On 2017 May 11, Alexis Frazier-Wood commented:

The key points section of this article, the purpose of which is to isolate the ‘key conclusion and implication based on the primary [study] finding(s)’, states that: “A randomized intervention that increased breastfeeding intensity was not associated with reduced obesity”. This is a selective interpretation of the study data on weight status, which show that maternal participation in the PROBIT intervention (which increased breastfeeding exclusivity and duration) was 1. associated with increased odds of offspring having adolescent overweight/obesity (odds ratio=1.14; 1.02-1.28) but 2. not associated having adolescent obesity (odds ratio=1.09; 0.92-1.29), although it can be seen that both associations were in the same direction. Body mass index (BMI) was also higher in the children from the intervention group by adolescence (mean difference Δ= 0.21, 0.06-0.36).

The reasons for the difference in significance (according to the specified alpha) between the results specifying BMI and overweight/obesity as outcomes vs. those specifying obesity likely arise from the differential power for the two outcomes. The relationship of breastfeeding to obesity vs. overweight/obesity had less power, largely due to the lower number of cases (obesity N=589 vs. overweight/obesity N=1868). Simulations in R v3.3.3, suggest the power for has “overweight/obesity” vs. has “obesity” was around 74% vs. 17%. These simulations did not account for the intention to treat procedure nor the correction for data clustering (since not enough data on e.g. ICC correlations was available), but due to the effects of these on power being equal across outcomes an assessment of relative power can be made. In addition, the alternative hypothesis (breastfeeding -> overweight/obesity) was formally tested, but the null hypothesis (breastfeeding ≠ obesity) was not, given the absence of any equivalence testing. Positive associations between breastfeeding and offspring adiposity have been reported before, but have not reached statistical significance (see Cope MB, 2008). Therefore, while the association of increased breastfeeding with significantly increased odds of overweight/obesity represents a novel finding which needs to be subjected to replication, without recourse to empirically stronger results, omitting this from the overall interpretation of the study in favor of a lesser powered, untested hypothesis represents a form of bias.

While the manifestation of bias in the article may be small, its effect can still be pernicious. Several organizations, including the World Health Organization and the American Heart Association, state that breastfeeding provides protection against offspring obesity (see WHO report and AHA Fact Sheets). However, this lacks strong statistical justification, given that any inverse associations between breastfeeding and offspring obesity are derived from observational designs and likely to reflect confounding (Kramer MS, 2002), and that probability theory suggests that the breastfeeding-offspring obesity data in the literature as a whole reflect one of two situations: (1) publication bias, or (2) a true positive association between breastfeeding and offspring obesity in at least one other published sample (Cope MB, 2008). That is not to deny that there may be a number of valid reasons to support breastfeeding, not related to obesity (see e.g. APA report). But perhaps it is this which has lead to a problem with ‘white hat bias’ in the breastfeeding-obesity literature - a term coined by Cope and Allison to denote ‘bias leading to the distortion of research based-based information in the service of what may be perceived as righteous ends (Cope MB, 2010). One such reason to support breastfeeding is to enable personal choice for parents and caregivers. However, this is incompatible with the practice of giving misleading information on the benefits of breastfeeding which actually deprives caregivers of their right to make informed decisions about feeding infants.

This is a problematic situation, and needs to be corrected. The causes are unknown, but distorted presentation of data has been identified in multiple reports of randomized clinical trials, often in only one section e.g. the abstract (Boutron I, 2010), and often in the secondary literature, such as press releases (Cope MB, 2010). Therefore all authors need express conclusions with great clarity and consistency, and not selectively include and exclude results without recourse to relative empirical strengths. To be accurate in reporting in this article, the results of this study as a whole are most consistent with either (1) an association between breastfeeding and increased offspring overweight/obesity, or (2) a lack of empirical strength in this study to contribute to the debate on whether there is an association between the two constructs.

On 2017 May 11, Alexis Frazier-Wood commented:

The key points section of this article, the purpose of which is to isolate the ‘key conclusion and implication based on the primary [study] finding(s)’, states that: “A randomized intervention that increased breastfeeding intensity was not associated with reduced obesity”. This is a selective interpretation of the study data on weight status, which show that maternal participation in the PROBIT intervention (which increased breastfeeding exclusivity and duration) was 1. associated with increased odds of offspring having adolescent overweight/obesity (odds ratio=1.14; 1.02-1.28) but 2. not associated having adolescent obesity (odds ratio=1.09; 0.92-1.29), although it can be seen that both associations were in the same direction. Body mass index (BMI) was also higher in the children from the intervention group by adolescence (mean difference Δ= 0.21, 0.06-0.36).

The reasons for the difference in significance (according to the specified alpha) between the results specifying BMI and overweight/obesity as outcomes vs. those specifying obesity likely arise from the differential power for the two outcomes. The relationship of breastfeeding to obesity vs. overweight/obesity had less power, largely due to the lower number of cases (obesity N=589 vs. overweight/obesity N=1868). Simulations in R v3.3.3, suggest the power for has “overweight/obesity” vs. has “obesity” was around 74% vs. 17%. These simulations did not account for the intention to treat procedure nor the correction for data clustering (since not enough data on e.g. ICC correlations was available), but due to the effects of these on power being equal across outcomes an assessment of relative power can be made. In addition, the alternative hypothesis (breastfeeding -> overweight/obesity) was formally tested, but the null hypothesis (breastfeeding ≠ obesity) was not, given the absence of any equivalence testing. Positive associations between breastfeeding and offspring adiposity have been reported before, but have not reached statistical significance (see Cope MB, 2008). Therefore, while the association of increased breastfeeding with significantly increased odds of overweight/obesity represents a novel finding which needs to be subjected to replication, without recourse to empirically stronger results, omitting this from the overall interpretation of the study in favor of a lesser powered, untested hypothesis represents a form of bias.

While the manifestation of bias in the article may be small, its effect can still be pernicious. Several organizations, including the World Health Organization and the American Heart Association, state that breastfeeding provides protection against offspring obesity (see WHO report and AHA Fact Sheets). However, this lacks strong statistical justification, given that any inverse associations between breastfeeding and offspring obesity are derived from observational designs and likely to reflect confounding (Kramer MS, 2002), and that probability theory suggests that the breastfeeding-offspring obesity data in the literature as a whole reflect one of two situations: (1) publication bias, or (2) a true positive association between breastfeeding and offspring obesity in at least one other published sample (Cope MB, 2008). That is not to deny that there may be a number of valid reasons to support breastfeeding, not related to obesity (see e.g. APA report). But perhaps it is this which has lead to a problem with ‘white hat bias’ in the breastfeeding-obesity literature - a term coined by Cope and Allison to denote ‘bias leading to the distortion of research based-based information in the service of what may be perceived as righteous ends (Cope MB, 2010). One such reason to support breastfeeding is to enable personal choice for parents and caregivers. However, this is incompatible with the practice of giving misleading information on the benefits of breastfeeding which actually deprives caregivers of their right to make informed decisions about feeding infants.

This is a problematic situation, and needs to be corrected. The causes are unknown, but distorted presentation of data has been identified in multiple reports of randomized clinical trials, often in only one section e.g. the abstract (Boutron I, 2010), and often in the secondary literature, such as press releases (Cope MB, 2010). Therefore all authors need express conclusions with great clarity and consistency, and not selectively include and exclude results without recourse to relative empirical strengths. To be accurate in reporting in this article, the results of this study as a whole are most consistent with either (1) an association between breastfeeding and increased offspring overweight/obesity, or (2) a lack of empirical strength in this study to contribute to the debate on whether there is an association between the two constructs.