention that included a PCD or to a 9-session group program of diabetes self-management education (DSME). Participants in the two groups were prescribed the same goals for energy intake (1250-1550 kcal per day) and physical activity (200 min per week). RESULTS: While both groups produced significant improvements in weight and HbA1c after 6 months of treatment, PCD participants lost 7.3 kg [95% confidence interval (CI): -5.8 to -8.8 kg], compared with 2.2 kg (95% CI: -0.7 to -3.7 kg) in the DSME group (P<0.0001). Significantly more PCD than DSME participants lost 5% of initial weight (54.0% vs 14.0%, P<0.0001) and 10% (26.0% vs 6.0%, P<0.0001). HbA1c declined by 0.7% (95% CI: -0.4 to -1.0%) in the PCD group, compared with 0.4% (95% CI: -0.1 to -0.7%) in DSME (P<0.026). Across both groups, larger weight losses were associated with greater reductions in HbA1c (r=0.52, P<0.0001). CONCLUSIONS: These findings demonstrate that a commercially available portion-controlled meal plan can induce clinically meaningful improvements in weight and glycemic control in obese individuals with type 2 diabetes. These data have implications for the management of obesity in primary care, as now provided by the Centers for Medicare and Medicaid Services.

Preventing excessive gestational weight gain: a systematic review of interventions.

Women who gain excessive weight during pregnancy have an increased risk of post-partum obesity, and retention of gestational weight gain (GWG) post birth is a strong predictor of maternal overweight/obesity a decade or more after the birth. The aim of the current review was to identify, and evaluate the effect of key variables designed to modify risk factors for excessive weight gain in pregnant women that have been targeted in interventions over the last decade. The 10 interventions focused primarily on behavioural changes in relation to physical activity and/or to eating. While six studies reported significantly less weight gain in the intervention women, only three showed that women in the intervention were significantly more likely to gain within recommended guidelines. GWG was reduced in only normal-weight, low-income, obese, or overweight women, or not at all. Only one study reported a reduction in GWG in women with body mass indexes spanning the normal, overweight and obese categories. The findings were inconsistent in relation to what factors need to be targeted in intervention programmes to reduce GWG. Consideration of psychological factors relevant to pregnancy, in addition to behavioural changes in relation to eating and physical activity, is suggested for future intervention studies.