depression
Schizophrenia and Bipolar disorder: The propensity towards psychosis
5 years ago
Schizophrenia, as we all know, is one of the most dibilating psychological disorder. It was primarily conceived of as a behavioral disorder, characterized by socially inappropriate and bizarre behavior, but much attention has been focussed nowadays on the cognitive component and the cognitive pathology underlying schizophrenia and it is not unusual for it to be characterized as a thought disorder nowadays .
Bipolar , or Manic Depressive disorder, on the other hand, has been primarily conceived of as a mood or affective disorder , characterized by excessive swings of emotion and motivation. One of my earlier post had tried to analyze the cognitive components involved in the Bipolar condition, and relate it to that found in unipolar depression.
While in my earlier posts, I have discussed the differences between the social and communicative difficulties of Autistic and Schizophrenic probands, especially in relation to their different cognitive styles, and how a milder form of such thinking can lead to different types of creativity, I had also promised for a similar dichotomous discussion of bipolarity at one end of the spectrum and depersonalization/ derealization/ ‘Alienation’ on the other hand- this time the important dimension being the feeling/emotion/motivation dimension.
While that discussion still awaits, I have come across a fascinating article by Lake et al(freely available, registration required) that tries to analyze the schizophrenic and bipolar type I disorders and concludes that there is no such thing as schizophrenia – the psychosis underlying schizophrenia, schizoaffcetive and Bipolar disorders is actually due to a not-yet-diagnosed Bipolar disorder in the patient. The extreme case of a Bipolar manic behavior would be a full-blown psychotic episode and in absence of proper assessment is likely to be diagnosed as schizophrenia. The article hopes, that identifying Bipolar in early stages would prevent unnecessary neuroleptics / anti-psychotics administration to the patient and prevent the significant side-effects of such medications and the rapid-cycling of the bipolar disorder itself, as mood stabilizers like Lithium and Valproate would not be given early on in the absence of bipolar diagnosis.
The other rationale for a single unified diagnosis of Bipolar is to prevent stigma associated with a diagnosis of schizophrenia. There has been well-documented research on the creativity-bipolar linkages; a similar research exists for creativity and schizotypal individuals- but due to the chronic, dibilating and adverse effects of a full-blown schizophrenic diagnosis , the literature about creativity and full-blown schizophrenia is limited (and perhaps inconclusive). The comprehensive ill-effects of a wrong diagnosis are given below:
For patient
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Less likely to receive a mood stabilizer or antidepressant
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Without a mood stabilizer, cycles increase and occur more rapidly; symptoms worsen
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More likely to receive neuroleptics for life, increasing risk for severe and permanent side effects
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Greater stigma with schizophrenia
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Less likely to be employed
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More likely to receive disability for life
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More likely to “give up”
??For clinician
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Increased risk of liability if patient given long-term neuroleptics instead of mood stabilizers develops tardive dyskinesia or commits suicide
The article takes a case study of a patient named Mr. C and tries to analyze how and why different diagnosis are made for the same patient depending on the presented symptoms and why Bipolar diagnosis occurs late in the cycle. Going through the case study may prove disheartening to many, and may make them skeptical of the whole psychiatry profession-leading to some anti-psychiatry rants too- yet one should realize that psychiatry is both an art as well as a science- asking the right question to get the patient (and disorder/ medication) history is very important. To appreciate this I would strongly recommend every body to read the “Selection of Antidepressant ‘ series on Corpus Callosum, which gives a fairly good idea of how psychiatrists make diagnosis in practice.
It is instructive to recall that we have earlier reported on a study that leads to common genetic markers for Psychosis and Mania- implying a single diagnosis, rather than a separate diagnosis of bipolarity or schizophrenia.
The article cites the following DSM-IV diagnostic criteria for Schizophrenia and explains how each is explicable as symptoms of extreme manic episode resulting in psychosis /depression.
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Schizophrenia diagnosis6 |
Seen in psychotic mood disorders |
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Criterion A |
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??Hallucinations and delusions |
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??Paranoia |
Hides grandiosity4 |
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??Catatonia |
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??Disorganized speech and behavior |
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??Negative symptoms |
All patients with moderate to severe depression4 |
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Criterion B |
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??Social and job dysfunction |
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Criterion C |
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??Chronic continuous symptoms |
Patients can have psychotic symptoms continuously for 2 years to life5,6,13 |
I would like to pause here and group the symptoms of schizophrenia according to the basis they have:
- A sensory basis (hallucinations etc, which may be due to senosrimotor gating as well as a lack of proper inhibition mechanisms; delusions of reference which may be due to inability to gate the inputs and thus end up treating everything as salient and consequently referring to self),
- A cognitive basis (delusions – which may be due to extremes of normal cognitive biases that we all have – a manic delusion of grandeur- that may also lead paradoxically to delusions of paranoia( fear and suspicion) as one thinks of oneself as very special and hence vulnerable to the evil out there in the world)
- A motor basis (catatonia – which may be due to problems with volitional control of motion- either too much control or too little- in one case ending up in the positions in which someone else has put them in- in the other remaining in the same position (samadhi in religious contexts) by exercising the will to move. Here again dopamine dysfunction would be relevant as it is involved in motor pathways.
- A social/theory of mind basis (disorganized speech(flight of ideas) as one assumes too much ToM abilities in others and believes that the specifics one has left unsaid- and the abstract way in which one is talking – is comprehensible to others; disorganized behavior- which may be due to not taking social appropriateness into account as one is presumably on a very important mission on Earth.
- An embodiment/ grounding basis and problems with agency(religiosity as one thinks of oneself as not grounded in the body and thus may lead to delusions of control and persecution (as a shadow that is embodied elsewhere is trying to control one) . Here metaphorical thinking and use of symbols as symbols for something else (an overarching idea) rather than referring to something out in the world may lead to loss with reality and magical thinking that takes too much correlation-is-causation kind of thinking and extends it to non-material and non-living things.
- An Affective basis ( related to the fifth point for those who believe that emotions are due to body states) : the characteristic anhedonia , alogia and avolition. Symptoms that are similar in many ways to the symptoms of depressive state.
- A Volitional basis (social and job dysfunction may be due to disturbances in the volitional system- too much goal direction (and where the goal happens to be not socially or work-place acceptable) leads to job dysfunction as does too less of goal-directed behavior.
- Chronic nature: once neuroleptics are started one gets caught in the downward vicious circle. Also the nature of the disorder is cyclic just like the Bipolar with Positive symptoms more prominent in one phase and negative symptoms more prominent in the other phase. In between there can be remission and proper functioning.
Thus, I agree with the broad assessment of Lake et al, that most cases of schizophrenia may be juts an undiagnosed psychotic bipolar episode. Yet, I believe that schizophrenia is a heterogeneous disorder and there may be one or more sub-types. In my view schizophrenia proper leans more towards ToM/ social/ cognitive/ agency dysfunctions while Manic depressive is more about affective and volitional and recurrent dimensions. In my developmental framework; while the schizophrenic struggle with the first five developmental tasks; the bipolar struggle with the next three. Yet their common psychotic style confers susceptibility to psychosis in both cases. This would be as opposed to the same developmental challenges also faced by those with Autism/ depersonalization/ derelaization etc., who have an entirely different take on these issues. While one leans towards science (whose utility is well established); the other leans towards arts (whose utility is doubted sometimes), but which in my view is very important.
We are getting evidence of how emotions can affect decisions towards a better outcome and how having a framework that gives one a sense of meaning and purpose is essential. Science and evolutionary thinking at times robs us of these finer appreciations of life- at that time we do need a counter-dose of Art to keep us more grounded and to make life more enjoyable and worth living- even if that costs some people their sanity!! Maybe we need both GOD and evolution; both science and faith to keep us sane and on the right course.
Hat Tip: Neurofuture
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Depression and Mania: The Bipolar thinking style
5 years ago
PsyBlog has recently posted an article on Cognitive Therapy (CBT) and how it is useful in Depression treatment. this therapy has been shown to be equally effective in Depression as is medication, though this woks in a top-down fashion in the brain (revealed by brain scans), while anti-depressants work in a bottom-up fashion.
PsyBlog quotes the following irrational beliefs , as outlined by Beck, that are prominent in Depression.
* Over-generalization. Drawing general conclusions from a single (usually negative) event. E.g. thinking that failing to be promoted at work means a promotion will never come.
* Minimalization and Maximization. Getting things out of perspective: e.g. either grossly underestimating own performance or overestimating the importance of a negative event.
* Dichotomous thinking – Thinking that everything is either very good or very bad so that there are no gray areas. In reality, of course, life is one big gray area.
To me all of these beliefs are equally relevant for Manic thinking, although in the Manic case these beliefs would be about positive events and have a different spin.
- Over-generalization: a single instance of success at some endeavor disposing one to think that one can achieve anything in unrelated fileds. Also more co-incidence detection and more correlation-is-causation type of thinking that may ultimately lead to the Magical Thinking of full-blown Psychosis.
- Minimalizations and Maximizations: Here, again, things go out of perspective: Overestimating one’s own performance and underestimating the importance of external happenstances that might have led to success.
- Dichotomous thinking: thinking that things are mostly good/bad and unfounded optimism/faith/trust – the opposite of the depressive feeling. Although the reverse thinking that things are mostly bad (external environment is bad, I am good) can also kick in. The point is seeing the world in Black/white but not in shades of gray.
PsyBlog also has an earlier post on depressive thinking style in which it elaborates on the internal-locus-of-control predisposition in depressive probands. Thus, the depressive style is marked by the following internal, global and stable attributions: :
* It is my fault that I didn’t get the job. Here I have made an internal attribution.
* I think I am worthless: a thought that is likely to affect all areas of my life. Now I am making this attribution global.
* I see no reason for the fact that I am worthless to ever change. Now the attribution is stable
It is clear that the Manic person too makes the similar attributions: His success (maybe a single, lucky success) is due to his genius(internal attribution). His genius is not limited to one field- he is generally the most valuable, productive and creative genius and is an all-rounder(global attribution). His genius is not a short-lived entity- he will continue to remain a productive genius no matter what external circumstances / reality (stable attribution). He may thus have no drive to learn about external reality as he suspects that the external reality is not relevant and he can predict outcomes (which are bound to be good) based on his skills, expertise, grandiosity alone. An extreme form of this thinking may lead to the loss of reality characteristic of a full blown Psychotic episode.
While the minimalisations and maximizations are explained by the internal locus of control, the over-generalization is explicable by a propensity of jumping-to-conclusions sort of thinking that leads to global, stable over-regularizations. Another feature important in my view would be the mixing of contexts, where things from one context are referenced in another, dissimilar context. One could call this mixing up of metaphorical thinking where wrong analogies are applied and thus wrong (positive or negative) conclusions are arrived at. The third factor of dichotomous thinking is also very important though hard to pin down. Why should everything appear black and white in depressive or manic thinking and why in one case(depressive ), black is the color of self, while in Manic white is the color of self, remains a mystery. Answering how and when the switch from a grayish-world to a black-me-world(I’m a piece of shit) or white-me-world(I’m the next Einstein) happens would go a long way in making the bipolar patient control his moods and if he has to be sick then enable him to go for a manic episode (where the price may be insanity- a psychotic episode) instead of a depressive one (where there is a real risk of life).
Although the other wrong attributions and thinking styles also need to be addressed, the mechanism of the switching of mood/ black-white world view would help the most and should be the first one targeted in CBT/ medications.
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Depression and Stress: their bland tastes and their differential mediation and remeidal mechanisms vis a vis HRV and yoga
5 years ago
As per an interesting new research article, the Human
Taste thresholds are modulated by Serotonin and Norepinepherine. As per the Abstract:
Circumstances in which serotonin (5-HT) and noradrenaline (NA) are altered, such as in anxiety or depression, are associated with taste disturbances, indicating the importance of these transmitters in the determination of taste thresholds in health and disease. In this study, we show for the first time that human taste thresholds are plastic and are lowered by modulation of systemic monoamines. Measurement of taste function in healthy humans before and after a 5-HT reuptake inhibitor, NA reuptake inhibitor, or placebo showed that enhancing 5-HT significantly reduced the sucrose taste threshold by 27% and the quinine taste threshold by 53%. In contrast, enhancing NA significantly reduced bitter taste threshold by 39% and sour threshold by 22%. In addition, the anxiety level was positively correlated with bitter and salt taste thresholds. We show that 5-HT and NA participate in setting taste thresholds, that human taste in normal healthy subjects is plastic, and that modulation of these neurotransmitters has distinct effects on different taste modalities. We present a model to explain these findings. In addition, we show that the general anxiety level is directly related to taste perception, suggesting that altered taste and appetite seen in affective disorders may reflect an actual change in the gustatory system.
What this means is that if you increase the amount of serotonin in the brain, then the capacity to detect sweet and bitter tastes is increased; if you increase noradrenaline levels those of detecting salty and bitter tastes is augmented; while a general increase in anxiety leads to better bitter taste detection. This also means that an anxiety state produces more bitter taste perception whereas a depressive state (characterized by low serotonin) is marked by bland sense of taste with marked inability to detect sweet and bitter tastes. A stressed state , marked by abundance of noradrenaline, would however lead to more salty and bitter taste perception.
It should be noted that different receptors and cells , in all taste regions of the tongue, for different human tastes have been found, and to me this seems evidence for five different flavors that have separate and distinct mechanisms and somehow model five different (chemical and taste) properties of the world.
Interesting to note that stress (which I loosely associate with noradrenaline) and depression which I loosely associate with serotonin) affect different taste receptors and thresholds. One can speculate that other major neurotransmitters like epinephrine (mediating stress and anxiety) may affect bitter taste; while GABA and dopamine may affect sour and ummami taste thresholds respectively.
Interesting again to note that generalized anxiety (most probably due to epinepherine levels) is tied to bitter taste and epinepherine acts on blood pressure, heart rate etc and so an epinepherine mediated response to stress could be via its effect on the Sympathetic Nervous System and affecting heart rate etc.
I would now like to rephrase the serotonin and norepinepherine distinction as that due to external lions haunting a zebra or internalized lions haunting an elephant and more generally in terms of Anxiety due to external stress and threat perception and Depression as a result of internalized stress and perceived threats. Please see discussion between me and Alvaro in comments on The Neugrogeneisis post for more perspective on this.
I’ll like to move the discussion here towards an article Alvaro mentions in his commnets regarding Heart-Rate Variability (HRV) and how that measure is related to emotional regulation.
But before I do that, let me, before leaving the Taste senses, briefly highlight another Nature article in the same series, that mentions the retronasal system of olfaction and its relation to flavor perception. As per that article (you can read Mind Hacks comment on the same article here) , when we exhale, the retro nasal olfactory system kicks in, and by smelling the internal smells (of food being chewed for example), it leads us to perceive a flavor or taste that is actually based on an activation of a sense of smell and not taste proper. This is just so that the reader keeps in mind that senses of taste and smell are linked (by flavor) and it may be the case that a sense of smell may also be involved/ affected by emotional disorders like Anxiety and Depression.
What I propose is that Anxiety is a short term reaction to external stress; while depression is a long-term reaction to stress that is subsequently internalized. Thus, it is my contention that their mechanisms are different and their remedies too need to be different.
Alvaro, of Sharbrains, on the other hand contends that both are emotional dys-regulations and that HRV is a good indicator of how fit a person emotionally is and that teaching people how to regulate their emotions by providing them feedback about their HRV can be an effcetive tool against both. (Although, the sharp brains product FreezeFramre is focussed around Anxiety and external stressors and is intended for normal populations and not for depressed subjects; yet theoretically he seemed to believe that emotional regulation as indicated by a good HRV, should suffice to take care of both (Please correct me If I have interpreted wrongly, Alvaro). Also for some background on heart rate variability and its benefits go read the Sharpbrains entry in the 11th Encephalon hosted by me or more on this link.
Alvaro has pointed me to an excellent article and I agree broadly with him that emotional regulation and HRV should take care of both anxiety and depression. Yet the purpose of this post is to show that there must be (and are) subtle differences.
First for definitions (from the excellent paper Alvaro refereed to me).
The ANS, SNS and PNS:
A key system involved in the generation of this physiological arousal is the autonomic nervous system (ANS). The ANS is subdivided into an excitatory sympathetic nervous system (SNS) and an inhibitory parasympathetic nervous system (PNS) that often interact antagonistically to produce varying degrees of physiological arousal. During physical or psychological stress, activity of the SNS becomes dominant, producing physiological arousal to aid in adapting to the challenge. An increased pulse, or heart rate, is characteristic of this state of arousal. During periods of relative safety and stability, the PNS is dominant and maintains a lower degree of physiological arousal and a decreased heart rate. The ease with which an individual can transition between high and low arousal states is dependent on the ability of the ANS to rapidly vary heart rate.The PNS and SNS act antagonistically to influence cardiac activity.
For Heart Rate Variability (HRV):
Heart rate variability (HRV) is a measure of the continuous interplay between sympathetic and parasympathetic influences on heart rate that yields information about autonomic flexibility and thereby represents the capacity for regulated emotional responding. HRV reflects the degree to which cardiac activity can be modulated to meet changing situational demands.
This line caught my attention:
Although both autonomic branches exert a constant influence on heart rate, parasympathetic influence is predominant at rest and serves to maintain resting heart rate well below the intrinsic firing rate of the sinoatrial node.
I interpret this to mean that there is an intrinsic firing rate of sinoatrial node that is independent of PNS and SNS activities. This rate may be modfied by SNS to yield the resting heart rate, but there exists an independent compononent too to the heart rate.
Please note that there is a temporal difference in the action of PSN and ASN.
Sympathetic influence on heart rate is mediated by neurotransmission of norepinephrine and possesses a slow course of action on cardiac function. That is, changes in heart rate due to sympathetic activation unfold rather slowly, with peak effect observed after about 4 s and return to baseline after about 20 s. In contrast, parasympathetic regulation of the heart is mediated by acetylcholine neurotransmission and has a very short latency of response, with peak effect at about 0.5 s and return to baseline within 1 s.Owing to the difference in their latencies of action, the oscillations in heart rate produced by the two autonomic branches occur at different speeds, or frequencies.
Now the linkage with the nasal and smell systems:
Breathing air into the lungs temporarily gates off the influence of the parasympathetic influence on heart rate, producing a heart rate increase (see Berntson, Cacioppo, & Quigley, 1993). Breathing air out of the lungs reinstates parasympathetic influence on heart rate, resulting in a heart rate decrease. This rhythmic oscillation in heart rate produced by respiration is called respiratory sinus arrhythmia. As only cardiac parasympathetic activity possesses a latency of action rapid enough to covary with respiration, respiratory sinus arrhythmia is a phenomenon known to be entirely mediated by the PNS. In fact, a large majority of parasympathetically mediated variation in heart rate is produced by respiratory sinus arrhythmia.
I believe this connection between depression/ stress / taste/ retronasal olfactory systems/ smell/ nose/ yoga or paranayama/ breathing exercises to regulate HRV may be a valid linkage and the key behind breathing relaxation techniques for emotional regulation.
HRV is measured by various geometric and statistical means. We’ll treat the simplest concept of HRV as implying the variance of heart beat rate (or interbeat interval) under different activities and spread over some interval to be a measure of HRV.
Statistical analyses are frequently reported and can be computed to represent overall HRV or HRV at different frequencies. For example, SDNN refers to the standard deviation of NN intervals, and SDANN refers to the standard deviation of the average NN interval computed across all 5-min recording segments.
Before discussing the hypothesized differences in HRV and emotional regulation in Depression Vs Anxiety/stress, I would like to briefly touch on one model of this HRV functionality that I find highly promising (it is a social and developmental model and takes into account evolutionary considerations).
Two major theories causally relate the autonomic flexibility represented by HRV with regulated emotional responding. Porges’s (1997, 2001) polyvagal theory is based within an evolutionary framework, which understands aspects of human functioning in terms of acquired, genetically based characteristics that are presumed to have aided in survival and/or reproduction throughout human phylogenetic history. Specifically, the polyvagal theory posits that the human ANS evolved in three stages, each characterized by the acquisition of an autonomic structure that plays a unique role in social processes. First acquired was the dorsal vagal complex, a slow-responding, unmyelinated vagus nerve that supports simple immobilization (e.g., freezing) in response to threat. This “vegetative vagus” slows heart rate through tonic inhibition of sinoatrial node activity. The capacity for active mobilization responses (e.g., fight or flight) became supported with the subsequent acquisition of the SNS. Most recently acquired was the ventral vagal complex, consisting of a fast-acting, myelinated vagus that can rapidly withdraw and reinstate its inhibitory influence on sinoatrial node activity.The polyvagal theory states that the ability of the ventral vagal complex to rapidly withdraw its inhibitory influence allows humans to rapidly engage and disengage with their environment without the metabolic cost of activating the slower responding SNS. The dynamic nature of many social processes (e.g., nonverbal communication, romantic courtship) requires this rapid management of metabolic resources. Only when ventral vagal complex withdrawal is insufficient to meet demands are other autonomic subsystems enlisted. In this respect, the polyvagal theory emphasizes the relation of respiratory sinus arrhythmia (which purportedly indexes ventral vagal complex activity) and the regulation of the emotional processes underlying social behavior.
Finally lets look at some of the emperical research with HRV and emotional regulation disorders. There apperas to be robust data suggesting HRV is low or dysfunctional in anxiety disorders etc.
Coping refers to a set of regulatory strategies that are motivated by emotions (often negative emotions) and that frequently serve an emotion regulatory function but generally involve either nonemotional actions or nonemotional goals, or both (Gross, 1998). Higher levels of resting respiratory sinus arrhythmia have been associated with greater self-reported emotion regulation and the use of constructive coping strategies in university students (Fabes & Eisenberg,1997). This relation between resting respiratory sinus arrhythmia and constructive coping was mediated by negative emotional arousal.Similarly, higher resting HRV was associated with reduced indices of distress in grade school children watching an upsetting film (Fabes,Eisenberg, & Eisenbud, 1993) and higher social competence in young children.
Recently bereaved individuals with higher resting respiratory sinus arrhythmia scored higher on measures of active coping and acceptance and lower on measures of passive coping. Female graduate students classified as repressive copers demonstrated lower resting LF and HF HRV near the time of a major examination than women classified as low anxious (Fuller, 1992), and women with lower parasympathetically mediated HRV (RMSSD) during experimentally induced fear states reported greater use of defensive coping (Pauls & Stemmler, 2003). Finally, those who exhibited submissive behavior during an interpersonal stressor had lower HRV (SDNN and RMSSD) at rest and during the task.
Now we come to Anxiety::
As predicted by the model, patients with generalized anxiety disorder have shown lower parasympathetically mediated HRV relative to controls during rest and during intense worry (Thayer, Friedman, & Borkovec, 1996). Lower overall and parasympathetically mediated HRV (aggregated across several tasks) have been observed in nonclinical panickers and blood phobics relative to controls (Friedman & Thayer, 1998a). Other manifestations of anxiety, such as trait anxiety (Fuller, 1992), social anxiety (Mezzacappa et al., 1997), and self-perceived stress induced anxiety (Sgoifo et al., 2003) have been associated with reduced resting parasympathetically mediated or overall HRV, suggesting the possibility that diminished autonomic flexibility may be an underlying causal factor.
It thus appears that in anxiety HRV is affected and is characterized by a simple low HRV value indicating lower emotional reactivity to external stress.
Now for depression (emphasis in article mine):
As with anxiety, it would be expected that diminished HRV would accompany depressive states given that a core feature of depression is the inability to generate appropriate positive and negative emotions . Consistent with this view, bereaved individuals and patients being treated for melancholic major depression with amitriptyline exhibited diminished resting parasympathetically mediated HRV, and patients with bibipolar depression showed reduced overall resting HRV . One study found decreased resting parasympathetically mediated HRV in depressed men, but increased HRV in depressed women . An inability to generate well-regulated autonomic responses to stress has been observed in depression, as those reporting greater depressive symptoms exhibited larger decreases from baseline in parasympathetically mediated HRV during a stressful speech task and smaller increases in parasympathetically mediated HRV during a cold pressor task , indicating a lessened capacity to regulate cardiac activity to meet the task demands. Resting overall and parasympathetically mediated HRV have interestingly been shown to increase with successful treatment of depression , suggesting that resting HRV is related to within-person variation in regulated emotional responding over time.
What I would like to emphasize is that depression is a second type of dis-regulation of Heart rate. While HRV captures the first rate variance that is ANS mediated, the baseline (or average) of heart rate variance may differ between people and within-a-person over time. In Manic episodes (when all the world is friendly and everyone an angel), the HRV may be very great; while in depressive episodes HRV may revert to a very low baseline level. It is my contention that this baseline Heart rate variability and the ability of heart to keep the HRV suited to task demands may be disrupted in depressive people as the baseline HRV has shifted. That is the depressive person will have a lower resting HRV than controls and given a control task would be unable to modify its HRV appropriately to meet task demand. To put matters simply while HRV measures the variance and flexibility in Heart rate and emotional regulation in response to an external event and low levels means inability to deal with external stress; The depression is characterized by low mean or baseline heart rate variability per se. This I suspect may be due to the lowered baseline firing rate of sinoarterial node an may have nothing to do with CNS, but might be directly influenced by CNS.
Hence my contention that we may need other tricks like CBT, RET for suitably modifying HRV and letting the HRV have a stable value over a long time period. Biofeedback, which would just indicate the variability with respect to current baseline , and would not reflect the cumulative history of the baseline Heart rates may not be helpful in treating depression thus.
Would love to hear other comments/ opinions.
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Markers for Psychosis and Mania
5 years ago
A recent review of the COMT genotype Met/VAL SNP on psychiatric phenotypes of schizophrenia, bipolar mood disorder and schizoaffective disorder seems to suggest that the SNP’s effcet mya be more of modifying the symptoms (with Val conferring positive symptom susceptibility and MET negative symptom susceptibility) of psychosis and mania, rather than conferring susceptibility to the diseases per se. Also the association, in European populations primarily, would be between both psychosis and mania (schizoaffcetive) present rather than juts a simple diagnosis of schizophrenia or bipolarity.
The narrowing of COMT linkages to the combination of Mania and Psychosis loks like a step forward and the distinction between symptom modifying effects and the distinction between symptoms based on their being positive (additions of functionality) or negative (deletion of functionality) seems to be a step in the right direction.
This differential effect of having a Met or Val allele on symptom type (positive and negative) is also inline with the inverted U model of dopamine levels that suggests that there is a range of dopamine levels that is good for the body(brain) and beyond either end there are deleterious effects. It could be that while a Met allele confers protective advantage for positive symptoms, it is an aggravator for negative symptoms. Depending on dopamine environmental levels, the person having Met allele may or may not show the symptoms of mania/ scizophrenia.
I am also intrigued by the BDNF met/val allele effect on anxiety susceptibility and forced to think whether there too the effect may be that of symptom modification rather than susceptibility?
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History in the making – the neurogeneisis discovery
5 years ago
There is an old article by Jonah Lehrer in the Seed magazine regarding the historical process via which the fact of neurogenesis in the humna brain was discovered and established.
One of the findings related to the stress/depression and the-lack-of-neurogenesis linkage and the underlying mechanisms that are involved (including sertonergic triggering of cascade reactions that lead to increase in trophic factors). A corollary finding was that enriched environments also lead to more neurogenesis and can help heal the scars formed due to depression/stress by stimulating neurogenesis in the adult brain. How neurogenesis (in areas like hippocampus and dompaminergic neurons) leads to recovery from depression/ stress is still not clear.
To briefly summarize the findings (though it is highly recommended that you read the original article which is very well written):
- Neurogenesis happens in adult brains (rats, primates and even humans).
- Stress reduces neurogenesis.
- Depression and reduced neurogenesis have been found to co-occur.
- Enriched environments lead to increase in neurogeneisis. (in rats, marmoset monkeys)
- Sertonin-based antidepressants primarily work by increasing neurogeneisis.
Hence inductively it seems probable that Low IQ is caused by Lower SES. (OK, this may seem like a joke…but do go and read the article and Gould’s views on the stress and poverty relationships- and I find her views (and her supporting experimental and observational facts) quite plausible.)
The scientists profiled in the article, at that time, were still wondering (and actively exploring) the exact mechanism between neurogenesis and depression/ stress.
My hypothesis of why depression leads to less nurogenesis in hippocampus would be related to the role of hippocampus in memory and learning and how, for example, repeated exposure to shocks in rats leads the rats to exhibit a phenomenon known as ‘learned helplessness’. Once the memory of a shockful and distressing repetitive experience is entrenched in the rat’s memory, in the hippocampal region, she may not try to explore the environment that much, to discover and learn what has changed regarding the environment, and whether the stressful conditions and environments are over. This may lead to reduced neurogenesis as the rat’s brain resigns itself to fate. This inability-to-learn or ‘learning helplessness’ (my slightly changed term for the same behavioral description) may lead to a vicious downward cycle leading to depression.
Once the neurogenesis is re-triggered, either due to administration of prozac or other antidepressants, or due to Cognitive behavioral therapy (and it had been found using brain scans that these two approaches seem to converge- one working in a top-down fashion (expecations and beliefs), while the other on a molecular and bottom-down fashion ), then the increased neurogenesis leads to an enhanced ability to learn and adapt and thus overcome the depressive epsiode and get rid of the symptoms. In both cases, the brunt of effort to get out of depression is still borne by the individual who is affected.
The other piece of information that caught my fancy was that of the dopimenergic neurogenesis and the potential cure of parkinson’s disease based on targetting this pathway. Whether neurogenisis is limited to hippocampal regions, or also happens in the substatntia nigra/ VTA region (where I guess all the dopaminergic neurons reside) is an important question and my lead to more insight as to which all areas of the brain (or all areas) are susceptible to neurogenesis.
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