Adverse childhood experiences, genes, and mental illness

Bob Fancher, PhD
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Since at least the time of Moses, we’ve wanted to believe that the “child is father to the man,” that to understand adults we need first look to their childhoods. In mental health care, this age-old folk notion takes the form of belief that your problems are all about your momma, or someone else who “bent the twig” and “shaped the tree.” Got problems? Look to your childhood.

In mental health care—and in psychology generally—the idea hasn’t fared so well in recent decades. The inaccuracy of childhood memories, the difficulty of scientists in finding robust correlations between early childhood and adult life, the rise of genetics in explaining such consistencies as turn up—these and other considerations have put the idea in ill repute.

Of late, mental health professionals still wedded to the idea have taken heart from the “ACE” research—adverse childhood events. People who suffer the distress we call mental illness have also suffered adverse childhood experiences at a far higher rate than “healthy” souls.  Vindication of our beliefs! Right?

We need to be careful to read this research accurately, and to understand what it does and does not say.

While studies of Adverse Childhood Experience (ACE) differ a bit, generally they indicate that such experiences occur roughly three times more often in the lives of people who suffer schizophrenia, affective psychosis, depression, and personality disorders than they do in healthy souls, and a bit more often than that to people who suffer PTSD or dissociative disorders. (Anxiety disorders seem to correlate with ACE less often.) Obviously, then, ACEs increase the risk of mental illness.

But that’s all they do—increase the risk. They don’t cause mental illness, in any straightforward sense of “cause.”

To understand the significance of the ACE literature, we must look at the numbers more carefully. About six percent of adults in America suffer some sort of severe mental illness in any given year. That means that out of 1000 American adults, 60 suffer serious mental illness.

Depending on the study you read, we can assume that roughly half of those suffered ACE—most studies that I know say the rate is less than that, but let’s keep things simple for the sake of clarity. That means that out of 1000 American adults, 30 suffered ACE and developed a severe mental illness.

But 940 of those 1000 adults do not suffer a serious mental illness. If they have suffered ACEs only one-third as often (that is, if ACEs are three times more likely to happen to persons who suffer mental illness), that means about 17% of them suffered ACEs. That’s about 160 people.

So totaling the 30 mentally ill people who suffered ACEs and the 160 healthy people who suffered ACEs, we see that 190 people suffered ACEs.

The overwhelming majority of people who suffer ACEs do not develop mental illness. Obviously, it is too simple, and mistaken, to say that ACEs cause mental illness.

And mental illness can happen without any reported ACE. Perhaps the best meta-analysis of ACE and schizophrenia, for example, shows that if all ACEs were eliminated, psychosis would most likely only be reduced by about one-third.

The ACE research also does not show that genes aren’t implicated in mental illness.  From behavioral genetics, we have reasonably good, well-evidenced knowledge of the heritability quotients of a great many mental disorders and other psychological characteristicsSchizophrenia and bipolar I—classic manic depression—are about 80% heritable. Major depression is much lower—about 40%. Panic disorder is a bit less heritable than that. Most psychological traits are heritable in the same range as depression and panic—30-40%. ACE research does not address, and does not contradict, that research.

Moreover, we do not know the extent to which ACEs themselves are due to genetic factors, so we cannot simply ascribe a particular level of significance to them. Most likely, they are less significant than the percentages suggest, because the correlation between ACEs and mental illness may be confounded, to some extent, by genetic factors. That is, the genetic factors that raise the probability of mental illness may themselves contribute to the occurrence of the ACEs.

A child and his or her father, for instance, may share whatever genetic material predisposes to major depression. The father may subject the child to neglect, abuse, or other harsh treatment because of traits associated with that genotype.

Or a child may be bullied because he or she shows early oddities due to the genetic predisposition.

Or the parents or children may suffer excessive risk-taking, or poor foresight, or impaired social perceptiveness, due to genetic factors, and these may result in conditions (e.g., poverty, instability) that promote ACEs.

In none of these cases could we say, then, to what extent the ACEs occur independently of the genetic predisposition that contributes to the mental illness.

We do not yet know how often genetic confounding occurs, or the extent of the effects. Research on confounding factors is only getting started; some early research claims to find no confounds. That’s a bit incredible, since we know that genetic factors mediate such things as a family’s socio-economic status, or parents’ tendencies to bad behavior, and other things which must surely sometimes contribute to ACEs. But we will have to see how this research develops over time.

We know, then, that ACEs increase the risk of developing mental illness, but we do not know just how much. We know that by themselves, ACEs cannot simply be said to cause mental illness. And we know that mental illness can occur in the absence of ACEs.

The distress that, rightly or wrongly, we call mental illness is real and terrible. Genetic factors contribute to it—and adverse childhood experience can, for some people, pose destructive challenges.

Neither genetics nor early childhood is the whole story, and the whole story will doubtless involve a great many other things—the progress and outcome of the story is assuredly not set, for most people, by one’s fifth or sixth or seventh birthday. In mental health care, we can continue to puzzle out the significance of childhood experience for mental distress. But the best research makes clear that we can’t rest content in easy, old superstitions about the power of the early years.

 

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62 COMMENTS

  1. Dr. Fancher,

    Good post.

    IMO, none of us are victims.
    We are not *victims* of our genes.
    Nor are we *victims* of our past.

    Unless we *choose* to be.

    No matter how much adversity any of us suffer, there are always options on how we choose to handle the situation, person or event.

    And how we choose to release and overcome – particularly fear and resentments.

    I don’t mean to sound preachy, but this is, IMO a *reality*.

    Duane

  2. Nice post Bob, although as you point out, understanding the cause of the experience varies with the material one reads. As you say;

    “In mental health care, we can continue to puzzle out the significance of childhood experience for mental distress. But the best research makes clear that we can’t rest content in easy, old superstitions about the power of the early years.”

    Yet how do we know which is the best research to read? Should it be a question of volume or quality? For example, you write;

    “the progress and outcome of the story is assuredly not set, for most people, by one’s fifth or sixth or seventh birthday.” Which reminds one of the old Jesuit maxim “Give me a child for for his first seven years and I’ll give you the man.”

    Yet highly respected researcher’s like Allan N Score, suggest that the truly critical period in human development may be as short as three years, and that early interactions between care giver and baby are crucial to the still maturing brain and nervous systems. Examples:

    “A major task of the first year is the evolution of affective tolerance for increasingly higher levels of arousal, and that this is facilitated by the mother’s modulation of the infants highly stimulated states. Indeed regulatory processes are the precursors of psychological attachment and its associated emotions, and psychobiological attunement is now thought to be the mechanism that mediates attachment bond formation. The positive emotions of pleasure and interest are the major indicators of affect attunement.
    (p, 8)

    It is now established that emotion expression changes developmentally as a function of the experience-dependant maturation of neural inhibitory mechanisms, and that the maturation of the frontal region in the second year is responsible for affect regulation and the development of complex emotions. The emergence of the adaptive capacity to self-regulate affect is reflected in the appearance of more complex emotions which result from the simultaneous blending of different affects, and in an expansion of the “affect array.” (p, 24)

    Developmental psychoanalytic researchers suggest that a psychic structural system involved in the self-regulation of affect and therefore an autonomous emotional functioning appears in the middle of the second year. At the same time an internal signaling system emerges in which affect, especially negative affect that conveys information about threat and lack of social success can be used as a signal function.

    Failures of early attachment invariably become sources of shame, that impairments in the parent-child relationship lead to pathology through an enduring disposition to shame, and this results in chronic difficulties in self-esteem regulation found in all developmental psychopathologies.

    If an attachment figure frequently rejects or ridicules the child’s requests for comfort in stressful situations, the child develops not only an experience of the parent as rejecting but also one of himself as unworthy of support. There is now compelling evidence, from a number of separate disciplines at different levels of analysis, that all early forming psychopathology constitutes disorders of attachment and manifests itself as failures of self and/or interact ional regulation. Loss of ability to regulate the intensity of feelings is the most far-reaching effect of early trauma and neglect. (p, 31)

    The developing infant is maximally vulnerable to non-optimal and growth inhibiting environmental events during the period of most rapid brain growth. During these critical periods of synapses overproduction followed by synapses elimination, the organism is sensitive to conditions in the external environment, and if these are outside the normal range a permanent arrest of development occurs. (p, 32)

    Social environments that provide less than optimal psychobiological attunement histories retard the “experience-dependant” development of fronto-limbic regions, areas of the cortex that are influenced by attachment experiences and prospectively involved in homeostatic functions. (p, 33)

    The casual relationship between these early experiences and the genesis of predispositions to pathology may be explained by the fact that the genetic systems that program the structural connections within the limbic system are extremely active during critical periods of infancy. Alterations in gene-regulating hormones, such as opioids, corticosteriods, and other neuropathies, are induced and indeed regulated by interacting with the “external environment,” and these changes trigger the activation of genetic programs and thereby the micro-architecture of growing brain regions in the “internal-environment.” (p, 33)”

    Exerts from “Affect Dysregulation & Disorders of The Self” by Allan N Schore.

    In my own 32 year experience of classic manic-depression, birth trauma compounded by emotional and physical abuse, which included maternal neglect as a generational pattern, lies at the root of my experience.

    Self education into how my autonomic nervous system is involved in affect/energy regulation, and using practical techniques for releasing a trauma conditioned response to life, has allowed me to find increasing conscious awareness and control over my affective disorder, otherwise known as bipolar type 1.

    What is interesting to note, when reading people like Schore, Porges and Damisio among others, is the references to the auto nervous system, which never seem to come up in the rather myopic focus on brain chemicals, in most research.

    Jaak Panksepp, points out other findings in neuroscience which are routinely ignored, in our prevailing intellectual zeitgeist, perhaps because such findings demand a further exploration of the nature of the human mind, for which we are not yet ready?

    Warm regards,

    David Bates.

  3. Bob – thanks for your blog post which is similar to how I see life and its variables.

    I don’t think there’s any easy answers as to why some people and families experience more mental distress than others. I say this from the viewpoint of being in a family that’s had most of us engaging with the psychiatric system at one point or another. And I had a happy childhood which I remember fondly. The resilience I developed in my earlier years helped me get out of the psychiatric system and recover from the experience.

    I do get annoyed when people assume that having more than one episode of mental ill health means ACE as you describe it, or a lifetime of ‘mental illness’. I’ve never believed this or accepted it. And so I’ve recovered, got over it and got back on with my life.

    I agree with you that we need to listen to the whole story. And for all of us the story is still unfolding.

    Regards, Chrys

  4. “We know that by themselves, ACEs cannot simply be said to cause mental illness. And we know that mental illness can occur in the absence of ACEs.”

    I’m not so sure that we actually know this, and the statement seems to me in itself to be a little simplistic. Just like saying something like, “We know mental illness is genetic”, or “We know childhood trauma is at the root of emotional distress”. The question is, what gets called an “ACE”. Is it having been beaten up several times a day, having been sexually abused, suffered obvious neglect, massive bullying, etc., during most of one’s childhood? And if no such obvious ACEs are reported, does that automatically mean that the person’s childhood was just perfect? And that if they develop what gets called a “mental illness”, it must be genetic?

    What I see looking at people labelled with a “mental illness” is, to put it in a simplistic way, somebody who hasn’t learnt to deal with one or the other, or several, aspect(s) of life in a grown-up manner. These people lack the tools and skills to deal in a grown-up manner with life, so they, of course, resort to whatever tools and skills are at their disposal, which are a kid’s tools and skills. What I see is people making use of the tools and skills we all would regard appropriate to use for a kid, but not for a grown-up person. And I also see a stunning correlation between which age-specific tools and skills people use and what their life story reveals at what point of time in their life an “ACE” had them get stuck in their personal, emotional development, which is what trauma does to people.

    The world isn’t perfect. Our culture isn’t perfect. Human beings aren’t perfect. None of us is ever born with the complete tool kit and the perfectionized skills to use it that enables them to navigate whatever life might have in store for them in the most constructive way imaginable. We all have to learn how to navigate life. One’s childhood may seem perfect from the perspective of a world, a culture, that tends to view itself/themselves as perfect, but that nevertheless in reality is pretty much imperfect, and from the perspective of whoever is looking at it – be it the person herself – who’s a member of this world/culture, and thus conditioned to view it as more perfect than imperfect. But if somebody ends up psychiatrically labelled, they have for one or the other reason not acquired the tools and skills necessary to navigate life without getting labelled. And whatever it otherwise is called that prevents people from acquiring these tools and skills, it is, essentially, an “ACE”, if it gets reported as such, or not.

    It is through the adversities we encounter in life that we learn, that we achieve personal development and growth. But sometimes we encounter adversities at a point of time in our life where we don’t have the necessary personal maturity yet to deal with them, and/or of a kind that would demand us to own extraordinary tools and skills, if we were to deal with them in a constructive way, and the result is trauma, i.e. we get stuck with this unresolved situation, i.e. we experience “mental illness”, our personal growth and development is stunted, and we won’t be able to move forward unless we find one or the other viable resolution for the situation we were overwhelmed by, which is what “recovery” is all about.

    An “ACE” isn’t easily defined. Although even the ACE-studies themselves seem to think they are. And in a way the ACE-studies, too, like virtually all the research in the field, fall short in that they, too, try to apply a somewhat narrow technological view on what life is, what it means to be a human being in the world (cf. the technological language used both in the above article, and especially one comment to it, in the ACE-studies themselves, alongside virtually all research in the field, and that we’ve become so used to ourselves that we hardly realize anymore how it dominates the discourse, let alone manage to free us from it). But at least the ACE-studies acknowledge what biopsychiatry entirely fails to take into account: that, while our experiences may and do shape our biology, too, who we are as a person is not our biology, but our experiences: mind over matter.

  5. Marian – this is an interesting response. Especially regarding psychiatric labels which in my experience were given to me without any consent or consultation. And remain in my medical notes indelibly. And all because I had an episode of mental distress and ended up in a psych ward. And had two more episodes over a 25 year period, meaning I was ‘mentally ill’ in the eyes of psychiatry.

    Now my episodes were not mainly about adversity or coping with life but, I believe, due to internal factors in my body, hormonally. After having a baby (twice) and at the menopause. I do think that having one postpartum psychosis predisposes you to another, if the circumstances are ‘right’. Which they were in my case. Factors which were beyond my control at the time.

    Life has a habit of throwing us a googly, or something unexpected and treacherous. And sometimes we have no choice but to bail out by going into an alternative space or into a psychosis or a nervous breakdown. It happens. And with the best will in the world we are in an alternative universe until the crisis passes.

    I would like the alternative universe to be a place of respite and refuge, without psychiatric drugs being forced on me, where people would take time to get to know me and work with me into recovery. This is what I’m hoping for in a transformed psychiatric system.

    And I agree with that it is our experiences that matter, not our biology,

    Regards, Chrys

  6. Chrys, especially in Germany there’s a growing interest in the medical field in general to look at even, at first glance, purely physiological problems from a more holistic perspective, and to, also!, see the body, the entire body, as a metaphor. So, in a way what they say is that even something like hormonal turbulences may in part be due to things like psychological stress. Unfortunately such a view carries the risk in it that, all of a sudden, whatever the physiological problem, it’s all in your head, and so in Denmark for instance an extreme version of this view that tries to bridge the dualistic mind-body gap, has led to a troubling trend to send everybody who complains about physiological problems without the doctors being able to provide an easy diagnosis and treatment, to a psychiatrist… who then will tell you that, whatever your problem, it’s your brain that’s broken. Which is paradoxical as it, once again, denies the existence of the mind as fundamentally different from (although inextricably connected with) the body, so it’s not bridging anything, but, once again, reducing what would be an actually holistic approach to a totally limited, purely technological one.

    I think, what we need to do is to sit down and listen to people as they speak about their problems in their own words.The more we try to reframe everything exclusively under the technological paradigm, the further we will move away from an actual understanding of life and ourselves. And it’s not that I don’t appreciate technology. It certainly is of importance, especially in regard to physiological problems. But I think that if we believe we just have to view everything, if it’s hormonal disturbances or ACEs or whatever, from a technological perspective, doing tons of randomized, double-blinded this and that studies that live up to all those technological standards, and, voilà, we’ve understood its true nature, we’re fooling ourselves big time. But maybe this, our tendency to hold on to an almost exclusive view of life and ourselves in technological terms is just another “adversity” thrown in our way for us to learn how to overcome, once it causes us enough suffering to have us look for different solutions…

  7. Hi Bob- I appreciate your comments, but do disagree with your data on the obvious genetic heritability of Schizophrenia. Here’s a section from a recent paper of mine on the issue; I’d love your thoughts if you have the chance:

    Since the famous twin studies, first appearing during the middle part of the 20th century, belief in a genetic cause for Schizophrenia has been repeatedly asserted by many within the field of medical psychiatry, and specific work has subsequently been done in an attempt to discover particular genetic abnormalities responsible for the condition (Karon & Vandenbos, 1981; Boyle, 1990; Tillman, 2008; Williams, 2012). A majority of medical schools teach their psychiatrists in training that evidence for genetic causes and the role of heritability in schizophrenia is all but definitive, and it is exclaimed in the popular press quite often that we are on the brink of the one big discovery needed to at last put this issue to rest (Leo & Joseph, 2002; Joseph, 2003; Tillman, 2008; Williams, 2012).
    Much of the evidence put forth alleging the major role of genetic phenomena in the etiology of Schizophrenia comes from the previously mentioned twin studies (Leo & Joseph, 2002; Joseph, 2003; Williams, 2012). In opposition to data repeatedly referenced by the NIMH, findings drawn from a meta-analysis of all twin studies after 1963 show that identical twins have a concordance rate for Schizophrenia of 22.4%, and that fraternal twins have a rate of 4.6 % (Leo & Joseph, 2002; Joseph, 2003; Williams, 2012). These numbers, while relatively small, do make a case for the influence of genes in the development of psychotic disorders. However, numerous methodological issues have been found with the pool of studies included in this meta-analysis, including “(1) lack of an adequate and consistent definition of schizophrenia; (2) non-blinded diagnoses, often made by investigators strongly devoted to the genetic position; (3) diagnoses made on the basis of sketchy informa¬tion; (4) inadequate or biased methods of zygosity determination (that is, whether twins are [identical or fraternal]); (5) unnecessary age-correction formulas; (6) non-representative sample populations; and (7) lack of ad¬equate descriptions of methods.” (Williams, 2012, Pg. 27).
    These issues aside, the concordance rates for identical twins have indeed been noted as higher than those for fraternal twins, a finding which has been said to indicate the substantial role of genetics in perpetuating psychotic disorders; but is this so? In conjunction with genes, the environmental conditions of both sets of twins must be examined for a verdict to be reached. It has been assumed that fraternal twins and identical twins share similar environments, and that the twins in each pair would be treated by this environment as separate individuals (Karon & Vandenbos, 1981; Karon, 2006; Williams, 2012). A contrary argument is that identical twins are more likely to be treated as one person, and that similar treatment by caretakers in their environment, as well as the lack of a well-defined identity, would likely contribute to the development of psychotic symptomatology (Karon & Vandenbos, 1981; Leo & Joseph, 2002; Joseph, 2003; Karon, 2006; Williams, 2012).
    The second group of sources of research on the role of genetics and heredity in Schizophrenia are adoption studies, of which there have only been 7 major examples to date (Williams, 2012). About half of these have involved cases in which offspring of biological parents diagnosed with Schizophrenia have been followed, having been adopted by parents either diagnosed or undiagnosed. (Karon & Vandenbos, 1981; Leo & Joseph, 2002; Joseph, 2003; Williams, 2012). The other half include cases where the biological parents of adopted children diagnosed with schizophrenia have been sought out so as to determine if they have passed on the condition to these offspring (Karon & Vandenbos, 1981; Leo & Joseph, 2002; Joseph, 2003; Williams, 2012). Along with methodological issues stemming from overly wide definitions of the term ‘psychotic’ that, if corrected, would have found many fewer persons fitting disorder criteria, scrutiny has been focused on the particular times and places in which these parents and children lived (Karon & Vandenbos, 1981; Leo & Joseph, 2002; Joseph, 2003; Williams, 2012). In all cases sterilization policies were in place for individuals who were deemed to have produced schizophrenic offspring, with their progeny almost definitely having been labeled as ‘defective’ and ‘schizophrenic’ (Karon & Vandenbos, 1981; Leo & Joseph, 2002; Joseph, 2003; Williams, 2012). It is likely that the most qualified sets of adoptive parents would not have jumped at the chance to adopt children so designated, meaning that much less fit parents would likely have reared these boys and girls; this issue was not addressed in any of the studies referenced above, significantly limiting validity (Karon & Vandenbos, 1981; Leo & Joseph, 2002; Joseph, 2003; Williams, 2012).
    Finally, much to the continued dismay of researchers the quest to discover specific genetic abnormalities associated with Schizophrenia has not delivered consistent, replicable and definitive findings (Karon & Vandenbos, 1981; Boyle, 1990; Leo & Joseph, 2002; Joseph, 2003; Petronis, et al, 2003; Williams, et al, 2007; Hamilton, 2008; Simons & van Winkle, 2012; Whitaker, 2012; Williams, 2012). The now familiar issues of universality and exclusivity again arise, highlighting the serious issues involved in current genetic research into psychotic conditions (Leo & Joseph, 2002; Joseph, 2003; Petronis, et al, 2003; Williams, et al, 2007; Hamilton, 2008; Simons & van Winkle, 2012; Whitaker, 2012; Williams, 2012). And perhaps most strikingly, many researchers who profess belief in the existence of genes linked to schizophrenic psychoses have voiced serious concern about the future of their discipline (Williams, 2012), with one even going so far as to state that “common genes of major effect…are unlikely to exist for schizophrenia” (Williams, et al, 2007, Pg. 30).
    In light of the major roadblocks that contemporary genetic research into Schizophrenia has encountered, an avenue of study into the effect of environmental phenomena on genetic function and expression has emerged; epigenetics. The term ‘epigenetics’ refers to “the reversible regulation of various genomic functions, occurring independently of DNA sequence, mediated principally through changes in DNA methylation and chromatin structure.” (Rutten & Mill, 2009, Pg. 1045). Many of these changes to the properties of genes have been seen as the result of exposure to insults from the human environment (van Winkle, et al, 2008; Rutten & Mill, 2009), an assertion that has finally given credence to decades of work by researchers and clinicians who have repeatedly pointed out the role of interpersonal phenomena in the development of psychotic conditions (Bettleheim, 1967; Karon & Vandenbos, 1981; Williams, 2012). Among these environmental insults are: maternal stress, one’s ‘rearing environment’, chronic stress in childhood, experience of trauma, living in an urban environment, the experience of migration, and drug abuse (van Winkle, et al, 2008; Rutten & Mill, 2009). The impacts of these negative experiences have been found to include biological and genetic changes, as well as the development of emotional, cognitive and behavioral symptomatology.

  8. I think we are missing one very important aspect of the research you are quoting, Bob. Namely, the arbitrary and subjective nature of the entities called “mental illnesses” that we are “measuring.” For instance, to say that “classic bipolar disorder” is “80% heritable” assumes that we can accurately define who does and does not have “classic bipolar” for the purposes of counting them. But we really have no way to consistently or accurately do this. If we go by whether the person receives such a diagnosis, we have the huge confounding factor of the assumption clinicians tend to make that “oh, his mom was bipolar, that must be what is happening.”

    Additionally, there are other sorts of “ACEs” that don’t occur in the family, such as bullying in school by peers OR by teachers (I got hit in the head by my second grade teacher for objecting when she threw a book across the room), being socially isolated due to race, appearance, economic status, etc., exposure to community violence, or even living in a world where nuclear holocaust is a daily possibility.

    That genetics play a role in behavior and emotional experience is not something I think most people would dispute. But defining what is “normal” is not a scientific process, and human reactions are SUPPOSED to be genetically varied in the interests of species survival. And a lot of expected behavior for kids and adults is far from “normal,” from the point of view of our species evolution – we are not genetically adapted to do these things. It’s not normal for a kid to be expected to sit in a chair most of the day working on written material. It’s not normal to expect babies to sleep separately from their parents or to eat on 4-hour schedules. It’s not normal for adults to spend all day sitting in a cubicle with no exercise or natural light. It’s not normal to have to get up at 6 in the morning and travel two hours in traffic to arrive at said cubicle, and then repeat the action at the end of the day. These cases of “mental illness” may occur at a certain rate in our society because a certain percentage of the population isn’t well suited to adapt to these abnormal expectations.

    Finally, while genetics and environment clearly both play a role, it’s even clearer that genetics is the one of the two that is much less amenable to change. Whatever a person’s genetic substrate may be, their own ability to succeed is far more dependent on what their environment demands of them and how capable they are of devising an adaptive response to those demands. There are skills that can be learned, even if genetics don’t make it easy for a particular person. And we can also re-think some of our weird expectations, especially for kids – for instance, research suggests that we could almost eliminate the “ADHD” epidemic by putting active kids in open classrooms instead of drugging them. But that option is not on the table as long as we blame their genes and not the environment they are expected to adapt to.

    Rather than spending a lot of time on “what causes mental illness,” I think we’re better served by figuring out what kinds of environments maximize the chances of our kids growing up feeling good and capable and successful. If you’ve looked at the overall environment lately, I daresay you have found a hell of a lot of room for improvement.

    Genetics are what they are – we all have our substrate of strengths and vulnerabilities. Let’s work on the part we DO control and I think we’ll be much more successful at improving outcomes, rather than attempting to classify certain genetic tendencies as “illnesses” that we can neither verify or substantially change by any means we are aware of.

    —- Steve

  9. Exposing questionable myths is often a more efficient way to better our society than new innovative ideas or treatments. Thanks for bringing light to the common issue of childhood trauma (any false assumption of determinism can doubly harm via the negative expectations it generates).

    I believe the research you mention does provide strong evidence for the conclusion (even if based on diagnoses with little validity): we cannot predict or explain mental illness either by genetics or childhood trauma. Does that justify the biopsychosocial model?

    Given the influences of our genes (in addition to the uniqueness of our history) on our brain and mind dynamics, would you agree that a focus on individualized education, versus a focus on “standardized” education which is quite common (even if the exact standard varies from family to family), could have as much influence on our future mental health than the presence of ACEs?

    Some of the linked research looks at psychotic episodes. In the same way that some classic illnesses can resolve themselves with a stronger immune system, MIA participants are familiar with the numerous stories of psychotic episodes leading to a positive transformation. Would you agree that putting all kind of psychotic episodes in the same category independently of their content and outcome can be misleading?

    In inheritability computations, as a thought experiment, if some component of the final influence on mental illness was mediated by society prejudices towards some slightly unusual facial feature (or any feature with no significant mind connection), would that count as environment or inherited influence?

  10. Thought provoking post, Bob. I wonder about the cost of the studies you reference, not to mention the time spent on them. I think it would be a great leap forward if we all agreed that the cause for suffering— every imaginable sort and most definitely the suffering caused when one is given a mental illness label; the cause of ALL this suffering is, BIRTH.

    Yes, I am yelling! and not just because you blew off Richard Lewis’ relevant questions, but because it makes no sense to quibble over the “nature v. nurture” chicken and egg parable, unless or until there is serious and dedicated effort towards improving the circumstances that amount to our shared existence as a community of human beings living in a society in a developed country.

    How can we become better human beings??? After we are born into this world ?

  11. Re: Genetics

    We are not *victims* in this life. We can literally change our genes.

    From PBS/Nova:

    “Once nurture seemed clearly distinct from nature. Now it appears that our diets and lifestyles can change the expression of our genes. How? By influencing a network of chemical switches within our cells collectively known as the epigenome.”

    More here –

    http://www.pbs.org/wgbh/nova/body/epigenetics.html

    I constantly read the battle… on this site, and especially on other sites… Not only *nature* versus *nurture* but *disease* versus *no disease*.

    Again, at the risk of being called a *heretic*, it matters not to me. *Mood disorders* could be the product of abusive childhoods, or poor functioning thyroid, or both.

    How do we encourage ourselves and others to find more peace in their lives, more calmness, better overall wellness and higher functioning, thriving?

    And how do we replace a *monopoly* (psychiatry) with a host of non-drug options, while putting an end to the use of force?

    That’s what I care about.
    And not much else.
    IMO, freedom with real choice is the priority.

    Duane Sherry, M.S.
    http://discoverandrecover.wordpress.com

    • Disease
      Dis-ease

      A person who is suffering at a severe level might be considered to be at *dis-ease*.

      So what?
      What difference does it make, if these conditions are viewed as *temporary* events that people can overcome?

      Once we begin to see *psychosis* as an EVENT and *not* a person, we can look beyond the *nature/nurture* and (dare I add) *genetic/non-genetic* debate.

      Because when we begin to see 85-90% of folks diagnosed with *severe mental illness* fully recover, the issue will be moot…The larger issue will be helping more people begin to fully realize this possibility.

      Duane

  12. Bob-
    Once again, I appreciate the clarity of your argument. It is instructive to be reminded once again about the distinction between correlation and causation and to walk through the actual numbers.
    You make reference to “folk notions” and I have observed the problems when “folk psychology/psychiatry” gets applied to practice . At the same time, I sometimes am reminded of Michael Pollan’s admonition to only eat things our grandmothers would recognize as food. In a similar vein, it strikes me that some of what we are saying: that our emotions and personalities are formed by some incredibly complex (albeit as yet not fully understood) interplay between our genetic endowment and our environment seems to be what our grandmothers might have said and seems to be supported by the emerging science. This interplay, however, is so complex it may be beyond our (or at least my) understanding.
    Sandy

  13. Bob

    You stated above in your last commnent to me:

    ” I think we should almost never tell or encourage a patient to believe (or believe ourselves) that his or her early childhood experiences explain his or her distress ”

    I believe this statement totally downplays the potential role of understanding early childhood experiences in general and, in particular, its potential therapeutic role for those who seek the counseling experience.

    Of course we should not assume we know exactly where someone’s distress came from or impose our view or opinion on a person engaging in therapy with us. But quite often there are very obvious connections between early trauma and the historical course of distress symptomology, and we should not ignor those connections or fail to help a person make those connections when there is clear evidence.. This would be to deny them some of the most profound discoveries they can make in the therapy process.

    Oppressed peoples find the tools to liberation by learning about and understanding their history. Just one example would be the influence of slavery on the history of the Black family unit and its effect on the concept of the emasculated Black male in society. Some individual achieve profound insights in therapy when they make the connections in their own life between their own early history and the development of distress symptomology. Sometimes these “aha” moments lead to other insights and positive practical changes in their current life

    When bad things happen to children they take on the badness as if it were their own. They end up believing they are bad, sometimes for a lifetime. Quite often the perpetrator of abuse tells them they are bad or deserved their abuse. They carry toxic shame and guilt into their adulthood. Even if they know deep down that they are not responsible, they end up thinking they are bad, because “why would God allow this to happen if he didn’t think I was bad.”

    I have treated people who were abused at age 12 and very shortly thereafter began drinking heavily at an early age. This is often no accidently succession of events. Trauma creates a hightened state of anxiety; people often “self medicate” with alcohol. Most children experiment with alcohol, but trauma victims find themselves repeating this experience often because it becomes the only coping mechanism that temporarily takes away their anxiety. It is no surprise that many trauma victims end up with various forms of addiction problems. Learning that someone’s addiction may have begun as a result of trauma does not by itself lead to recovery. But some times it gives them the courage and motivation to finally address these past issues of trauma instead of investing more energy running from them; something they may have done almost their entire lifetime.

    I do EMDR trauma treatment in my work. At times I have seen profound transformations in just a few sessions when some clients have finally revisited and ultimately reprocessed their trauma in a safe and controled environment.

    Bob, why should we downplay the potential significance of these adverse events in childhood for those of us trying to better understand the etiology of experiences that can lead to thoughts and beahvior that gets labeled as “mental illness” AND (for emphasis only) why should we deny people in counseling the opportunity to make critical leaps in understanding their own deveplopment of distress symptomology? Especially when this knowledge can sometimes become truly liberating in their own journey.

    Richard

  14. And the RCTs conducted by PHARMA don’t support the Adverse Drug Reactions reported by millions of people… and so, some ‘experts’ have continued to discount patient reports of side effects as related to the drug they were taking! Who do YOU believe?

    If the mental health experts had a reputation for withholding their *treatments* until irrefutable evidence supported them, there would be nothing to talk about here; no distinguished profession known as psychiatry, to say the least!

    If there weren’t countless studies whose outcomes target our own individual self perceptions; cause us to doubt our intuition and insight, there would be market for 98% of our health care
    industry!

    There is but one method for healing mental/emotional anguish , that is; support the person suffering throughout his journey to self mastery. that will entail an infinite number of ways and means as each person is a truly unique individual,–. the polar opposite of relying on the rigorous study of those who seek financial gain and personal recognition from their efforts, it’s about trusting in and developing our own humanity.

    Gotta run. I am NOT off tonight !!

  15. I am having a very hard time with the speculation that the behavior of people who abuse or neglect children is genetically determined in any identifiable fashion.

    Behaviors, language, and attitudes are also passed down from generation to generation in family culture. It’s not necessary to invoke genetics to explain it.

    The logic of behavioral genetics tends to break down when attempting to describe complex human behaviors. I agree with the commenters above who expressed skepticism about distinguishing nature from nurture in much of human emotional life.

  16. Bob,

    The only thing that is bugging me in your presentation is the 80% heritability number for schizophrenia/bipolar. That number is not fundamental to your argument or conclusion, which are both important and appreciated. But here are my thoughts anyway: what I find strange is not the number itself, but the fact that we can compute such a number at all for such complex behavioral traits.

    Looking at SEP, http://plato.stanford.edu/entries/heredity/ , it seems there are serious controversies about whether heritability can be measured in situations where the COV(G,E) factor cannot be ignored (normally heritability computations rely on the assumption that genes and environment are mostly additive, i.e. their contributions are not interfering too much with each other). I could imagine measuring heritability for simple traits as anxiety, intelligence, compulsivity, memory or for many other illnesses or behavioral problems, but for the purpose of complex mental illnesses occurring in adult age, COV(G,E) could well be the most significant factor (and probably some very non-linear chaotic component as complex as life itself).

    SEP says: “There is something of a consensus in most fields (e.g. philosophy of biology, evolutionary biology, psychology and behavioral genetics) that heritability measures (particularly hb2 measures) only have a very limited use. The consensus among philosophers of biology is that broad heritability measures are uninformative but there are a few dissenting voices”.

    I was wondering if you think that is relevant to the validity of the 80% number you mentioned, more specifically if the COV(G,E) (or other problems mentioned in the SEP text) are obsolete or irrelevant in this case (rather than just ignored).

  17. Bob, thanks again for bringing your knowledge here in the blog and the comment section. On your main subject, argument, and conclusion, I think your point is well understood by everybody (and agreed by most, and definitely by me).

    Which is I am continuing on the side topic of heritability.

    Twin and adoption studies are shedding important light on the heritability problem, and few if any are contesting those numbers (even if there is still room for interpretation).

    Computing heritability quotient seems a different game, it is currently based on a mathematical model with many assumptions that are not always explicited. The result is only as good as those assumptions. I do believe the heritability quotient of height is meaningful and computable (and yes I did understand the full statistical meaning and implications, the population scope of the interpretation before I started to comment).

    If the mathematical model works for height, it’s easy to assume the same model should work for bipolar, but that’s only the case if we assume there is no feedback loops between the trait studied, and the environment in which the trait develops (the math model is simply completely inadequate if there are feedback loops, and the final result meaningless).

    To use that heritability computation for bipolar, one has to argue that there is no social vicious circles involved in the development of aggressiveness, paranoia, mistrust, conflict, isolation or that those traits and dynamics have no influence on the development of bipolar. One has to argue that a family with a aggressive child will not be affected the least in their mood and behavior, and will provide the same environment than they would with a easy child. One has to argue that a partner with an aggressive moody spouse/significant-other will be as loving and happy than one with the “perfect” partner.

    At the extreme, in some very dynamic environments, the mere notion of heritability quotient will become meaningless like would the notion of trying to assign a responsibility quotient between speaker, amplifier and micro in a larsen effect.

    My gut feeling is the concept of heritability quotient is meaningful in bipolar, but that we don’t have the knowledge to compute it, and after looking at it again, I am pretty confident the math model currently used is complete junk unless making very unusual assumptions.

  18. This from the same guy whose earliest posts were arguing that talk therapies could be at least as dangerous as psychotropic drugs and that people should lean on the side of caution until scientists begin studying the side effects of talk therapy.

    I didn’t even bother reading much past your made up statistics, but I do wonder, what exactly are you trying to do? Are you a psychiatric apologist or something?

  19. “But the best research makes clear that we can’t rest content in easy, old superstitions about the power of the early years.”

    Really? Are you serious? The best research clearly shows that experiences from the womb through childhood influence brain development and that this will cause the brain to function a certain way for the rest of a persons life. For instance, not receiving physical stimuli as a baby (as studied using babies kept in germ-free environments due to immune system problems) will cause the brain to develop abnormally in ways that affect social behavior and affection.

    I strongly suggest that you look into the works of Robert Sapolsky.

    • And the best research (Bruce Perry, for instance) also indicates that the brain can be healed from early trauma, and the best way to heal that trauma is through SUPPORTIVE RELATIONSHIPS WITH HEALTHY ADULTS!!!! Sounds like even from the perspective of pure physiology, brain health depends on relationships, which affect all the neurotransmitters psychiatrists are so hot about manipulating. It seems a hug and some quality time with a good listener whom you trust is the best prescription, regardless of this pointless argument about the “causes of mental illness.”

      An interview with Bruce Perry can be read here:

      http://www.healingresources.info/video_bruceperry.htm

      Again, I think we worry too much about defining the “causes of mental illness.” We’re not even sure what “mental illness” is or whether it’s actually an illness at all. Instead, we need to look at what actually promotes healing and recovery in the long term, and when we compare the outcomes for the drug approach and for Perry’s relationship research, it’s pretty clear who wins out.

      —- Steve

      • But to one of the babies who received no physical stimuli, a hug later in life will produce no sensation different than leaning against a wall. The part of their brain that would allow them to experience physical affection just simply did not develop to function normally so they will live their entire life without it.

        That’s just one example.

        • This is true. However, that would be a very extreme case. The vast majority of infants, toddlers, and even older kids can and do respond to appropriate intervention by caring adults. They may not ever behave in what we would consider a “normal” fashion, but the dire outcomes predicted by their early brain damage from trauma can be avoided to a significant extent.

          My point would be that even if we focus ONLY on modifying the brain, and leave out all the other spiritual aspects of “mental health problems,” focusing on relationships is superior by far to using drugs as a brain-healing measure. Does it work for everyone? Nope. But when it does work, the positive changes are permanent, and the adverse effect profile for a series of hugs is certainly much more benign!

          — Steve

  20. As I get bits and pieces of memory, I have wondered if I was born this way, or if I am the culmination of everything I endured. We can over complicate things with different schools of thought, but it’s really quite logical. Yes, I was anxious, fearful child, but after years of blaming myself, I know my mother was and is very ill. Most of the time, I hope she is psychopathic because then I can tell myself she is unaware of the things she has done. There is some comfort in that. I can’t say that she is souly responsible, but I can say I can’t separate those early childhood fears from the few memories I have of my mother at that time, and that degree of illness has a long reach. You become “crazy” to survive, but you have to be a little crazy to stay, too.