Clinical Trial Details
— Status: Completed
Administrative data
| NCT number |
NCT04076722 |
| Other study ID # |
AS1965 |
| Secondary ID |
|
| Status |
Completed |
| Phase |
N/A
|
| First received |
|
| Last updated |
|
| Start date |
December 4, 2019 |
| Est. completion date |
December 11, 2020 |
Study information
| Verified date |
March 2021 |
| Source |
Oklahoma State University |
| Contact |
n/a |
| Is FDA regulated |
No |
| Health authority |
|
| Study type |
Interventional
|
Clinical Trial Summary
Adverse childhood experiences (ACEs) are repeatedly shown to predict negative biopsychosocial
health outcomes, including obesity. High rates of ACEs in communities are often paralleled by
high obesity rates, and higher ACEs, such as child abuse, have been shown to positively
predict later obesity and use of unhealthy weight control behaviors. Thus, in light of the
high prevalence of and potential causal links between early-life stress and obesity, there is
a critical need to further explore the ACEs-obesity relationship in order to understand and
to improve obesity outcomes. Given the adverse impact of ACEs and obesity on brain health,
two potential high impact treatment targets of the ACEs-obesity relationship will be explored
in the proposed pilot study: 1) markers of neurocognition (i.e., executive function; EF) and,
2) brain health/plasticity (i.e., neurotrophins like brain-derived neurotropic factor; BDNF
and glial cell derived neurotrophic factor; GDNF).
Specifically, this trial will be the first to 1) Identify whether brain markers of neural
health (e.g., neurotrophins) are related to ACES and/or neurocognitive EF performance, and 2)
Test whether neuronal or glial neurotrophins predict or change in response to weight loss.
Addressing these two needs advances the science of whether ACEs and EF levels are
differentially related to brain indices of neural and glial health/plasticity. Results of
this pilot may identify a neural substrate and/or profile by which ACEs promote obesity that
may ultimately be more amenable to pharmacologic intervention in order to promote weight loss
outcomes.
This group-treatment trial will assess 48 obese adults randomized to either an 8-week
behavioral weight loss treatment group (n=24) or a wait list control (n=24). Our primary
endpoints are percent reductions in body weight and changes in neurotrophins (e.g., BDNF,
GDNF). Weight and blood specimens will be assessed at baseline, post-treatment (8-weeks), and
follow-up (12-weeks). In testing these endpoints, we will meet the following aims: 1) To test
whether neurotrophins are related to ACEs and executive function (EF), and 2) To test if
neurotrophins predict or change in response to weight loss trajectory.
****The above description describes the study design that was terminated prematurely due to
Covid-19. The following description is the modified protocol.
The treatment described above was canceled and the present study focused on the baseline
visit. In this visit, participants participated in a stress reactivity protocol, so instead
of looking at change in BDNF, GDNF, and inflammatory markers after weight loss treatment, we
looked at change in BDNF, GDNF, and inflammatory markers after the stress activity task. This
information will tell us about how ACEs status is related to these biomarkers at baseline and
in response to stress.
Description:
Adverse childhood experiences (ACEs) are repeatedly shown to predict negative biopsychosocial
health outcomes, including obesity. High rates of ACEs in communities are often paralleled by
high obesity rates, and higher ACEs, such as child abuse, have been shown to positively
predict later obesity and use of unhealthy weight control behaviors. Thus, in light of the
high prevalence of and potential causal links between early-life stress and obesity, there is
a critical need to further explore the ACEs-obesity relationship in order to understand and
to improve obesity outcomes. Given the adverse impact of ACEs and obesity on brain health,
two potential high impact treatment targets of the ACEs-obesity relationship will be explored
in the proposed pilot study: 1) markers of neurocognition (i.e., executive function; EF) and,
2) brain health/plasticity (i.e., neurotrophins like brain-derived neurotropic factor; BDNF
and glial cell derived neurotrophic factor; GDNF).
Specifically, this trial will be the first to 1) Identify whether brain markers of neural
health (e.g., neurotrophins) are related to ACES and/or neurocognitive EF performance, and 2)
Test whether neuronal or glial neurotrophins predict or change in response to weight loss.
Addressing these two needs advances the science of whether ACEs and EF levels are
differentially related to brain indices of neural and glial health/plasticity. Results of
this pilot may identify a neural substrate and/or profile by which ACEs promotes obesity that
may ultimately be more amenable to pharmacologic intervention in order to promote weight loss
outcomes.
This group-treatment trial will assess 48 obese adults randomized to either an 8-week
behavioral weight loss treatment group (n=24) or a wait list control (n=24). Our primary
endpoints are percent reductions in body weight and changes in neurotrophins (e.g., BDNF,
GDNF). Weight and blood specimens will be assessed at baseline, post-treatment (8-weeks), and
follow-up (12-weeks). In testing these endpoints, we will meet the following aims: Aim 1 - To
test whether neurotrophins are related to ACEs and executive function (EF), and Aim 2: To
test if neurotrophins predict or change in response to weight loss trajectory. To ensure the
success of the trial, we have assembled a team of experts in adult behavioral obesity
treatment (PI: Hawkins, PhD), neurotrophins (Consultant: Vasquez, PhD), and biostatistics
(Consultant: Washburn, PhD). The results of this study will advance the science of
neurocognitive risk of weight loss difficulties and their potential treatment. Our approach
ensures that the neurocognitive testing and weight loss protocol can be delivered by trained
non-experts, improving its scalability and future dissemination potential. The results could
ultimately be used to tailor weight loss treatments such that neurocognitive risk factors
related to ACES are identified early and may ultimately be proactively mitigated early in
treatment to maximize participants' lasting weight loss outcomes.
****The above description describes the study design that was terminated prematurely due to
Covid-19. The following description is the modified protocol.
The treatment described above was canceled and the present study focused on the baseline
visit. In this visit, participants participated in a stress reactivity protocol, so instead
of looking at change in BDNF, GDNF, and inflammatory markers after weight loss treatment, we
looked at change in BDNF, GDNF, and inflammatory markers after the stress activity task. This
information will tell us about how ACEs status is related to these biomarkers at baseline and
in response to stress.
