14 replies to this topic

[wccaguy]

The systematic study of the Vagus Nerve, Heart Rate Variability, and Cholinergic Anti-Inflammatory Pathway Nexus has been among the most profound developments in disease and aging research since the year 2000.

I've established this thread to describe and discuss the science underlying this development.  I believe Dr. Kevin Tracey to be the leading student of the Vagus Nerve and the Cholinergic Anti-Inflammatory Pathway (hereafter CAIP).  The literature about Heart Rate Variability (HRV) has a longer history.  Lower HRV is inversely correlated with disease incidence of most of the most serious diseases, morbidity, and mortality.  

I first began to examine the literature of HRV in 2008.  At that time, I hadn't come across the literature, which had already been published, about the Vagus Nerve and the CAIP which is associated by causation to higher and lower HRV.  When I stumbled on the literature of the Vagus Nerve and the CAIP I was astounded.  I couldn't believe that, in all my health science related travels, I had never come across it.  I think it must be one of the most important topics that many of us don't know anything about.

I've written a great deal about this topic at Dr. William Davis' Track Your Plaque Forum, totaling more than 100 detailed posts about it by this date I think.  It has seemed to me that the Longecity forum needed a thread about the topic and I've decided to make a go of writing about the topic here.  I'm hoping to cover the entire range of the topic at a high level over the course of the next few weeks.

I'll begin to lay out the literature about it by referencing the abstracts and graphic figures of Dr. Kevin Tracey and his colleagues.  His primary focus is on the Vagus Nerve and the CAIP.  Remember, while you're looking at his work, that Low HRV is strongly, inversely related to serious disease incidence, morbidity, and mortality.

I look forward to discussion and new insight about this biological lever we have to improve our lives and our health!

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The Cholinergic Anti-inflammatory Pathway: A Missing Link in Neuroimmunomodulation

This review outlines the mechanisms underlying the interaction between the nervous and immune systems of the host in response to an immune challenge. The main focus is the cholinergic anti-inflammatory pathway, which we recently described as a novel function of the efferent vagus nerve. This pathway plays a critical role in controlling the inflammatory response through interaction with peripheral α7 subunit–containing nicotinic acetylcholine receptors expressed on macrophages. We describe the modulation of systemic and local inflammation by the cholinergic anti-inflammatory pathway and its function as an interface between the brain and the immune system. The clinical implications of this novel mechanism also are discussed.

Edited by wccaguy, 24 May 2012 - 11:48 PM.

[wccaguy]

Kevin Tracey and a collegue wrote an overview of the literature about this topic, published in 2007.  This post contains the abstract from the overview article and 3 graphic figures from it.  I recommend studying the article, which is available in its entirety for free, and the figures in detail.

Dr. Tracey did a video presentation of the content of this article in an hour lecture to the NIH a few years ago.  The video quality is not great but, if you're like me, and once it dawns on you how important this topic is, you'll want to see it... Or so I'd bet...  Here's the link to the video...

http://videocast.nih...y.asp?live=6197


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2007
The entire article is available for free at the link

Physiology and immunology of the cholinergic antiinflammatory pathway

Cytokine production by the immune system contributes importantly to both health and disease. The nervous system, via an inflammatory reflex of the vagus nerve, can inhibit cytokine release and thereby prevent tissue injury and death. The efferent neural signaling pathway is termed thecholinergic antiinflammatory pathway. Cholinergic agonists inhibit cytokine synthesis and protect against cytokine-mediated diseases. Stimulation of the vagus nerve prevents the damaging effects of cytokine release in experimental sepsis, endotoxemia, ischemia/reperfusion injury, hemorrhagic shock, arthritis, and other inflammatory syndromes. Herein is a review of this physiological, functional anatomical mechanism for neurological regulation of cytokine-dependent disease that begins to define an immunological homunculus.

Edited by wccaguy, 24 May 2012 - 11:31 PM.

[wccaguy]

Among the first and most important articles Dr. Tracey has written about the Cholinergic Anti-Inflammatory Pathway (CAIP) is the one that appeared in Nature in 2002.

It's a free and truly great introduction to the topic and contains graphics that make the scientific concepts he's communicating clear.  A must read...

Be sure to open the document to view the graphic figures...

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2002
A downloadable PDF

The Inflammatory Reflex

Inflammation is a local, protective response to microbial invasion or injury. It must be fine-tuned and regulated precisely, because deficiencies or excesses of the inflammatory response cause morbidity and shorten lifespan. The discovery that cholinergic neurons inhibit acute inflammation has qualitatively expanded our understanding of how the nervous system modulates immune responses. The nervous system reflexively regulates the inflammatory response in real time, just as it controls heart rate and other vital functions. The opportunity now exists to apply this insight to the treatment of inflammation through selective and reversible ‘hard-wired’ neural systems.

Edited by wccaguy, 24 May 2012 - 11:36 PM.

[wccaguy]

Ok... Enough of the overviews of the literature for now, right?  How about some actual, harder scientific studies of the subject...

I first came across the literature of the Cholinergic Anti-Inflammatory Pathway because I was increasing my Acetylcholine precursor dose while using HeartMath's emWave2 product to practice increasing my Heart Rate Variability.  I noticed that it was dramatically easier to raise my HRV while supplementing Acetylcholine than when I wasn't.  I didn't understand why that should be.  So I began to investigate and that led me to find the work of Kevin Tracey...  8-)

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2002
Complete study is available for review for free


Pharmacological Stimulation of the Cholinergic Antiinflammatory Pathway

Efferent activity in the vagus nerve can prevent endotoxin-induced shock by attenuating tumor necrosis factor (TNF) synthesis. Termed the “cholinergic antiinflammatory pathway,” inhibition of TNF synthesis is dependent on nicotinic α-bungarotoxin-sensitive acetylcholine receptors on macrophages. Vagus nerve firing is also stimulated by CNI-1493, a tetravalent guanylhydrazone molecule that inhibits systemic inflammation. Here, we studied the effects of pharmacological and electrical stimulation of the intact vagus nerve in adult male Lewis rats subjected to endotoxin-induced shock to determine whether intact vagus nerve signaling is required for the antiinflammatory action of CNI-1493. CNI-1493 administered via the intracerebroventricular route was 100,000-fold more effective in suppressing endotoxin-induced TNF release and shock as compared with intravenous dosing. Surgical or chemical vagotomy rendered animals sensitive to TNF release and shock, despite treatment with CNI-1493, indicating that an intact cholinergic antiinflammatory pathway is required for antiinflammatory efficacy in vivo. Electrical stimulation of either the right or left intact vagus nerve conferred significant protection against endotoxin-induced shock, and specifically attenuated serum and myocardial TNF, but not pulmonary TNF synthesis, as compared with sham-operated animals. Together, these results indicate that stimulation of the cholinergic antiinflammatory pathway by either pharmacological or electrical methods can attenuate the systemic inflammatory response to endotoxin-induced shock.

Edited by wccaguy, 24 May 2012 - 11:42 PM.

[wccaguy]

Another harder science post about the CAIP...  The control of the bodies innate, systemic and organ specific immune system inflammation fighting effort is controlled by acetylcholinesterase...

2009
Haven't found a free version of entire study

Brain acetylcholinesterase activity controls systemic cytokine levels through the cholinergic anti-inflammatory pathway

The excessive release of cytokines by the immune system contributes importantly to the pathogenesis of inflammatory diseases. Recent advances in understanding the biology of cytokine toxicity led to the discovery of the “cholinergic anti-inflammatory pathway,” defined as neural signals transmitted via the vagus nerve that inhibit cytokine release through a mechanism that requires the α7 subunit-containing nicotinic acetylcholine receptor (α7nAChR). Vagus nerve regulation of peripheral functions is controlled by brain nuclei and neural networks, but despite considerable importance, little is known about the molecular basis for central regulation of the vagus nerve-based cholinergic anti-inflammatory pathway. Here we report that brain acetylcholinesterase activity controls systemic and organ specific TNF production during endotoxemia. Peripheral administration of the acetylcholinesterase inhibitor galantamine significantly reduced serum TNF levels through vagus nerve signaling, and protected against lethality during murine endotoxemia. Administration of a centrally-acting muscarinic receptor antagonist abolished the suppression of TNF by galantamine, indicating that suppressing acetylcholinesterase activity, coupled with central muscarinic receptors, controls peripheral cytokine responses. Administration of galantamine to α7nAChR knockout mice failed to suppress TNF levels, indicating that the α7nAChR-mediated cholinergic anti-inflammatory pathway is required for the anti-inflammatory effect of galantamine. These findings show that inhibition of brain acetylcholinesterase suppresses systemic inflammation through a central muscarinic receptor-mediated and vagal- and α7nAChR-dependent mechanism. Our data also indicate that a clinically used centrally-acting acetylcholinesterase inhibitor can be utilized to suppress abnormal inflammation to therapeutic advantage.

Edited by wccaguy, 25 May 2012 - 12:14 AM.

[wccaguy]

Ok.  I confess.  I've been meaning to establish this thread for a while.  I understand a good deal about the subject and seeing as how doing good deeds would increase my Positivity and that, in itself, stimulates the Vagus Nerve, I should have gotten to it earlier...  But I didn't until...

I've been participating in that Buckyball/Olive Oil Study thread about doubling rat life spans and I came across a study of the Cholinergic Anti-Inflammatory Pathway and ... you guessed it... Olive Oil...  It seems that Olive Oil is a powerful Vagus Nerve trigger....  (And immediately your mind thinks "ah, so positive Mediterranean Diet health effects are caused, perhaps, by Vagus Nerve stimulation?  Mine did...)  And that led to some looking around and I came across this Kevin Tracey study from 2005.  I might eventually get around to posting the Olive Oil studies here.  For now, I'll post them in the Buckyball/Olive Oil study thread...

Enjoy!

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2005
Free access to complete text

Fat meets the cholinergic antiinflammatory pathway

The cholinergic antiinflammatory pathway is a neural mechanism that is controlled by the vagus nerve and inhibits local cytokine release, thereby preventing the damaging effects of cytokine overproduction. A new study now shows that dietary fat can activate this pathway, a finding that may help explain the immune system's failure to react to food antigens and commensal bacteria. Here we discuss this new data and its potential implications for dietary intervention in the treatment of inflammatory diseases.

Edited by wccaguy, 25 May 2012 - 12:05 AM.

[wccaguy]

Evidence from someone other than Kevin Tracey that this CAIP exists and has a relationship to Heart Rate Variability...

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2009
Free access

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

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.

Edited by wccaguy, 25 May 2012 - 12:22 AM.

[wccaguy]

An attempt to falsify Tracey's CAIP hypothesis finds that, indeed, HRV varies inversely with inflammation...

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2007
Free access to study text available

Stimulated Production of Proinflammatory Cytokines Covaries Inversely With Heart Rate Variability

Objective: To examine whether high-frequency heart rate variability, an indirect measure of parasympathetic (vagal) control over variations in heart rate, is associated with immune reactivity to an in vitro inflammatory challenge. Convergent evidence from the animal literature shows that the autonomic nervous system plays a key role in regulating the magnitude of immune responses to inflammatory stimuli. Signaling by the parasympathetic system inhibits the production of proinflammatory cytokines by activated monocytes/macrophages and thus decreases local and systemic inflammation. As yet, no direct human evidence links parasympathetic activity to inflammatory competence.
Methods: We examined the relationship of variations in heart rate, recorded during paced respiration, to lipopolysaccharide-induced production of the inflammatory cytokines interleukin (IL)-1ß, IL-6, tumor necrosis factor (TNF)-α, and IL-10 among a community sample of 183 healthy adults (mean age = 45 years; 59% male; 92% White, 7% African-American).
Results: Consistent with animal findings, higher derived estimates of vagal activity measured during paced respiration were associated with lower production of the proinflammatory cytokines TNF-α and IL-6 (r = –.18 to –.30), but were not related to production of the anti-inflammatory cytokine IL-10. These associations persisted after controlling for demographic and health characteristics, including age, gender, race, years of education, smoking, hypertension, and white blood cell count.
Conclusions: These data provide initial human evidence that vagal activity is inversely related to inflammatory competence, raising the possibility that vagal regulation of immune reactivity may represent a pathway linking psychosocial factors to risk for inflammatory disease.

Edited by wccaguy, 25 May 2012 - 12:29 AM.

[wccaguy]

All that we are is the result of what we have thought.  The mind is everything.  What we think we become.  -- Gautama Siddharta, the Buddha

Among the most amazing things to me about the science of the CAIP is this... In the years between 1000 BCE and 400 BCE, the peoples inhabiting current day South Central India had discovered profound truths about human life and health.

• the Buddha and his spiritual comrades had discovered the meditation and mindfulness practices that our science only in the last 10 years has receognized as being valid.

• religious texts of this period also began to describe the healthful effects of the gum resin of the Frankincense tree (Boswellia Serata (AKBA)).  (I've spent a lot of time studying the science of Boswellia and how it inhibits the 5-Lipoxygenase Inflammatory Pathway.  Just a few months ago, the LEF, for the first time, published an editorial stating that 5-LO was involved in 7 out of the 10 most lethal diseases in the US.

Here is Dr. Barbara Fredrickson, the leading student in the world of Positive Human Emotions, about Positive Emotions and "Vagal Tone"...

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2010
free download

Upward spirals of the heart: Autonomic flexibility, as indexed by vagal tone, reciprocally and prospectively predicts positive emotions and social connectedness

Vagal tone (VT), an index of autonomic flexibility, is linked to social and psychological well-being. We posit that the association between VT and well-being reflects an “upward spiral” in which autonomic flexibility, represented by VT, facilitates capitalizing on social and emotional opportunities and the resulting opportunistic gains, in turn, lead to higher VT. Community-dwelling adults were asked to monitor and report their positive emotions and the degree to which they felt socially connected each day for 9 weeks. VT was measured at the beginning and end of the 9-week period. Adults who possessed higher initial levels of VT increased in connectedness and positive emotions more rapidly than others. Furthermore, increases in connectedness and positive emotions predicted increases in VT, independent of initial VT level. This evidence is consistent with an “upward spiral” relationship of reciprocal causality, in which VT and psychosocial well-being reciprocally and prospectively predict one another.

Edited by wccaguy, 25 May 2012 - 12:48 AM.

[wccaguy]

There's more to come... The devil is in the details right?  And there are lots more details...

When I have more time, I'll talk about my experience with HeartMath's emWave2 product...  An amazing tool.  It was the tool that led me to try to figure out why Acetylcholine helped me raise my HRV and keep it high...

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In the meantime, has your mind gone there yet?  I mean, you know, about the Placebo Effect?  Take the scientific findings of folks like Kevin Tracey and combine it with the insight and findings of Barbara Fredrickson and you can derive something close to a relatively strong Hypothesis about what lies behind the Placebo Effect.  And studies could be done to try to Falsify the Hypothesis.

So help me out... Before I go and post the following Figure as my Facebook Cover Photo, tell me what I got wrong, so I don't embarrass myself...

Enjoy healing yourself!





Explanations that transform the world are the beginning of Infinity -- David Deutsch

Edited by wccaguy, 25 May 2012 - 01:13 AM.

[wccaguy]

Two pics that didn't make the post about Fredrickson's Positive Emotions point before I lost edit capability on the post....

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A great figure illustrating "upward positive" and "downward negative" spirals of the mind and heart.  I believe the science is established and actual practiced has confirmed that autonomic flexibility (aka "positive vagal tone" or "parasympathetic nervous system dominance") is difficult or impossible to achieve without some degree of Positive Mental State...

These figures are from the Fredrickson, et al, study...


Upward spirals of positive emotions counter downward spirals of negativity: Insights from the broaden-and-build theory and affective neuroscience on the treatment of emotion dysfunctions and deficits in psychopathology


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That image of the chalkboard with Fredrickson's list of Positive Emotions was fuzzy.  Here's a better one...

Edited by wccaguy, 25 May 2012 - 02:13 AM.

[niner]

wccaguy, on 25 May 2012 - 12:31 AM, said:

Before I go and post the following Figure as my Facebook Cover Photo, tell me what I got wrong...

Is the wording right on the 7/8 box?  It sounds odd...

[wccaguy]

niner, on 25 May 2012 - 02:18 AM, said:

Is the wording right on the 7/8 box?  It sounds odd...

Hey niner... Thanks, you're right.  I'm thinking it should be "Reducing Serious Disease, Morbidity, and Mortality".

Thanks for spotting that!

[wccaguy]

Heart Rate Variability (HRV) is computed and measures "Vagal Tone," "Parasympathetic Dominance," "Autonomic Balance," etc.

Higher HRV is healthier and indicative of Vagus Activation/Stimulation. Lower HRV is implicated in more serious disease, morbidity, and death. Kevin Tracey's work on the Vagus/CAIP Nexus explains the physiology and biology of HRV.

In fact, the scientific evidence is clear that numerous vagus mutations must have arisen over thousands of years (because they exist in other mammals)  and it is recognized as an independent predictor of extreme longevity, by means of Heart Rate Variability measurement.

What follows below are snippets from numerous studies about the importance of HRV in aging, disease, and mortality.

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Relation of high heart rate variability to healthy longevity

The population's aging underscores the need to understand the process and define the physiologic markers predictive of healthy longevity. The findings that aging is associated with a progressive decrease in heart rate variability (HRV), an index of autonomic function, suggests that longevity might depend on preservation of autonomic function. However, little is known about late life changes.... The HRV-sympathetic function continues to decrease throughout life. In contrast, the decrease in HRV-parasympathetic function reaches its nadir in the eighth decade, followed by reversal and a progressive increase to higher levels (p <0.05), more characteristic of a younger population. In conclusion, healthy longevity depends on preservation of autonomic function, in particular, HRV-parasympathetic function, despite the early age-related decrease. The eighth decade reversal of the decrease in HRV-parasympathetic function and its subsequent increase are key determinants of longevity. Persistently high HRV in the elderly represents a marker predictive of longevity.

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We studied the significance for further survival of heart rate variability and other variables in the very elderly...
Logistic regression analysis using backward elimination detected three factors, dementia, LF/HF , and age, that independently influenced mortality. Mortality risk increased with greater age..., more severe dementia, or lower LF/HF [i.e., HRV].

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Consequently, the low-frequency/high-frequency ratio (0.43±0.07 compared with 0.91±0.05; P < 0.02) was also lower in the healthy centenarians than in the aged subjects. Our study demonstrates that the basal low-frequency/high-frequency ratio, an indirect index of cardiac sympathovagal balance, is lower in healthy centenarians than in aged subjects.

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These data confirm an age-related decline in sympathetic activity. Compared with elderly subjects from 81 to 100 years of age ultra-centenarians have significantly higher spectral parasympathetic indexes. Parasympathetic predominance may be the neuroautonomic feature that helps to protect ultra-centenarians against cardiovascular disease.

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This study demonstrated that age had a greater impact on HRV than sex. The older age group had consistently lower HRV than younger people. The values generated in this study may be useful in health care settings to determine abnormal ranges of HRV under different clinical and experimental conditions.

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Power-law relationship of 24-hour HR variability is a more powerful predictor of death than the traditional risk markers in elderly subjects. Altered long-term behavior of HR implies an increased risk of vascular causes of death rather than being a marker of any disease or frailty leading to death.

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HR variability remained a significant predictor of mortality after adjusting for clinical, demographic, other Holter features and ejection fraction. A hypothesis to explain this finding is that decreased HR variability correlates with increased sympathetic or decreased vagal tone, which may predispose to ventricular fibrillation.

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Decreased heartratevariability (HRV) is associated with congestive heart failure, post-myocardial infarction, ventricular arrhythmias, sudden cardiac death, and advancing age.

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Physiological ageing is associated with a reduction in parasympathetic control of the heart; this decline in parasympathetic activity can be reduced by regular endurance exercise.

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Intensive endurance training in elderly men enhanced parasympathetic parameters of HRV and, interestingly, of SBR. Physiological mechanisms and long-term clinical effects on health status should be further investigated.

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Low HRV was associated with increased risk of CHD and death from several causes. It is hypothesized that low HRV is a marker of less favorable health.

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ATRAMI provides clinical evidence that after myocardial infarction the analysis of vagal reflexes has significant prognostic value independently of LVEF and of ventricular arrhythmias and that it significantly adds to the prognostic value of heart-rate variability.

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CHF is associated with autonomic dysfunction, which can be quantified by measuring HRV. A reduction in SDNN identifies patients at high risk of death and is a better predictor of death due to progressive heart failure than other conventional clinical measurements.

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During a mean follow-up of 3.5 years, cardiac events occurred in 58 subjects. After adjustment for age, sex, cigarette smoking, diabetes, left ventricular hypertrophy, and other relevant risk factors, all HRV measures except the ratio of low-frequency to high-frequency power were significantly associated with risk for a cardiac event.

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Relationships between measures of inflammation and autonomic function are stronger among depressed than non-depressed cardiac patients. Interventions targeting regulation of both autonomic control and inflammation may be of particular importance.

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Substantial evidence exists to support the notion that decreased HRV precedes the development of a number of risk factors and that lowering risk profiles is associated with increased HRV. We close with a suggestion that a model of autonomic imbalance may provide a unifying framework within which to investigate the impact of risk factors, including psychosocial factors and work stress, on cardiovascular disease.

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heart rate variability may offer an inexpensive, non-invasive method of monitoring neuropathological processes following CA. The inverse linear relationships between heart rate variability and brain damage after CA also may partially explain why low heart rate variability is associated with increased morbidity and mortality in myocardial infarction patients.

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The components of the heart rate variability indicated that men with a large prostate had increased sympathetic activity.

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Exposures to Air Pollution is associated with decreased HRV, and history of IHD, hypertension, and diabetes may confer susceptibility to autonomic dysfunction by air pollution.

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TNF is an independent predictor of depressed heart rate variability in patients with heart failure.

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We concluded that power spectral analysis of heart rate variability offers a possible means of identifying episodes of sleep-related breathing disorders or periodic leg movements.

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Hemispheric brain infarction seems to cause significant long-lasting damage to the cardiovascular autonomic regulatory system manifested as abnormalities of heart rate variability. Distorted heart rate variability in the acute phase of stroke may be prognostically unfavorable.

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During the awakening period, global HRV and the parasympathetic tone were significantly lower in the worsened neurologic state group. In conclusion, HRV could be helpful as a predictor of imminent brain death and a useful adjunct for predicting the outcome of patients with severe head injury.

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HRV time and domain parameters were lower in patients with AD than in patients with MCI and controls.... QTD and HRV were found to be significantly correlated with the degree of cognitive impairment.

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Habitual tuna/other fish and marine ω-3 consumption are associated with specific HRV components in older adults, particularly indices of vagal activity, baroreceptor responses, and sinoatrial node function.

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These findings suggest that higher intake of green leafy vegetables may reduce the risk of cardiovascular disease through favorable changes in cardiac autonomic function.

Edited by wccaguy, 27 May 2012 - 08:35 PM.

[wccaguy]

This topic of the Vagus Nerve and the Cholinergic Anti-Inflammatory Pathway explains a lot of what health science we see floating around...

I made the followings posts at Dr. William Davis' TrackYourPlaque Forum...  It's the place I go to help me manage my Coronary Artery Disease... I think Dr. Davis is THE MAN on this topic...

At any rate, these posts are relevant to this topic.  My posts are about the bad science underlying the work of Dr. Dean Ornish...  The scientific work of Dr. Tracey explains how the bad diet advice of Dr. Ornish is compensated for by lifestyle change and stress reduction...

Enjoy...


wccaguy

Master Contributor

Posted: 5/28/2012 10:03:47 AM
Ornish is a master at confounding of independent variables in his studies.  I believe any positive health effects his experiments have had can be explained now by a look at the science of the variables he confounds.  There is something profound we can learn here by taking his experiments apart.

• Notice that his studies always include, not just low fat diets, but also "lifestyle change."  The kinds of lifestyle change he advocates always amount to the same thing:  stress reduction.

• He's a slippery guy... If you watch closely, in his writing and speaking engagements, he always talks about the importance of the lifestyle change independent variable but then he quickly shifts to talk about low fat diets.  That's his schtick...

• So what is this independent variable "lifestyle change" (aka stress reduction).  How can that, per se, possibly compensate for the negative health effects of the low fat diet?  That question has been among the puzzling questions right?  Well, it need no longer be a puzzling question because now we understand the science of what's going on.

• We now know that stress reduction techniques shift the balance of Autonomic Nervous Systems:  the Parasympathetic Nervous System more dominates the Sympathetic.  And we now know that shift is correlated with Vagus Nerve Stimulation and Activation of the Cholinergic Anti-Inflammatory Pathway (CAIP).

• Thanks to the work of Dr. Kevin Tracey and others about the CAIP, we now understand the profoundly positive health effects the CAIP can have.  Thanks to the work of Dr. Barbara Fredrickson we now understand that Positive Emotions, (aka, per Ornish as "lifestyle change") increase "Vagal Tone" and that leads to the activation of the CAIP.

• Swinging the point back around to Ornish now...  We now know that the "lifestyle changes" his work always includes are so powerful via the CAIP that they compensate for the ill health effects of the low fat diet.

I've established threads about the Vagus Nerve and the CAIP here at the TYP Forum and here at the longecity forum.  The posts at the longecity forum provides a more systematic introduction to the topic because, here at the TYP Forum, I was posting as I was getting a handle on the topic.

But back to the discussion of diet just for a moment... Check this out...  It turns out that a High Fat Diet, per se, stimulates the Vagus Nerve...

Why are specially chosen fats healthy... I think what follows below explains much of the reason...

Enjoy!

Steve

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Fat meets the cholinergic antiinflammatory pathway

The cholinergic antiinflammatory pathway is a neural mechanism that is controlled by the vagus nerve and inhibits local cytokine release, thereby preventing the damaging effects of cytokine overproduction. A new study now shows that dietary fat can activate this pathway, a finding that may help explain the immune system's failure to react to food antigens and commensal bacteria. Here we discuss this new data and its potential implications for dietary intervention in the treatment of inflammatory diseases.

Tags: wccaguy

Master Contributor

Posted: 5/28/2012 10:19:17 AM You heard it hear first...

Kevin Tracey is going to win the Nobel Prize in Medicine for his work on CAIP.  That's how important it is.

And look, Dr. Davis has already pointed the TYP program in that direction by providing us with a means of purchasing a powerful tool to increase our Vagal Tone and activate the CAIP at a price better than the one at Amazon...  Use of THAT tool (the PSR version) is what lead me to discover the literature about the CAIP.  IMHO, it's an essential component of a CAD fighting strategy.  Buy it here at TYP...

https://shop.trackyo.../heartmath.aspx

My hope is that Dr. Davis will soon author an easy to understand article about the CAIP for a wider audience.  I've told him he should...  He's the guy to do it!

Not that he should increase his stress level or anything like that...  I want Dr. Davis to write the article about the CAIP so it will give HIM and TYP more visibility...

8-)
Tags: wccaguy

Master Contributor

Posted: 5/28/2012 10:31:24 AM
You know.... I went from making those posts above to my email inbox and came across a study summary from Kurzweilai.net...  You gotta check this out.  It makes the point about positive emotions...


‘Personality genes’ may help account for longevity

It's about the Positive Emotions that I was just mentioning that Barbara Fredrickson has written about...   Here...

Kok, B.E. & Fredrickson, B.L. (2010). Upward spirals of the heart: Autonomic flexibility, as indexed by vagal tone, reciprocally and prospectively predicts positive emotions and social connectedness Biological Psychology, 85, 432-436.

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Is it any wonder now how Ornish, THE master confounder of independent variables, has gotten away with promoting low fat diets by including "lifestyle change" as part of his program?

8-)