Currently, many patients are turning to meditation as an alternative approach to reduce stress and anxiety. Meditation offers a therapeutic and often spiritual approach that avoids side effects of medications and the stigma of psychiatric treatments.
The potential regulatory functions of meditation practices on attention and emotion processes have a long-term impact on the brain and behavior. Stress reduction is associated with slow, deep, regular, and diaphragmatic-abdominal breathing during meditation (Chapell, 1994).
Activation of the anterior PFC and 5-HT system may be responsible for the improvement of negative mood observed during focused attention (FA) on abdominal breathing (Yu et al., 2011).
Loving-kindness meditation (LKM) is a mind-training practice used to cultivate positive emotions, such as friendliness and compassion (Salzberg, 1995). The practice of LKM has significant beneficial effects, such as reduced psychological distress, reduced anger, and increased social connectedness (Carlson et al. 2004; Hutcherson et al., 2008).
There is also evidence that through the cultivation of positive emotions with LKM practice, individuals experience decreased illness symptoms as well as an increase in a broader range of personal resources such as social support, purpose in life, and increased mindfulness. (Fredrickson et al., 2008)
Yoga has been shown to have psychological effects: decreasing anxiety and increasing feelings of emotional, social, and spiritual well-being. Yoga also reduced sleep disturbances following 6 months of practice in a geriatric population (Manjunath et al., 2005; Shelov et al., 2009).
Women with breast cancer have experienced less anxiety following Yoga. Self reported state anxiety and trait anxiety were significantly decreased in Yoga group compared to the control group (Rao et al., 2009).
In breast cancer patients, weekly Yoga sessions similarly led to improved quality of life and reduced anxiety (Speed-Andrews et al., 2010; Ulger et al. 2010).
The psychological effect of Yoga is mediated via down-regulation of the hypothalamic-pituitary-adrenal (HPA) axis and the sympathetic nervous system. Yoga decreases levels of salivary cortisol and urine catecholamine levels , resulting in reduced heart rate and systolic and diastolic blood pressure (Damodaran et al., 2002; Gokal et al., 2007).
Tai-chi has been shown to positively influence quality of life for those with a wide variety of medical illnesses, including multiple forms of cancer, hypertension, and chronic pain (Lee et al. 2007; Taylor-Piliae et al., 2007).
Tai-chi appears to be effective as a non-pharmacological approach to sleep enhancement for sleep-disturbed elderly individuals (Li et al., 2004).
Incorporating Qi-gongand Tai-Chi into the treatment may support the potential efficacy for survivors of torture and refugee trauma (Grodin et al., 2008).
After Tai-chi practice, the parasympathetic activity increased, while sympathetic activity decreased. Heart rate, systolic blood pressure and diastolic blood pressure also decreased sequentially after Tai-chi. These suggest that Tai-chi enhances the vagal modulation and tilt the sympatho-vagal balance (Lu et al., 2003).
Placebo effects on depression
In depression, there are clinical evidences that different regions of the brain linked to serotonin (5-HT) are involved in the placebo response for depression. The placebo group manifests a mean therapeutic effect of 30%, while the active group manifested 50% (Walsh et al., 2002; Sysko et al., 2007).
Recent meta-analyses evaluation of the clinical efficacy of antidepressant medications in the treatment of major depressive disorders concluded that there was no significant difference in comparison to placebo in the patients with moderate depression, and only a relatively small difference for patients with very severe depression (Kirsch et al., 2008; Fournier et al., 2010).
Using PET, Mayberg et al. (2002) studied the effects of anti-depressant (fluoxetine) and placebo. Remission of symptoms was observed in approximately half of each group. The placebo response was associated with an increased glucose metabolism in the PFC, parietal cortex, anterior cingulate cortex (ACC), and posterior cingulate cortex (PCC). Subjects who responded to fluoxetine showed a similar metabolic pattern, suggesting a possible involvement of serotonin (5-HT) in the antidepressant effects of placebo induction (Mayberg et al. 2002).
Central OXT seems to be involved in mediating placebo effects. Social interaction stimulates OXT release and that OXT mediates trust, analgesic and anti-depressive effects.It is, therefore, conceivable that a reliable patient-doctor relationship increases OXT expression in the patients’ brain, resulting in analgesic and anti-depressive effects.
Further studies are needed whether the hypothalamic OXT stimulation is initiated via the activation of the PFC in response to a reliable patient-doctor relationship.
OXT may be the central mediator of the placebo response (Enck et al. 2008). It is likely that that emotional impact (whatever non-specific or psychological) can alter the brain activity, especially OXT neurons, which leads to the beneficial effects.
Depression and OXT
Plasma OXT levels are reduced in patients who are suffering from major depression (Frasch et al., 1995). Cyranowski et al. (2008) compared patterns of peripheral OXT release exhibited by depressed and non-depressed women. Depressed women were more likely than controls to display a dysregulated pattern of peripheral OXT release (Cyranowski et al., 2008).
One of the actions of SSRIs is through increased OXT release. Administration of SSRIs increased plasma OXT levels in rats (Uvnas-Moberg et al., 1999). OXT may regulate 5-HT release and exert anxiolytic effects via direct activation of OXT receptor expressed in 5-HT neurons of the raphe nuclei (Yoshida et al. 2009).
The inhibitory effect of OXT on CRF expression is mediated by GABAA receptors at the PVN (Bulbul 2011). The anxiolytic agent (diazepam) is a GABAA receptor agonist. Subcutaneous administration of low dose of OXT has an anxiolytic effect in rats (Uvnas-Moberg et al., 1994). It is likely that the anxiolytic affect of OXT is mediated via GABAA receptors at the PVN.