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Depression, Anxiety, Stress, and Spirituality in Cardiovascular Disease
Published in Stephen T. Sinatra, Mark C. Houston, Nutritional and Integrative Strategies in Cardiovascular Medicine, 2022
Erminia Guarneri, Shyamia Stone
Exercise is perhaps the most beneficial treatment for both depression and cardiovascular health.152 Regular exercise works to prevent obesity, a risk factor for both depression and CVD, and to lower systemic inflammation.70 Exercise has been shown to decrease cortisol levels and increase levels of mood-boosting beta-endorphins.153 Recent research on exercise has elucidated the ability of exercise to increase brain-derived neurotrophic factor (BDNF), a growth factor responsible for cell growth and regeneration, synaptic remodeling and plasticity, while also impacting hypothalamic pathways of homeostasis, central metabolism, and regulation of angiogenesis and muscle regeneration.154 A study performed by Zembron-Lacny and colleagues154 showed that individuals who were more active had higher BDNF and better lipoprotein profiles with less oxidative stress and inflammation.
Hormones as Immune Modulating Agents
Published in Thomas F. Kresina, Immune Modulating Agents, 2020
Beta-endorphin (β-END) is derived in the pituitary gland and in other tissues from the POMC peptide by enzymatic cleavage. The production and secretion of β-END in the pituitary gland are regulated by CRF and immune-derived cytokines, such as IL-1β and TNFα [164,165]. Beta-endorphin is also produced in lymphoid cells, especially those infiltrating inflamed tissues. There is evidence to suggest that opioids in general and β-END in particular exert an antiinflammatory effect and down-regulate the immune response [166,167], In vitro, both μ and κ opioid agonists exhibit immunosuppressive activity for antibody responses [168]. The κ opioid agonist agent U50.488H suppressed the production of IL-1 and TNFα by mouse perito-neal macrophages at 1 nM and IL-6 at 10 nM concentrations. This suppressive effect could be completely reversed by the κ-selective antagonist norbinaltorphimine [169].
Central Stress-Limiting Systems and Cardioprotective Effects of their Mediators and Activators
Published in Felix Z. Meerson, Alexander V. Galkin, Adaptive Protection of The Heart: Protecting Against Stress and Ischemic Damage, 2019
Felix Z. Meerson, Alexander V. Galkin
As shown in recent years, OPs can restrict the adrenergic regulation and other links of the stress reaction by several concrete mechanisms. First, at the presynaptic level the norepinephrine release from sympathetic terminals in the CNS and in the periphery can be suppressed by the action of OPs on the opiate receptors on the terminals.6,68,69 Second, OPs can also inhibit the adrenergic neurons themselves in the CNS and in the peripheral sympathetic ganglia,63,70 and block liberation of catecholamines from the adrenal glands and their action on the effector organs, which takes place through the postsynaptic opiate receptors.63,70 Third, besides restricting the activity and the effects of the adrenergic system, OPs can modulate the release of hormones. Beta-endorphin produced in the pituitary body has been shown to locally inhibit there the liberation of a stress hormone vasopressin.71 OPs inhibit the biosynthesis and liberation of corticosteroids, including glucocorticoids.72 On the other hand, OPs can activate the secretion of insulin,73 usually depressed in stress, and secretion of thyrocalcitonin and somatotropin74 participating in the adaptive effects of stress reaction (see Chapter 1).
British Journal of Biomedical Science in 2021. What have we learned?
Published in British Journal of Biomedical Science, 2021
Also in this issue, Albonaim et al [19] examined the effects of polymorphisms in the opioid receptor kappa type 1 (OPRK1) which has a role in nicotine dependence. This receptor affects the activity of brain reward systems to the beta-endorphins and enkephalins so has a proposed role in addiction. The authors noted significant differences in the SNPs tested and propose that opioid receptor antagonists may assist in reducing the negative impact of nicotine withdrawal. However, the literature is confusing, with many confounding factors (for example addiction to other substances) and in this study a small sample size and a limited number of SNPs studied. This area is of importance given the adverse effects of nicotine which can cause an increase in blood pressure, heart rate, flow of blood to the heart and a narrowing of the arteries. Nicotine may also contribute to the hardening of the arterial walls, which in turn, may lead to a heart attack (and other) addictions on health in general.
Laughter Yoga as a Social Work Intervention
Published in Smith College Studies in Social Work, 2020
Laughing or simply smiling on a daily basis as a form of stress relief is not a new idea, “dated back at least to biblical times” (Roscoe, 2017, p. 1438). Commonly known, laughter increases the beta-endorphin secretion in a human body. Beta-endorphin is a chemical that connects to relaxation and good mood through positive physiological and biochemical changes, particularly through exercising (Goldfarb & Jamurtas, 1997). Since 1995, research has documented scientific evidence on laughter in terms of its transmission of positivity to the brain for endorphin production (MacDonald, 2004; Shahidi et al., 2011; Yim, 2016). Similar to aerobic exercises, laughing makes these muscles contract and relax, which can increase the oxygen level in the blood (Čokolič, Stangler Herodež, Sternad, & Krebs, 2013). Recent research has focused on the benefit of laughter to promote physical and emotional health in different cultural environments (Wagner, Rehmes, Kohle, & Puta, 2014; Wu, Wong, Mak, Yip, & Mak, 2019). However, research on laughter yoga as an exercise has focused more on its effect on improving physical health problems (Čokolič et al., 2013; Lynes, 2019). We found very few empirical data linking client outcomes to the use of laughter yoga as a mental health intervention. This article aims to discuss whether the use of laughter yoga initiated from the East can be applied universally to all clients as their social work intervention.
The effect of tramadol on blood glucose concentrations: a systematic review
Published in Expert Review of Clinical Pharmacology, 2020
Samaneh Nakhaee, Jeffrey Brent, Christopher Hoyte, Khadijeh Farrokhfall, Farshad M Shirazi, Masoumeh Askari, Omid Mehrpour
Tramadol is an analgesic that has diverse pharmacological actions and a concomitant capability for numerous adverse effects. Blood glucose impairments, especially hypoglycemia, should be regarded as one of the consequential side effects of tramadol. Studies conducted on diabetic subjects universally reported hypoglycemia. Tramadol-induced hypoglycemia may be severe in some cases. Based on the results of this study, glycemic changes, particularly hypoglycemia, should be considered a potential side effect of tramadol use. Mechanisms of hypoglycemia due to tramadol may include 1. Activation of pancreatic opioid receptors. 2. Increased hepatic insulin sensitivity 3. A decrease in the liver’s expression of lPEPCK. 4. Activation of the insulin signaling pathway. 5. Increasing insulin receptor expression. 6. Activation of serotonin-induced increase in insulin concentrations. 7. The release of beta-endorphin. 8. Stimulation of glucose uptake by muscles. 9. Activation of peripheral opioid µ-receptors, which can increase glucose uptake. Very few studies evaluated tramadol-induced hyperglycemia, nor have they studied any possible tramadol dose effect. Therefore, conclusions regarding hyperglycemias should be regarded as speculative.