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Acupressure as a Non-Pharmacological Treatment for Neurological Insult and Stress Reduction: Theory, Mechanisms, and Efficacy
Acupressure is a form of complementary and alternative medicine (CAM) that involves stimulation of acupoints using fingertip pressure. Acupoints are areas of skin designated as such by Traditional Chinese Medicine, with stimulation thought to elicit distinct effects from stimulation of non-acupoints. As such, the studies in this thesis compare effects of active acupressure treatments (with stimulation of acupoints) to those of placebo acupressure treatments, which control for all aspects of active acupressure treatments, but stimulate non-acupoints rather than acupoints. Specifically, the effects of acupressure on cognitive function following traumatic brain injury (TBI) were investigated, as well as the efficacy of acupressure for stress reduction in healthy college students. A series of eight acupressure treatments were found to improve cognitive function and reduce perceived stress over and above improvements seen following placebo acupressure in TBI survivors. The cognitive benefits seen could be a result of active acupressure-associated stress reduction, possibly mediated via the autonomic nervous system. No group differences in stress response reduction were found after a single administration of active acupressure, placebo acupressure or a relaxation CD in the stress study, possibly due to insufficient \u22dosing\u22. As attitudes can contribute to placebo effects in both active and placebo interventions, the impact of attitudes towards CAM and conventional medicine on treatment outcome in both studies were assessed, to further delineate possible placebo effects. Although having less of an influence on outcome than hypothesized, attitudes towards both CAM and conventional medicine did affect a number of outcome measures, as well as measures at baseline and during the intervention itself, suggesting that attitudes towards CAM and conventional medicine should be taken into account both in clinical studies and regular clinical practice. These studies highlight the importance of rigorous scientific research of CAM therapies, incorporating randomization, blinding procedures, and appropriate control conditions
Propensity to obesity impacts the neuronal response to energy imbalance
The mechanisms responsible for the propensity to gain weight or remain normal weight are poorly understood. The objective of this study was to study the neuronal response to visual food cues during short-term energy imbalance in healthy adults recruited as obesity-resistant (OR) or obesity-prone (OP) based on self-identification, BMI, and personal/family weight history. 25 OR and 28 OP subjects were studied in underfed (UF) and overfed (OF) as compared to eucaloric (EU) conditions in a randomized crossover design. Each study phase included a 3 day run-in diet, 1 day of controlled feeding (basal energy needs for EU, 40% above/below basal energy needs for OF/UF), and a test day. On the test day fMRI was performed in the acute fed stated (30 minutes after a test meal) while subjects viewed images of foods of high hedonic value and neutral non-food objects. Measures of appetite and hormones were also performed before and every 30 minutes after the test meal. UF was associated with significantly increased activation of insula, somatosensory cortex, inferior and medial prefrontal cortex, parahippocampus, precuneus, cingulate and visual cortex in OR. However, UF had no impact in OP. As a result, UF was associated with significantly greater activation, specifically in the insula, inferior prefrontal cortex, and somatosensory cortex in OR as compared to OP. While OF was overall associated with reduced activation of inferior visual cortex, no group interaction was observed with OF. In summary, these findings suggest that individuals resistant to weight gain and obesity are more sensitive to short-term energy imbalance, particularly with UF, than those prone to weight gain. The inability to sense or adapt to changes in energy balance may represent an important mechanism contributing to excess energy intake and risk for obesity