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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