Importance
Counseling and active behavioral interventions to limit excess gestational weight gain (GWG) during pregnancy may improve health outcomes for women and infants. The 2009 National Academy of Medicine (NAM; formerly the Institute of Medicine) recommendations for healthy GWG vary according to prepregnancy weight category.
Objective
To review and synthesize the evidence on benefits and harms of behavioral interventions to promote healthy weight gain during pregnancy to inform the US Preventive Services Task Force recommendation.
Data Sources
Ovid MEDLINE and the Cochrane Library to March 2020, with surveillance through February 2021.
Study Selection
Randomized clinical trials and nonrandomized controlled intervention studies focused on diet, exercise, and/or behavioral counseling interventions on GWG.
Data Extraction and Synthesis
Independent data abstraction and study quality rating with dual review.
Main Outcomes and Measures
Gestational weight–related outcomes; maternal and infant morbidity and mortality; harms.
Results
Sixty-eight studies (N = 25 789) were included. Sixty-seven studies evaluated interventions during pregnancy, and 1 evaluated an intervention prior to pregnancy. GWG interventions were associated with reductions in risk of gestational diabetes (43 trials, n = 19 752; relative risk [RR], 0.87 [95% CI, 0.79 to 0.95]; absolute risk difference [ARD], −1.6%) and emergency cesarean delivery (14 trials, n = 7520; RR, 0.85 [95% CI, 0.74 to 0.96]; ARD, −2.4%). There was no significant association between GWG interventions and risk of gestational hypertension, cesarean delivery, or preeclampsia. GWG interventions were associated with decreased risk of macrosomia (25 trials, n = 13 990; RR, 0.77 [95% CI, 0.65 to 0.92]; ARD, −1.9%) and large for gestational age (26 trials, n = 13 000; RR, 0.89 [95% CI, 0.80 to 0.99]; ARD, −1.3%) but were not associated with preterm birth. Intervention participants experienced reduced weight gain across all prepregnancy weight categories (55 trials, n = 20 090; pooled mean difference, −1.02 kg [95% CI, −1.30 to −0.75]) and demonstrated lower likelihood of GWG in excess of NAM recommendations (39 trials, n = 14 271; RR, 0.83 [95% CI, 0.77 to 0.89]; ARD, −7.6%). GWG interventions were associated with reduced postpartum weight retention at 12 months (10 trials, n = 3957; mean difference, −0.63 kg [95% CI, −1.44 to −0.01]). Data on harms were limited.
Conclusions and Relevance
Counseling and active behavioral interventions to limit GWG were associated with decreased risk of gestational diabetes, emergency cesarean delivery, macrosomia, and large for gestational age. GWG interventions were also associated with modest reductions in mean GWG and decreased likelihood of exceeding NAM recommendations for GWG.
The prevalence of overweight and obesity is increasing among women of childbearing age and pregnant women in the US, similar to trends observed in nonpregnant populations. Data suggest that obesity rates during pregnancy in the US increased from 13% in 1993 to 24% in 2015, and in the same year, nearly half of all women entered pregnancy with a body mass index (BMI) category of overweight (24%) or obese (24%).1,2
Gestational weight gain is usually defined as change in weight measured before pregnancy (prepregnancy) or during the first trimester to weight measured at the end of pregnancy (eg, prior to delivery). Prepregnancy BMI is independently associated with many adverse pregnancy outcomes. Many observational studies report strong associations between elevated prepregnancy BMI and adverse pregnancy outcomes.3-11 In 2009, the National Academy of Medicine (NAM; formerly the Institute of Medicine) recommended that women begin pregnancy with a normal BMI and made recommendations for healthy gestational weight gain (GWG), which varied according to prepregnancy weight category (25-35 lb for normal weight, or BMI 18.5-24.9 [calculated as weight in kilograms divided by height in meters squared]; 15-25 lb for overweight, or BMI 25.0-29.9; and 11-20 lb for obese, or BMI ≥30.0).12 Approaches to achieving recommended GWG include preconception counseling and weight loss for women with overweight or obesity; counseling about healthy weight gain during pregnancy; adherence to NAM recommendations for GWG; and/or providing women at risk of excess GWG with lifestyle interventions.13 Guidelines also note that abnormally high or low BMI and excessive GWG is associated with pregnancy complications. In response to NAM and other recommendations on GWG, there has been a proliferation of randomized clinical trials on the effect of interventions on GWG published in the last decade.14,15
The US Preventive Services Task Force (USPSTF) has not previously made a recommendation on healthy weight gain during pregnancy. This review synthesizes current evidence to inform a USPSTF recommendation on this topic.
This review addressed 3 key questions (KQs) (Figure 1) examining the effectiveness of counseling and active behavioral interventions to promote healthy weight gain during pregnancy on health-related outcomes (KQ1), weight-related outcomes (KQ2); and potential harms of interventions (KQ3). Full methods, including data analysis methods, are available in the full evidence report.17
Data Sources and Searches
Searches of Ovid MEDLINE, the Cochrane Central Register of Controlled Trials, and the Cochrane Database of Systematic Reviews through February 2021 (eMethods 1 in the Supplement). Reference list review of relevant systematic reviews supplemented the searches. Ongoing surveillance was conducted to identify major studies published since March 2020 that may affect the conclusions or understanding of the evidence and related USPSTF recommendation. The last surveillance, conducted on February 5, 2021, identified no additional studies. All searches were limited to articles published in English.
Two investigators independently reviewed titles, abstracts, and full-text articles using predefined eligibility criteria (eTable 1 in the Supplement). Populations included adolescent and adult women who were pregnant or planning a pregnancy, with normal weight (BMI of 18.5-24.9), overweight (BMI of 25-29.9) or obesity (BMI ≥30), based on prepregnancy weight categories as defined by the World Health Organization. Women with low prepregnancy BMI (underweight) were outside the scope of this review. Studies of interventions vs controls (eg, usual care, attention control, minimal intervention) were included (eTable 7 in the Supplement). Interventions were categorized as active (consisting of a structured, physical element that could include a counseling component [eg, supervised exercise programs, prescribed exercise or dietary programs, or intensive weight management] or counseling only. Intervention intensity was categorized as low (<2 contacts during the intervention period), moderate (3-11 contacts), or high (≥12 contacts). Outcomes were classified as weight-related intermediate outcomes (GWG, exceeding or adhering to NAM GWG recommendations, and postpartum weight loss or retention) or health outcomes (maternal morbidity or mortality, infant morbidity or mortality). Harms were anxiety, depression, maternal musculoskeletal injuries, stigma, and those related to insufficient weight gain, including infants small for gestational age. Randomized clinical trials (RCTs) and nonrandomized controlled intervention studies were considered for harms; only RCTs were eligible for analysis in all other outcomes.
Data Abstraction and Quality Rating
One investigator abstracted details about each study’s design, patient population, setting, interventions, analysis, follow-up, and results. A second investigator reviewed abstracted data for accuracy. Two investigators independently assessed the quality of each study as good, fair, or poor using predefined criteria developed by the USPSTF (eMethods 2 in the Supplement).16 Discrepancies were resolved through consensus. In accordance with the USPSTF Procedure Manual, poor-quality studies with critical methodological limitations were excluded.16
Data were synthesized separately for each KQ by outcome. Only RCTs were considered for meta-analysis. Nonrandomized controlled intervention studies were not pooled; these studies did not affect the findings that are described in the full report. For both continuous and dichotomous outcomes, random-effects meta-analyses were conducted using the profile likelihood method using Stata version 14 (StataCorp).
For continuous data, meta-analysis of RCTs was conducted to combine the mean difference between the intervention and the control groups. For mean GWG, the mean difference adjusted for baseline characteristics was used in the meta-analysis when available; otherwise, the mean difference in weight change from baseline to follow-up was used. Because imbalance in baseline weight was generally not observed, sensitivity analysis was not conducted using the difference in follow-up weights. If necessary, mean weight change was calculated based on reported baseline and follow-up weights; when not reported, the correlation between baseline and follow-up weights was assumed to be the average correlation calculated from studies that reported this information. Missing standard deviations were imputed, if necessary, by assuming the same coefficient of variation at baseline and follow-up; the standard deviations at baseline and follow-up were similar in studies that reported both. For dichotomous outcomes with at least 5 trials, sufficient sample size, and comparable outcomes, risk ratios were combined across eligible studies.
Stratified analyses were conducted when sufficient data were available on BMI category (normal, overweight, obese, overweight or obese combined, or mixed BMI populations), GWG assessment time point (28 weeks, 34-36 weeks, 36 weeks up to delivery, and at delivery), intervention type (counseling-only or active), intervention intensity (low, moderate, or high), and study quality (good or fair). Statistical heterogeneity was assessed with the Cochran Q-test and the I2 statistic to detect the proportion of total variability in point estimates.18 The P value for subgroup interaction was calculated to test for subgroup differences. Interactions between interventions and sociodemographic characteristics could not be assessed because of sparse data. Results were considered statistically significant if the P value was less than .05, based on 2-sided testing.
A total of 8511 unique citations and 845 full-text articles were reviewed. Across all KQs, 64 RCTs (N = 24 829)19-82 and 4 nonrandomized controlled intervention studies (N = 960)83-86 met criteria for this systematic review (Figure 2).
Across all studies, sample sizes ranged from 50 to 2261 (N = 25 789; median n = 230). Mean sample ages ranged from 18.6 years to 33.8 years (median, 30.4 [SD, 2.8] years), with study eligibility criteria ranging from 14 to 49 years (eTable 2 in the Supplement). Twenty-eight of 68 included studies (41%) enrolled more than 20% of patients from diverse backgrounds, including those who were socioeconomically disadvantaged, racial or ethnic minorities, rural populations, or others defined by the National Institute on Minority Health and Health Disparities as populations adversely affected by disparities.87 There were no studies exclusively of pregnant adolescents or women with advanced maternal age. Studies enrolled women in 3 prepregnancy BMI categories: mixed (all BMI categories), overweight and obesity only, and obesity only.
All studies evaluated pregnancy interventions except for 1 study of a prepregnancy intervention; 1 study included a preconception component.70,88 The majority of interventions were counseling-only (45 studies),20-24,31-36,38-40,46-48,51-58,60,62,64-70,74-79,81,82,84-86,89-99 and were rated as moderate-intensity (23 studies)20,22,31,33,38,39,46,47,51-54,57,58,62,69,70,74-76,82,84,85,89,91,93-96 or high-intensity (34 studies)19,21,25-30,34,37,40-45,48-50,56,59,61,63,66,67,71-73,77-81,83,86,90,92,98-105 (eTable 3 in the Supplement). The remaining 22 studies19,25-30,37,41-45,49,50,59,61,63,71-73,80,83,100-105 used active interventions (eTable 3 in the Supplement).
The duration of follow-up ranged from 14 weeks to 12 months postpartum; the majority (77%) of studies enrolled pregnant women early in their second trimester and followed them up until at least 36 weeks’ gestation (eTable 4 in the Supplement). Fifteen RCTs and 1 nonrandomized controlled intervention study were rated good-quality, and 49 RCTs and 3 nonrandomized controlled intervention studies were rated fair-quality (eTables 5 and 6 in the Supplement). Given the nature of the interventions and comparisons, many participants and clinicians could not be blinded. Methodological limitations included unclear reporting of randomization and allocation concealment (eMethods 2 in the Supplement).
Benefits for Health Outcomes
Key Question 1a. Do interventions to limit excess gestational weight gain improve health outcomes among pregnant women and their infants?
Key Question 1b. Do interventions to reduce prepregnancy weight in women who are overweight or obese improve health outcomes among women who become pregnant and their infants?
Key Question 1c. Does the effectiveness of these interventions differ by age, race/ethnicity, socioeconomic status, parity, smoking status, or BMI category?
Forty-three trials (n = 19 752) of counseling-only and active interventions vs controls reported on gestational diabetes (Table 1; eFigure 1 in the Supplement).20,24,26,28-34,36-39,41,44,46,48-53,55-60,62-65,67,69-74,78-80,82 Gestational diabetes criteria varied among studies and included criteria based on country-specific guidelines (15 trials)29,31,39,44,49-51,53,55,59,65,67,72,80,82; International Association of Diabetes and Pregnancy Study Groups criteria using the 1-step approach to diagnosis with a 75-g glucose load (18 trials)20,24,30,33,34,37,38,41,46,52,56,60,63,69,70,73,74,78; and review of medical records (8 trials).28,36,57,58,62,64,71,79 Two trials used unclear criteria to define gestational diabetes.26,32
Gestational weight gain interventions were associated with decreased risk of gestational diabetes vs control (43 trials; relative risk [RR], 0.87 [95% CI, 0.79 to 0.95]; I2 = 16.4%; absolute risk difference [ARD], −1.6% [95% CI, −2.5% to −0.7%]) (Table 1; eFigure 1 in the Supplement). In stratified analyses, there were no statistically significant interactions between effects of GWG interventions on likelihood of gestational diabetes and BMI category, intervention type, or intensity.
Twenty-eight RCTs (n = 14 875) reported rates of gestational hypertension (Table 1; eFigure 2 in the Supplement).24,28,31-34,38,39,41,51,52,55-58,60,62-64,67,69-71,73,77,79,80,82 Gestational hypertension was defined as persistent or repeated measures of blood pressure greater than or equal to 140/90 mm Hg after 20 weeks’ gestation (a definition generally consistent with the US guideline).106
Gestational weight gain interventions were not associated with reduced likelihood of gestational hypertension compared with controls (28 trials; RR, 0.87 [95% CI, 0.70 to 1.04]; I2 = 32.5%; ARD, −0.8% [95% CI, −1.9% to 0.2%]) (Table 1; eFigure 2 in the Supplement). However, stratified analysis showed statistically significant interactions between effects of GWG interventions on risk of gestational hypertension and intervention type and intensity (P<.001 for interactions) but not BMI category. There were statistically significant effects in the active (7 trials; RR, 0.60 [95% CI, 0.41 to 0.82]; I2 = 0%; P < .001) and high-intensity (12 trials; RR, 0.69 [95% CI, 0.50 to 0.91]; I2 = 23.5%; P = .006) intervention subgroups.
Forty-six RCTs (n = 19 573) reported effects of GWG interventions on rates of cesarean delivery (Table 1; eFigure 3 in the Supplement).20,22-24,26,28-34,36-40,44,49-52,55-59,61-65,67,69,71-73,75,77-80,82,100 Thirty-four trials20,22,26,28-30,33,34,36,38-41,44,49-52,56-59,61-65,67,69,71,73,78,79,82 reported on the outcome of cesarean delivery not specified as emergency or elective (n = 15 908); 12 trials24,31,32,37,44,52,55,72,75,77,80 specified elective cesarean delivery (n = 6222); and 14 trials24,31,32,37,38,44,52,55,56,67,72,75,77,80 reported emergency cesarean delivery (n = 7520), though only 1 trial78 reported indications for emergency cesarean delivery (eTable 4 in the Supplement).
Gestational weight gain interventions were not associated with decreased likelihood of cesarean delivery (not specified as emergency or elective) vs controls (34 trials; RR, 0.98 [95% CI, 0.91 to 1.04]; I2 = 10.8%; ARD, −0.7% [95% CI, −2.4% to 0.8%]) (Table 1; eFigure 3 in the Supplement). However, GWG interventions were associated with reduced risk of emergency cesarean delivery (14 trials; RR, 0.85 [95% CI, 0.74 to 0.96]; I2 = 0%; ARD, −2.4% [95% CI, −4.2% to −0.3%]) (Table 1). A separate analysis was not conducted for elective cesarean delivery alone because of lack of reporting on indication. In stratified analyses, there were no statistically significant interactions between associations of GWG interventions with likelihood of cesarean delivery and BMI category, intervention type, or intensity.
Twenty-seven RCTs (n = 17 538) reported effects of GWG interventions on rates of preeclampsia (Table 1; eFigure 4 in the Supplement).20,24,28,31,36,38,39,44,51-53,55,57,58,62-64,67,69,70,72,73,77,79,80,82 Most studies defined preeclampsia as gestational hypertension accompanied by proteinuria (greater than 300 mg/24 h). The remaining 6 trials57,58,62-64,82 reported preeclampsia as clinically distinct from gestational hypertension but did not provide a formal definition.
Interventions for GWG were not associated with reduced risk of preeclampsia vs controls (27 trials; RR, 0.98 [95% CI, 0.84 to 1.13]; I2 = 0%; ARD, 0.1% [95% CI, −0.6% to 0.5%]) (Table 1; eFigure 4 in the Supplement). In stratified analyses, there were no statistically significant interactions between effects of GWG interventions on likelihood of preeclampsia and BMI category, intervention type, or intensity.
There were no effects of GWG interventions on the remaining maternal outcomes (postpartum hemorrhage, perineal trauma, or maternal death); events were uncommon and estimates were imprecise. See the full report for details.17
Twenty-five trials (n = 13 990) evaluated effects of GWG interventions on risk of macrosomia. Macrosomia was defined as term infants weighing more than 4 kg (21 RCTs22,25,27,28,30,33,38,53,57,59,62-64,67,71-73,77,79,80,107) or 4.5 kg (6 RCTs),24,37,38,51-53 with 2 trials38,53 reporting outcomes using both definitions (eTable 4 in the Supplement).
Gestational weight gain interventions were associated with decreased risk of macrosomia vs controls (25 trials; RR, 0.77 [95% CI, 0.65 to 0.92]; I2 = 38.3%; ARD, −1.9% [95% CI, −3.3% to −0.7%]) (Table 2; eFigure 5 in the Supplement). Stratified analyses showed statistically significant interactions between effect of GWG interventions on risk of macrosomia and intervention intensity (P = .03 for interaction) but not BMI category or intervention type. Statistically significant effects were demonstrated in the high-intensity intervention subgroup (14 trials; RR, 0.65 [95% CI, 0.49 to 0.84]; I2 = 37%).
Large for Gestational Age
Twenty-six RCTs (n = 13 000) reported the outcome of large for gestational age (LGA) infants, defined as birth weight greater than the 90th percentile for gestational age (Table 2; eFigure 6 in the Supplement).20,24,32-34,37-40,44,49,50,52,53,56,58,65,67,69,72-74,77-80 Gestational weight gain interventions were associated with decreased risk of LGA (26 trials; RR, 0.89 [95% CI, 0.80 to 0.99]; I2 = 0%; ARD, −1.3% [95% CI, −2.3% to −0.3%]) (Table 2; eFigure 6 in the Supplement). In stratified analyses, effect estimates of GWG interventions on likelihood of LGA did not differ by BMI category, intervention type, or intensity.
Thirty-three RCTs (n = 16 974) reported on the outcome of preterm birth (Table 2; eFigure 7 in the Supplement). Preterm birth was defined as delivery at less than 37 weeks in 24 trials20,22,24,25,27-30,34,36-40,52,56,57,67,69,73,77-79,102 and less than 36 weeks in 4 trials62-64,71; 5 trials did not report a definition (eTable 4 in the Supplement).33,44,60,65,75 Gestational weight gain interventions were not associated with a lower risk of preterm birth (33 trials; RR, 0.93 [95% CI, 0.81 to 1.07]; I2 = 2.2%; ARD, −0.2% [95% CI, −1.1% to 0.7%]) (Table 2; eFigure 7 in the Supplement). In stratified analyses, effect estimates of GWG interventions on likelihood of preterm birth did not differ by BMI category, intervention type, or intensity.
There were no associations of GWG interventions with the remaining infant outcomes (respiratory distress syndrome, shoulder dystocia, neonatal intensive care unit admission, neonatal death, or infant growth during the first year); events were uncommon and estimates were imprecise. See the full report for details.17
Benefits for Weight Outcomes
Key Question 2a. Do interventions to limit excess gestational weight gain reduce gestational weight gain, postpartum weight retention, or obesity-related adverse perinatal conditions among pregnant women and their infants?
Key Question 2b. Do interventions to reduce prepregnancy weight in women who are overweight or obese improve weight outcomes or reduce obesity-related adverse perinatal conditions among women who become pregnant and their infants?
Key Question 2c. Does the effectiveness of these interventions differ by age, race/ethnicity, socioeconomic status, parity, smoking status, or BMI category?
Fifty-five trials evaluated effects of GWG interventions on mean GWG (Table 3, Figure 3).19,20,22-31,33-41,43,45-53,55-60,62-68,71-76,78-82 Gestational weight gain interventions were associated with reduced GWG during pregnancy of approximately 1 kg vs controls (55 trials; n = 20 090; pooled mean difference [MD], −1.02 kg [95% CI, −1.30 to −0.75]; I2 = 60.3%) (Table 3, Figure 3).
High-intensity interventions were associated with greater effects on GWG (28 trials; MD, −1.47 kg [95% CI, −1.78 to −1.22]; I2 = 13.0%) than were moderate-intensity (18 trials; MD, −0.32 kg [95% CI, −0.71 to −0.04]; I2 = 17.6%) or low-intensity (9 trials; MD, −0.64 kg [94% CI, −1.44 to 0.02]; I2 = 48.4%; P < .001 for interaction) interventions. Subgroup analyses according to BMI category demonstrated slightly higher effect estimates among women with obesity (18 trials; MD, −1.63 [95% CI, −2.45 to −0.91]; I2 = 63.0%) compared with other BMI categories (overweight, 10 trials; MD, −0.89 [95% CI, −1.54 to −0.32]; I2 = 15.5%; overweight and obesity combined, 20 trials; MD, −0.90 [95% CI, −1.38 to −0.46]; I2 = 31.1%; mixed weight categories, 28 trials; MD, −0.81 [95% CI, −1.16 to −0.46]; I2 = 60.7%; or normal weight, 8 trials; MD, −0.48 [95% CI, −96 to −0.21]; I2 = 0.0%) (Table 3). There was no association between effects of GWG interventions and overall prepregnancy BMI category (Table 3, Figure 3).
In stratified analyses, the were no statistically significant interactions between effects of GWG interventions on mean GWG and intervention type, study quality, or timing of weight gain assessment.
Exceeding NAM Recommendations for GWG
Thirty-nine RCTs (n = 13 955) reported the outcome of GWG in excess of NAM recommendations (Table 3; eFigure 8 in the Supplement).21-23,25,27-30,32,34-37,41,43,48-50,52,54,55,57,59,61-66,68,71,74-76,78-81,95 Interventions were associated with decreased likelihood of gaining weight in excess of NAM recommendations (39 trials; RR, 0.83 [95% CI, 0.77 to 0.89]; I2 = 63.8%; ARD, −7.6% [95% CI, −11.0% to −4.6%]) (Table 3; eFigure 8 in the Supplement). Stratified analysis showed statistically significant interactions between effects of GWG interventions on excess weight gain and intervention type (P = .003) and intensity (P<.001 for interaction) but not for BMI category. There were statistically significant effects in the active (15 trials; RR, 0.73 [95% CI, 0.67 to 0.80]; I2 = 0%) and high-intensity (22 trials; RR, 0.74 [95% CI, 0.69 to 0.79]; I2 = 0%) intervention subgroups.
Adherence to NAM Recommendations for GWG
Nineteen RCTs (n = 5835) reported on the outcome of rates of adherence to GWG guidelines by prepregnancy BMI category according to ranges recommended by the NAM (ie, neither gaining excessive weight nor failing to gain sufficient weight (Table 3; eFigure 9 in the Supplement).23,29,32,36,38,43,55,58,60-62,64,68,71,74,75,77,79,80 There was no difference between GWG interventions and controls in likelihood of adherence to NAM recommendations for GWG (19 trials; RR, 1.10 [95% CI, 0.89 to 1.35]; I2 = 84.3%), although statistical heterogeneity was substantial (Table 3; eFigure 9 in the Supplement). In stratified analyses, there were not statistically significant interactions between effects GWG interventions and adherence to NAM recommendations by BMI category, intervention type, or intensity.
Postpartum Weight Retention
Thirteen RCTs (n = 4841) evaluated the effects of GWG interventions on postpartum weight retention (PPWR) (Table 3; eFigure 10 in the Supplement). Gestational weight gain interventions were associated with statistically significantly less PPWR at 12 months (10 trials; MD, −0.63 kg [95% CI, −1.44 to −0.01]; I2 = 65.5%)22,90,92-94,96,97,99,101,102 but not at 6 months postpartum (3 trials; MD, −0.85 kg [95% CI, −3.67 to 0.81]; I2 = 70.6%)62,92,105 or less than 6 months postpartum (9 trials; MD, −0.81 kg [95% CI, −2.40 to 0.55]; I2 = 84.4%).42,64,65,82,91,93,94 In stratified analyses, effect estimates of GWG interventions on likelihood of PPWR did not differ by BMI category at follow-up time of up to 6 months or 12 months.
Key Question 3a. What are the harms of interventions to limit excess gestational weight gain among pregnant women and their infants?
Key Question 3b. What are the harms of interventions to reduce prepregnancy weight among women who are overweight or obese?
Key Question 3c. Do the harms of these interventions differ by age, race/ethnicity, socioeconomic status, parity, smoking status, or BMI category?
Evidence on harms associated with GWG interventions was very limited, with most studies not reporting harms (Table 4; eTable 4 in the Supplement). In general, there were no serious harms related to the interventions, including depression or anxiety, and most trials noted no differences between groups in the rates of adverse events, including SGA.
The evidence from this report is summarized in Table 4. Evidence on effects of GWG interventions on maternal outcomes was most robust for gestational diabetes, gestational hypertension, preeclampsia, and cesarean delivery. Active or counseling-only GWG interventions were associated with decreased risk of GDM and emergency cesarean delivery. While there was no overall association between GWG interventions and risk of gestational hypertension, stratified analyses indicated that high-intensity and active interventions were associated with decreased rates of gestational hypertension, suggesting a possible dose effect. There was no association of GWG interventions with preeclampsia, a multisystem syndrome with less clear associations with BMI.108 Evidence on effects of GWG interventions on infant outcomes was most robust for macrosomia, LGA, and preterm birth. Gestational weight gain interventions were associated with decreased risk of macrosomia and LGA.
Gestational weight gain interventions were associated with slightly less overall gestational weight gain vs controls. The effects of interventions on GWG were greater in trials of high-intensity interventions compared with moderate- or low-intensity interventions. The effects of GWG interventions on gestational weight gain also were greater in women in the obese and overweight categories compared with women with normal prepregnancy BMI, although the overall interaction between BMI and GWG was not statistically significant.
Gestational weight gain interventions were associated with decreased likelihood of weight gain in excess of NAM recommendations vs controls, with some evidence of a dose-response relationship. The findings support the obesity and behavioral intervention literature that demonstrates more promising effects of interventions that offer more frequent patient contact.109,110
There was no significant association between GWG interventions and likelihood of adhering to NAM recommendations for GWG. The discrepancy between the effects of GWG interventions on exceeding guidelines vs adhering to guidelines could be attributable to an increased likelihood of some women not adhering to NAM recommendations because they did not gain enough weight. However, data were not available to verify this, as most studies did not report the proportion of women with less GWG than recommended. Gestational weight gain interventions were associated with effects on PPWR at 12 months; effects on PPWR at 6 months were not statistically significant, but data were more limited and imprecise. Evidence on harms of GWG interventions was limited, but there was no association with increased risk of small for gestational age and no indication of serious harms.
Trials should be designed to examine the effects of weight loss interventions in diverse populations stratified by BMI and report outcomes according to population categories, including adolescents and women with advanced maternal age. Additional studies examining the effect of prepregnancy weight loss interventions are also an important next step.
This review had several limitations. First, data were often not available for important groups defined by race or ethnicity, age (eg, adolescents, advanced maternal age), or socioeconomic status; study results were not stratified by these factors. No study was conducted exclusively in pregnant adolescents or women of advanced maternal age, and only 1 study conducted a weight loss intervention prior to pregnancy. Trials did not address issues of health care disparities, access to prenatal care (or lack thereof), or feasibility of interventions in settings where access to care is limited or arrival to care is delayed. More studies of underrepresented populations who may have higher risk of adverse outcomes are needed.111,112
Second, there was statistical heterogeneity in some pooled analyses due to variability in intervention components, comparison groups, and timing and method of assessment of outcomes, but results were consistent with stratified analyses. Because of anticipated heterogeneity, random-effects models were used, which results in wider confidence intervals than fixed-effects models when statistical heterogeneity is present, reflecting the greater uncertainty in estimates. In addition, the profile-likelihood method was used for conducting meta-analyses, which may be more reliable when statistical heterogeneity is present.113
Third, there were methodological limitations in the literature. Poor-quality trials were excluded because of serious flaws; results were similar in analyses stratified by study quality. Trials primarily focused on the effects of GWG interventions on mean GWG, an intermediate outcome, with less evidence on the direct effects of GWG interventions on maternal and infant health outcomes. Some stratified analyses were underpowered to evaluate subgroup effects. Additionally, some trials enrolled mixed populations of women with different BMI categories, limiting the usefulness of stratified analyses. Other factors could define intervention intensity (eg, session duration or frequency or type of intervention) but were difficult to categorize. Fourth, evidence on harms was limited, particularly for effects on psychological well-being and quality of life.
Counseling and active behavioral interventions to limit GWG were associated with decreased risk of gestational diabetes, emergency cesarean delivery, macrosomia, and large for gestational age. Gestational weight gain interventions were also associated with modest reductions in mean GWG and decreased likelihood of exceeding NAM recommendations for GWG.
Corresponding Author: Amy G. Cantor, MD, MPH, Oregon Health & Science University, 3181 SW Sam Jackson Park Rd, Mail Code BICC, Portland, OR 97239 (cantor@ohsu.edu).
Accepted for Publication: March 5, 2021.
Author Contributions: Dr Cantor had full access to all of the data in the study and takes responsibility for the integrity of the data and the accuracy of the data analysis.
Concept and design: Cantor, Jungbauer, McDonagh, Marshall, LeBlanc, Chou.
Acquisition, analysis, or interpretation of data: All authors.
Drafting of the manuscript: Cantor, Jungbauer, McDonagh, Blazina, Marshall, Weeks, Fu, Chou.
Critical revision of the manuscript for important intellectual content: Cantor, Jungbauer, Blazina, Marshall, LeBlanc, Chou.
Statistical analysis: Cantor, Jungbauer, Blazina, Marshall, Fu.
Obtained funding: Cantor, Chou.
Administrative, technical, or material support: Cantor, Jungbauer, McDonagh, Blazina, Marshall, Weeks.
Supervision: Cantor, Jungbauer, McDonagh, Chou.
Conflict of Interest Disclosures: None reported.
Funding/Support: This research was funded under contract HHSA 290201500009-I, Task Order 14, from the Agency for Healthcare Research and Quality (AHRQ), US Department of Health and Human Services, under a contract to support the US Preventive Services Task Force (USPSTF).
Role of the Funder/Sponsor: Investigators worked with USPSTF members and AHRQ staff to develop the scope, analytic framework, and key questions for this review. AHRQ had no role in study selection, quality assessment, or synthesis. AHRQ staff provided project oversight, reviewed the report to ensure that the analysis met methodological standards, and distributed the draft for peer review. Otherwise, AHRQ had no role in the conduct of the study; collection, management, analysis, and interpretation of the data; and preparation, review, or approval of the manuscript findings. The opinions expressed in this document are those of the authors and do not reflect the official position of AHRQ or the US Department of Health and Human Services.
Additional Contributions: We thank the following individuals for their contributions to this project: AHRQ Medical Officer Iris Mabry-Hernandez, MD, MPH; EPC staff member Tracy Dana, MLS; and the USPFTF. We also acknowledge past and current USPSTF members who contributed to topic deliberations. The USPSTF members, external reviewers, and federal partner reviewers did not receive financial compensation for their contributions.
Additional Information: A draft version of this evidence report underwent external peer review from 4 federal partners representing the Centers for Disease Control and Prevention, US Food and Drug Administration, and the National Institutes of Health and 3 content experts (Patrick Catalano, MD [Tufts University School of Medicine]; Rebecca Clifton, PhD [Milken Institute School of Public Health, George Washington University]; and Alan Peaceman, MD [Feinberg School of Medicine, Northwestern University]). Comments were presented to the USPSTF during its deliberation of the evidence and were considered in preparing the final evidence review.
Editorial Disclaimer: This evidence report is presented as a document in support of the accompanying USPSTF Recommendation Statement. It did not undergo additional peer review after submission to JAMA.
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