Heart rate variability biofeedback: how and why does it work?

Bekrefter alle elementer jeg jobber med i Autonom pust: vagus, betennelse, m.m.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4104929/

In recent years there has been substantial support for heart rate variability biofeedback (HRVB) as a treatment for a variety of disorders and for performance enhancement (Gevirtz, 2013). Since conditions as widely varied as asthma and depression seem to respond to this form of cardiorespiratory feedback training, the issue of possible mechanisms becomes more salient. The most supported possible mechanism is the strengthening of homeostasis in the baroreceptor (Vaschillo et al., 2002Lehrer et al., 2003). Recently, the effect on the vagal afferent pathway to the frontal cortical areas has been proposed. In this article, we review these and other possible mechanisms that might explain the positive effects of HRVB.

ANTI-INFLAMMATORY EFFECTS

It is known that the vagal system interacts closely with the inflammatory system, such that increases in vagus nerve traffic (usually produced by electrical vagal stimulation) are associated with decreases in serum levels of various inflammatory cytokines (Borovikova et al., 2000Tracey, 2002). One study did find a decrease in C-reactive proteins among hypertensive patients treated with HRV biofeedback (Nolan et al., 2012). In another study, we experimentally exposed healthy subjects to an inflammatory cytokine, lipopolysaccharide (Lehrer et al., 2010). Usually both sympathetic and parasympathetic activity is blocked by lipopolysaccharide. Although no biofeedback-induced decreases in inflammatory cytokines were found, the autonomic effects of inflammation were greatly modulated, indicating that a greater resiliency was preserved among individuals given HRV biofeedback.

Matoverfølsomhet – et paradigmeskifte

Artikkel skrevet i 2011 som nevner mange viktige poenger. Blandt annet at vagus svekkes ved IBS og at det gir andre plager, spesielt hudplager.

http://www.naaf.no/Documents/Allergi%20i%20Praksis/matoverfoelsomhet_aip_1_2011w_v2.pdf

Dessuten hadde mange pasienter ekstra-intesti- nale symptomer og skåret høyt på «Subjective Health Complaints» (1). Påfallende mange anga at de hadde kronisk tretthet samt leddsmerter med morgenstivhet uten påvisbar artritt. Livskvaliteten var til dels be- tydelig redusert (2).

Over 50% av pasientene tilfreds- stilte kravene til en psykiatrisk diag- nose. Men hvor mye av de psykologiske problemene kan være sekundære? Inntil for knapt 20 år siden ble også magesårsykdommen regnet som en psykosomatisk sykdom. De psykolo- giske problemene vi så hos ulcuspasi- entene var ganske like de vi nå finner hos de matoverfølsomme, og vi har enda friskt i minnet hvordan alle pro- blemene hos ulcuspasientene, in- kludert de psykologiske, «blåste bort» etter fjerning av magesårbakterien Helicobacter pylori (4).

Kun sykdomspesifikk angst eller for- ventninger om plager var signifikante uavhengige prediktorer. Disse pre- diktorene forklarte dog til sammen ikke mer enn 10% av variansen i mageplagene, og alder var eneste signifikante prediktor av ekstra- intestinale plager. Det vil si at 90% av variansen i grad av somatiske plager ikke kunne forklares av psyko- logiske faktorer. Vi tror derfor nå at mange av de psykologiske problemene ved matoverfølsomhet er sekundære og at betydningen av psykologiske faktorer som årsak til matoverfølsomhet kan være betydelig overdrevet.

Vi kunne vise at et tungt fordøyelig, men fermenter- bart karbohydrat, som laktulose, ofte reproduserte pasientens plager (6). tester på klassisk IgE-sensitivisering mot spesifikke kostproteiner, deri- mot, var sjeldent positive. Det virker som om mageplagene først og fremst trigges av tungt fordøyelige karbo- hydrater og ikke spesielt av proteiner i kosten. Dessuten, at plagene kunne reproduseres av mat, viser at pasien- ten har rett – plagene kan skyldes maten! Det passer med at pasientene ikke har plager om natta, når de faster, etter tarm- skylling eller når de får tømt seg fullstendig.

Over 60% av pasientene hadde indikasjon på atopisk sykdom (Dette er hud- og slimhinnerelaterte sykdommer som allergi, tørr hud, kløe, m.m.)

Histamin øker sympatisk og redusert para- sympatisk (vagal) tonus, som også er karakteristisk for pasienter med funksjonelle mageplager (16, 17). Slik endret autonom aktivitet kan være et resultat av IgE-mediert histaminfrigjøring fra lokalt sensibili- serte mastceller (18).

Systemiske symptomer som kro- nisk tretthet og leddsmerter hos pasi- enter med IBS har tidligere ofte blitt forklart som somatisering av psykolo- giske problemer, men det finnes andre muligheter. For eksempel er det nylig rapportert at symptomer ved kronisk tretthetssyndrom kan behandles med en B-celle-antagonist (rituximab) (21). I likhet med de matoverfølsomme, har pasienter med kronisk tretthets- syndrom ofte IBS og endret mikro- flora som kan være av betydning for immunaktiveringen hos disse pasi- entene (22). Hos matoverfølsomme med IBS har vi nylig påvist økt nivå av B-celle aktiverende faktor (BAFF) i blod og tarmskyllevæske (23). BAFF er relatert til autoimmunitet og lokal immunaktivering i tarmen («lokal allergi») (24).

At karbohydrater kan reprodusere mageplagene hos pasienter med IBS og matoverfølsomhet, er verdt å merke seg, og mye tyder på at dette allerede nå bør få terapeutiske konsekvenser (27). Vi ser med andre ord for oss et paradigmeskifte når det gjelder utredning og behandling av pasienter med IBS og matoverfølsomhet.

Efficacy of paced breathing for insomnia: Enhances vagal activity and improves sleep quality.

Nevner at 0,1 Hz pust (5x minuttet) styrker vagusnerven slik at søvnen blir bedre for de som har insomnia. Her gjorde de det i 20 minutter før de la seg til å sove.

http://www.ncbi.nlm.nih.gov/pubmed/25234581

Abstract

Fourteen self-reported insomniacs (SRI) and 14 good sleepers (GS) had their cardiac neuronal activity assessed by heart rate variability (HRV) under controlled respiration at a slow frequency rate of 0.1 Hz, and a forced rate of 0.2 Hz during daytime rest. Nighttime sleep was measured by polysomnography. The SRI showed depressed high frequency power of HRV compared to the GS. An increased total power of HRV was observed among the SRI during slow, paced breathing compared with spontaneous breathing and 0.2 Hz. Sleep onset latency, number of awakenings, and awakening time during sleep were decreased and sleep efficiency was increased if SRI practiced slow, paced breathing exercises for 20 min before going to sleep. Our results indicate that there is autonomic dysfunction among insomniacs, especially in relation to vagal activity; however, this decreased vagal activity can be facilitated by practicing slow, paced breathing, thereby improving sleep quality.

RR interval-respiratory signal waveform modeling in human slow paced and spontaneous breathing.

Enda en bekreftelse på at pusten påvirker vagusnerven, og vagusnerven påvirker betennelser. Og at 0,1Hz (6 pust i minuttet) gir sterkest påvirkning på vagusnerven.

http://www.ncbi.nlm.nih.gov/pubmed/25139803/

Denne studien var en datamodell av hvordan forskjellige elementer av pusten (dybde og hastighet i dette tilfellet) påvirker hjerterytmen, som uttrykker vagusnerven. De fant at pustefrekvensen påvirket mest, altså hastigheten i dette tilfellet. 

The model’s results depended on breathing frequency with the least error occurring during slow paced breathing.

Deres forklaring på hvorfor pusten påvirker hjerterytmen er at strekk-reseptorer i lungene sier ifra om lungevolum som hjernen så bruker til å vurdere kardiovagale (vagusnervens påvirkning på hjertet) signaler.

Assuming that a0 represents slowly adapting pulmonary stretch receptors (SARs) and a1 SARs in coordination with other stretch receptors and central integrative coupling; then pulmonary stretch receptors relaying the instantaneous lung volume are the major factor determining cardiovagal output during inspiration.

De sier at ved forskjellige sykdommer blir det dårligere forbindelse mellom blodstrømning, blodtrykk, hjerterytme og pust, som gir ustabil kardivagal styring.

The role of vagal afferent neurons in cardiorespiratory coupling may relate to neurocardiovascular diseases in which weakened coupling among venous return, arterial pressure, heart rate and respiration produces cardiovagal instability.

Dette kan bidra til saktere, eller manglende, helbredelse av sykdom. Når man lærer å bruke pusten til å styrke vagusnerven er man i det minste én faktor nærmere helbredelse.

 

Respiratory effects on experimental heat pain and cardiac activity.

Her viser de hvordan HRV pust (6 bpm) resuserer smerte og påvirker hjerterytmen. De sammenlignet med hvordan distraksjon reduserer smerte of fant at pusten fungerer litt bedre. De nevner at pustens smertereduserende effekt virker gjennom andre mekanismer enn distraksjon.

http://www.ncbi.nlm.nih.gov/pubmed/19671085

http://www.researchgate.net/publication/26732610_Respiratory_effects_on_experimental_heat_pain_and_cardiac_activity

Abstract

OBJECTIVE:

Slow deep breathing has been proposed as an effective method to decrease pain. However, experimental studies conducted to validate this claim have not been carried out.

DESIGN:

We measured thermal pain threshold and tolerance scores from 20 healthy adults during five different conditions, namely, during natural breathing (baseline), slow deep breathing (6 breaths/minute), rapid breathing (16 breaths/minute), distraction (video game), and heart rate (HR) biofeedback. We measured respiration (rate and depth) and HR variability from the electrocardiogram (ECG) output and analyzed the effects of respiration on pain and HR variability using time and frequency domain measures of the ECG.

RESULTS:

Compared with baseline, thermal pain threshold was significantly higher during slow deep breathing (P = 0.002), HR biofeedback (P < 0.001), and distraction (P = 0.006), whereas thermal pain tolerance was significantly higher during slow deep breathing (P = 0.003) and HR biofeedback (P < 0.001). Compared with baseline, only slow deep breathing and HR biofeedback conditions had an effect on cardiac activity. These conditions increased the amplitude of vagal cardiac markers (peak-to-valley, P < 0.001) as well as low frequency power (P < 0.001).

CONCLUSION:

Slow deep breathing and HR biofeedback had analgesic effects and increased vagal cardiac activity. Distraction also produced analgesia; however, these effects were not accompanied by concomitant changes in cardiac activity. This suggests that the neurobiology underlying respiratory-induced analgesia and distraction are different. Clinical implications are discussed, as are the possible cardiorespiratory processes responsible for mediating breathing-induced analgesia.

 

In conclusion, this is the first experimental study to systematically control for breathing frequency and distraction effects and to show that respiratory-induced analgesia reduces pain in healthy subjects. The combined cardiorespiratory and antinociceptive effects observed during slow deep breathing suggest that the modulation of HR and pain share a common neurophysiological pathway. Our results, therefore, support the use of slow deep breathing as an inexpensive and valuable adjunct to the current treatment of pain.

Heart rate variability, overnight urinary norepinephrine and C-reactive protein: evidence for the cholinergic anti-inflammatory pathway in healthy human adults.

Stor studie med 611 friske arbeidere som viser at lav HRV assosieres med betennelser (CRP).

http://www.ncbi.nlm.nih.gov/pubmed/19019182

Abstract

OBJECTIVES:

C-reactive protein (CRP) has been identified as an independent predictor of cardiovascular mortality and morbidity in population-based studies. Recent advances have suggested a prominent role for the autonomic nervous system (ANS) in the regulation of inflammation. However, no in vivo human studies have examined indices of sympathetic and parasympathetic nervous system activity simultaneously in relationship to inflammatory markers in apparently healthy adults. Therefore, the objective of this study was to assess the immunomodulatory effects of the ANS.

METHODS AND RESULTS:

The study population comprised 611 apparently healthy employees of an airplane manufacturing plant in southern Germany. Urinary NE was positively associated with white blood cell count (WBC) in the total sample. We found an inverse association between indices of vagally mediated heart rate variability and plasma levels of (CRP), which was significantly larger in females than in males after controlling for relevant covariates including NE. Similar results were found using the percentage of interbeat interval differences >50 ms and WBC.

CONCLUSIONS:

We report here for the first time, in a large sample of healthy human adults, evidence supporting the hypothesis of a clinically relevant cholinergic anti-inflammatory pathway after controlling for sympathetic nervous system activity. This suggests an important role for the vagal control of systemic inflammatory activity in cardiovascular disease.

The relationship between heart rate variability and inflammatory markers in cardiovascular diseases.

Om hvrodan lav HRV bidrar til hjerte/kar problematikk og betennelser.

http://www.ncbi.nlm.nih.gov/pubmed/18819754

INTRODUCTION:

Recent evidence implicates a cholinergic anti-inflammatory pathway. Because vagus nerve activity mediates some heart rate variability (HRV), this qualitative review examines the literature concerning circulating cytokines and HRV in cardiovascular function in humans. This qualitative review examines the literature concerning circulating cytokines and HRV in cardiovascular function in humans.

METHODS:

Thirteen studies on HRV, inflammation, and cardiovascular function were located by electronic library search and descriptively reviewed.

RESULTS:

The relationship between HRV and inflammation was studied in healthy controls, patients with acute or stable coronary heart disease (CHD), patients with metabolic syndrome or impaired glucose tolerance and patients with kidney failure. Investigations focused mainly on Interleukin-6 (IL-6) and C-reactive peptide (CRP). The majority of reviewed studies reported that parasympathetic nervous system tone as inferred from heart rate variability is inversely related to inflammatory markers (r values between -0.2 and -0.4). The relationships with inflammatory markers were similar whether derived from ECG signals as short as 5-30min or from 24-h ECG readings for HRV analyses. While inflammatory markers appear to be related to HRV, it is a mistake to assume that the traditional «vagal measures» of HRV (such as high frequency heart rate variability) are the driving factors. Indeed, low frequency heart rate variability, a complex measure reflecting both parasympathetic and sympathetic activity, is the more commonly associated measure linked to inflammatory markers.

DISCUSSION:

Heart rate variability is inversely correlated with inflammatory markers in healthy individuals as well as in those with cardiovascular diseases.