More threads by Daniel E.

Daniel E.

daniel@psychlinks.ca
Administrator
The Upside of Feeling Down
by Sharon Begley
Newsweek

November 2, 2009

Depression might be evolution's way of fixing what ails us

Happiness has had a tough time of it lately. The backlash against the seemingly endless stream of books about the subject (Amazon returned 426,789 titles when I used that search term, including one that calls happiness "life's most important skill") had already set in last year. At the time, I pointed out that "among people with late-stage illnesses, those with the greatest sense of well-being were more likely to die in any given period of time than the mildly content were. Being 'up' all the time can cause you to play down very real threats," and channeled the arguments of scholars who lamented the medicalization of the normal human emotion of sadness. (Click here to follow Sharon Begley)

These and other critiques of happiness and the happiness industry, however, came mostly from psychologists, philosophers, and sociologists who are concerned about the effect of a message that says modest levels of well-being aren't enough, and that we all practically have a duty to be really, really happy—and that what was once considered normal sadness is something to be smothered, even shunned. I was therefore interested to see a new scientific paper taking a more brain-based perspective. (My thanks to The Psych Student blog for drawing my attention to it.)

Writing in the journal Psychological Review, postdoctoral fellow Paul Andrews of Virginia Commonwealth University and psychiatrist J. Anderson Thomson Jr. of the University of Virginia present research suggesting that depression is present in the species, and in individuals, for a purpose, and we're playing with fire if we try to eradicate it. In evolution-speak, depression is an "adaptation," they argue. That is, it evolved because it made individuals who experienced it fitter, under natural selection, than individuals who did not experience it. Andrews and Thomson—who is best known for research on the psychology of religious belief, and who has also studied whether antidepressants threaten love and fidelity—offer as evidence the presence of a molecule in the brain called the 5HT1A receptor. This serves as a docking port for the neurochemical serotonin, which the Prozac/Zoloft/Paxil class of antidepressants targets. Human brains are not the only ones with the 5HT1A receptor. Rats also have it.

Here's the really interesting part: the rat version is 99 percent identical to the human one. This suggests that in the evolution from the shared ancestor of rats and people (hold those creationism letters!), natural selection did not mess with the receptor much. That leave-well-enough-alone history tends to happen when the function of some trait is so important that tinkering with it evolutionarily would produce more harm than good. What kind of harm? Rodents that have a mutation causing them to lose this receptor exhibit fewer symptoms of depression when they suffer some stress, a 1998 paper reported. In other words, losing the receptor that promotes depression in response to stress is something evolution thought would be a very bad move. Ergo: depression is not something to be thrown out lightly.

Why not? Because, argue Andrews and Thomson, depression alters thinking and behavior in beneficial ways. For instance:

*People in the grip of depression tend to ruminate, to turn an issue over and over in the mind. If they're ruminating on why they can't get a date, that might seem bad—since it keeps the person depressed. But this way of thinking, note the scientists, is "often highly analytical." That can be useful, producing solutions to what tipped the person into depression in the first place, not to mention "Eureka!" moments such as discovering fire. Evidence: people who felt depressed before tackling challenging math problems tend to score higher than happier test-takers, Andrews and Thomson reported in a 2007 study.

*Depression tends to focus thinking. That 5HT1A receptor, it turns out, also supplies neurons with fuel, allowing them to fire without flagging. That includes neurons in the ventrolateral prefrontal cortex, which have to fire continuously to keep the mind from wandering. (It's an attention circuit.) Focused thinking, like analytical thinking, might help someone overcome depression.

*Depression tends to make sufferers seek isolation, and keeps them from deriving pleasure from sex, food, or life itself. Obviously this can be crippling (and even fatal) to the sufferer. But it may also be adaptive: these behaviors foster the kind of focused and deliberative thinking that might solve the problem that triggered the depression in the first place. Evidence: a 2006 study found that when people suffering from depression engage in expressive writing, which forces them to focus on their troubles, their depression tends to lift sooner than otherwise. A 2008 study reached the same conclusion.

Thomson, who has a private psychiatry practice in Charlottesville, Va., has described how his views on the mind have been shaped by evolutionary psychology, the discipline that (among other things) floats hypotheses about the evolutionary roots of illness. Evo psych changed the way he viewed life and practiced psychiatry, Thomson has said. He's putting theory into practice, going so far as to suggest that people suffering from depression might benefit from more rumination, not less. "Therapies should try to encourage depressive rumination rather than try to stop it, and they should focus on trying to help people solve the problems that trigger their bouts of depression," he and Thomson write in a popularized version of their paper.

The question of whether depression has adaptive value is obviously far from settled. One criticism: the argument that depression fosters rumination and analytical thought seems problematic, since many people with depression report that although they indeed ruminate on their problems, their thinking is far from clear, focused, and analytical, and thus provides little insight into—let alone a remedy for—their illness. Nevertheless, as philosophers and sociologists harrumph about the pernicious effect of the happiness industry, it's useful to throw some neuroscience into the mix.

Sharon Begley is NEWSWEEK's science editor and author of The Plastic Mind: New science reveals our extraordinary potential to transform ourselves and Train Your Mind, Change Your Brain: How a New Science Reveals Our Extraordinary Potential to Transform Ourselves .
 
Going over and over what has happened sometimes helps in that one can see perhaps how their thinking was distorted. They can see perhaps how they could have changed things for a better outcome Ihave been going over things and over in hope i can learn something from all of my past. I can see some truth to what is being said.
 

unionmary

Member
Wonderfully thought out and well written article Daniel, I thoroughly enjoyed the read!

Got me wondering what shape my "5HT1A receptor" is in?

thank you for sharing this.:2thumbs:
 

Daniel E.

daniel@psychlinks.ca
Administrator
From a related article:

Other scientists, including Randolph Nesse at the University of Michigan, say that complex psychiatric disorders like depression rarely have simple evolutionary explanations. In fact, the analytic-rumination hypothesis is merely the latest attempt to explain the prevalence of depression. There is, for example, the “plea for help” theory, which suggests that depression is a way of eliciting assistance from loved ones. There’s also the “signal of defeat” hypothesis, which argues that feelings of despair after a loss in social status help prevent unnecessary attacks; we’re too busy sulking to fight back. And then there’s “depressive realism”: several studies have found that people with depression have a more accurate view of reality and are better at predicting future outcomes. While each of these speculations has scientific support, none are sufficient to explain an illness that afflicts so many people. The moral, Nesse says, is that sadness, like happiness, has many functions.

Depression’s Upside - NYTimes.com
 

Daniel E.

daniel@psychlinks.ca
Administrator
More criticism:

“The idea that depression might enhance creativity is a myth, often based on the life stories and statements of deceased artists and writers… Contemporary poets who are alive and can tell us about their experience with depression are consistent in reporting that it was only after effective psychiatric treatment that they were able to create at their highest levels.” (R.M. Berlin M.D., personal communication, 1/27/08).

The Myth of Depression’s Upside | World of Psychology
 

Daniel E.

daniel@psychlinks.ca
Administrator
The Evolutionary Calculus of Depression
By Jerry A. Coyne, PhD
Psychiatric Times
May 26, 2010

...The ARH [adaptive rumination hypothesis] is unsatisfactory for three reasons:

Depression is not an adaptation in the evolutionary sense. Andrews and Thomson consider depression an ?adaptation? because it supposedly helps the sufferer solve problems. But an evolutionary adaptation is more than something that is merely useful. Biologists consider a trait adaptive only if that behavior, and the genes producing it, enhance an individual?s fitness?the average lifetime output of offspring. It is this genetic advantage, and the evolutionary changes in behavior it promotes, that is the essence of adaptation by natural selection. To demonstrate that depression is an evolved adaptation, then, we must show that it enhances reproduction.

Andrews and Thomson don?t do this, or even try. And if they did try, they probably wouldn?t succeed, for everything we know about depression suggests that rather than enhancing fitness, it reduces it. The most obvious issue is suicide, a word that, curiously, does not appear in Andrews and Thomson?s text. Statistics show that those with major depression are 20 times more likely to kill themselves than are individuals in the general population.4 Evolutionarily speaking, this is a strong selective penalty. Depression also appears to reduce libido and may make one unattractive as a sexual partner. Andrews and Thomson point out depression?s ?adverse effect on women?s fertility and the outcome of pregnancy.?1,p.638 Other health problems are comorbid with depression, although it?s not clear whether depression is the cause or consequence of these problems. Finally, studies show that depressed mothers provide poorer care of their children.

If there is counterevidence that depressive rumination outweighs all these problems and enhances reproduction, Andrews and Thomson don?t provide it. The evolutionary calculus for depression?as for any psychological ?adaptation??demands an answer to this question: how does that condition affect your expected number of offspring? It is odd that evolutionary psychiatrists neither answer this question nor, with rare exceptions, consider it, especially because data on reproductive output are not hard to gather.

If the evolutionary calculus is not favorable, one can still appeal to history: while depression may not be adaptive now, maybe it was reproductively advantageous in our ancestors. Perhaps the symptoms of depression were less debilitating in the past, or there was a lower possibility of suicide. Such appeals often smack of ad hoc special pleading, especially because we?re largely ignorant of the conditions under which our ancestors lived. Andrews and Thomson try this plea:

"A design analysis does not require depressive rumination to be currently adaptive because modern and evolutionary environments may differ in important ways. . . All that is required is that on average, depressive rumination helped people analyze and solve the problems they were ruminating about in ancestral environments."1,p.644

This is wrong. Appeals to problem solving in the past, as to the present, must ultimately involve reproduction. Note too that if depressive rumination no longer helps us solve problems, we can ignore Andrews and Thomson?s suggested therapies.

But we need to consider other data as well?data about the genetic basis of depression. And here the ARH also fails.

The ARH does not explain the existence of genetic variation for depression. No evolutionary hypothesis about depression is credible without specifying the nature of genetic variation. It is most crucial to propose whether the genes producing depression are fixed or segregating. And both hypotheses come with problems.

?Fixed? genes are those for which all individuals have the same genes, presumably those genes produced a form of depressive rumination that was favored in all human populations. Under this scenario, individuals do not vary genetically in their liability to depression, so variation in the disorder reflects only the different environments faced by different individuals (these environments include nongenetic accidents of development).

Under the fixed-gene model it is impossible to show by pedigree analysis that there is a ?genetic basis? to depression, for those methods require the existence of genetic variation among individuals. For the same reason one could not demonstrate an evolutionary advantage of genes causing depression, since everyone currently carries the same ?depression genes.?

Thomson and Andrews apparently reject this model because they recognize that individuals do differ genetically in their susceptibility to depression. They thus accept the second scenario: segregating ?depression genes,? in which variation among individuals results from variation in both genes and the environmental circumstances that precipitate the disorder.

But adopting the ?segregating-gene? hypothesis creates other problems, for now one has to explain not only the selective advantage of depression but also why genes producing it are segregating. Genes with a uniform advantage should not show this kind of variation. And population genetics theory tells us that the biological conditions under which natural selection maintains genetic variation for a trait are quite restrictive. One requires either that heterozygotes (individuals carrying one copy of a ?depression? gene and one copy of a ?nondepression? gene) have a higher fitness than individuals having two identical copies of either gene, or that environments vary over time or space in a way that depression genes are favored at some times or places, and disfavored at others. And even in this latter scenario, different environments have to appear in precisely the correct frequency or spatial distribution lest a single, generally adaptive form of the gene become fixed.

Neither Andrews and Thomson?nor, as far as I know, any proponent of adaptive explanations for mental disorders?describes what form of selection they see as maintaining genetic variation. Without such a hypothesis, any adaptive theory cannot be taken seriously, much less experimentally tested.

There is no reason to think that depression is an adaptation rather than a pathology. Lacking evidence for a reproductive advantage of depression, Andrews and Thomson see the malady as an evolutionary adaptation for three other reasons: it is an ?orderly? syndrome (?there is a neurological orderliness [anhedonia and biochemical effects on serotonin concentration that affects rumination] that appears to specifically and proficiently promote analysis in depressive rumination and is not likely to have evolved by chance?1,p.622; it is relatively common both within and among cultures; and it has a partial genetic basis.

None of this suggests that depression is an adaptation rather than a pathology. The ?coordination? of symptoms is a post facto rationalization: with sufficient imagination, one can view nearly any mental illness as an orderly and useful syndrome. Schizophrenia, for example, could be considered a cluster of ?coordinated? symptoms that enable individuals to discard a reality that is simply too painful to bear. Without information that depression enhances reproduction, the idea of adaptive ?coordination? is mere storytelling.

More importantly, there are alternative explanations for disorders that are fairly common and have some genetic underpinning. Take alcoholism, which has an incidence similar to that of depression (about 7%), and appears to have some genetic basis. But nobody maintains that alcoholism is adaptive. Rather, it?s almost certainly a pathological effect of an environmental change (the discovery of fermentation and distillation) on an adaptive trait (the evolved wiring and pleasure centers of our brain). Like the painful and sometimes fatal childbirth that is the byproduct of selection for larger human brains, depression could simply be a maladaptive byproduct of a feature that is generally adaptive?perhaps the wiring of those brains. Viewed in this way, depression could be a ?spandrel,? a genetic hitchhiker that is a byproduct of something else.5

Alternatively, genes that cause depression might have some advantage when they are present but do not produce the disorder. This can happen if the condition has what geneticists call ?variable penetrance?: 10% of individuals carrying the dominant gene for retinoblastoma, for instance, don?t develop the disease. Or, genes that cause depression only when present in two copies could, when present in heterozygous (one-copy) condition, have another, unknown advantage. Note that these two scenarios offer an adaptive explanation for depression genes that do not view the condition itself as adaptive. And both can be tested, for they predict that the non-depressed relatives of depressives (who carry but don?t express ?depression genes?) should have higher reproductive output than do non-depressed people whose relatives are also not depressed.

This critique of the ARH applies, of course, to other adaptive explanations of depression, including the plea for help theory,6 the social rank theory,7 and the depressive realism theory.8 Further, some have suggested that depression is adaptive because it and other affective disorders are associated with high creativity.9 This suggestion is also dubious, as there is no evidence that depressed people who are creative have a higher reproductive output than other members of the population.

Andrews and Thomson conclude that, in view of the ARH, problem-solving therapies like cognitive behavioral therapy are the go-to treatments for depression. Further, they say, doctors should not be too hasty in prescribing antidepressant medication because the afflicted should be willing to ?endure the pain?1,p.645 in hopes of a more permanent, evolution-based cure. Indeed, one could read the ARH as suggesting that depression should not be cured, but cultivated!

But Andrews and Thomson?s prescriptions lose force to the extent that they rest on a flawed biological premise. Of course researchers should continue to compare talk therapies and to determine which, if any, drugs are useful in alleviating depression. But in the meantime, let?s not expropriate and distort evolutionary theory in a misguided attempt to claim mental disorders as ?adaptations.?

References
1. Andrews PW Thomson JA Jr. The bright side of being blue: depression as an adaptation for analyzing complex problems. Psychol Rev. 2009;116:620-654.
2. Lehrer J. Depression?s upside. New York Times, Feb. 25, 2010.
3. Coyne JA. Is depression an evolutionary adaptation? Available at: [Part 1] Is depression an evolutionary adaptation? Part 1. ? Why Evolution Is True. [Part 2] Is depression an evolutionary adaptation? Part 2. ? Why Evolution Is True. Accessed May 25, 2010.
4. Lonnqvist JK. Suicide. In: Gelder MN, Andreasen, Lopez-Ibor J, Geddes J, eds. New Oxford Textbook of Psychiatry, 2nd ed. Oxford: Oxford University Press, 2009:951-957.
5. Pies RW. The myth of depression?s upside. Available at: The Myth of Depression?s Upside | World of Psychology. Accessed May 25, 2010.
6. Keedwell P. How Sadness Survived: The Evolutionary Basis of Depression. Oxford: Radcliffe Publishing; 2008.
7. Gilbert P, Allan S. 1998. The role of defeat and entrapment (arrested flight) in depression: an exploration of an evolutionary view. Psychol Med. 1998;28:585-598.
8. Taylor SE. Positive Illusions: Creative Self-deception and the Healthy Mind. New York: Basic Books; 1991.
9. Andreasen NC. Creativity and mental illness: prevalence rates in writers and ttheir first-degree relatives. Am J Psychiatry. 1987;144:1288-1292.
 

Daniel E.

daniel@psychlinks.ca
Administrator
Depression Defies the Rush to Find an Evolutionary Upside

...Even if depression is “natural” and evolved from an emotional state that might once have given us some advantage, that doesn’t make it any more desirable than other maladies. Nature offers us cancer, infections and heart disease, which we happily avoid and do our best to treat. Depression is no different.
 
Replying is not possible. This forum is only available as an archive.
Top