Følelser og fysiologi

Filosofen Descartes skapte et kunstig skille mellom hode og kropp på 1600-tallet. Det at hjernen påvirker resten av kroppen kroppen er et eget fagfelt og kalles for Psychoneuroimmunology (PNI). Beskrivelsen ligger til sist på denne teksten; for øyeblikket på engelsk, men det kommer en norsk versjon etterhvert.

Følelser

Følelser eller emosjoner henger sammen med det ubevisste og tankene vi tenker uten bestandig å være klar over. Disse tankene lar seg ikke bestandig kontrollere av selve individet, f.eks. at ingen kan være lykkelig når man ønsker det selv. Det som er med på å påvirke det ubevisste, er andre menneskers reaksjoner på oss. Dette gjelder spesielt mennesker som har betydning for våre liv. Følelser spiller en avgjørende rolle i menneskenes liv, enten det gjelder samarbeid i sosiale grupper, seksualitet og reproduksjon eller som motivasjon for handlinger og valg. Ifølge den biologiske utviklingslæren har følelser derfor vært nødvendige for menneskers og dyrs overlevelse som arter.

Følelser kan psykologisk defineres som «positive eller negative evaluerende reaksjoner på stimuli». De er med andre ord følelsesmessige reaksjonstilstander. Det finnes utallige følelsesregister hos mennesker. Ved siden av intelligens og adferd utgjør følelser personligheten. Vi kan identifisere seks grunnleggende følelser, som har utallige variasjoner, og som også spedbarn kan uttrykke

Frykt, Hat, Glede, Sorg, Sinne, Redsel

Hver av disse følelsene setter i gang ulike fysiologiske prosesser. Dette kan være sunne reaksjoner på ytre stimuli som har vært livsviktige for huleboere og andre primitive skapninger. Følelsene kan imidlertid også føre til sykdom dersom de ikke kontrolleres, noe som også kjennetegnes ved endret adferd og intelligens. Følelsene utløses av en stimulus, de påvirkes av vår vurdering av stimulusen, de skaper fysiologiske reaksjoner i kroppen, og de kan endre adferd.

Følelser oppstår ubevisst ved opplevelser som følge av tidligere erfaringer. Hjernen registrerer alle sanseinntrykk og lagrer dem i hukommelsen. Det dannes da et biokjemisk spor i forhold til denne opplevelsen, og ved gjentagelse av samme sanseinntrykk vil hjernen sende ut signaler til nervesystemet i henhold til erfaringene. Mørke, trange rom kan eksempelvis være et faresignal som setter igang en fryktreaksjon.

Det synaptiske system i hjernen inneholder visse signalstoffer som styrer emosjonene: dopamin og seratonin er de viktigste av disse.

Følelsenes hovedkomponenter

Den utløsende stimulus kan være både intern og ekstern. Eksterne stimuli kan være alt fra synet av sin mor til lyden av gråt. Interne stimuli, som tanken på noe en gleder seg til, kan også utløse følelser. Med andre ord kan alt som betyr noe for oss være utløsende stimuli.

Den kognitive evalueringen er ens vurdering av stimulusen. Hvis man ikke oppfatter stimulus som viktig, vil den ikke utløse emosjoner. Man vil i tillegg evaluere om en stimulus er positiv eller negativ.

De fysiologiske responsene er kroppens reaksjoner på emosjonene. Disse er viktige blant annet fordi de kan måles med objektive metoder. For eksempel vil produksjon av svette lett kunne måles ved hjelp av EDA. Andre eksempler på fysiologiske responser er økt hjerterytme og produksjon av ulike hormoner.

Adferdskomponentene finnes det to typer av. Instrumentell adferd er å gjøre noe med stimulusen. Hvis stimulusen er noe negativt kan instrumentell adferd være å for eksempel fjerne den, eller å fjerne seg fra den. Ekspressiv adferd er å uttrykke følelsene sine, for eksempel ved å smile eller å gråte.

Emosjonskomponentene er preget av et gjensidig påvirkningsforhold.

Nevrologi

Følelser kan i visse tilfelle føre til varige endringer som kan observeres ved nevrologiske undersøkelser. [1]

Psychoneuroimmunology (PNI) is the study of the interaction between psychological processes and the nervous and immune systems of the human body.[1] PNI takes an interdisciplinary approach, incorporating psychology, neuroscience, immunology, physiology, pharmacology, molecular biology, psychiatry, behavioral medicine, infectious diseases, endocrinology, and rheumatology.

The main interests of PNI are the interactions between the nervous and immune systems and the relationships between mental processes and health. PNI studies, among other things, the physiologicalfunctioning of the neuroimmune system in health and disease; disorders of the neuroimmune system (autoimmune diseases; hypersensitivities; immune deficiency); and the physical, chemical and physiological characteristics of the components of the neuroimmune system in vitro, in situ, and in vivo.

PNI may also be referred to as psychoendoneuroimmunology (PENI).

PNI research is looking for the exact mechanisms by which specific brainimmunity effects are achieved. Evidence for nervous system–immune system interactions exists at several biological levels.

The immune system and the brain talk to each other through signaling pathways. The brain and the immune system are the two major adaptive systems of the body. Two major pathways are involved in this cross-talk: the Hypothalamic-pituitary-adrenal axis (HPA axis) and the sympathetic nervous system (SNS). The activation of SNS during an immune response might be aimed to localize the inflammatory response.

The body’s primary stress management system is the HPA axis. The HPA axis responds to physical and mental challenge to maintain homeostasis in part by controlling the body’s cortisol level. Dysregulation of the HPA axis is implicated in numerous stress-related diseases. HPA axis activity and cytokines are intrinsically intertwined: inflammatory cytokines stimulate adrenocorticotropic hormone (ACTH) and cortisol secretion, while, in turn, glucocorticoids suppress the synthesis of proinflammatory cytokines.

Molecules called pro-inflammatory cytokines, which include interleukin-1 (IL-1), Interleukin-2 (IL-2), interleukin-6 (IL-6), Interleukin-12 (IL-12), Interferon-gamma (IFN-Gamma) and tumor necrosis factor alpha (TNF-alpha) can affect brain growth as well as neuronal function. Circulating immune cells such as macrophages, as well as glial cells (microglia and astrocytes) secrete these molecules. Cytokine regulation of hypothalamic function is an active area of research for the treatment of anxiety-related disorders.[11]

Cytokines mediate and control immune and inflammatory responses. Complex interactions exist between cytokines, inflammation and the adaptive responses in maintaining homeostasis. Like the stress response, the inflammatory reaction is crucial for survival. Systemic inflammatory reaction results in stimulation of four major programs[12]:

These are mediated by the HPA axis and the SNS. Common human diseases such as allergy, autoimmunity, chronic infections and sepsis are characterized by a dysregulation of the pro-inflammatory versus anti-inflammatory and T helper (Th1) versus (Th2) cytokine balance.

Recent studies show pro-inflammatory cytokine processes take place during depression, mania and bipolar disease, in addition to autoimmune hypersensitivity and chronic infections.

Chronic secretion of stress hormones, glucocorticoids (GCs) and catecholamines (CAs), as a result of disease, may reduce the effect of neurotransmitters, including serotonin, norepinephrine and dopamine, or other receptors in the brain, thereby leading to the dysregulation of neurohormones. Under stimulation, norepinephrine is released from the sympathetic nerve terminals in organs, and the target immune cells express adrenoreceptors. Through stimulation of these receptors, locally released norepinephrine, or circulating catecholamines such as epinephrine, affect lymphocyte traffic, circulation, and proliferation, and modulate cytokine production and the functional activity of different lymphoid cells.

Glucocorticoids also inhibit the further secretion of corticotropin-releasing hormone from the hypothalamus and ACTH from the pituitary (negative feedback). Under certain conditions stress hormones may facilitate inflammation through induction of signaling pathways and through activation of the Corticotropin-releasing hormone.

These abnormalities and the failure of the adaptive systems to resolve inflammation affect the well-being of the individual, including behavioral parameters, quality of life and sleep, as well as indices of metabolicand cardiovascular health, developing into a “systemic anti-inflammatory feedback” and/or “hyperactivity” of the local pro-inflammatory factors which may contribute to the pathogenesis of disease.

This systemic or neuro-inflammation and neuroimmune activation have been shown to play a role in the etiology of a variety of neurodegenerative disorders such as Parkinson’s and Alzheimer’s disease, multiple sclerosis, pain, and AIDS-associated dementia. However, cytokines and chemokines also modulate central nervous system (CNS) function in the absence of overt immunological, physiological, or psychological challenges.[13]

 

Psychoneuroimmunological effects

There is now sufficient data to conclude that immune modulation by psychosocial stressors and/or interventions can lead to actual health changes. Although changes related to infectious disease and woundhealing have provided the strongest evidence to date, the clinical importance of immunological disregulation is highlighted by increased risks across diverse conditions and diseases.

Link between stress and disease

Stressors can produce profound health consequences. In one epidemiological study, for example, all-cause mortality increased in the month following a severe stressor – the death of a spouse.[14] Theorists propose that stressful events trigger cognitive and affective responses which, in turn, induce sympathetic nervous system and endocrine changes, and these ultimately impair immune function.[15][16] Potential health consequences are broad, but include rates of infection[17][18] HIV progression[19][20] and cancer incidence and progression.[21][22][23]

Stress is thought to affect immune function through emotional and/or behavioral manifestations such as anxiety, fear, tension, anger and sadness and physiological changes such as heart rate, blood pressure, and sweating. Researchers have suggested that these changes are beneficial if they are of limited duration,[24] but when stress is chronic, the system is unable to maintain equilibrium or homeostasis.

Immune changes in response to very brief stressors have been a central theme in the last decade of PNI research, but older literature also provides early illustrations. In a study published in 1960, subjects were led to believe that they had accidentally caused serious injury to a companion through misuse of explosives.[25]

Two meta-analyses of the literature show a consistent reduction of immune function in healthy people who are experiencing stress.

In the first meta-analysis by Herbert and Cohen in 1993,[26] they examined 38 studies of stressful events and immune function in healthy adults. They included studies of acute laboratory stressors (e.g. a speech task), short-term naturalistic stressors (e.g. medical examinations), and long-term naturalistic stressors (e.g. divorce, bereavement, caregiving, unemployment). They found consistent stress-related increases in numbers of total white blood cells, as well as decreases in the numbers of helper T cells, suppressor T cells, and cytotoxic T cells, B cells, and Natural killer cells (NK). They also reported stress-related decreases in NK and T cell function, and T cell proliferative responses to phytohaemagglutinin [PHA] and concanavalin A [Con A]. These effects were consistent for short-term and long-term naturalistic stressors, but not laboratory stressors.

In the second meta-analysis by Zorrilla et al. in 2001,[27] they replicated Herbert and Cohen’s meta-analysis. Using the same study selection procedures, they analyzed 75 studies of stressors and human immunity. Naturalistic stressors were associated with increases in number of circulating neutrophils, decreases in number and percentages of total T cells and helper T cells, and decreases in percentages ofNatural killer cell (NK) cells and cytotoxic T cell lymphocytes. They also replicated Herbert and Cohen’s finding of stress-related decreases in NKCC and T cell mitogen proliferation to Phytohaemagglutinin (PHA) and Concanavalin A (Con A).

Communication between the brain and immune system

  • Stimulation of brain sites alters immunity (stressed animals have altered immune systems).
  • Immune cells produce cytokines that act on the CNS.
  • Immune cells respond to signals from the CNS.

Communication between neuroendocrine and immune system

  • Glucocorticoids and catecholamines influence immune cells.[28]
  • Endorphins from pituitary & adrenal medulla act on immune system.
  • Activity of the immune system is correlated with neurochemical/neuroendocrine activity of brain cells.

Connections between glucocorticoids and immune system

  • Anti-inflammatory hormones that enhance the organisms response to a stressor.
  • Prevent the overreaction of the body’s own defense system.
  • Regulators of the immune system.
  • Affect cell growth, proliferation & differentiation.
  • Cause immunosuppression.
  • Suppress cell adhesion, antigen presentation, chemotaxis & cytotoxicity.
  • Increase apoptosis.

Corticotropin-releasing hormone (CRH)

Release of corticotropin-releasing hormone (CRH) from the hypothalamus is influenced by stress.

  • CRH is a major regulator of the HPA axis/stress axis.
  • CRH Regulates secretion of Adrenocorticotropic hormone (ACTH).
  • CRH is widely distributed in the brain and periphery
  • CRH also regulates the actions of the Autonomic nervous system ANS and immune system.

Furthermore, stressors that enhance the release of CRH suppress the function of the immune system; conversely, stressors that depress CRH release potentiate immunity.