No, I am not speaking metaphorically. Quite literally,there has been accumulating evidence that sense are sharpened and have great acuity in mania while they are dulled in depression and the effects can be seen within the same individual over time as he/she suffers from manic/depressive episodes.
The latest study to add to this literature is by Bubl et al that found that depressive people’s brain registered lesser contrast than that registered by normal control brains when presented with same black and white images. They used pattern electroretinogram (PERG) to find whether the contrast gains registered by depressive retinas (those suffering from MDD) were different from those of controls and they found a strong and significant association with the severity of the depression.
I have covered earlier studies that found that sense of taste was compromised in depression (and enhanced in mania) and similarly that the sense of smell showed similar effects. Some snippets from the earlier posts:
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.
In one of my earlier post on depression, I had commented on the fact that those suffering from depression have less sensitivity to sweet and bitter tastes and as such may compensate by eating more sugar thus leading to the well documented diabetes – depression linkage.
In a new study it has just been discovered that not only depressives have bland sense of taste, their sense of smell is also diminished and they may make compensations by using greater amounts of perfume. Overall it seems that those suffering from depression will have bland subjective experience of flavor(which is a combination of both smell and taste) and thus may even not really find what they eat to be tasty.
Further on, I speculate prophetically that blander vision will also be found:
To me, this is an important finding. To my knowledge no research has been done in other sense modalities (like vision), but there is every reason to think that we may discover a bland sense of vision in depression. Why do I surmise so? this is because there is extensive literature available regarding the manic state and how things seem ‘vivid’ during that state including visual vividness. If depression is the converse of Mania, it follows that a corresponding blandness of vision should also be observed in those who are clinically depressed.
We also know that in extreme or psychotic forms of Mania, auditory hallucinations may arise. I am not suggesting that hallucinations are equal to vividness, but I would definitely love to see studies determining whether the auditory sense is heightened in Mania (maybe more absolute pitch perception in Mania) and a corresponding loss of auditory absolute pitch perception in depression. If so found, it may happen that music literally becomes subdued for people with depression and they sort of do not hear the music present in everyday life!
Whether other sense like touch, vestibular/ kinesthetic , proprioception (a heightened sense of which may give rise to eerie out-pf-body experiences in Mania) are also diminished in depression is another area where research may be fruitful.
Of course I have also speculated about the others senses and would love to hear studies supporting/contradicting this thesis. But given that senses are attenuated in depression and exaggerated in mania the question remains why? Which brings me to the topic of this post- why is the world bleak /bland to a depressive and vivid for a manic?
This was also the question asked by Mark Changizi (@Mark_Changizi) on twitter with respect to this new study uncovered today and I replied that this may be due to broaden-and-build theory being applied to sensory domain or sensory gating phenomenon differentially acting in manic/ depressive states, while Mark was of the opinion that it might be the result of physiological arousal with arousal being the variable of interest controlling whether the sense remain acute or dull?
I do not see the two views necessarily contradictory and it may be that chronic affect per se activates arousal and that is the mediating variable involved in its effect on senses; and we can design experiments to resolve this by measuring the effect of state sadness/ happiness/arousal on visual acuity (if the effects of state manipulations are big enough); howsoever, I woudl like to elaborate on my broaden and build theory.
In the cognitive, psychological and psychosocial domains the broaden and build theory of positive affect is more or less clearly elaborated and delineated. I wish to extend this to the sensory domain. I propose that chronic positive affect signals to our bodies/brains that we can afford to make our attention more diffuse, let senses be perceived more vividly as we have more resources available to process incoming data; conversely in a chronic low affect state we might like to conserve resources by narrowing focus/ literally narrowing the range of sensory inputs/reducing the sensitivity of sense organs and pool those resources elsewhere.
I know this is just a hypothesis , but I am pretty convinced and would love to hear the results of experiments anyone conducts around this theory.
Bubl, E., Kern, E., Ebert, D., Bach, M., & Tebartz van Elst, L. (2010). Seeing Gray When Feeling Blue? Depression Can Be Measured in the Eye of the Diseased Biological Psychiatry, 68 (2), 205-208 DOI: 10.1016/j.biopsych.2010.02.009
Chronic stress in mice leads to the ‘learned helplessness‘ model of depression in mice. Also, from studies in humans as well as other animals we know that chronic stress is a risk factor and cause for depression and this is mediated by the interactive effects of two stress related systems: “the neural substrate for the organism’s stress response comprises two anatomically distinct but functionally integrated circuits, the corticotropin-releasing hormone CRH system and the locus coeruleus–norepinephrine LC-NE system.”
The relation between cortisol level/ activity in the CRH/LE-NE system and stress related maladaptation is not simple , but the relationship is complex.
There are many theories of depression. A finding that has gained ground in recent years is the enhanced neurogenesis due to administration of anti-depressants and how the action of anti-depressants may be due to their enhancing neurogenesis effects.
However this new study in PNAS, conducted on mice, casts doubt that the relation between stress/depression and neurogenesis is simple. It seems the relation is as complex as that between stress/depression and the cortisol levels.
I would first like to briefly summarize the findings of the study:
- chronic stress paradigm used was that of social defeat (cohabitation with a socially dominant conspecific). 10 days of this social defeat were administered. this typically leads to social avoidance behaviors and these behaviors are correlated with other depressive phenotypes.
- after 10 days when social avoidance (time interacting with a potential friendly con-specific) was measured it was found that about half the mice exhibited social avoidance and were sensitive to the stress; the rest of the half were ‘resilient’ and did not differ from control mice (not exposed to chronic social defeat) in their social avoidance.
- all mice, both resilient and sensitive , showed decreased proliferation in subgranular zone (SGZ) for new cells immediately after stress exposure. This effect disappeared / normalised after 24 hrs.
- Cell survival for cells created before stress exposure was not affected by stress exposure.
- cell survival for neurons created 1 day after stress exposure was enhanced selectively for those mice that were susceptible or sensitive to stress, but was not enhanced for the resilient mice or the mice taken as a whole.
- when the mice were irradiated, before stress exposure, to prevent neurogenesis, then the social avoidance behavior, even in susceptible mice disappeared. It is thus evident that social avoidance is mediated by increased neurogenesis post-stress exposure in the susceptibel mice.
Overall, the results I believe are clearly in favor of conceptualizing the susceptible mice as ‘orchid’ mice – having enhanced tendency for neurogenisis following positive/negative events of interests. they are biologically sensitive to context and exhibit neurogenesis reactivity similar to stress reactivity shown by orchid children. Given a positive life experience the increased neurogenesis post-event helps in having happy memories and cognition s and better functioning; preponderance of negative life vents in contrast lead to more negative and longlasting cognitions and memories leading to reduced functioning. Of course the dandelion mice are resilient and not that much affected by chronic stress. However, they would also not be able to make best use of environment in good conditions.
The only hiccup I see in the whole scheme of things is the effect of anti-depressants on neurogenesis and my earlier theorizing that cells may die under repetitive stress and reduced or absent neurogenisis would be a prime factor in depression. However, the relation between neurogenesis and stress will be , I am sure, complex and needs to be settled empirically, rather than theoretically. However one thing is clear, neurogenesis has a rpime role to play in depression , mediated perhaps by, chronic stress exposure and genetic diatheisis (orchid-dandelion effect).
I am excited and would love to hear of more papers that are addressing this new trend in depression – neurogenesis research keeping in mind the biological sensitivity to context thing too.
Lagace, D., Donovan, M., DeCarolis, N., Farnbauch, L., Malhotra, S., Berton, O., Nestler, E., Krishnan, V., & Eisch, A. (2010). Adult hippocampal neurogenesis is functionally important for stress-induced social avoidance Proceedings of the National Academy of Sciences, 107 (9), 4436-4441 DOI: 10.1073/pnas.0910072107
Chronically stressful life events have been shown to lead to depression. Chronic stress leads to hyperactivity of HPA axis leading to more glucocorticoids (cortisol) in the human body. This excess cortisol in term is proposed to underlie the affective symptoms of depression. Also, depressive people have been found to have up to 20% smaller hippocampal volume, and a recent theory is gaining ground that depression is due to reduced neurogenesis. Even if the entire spectrum of depressive symptoms is not due to reduced neurogenesis and atrophied or smaller hippocampus, at least the cognitive symptoms of depression are largely due to this.
I stumbled upon a commentary by Robert Sapolsky that although is 10 years old, but I still found interesting and worth bringing to notice of my dear readers. In it Sapolsky looks at a study by Czeh et al that found evidence linking reduced proliferation in dentate gyrus and a shrunken hippocampus to depressive stress as modeled by psycho-social stress paradigm in tree shrew. Also, they found that an antidepressant, tianeptine, reversed the effects of stress by restoring proliferation and hippocampus size and thus reversing symptoms of depression. However the level of glucorticiods were still higher, after anti-depressant treatment, and thus it is apparent that anti-depressants work downstream of stress induced increase in glucorticoids.
Sapolsky believes that the data support either of models presented in figure 1A or figure 1B i.e. the increased glucocrticoids can lead to shrinkage of hippocampus directly or through their effect on affective symptoms. I believe figure 1C is also possible and its not necessarily incompatible with 1A or 1B and that increased stress may lead to increased cortisol- may lead to reduced neurogenesis may lead to shrinkage of hippocampus and which may in turn lead to affective and cognitive symptoms.
An alternative to reduced neurogenesis/ proliferation theory is the dendritic atrophy/ neurotoxicity theory that posits that shrinkage of hippocampus is due to cell death/ white matter loss. This again is a possibility but the evidence in favor of reduced neurogenesis is growing and becoming strong by the day.
Overall the new paradigms in depression research that look beyond serotonin or mono amine imbalance is a welcome trend and hopefully would lead to better interventions and prevention strategies and not just better pharmaceutical innovations. Its time one realized the rile chronic stress play sin depression and how that can be easily prevented to reduce the mental health burden.
Sapolsky, R. (2001). Depression, antidepressants, and the shrinking hippocampus Proceedings of the National Academy of Sciences, 98 (22), 12320-12322 DOI: 10.1073/pnas.231475998
Czeh, B. (2001). Stress-induced changes in cerebral metabolites, hippocampal volume, and cell proliferation are prevented by antidepressant treatment with tianeptine Proceedings of the National Academy of Sciences, 98 (22), 12796-12801 DOI: 10.1073/pnas.211427898
Let us see how they describe thought speed and variability and what their hypothesis is:
1. The principle of thought speed. Fast thinking, which involves many thoughts per unit time, generally produces positive affect. Slow thinking, which involves few thoughts per unit time, generally produces less positive affect. At the extremes of thought speed, racing thoughts can elicit feelings of mania, and sluggish thoughts can elicit feelings of depression.
2. The principle of thought variability. Varied thinking generally produces positive affect, whereas repetitive thinking generally produces negative affect. This principle is derived in part from the speed principle: when thoughts are repetitive, thought speed (thoughts per unit time) diminishes. At its extremes, repetitive thinking can elicit feelings of depression (or anxiety), and varied thinking can elicit feelings of mania (or reverie).
Let me clarify at the outset that they are aware of the effects of though speed on variability and vice versa; as well as the effects of mood on felt energy and vice versa; thus they know that one can confound the other. Another angle they consider is the relationship between thought speed/variability i.e the form of thought and the contents of thought (whether having emotional salience or neutral) and investigated whether the effects of speed and variability were confounded with though content; they found negative evidence for this inetrcationist view.
Let me also clarify that I differ slightly (based on my interpreation of their data) from their original hypothesis, in the sense that I believe that their data shows that speed affects felt energy and variability affects affect and that the effects of speed on mood may be mediated by the effect of speed on felt energy and similarly the effect of variability on felt energy may be mediated by its effects on mood.
Thus my claim is that:
- Thought speed leads to more felt energy. Extremes of ‘racing thoughts’ leads to the manic feeling of being very energetic (when accompanied with positive mood, this may give rise to feelings of grandiosity- I have the energy to achieve anything), while also may lead to anxiety states (when accompanied with negative affect) in which one cannot really suppress a negative chain of thoughts – one following the other in fast succession, regarding the object of ones anxiety. The counterpart to this the state where thoughts come slowly (writer’s block etc) and when accompanied with negative affect, this can easily be viewed as depression.
- Thought variability leads to more positive affect: Extremes of ‘tangential thoughts’ leads to the manic feeling of being in a good mood (when accompanied with high energy , this manifest as feelings of euphoria); while the same tangential thoughts when accompanied by low felt energy may actually be felt as serenity/ calmness/ reverie. The counterpart to this is the state of thoughts that are stuck in a rut – when accompanied with low energy this leads to feelings of depression and sadness.
Thus, to put simply : there are two dimensions one needs to take care of – mood (thought variability) x energy (thought speed) and high and low extremes on these dimensions are all opposites of their counterpart.
Before we move on, I’ll let the authors present their other two claims too:
3. The combination principle. Fast, varied thinking prompts elation; slow, repetitive thinking prompts dejection. When speed and variability oppose each other, such that one is low and the other high, individuals’ affective experience will depend on factors including which one of the two factors is more extreme. The psychological state elicited by such combinations can vary apart from its valence, as shown in Figure 1. For example, repetitive thinking can elicit feelings of anxiety rather than depression if that repetitive thinking is rapid. Notably, anxious states generally are more energetic than depressive states. Moreover, just as fast-moving physical objects possess more energy than do identical slower objects, fast thinking involves more energy (e.g., greater wakefulness, arousal, and feelings of energy) than does slow thinking.
4. The content independence principle. Effects of thought speed and variability are independent of the specific nature of thought content. Powerful affective states such as depression and anxiety have been traced to irrational and dysfunctional cognitions (e.g., Beck, 1976). According to the independence principle, effects of mental motion on mood do not require any particular type of thought content.
They review a number of factors and studies that all point to a causal link between thought speed and energy and between thought variability and mood. More importantly they show the independent effects of though speed and variability from the effects of thought content on mood. I’ll not go into the details of the studies and experiments they performed, as their article is available freely online and one can read for oneself (it makes for excellent reading); suffice it to say that I believe they are on the right track and have evidence to back their claims.
What are the implications of this:
The speed and repetition of thoughts, we suggest, could be manipulated in order to alter and alleviate some of the mood and energy symptoms of mental disorders. The slow and repetitive aspects of depressive thinking, for example, seem to contribute to the disorder’s affective symptoms (e.g., Ianzito et al., 1974; Judd et al., 1994; Nolen-Hoeksema, 1991; Philipp et al., 1991; Segerstrom et al., 2000). Thus, techniques that are effective in speeding cognition and in breaking the cycle of repetitive thought may be useful in improving the mood and energy levels of depressed patients. The potential of this sort of treatment is suggested by Pronin and Wegner’s (2006) study, in which speeding participants’ cognitions led to improved mood and energy, even when those cognitions were negative, self-referential, and decidedly depressing. It also is suggested by Gortner et al.’s (2006) finding that an expressive writing manipulation that decreased rumination (even while inducing thoughts about an upsetting experience) rendered recurrent depression less likely.
There also is some evidence suggesting that speeding up even low-level cognition may improve mood in clinically depressed patients. In one experiment, Teasdale and Rezin (1978) instructed depressed participants to repeat aloud one of four letters of the alphabet (A, B, C, or D) presented in random order every 1, 2, or 4 s. They found that those participants required to repeat the letters at the fastest rate experienced the most reduction in depressed mood. Similar techniques could be tested for the treatment of other mental illnesses. For example, manipulations might be designed to decrease the mental motion of manic patients, perhaps by introducing repetitive and slow cognitive stimuli. Or, in the case of anxiety disorders, it would be worthwhile to test interventions aimed at inducing slow and varied thought (as opposed to the fast and repetitive thought characteristic of anxiety). The potential effectiveness of such interventions is supported by the fact that mindfulness meditation, which involves slow but varied thinking, can lessen anxiety, stress, and arousal.
hat tip: Ulterior Motives
Pronin, E., & Jacobs, E. (2008). Thought Speed, Mood, and the Experience of Mental Motion Perspectives on Psychological Science, 3 (6), 461-485 DOI: 10.1111/j.1745-6924.2008.00091.x
Pronin, E., & Wegner, D. (2006). Manic Thinking: Independent Effects of Thought Speed and Thought Content on Mood Psychological Science, 17 (9), 807-813 DOI: 10.1111/j.1467-9280.2006.01786.x
Daniel Nettle, writes an article in Journal Of Theoretical Biology about the evolution of low mood states. Before I get to his central thesis, let us review what he reviews:
Low mood describes a temporary emotional and physiological state in humans, typically characterised by fatigue, loss of motivation and interest, anhedonia (loss of pleasure in previously pleasurable activities), pessimism about future actions, locomotor retardation, and other symptoms such as crying.
This paper focuses on a central triad of symptoms which are common across many types of low mood, namely anhedonia, fatigue and pessimism. Theorists have argued that, whereas their opposites facilitate novel and risky behavioural projects. These symptoms function to reduce risk-taking. They do this, proximately, by making the potential payoffs seem insufficiently rewarding (anhedonia), the energy required seem too great (fatigue), or the probability of success seem insufficiently high (pessimism). An evolutionary hypothesis for why low mood has these features, then, is that is adaptive to avoid risky behaviours when one is in a relatively poor current state, since one would not be able to bear the costs of unsuccessful risky endeavors at such times .
I would like to pause here and note how he has beautifully summed up the low mood symptoms and key features; taking liberty to define using my own framework of Value X Expectancy and distinction between cognitive(‘wanting’) and behavioral (‘liking’) side of things :
- Anhedonia: behavioral inability to feel rewarded by previously pleasurable activities. Loss of ‘liking’ following the act. Less behavioral Value assigned.
- Loss of motivation and interest: cognitive inability to look forward to or value previously desired activities. Loss of ‘wanting’ prior to the act. Less cognitive Value assigned.
- Fatigue: behavioral inability to feel that one can achieve the desired outcome due to feelings that one does not have sufficient energy to carry the act to success. Less behavioral Expectancy assigned.
- Pessimism: cognitive inability to look forward to or expect good things about the future or that good outcomes are possible. Less cognitive Expectancy assigned.
The reverse conglomeration is found in high mood- High wanting and liking, high energy and outlook. Thus, I agree with Nettle fully that low mood and high mood are defined by these opposed features and also that these features of low and high mood are powerful proximate mechanisms that determine the risk proneness of the individual: by subjectively manipulating the Value and Expectancy associated with an outcome, the high and low mood mediate the risk proneness that an organism would display while assigning a utility to the action. Thus, it is fairly settled: if ultimate goal is to increase risk-prone behavior than the organism should use the proximate mechanism of high mood; if the ultimate goal is to avoid risky behavior, then the organism should display low mood which would proximately help it avoid risky behavior.
Now let me talk about Nettle’s central thesis. It has been previously proposed in literature that low mood (and thus risk-aversion) is due to being in a poor state wherein one can avoid energy expenditure (and thus worsening of situation) by assuming a low profile. Nettle plays the devil’s advocate and argues that an exactly opposite argument can be made that the organism in a poor state needs to indulge in high risk (and high energy) activities to get out of the poor state. Thus, there is no a prior reason as to why one explanation may be more sound than the other. To find out when exactly high risk behavior pay off and when exactly low risk behaviors are more optimal, he develops a model and uses some elementary mathematics to derive some conclusions. He, of course , bases his model on a Preventive focus, whereby the organism tries to minimize getting in a state R , which is sub-threshold. He allows the S(t) to be maximized under the constraint that one does not lose sight of R. I’ll not go into the mathematics, but the results are simple. When there is a lot of difference between R (dreaded state) and S (current state), then the organism adopts a risky behavioral profile. when the R and S are close, he maintains low risk behavior, however when he is in dire circumstances (R and S are very close) then risk proneness again rises to dramatic levels. To quote:
The model predicts that individuals in a good state will be prepared to take relatively large risks, but as their state deteriorates, the maximum riskiness of behaviour that they will choose declines until they become highly risk-averse. However, when their state becomes dire, there is a predicted abrupt shift towards being totally risk-prone. The switch to risk-proneness at the dire end of the state continuum is akin to that found near the point of starvation in the original optimal foraging model from which the current one is derived (Stephens, 1981). The graded shift towards greater preferred risk with improving state is novel to this model, and stems from the stipulation that if the probability of falling into the danger zone in the next time step is minimal, then the potential gain in S at the next time step should be maximised. However, a somewhat similar pattern of risk proneness in a very poor state, risk aversion in an intermediate state, and some risk proneness in a better state, is seen in an optimal-foraging model where the organism has not just to avoid the threshold of starvation, but also to try to attain the threshold of reproduction (McNamara et al., 1991). Thus, the qualitative pattern of results may emerge quite generally from models using different assumptions.
Nettle, then extrapolates the clinical significance from this by proposing that ‘agitated’ / ‘excited’ depression can be explained as when the organism is in dire straits and has thus become risk-prone. He also uses a similar logic for dysphoric mania although I don’t buy that. However, I agree that euphoric mania may just be the other extreme of high mood and more risk proneness and goal achievements; while depression the normal extreme of low mood and adverse circumstances and risk aversion. To me this model ties up certain things we know about life circumstances and the risk profile and mood tone of people and contributes to deepening our understanding.
Nettle, D. (2009). An evolutionary model of low mood states Journal of Theoretical Biology, 257 (1), 100-103 DOI: 10.1016/j.jtbi.2008.10.033