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Depression Re-examined: A New Way to Look at an Old Puzzle

Depression affects approximately 10% of Americans. It can be fatal; I found estimates of suicide rates ranging from 2-15% of patients with major depression. When it doesn’t kill, it impairs functioning and can make life almost unbearably miserable. It is a frustrating condition because there is no lab test to diagnose it, no good explanation of its cause, and the treatments are far from ideal.

Jonathan Rottenberg is a psychologist and research scientist who began to study depression after his own recovery from a major depressive illness. He teaches psychology at the University of South Florida, where he is the director of the Mood and Emotion laboratory. He has launched the Come Out of the Dark campaign to start a better, richer national conversation about depression. In a new book The Depths: The Evolutionary Origins of the Depression Epidemic, he reviews insights from recent experiments and asks a number of difficult questions, such as why humans evolved to be subject to incapacitating depressions. He comes up with some startling hypotheses, including the idea that evolution favored depression because of its survival value and that depression is essentially a good thing. He offers his ideas as the basis of a paradigm shift.

Is there an epidemic of depression? Rates of depression have been rising in most but not all countries. Is it a real epidemic, or might we be seeing the influence of increased awareness through the media and better diagnosis? I’m not sure we have enough evidence to be certain at this point.

What is depression? Is it:

  • A defect in brain chemistry? This is the basis of drug therapy. The chemistry imbalance hypothesis is simplistic, misleading, and essentially wrong. Antidepressants do indeed alter brain chemistry as they relieve symptoms, but that doesn’t necessarily mean that a chemical imbalance caused the problem, and it doesn’t explain what caused the imbalance or why it happened when it did.
  • A defect in thoughts? This is the basis of cognitive behavioral therapy (CBT). Is mere thinking enough to think yourself into a depression or out of one? The evidence suggests otherwise.
  • A defect in childhood experience? This is the basis of psychoanalysis. Freud’s theories have been largely discredited, and people with the most appalling childhoods can have normal adulthoods.
  • Not a defect at all? This is what Rottenberg proposes.

Evolution did not design us to be happy. It designed us to survive and reproduce. The function of mood is to integrate internal with external information to enhance fitness. Mood affects behavior: an anxious mood focuses attention on threats; a good mood broadens attention and leads people to seek out variety; and a negative mood first mobilizes effort, then eventually de-escalates effort when a task proves hopeless, conserving resources that can later be used to better purpose. Our moods occur first: we feel happy or sad, we feel a need to explain why we feel that way, and we think of a reason that would explain the mood. The reasons we come up with are not necessarily the right ones, and often they are mere confabulations.

Low mood has its benefits. Non-depressed people tend to overestimate their abilities, are prone to positive illusions, and demonstrate overconfidence and blindness to faults. When depressed, people are more realistic; they are more deliberate, skeptical, and careful in processing information from the environment.

Low mood can be triggered in animals and humans by factors such as separation from the group, removal to an unfamiliar environment, the inability to escape from a stressful situation, the death of a significant other, scarce food resources, prolonged bodily pain, and social defeat. Low mood serves as an alarm system. It gets our attention and lets us know something is wrong. Depression allows us to stop, retreat to an emotional cocoon, analyze what went wrong, and hopefully change course to avoid future calamities.

But low mood has its costs, too. Whatever the benefits, there are plenty of negative effects like distorted thinking, delusions, suicide, difficulty in concentrating and functioning, and weakened executive functions in the brain.

A shallow depression can be adaptive, but a deep depression is maladaptive. There’s a continuum, and any cut-off point to divide normal from abnormal is arbitrary. Rottenberg thinks low moods used to be helpful in the environment where humans evolved, but that the environment has changed in ways that make low moods less advantageous today.

He describes animal and human experiments that shed light on depression. Animals show signs of depression too. Animals often act as if they are mourning after they lose a significant other. In the “tail test,” rats suspended by their tails conserve their resources better if they give up quickly and stop struggling. Their low mood resolves quickly when the stress is over. Adolescent girls who had depressive symptoms became more disengaged from goals over time, but the more disengaged they were, the better off they were in later assessments, reporting lower levels of depression. In another study, a negative mood was found to enhance the quality and concreteness of persuasive arguments. In a starvation experiment, subjects developed the signs of depression as their bodies reacted to conserve the insufficient calories. Their energy and concentration diminished, they lost all interest in sex, and they ruminated obsessively about food. By preventing action they couldn’t afford, depression contributed to their survival on scanty rations. Their depression lasted longer than the experiment; Rottenberg hypothesizes that this strategy is effective because it holds behavior in place until depleted resources can be rebuilt.

How does this normally-resilient mood system fall into deep depression? Prolonged shocks produced helpless behavior in dogs, so they didn’t even try to escape from shocks when it was possible to escape. Chronic mild stress in rats reduces their pleasure-seeking behavior for months afterwards; their responsiveness to rewards returns when they are given antidepressants. Undergoing several stressors at once increases the likelihood of depression in both animals and humans. Not every animal shows prolonged depression, just as not every human becomes depressed under equivalent stresses. Genetic variation is likely the reason: it has been estimated that 30-40% of susceptibility to depression in humans is genetic.

Some kind of loss is always present in depression, whether it be the death of a child or an imagined loss of status. Bereavement is one kind of depression, once thought to be a separate entity but now considered to be part of the same continuum.

How long do minor depressions last? There are no good treatments for minor depression, and doctors often resort to “watchful waiting.” This may be a mistake: a study showed that after a month, only 6% of patients had recovered. Another study found that 72% of people who had a minor depression were still bothered by one or more symptoms of depression when interviewed a year later. At any given time, 22% of the population has at least one significant symptom of depression. Mild depressions outnumber deep ones six to one. Low-level sadness is so ordinary it is often overlooked. But having a mild depression quintuples the risk of a later major depression.

Depression can be triggered by events, temperaments, and routines such as sleep patterns, night shifts, and artificial light. Fish with different temperaments have different success in different environments; the bold fish are more likely to enter a trap, while wary fish are slower to adapt to changing conditions. Humans have an additional problem: Rottenberg says “Homo sapiens has the distinction of being a species that can become depressed without a major environmental insult.” We think our way into deeper depressions by rumination and self-flagellation. We worry about remote or nonexistent possibilities. When we are depressed we think we ought to be able to fix ourselves; but we can’t, and that makes us even more depressed.

Sometimes depressed people can’t even get out of bed. This reflects a lack of goals. They don’t see any good reasons that would motivate them to get up. Humans can set goals in abstract domains where progress is hard to measure. When they hold on to failing goals, they become depressed. They need to disengage from the failing goals. Self-help books and the ideals of happiness in our society create high expectations and perceived failures. In the West the idea of happiness usually involves high levels of arousal like enthusiasm and excitement; in general, those who place the highest values on that kind of happiness tend to be the least happy. Asians tend to place greater value on low arousal states like calm and serenity.

According to Rottenberg, depression arises not from a defect, but from what we do well: thinking, using language, holding onto ambitious goals, and even our drive to be happy. Rottenberg says “The picture of depression that emerges is richer, more interesting, and in some ways more troubling than defect-model approaches would allow.”

He offers clues about how low moods can be better managed: appreciating the costs of thinking, sometimes accepting a low mood with equanimity, aiming for goals that are high but not too high, knowing when it is time to give up on a goal, and realizing that happiness is not itself a goal but “a fleeting byproduct of progress towards other goals.” Despite the evolutionary directive to become depressed, we retain a margin of control to shape its course.

We have learned that depression comes on more gradually and lifts more gradually than we once thought. We can’t predict whether a patient will respond to any treatment, but that doesn’t mean we shouldn’t keep trying. We used to think antidepressants took 6 weeks to show an effect, but we often see patients improving in the first two weeks, even those taking a placebo! Early improvement doesn’t predict final outcome. Early improvers may face fewer life problems, have an innate resilience, or maybe they are just lucky. Recovered patients may still have some residual depression and fear that a relapse could happen any time. A deep depression can re-program our mood system so that it favors a return to low mood states; but the same brain plasticity also allows for re-re-programming to a more normal state with treatments like mindfulness-based cognitive therapy, which attempts to disconnect sad moods from negative thoughts about the self. Mood can be rebuilt by changing the way we think, our environment, our relationships, and our health habits like sleep, diet, and exercise.

“Just like hunger or pain, moods are survival-relevant mental states that can bind together thoughts, feelings, and memories [and] change our mental priorities.” But they lead to mood-congruent memory, where we retrieve memories that match our current mood and are unable to call up contradictory memories. This can fortify us to change our situation, but it also tends to deepen the depression and makes us mentally less nimble.

Depression can be viewed as an opportunity. Rottenberg describes a patient who used her depression as a lens to re-evaluate everything in her life and re-set her priorities. Her life was better after the depressive episode than before.

Conclusion

Rottenberg calls his ideas the “mood science approach” to depression. He says:

The evolutionary perspective asks us to be patient, to learn to tolerate some degree of low mood, and to listen to what it is that low mood can tell us.

I don’t think his approach qualifies as a “paradigm shift,” but he does provide some valuable insights about this frustrating condition. Some of these insights are speculative, but most are based on recent animal and human research.

I used to try to reduce the stigma and guilt of obesity by telling obese patients that their tendency to store calories as fat was not a bad thing per se: it would give them a survival advantage over thinner people in a starvation environment or an environment of alternating feast and famine. But in our modern environment, where food is plentiful, the survival advantage is with the non-obese. I don’t think what I said made them lose weight more successfully, but I hope it provided some degree of comfort and reduced guilt. In the same way, Rottenberg’s concepts may help destigmatize depression. Depressed patients may feel better about their condition if they are told that it is a result of evolutionary traits that are basically good for us but that sometimes overdo it. If nothing else, the ideas and the experimental evidence Rottenberg presents provide plenty of food for thought.

Posted in: Book & movie reviews, Evolution, Neuroscience/Mental Health

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84 thoughts on “Depression Re-examined: A New Way to Look at an Old Puzzle

  1. Dr Robert Peers MBBS [UniMelb] says:

    Oscar Wilde once said “Life is too important to be taken seriously.” Genuine depression seems to be very rare in Nature–most critters enjoy their “Funktionslust” with hearty gusto–like a soaring eagle twitching its wing-tip feathers. It also seems to be rare in traditional non-Western societies, like the Kaluli people in Papua, or in Japanese fishing villages.

    Westerners seem particularly prone to clinical depression. In 1870, pioneering British psychiatrist Dr Henry Maudsley noted a familial link between diabetes and mental disorders. In 1916, London psychological medicine consultant Dr Charles Mercer, appalled by his patients’ fatty diet, tested a low-fat diet, and found that “all were cured, bar one”. ["Diet As A Factor In The Causation Of Mental Disorders". Lancet, 1916].

    Next, in 1925, London chemical pathologist S A Mann reported glucose intolerance in melancholics, manics, psychotics etc.. [J Mental Science]. In 1936, Prof Sir Harry Himsworth pinned down the cause of this pre-diabetic glucose intolerance: dietary saturated fat.

    In the US, in 1939, Conn and Newburgh reported complete reversal of maturity-onset diabetes with diet [JAMA]. Must have been a good diet, but not described in detail.

    In England, in 1956, Oxford essential fatty acid pioneer Dr Hugh Sinclair proposed that the fatty Western diet created faulty cell membranes–including mitochondrial membranes, which, when less “unsaturated” caused respiratory uncoupling [P Klein, Detroit, 1954]; uncoupling means oxidation and inflammation.

    And a “fattier” plasma membrane means insulin resistance and glucose intolerance, as shown by Alberta’s Dr M T Clandinin in 1988. In the same year, US scientist Dr Stephen Koslow found glucose intolerance in both unipolar and bipolar depression.

    I first noted, in the 1980s, that my routine low-fat diet reduced depression in my own patients–but left them strangely anxious! I later noted, from my habit of taking dietary histories, that calm fat-eating parents produced shy, anxious offspring.

    Anxiety disorder has long been known to precede and underlie depression: my calm patients eating fatty diet report only mild mental and physical tiredness, not depression.

    In 1995, my scientist daughter helped me to work out how fatty maternal diet causes offspring anxiety: the mild placental inflammation allows maternal cortisol to reach the foetal brain, where the forbidden hormone programmes enduring anxiety.

    This surprising effect has now been confirmed in monkeys and mice [E Sullivan; S Bilbo].

    Anxiety affects 25% of Aussies, 30% of New Zealanders, and 32% of US citizens [including over 50% of medical students and practitioners]. A New Zealander has 10 times the bipolar risk of a Hong Kong resident [M Weissman].

    Depression is more common and more severe in Northern Europe, than in the South, where Mediterranean diet is eaten.

    Genetic estimates for depression risk are grossly inflated, due to failure to control for both personal diet and maternal diet, in twin and family studies. A calm fat-eating grandmother often produces a string of anxious, depressed female offspring and grand-daughters, whose pregnancy diets render genes unnecessary.

    While low-fat diet usually clears depression, the underlying anxiety responds well to the natural serotonin 2A receptor blocker, myo-inositol [Levine J, 1997].

    The actual mechanisms driving depression may include:

    1. Pre-natal induction of predisposing lifelong anxiety, by fatty maternal diet.

    2. Conversion of anxiety to depression by fatty personal diet [dairy fat, meat fat, bakery fat, chocolate, cooking fat]:

    a) Fatty diet, via faulty mitochondrial membranes, causes oxidation and inflammation: pro-inflammatory cytokines [e.g. interleukin 6] cause both “sickness behaviour” and a further rise in cortisol, by activating the “stress axis”. Cortisol can suppress ongoing neurogenesis in the hippocampus, with depressing results.

    b) The same diet causes insulin resistance, which in the brain causes impaired neuronal and synapse survival, and also reduced glucose uptake.

    c) Both inflammation and cortisol divert dietary tryptophan away from healthy serotonin formation, towards the formation of neurotoxic tryptophan metabolites, like kynurenic acid, that is known to inhibit cognition, by affecting certain neuronal receptors in the hippocampus and prefrontal cortex [H Y Meltzer].

    Thus, the typical depression we see in the fat-eating West has a nutritional cause, and also a nutritional treatment. Inositol is abundant in grains, nuts, legumes and citrus, while powder supplement [5 g/d] may be needed for complete anxiety reversal.

    1. MadisonMD says:

      “Life is too important to be taken seriously.”

      Thus, the typical depression we see in the fat-eating West has a nutritional cause, and also a nutritional treatment. Inositol is abundant in grains, nuts, legumes and citrus, while powder supplement [5 g/d] may be needed for complete anxiety reversal.

      Thus life is too short to take you seriously.

      You lack evidence to support your wild claims.

      Inositol is not a panacea

      1. mousethatroared says:

        No, No – life is too long to take him seriously.

        1. mousethatroared says:

          darn, that why I seldom use tags in my comments. I did close that italics tag after “long” but it didn’t work. The graphic designer in me is appalled.

    2. LeZ says:

      What a relief! Dr. Hall’s succinct exposition of Rottenberg’s analysis made it seem as if we were talking about a complex phenomenon. I’m happy to see reconfirmed that for every complex problem there is an answer that is clear and simple.

      However, to make your comment fit in better with the SBM theme of this blog, could you please qualify some of your assertions?

      While low-fat diet usually clears depression [...]

      The word “usually” is a bit vague but suggests the majority of cases, which is a strong claim, even if we interpret “clearing depression” as temporary relief (for instance due to psychological effects of switching diets). Please quantify and provide evidence, as in “In x% of cases a low-fat diet was shown to cure depression. [citation, ...]“, with a quantified definition of “cure”.

      [T]he typical depression we see in the fat-eating West has a nutritional cause [...]

      The word “typical” has the same vagueness issue as the word “usually”, but now suggests the modality of cases, which is an even stronger claim, certainly in the light of Rottenberg’s research, which points to both a wider range of causes and different primary causes[1]. Please reformulate after the same fashion as above.

      Several other claims you make would look better with evidence, but then the duo “food is the primary cause of depression” and “food cures most depressions” seem to capture most of your theory, so let’s start with those.

      [1] Unless you would claim that nutritional causes for depression are a phenotypical manifestation of the evolutionary traits favouring depression, which you don’t, given that you state that “genetic estimates for depression risk are grossly inflated”.

    3. WilliamLawrenceUtridge says:

      “Oh look, a nail! Good thing I’ve got this convenient hammer!”

      “Oh look, a screw! Good thing I’ve got this convenient hammer!”

      “Oh look, meningitis! Good thing I’ve got this convenient hammer”

      Disparate diseases rarely have single causes, particularly at population levels. However, when you think you’ve got the One True Cause Of All DiseaseTM, it’s amazing how you can convince yourself that you’ve also got the One True SolutionTM.

      You’ve perhaps got a solution to constipation. I doubt it’s much else. But hey, the nice thing is – if you’re right, eventually the data will arise to support it. Of course, in the meantime what you are doing is unethical, but whatever. It’s not like you care.

      Tell me again about how quacks are unethical for selling unproven remedies to children with cancer, but you selling a single unproven remedy is fine because it’s cheap? I thought it was naked hypocrisy the last time, maybe I’ll be convinced this time.

    4. Thor says:

      Anecdote alert: When it comes to applying different diets over an extended amount of time, I’ve tried more approaches than most. By far the best food intake ‘plan’ for me is balance of macronutrients. Not low or high anything. On the contrary, whenever I did apply low-fat, I could practically bank on a negative outcome, including depression and anxiety. And having had interaction with hundreds of people concerned with diet, my experience doesn’t seem to be unique. Fat-deprived people generally seem less happy and fulfilled, and more uppity and repressed.

      1. mousethatroared says:

        Years ago I tried some sort of GABA supplement. It seemed like it made me irritable. I’ve tried Omega Acid supplements and I thought I might feel mildly more relaxed, but my skin broke out*…On the other hand, I think I’m been in perimenopause for many years now. Trying to track any preventative interventions effect on mood, skin, etc with such erratic cycles is a bit like doing calligraphy in a pick-up truck on a dirt road. This is why I tend toward cognitive interventions that one can use in response to a symptoms rather than an experimental prevention.

        *Ultimately, I gave up the Omega Acid, though I do try to eat more fish.

        1. Thor says:

          Yes, ma’am. Clever (and funny) analogy! When it comes to nutritional claims: show me the money. Experiment on plausible ideas, then verify. Nice to know talented, dedicated professionals are working on this, like Angora Rabbit. The one thing doomed for failure is the ‘one diet for all approach’. Generally, for most healthy people, a balanced macro-nutrient diet is best (with minor individual modifications), minimizing processed carbs, sugar and junk-fat laden foods, and incorporating as many vegetables as possible.

          For specific conditions, though, this may have to be modified, such as diabetes, epilepsy and other neurological disorders, and cancers. In particular, I’m interested to see how the ketogenic diet effects cancers. We know pretty much for sure about its efficacy in epilepsy. Regarding probiotics, this is obviously an exciting emerging field of medicine. But thus far, definitely “more studies are needed”. For various forms of diarrhea it seems to excel. Initial findings are hopeful for IBS. Beyond that, not quite ready for claims.

  2. mousethatroared says:

    @Harriet Hall – Sounds like a very interesting book. Thanks so much for reading it and giving us that summary and excellent review!

  3. windriven says:

    “Low mood has its benefits. Non-depressed people tend to overestimate their abilities, are prone to positive illusions, and demonstrate overconfidence and blindness to faults. When depressed, people are more realistic; they are more deliberate, skeptical, and careful in processing information from the environment.”

    How does one determine where a realistic assessment ends and clinical depression begins? Or do they even exist on the same continuum?

    1. mousethatroared says:

      Windriven – I know this is more a question for Harriet Hall, but I’ll add my two cents and point out that some research indicates that clinical depressed people ARE more realistic…that non-depressed people tend to be slightly unrealistically optimistic. So in those cases, the realism co-exists with the depression, rather being on a spectrum that gradates from realism to depression.

      1. mousethatroared says:

        Anecdote alert – Being more deliberate, skeptical, and careful in processing information from the environment may sound good, but it’s got a downside. When suffering from mild depression for a time after my mother’s death and a job shift, I dreaded going into a grocery store. I needed food, but between figuring out appropriate nutrition, price, convenient cooking and what I actually wanted to eat, and weighing how to compromise on the variables, it took me forever to select items. Sometimes I would get so bogged down, I’d just leave without finishing shopping. Analytical without some sort positive emotional pay-off is often not particularly productive.

        In a typical mood, it’s much easier for me to say “Hey, rice, like jasmine, that’s the cheapest, cart, next aisle.”

        Although I can’t say if that was entirely depression, it may have been some sort of anxiety/depression combo phenomenon.

    2. Thor says:

      Might have to do with degree. While ‘normal’ depression appears to have the benefits Dr. Hall eluded to, major clinical depression is uncontrollable, compulsive, and obsessive, leading to harm. The benefit of evoking realistic assessment and perspective, develops and transforms into incapacitating mental/emotional pathology. It seems the mechanism has gone awry, that the evolutionary benefit is lost and the condition becomes harmful and counter-productive. But, why/how does ‘normal’ depression switch to a major psychiatric disorder? Again, so much for evolution being an ordered design.

  4. Kevin Moore says:

    New studies suggest that depression may be even more complex than entertained in Rottenberg’s analysis. Animal experiments have indicated striking connections between gut flora composition and mind states.

    1. WilliamLawrenceUtridge says:

      See my comment above. Seriously, you guys could be competing clones.

      Say, since you’ve both got the One True Cure For All Disease, could you test them in a clinical trial, so we know which one is really the One True Cure? Because doing both seems like a pain in the ass.

      1. Sawyer says:

        But he used the word “complex” WLU. That clearly means he’s NOT supporting some sort of overly simplistic model of gut chemistry / brain chemistry.

        :)

      2. Kevin Moore says:

        Don’t know how to respond to someone who misreads my post. The only cure I know for all disease puts one six feet under.

        1. WilliamLawrenceUtridge says:

          Try to treat depression with gut bacteria and I think you’ll cure a lot more people.

          Ambiguity intended.

    2. MadisonMD says:

      That’s great, Kevin. Brings new meaning to the term ‘poopy head.’

      Mechanism?

    3. mousethatroared says:

      I’m a layperson, but I will say read some reports that indicated some possible connections between gut flora and some anxiety, depression disorders….but I got the distinct impression that it’s still in the hypothesis testing, not ready for prime time. Look forward to hearing what happens in the future, though.

      Here’s a summary, Not the original studies, but I think one could track them down from here if anyone is interested.

      http://www.sciencedaily.com/releases/2013/11/131114094754.htm

    4. MadisonMD says:

      Mechanism and plausibility.

      Plausibility: I wonder how my gut flora changes over the course of a day… when I go from happy to angry to sad to exhausted?

      Mechanism: So I eat yogurt with lactobacillus and strep thermophillus. Somehow, the strep makes it to my colon and alters the balance of E coli/strep in my gut that day.
      The increased strep releases increased a significant amount of X.
      X reaches pharmacological effective levels, travels to my brain, modifies some receptors, and relieves stress.

      Well, somehow all this seems like a hypothesis not worth testing– does not have the requisite plausibility or mechanism. But hey, find X or tell me what it is and I’ll eat my words*.

      ——————————
      *Don’t try to tell me its a vitamin unless you have damn good evidence** about neurologic effects of the vitamin at levels above that required to avoid deficiency.
      **There is no such evidence for any vitamin. (and, moreover, if there were, you could take the vitamin instead of eating yogurt.)

      1. mousethatroared says:

        Hey MadisonMD – If you (or anyone else interested) gets some time I’d love to hear some opinions on the papers in the science daily release that I posted. Does it seem like complete bosh to you or possibly something with promise?

        The mechanism as far as my not so science educated reading seems to be that tightly controlled doses of probiotics (not your average yogurt at the grocery store) can change the gut flora and, if done correctly reduce inflammation, even systemically. Chronic inflammation, immune response has been tied to some mental disorders…so possibly if probiotics reduce inflammation, they may reduce mental symptoms tied to inflammation.

        I’m not trying to sell this idea. It’s just that it seems to be that I had heard that some SSRI also had an anti-inflammatory effect and even (sorry, I might be misremembering) that some anti-inflammatories sometimes seemed to have some mild effect on depression….blah, blah, blah (citation needed, but I don’t have time to go on that med pub, google hunt).

        Clearly, I’m not talking one true cause here, just one approach to some cases.

        I wish I could remember where I read it, but it seems to me that I had heard this theory as legit…not complete claptrap, but also not that it had huge promise (we’re not talking curing bipolar here.)

        Maybe it warrants an article.

      2. MadisonMD says:

        @MTR

        The mechanism as far as my not so science educated reading seems to be that tightly controlled doses of probiotics (not your average yogurt at the grocery store) can change the gut flora and, if done correctly reduce inflammation, even systemically. Chronic inflammation, immune response has been tied to some mental disorders…so possibly if probiotics reduce inflammation, they may reduce mental symptoms tied to inflammation.

        There are somewhat tenuous linkages here but at least it is testable. Here are some (rather straightforward) tests which could establish this:
        (a) Link depression and systemic inflammation Case-control establishing the link between depression and systemic inflammation. [say major depression as defined by DSM-V and CRP/ESR].
        (b) Link systemic inflammation with gut inflammation There are many sources of systemic inflammation so this one is tough, but you could try to etablish.
        (c) Strength of correlation with depressionEstablish that gut and systemic inflammation are both highly prevalent in people with depression.
        (b) Establish non-pathogenic flora as a likely cause of gut and systemic inflammation You need to establish what you think is inflammatory in gut flora e.g. is it a ratio of two species? The % of one species? Then measure systemic inflammation, say by CRP/ESR and gut inflammation by biopsy (careful– sampling error will come into play).
        (c) Validate link between flora and depressionCorrelate the “inflammatory gut flora” with depression in a prespecified way (no post-hoc correlations allowed).
        (d) Experiment–RCTUltimately, probiotics will have to be shown to modify gut flora, inflammation and depression in a predictive and positive way in randomized double blind placebo-controlled trials. (you know– placebo effect and all that)

        Personally, I find the mechanism and the prediction doubtful*. But I would accept data that demonstrates otherwise.

        ————–
        An obvious scientific problem with this new field is the degrees of freedom it provides researchers to find correlation between bacterial flora pattern (since any researcher can select any arbitrary pattern which is believed or found to correlate with psychology), and the number and subjectivity of endpoints (e.g. inferring depression from mouse behavior). This provides many, many, many opportunities to obtain spurious positive findings– allowing one to publish and keep the grant $ coming. So I think a prespecified gut flora pattern, mechanism, and endpoints are critical to consider when reviewing the literature.

        The press release you linked to refers to a review article which refers to many other references. At least some seem to establish correlations between gut flora and mental states or behavior of mice. In particular, I am concerned that behavior of mice can be (a) quite subjective; and (b) lend itself to measuring multiple behavioral parameters. So reviewing these articles would require careful attention to how the observers were blinded as well as an assurance that “positive endpoint” was prespecified (to avoid multiple hypothesis testing/degrees of freedom in selecting the most postive outcome measure). Even the correlation wouldn’t establish causation, nor would the findings in mice be automatically extrapolatable in humans.

        I haven’t read the primary articles, but if you point to one or two that you find particularly compelling, I might find the time to have a look.
        ————–
        *Not only mechanistically implausible. Also, my skeptical antennae are alerted to this topic b/c: (i) The autism-gut hypothesis which is simply infiltrated with junk science, and (ii) alt med types are pushing the probiotics which are big money makers without compelling clinical evidence of effectiveness.

        1. Kevin Moore says:

          Thanks for your quick overview. Personally I find discussion of actual science research on SBM more compelling than ferreting out the woo, which though laudable, to me is shooting fish in a barrel. If junk science is infiltrating gut flora research and grant funds are driving spurious findings more examination is needed.. I hope to see more inquiry into the new microbiome research on SBM in the future, especially in light of a seemingly growing interest among researchers and the public in the subject.

          1. S.A. says:

            I’m not sure I would call probiotics big money makers compared to the millions of dollars people spend sitting on a couch re-examining their childhood for year after year just because their stomach hurts and they’re tired all the time. Not saying that probiotics will cure anybody except for people who have chartable bacterial infections, but I certainly know talking about childhood doesn’t cure stomach pain that comes from a host of treatable and confirmable intestinal illnesses. Yet stomach pain remains a symptom of depression. Weird.

            1. Andrey Pavlov says:

              et stomach pain remains a symptom of depression. Weird.

              Only weird if you take it completely out of context like you have and fail to understand how and why the diagnostic criteria work the way they do.

              Depression is a syndromic diagnosis. We do not have an objective standardized test to check and see if you are depressed. It is a constellation of symptoms, some of which are conflicting (know what’s weird? Both increased and decreased appetite are symptoms of depression). The point is that in light of the lack of a confirmatory test we look for every possible common symptom of depression, create a list, and then require a certain number of criteria be met (increased or decreased appetite) in order to call it “depression.” By changing the number of criteria necessary we increase or decrease sensitivity and specificity of our diagnosis.

              But at the end of the day there is always clinical judgment and – most importantly – patient context. We may diagnose someone as depressed if they meet only 4 criteria (5 is technically necessary) given the correct patient centered context. Or we may not diagnose someone with 6 criteria met.

              Clearly, gray areas like this make it difficult to really accurately diagnose and so, as with most if not all DSM criteria, it is specifically noted that it must have some sort of negative effect on the patient’s life and/or activities of daily living in order to be diagnostic. That can be either from the patient’s own subjective opinion (doc, I know it doesn’t seem like a big deal but it is really causing me problems!) or from objective criteria (no doc! me losing all of my money and spending my kids’ college fund on gambling isn’t really a problem, doesn’t bother me at all!)

              We aren’t as stupid as you seem to imply by insinuating that we could be hoodwinked into misdiagnosing an ulcer as depression.

            2. WilliamLawrenceUtridge says:

              Yet stomach pain remains a symptom of depression. Weird.

              Why is it weird? Most of the receptors in the body are duplicated, having at least two functions. The main reason for this is the blood-brain barrier; it allows the same receptor and signalling molecules to be used in the central nervous system (brain and spinal cord, on one side of the BBB) and again in the rest of the body (on the other side of the BBB). This happens because evolution is “efficient” in a lazy, half-assed, poorly-executed way. It’s the reason so many “brain” drugs have gut side effects. There are more serotonin receptors (and more serotonin) in the gut than there are in the brain. Not to mention the GI tract is heavily inveseted with nerves that allows some degree of central control over its functioning. For instance – people who crap their pants in fear. Or people who overeat as as form of self-medication.

              If one adopts the idea that there is the “brain” and there is the “body” and the two are totally separate, yes it might seem weird. But they’re not, they’re intimately joined in complicated ways.

              And now Andrey will prove me wrong, ’cause he’s a doctor and I ain’t :)

              1. Andrey Pavlov says:

                LOL. I would argue that S.A.’s point is not precisely that (hence my own answer) and would point out that there are a couple of useful and important details and nuance that are missing in yours, along with perhaps a bit of “just so” story from an evolutionary perspective, but overall no. Nothing to prove wrong. Just a few trivialities we could discuss over beers. (though the serotonin thing could be pounced on by someone with an agenda, as it is neither wrong nor specifically relevant)

            3. mousethatroared says:

              Darn – Does anybody actually do psychotherapy anymore? I mean I’ve done therapy three times and there was never a couch in sight and it was never countless hours. The was always a definitive number of sessions covered for the particular complaint. Much like physical therapy….although with less movement, I will admit.

              Like physical therapy – I don’t think that one should continue with a psychologist (clinical social worker, etc) unless you are seeing some improvement in symptoms within a reasonable amount of time. It suggests, to me, that another approach, consult for medication, different CBT or another therapeutic approach, etc may be in order.

              Although I can see how there is a need for long term maintenance sessions in some conditions.

              Although, that’s just a patient perspective, I don’t know professional recommendations.

            4. mousethatroared says:

              This is a confusing statement. I do get a stomach ache from my anxiety, sometimes. It’s clearly tied to my anxiety and controlling the intensity of my anxiety does help that stomach ache.

              People also get stomach pain from bacteria, such as H Pylori. Clearly the best route to such an issue is to treat the H Pylori. or other bacterial problem.

              There are also cases of functional abdomin pain. which (from my understanding) appear to be caused by increased sensitivity to normal stimuli. I have read that sometime this is treated with low doses of SSRI, because serotonin seems to effect how our brains process pain.

              Stress levels (such as anxiety) or depression can effect how our brains process pain also. But, from my recall of reading on the subject, many people with functional abdomen pain do not have coexisting depression or anxiety disorders, but the SSRI may still help them.

              For those who do have coexisting anxiety or depression – there could be some hope for dimished functional abdomen pain through a successful CBT approach for anxiety or depression (but what does the research indicate? I don’t know). But I have never heard of a science based approach that recommended treating functional abdomen pain by discussing your childhood.

              Ha – put me on a couch and have me discuss my childhood and I’m bound to end up WITH a stomachache. That would be a crock, avoid any therapist who recommends it!

            5. MadisonMD says:

              Yet stomach pain remains a symptom of depression. Weird.

              I took this to imply that there might be something to the microflora-brain connection. However, the known mechanism involving serotonin receptors and vagal stimulation (per WLU) is more plausible than the unknown and tenuous link between microflora and mental state.

              The timescale for microflora change (slow) and changes in mental state (fast) do not even match. (Though admittedly this alone could not rule out a chronic undercurrent of mood or mental illness.)

              1. mousethatroared says:

                “I took this to imply that there might be something to the microflora-brain connection. ”

                Yeah, I had the same reading. But there is also a mention of that form of mind/body/Freudianish woo that likes to suggest that repressed childhood feelings or memories can cause all manner of physical symptoms. S.A. seems to have the right idea in dismissing that.

        2. mousethatroared says:

          Thanks MadisonMD for the excellent tutorial! I don’t have time to track down studies now. But this will be really useful in looking through them later and evaluating how they measure up to your thoughts. If I find something that seems like an example of good or bad, I’ll post it.

          Thanks again

    5. Angora Rabbit says:

      For those curious about the topic, search PubMed (not Google, please) for “acylethanolamines” and “oleoylethanolamine”. Very hot research topic right now. OEA, a gut fatty acid derivative, can activate PPAR-alpha and GPR119 at reasonable biological profiles. The emphasis here is upon satiety control, which is brain-mediated through the dorsal striatum. There is great scientific interest currently on how dietary lipids and gut lipids may control eating behaviors, metabolism, and the like.

      An interesting starting point for reading might be “LA Tellez et al., Science 341:800-802 (16 Aug 2013), “A gut lipid messenger links excess dietary fat to dopamine deficiency.” Follow the references from there. Not ready for clinical translation but a fascinating intro to a fascinating topic.

  5. Jay says:

    I have MS. I also have malignant hypertension, which may be from a pheochromocytoma, but no one has found the pesky clump of cells that make my adrenaline levels spike…so far. It’s only been 20 years, so I’m not expecting a miracle.
    I take Escitalopram 20 mgs per day, along with 4 BP medications and Thyroxine and beta-inteferon 1a.
    I have not depression, but anxiety. I’m not depressed, but I spent a few years living with a seriously depressed person.
    I lived on the edge of flight/fight for so long that I found after 10 years, that my anxiety had suddenly changed into fantasies of suicide.
    The Escitalopram stopped these thoughts. My panic attacks disappeared and my life improved.
    I’m not classed as disabled and you wouldn’t know I have MS.
    My husband has hemiplegic migraines and his attacks start with a surge of either euphoria or anxiety, then a total lack of awareness, followed by hemi-paresis.

    Depression per se, is not an easy tag. Yes, for about 5 years, I was convinced that my wonderful marriage was over. I didn’t know that my husband was delusional. I realised this quite suddenly – that his anger was based on something imagined. He sought help, but is allergic to SSRIs. In fact, Venlafaxine almost killed him.
    Yes, I was depressed. I wished that I was invisible and just endured each day.

    Rottenburg may be correct. I responded well to an SSRI. I still take it after a year and life is pretty good.
    I’m not sad. I’m not even slightly sad. I live with a horrible, incurable disease and know that at sometime, there is a possibility that it will rob me of something really important.
    I’m aware – super aware.

    Am I depressed? I don’t think so, just a realist who lives a difficult life. I wouldn’t like to face it again with my SSRI.

    Diet? Am I anxious because of my ‘fatty Western diet?”
    In my case, I can’t eat wheat, (gluten increases my nerve pain) legumes (lectins are very bad for the blood/brain barrier and increase inflammation in MS), oats (no way, totally allergic) nuts? good.
    Life isn’t that simple. Just live in the MS world and you’ll see that life ain’t that simple and MS is a whole new world of confusion and dodgy treatments or cures.

  6. Peter S. says:

    “What is depression? Is it:
    A defect in brain chemistry? This is the basis of drug therapy. The chemistry imbalance hypothesis is simplistic, misleading, and essentially wrong. Antidepressants do indeed alter brain chemistry as they relieve symptoms, but that doesn’t necessarily mean that a chemical imbalance caused the problem, and it doesn’t explain what caused the imbalance or why it happened when it did.”

    I cannot thank you enough for saying this. As you well know, for some reason a huge number of practitioners both conventional and alternative still do not understand this. If I see one more reference to “low serotonin” I may lose it.

  7. Walter says:

    A great part of the stigmatization of depression proceeds directly from the notion that it is more than superficially goal-oriented. Propagation of this untruth is profoundly upsetting to sufferers, and has a terrible impact on many dimensions of treatment, including regimen compliance and suicidality.

    A debilitating depressive episode reduces the patient’s ability to accomplish goals in much the same way a horrific chainsaw accident tends to put a damper on a person’s plans. That is, it’s not a question of “I won’t,” but rather a question of “I cannot.” And this “inability to will to will” runs even deeper, into currently (unfortunately) ineffable territory.

    It seems Dr. Hall and the author of the book she profiled need to first come up with a far more accurate working definition of this phenomenon before they can give it meaningful attention.

    1. MadisonMD says:

      A great part of the stigmatization of depression proceeds directly from the notion that it is more than superficially goal-oriented.

      So it is your position that depression is superficially goal oriented and nothing more? Would you also claim that your chainsaw analogy is also just superficially goal oriented? After all you point out that it has the same effect.

      Dr. Hall and the author of the book… need …a far more accurate working definition of this phenomenon

      Agree that it is best to define the terms. (DSMV?) But, what is the gold standard for accuracy?

      1. Walter says:

        So it is your position that depression is superficially goal oriented and nothing more?

        Yes. Put another way, it is only about agency to the extent that agency is curtailed. As it would be if one had a limb-lopping logging accident.

        But, what is the gold standard for accuracy?

        I’m sure I don’t know. Neither do they. Worse, they’re spreading and reinforcing untruths with aggressively implied authority.

        1. MadisonMD says:

          Somehow I think cutting off my arm would have a greater effect on my life than simply curtailing my ability to use my arm. I also think that depression goes a bit deeper than superficially affecting my goals… it could affect my mood, my sleep, my appetite, my thoughts, my life. But perhaps you are a strict behavioralist who rejects the notion of unobservable psychologic states?

          Regarding holding an operational definition to a gold standard, this seems to be a paradox in terms. An operational definition is, by its very nature, practical and somewhat arbitrary. The DSMV definitions are as good as any, unless you would argue depression does not exist at all.

          1. Walter says:

            Somehow I think cutting off my arm would have a greater effect on my life than simply curtailing my ability to use my arm.

            Now you’re just playing games with semantics and (hopefully) faux naivete.

            I also think that depression goes a bit deeper than superficially affecting my goals….

            Of course it does. That’s pretty much the entirety of my assertion.

            But perhaps you are a strict behavioralist who rejects the notion of unobservable psychologic states?

            Sigh. Your wires are tangled. Or perhaps mine are.

            Depression is more than Dr. Hall’s review would have us believe. Full stop.

  8. Norman says:

    Maybe to get away a little from this gut flora issue…

    “A defect in childhood experience? This is the basis of psychoanalysis. Freud’s theories have been largely discredited, and people with the most appalling childhoods can have normal adulthoods.”

    I´m quite astonished by this statement. As far as I know, both Freud and the concept of childhood traumas is widely thaught worldwide in universities and everything related to psychology. Of course, nowadays the concept of “resilience” or ability to cope with adversities in life is seen as more important than childhood experiences itself, so that people with negative experiences but good resilience are better off than people with no negative experiences but also no resilience. This is why, from my impression, behavioral therapeutic approaches are being used more and more in detriment of psychoanalitical ones. To teach people resilience.

    But still, just saying that his theories have been largely discredited seems exaggerated, altough I would be grateful if you could point me to some authors/books. Or maybe it´s just that you are talking about severe disorders like depression and I am thinking more about lighter personality issues/Neurosis?

    1. Harriet Hall says:

      While some people think some of Freud’s ideas are still viable, he has been widely criticized because his approach was not scientific, he didn’t attempt to test his hypotheses, and indeed, most of his claims are not even testable by scientific methods. He has even been accused of fabricating some of his case histories, or at least naively assuming that a patient’s fantasies were actual childhood events. Books that discredit him? Here’s a start:
      http://www.nytimes.com/books/97/08/10/reviews/970810.10boxert.html

  9. Bill Anderson says:

    In daily parlance what makes us depressed? Disappointment. We have expectations which are not fulfilled. Modern society is submerged in a tsunami of hype, of proffered delights via advertising, the media etc. The vast majority do not materialise. We encounter disappointment on an unprecedented scale. It would not be surprising thus if some of us experienced serious depression. Its worth a look . In the field of grand unsubstantiated theories it is not outstandingly bizarre.

    1. WilliamLawrenceUtridge says:

      That suggests a purely intrapsychic, purely mental, purely life and life satisfaction cause to all depression. I think that is a bit simplistic. There are people who have no “objective” reason to be depressed, with rewarding and challenging jobs, loving friends and family, and adequate resources to live their lives, who are still depressed. I don’t think you can blame all depression on watching too much TV with unrealistically attractive actors and actresses, that seems like a gross oversimplification.

    2. Chris says:

      “In daily parlance what makes us depressed? Disappointment.”

      Um, no. Having known those who have suffered severely with depression, even though as teenagers they had many friends, did well in school without much effort and were in very functional families.

      One of them committed suicide when she was seventeen years old. Please don’t tell me that this honor student who had a job, many friends, participated in several activities, lived with two loving parents, and who facing a very bright future had over extended expectations.

      In contrast, my family was pretty dysfunctional. Before and after my mother died in a plane crash when I was eleven years old. Yes, there were issues with my stepmother, and sometimes my stepsister (though I actually feel more connected to her than my younger sister). But, then again, in our family we just say that our dad puts the “fun” into dysfunctional (example we were told that our paternal grandparents were dead, except after my mother’s death my brother picked up the phone to find himself speaking to our very much alive paternal grandfather… apparently there had been a rift in relations, and our dad decided the less we knew the better).

      So, yes, I have times when I am depressed. But I know they are temporary, and will soon pass in less than a day. Dear hubby knows this, and I will warn him if it causes me to be short tempered. It really only happens a couple three times of year. One of those was about a week ago when I was thinking about a relative who committed suicide due to reading an article on the web, so I decided to do some dishes. Unfortunately I woke up hubby (who went to bed oddly early), he was at the top of the stairs when I was coming up to yell at me, but saw me silently crying and decided to just let things be. The next day, all was well.

      He is more understanding due to also losing a parent do death at around the same age. We both hate the movie Terms of Endearment. It was wrongly advertised as comedy. But I had to go into the lobby to get napkins to mop up spousal tears. I am pretty sure all of those folks still sitting in the theater crying had lost a parent, and not just my hubby and myself. I am sorry, but this is something that never leaves you. But it does not in itself lead to depression.

      These anecdotes are just to show the difference between the types of depression. Someone told me that the ones I have are “situational.”. Meaning they are do to things that have actually happened to me. It is not “deep” or “severe” depression that can happen for no apparent reason.

      But do not despair! Or become depressed! Someone who has experienced this has put pen to paper to describe what it is like:
      http://hyperboleandahalf.blogspot.com/2011/10/adventures-in-depression.html

      1. Chris says:

        One of the perks (or problems) of having a child going to college still living at home who takes psychology courses, is that one gets corrected.

        I have just been told that the above link only describes on type of severe depression. There are many others, including a form of depression coupled with anxiety. Woo hoo!

        Though one would have known that if they had read what Dr. Hall wrote:

        There’s a continuum, and any cut-off point to divide normal from abnormal is arbitrary.

        You can actually buy stuff that expresses this reality: “I think you’ll find it’s a bit more complicated than that…” and other excellent Christmas gifts.

        Simplistic platitudes have no place in human biology, or any real science.

    3. windriven says:

      “In daily parlance what makes us depressed? Disappointment.”

      No, you confuse dissatisfaction with clinical depression.

    4. weing says:

      “In daily parlance what makes us depressed? Disappointment.”
      Sorry to disappoint you. I hope this doesn’t make you depressed. I’ll add Simon and Garfunkel’s version of “Richard Cory”.

  10. Xplodyncow says:

    Thanks for this review, Dr. Hall. I admire Rottenberg for starting the Come Out of the Dark campaign. The stigma needs to disappear. It’s 2014.

    I haven’t yet read this book, but I’m always wary of evo psych explanations of anything. I’m guessing the thrust of the book agrees with this quotation from a recent blog post:

    Our main approach to depression is biomedical and assumes that depression is an illness. Yet the search to discover a fundamental defect in the brain that causes depression has foundered. There remains no biological test to diagnose depression, despite hundreds of physical assays, nor are there any genes that strongly predict it. Brilliant scientists cannot find the defect—even if they look with different or more expensive toys—because their search is animated by the wrong question: Where is the disease?

    Just because medical science hasn’t found all the biological answers yet doesn’t mean they don’t exist. Swap out “depression” for any other disease state — do his statements still make sense?

    Rottenberg’s hypotheses “that evolution favored depression because of its survival value and that depression is essentially a good thing” were proposed at least five years ago by Andrews and Thomson. I used to agree with these hypotheses, but reading (and attempting to understand) journal articles about the tedious, painstaking search for answers to mood disorders has changed my mind.

    I worry that instead of destigmatizing depression, Rottenberg’s ideas will reinforce the stigma, either by making patients feel like prisoners of genetics or by inadvertently promoting the idea that patients can just snap — er, evolve out of it.

  11. Jchag says:

    There is research being done now which is showing a clear link between unhealthy gut and psychiatric illnesses such as depression and anxiety, which may lead to a new form of medication known as psychobiotics. In other words, the probiotic strong diet that is put forth in the GAPS diet, or any diet that is based on reducing inflammation and creating a healthy gut is taken seriously by the mainstream medical community. Why is it so hard to fathom that what we put into our bodies affects all aspects of our well being? A healthy, nutrient filled diet is the best medicine.

    http://www.ncbi.nlm.nih.gov/m/pubmed/23759244/

    1. WilliamLawrenceUtridge says:

      Preclinical data in rodents, limited data in humans for conditions where the relevance to people with depression and anxiety is questionable. Irritable bowel syndrome has a psycogenic component, so there’s considerable confound there. CFS is a syndrome, it’s basically a crap shoot. Whether probiotics end up having specific effects on DSM-defined depression and anxiety is a very open question.

    2. MadisonMD says:

      There is research being done now which is showing a clear link between unhealthy gut and psychiatric illnesses such as depression and anxiety, which may lead to a new form of medication known as psychobiotics

      It may. But it may not. Since most research leads to dead ends, I don’t think “research being done now” is a good indication that something is true. In this case, the cause-effect link is implausible, yet the very idea has caught fire with the public. We know from experience that when the public latches onto an idea, it is loathe to let it go and research on implausible treatments can limp on for decades. My point is ongoing research on a hypothesis that catches the public attention actually indicates a decreased liklihood of actual truth– bad ideas are falsified and rejected more quickly when they don’t catch the favor of the public.

      In other words, the probiotic strong diet that is put forth in the GAPS diet, or any diet that is based on reducing inflammation and creating a healthy gut is taken seriously by the mainstream medical community.

      I’m about as mainstream as I get but am doubtful. What diet reduces inflammation? Inflammation where? How do you know this? Why do you think inflammation would have a direct and strong link with DSMV illness? And which illness exactly are we speaking of?

      1. MadisonMD says:

        Meant to close the link after “decades.”

  12. AlisonM says:

    I’m sorry, but as a person who has a wonderful life and is still too depressed to function, I take issue with this characterization of depression as some sort of evolutionary advantage, just a little further along the continuum.

    Maybe it’s not caused by a “chemical imbalance,” but I can tell you for certain that when you’re trying to find a way to kill yourself that will be the least traumatic to your loved ones, a chemical that makes you stop thinking of that is a good thing to have even if it isn’t “proven” to be the thing that “causes” the depression.

    I agree with Xplodyncow that this kind of thinking will bring about further stigmatization. It’s already hard enough to get people to understand that thinking about my comfortable home, wonderful husband, great kids, and supportive friends actually makes me feel worse – not only am I depressed, but I’m ungrateful because I’m not made happy by the good things in life. Thanks for that. People already think that the cure to depression is to cheer up. If it’s just a smidge more than “unhappy,” then you really are a self-absorbed ingrate for not being happier.

    1. Andrey Pavlov says:

      AlisonM:

      I can sympathize.

    2. mousethatroared says:

      I’ve had that experience. When I started taking medication for anxiety/depression, my brother called me and started in with “You have such a great life, you have everything to be thankful for…” I basically told him “Yet, I feel like sh*#t, Duh, that’s what depression is.”

      But, I didn’t read Harriet Hall’s summary to be suggestive that this approach would lead to that old “snap out of it” approach as you and xplodncow* did. I think I must have sort of confirmation bias going on that’s causing me to miss something.

      Maybe it’s because I’m avoiding medication because I don’t like the side effect. Denial? I don’t know.

      *oh jeez, I didn’t get that until I typed it. :)

      1. AlisonM says:

        I’ve spent a lot of time being depressed. I’ve spent a lot of time on discussion forums with other people who are depressed (ADHD almost makes that a given.) I can imagine that makes me a little more sensitive to the feeling of MDD being marginalized even by people who feel that they have the best of intentions. Sometimes especially by people who have the best of intentions.

        From that perspective, I find the attitude that it’s just another evolutionary adaptation and we should just accept it and wait it out to be pretty patronizing and condescending. For many of us, waiting it out is not an option, because it simply Does. Not. Go. Away. And someone who tells us we should accept it and wait it out is cruel and unsympathetic.

        1. Harriet Hall says:

          No one suggested you should “just accept it and wait it out.” In fact, I described how Rottenberg points out the dangers of “watchful waiting.” Read the article again, more carefully. Or better still, read the book.

          1. AlisonM says:

            Dr. Hall, I do respect you, and have linked to your writing on numerous occasions. . .and I have now read the article three times. My feeling has not changed that there seems to be no understanding that there is a distinct difference between temporary or situational depression – or, as it’s described, “low mood” – and Major Depressive Disorder. This is really where the problem seems to be. I fully agree that a mood dip that is triggered by an event or a situation or any factor that is transient in nature fits this particular model.

            However, the idea of Major Depressive disorder in the post seems to be presented as simply another step on the continuum that would respond to the same attitude as treatment, when it is most certainly not the case. The impairment and loss of function of MDD is a definite dividing line, and it cannot be helped by this approach at all. I mean no disrespect, but I speak for myself and many others I know who have a clear understanding of the difference between “low mood” and MDD through (unfortunately) personal experience.

            Because of this problem that is inherent in the post, which does indeed seem to imply that “low mood” and MDD are similar situations with similar outcomes and similar expectations, there is really no inspiration to read the book, because the post makes it seem as if the book is dismissive of the much more serious problems conferred by MDD. No disrespect, just trying to point out that those of us who truly suffer with depression are acutely aware of the pooh-poohing of our problems, and that makes us perhaps a little more defensive when faced with something that appears to be doing the same.

            1. Harriet Hall says:

              Low mood can be transient or it can be recurrent or prolonged, and the line between it and “dysthymia” can be hard to draw. How can you define what is “normal” for an individual? Similarly, the line between dysthymia and mild depression is fuzzy. Depressions triggered by life events were previously thought to be “reactive” depressions categorically different from unprovoked depressions, but the thinking is changing and the author makes the point that they are now considered to be essentially the same illness and their treatment need not differ. He also makes the point that mild depressions are risk factors for major depressions. I don’t see any compelling reason to separate out any component as not being part of a continuum. I think it is reasonable to think of a continuum from low mood through dysthymia and mild depression to major depressive illness. I don’t think we have the tools yet to categorize them any better or to decide where the cut-offs should be. Also, I thought I had made it clear by my analogy with overweight patients that I didn’t think that having an evolutionary explanation for depression would speed recovery, just that it might offer some degree of comfort and reduce any self-blame or rumination about “why” that might be an additional source of stress. Neither I nor the author think that “attitude” about evolution could be considered “treatment.” And the author is clearly not dismissive of the serious problems of MDD, since he had it himself and was slow to recover.

        2. mousethatroared says:

          “For many of us, waiting it out is not an option, because it simply Does. Not. Go. Away. And someone who tells us we should accept it and wait it out is cruel and unsympathetic.”

          I completely agree with this. I sounds like Harriet is saying that Rottenberg would agree with you as well. So I’ll leave that aside.

          Here is my thing. As much as I hate having anxiety and the occasional depression, I actually see some advantages in some of the ways my brain works over how I see other people approaching problems. The problem is, those tendencies can get me in trouble and sometimes they are just too much work and it all doesn’t seem worth it. So the my brain’s got good sides and bad sides and when the bad tendencies start outweighing the good and I feel like I’m over my head, I look for help through therapy or medication. I took this to be what Rottenberg was saying…and like I said, because that’s my attitude there may be some confirmation bias.

          Do you ever feel that way? Like your brain, in spite of the hell it’s putting you through is better at some things than “typical” people’s are?

          Sorry if that’s a bizarre question.

          1. AlisonM says:

            My brain is better at a lot of things than other people’s brains are. It’s also worse at a lot of things. And I do a pretty darned good job of “waiting it out” when I have to – because I know that once I get back on the right medication, the good things get better and the bad things aren’t so much of a problem. However, I don’t think that it’s my depression or ADHD that are giving me the advantages.

            1. mousethatroared says:

              It’s understandable then – I appreciate your answer AlisonM – From people’s responses here, it seems like it’s reasonable to expect that many people with severe depression (and maybe mild/moderate) will NOT find the concept of depression as an evolutionary adaption helpful.

              It is good to consider how/if the concept could be used to stigmatize people with depression. If only so as to be prepared to defend against that.

              1. AlisonM says:

                The stigma actually comes from the inability to snap out of it, which far too many people seem to perceive as deliberate or due to a lack of effort to help oneself. When you tell people you’re depressed, they bombard you with advice and positive thinking (Oh, you’re so strong/smart/powerful/whatever – you’ll pull yourself out of it!!!) and when you don’t because you can’t, they kind of take it as a personal affront.

                Being told it’s an evolutionary adaptation and we should accept it, and that will help us pull out of it, is not far removed from these other admonitions. Being depressed is not the stigma that it used to be; not pulling yourself up by the bootstraps, OTOH, is. The strategies that may work for a low mood are pretty much guaranteed to fail with MDD – so those who’ve pulled themselves out of low mood by using them are particularly critical of others with MDD who haven’t been able to.

              2. mousethatroared says:

                AlisonM “The stigma actually comes from the inability to snap out of it, which far too many people seem to perceive as deliberate or due to a lack of effort to help oneself. ”

                Do you know what’s funny (not haha, funny). I belong to an online group of people with Lupus and similar diagnoses…often called invisible illnesses. They have kinda similar complaints. Many of their friends, co-workers or family think they are making a bigger deal of being ill than nessasary or are just using the diagnoses as an excuse to avoid some obligation or would get better if they just followed some well intended advice. I get the same thing with anxiety. People think I can just make it go away (instantly) if they just give me a logical explaination of why I shouldn’t be afraid.

                I think this is some sort on cognitive social bias, but I’m not sure which. If I were to name it, it would be the “You must be doing it wrong bias”.

        3. mousethatroared says:

          Maybe this is a side note, but I think there are evolutionary adaptions that do create harm to the…recipient (?). Isn’t sickle cell anemia suppose to be an evolutionary adaption to malaria? No one* would suggest that people should just sit by and accept sickle cell anemia. So I guess that would be my argument to any “helpful” person who made a similar suggestion to a depressed person.

          *Actually, there is alway at least one person who will suggest the most preposterous things. But what are we to do with those people.

        4. Andrey Pavlov says:

          From that perspective, I find the attitude that it’s just another evolutionary adaptation

          It may well be an evolutionary adaptation. I don’t know that it can really be demonstrated robustly one way or another, but it can be entertained as a possibility.

          But that doesn’t matter. Every process we have and every evolutionary adaptation (or non-adaptive change) can go haywire. Which is why we have a term called “dysthymia” and another called “depression.” Dysthymia is just a low mood, not harmful to the person, and happens to everyone. We could consider that to be adaptive (possibly) and it can then go haywire into “depression” which is when it become maladaptive.

          We make it a point to try and differentiate between the two (medically/psychiatrically speaking) but of course it is a clinical and subjective (on both patient and physician’s parts) diagnosis so the extremes are obvious but the middle can get murky. And of course, there is no reason to think it is a quantized state so it can be very easy to slip back and forth over where ever that threshold actually “is.”

          1. mousethatroared says:

            Hey AP – sorry for the nitpick, but I believe that dysthymia is actually considered a form of chronic mild/moderate depression, not a temporary low mood. I think it’s considered a disorder, not a typical flucuation in mood. At least that’s what my psychiatrist told me. ;)

            They do like to change around that DSM, though.

            http://www.nlm.nih.gov/medlineplus/ency/article/000918.htm

            Just so as not to confuse people with that diagnoses or their friends or family.

          2. AlisonM says:

            Exactly, Andrey – and that’s where I see the problem. Dysthymia is distinctly different from Depression, and a line really *must* be drawn. I was responding earlier to a Quora user who wanted to know what medication to take to get over the death of a loved one, and expressed my feeling that medication should not be used for a depression that had a specific cause like that because the costs outweighed the benefit. And just as a depression that’s triggered by an event or situation should first be addressed by trying to learn to cope and compensate, a depression that’s idiopathic and deep and debilitating shouldn’t be taken as something that will simply pass on its own.

  13. Kultakutri says:

    Every day, I get up, go to work, hope for boring uneventful days so that I can shuffle papers and stare into the wall and being a manager, sometimes I end up banging the table with my fists and crying in frustration. I do stuff. And, that’s it. Memory impairments – hey, I forgot that I actually own an apartment. Lack of appetite bordering on eating disorder. Attention span of ten seconds. Odd blend of anxiety and apathy. No orientation in time – often I have no idea what day in the week it is or whether something happened yesterday or two weeks ago as most likely, both is forgotten, or rather pushed aside to be dealt with later. I need three different medications to have a bit of decent sleep, one to switch me off, one to keep me sleeping and one somethingzepam to calm me down so that the former would work.

    I’m not retreated in my cocoon, comfortably slowed down and rethinking my priorities. I’m slowed down but restless and given the chance, I plop on my bed and lie with my mind mostly blank. There may or may not be some evolutionary advantage to this but personally, I don’t care, I just wish I could get rid of that crap and live normally, for a given value of normal. Or, actually, whatever that normal may be, I’ve had depressions, on and off, since I was 14 or 15 and what was before was mostly childhood.

    While I agree that low mood in the common sense of the word is well within the borders of normal – it’s normal to be distressed, in mourning, or just down because the weather sucks – I hate when anyone conflates low mood with depression and consequently tries to cheer me up or forces useless advice. Also, I find the description of depression as some sort of yoga retreat for the mind pretty condescending. It’s not fortifying or making me reconsider all the life’s possibilities, the thing I’d love most is to lie splatted on my bed, under a heap of comforters, with my mind blank, asleep or awake, no difference.

    And no, it doesn’t make me feel any better that it may have evolutionary advantages. It’s a food for thought but it’s not helping at all.

    I admit to conflating minor and deep depression but in the review, it’s not always clear what’s being discussed. I’m being mean today.

  14. Alonso says:

    Hi, Jerry A. Coyne refuted this some 4 years ago, read his refutation here:

    http://whyevolutionistrue.wordpress.com/2010/05/27/is-depression-an-adaptation/

    Let us know what you think

    1. Harriet Hall says:

      @ Alonso,
      Thanks for posting that link. Coyne makes a lot of sense. Evolutionary explanations are only hypotheses: it’s hard enough to test whether they realistically represent what “could” have happened or what “probably” happened, and without a time machine it is impossible to be certain that they “are” what happened. Coyne offers a more scientific way to think about them than Rottenberg does. I guess one of the biggest problems is where to draw the line between extreme “normal” sadness and mild clinical depression, and I don’t think we know enough yet to say the two are not part of the same continuum. But if you read Rottenberg’s book thinking he is wrong about the evolutionary explanation, you will still find much of value there. He recounts his personal experience with severe depression, he covers a lot of recent research that should inform any thinking about depression, coping behaviors, and treatment, and he offers patients hope that something positive may come out of their suffering, in the sense that they may end up a better person for it, better able to cope with life’s vicissitudes and better able to set priorities realistically and spend less time ruminating about minor issues that they can’t control. I think there is value in trying to find something good to hang onto in any bad situation. The worst thing a depressed person can do is ruminate that it is all his own fault, that he is a bad or defective person, and that he should be able to “snap out of it” without help.

  15. CyABD says:

    On the gut/brain connection: after a year of increasing abdominal pain, fatigue, cloudiness, sleep problems, and monthly middle-of-the-night pre- or actual syncope, I was finally diagnosed with alpha-gal allergy (no mammalian meat for me :( ) and mast cell activation syndrome. It is not an exaggeration to say that it very nearly killed me. But! Once I started my medication regimen (so…many…antihistamines) and avoiding delicious beef and pork products, I got so much better. Except for a couple things: I couldn’t seem to shake the alternating in/hypersomnia, even though I felt physically orders of magnitude better; I was still procrastinating chronically at my job of PhD student in evolutionary biology; and I couldn’t focus more than like five minutes at a time even on things I desperately wanted to do. My adviser, during a particularly frustrating meeting of me trying to explain that I don’t understand why I hadn’t finished my manuscript, finally realized (it hadn’t crossed my mind) that depression was probably in play. Turns out, years (I’ve been having MCAD symptoms my entire adult life, it was just exacerbated by the alpha-gal allergy) of my gut mast cells spewing histamine unnecessarily all over the place can screw with your brain chemistry. It took a four-month leave from my grad program, but with an excellent psychiatric RN and some patience in titering SSRI dosage, my brain is back to (my) normal. Then again, was it really histamine? Serious illness and the scare of potential job loss (in this case, it would’ve been losing a career, since I have to successfully complete this whole PhD thing first) are certainly enough to trigger a depressive event on their own. Either way, I’m just glad the drugs exist, because I wouldn’t still be in grad school without them.

    (turns out the sleep crap wasn’t depression. i have sleep apnea too, because my life is actually ridiculous, and there were still a couple departments at my hospital/university i hadn’t met yet)

    1. mousethatroared says:

      I’m not really sure why, but I kinda love this comment…still need a like button.

      Glad your are doing better CyABD

      1. irenegoodnight says:

        “Like”

    2. irenegoodnight says:

      “…,it was just exacerbated by the alpha-gal allergy) of my gut mast cells spewing histamine unnecessarily all over the place can screw with your brain chemistry.”

      This is interesting. I have severe allergic asthma and after two consecutive “flare ups”, I find myself with persistent low mood (at least). I have attributed this to the unending winter, but….

      I am not compliant with treatment; antihistamines because they have unpleasant side effects, and steroid inhalers because they stimulate my appetite.

  16. George Locke says:

    A defect in brain chemistry? This is the basis of drug therapy. The chemistry imbalance hypothesis is simplistic, misleading, and essentially wrong. Antidepressants do indeed alter brain chemistry as they relieve symptoms, but that doesn’t necessarily mean that a chemical imbalance caused the problem, and it doesn’t explain what caused the imbalance or why it happened when it did.

    Your assertion that the defect hypothesis is the basis of drug therapy appears to be contradicted by the rest of this paragraph.

    Suppose that the alterations in brain chemistry caused by drugs are the direct cause of their efficacy. This does not imply that depression (or other mental illnesses) is caused by a defect in brain chemistry. So how is the chemical defect hypothesis the “basis of drug therapy”? I thought the “basis of drug therapy” was the hypothesis that alterations in brain chemistry can shape consciousness, regardless of how consciousness got misshapen in the first place. Maybe I’m mistaken, but afaict, my characterization is both true and a sufficient basis for drug therapy.

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