Investigating the Efficacy of Genetic, Environmental, and Multifactorial Risk Information When Communicating Obesity Risk to Parents of Young Children.

BACKGROUND: Effectively communicating with parents about children's obesity risk is of critical importance for preventive medicine and public health. PURPOSE: The current study investigates the efficacy of communications focused on two primary causes of obesity: genes and environment. METHODS: We compared parental feeding responses to messages focused on (i) genetics alone, (ii) family environment alone, (iii) genetics-family environment interaction (G × FE), and (iv) no causal message. We also examined whether parental guilt mediates the effect of message type on feeding. Our sample consisted of 190 parents, half mothers and half fathers, of children 3-7 years old. After receiving one of the four types of messages, parents chose foods for their child using the Virtual Reality Buffet measure. Parents responded to questionnaires in the lab and at 1-week follow-up. RESULTS: In the VR Buffet, parents did not feed their children differently in message provision conditions versus control. There were, however, differences among message provision conditions wherein mothers who received any genetic information chose higher-calorie meals in the VR Buffet. At 1-week follow-up, parents who received information about genetics alone reported feeding their child more junk food and fatty meat on self-report food frequency assessments; there were no such differences for sugary beverages, sugary foods, or fast foods. Parental guilt was typically higher for participants who received family environment information alone but did not mediate the relation between information provision and feeding outcomes. CONCLUSIONS: While none of the messages improved feeding above the control condition, GxFE messages were associated with a better overall profile of outcomes. As such, it may be beneficial for messaging for parents about children's obesity risk to include content that reflects the complexity of genetic and environmental contributions to obesity risk.

Diabetes causal attributions among affected and unaffected individuals.

Objective: The present study aims to describe and compare causal attributions for type 1 diabetes (T1D) and type 2 diabetes (T2D) among affected and unaffected individuals and to investigate the relationships among attributions, attitudes, and beliefs. Research design and methods: Adults with no diabetes (N=458), T1D (N=192), or T2D (N=207) completed an online survey. Measures assessed diabetes conceptual knowledge, causal attributions for T1D and T2D, perceived control over diabetes onset, and favorability judgements of individuals affected by each type. Results: Results indicate general agreement on causal attributions for T1D and T2D among all respondent groups, with some divergences by disease status. All respondents attributed both T1D and T2D to genetics, and genetic attributions were positively associated with favorability judgements of individuals with T2D, but not those with T1D. Conclusions: This report sets the stage for investigations into how and why attributions for T1D and T2D differ and the implications of these differences including stigmatization of individuals with diabetes and diabetes-related self-concept. Additionally, this work can inform efforts towards clinical and public health education to prevent and optimize treatment of T1D and T2D.

Validation of Matrix Metalloproteinase-9 (MMP-9) as a Novel Target for Treatment of Diabetic Foot Ulcers in Humans and Discovery of a Potent and Selective Small-Molecule MMP-9 Inhibitor That Accelerates Healing.

Diabetic foot ulcers (DFUs) are a significant health problem. A single existing FDA-approved drug for this ailment, becaplermin, is not standard-of-care. We previously demonstrated that upregulation of active matrix metalloproteinase (MMP)-9 is the reason that the diabetic wound in mice is recalcitrant to healing and that MMP-8 participates in wound repair. In the present study, we validate the target MMP-9 by identifying and quantifying active MMP-8 and MMP-9 in human diabetic wounds using an affinity resin that binds exclusively to the active forms of MMPs coupled with proteomics. Furthermore, we synthesize and evaluate enantiomerically pure ( R)- and ( S)-ND-336, as inhibitors of the detrimental MMP-9, and show that the ( R)-enantiomer has superior efficacy in wound healing over becaplermin. Our results reveal that the mechanisms of pathology and repair are similar in diabetic mice and diabetic humans and that ( R)-ND-336 holds promise for the treatment of DFUs as a first-in-class therapeutic.