Mind/Body Connection: How Emotions Affect Health
Mind/Body Connection: How Your Emotions Affect Your Health can help you achieve this goal with cognitive behavioral therapy (CBT). There are multiple associations between mental health and chronic physical conditions that Understanding the links between mind and body is the first step in. the mind and body work together to promote health and well-being. The Mind-Body Connection: How Mental and Physical Wellness Are.
Having or adopting a baby. How can my emotions affect my health? Your body responds to the way you think, feel, and act. Path to improved health There are ways that you can improve your emotional health. First, try to recognize your emotions and understand why you are having them. Following are some other helpful tips. Express your feelings in appropriate ways If feelings of stress, sadness, or anxiety are causing physical problems, keeping these feelings inside can make you feel worse.
However, keep in mind that your family and friends may not always be able to help you deal with your feelings appropriately. At these times, ask someone outside the situation for help. Try asking your family doctor, a counselor, or a religious advisor for advice and support to help you improve your emotional health. Live a balanced life Focus on the things that you are grateful for in your life. Try not to obsess about the problems at work, school, or home that lead to negative feelings.
You may want to use a journal to keep track of things that make you feel happy or peaceful.
Some research has shown that having a positive outlook can improve your quality of life and give your health a boost. Those modest but significant differences were also observed in patients with anxiety disorders Vreeburg et al. In line with clinical findings, the circadian pattern of corticosterone has been reported to be disrupted in rodent models of depression Touma et al. In rats, chronic stress induces a depressive-like phenotype, associated with dysregulation of the HPA axis and reductions in dopaminergic and serotonergic transmissions in the PFC Mizoguchi et al.
Affective-like behavioral deficits have been reported in mouse mutants with altered HPA axis function [see Renoir et al. Chronic treatment with corticosterone as well as isolation rearing increase the depressive-like behavior in GR-dependent and independent manners Ago et al. Chronic elevation of corticosterone creates a vulnerability to a depression-like syndrome that is associated with increased expression of the serotonin synthetic enzyme tryptophan hydroxylase 2 tph2similar to that observed in depressed patients Donner et al.
Interestingly, the effects of chronic corticosterone administration in animal models have also been studied in the context of affective and systemic disorders. Chronic antidepressant treatment reversed those behavioral impairments. Furthermore, relevant to the relationship between stress and metabolic syndrome, 4-wk exposure to high doses of corticosterone in mice, has been found to increase weight gain and plasma insulin levels as well as reduce home-cage locomotion Karatsoreos et al.
However, these elevated corticosterone levels returned to baseline levels after 6 weeks of CMS.
Mind-Body Health Connection
Similarly, Adzic et al. Interestingly, this study suggests a recovery of diurnal corticosterone rhythm after 8 weeks of CMS. Taken together, these observations suggest an adaptive capacity for the HPA axis to cope with prolonged stress. The effects of chronic stress on HPA axis function have been widely studied in both animal models and clinical populations.
Many of those investigations have focused on the negative feedback part of the HPA axis mainly mediated by the GR. Further regression analyses showed that low social support at work and high job strain were associated with more cortisol suppression after the dexamethasone suppression test Holleman et al. In rodents, social isolation decreased the feedback sensitivity of the HPA axis to dexamethasone Evans et al.
Another animal study reported that socially deprived mice had increased adrenal weights as well as a greater increase in corticosterone levels in response to acute stress Berry et al. Polymorphisms in genes controlling the activity of the HPA axis are also associated with differential risk of psychiatric disease. Polymorphisms in the GR gene have been associated with major depression in multiple cohorts van West et al.
Interestingly, some GR polymorphisms are also a predictor of the HPA axis response to psychosocial tests Kumsta et al. Genotype-phenotype associations have also been identified in terms of response to antidepressant response Ellsworth et al. Evidence of gene-environment interactions in the stress response and psychiatric susceptibility comes from a study of the corticotrophin-releasing factor receptor CRF-R Bradley et al.
Individuals with a particular CRF-R genotype who had experienced child abuse had enhanced risk of depression as adults, an observation repeated in two ethnically different populations. Overall, studies suggest that the degree of HPA axis hyperactivity can vary considerably across psychiatric patient groups, likely due to genetic and environmental factors during early development or adult life.
In that regard, two separate studies reported that polymorphisms of the FKBP5 gene that potentially modify the sensitivity of the GR are associated with an increased likelihood of adult depression for individuals exposed to adverse life events Zimmermann et al.
Genes involved in other pathways may also potentiate an aversive response to stress. A landmark early study described an association between a variant in the serotonin transporter gene and the response to stressful life experiences Caspi et al.
This functional variant in a major target of antidepressant therapies is associated with an elevated response to fearful stimuli, elevated hormonal responses to stress, and increased risk of depression in response to stress exposure Lesch et al.
Variants in multiple genes in the serotonergic pathway have also been associated with altered behavioral phenotypes in animal models [reviewed in Holmes ].
Critically, changes in circulating corticosteroids can regulate the activity of the rate-limiting serotonin synthetic enzyme tryptophan hydroxylase 2 in the brain Clark et al. In rodent models, acute restraint stress up-regulates serotonin production in the amygdala Mo et al.
Taken together these findings demonstrate that alterations in HPA axis function can directly impact on CNS systems known to be associated with psychiatric disease. Peripheral disorders associated with HPA changes and psychiatric disease A wealth of evidence is now emerging to illustrate the link between stress and risk factors for physiological disorders, in particular metabolic disorders.
Hyperactivity of the HPA axis and hypercortisolaemia is associated with the metabolic syndrome Anagnostis et al. Similarly, both chronic stress and chronic treatment with glucocorticoids are associated with central adiposity, dyslipidaemia, atrophy of skeletal muscles, insulin resistance, and glucose intolerance: Elevations of circulating glucocorticoids have also been linked with an increased risk of depression in those with metabolic disorder Vogelzangs et al.
On the other hand, disturbances in fatty acid metabolism have been observed in cohort studies of depression Assies et al. Fatty acid levels appear to have a bidirectional relationship with HPA axis activity, with glucocorticoids modulating fatty acid metabolism Brenner et al. A study examining this relationship in more detail has shown that the circadian changes in cortisol have a different association with the major fatty acid forms in major depression patients compared to controls Mocking et al.
Other studies have demonstrated both changes in visceral fat levels and adrenal gland volume in women with major depressive disorders Ludescher et al. Some of these associations appear to have developmental antecedents, with exposure to dietary high fat in the perinatal period being linked with both altered HPA axis function and mood changes Sasaki et al.
If metabolic disorders are considered as a spectrum, then diabetes is arguably positioned as the end point of this decline in function. Chronic stress and sustained dysregulation of corticosteroid production are strongly associated with the development of type 2 diabetes mellitus in both human cohorts and in animal models Chan et al.
As an example in mice, streptozotocin STZ -induced diabetes resulted in increased depressive-like behavior as well as increased corticosterone levels Ho et al. The convergence of the associations between HPA axis dysfunction and both diabetes and depression is striking, with compelling evidence for links between the two disorders and this central underlying risk factor [reviewed in Champaneri et al.
Dysfunction of HPA signaling also appears to interact with the autonomic nervous system to influence cardiovascular function. Components of the HPA axis act outside the hypothalamus to regulate sympathetic outflow, and thus heart rate.
Elevated heart rate has been associated with depression in multiple studies Forbes and Chaney, ; Carney et al. Depression is associated with an increased risk of mortality in patients with cardiovascular disease Mann and Thakore,and this increased risk is strongly linked with hypercortisolaemia Jokinen and Nordstrom, Taken together, these studies speak to the accumulating evidence suggesting a link between disorders which involve HPA dysregulation and the risk of developing psychiatric disease.
This is illustrative of the bidirectional relationship between peripheral illness and mental health: HPA axis changes may be either contributors to or consequences of peripheral disorders but also have the capacity to modulate brain function and predispose to psychiatric disease. Pharmacological targeting of the HPA axis The GR antagonist mifepristone has been tested as an adjunctive treatment for psychiatric disorders Schatzberg and Lindley, Most recently, a randomized controlled trial of adjunctive mifepristone in patients with bipolar disorder demonstrated alterations in cortisol levels which were correlated with improvements on neuropsychological tests of working memory Watson et al.
An earlier, smaller scale trial by the same group showed improvements in both neurocognitive function and depression rating scores Young et al. However, a similar study in schizophrenia showed alterations in plasma cortisol but no significant change in symptoms Gallagher et al. These mixed findings do highlight the potential utility of therapeutics targeting HPA axis function, but also are suggestive of the heterogeneity in the role of the HPA axis across, and potentially also within, psychiatric disorder diagnoses.
The main challenge in pharmacological targeting of the HPA axis is that blockage of all GR-dependent processes could ultimately lead to counteractive effects such as elevated endogenous corticosterone levels. In that context, a newly developed high-affinity GR ligand C shows promising characteristics in rats Zalachoras et al.
Indeed, C displays partial agonistic activity for suppression of CRH gene expression and potently enhances GR-dependent memory consolidation. This compound, which does not lead to disinhibition of the HPA axis, could help in dissecting the molecular signaling pathways underlying stress-related disorders. In recent years, other therapeutic strategies interacting at different levels of the HPA axis have been developed.
In patients who were successfully treated with fluoxetine, the secretion of cortisol decreased Piwowarska et al.
Furthermore, recent data suggest that GR levels in lymphocytes could be used to predict response to antidepressant treatment in major depressive patients Rojas et al. However, it should be noted that GR levels seemed inconsistent over time in this study.
Also, measuring cortisol levels in depressed patients before and following treatment with SSRI, Keating et al. The variation in findings from these studies may reflect differing modes of activity of the different antidepressant drug classes, superimposed on a heterogeneous patient population.
This was illustrated in a study examining changes in daily cortisol patterns in patients using SSRIs, tricyclic antidepressants, other therapeutics or no medications Manthey et al. A complex pattern emerged, with some antidepressants suppressing the morning peak in cortisol, and others altering the response to the dexamethasone suppression test.
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However, the challenges inherent to measuring a circulating factor which is both diurnally regulated and acutely sensitive to environmental cues should not be underestimated.
Immune dysregulation, inflammation and psychiatric health There is strong evidence that peripheral growth factors, pro-inflammatory cytokines, endocrine factors, and metabolic markers contribute to the pathophysiology of major depressive disorders and antidepressant response Schmidt et al. Similarly, many of the systemic disorders associated with a higher incidence of psychiatric disease involve a significant inflammatory component. In fact, as our understanding of the aetiology of these disorders deepens, it has become apparent that there is significant overlap between the factors driving peripheral inflammatory disease and psychiatric disorders.
Elevations of pro-inflammatory cytokines have been observed in both clinical populations and animal models of heart failure Levine et al. Importantly, the pathogenesis of atherosclerosis is intrinsically inflammatory Koenig,with elevated local and circulating pro-inflammatory cytokines. In addition, the acute-phase marker C-reactive protein CRP is strongly associated with cardiovascular disease van Holten et al.
As discussed above, cardiovascular disease is strongly associated with changes in psychiatric health, in particular depression. Cardiovascular disease is in turn closely linked with obesity, dyslipidemia, diabetes and metabolic disease. The elevated frequency of anxiety and depression in these disorders may in part underlie the association between cardiovascular and psychiatric risk factors.
In studies of diabetic patient cohorts, the inflammatory marker CRP was consistently predictive of direct associations between depression severity, lipid profiles and obesity levels van Reedt Dortland et al.
Similarly, increased risk of depression in a cohort of patients with diabetes was associated with a higher BMI, illustrating the link between depression and poor control of cardiovascular risk factors Kimbro et al. Obesity itself is considered to be a state of low-grade inflammation, and is linked with elevated depressive symptoms.
In addition, in a longitudinal study CRP levels at baseline were statistically associated with depression scores Daly, Other disease states involving inflammatory processes are associated with elevated risk of depression. Likewise, although the incidence rate varies significantly between studies, an elevated incidence of depression has been documented in systemic lupus erythematosus Palagini et al.
Common to all of these disorders is an autoimmune-mediated elevation of inflammatory signaling, with increased circulating pro-inflammatory cytokines observed in the periphery and in the CNS. Large case-control studies have described increased rates of anxiety and depression in patients with inflammatory bowel disease Kurina et al.
Altered gut permeability to enteric bacteria has also been associated with depression. Translocation of bacterial allergens [in particular lipopolysaccharide LPS ], stimulates a systemic immune response characterized by elevated IgM and IgA antibodies reactive to the bacteria.
Individuals with chronic depression are more likely to display increased LPS-reactive IgM and IgA than control subjects, indicating that elevated gut permeability may be potentiating a systemic inflammatory state Maes et al.
Mind/Body Connection: How Your Emotions Affect Your Health
The case for altered peripheral inflammation in psychiatric disease is strong, perhaps most so for major depression. Individuals with clinically classifiable major depression exhibit a wide range of changes in inflammatory markers, including elevated cytokines, chemokines, and acute phase proteins, findings which have been replicated in several meta-analyses and which in some studies appear to be correlated with specific depressive symptoms Miller et al.
I was astonished by how physically unwell I became. My heart sped up. Every bit of me hurt. I was suicidal, because I felt so rotten. Try this for a moment. Take a deep breath. Let your shoulders drop. And notice something interesting. When we become physically relaxed, we become mentally relaxed. Equally, if you feel stressed and tense, your body follows. In repressive cultures where expressions of the thought are not allowed, the mind can manifest itself in symptoms of pain.