Relationships between depression, gender, and unhealthy weight loss practices among overweight or obese college students.

INTRODUCTION: Unhealthy weight loss practices are common among female college students. It is unknown if these practices are also most common among women in the subset of overweight or obese college students or if these practices are related to depression. We examined the relationship between gender, depression, and unhealthy weight loss practices among overweight or obese college students. METHODS: Students (body mass index between 25.0 and 34.9 kg/m(2)) from three Southern California universities (M(age) = 22 years, SD = 4; 70% women) were recruited from May 2011 to May 2012 for participation in a weight loss clinical trial (N = 404). Logistic regressions were performed with baseline data to assess the cross-sectional relationship between self-reported unhealthy weight loss practices and gender and depression as measured by the Center for Epidemiologic Studies Depression short form. RESULTS: Twenty-nine percent of participants reported engaging in at least one unhealthy weight loss behavior (e.g., fasting, purging) over the last 30 days, with no differences by gender. Self-report of at least one unhealthy weight loss behavior was associated with report of symptoms of depression (e(B) = 1.14 [confidence interval, CI: 1.08-1.20]), adjusting for potential confounders. Interactions between gender and depression were not significant (e(B) = 1.04 [CI: 0.93-1.16]). CONCLUSION: Among an overweight or obese sample of college students, unhealthy weight loss practices were equally common in both genders, and students with depressive symptomatology were at greatest risk. Obesity interventions targeting overweight or obese college students should educate both men and women about the dangers of unhealthy weight loss practices. In addition, screening for depression can help identify students who would benefit from additional supportive and coping strategies and resources.

Design and implementation of a randomized controlled social and mobile weight loss trial for young adults (project SMART).

PURPOSE: To describe the theoretical rationale, intervention design, and clinical trial of a two-year weight control intervention for young adults deployed via social and mobile media. METHODS: A total of 404 overweight or obese college students from three Southern California universities (M(age) = 22( ± 4) years; M(BMI) = 29( ± 2.8); 70% female) were randomized to participate in the intervention or to receive an informational web-based weight loss program. The intervention is based on behavioral theory and integrates intervention elements across multiple touch points, including Facebook, text messaging, smartphone applications, blogs, and e-mail. Participants are encouraged to seek social support among their friends, self-monitor their weight weekly, post their health behaviors on Facebook, and e-mail their weight loss questions/concerns to a health coach. The intervention is adaptive because new theory-driven and iteratively tailored intervention elements are developed and released over the course of the two-year intervention in response to patterns of use and user feedback. Measures of body mass index, waist circumference, diet, physical activity, sedentary behavior, weight management practices, smoking, alcohol, sleep, body image, self-esteem, and depression occur at 6, 12, 18, and 24 months. Currently, all participants have been recruited, and all are in the final year of the trial. CONCLUSION: Theory-driven, evidence-based strategies for physical activity, sedentary behavior, and dietary intake can be embedded in an intervention using social and mobile technologies to promote healthy weight-related behaviors in young adults.

Social network determinants of depression.

The etiology of depression has long been thought to include social environmental factors. To quantitatively explore the novel possibility of person-to-person spread and network-level determination of depressive symptoms, analyses were performed on a densely interconnected social network of 12,067 people assessed repeatedly over 32 years as part of the Framingham Heart Study. Longitudinal statistical models were used to examine whether depressive symptoms in one person were associated with similar scores in friends, co-workers, siblings, spouses and neighbors. Depressive symptoms were assessed using CES-D scores that were available for subjects in three waves measured between 1983 and 2001. Results showed both low and high CES-D scores (and classification as being depressed) in a given period were strongly correlated with such scores in one's friends and neighbors. This association extended up to three degrees of separation (to one's friends' friends' friends). Female friends appear to be especially influential in the spread of depression from one person to another. The results are robust to multiple network simulation and estimation methods, suggesting that network phenomena appear relevant to the epidemiology of depression and would benefit from further study.

Alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid-mediated excitotoxic axonal damage is attenuated in the absence of myelin proteolipid protein.

In vivo and in vitro studies have shown that alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA)-receptor-mediated excitotoxicity causes cytoskeletal damage to axons. AMPA/kainate receptors are present on oligodendrocytes and myelin, but currently there is no evidence to suggest that axon cylinders contain AMPA receptors. Proteolipid protein (PLP) and DM20 are integral membrane proteins expressed by CNS oligodendrocytes and located in compact myelin. Humans and mice lacking normal PLP/DM20 develop axonal swellings and degeneration, suggesting that local interactions between axons and the oligodendrocyte/myelin unit are important for the normal functioning of axons and that PLP/DM20 is involved in this process. To determine whether perturbed glial-axonal interaction affects AMPA-receptor-mediated axonal damage, AMPA (1.5 nmol) was injected into the caudate nucleus of anesthetized Plp knockout and wild-type male mice (n = 13). Twenty-four hours later, axonal damage was detected by using neurofilament 200 (NF 200) immunohistochemistry and neuronal damage detected via histology. AMPA-induced axonal damage, assessed with NF 200 immunohistochemistry, was significantly reduced in Plp knockout mice compared with wild-type mice (P = 0.015). There was no significant difference in the levels of neuronal perikaryal damage between the Plp knockout and wild-type mice. In addition, there was no significant difference in the levels of glutamate receptor subunits GluR1-4 or KA2 in Plp knockout compared with wild-type littermates. The present study suggests that PLP-mediated interactions among oligodendrocytes, myelin, and axons may be involved in AMPA-mediated axonal damage.

The types of neuron which contain protein kinase C gamma in rat spinal cord.

Protein kinase C (PKC) is thought to have a role in sensitization of dorsal horn neurons in certain pain states, and a recent study has reported that mice which lack the gamma isoform (PKCgamma) show reduced neuropathic pain after peripheral nerve injury. Although PKCgamma is present at high levels in the ventral part of lamina II we have limited information concerning the types of neuron in which it is located. In this study we have used immunocytochemistry to characterise the neurons which contain PKCgamma. Immunoreactive neurons were concentrated in ventral lamina II, but were also present in lamina III. Some weakly-immunoreactive neurons were located in the dorsal part of lamina II and in lamina I. The great majority (92%) of cells with PKCgamma were not GABA-immunoreactive, and these cells are likely to be excitatory interneurons. Dual-immunofluorescence labelling showed that PKCgamma was not randomly distributed amongst non-GABAergic neurons, since it was present in 76% of cells with neurotensin and 45% of those with somatostatin, but only 5% of those with the mu-opioid receptor (MOR-1). Cells with the neurokinin 1 receptor are found in lamina I and lamina III, and PKCgamma was present in 22% and 37% of these populations, respectively. These results suggest that excitatory interneurons in laminae II and III which lack the micro-opioid receptor may have a significant role in generating neuropathic pain.