Posttraumatic growth in head and neck cancer survivors: Is it possible and what are the correlates?

OBJECTIVES: Posttraumatic growth (PTG) is a possible positive consequence of a traumatic event, such as cancer. Head and neck cancer (HNC) may be particularly traumatic, given its adverse effects on functional, psychological, and social wellbeing. We investigated the extent of PTG, factors associated with PTG, and associations between PTG and health-related quality-of-life (HRQoL) in HNC survivors. METHODS: HNC survivors (ICD10 C00-C14, C32), identified from the population-based National Cancer Registry Ireland, completed a postal survey. PTG was assessed using the Posttraumatic Growth Inventory (PTG-I) and HRQoL with FACT-G and FACT-H&N. Associations between socio-economic characteristics, social support, and clinical variables and PTG were examined using multivariable linear regression. Total HRQoL scores were compared in those with none-low PTG vs moderate-high PTG. RESULTS: A total of 583 survivors participated (response rate = 59%). The mean PTG score was 55.74 (95%CI 53.15-58.33); 60% had moderate-high PTG. Survivors scored highest in the PTG-I domain appreciation of life. In multivariable analysis, being female, being younger, having more social support, and having cancer-related financial stress were significantly associated with more PTG. HRQoL was significantly higher in those with moderate-high than no-little PTG (P < .01). CONCLUSIONS: A notable proportion of HNC survivors report PTG but growth is, on average, lower than reported for other cancers. Nonetheless, higher PTG appears related to better HRQoL. Further research would be valuable to understand the pathways by which HNC may lead to PTG and inform development of strategies to support and encourage PTG in this survivor population.

A Leptin Fragment Mirrors the Cognitive Enhancing and Neuroprotective Actions of Leptin.

A key pathology of Alzheimer's disease (AD) is amyloid ß (Aß) accumulation that triggers synaptic impairments and neuronal death. Metabolic disruption is common in AD and recent evidence implicates impaired leptin function in AD. Thus the leptin system may be a novel therapeutic target in AD. Indeed, leptin has cognitive enhancing properties and it prevents the aberrant effects of Aß on hippocampal synaptic function and neuronal viability. However, as leptin is a large peptide, development of smaller leptin-mimetics may be the best therapeutic approach. Thus, we have examined the cognitive enhancing and neuroprotective properties of known bioactive leptin fragments. Here we show that the leptin (116-130) fragment, but not leptin (22-56), mirrored the ability of leptin to promote AMPA receptor trafficking to synapses and facilitate activity-dependent hippocampal synaptic plasticity. Administration of leptin (116-130) also mirrored the cognitive enhancing effects of leptin as it enhanced performance in episodic-like memory tests. Moreover, leptin (116-130) prevented hippocampal synaptic disruption and neuronal cell death in models of amyloid toxicity. These findings establish further the importance of the leptin system as a therapeutic target in AD.