Phew! So it’s going much better than I thought!?

I have often written about all the difficulties I have had with reading my emotions. Especially in early recovery when I could not even identify and label the most intense negative emotions.

That experience has set me on a near decade-long search to better understand emotions and the way a lack of awareness of emotions plays in addiction and in recovery.

Today I would say the effective and rational/reasonable control of emotions is one area that has become noticeably better.

I tolerate negative emotions better, their intensity is much reduced compare to early recovery, the duration of these emotions is much much shorter than before. I seem to also make better decisions in my life based on not being overwhelmed by my emotions, particularly negative emotions.

It is said by much research that addicts, alcoholics and those with behavourial addictions have something skin to alexithymia, an impaired ability to read emotions and act on them in making decisions.

Humans seem to use emotions to make decisions which is something I never realized before.

When I ask my wife how have I changed she always says I have become more considerate and more mature in my emotional reactions.

This to me shows recovery as a process of handling emotions better, in a more emotional mature as opposed to immature way.

I also have looked at lots of research that says this emotional immaturity is there for many pre-using drugs or alcohol or engaging in unhealthy behaviours. So it may be a part of the aetiology of addictive behaviours.

When I first came into recovery I remember my wife would drive me to AA meetings. This was before my sponsor said I would be either walking or getting the bus from now on!

I was mortified?

ME!? Doesn’t he know who I am?

I have chauffeur, thank you very much?.

I had become so emotional dependent on my wife. It was like another addiction/dependency.

Recovery has been a long, at times painful, process of growing up, however reluctantly at times!

I was not only powerless over alcohol but fairly hopeless too when it came to living life on lives terms.

The more chronic my addictions became the more I regressed emotionally.

The more I recovered the more I matured emotionally,  is my point.

Even today I often have to “talk my emotions out” to see what I feel really, before I can label and identify what I am feeling really.

Before I can act maturely on what I am feeling instead of emotionally reacting which is what I always used to do.

As a fellow recovering person said in this article (1)  . . “. sit down with people and bounce some ideas off each other and get it off your chest and stuff. That’s very helpful and that kind of helps me, like saying it out loud to identify where I’m actually at.”

This is why ringing sponsors and talking to fellow recovering people is essential  especially in early recovery.

We do not how we feel clearly what we are really feeling otherwise, delude ourselves everything is fine, continue to make poor decisions to the point of becoming emotionally  drunk and then often relapsing to physically drunk.

We do all of this sometimes not because we want to drink but because we think we can do it alone when we cannot.

Sometimes in early recovery we haven’t go a clue what is going on, our arrogant pride however resists this idea and keeps missing the point of what is really going on.

Our errant emotion processing does not result in clear thinking, it results in negative, strangely deluded thinking.

By deluded I mean divorced from the reality of things as they really are. It takes some weeks and months to realize we cannot fully rely on our own thinking and this can be a blow to the pride.

The concluding part of this study (1) was very revealing to me and explained part of the “feeling” that often accompanies early recovery, the feeling of not recovering fast enough of not recovering NOW!

Addicts and alcoholics want everything NOW even recovery, they want the recovery of ten years in ten weeks!

” …some  participants interpreted negative feelings as global markers of overall emotional ill health and poor progress in recovery, for example, “I think I should be feeling better now” and “I thought I was progressing but in a lot of ways I haven’t and that’s not good.”

Here, participants realize they are experiencing negative feelings and understand it as suggestive of a larger negative phenomenon, for example, that they are not “better now” and not “progressing” as previously thought. This type of negative globalization is a type of cognitive distortion.”

A cognitive distortion is a deluded thought like those mentioned above. Our errant negative emotions produce distorting thinking.

Our negative feelings rarely tell us the truth. They give some jaundiced view of reality.

This is why we need to have constant contact with others in recovery to offload these negative feelings.

Just as with sharing with a sponsor or a friend to find out what we feel, we need to share with others to undistort our negative thinking. Negative emotions often give rise to negative thinking.

“As one participant said “And I know [recovery] is not a magic fix either because I didn’t expect, if you get sober to be all of a sudden everything is perfect. That’s not the way it works. . . . So it’s going to take you a little longer to feel better.””

I would add to this that it is  progress not perfection.

I would also add that we can feel better quicker than we think on a basis, one day at a time.

Ring someone, talk to someone and try to verbalise how you feel.

This straightens out your thinking and you will feel better right away.

We drank to go “phew!” a release from our thinking and negative heads, now we “share” with others what is really going on with us, to get to understanding what emotions ail us and this leads to the same feeling of release, to the same feeling of “phew!”

We never have to drink again to go “phew”, talk to someone instead.

We will discover things are never as negative as our thinking has lead us to believe, and are usually a whole better in fact!

We recover together.

 

References

1. Krentzman, A. R., Higgins, M. M., Staller, K. M., & Klatt, E. S. (2015). Alexithymia, Emotional Dysregulation, and Recovery From Alcoholism Therapeutic Response to Assessment of Mood. Qualitative health research,25(6), 794-805.

The terror of “Locked In” Attention!

I remember when I was in the first days, weeks and months of early recovery I used to give myself such a hard time when my attention was drawn to some alcohol-related cue, like someone drinking ,or finding it difficult not dealing with some  reminder of people places and things from my alcohol abusing past; finding that I found it nigh on impossible dragging my attention away from these and related memories associated with my drinking past.

It was as if I was entranced by it, in some of tunnel vision. It used to scare the life out of me.

I rarely found these thoughts appetitive but if I dwelt on these thoughts or trained my attention on cues I would find that the adverse, fearful things would turn to more desire based physiological reactions like salivating and so on.

I took these to mean that I actually wanted to drink and not stay sober. My sponsor at the time said two things which helped – a. I have an alcoholic brain that wants to drink period, 2. cues from my past may always have this effect on me. Accept it, don’t fight it.

That was what I had been doing in fact. Fighting it, these cues reminders and their automatically occurring intrusive thoughts about the past. It is in fighting these thoughts that they proliferate and then become “craving”.

Years later after much research I found that all alcoholics seem to have an attentional bias towards alcohol-related cues which leads to a cue reactivity.

Originally I thought this meant that I simply wanted to drink but found out that in  any manifestation of urge to drink (which is slightly different from a craving which requires an affective response on the part of the alcoholic in order to become a craving similar to mental obsession of the Big Book ) there is a stress reponse like the hear beat quickening, differences in galvanic skin conductance, increased saliva production etc .

Thus this cue reactivty seems to involve not only appetitive or desire states, i.e. it activates the reward system in the brain to motivate one to drink but also contains a stress based reactivity.

Any so-called “craving” state also manifests as either an anxiety state in simple cue reactivity e.g. the sight of alcohol or in negative emotions such as fear, anger and sadness in terms of a stress based craving.

Together, i.e. a cue based reactivity in the face stress/distress leads to a greater urge to drink than by either alone. By reacting to these one is increasing the stress/distress.

To the alcoholic brain having a drink or the desire to drink is the brain suggesting to us as alcoholics that this is the best way to attain transient homeostasis from an allostatic state of distress because this is how we used to balance the effects of emotional distress when we were drinking. We experience distress and automatically had thoughts about drinking. Thus alcoholism is a distress-based condition. We think it is us wanting the drink but it is the distress prompting the wanting of the drink!!

The distress does the drinking for us, itgets us out of our seats and down the street to the bar, it gets us on the bar stool….We may think it is our actions as we use rationalisng and justifying schemata afterwards to justify behaviour that had, in fact, been automatic or compulsive, compulsive meaning to relieve a distress state.

As a schema, which is implicit, i.e. it is automatically prompted and activated by distress also. We are not even in charge of this. We feel and think that we are in control over behaviour bit this is not the case as self control has become so impaired and limited it is distress doing the action and the subsequent rationalising.

The compusive part of the brain, the dorsal striatum, is the only part of the brain that requires us to make a post hoc rationalisation of why we did an action that was essentially automatic and compulsive.

We have become passengers in our own lives. Distress is now doing the driving.

So the brain thinks it is simply telling us the best way to survive this distress or in other words to regulate this distress. Thus it is an incredibly impaired way to regulate stress and emotional distress.

I want to further explain how some of this is linked to low heart rate variability. If we have low HRV we find it difficult inhibiting automatic responses and in changing behaviour. We become behaviourally rigid, and locked into attending to things like cues when we don’t really want to.

This is often the result of distress reducing the ability of the heart rate variability to inform and change our responses.

I cite and use excerpts form one of my favourite articles again by co-authored by Julian Thayer (1).

 

“The recovering alcoholic must face the difficulty of having his or her ambition to remain abstinent challenged in various situations in which memories about the pleasurable effects of alcohol are activated and the striving for abstinence no longer seems meaningful (Anton 1999; Marlatt and Gordon 1985). The odds for successful coping with such temptations are related to numerous factors, such as one’s subjective affective state and the ability to shift one’s focus from the automatic impulse to drink toward a cognitive reconstruction of the situation (Palfai et al 1997b; Tiffany 1990). Despite the importance of  attentional flexibility in effectively modulating such “highrisk” situations, research on the topic is scarce.

Thayer and Lane (2000) suggested that the interplay between positive (excitatory) and negative (inhibitory) feedback circuits in the nervous system (NS) allows for flexible and adaptive behavior across a wide range of situations. The uniqueness of this model lies with its emphasis on the importance of inhibitory processes in effective modulation of affective experience. In short, these researchers propose that the defects in neurovisceral regulation of affective experience seen in various psychiatric conditions (e.g., anxiety disorders) may be better explained by faulty inhibitory function in the NS than by unitary arousal models.

Tonic heart rate variability (HRV) may be a physiologic indicator of such inhibitory processes (Friedman and Thayer 1998a; Porges 1995). Heart rate variability refers to the complex beat-to-beat variation in heart rate produced by the interplay of sympathetic and parasympathetic (vagal) neural activity at the sinus node of the heart.

Importantly, heart rate (HR) is under tonic inhibitory control via the vagus nerve (Levy 1990). These neural connections to the heart are linked to brain structures involved in goal-directed behavior and adaptability (Thayer and Lane 2000). Compelling evidence now exists to show that high levels of HRV are related to cognitive flexibility (Johnsen et al 2003), modulation of affect and emotion (see Bazhenova 1995, cited in Porges 1995), and increased impulse control (Allen et al 2000; Porges et al 1996).

The hypothesis that reduced HRV is related to defective affective and emotional regulation has been supported in recent research in which reduced HRV was present in clinical disorders such as generalized anxiety disorder (Thayer et al 1996), panic disorder (Friedman and Thayer 1998b), posttraumatic stress disorder (Cohen et al 1997) several scientific arguments suggest that impaired inhibitory function may play a role in chronic alcohol abuse.

First, alcoholics have repeatedly been shown to have problems shifting attention and directing their attention away from task-irrelevant information (Johnsen et al 1994; Setter et al 1994; Stormark et al 2000). Second, frontal areas of the brain are most affected by the acute and chronic effects of alcohol, and these structures are of crucial importance in inhibitory functioning and self-control (Lyvers 2000). Third, acute effects of alcohol ingestion result in reductions in HRV, implying that chronic alcohol ingestion may result in a long-lasting impairment of the vagal modulation of HR (Reed et al 1999; Weise et al 1986)

Fourth, severely dependent alcoholics show a sustained phasic HR acceleration when processing alcohol information, indicating defective vagal modulation of cardiac function (Stormark et al 1998). Tonic HRV has similarly been found to be a useful measure of physiologic activity in challenging situations (Thayer and Lane 2000). Appropriate modulation of HRV (increases, decreases, or no change) depends on the type of challenge and the characteristics of individuals as they interact with specific contextual manipulation (Friedman and Thayer 1998a; Hughes and Stoney 2000; Porges et al 1996; Thayer et al 1996).

For example, during attention demanding tasks, healthy individuals show appropriate reductions in HRV (Porges 1995). In general, high tonic levels of HRV allow for the flexible deployment of organism resources to meet environmental challenges. With respect to attention, it is suggested that high levels of HRV reflect flexible attentional focus, whereas low HRV is related to “locked in attention” (Porges et al 1996). Moreover, increased tonic vagal activity is related to adaptive development and lack of behavioral and emotional problems (Hughes and Stoney 2000; Porges et al 1996).

Furthermore, it has been demonstrated that increases in vagal activity during challenging tasks discriminates between individuals who have experienced traumatic events and managed to recover from them and those who still suffer from chronic symptoms of posttraumatic stress (Sahr et al 2001). Such increases in vagal activity during challenging tasks are particularly interesting because studies on alcohol abusers have found increases in HRV after exposure to alcohol-related cues (Jansma et al 2000; Rajan et al 1998).

One could speculate that such enhanced vagal activity could be a sign of compensatory coping aimed at taming automatic drinking related processes (Larimer et al 1999). Such an interpretation is in agreement with cognitive theories predicting that alcoholics and other drug users do not simply respond passively to exposure to drug-related cues, but, on the contrary, in such situations conscious processes are invoked, inhibiting execution of drug-related cognition (Tiffany 1990, 1995). If this explanation is correct, alcoholics who have more effective coping resources should show stronger increases in vagal activity during such challenging exposure than alcoholics who express greater difficulty in resisting drinking-related impulses.

Also  general differences in HRV between alcoholics and nonalcoholics are interesting indicators of defective inhibitory functioning, a measure of rigid thought-control strategies and lack of cognitive control should be an important indicator of defective inhibitory function and “positive feedback loops” reflected as low HRV (Wegner and Zanakos 1994).

Linking these measures to the physiologic index of HRV makes a stronger case for attributing reduced vagal tone (HRV) to a defective regulatory mechanism resulting in unpleasant affective states and maladaptive coping with psychologic stressors

The main results of our study may be summed as follows. First, as expected, alcoholic participants had lower HRV compared with the nonalcoholic control group. Second, the imaginary alcohol exposure increased HRV in the alcoholic participants. Third, across the groups, an inverse association was found between HRV and negative mood and a positive association between positive mood and HRV. Fourth, HRV was negatively correlated with compulsive drinking during the imaginary alcohol exposure in the alcoholic participants. Fifth, within the alcoholic group, HRV was negatively associated with chronic thought suppression (WBSI).

Generally, these findings are in agreement with the neurovisceral integration model and the polyvagal theory that suggests HRV is a marker of the level of cognitive, behavioral, and emotional regulatory abilities (Thayer and Lane 2000).

The fact that the alcoholic group had generally lower tonic HRV compared with the nonalcoholic control group indicates that such reduced HRV may also be a factor in alcohol abuse; however, such group differences in HRV provide only indirect support for the theory that low HRV in alcoholics may be related to impaired inhibitory mechanisms

Because HRV is related to activity in frontal brain areas involved in cognition and impulse control (Thayer and Lane 2000), we speculated that tonic HRV would be an index of nonautomatic inhibitory processes aimed at suppressing and controlling automatic drug-related cognitions. To test this hypothesis more directly, the association between HRV and problems with controlling drinking-related impulses were studied.

Consistent with this hypothesis, the compulsive subscale of the OCDS was found to be inversely associated with HRV in the alcohol-exposure condition, thus suggesting that HRV may be an indirect indicator of the level of impulse control associated with drinking. These findings are therefore consistent with Stormark et al (1998), who found that sustained HR acceleration (lack of vagal inhibition) when processing alcohol-related information was related to compulsive drinking and “locked-in attention.”

Post hoc analysis further suggested that alcoholics who expressed a relatively high ability to resist impulses to drink (OCDS) had the clearest increase in HRV under the alcohol exposure this study suggests that alcoholics may actively inhibit or compensate for their involuntary attraction to alcohol-related information by activation of higher nonautomatic cognitive processes (Tiffany 1995). Such conscious avoidance has previously been demonstrated in studies on attentional processes in alcoholics (Stormark et al 1997) and by the fact that frontal brain structures involved in inhibition and control of affective information are often highly activated in the processing of alcohol related cues (Anton 1999). Furthermore, this interpretation is in agreement with other studies suggesting that high HRV during challenging tasks is associated with recovery from acute stress disorders (Sahr et al 2001).

Several studies have indicated that low HRV is associated with impaired cognitive control and perseverative thinking (Thayer and Lane 2002). Consistent with these reports a negative association was found between HRV and chronic thought suppression. The WBSI assesses efforts to eliminate thoughts from awareness while experiencing frequent intrusions of such “forbidden” thoughts and thus represents an interesting and well-validated measure of ineffective thought control (Wegner and Zanakos 1994). Thought suppression has been found to be an especially counterproductive strategy for coping with urges and craving (Palfai et al 1997a, 1997b) and may even play a causal role in maintaining various clinical disorders (Wenzlaff and Wegner 2000).

To our knowledge, this is the first time a link between physiologic indicators of a lack of cognitive flexibility (low HRV) and chronic thought suppression has been demonstrated.

Thayer and Friedman (2002) have reviewed evidence indicating that there is an association between vagally mediated HRV and the inhibitory role of the prefrontal cortex. Consistent with Thayer and Lane (2000), this study suggests that impaired inhibitory processes are significantly related to ineffective thought control.

The fact that this association between HRV and WBSI was only found in the alcoholics may be related to the fact that only this clinical group shows signs of such faulty thought control.

Wegner and Zanakos (1994) suggested that thought suppression is particularly ineffective when the strategic resources involved in intentional suppression are inhibited or blocked (Wegner 1994). Consistent with this hypothesis, our findings show that those reporting high scores on WBSI show signs of impaired inhibitory functioning as indexed by low vagally mediated HRV.”

This excellent article fro me is also alluding to the fact that those with increased HRV was related to successfully related to regulating negative emotion,  stress/distress and affect, not just the thoughts that these affective states gave rise to .

Thus any strategies that help with improving  the ability to increase HRV will likely have positive results in coping with cue associated materials.

We look at one of these therapeutic strategies next…that of mindfulness meditation.

 

References

1. Ingjaldsson, J. T., Laberg, J. C., & Thayer, J. F. (2003). Reduced heart rate variability in chronic alcohol abuse: relationship with negative mood, chronic thought suppression, and compulsive drinking. Biological Psychiatry54(12), 1427-1436.

 

 

 

The Heart of Recovery

How is low HRV related to longer term recovering alcoholics?

We cited and use excerpts from a study (2) into short term and longer term (3) of up to six months which shows that alcoholics with years of recovery still have low HRV although it improves although this is dependent of severity of the alcoholism.

“It is known that chronic and heavy alcohol use has a toxic effect on the nervous system,[2] including effects on autonomic nervous system.[3] Specifically, heavy alcohol use can cause cardiac autonomic neuropathy,[4] which in turn, is associated with greater mortality.

Resting cardiac autonomic function reportedly favors energy conservation by way of parasympathetic dominance over sympathetic influence. Heart rate is characterized by beat-to-beat variability over a wide range, which has been reported to indicate vagal dominance and thereby parasympathetic dominance.[5]

In those with alcohol dependence, HRV is lower than in healthy individuals even after several days of abstinence.[13,14] This decrement may improve with abstinence for long periods of time.[15,16]

A study of 24-h ambulatory HRV found significantly reduced HRV in alcohol-dependent men with established vagal neuropathy and in some without.[17] Alcohol dependence has been shown to compromise vagal output measured before sleep onset, which correlates with loss of delta sleep and morning sleep impairments.[18]

Reduced HRV was found in alcohol-dependent patients with negative mood states and compulsive drinking.[19] Rechlin et al.,[20] reported reductions in HRV in patients with alcohol dependence, and this has been consistently reported in subsequent studies.[21,22]”

 

“Heart rate variability (HRV) was studied in 11 chronic alcoholic subjects, 1–30 days after the beginning of abstinence and again 5, 12 and 24 weeks later. Two patients could be re-examined after 19 and 22 months, respectively. In the follow-up study, the total patient group showed a statistically significant increase in HRV with prolonged abstinence of at least 6 months.

No recovery of efferent vagal function was found in 4 patients. It is suggested that the vagal neuropathy may improve in chronic alcoholics, but perhaps only in patients with a short to moderately long duration of drinking history (3)”.

Thus it seems thee is a partial recovery in HRV as recovery proceeds although there may be work required depending on severity of one’s alcoholism.

In our next blog on HRV we will cite and use excerpts from one of the best articles authored by Thayer which is the best explanation of how low HRV keeps an alcoholics attention “locked in” to stuff he/she would rather it didn’t get locked into such as alcohol-related cues.

References

1. THAYER, J. F., AHS, F., FREDRIKSON, M., SOLLERS, J. J., & WAGER, T. D. (2012). A meta-analysis of heart rate variability and neuroimaging studies: Implications for heart rate variability as a marker of stress and health.Neuroscience and biobehavioral reviews, 36(2), 747-756.

2. Ganesha, S., Thirthalli, J., Muralidharan, K., Benegal, V., & Gangadhar, B. N. (2013). Heart rate variability during sleep in detoxified alcohol-dependent males: A comparison with healthy controls. Indian journal of psychiatry, 55(2), 173.

3. Weise, F., Müller, D., Krell, D., Kielstein, V., & Koch, R. D. (1986). Heart rate variability in chronic alcoholics: a follow-up study. Drug and alcohol dependence, 17(4), 365-368.

Recovery is a Journey from the Head to the Heart (and back)!

PART 2 

So what does this low HRV mean for the recovering alcoholic?

I have explained this to show that HRV is directly connected to areas of the the brain implicated in stress and emotion regulation.

If, via recovery practices, we can still our beating heart, become serene as well as clean, it will have neuroplastic effects on our brain and the regulation of emotion and stress.

Equally if we meditate and alter the functioning of areas implicated in this study such as areas of the medial PFC and cingulate gyrus we improve our control over our heart. Ultimately if we can learn to relieve the inherent distress at the heart of addiction we can recovery function of not only the heart but also of areas in the brain which interact with the heart in producing heart rate variability.

So ultimately we need only to know how to quell a distressed heart via prayer, meditation, loving others.

If we can do so, we improve our emotion and stress regulation.

But do we need to do this if we have been in recovery long term?

Let me give you an example of allostasis in action.

In an allostatic system like addiction there is stress dysregulation coupled with reward dysfunction (I believe there is a pre-morbid allostasis in those addicts who have experienced abuse, trauma and insecure attachment also which means there is a stress and emotion dysregulation from an early age which leads to a heightened reward sensitivity which means we start to regulate negative emotions from an early age via impulsively  using or consuming stuff we really really like, or seem to like more than healthy people, to make ourselves feel better).

These adolescents at risk also have low HRV and the effects of alcohol have a pronounced effect on HRV.

This sets the chain of addiction in action from the start for many addicts.

So when we decide we want something this leads to a feeling of pathological wanting and then needing simply because we have altered reward systems as they are linked to our “out of kilter” stress systems .

Buying something in the store, if thwarted, soon becomes a life and death like struggle. Ever had that feeling?

I remember a 75 year old recovering person with 30 odd years of recovery  sharing in a meeting how she went to a store to get something, to find that something wasn’t there, so she was instructed to drive somewhere else to get that something, and when she got there they didn’t have it, so she had an argument with them and then with her husband in the car, then off to another store which did not have the something either, then back home on the internet, found a online store that stocked the something and ordered it.

It arrived the next day because she paid a lot of money for it to arrive the very next day! When it arrived she found that she had not only completely forgot about ordering the something but did not really want the something even. So off she sloped to apologise to her husband for being so emotionally abusive and immature over the something on her way to the Post Office to post back the something that she never really wanted in the first place!!?

This is also my head still, even after a few years of recovery. It is not as bad it was, by a long shot! It does, however, get distressed, I become impulsive and  want, need, that thing now!!! On occasion.

So I think this is one area recovery people always need to be aware of. Wanting stuff.

As it can lead to pathological wanting fairly quickly – then people get in the way of those things and we get angry, frustrated, distressed, our emotions overwhelm us or we are mean to our fellow human beings all because they are getting in the way of the thing I really really want.. NEED God damn it!…

We lose our emotional sobriety.

When we have either got it, regardless of the the human or emotional cost, we often find we do not want it or never really wanted it…that much….

Not compared to the cost of getting it!?

How do we solve this problem? We let go, we calm down, talk to someone, express our feelings, try to establish a transient homeostasis, let our stress systems subside and start again, trying to managing these chaotic brain systems.

Amends time.

If you are like that you have a low HRV and a stress/emotion regulation problem and probably always will.

But if can be manged and it can vastly improve. Then one day we learn that it is in living with our hearts forefront to our decisions and not our heads that brings lasting everyday happiness.

That is why in recovery we travel from our at times over zealous heads to our hearts. The wisdom and direction and basis of our decision making lives their not in our heads. It is not to say we do not use these wondrous instruments but we incorporate the help of our hearts in activating the reasoning of the brain.

Solve the heart issue, and the rest comes.

 

Neural structures associated with HRV

Over the past several years however a number of human neuroimaging studies have appeared in which researchers have explicitly examined the brain structures associated with HRV. In the present paper we provide a meta-analysis of eight published studies in which HRV has been related to functional brain activity using either PET or fMRI

The goal of this meta-analysis was to identify areas that were consistently associated with HRV.

In the overall analyses three regions show significant activations One region in the medial PFC (MPFC) is the right pregenual cingulate (BA 24/32).

Brodmann Cytoarchitectonics 24.pngBrodmann Cytoarchitectonics 32.png

 

Another MPFC region is the right subgenual cingulate (BA 25).

Brodmann Cytoarchitectonics 25.png

The third region is the left sublenticular extended amygdala/ventral striatum (SLEA). This region extends into the basolateral amygdalar complex, and also covers the superior amygdala (central nucleus) and extends into the ventral striatum.

 

 

More generally, the pgACC/rmPFC correlation with HRV in our meta-analysis suggests thatthis region is part, and the most reliably activated part in studies to date, of a descending “visceromotor” system that controls the autonomic nervous system and possibly other responses (neuroendocrine) based on emotional context.

The meta-analysis provides supportfor the idea that HRV may index the degree to which a mPFC-guided “core integration” system is integrated with the brainstem nuclei that directly regulate the heart. Thus these results support Claude Bernard’s idea that the vagus serves as a structural and functional link between the brain and the heart. We have proposed that this neural system essentially operates as a “super-system” that integrates the activity in perceptual, motor, interoceptive, and memory systems into gestalt representations of situations and likely adaptive responses. These findings suggest that HRV may index important organism functions associated with adaptability and health.”

References

1. THAYER, J. F., AHS, F., FREDRIKSON, M., SOLLERS, J. J., & WAGER, T. D. (2012). A meta-analysis of heart rate variability and neuroimaging studies: Implications for heart rate variability as a marker of stress and health.Neuroscience and biobehavioral reviews, 36(2), 747-756.

Journey from the Head to the Heart (and back)!

Part 1

Over this week leading up to my interview/podcast with sincerightnow http://www.sincerightnow.com/upcoming/ http://www.sincerightnow.com/pdcst/

I want to look at the “neuroscience of alcoholism and addiction from another angle. I want to look at the evident difficulties seen in alcoholics in terms of impaired self and emotion regulation by looking at the relationship of the heart to the brain.

Some may find this a more clear, easier way to understand what is impaired in terms of brain functioning in alcoholics. I know I do and looking at the role of the heart in alcoholism has helped me understand the issues more clearly. I hope it does for you too.

I will seek to explain how the emotional, stress and thus self dysregulation seen in alcoholics and addicts is indexed or can be seen clearly in terms of a reduced heart rate variability  compared to normal healthy individuals.

I will explain as we go, how low HRV is linked to this dysregulation gives rise to a stress and emotion reactivity and an impulsivity seen commonly in alcoholics in particular.

This low HRV has a interactive effect in the emotion regulation  parts of the brain also with one effecting the other. So in terms of say reducing distress, stress and thus craving, for example, we could suggest instead use measures to improve low HRV such as mediation and so on. If we get the heart under more control, the neurotransmission of the brain and stress chemicals too seem also to be affected.

It certainly ties in with treatment regimes which advocate strategies of letting go of distress and maintaining balance and serenity.

Personally I find it fascinating how the heart can affect the workings of the brain.

Before we look at the concept of heart rate variability in relation to alcoholism we need to first to look at the interaction between the head and the heart.

We cite and use excerpts from a review (1) by Julian Thayer, one of the leading experts on the subject of heart rate variability (HRV) and it’s relationship to impaired self and emotion regulation.

“The intimate connection between the brain and the heart was enunciated by Claude Bernard over 150 years ago.

Heart rate variability may provide an index of how strongly ‘top–down’ appraisals, mediated by cortical-subcortical pathways, shape brainstem activity and autonomic responses in the body.

Thus, HRV may serve as a proxy for ‘vertical integration’ of the brain mechanisms that guide flexible control over behavior.

We have proposed that a core set of neural structures provides an organism with the ability to integrate signals from inside and outside the body and adaptively regulate cognition,perception, action, and physiology.

This system essentially operates as a “super-system” that integrates the activity in perceptual, motor, interoceptive, and memory systems into gestalt representations of situations and likely adaptive responses. Thus, it is undoubtedly extremely complex. However, it is still possible that physiological measures exist that can serve as indices ofthe degree to which this system provides flexible, adaptive regulation of its component systems. In a number of papers (Thayer and Brosschot, 2005; Thayer and Lane, 2000, 2009), we have proposed that heart rate variability (HRV) may provide just such an index.

However if component systems are become unbalanced, and a particular process can come to dominate the system’s behavior, rendering it unresponsive to the normal range of inputs. In the context of physiological regulation, and regulation of the heart specifically, a balanced system is healthy, because the system can respond to physical and environmental demands (Thayer and Sternberg, 2006). A system that is “locked in” to a particular pattern is dysregulated. This is why the heart rate of a healthy heart oscillates spontaneously (i.e., shows high HRV), whereas a diseased heart shows almost no variability under certain conditions. A critical idea is that HRV may be more than just an index of healthy heart function, and may in fact provide an index of the degree to which the brain’s “integrative” system for adaptive regulation provides flexible control over the periphery. Thus, HRV may serve as an easily measured output of this neural network that may provide valuable information about the capacity of the organism to effectively function in a complex environment.

 

Hear Rate Variability

Like many organs in the body, the heart is dually innervated. Although a wide range of physiologic factors determine cardiac functions such as heart rate (HR), the autonomic nervous system (ANS) is the most prominent with Although a wide range of physiologic factors determine cardiac functions such as heart rate (HR), the autonomic nervous system (ANS) is the most prominentwith  both cardiac vagal (the primary parasympathetic nerve) and sympathetic inputs.

 

 

The heart is under tonic inhibitory control by parasympathetic influences. Thus, resting cardiac autonomic balance favors energy conservation by way of parasympathetic dominance over sympathetic influences. In addition, the HR time series is characterized by beat-to-beat variability over a wide range, which also implicates vagal dominance as the sympathetic influence on the heart is too slow to produce beat to beat changes.

Low heart rate variability (HRV) is associated with increased risk of all-cause mortality, and low HRV has been proposed as a marker for disease (Thayer and Lane, 2007; Thayer et al., 2010b). The basic data for the calculation of all the measures of HRV is the sequence of time intervals between heart beats. This interbeat interval time series is used to calculate the variability in the timing of the heart beat. As mentioned earlier the heart is dually innervated by the autonomic nervous system such that relative increases in sympathetic activity are associated with heart rate increases and relative increases in parasympathetic activity are associated with heart rate decreases.

Thus relative sympathetic increases cause the time between heart beats (the interbeat interval) to become shorter and relative parasympathetic increases cause the interbeat interval to become longer.

The differential effects of the ANS on…s the timing of the heart beats, are due to the differential effects of the neurotransmitters for the sympathetic (norepinephrine) and parasympathetic (acetylcholine) nervous systems. The sympathetic effects are slow, on the time scale of seconds, whereas the parasympathetic effects are fast, on the time scale of milliseconds. Therefore the parasympathetic influences are the only ones capable of producing rapid changes in the beat to beat timing of the heart.

In summary, the heart and the brain are connected bidirectionally. Efferent outflow from the brain affects the heart and afferent outflow from the heart affects the brain. Importantly, the vagus is an integral part of this heart–brain system and vagally mediated HRV appears to be capable of providing valuable information about the functioning of this system.

 

HRV and emotional regulation In addition to being linked to vmPFC and amygdala modulation, emotion regulation is linked to HRV (Appelhans and Luecken, 2006; Thayer and Brosschot, 2005). Individuals with greater emotion regulation ability have been shown to have greater levels of restingHRV(Appelhans andLuecken,2006; Thayer andLane,2009). In addition, during successful performance on emotion regulation tasks HRV appears to be increased (Butler et al., 2006; Ingjaldsson et al., 2003; Smith et al., 2011).

We have investigated the role of HRV in emotional regulation attwo differentlevels of analysis. One level is at the trait or tonic level where individual differences in resting HRV have been associated with differences in emotional regulation. We have shown that individuals with higher levels of resting HRV, compared to those with lower resting levels, produce context appropriate emotional responses as indexed by emotion-modulated startle responses, fear-potentiated startle responses, and phasic heart rate responses in addition to behavioral and self-reported emotional responses (Melzig et al., 2009; Ruiz-Padial et al., 2003; Thayer and Brosschot, 2005). In addition, we have recently shown that individuals with low resting HRV show delayed recovery from psychological stressors of cardiovascular, endocrine, and immune responses compared to those with higher levels of resting HRV (Weber et al., 2010). Thus, individuals with higher resting levels of HRV appear more able to produce context appropriate responses including appropriate recovery after the stressor has ended.

Another level of analysis is at the state or phasic level where HRV values increase during the successful regulation of emotion during emotion regulation tasks. Thus, it has been shown that phasic increases in HRV in response to situations that require emotional regulation facilitate effective emotional regulation. In an early study, we showed that HRV increased in recovering alcoholics in response to alcohol cues but only if they later reported an increased ability to resist a drink. Those recovering alcoholics that later reported an urge to drink did not exhibit increased HRV during the alcohol cues (Ingjaldsson et al., 2003). A recent replication and extension of this work reported increased HRV during the successful regulation of emotion by either reappraisal or suppression (Butler et al., 2006). We have recently shown that the increase in HRV associated with emotional regulation is accompanied by concomitant cerebral blood flow changes in areas identified as being important in emotional regulation and inhibitory processes (Lane et al., 2009).

, the amygdala, which has outputs to autonomic, endocrine, and other physiological regulation systems, and becomes active during threat and uncertainty, is under tonic inhibitory control via GABAergic mediated projections from the prefrontal cortex (Davidson, 2000; Thayer, 2006).

. Thayer and Lane (2000) suggested that a common reciprocal inhibitory cortico-subcortical neural circuit serves as the structural link between psychological processes like emotion and cognition, and health-related physiological processes, and that this circuit can be indexed with HRV. Thus, because of these reciprocally interconnected neural structures that allow prefrontal cortex to exert an inhibitory influence on sub-cortical structures, the organism is able to respond to demands from the environment, and organize their behavior effectively. In the next section we briefly review the evidence for the relationship of HRV to this network of neural structures and further specify the prefrontal regions involved in the inhibitory control of the heart.

 

TBC

References

1. Thayer, J. F., Åhs, F., Fredrikson, M., Sollers, J. J., & Wager, T. D. (2012). A meta-analysis of heart rate variability and neuroimaging studies: implications for heart rate variability as a marker of stress and health. Neuroscience & Biobehavioral Reviews, 36(2), 747-756.