Adverse childhood experiences, genes, and mental illness
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 characteristics. Schizophrenia 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.
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
Report comment
And this *reality* did not come from books, but real life, personal experience, traumas along the way.
I don’t have it down to a science yet, but hope to get a little better each day…
I’m still learnin’.
Duane
Report comment
“Life is not what it’s supposed to be. It’s what it is. The way you cope with it is what makes the difference.” – Virginia Satir
Report comment
Thanks, Duane.
Report comment
Why do you always respond to yourself? I never see a post from you that isn’t immediately followed by at least two more from you.
Report comment
I apologize. I should gather my thoughts and put them down in one comment. Will work on it.
Duane
Report comment
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.
Report comment
That’s a lot of useful information, David. I’m a big fan of Panksepp and Damasio–and I completely agree that the focu on neurotransmitters in the psychiatric literature is myopic–just weird, except, of course, for the fact that neurotransmitters are the only thing psychotropic meds can affect.
Report comment
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
Report comment
Thanks, Chrys. That’s instructive, and especially meaningful.
Report comment
“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.
Report comment
My response is below Marian, apologies for putting it in the wrong place, Chrys
Report comment
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
Report comment
Chrys,
Re: Hormones/Menopause
I think that *many* people are labeled with *mental* disorders, while the underlying *physical* cause is overlooked, ignored, or dismissed -
http://discoverandrecover.wordpress.com/root-causes-of-mental-illness/
IMO, *nobody* should be given a psychiatric diagnosis before looking for these underlying conditions.
And IMO, nobody should be given conventional psychiatric treatment before being provided informed consent, and being shown safer, more effective non-drug options… which would put conventional psychiatry out of business pretty quickly.
Duane
Report comment
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…
Report comment
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.
Report comment
I resisted the results of behavioral genetics for many years, and finally realized I was simply being obdurate, looking for reasons to disbelieve rather than considering the issue disinterestedly. Certainly behavioral genetics, like all inquiry, is limited by human finitude and where we happen to be at a given point in the history of science, and subject to further development; but it is a serious science, conscientiously pursued by excellent minds, not notably corrupted by corporate money. If anything, BG studies probably underestimate the influence of heritability, for at least two reasons: (1) we know that, depending on the specific geographical region, the actual father is not the father of record in 5% to 20% of cases, and (2) it may be the case that more is inherited than is captured by the simple calculations of what identicals, 1st, and 2nd degree relatives have in common. I am not adept enough on current research into epigenesis, and the ways that germ lines are being discovered to contain a great deal more than the simple picture that obtained before the Human Genome project and ENCODE, to be sure about the latter point. But I’m sure about the first point.
Report comment
Thankyou Guru3522 for challenging Bob’s over emphasis on genetics. There seems to be a significant theme of genetic determinism meandering through this blog article and I was about to put out a call to the readers at MIA: WHERE ARE ALL YOU SCIENTISTS AND CRITICAL THINKERS? WHEN WE NEED YOU?
Bob, what is your real point? Are we fooling ourselves to focus attention on various forms of oppression and psychological stress in our envirionment including bad childhoods or even the lack of nurturance given to young people? Is it silly of us to want a dramatically different and more humane world than the one we currently have? Should we shift our focus and all our resources to finding the genetic “Holly Grail” or other genetic examples of “original sin?” Should we forget about dismantling Biological Psychiatry’s hold on the treatment of those people labeled as “mentally ill?” Are we deluding ourselves to think that revolutionary type changes in our environment and in mental health treatment models would make a significant difference in today’s world?
Bob, where do YOU want us to go with our time, energy, and resources?
Robert Sapolsky the popular Standford neuroscientist and primatologist makes a most important statement in his “Peace Among Primates” essay in 2007 (a must read):
“To an overwhelming extent, the age-old “nature vs nurture” debate is silly. The action of genes is completely intertwined with the environment in which they function; in a sense, it is pointless to even discuss what gene x does, and we should consider instead only what gene x does in environment y. Nonetheless, if one had to predict the behavior of some organism on the basis of only one fact, one might still want to know whether the most useful fact would be about genetics or about the environment.”
Sapolsky then goes on to show one remarkable example in the primate world where the environment, contrary to formerly very strong held theories, clearly trumped genes.
Bob, when you uncritically use the constructs schizophenia and Bipolar 1, and then say they are “…about 80% heritable” I say, HERITABLE IN WHAT ENVIRONMENT? Your use of genetics in this context seems very much opposed to the point Sapolsky made in the above quote and it seems to have a tilt towards genetic determinism.
I bet its possible for us to create an environment ( a very nast one) that is perhaps combined with the use of certain substances where every human being in it might end up displaying the symptoms that get labeled as schizophenia, or another where it might be like Bipolar Disorder.
Bob, you say “Neither genetics nor early childhood is the whole story…” You are right about this. But based on the content of your above blog I’m not sure what story you want to be apart of writing and how you want the ending to turn out.
Richard
Report comment
My point was very clear, Richard:
1. A certain proposition which was once widely believed has fallen into scientific disrepute.
2. Some people think the ACE research has rehabilitated that proposition.
3. A correct reading of the ACE research shows that it does not say nearly so much as that.
4. Therefore, it does not rehabilitate the old notion.
Which part is not clear?
Report comment
“What part is not clear?”
Bob, what point are you trying to make by making that point?
It might help me understand you better if you address some of the questions made in my second paragraph, and also my question raised; where do YOU want us to go with our time, energy, and resources?
Richard
Report comment
I’d really rather address the topic I set out to address, not some more wide-ranging set of issues. On the latter, I’m only willing to reiterate the “mission statement” of my blog here says: I want us to know the difference between what we know and what we don’t, and to try to know more, while helping patients without claiming more for our beliefs than is warranted.
In this particular case, 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. To tell someone that seems to me an intellectually unsound, unjustified position to take.
My personal wishes are surely beside the point. If we are going to hold our opponents to high standards of proof, we must hold ourselves to the same ones. What we might personally want to believe is no more relevant to what’s right for us to say than the personal wishes of the head of the DSM committee are relevant to what it is right for him to say.
I would say that you seem to be misreading Sapolsky or misunderstanding the behavioral genetics literature, and certainly attributing to me something I never implied nor believe. Hardly one denies that the “nature/nurture” dichotomy is wrong. The behavioral genetics literature is all about parsing the respective contributions of genes and environment. Certainly nothing I said involves “genetic determinism.”
As for wanting a better world, with less oppression–well, of course we should want that, because it would be better. That does not depend on any link to mental illness.
And BTW–all caps is generally considered shouting on the internet. There’s really no need to shout at me.
Report comment
Hi Bob- Thanks for your reply. I was hoping that you might address the data that I provided in light of your bold claims re: heritability of Schizophrenia. The two points that you make, after what appears to be a subtle intimation that I may be ‘obdurate’, do not address anything that I put forth, as well as have no associated citations. Further, these is a wealth of literature that makes what I view to be a compelling case for the role of childhood trauma, as well as other painful early life experiences, in the etiology and development of human suffering (i.e. “mental illness”). I agree that the answers we seek most definitely include biological, genetic, intrapsychic and interpersonal factors; however I do not feel that some of the information in your original post stands up to the types of scrutiny you make it a point to discuss. I do not say any of this with ill will, or as an attack on anything other than your conclusions and cited evidence. I only do so to ask that you more fully explain how you have reached these conclusions in light of much of the literature which, in my eyes, provides contrary evidence.
Report comment
While I remarked in passing that we know schizophrenia to be about 80% heritable, I didn’t understand myself to be making any “bold claim.” I’m just reporting the very-widely-accepted state-of-the-art in research.
The purpose of my post is specifically to address the notion that the ACEs literature rehabilitates a certain idea–call it “p,” for brevity’s sake. “p” has fallen into disrepute. To say that ACEs does not rehab “p,” it is certainly not necessary for me to rehash the arguments that have put “p” in disfavor.
It’s also not my job, in pointing out that the ACE’s literature doesn’t challenge the behavior genetics literature, to repeat all the reasons that the behavior genetics literature is reliable. It’s simply to point out that ACEs isn’t even about behavior genetics, and it is not inconsistent with it. Which is to say, again, that the ACEs literature does not rehab “p.”
I’m sorry that I’m not available for the particular debate you seem to want to have. But I’m just not.
Report comment
Understood. I must say in closing that I feel you often subtly (and at times overtly) insult those persons which want so badly to discuss real issues with you, and seem to minimize or disregard worthwhile information that runs counter to the ‘state of the art’ research you condescendingly referred to above. I would only ask that you reflect upon the reactions you have received from many of us on this site as you continue putting your ideas out for public comment. Again, I was hoping to speak to real issues and to hopefully learn things from you that I apparently have been unaware of. It seems that I did learn from you; however this knowledge was not related to behavioral genetics. I genuinely wish you well with your work.
Report comment
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
Report comment
“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.” — hear, hear!
Report comment
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?
Report comment
Stanley–
I certainly believe that at this point in the history of our knowledge, we should be looking at all three “legs” of the “biopsychosocial” stool.
As for “education,” I’m not sure what you’re referring to–are you talking about educational institutions, or how a kid gets taught about the world? It’s not my job here to address education policy–though I did work in that field, and publish in it, for awhile. But I certainly think that one way or another, kids need to learn things specific to their particular temperaments and interests, as well as the general things we all need to know, and it would be nice if everyone had people in their lives attentive enough to personalize that learning for them.
The question of one’s appearance and how it’s received in the environment is usually referred to as a “gene-environment interaction.” It may sometimes be the case that the sort of example you give confounds parsing the respective roles of genes and ACEs. If the child’s physiognomy were a function of the same genetic factors that dispose toward mental illness, we would not know to what extent the prejudice effected the outcome, versus how likely the outcome would have been anyway.
A genetic confound is a genetic factor that is involved in both of the phenomena in a correlation. It can be fairly indirect–e.g., a parent and child may share the genes that mediate depression, and the action of those genes in the father may lead to mistreatment of the child, or even to social circumstances that cause the child problem. An ACE that was due to such factors–again, perhaps bullying at school, if the family were very poor in a wealthy district, or if the dad had disgraced the family–would confound our understanding of the what role the bullying played in the genetically-mediated depression the child suffered in later life.
Report comment
Thanks for taking the time to reply. You certainly point at a lot of things to think about, and you have strong credentials in the subject.
Report comment
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 ?
Report comment
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
Report comment
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
Report comment
*Full* recovery – living in the community, working, paying taxes (aka, having a *life!)
Report comment
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
Report comment
Sandy, I frequently–maybe nearly always–feel the same way. The more I learn about emerging science, and the longer I practice, the less I think I understand.
Report comment
The ability to overcome profound injury and deeply heal may be beyond our understanding as well.
It’s part of the history of our humanity (the better part). It took place long-before there were mental health “experts”.
Duane
Report comment
Truer words were never spoken, Duane.
Report comment
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
Report comment
Richard, when you ask, “Why should we downplay . . . ” or “why should we deny our patients . . . ” you are begging the question–assuming as true what’s under debate. If we knew it to be the case that the “obvious connections” were in fact real connections, your formulations would be correct. But we do not know that what’s obvious is correct. Indeed, we know quite well from cognitive neuroscience that humans’ inveterate pattern-making is quite routinely powerful, convincing, and wrong. The obvious connections we see are often mythical.
Similarly, we do not know that what you refer to as “transformation” or “profound discovery” are in fact either of those things. People can have emotionally powerful experiences, interpreted to them or by them in certain ways which change how they live, while misunderstanding the source of the emotion, and shaping the emotion into satisfying but false narratives.
I am not saying that adverse experiences do not have bad effects. I am not saying that people do not need to talk through bad experiences with a sympathetic listener. I am not saying that we do not need to make to make sense of our lives. But I am saying that the ACEs literature cannot be correctly interpreted as vindicating therapeutic practices and mythologies that fell into disrepute precisely because they are often destructive and generally poorly evidenced, despite being emotionally pleasing to patients and therapists.
Report comment
Bob
I have to be brief because unfortunately I’m off for the day.
Everything is not relative. There are truths that can be told and discovered and are absolute representations of what happened in the real world. And it is important to know that truth and work with that truth.
Let’s not forget what happened when Freud made the cowardly and opportunist decision to not believe what his patients were telling him about their terrible histories of sexual abuse.
Richard
Report comment
I certainly agree that not everything is relative, that there are truths, and that we need to know and work with them. But I also believe that we can only distinguish truths from pleasing myths on the basis of evidence and rigorous inquiry. My point is that the evidence does not support a wide variety of pleasing therapeutic practices, and the ACEs literature doesn’t change that.
When you teach people that their adverse experiences have a significance that, in fact, the evidence does not support, you teach them modes of self-understanding, and of understanding events and other people, that are unlikely to be true. Truth, not relativity, is precisely the issue.
Report comment
Hi, Bob!
I have found that the crux of what I consider to be good therapeutic practice is something different that what you seem to be describing above. I don’t teach people ANYTHING about what significance their past experiences have. I assist THEM in deciding what significance past or present experiences may have FOR THEM. I consider it poor practice indeed to inform someone else what is wrong with them, and that’s actually my biggest objection to the whole DSM/psychiatric worldview. Who the hell are the psychiatrists or “medical science” or psychologists or anyone else to tell me what is wrong with me and my life? Isn’t it MY job to determine what is and is not important and what does and does not have significance for me?
I have had some clients who readily see their past experiences as having influenced how they decided to see the world, and used that insight to change their viewpoint. I’ve had others who have focused on current events and challenged themselves to overcome their anxiety/depression/anger by confronting their current view of the situation. I’ve had others heal through finding purpose that was lacking in their lives, or through leaving a bad relationship or job and finding a better situation, or through exercising and meditation, or through eating better or learning to manage their kids’ behavior or going back to school… There is an endless array of possible sources of distress and of solutions to those distressing experiences. We will NEVER find one approach that works for everyone or one cause that explains human distress and healing. No amount of scientific study will change this hard fact – human beings are all unique and require unique approaches if we want to help assist them in their journey.
An effective therapist, in my experience, is humble and does not tell his/her client what to think, believe or do. S/he helps the client find his/her own path and the power to follow it. There is no magic technique to make this happen, just as there is no explanation, genetic or otherwise, why certain people react one way to a certain stressful situation, and certain people act another way. Experience has taught me what kinds of questions to ask, but I always have to be open to the answers. I guess believe the answers aren’t scientifically accessible per se, because I don’t think they exist in the world of matter and energy. I think they exist in the world of the spirit, and that will always remain a mystery. Of course, many “scientists” will deny the existence of the human spirit, or consider it a sub-creation of the brain. But I don’t see one shred of scientific evidence for that theory, either.
Science is great for physical objects. Life forms may very well transcend the scope of science. I think humans certainly do.
—- Steve
Report comment
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 !!
Report comment
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.
Report comment
Surely you would not have trouble with the notion that one’s genetically-mediated temperament may dispose one to irritability, poor impulse control, sensation-seeking, and the like, would you? And surely you would not have trouble with the idea that within a family culture, under various sorts of stresses, those genetically-mediated traits might incline one toward intemperate behaviors? No one of any repute, to my knowledge, has ever said that one is genetically determined to abuse children. But it seems unreasonable to insist that genetically-mediated traits cannot be among the significant risk factors involved in the emergence of conditions difficult for or harmful to kids.
Report comment
Maybe, maybe not, Bob, but there are so many dimensions to personality, behavior, and relationships that I don’t believe you can separate out the genetic component.
On one level, everything is genetically determined, on another, not much is genetically determined. Even clear evidence of genetically determined diseases has shown the existence of a genetic anomaly is not predictive; many individuals with the same genetic structure do not go on to develop the disease.
The pursuit of a genetic basis to complex human behaviors is another form of biological reductionism. It may be interesting intellectually but not applicable due to wide human variation.
Report comment
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).
Report comment
Stanley–
The heritability quotients I quoted are h(squared) numbers, which measure the proportion of variance within a population that can be accounted for by additive genetic variance. By definition, this does not include COV (G,E). COV (G,E) would be a source of confounds, in the context of this discussion.
The h (squared) heritability quotient also does not include nonadditive genetic factors or epigenetic factors. That means the number probably underestimates heritability.
No one in behavioral genetics would ever claim that a heritability quotient is predictive for an individual. I think of these numbers as the scouting party’s finding out whether there’s a reason to send out an exploratory team: we will really only understand what is and isn’t inherited from a fine-grained exploration, including molecular biologists and others, but we need to know whether to bother. Your perplexity at how we could measure the relative contributions of genes vs environment is well-taken; but remember that these measures are taken at the population level, not the level of individual development, and all we have to do is count the instances within the population. Thus, the issue is not so much how complex the phenomenon is, as that we set a clear definition as to what will count as an instance of it within the body of research.
There are all sorts of things that we can’t tease out at the individual level, but looking at the level of the population enables us to get at the issues. For instance, in an individual’s case, we would have a hard time discerning the relative roles of income, marital satisfaction, professional success, and the like in his general state of mind. But looking at population numbers enables us to begin to see what sorts of roles those factors generally play.
It is certainly true that for individuals, gene/environment interaction is most important in phenotypic development, especially where heritability quotients are low to moderate. Note, though, that “environment” includes everything from the amniotic sac and the mother’s health during pregnancy to childhood illness to nutrition to family SES, etc., and positive as well as negative factors–not just, or mainly ACEs.
I had not read the SEP article until you referenced it, and honestly it surprised me. I haven’t kept up with the intra-disciplinary fights of philosophers in years, but I was under the impression that Lewontin et al had long since been surpassed. They certainly have in the broader community of scientists who study heritability. I don’t know what to say about that particular portrayal of the fights within philosophy–except to underline the article’s point that it is very odd to find philosophers of biology arguing against heritability calculations.
I know that I don’t need to say this to you, but since people seem to be having such a hard time getting my point, let me reiterate nonetheless: my point is that we know quite well that genetics plays a strong role in development, that the ACEs literature neither addresses nor contradicts this knowledge, and genetic confounds increase the difficulty of knowing what proportion of the correlation between ACEs and mental ilness reflection a causal relation vs a spurious correlation because of confounding factors.
And let me reiterate that I did not lead with the genetic material, since that was not my main point. I led with the more fundamental issue, that according to the ACEs literature itself, only a small minority of people who suffer ACEs develop mental illness, and mental illness often develops in the absence of ACEs.
Report comment
Good point. The definition of ACEs case by case cannot take into account every factor affecting the individual. You have a population with X identified factors in common, some but not all develop Y.
The difference might be genetic (a factor that was not identified) or it could be that the individuals developing Y had other experiences not captured by the survey.
Report comment
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.
Report comment
You may well be right, Stanley. I would rephrase your analysis as saying that the heritability quotient abstracts too far to be meaningful. Would that be apt?
What gives me pause is your particular example of bipolar. In classic bipolar, we generally only see that develop in adulthood–the idea that kids can be bipolar was largely the work of Joseph Biederman, right, who has been pretty well disgraced? So I’m not sure how the feedback loop you offer would apply to early childhood.
Report comment
When we know it, a percentage of contribution to covariance is still a very abstract concept (I find the name heritability quite misleading). I like the explication of the limits of its meaning at:
http://mancpsychsoc.blogspot.com/2011/10/schizophrenia-is-arguably-80-heritable.html
Report comment
Thank you for this link.
Report comment
Just in case, I’d like to clarify that in my view, the limitations explained in the above link are not incompatible with Bob’s usage of heritability for his specific point (although less cautious people might be more prone to abuse the concept for bolder assertions).
And I want to clarify that my main issue about heritability is not addressed in that link, and is about how the numerical values are computed: more specifically about the additive math model in use. I am afraid the simplification of that model (ignoring cov(g,e)) ends up attributing to the gene covariance pool complex interactions. For instance, let say there exists a gene that is protective in most environments, but act as an amplifier of some specific environmental risk factor, and that overall that gene is risk neutral. The existence of that gene will nevertheless increase the heritability result of the trait, in spite of being risk neutral (that type of influence should be part of the ignored cov(g,e)). Theoretically, a high heritability result could still be obtained with a situation where all genes and genotypes are risk neutral for the phenotype studied (which is a limitation that goes much further than the “smoking/cancer” example in the link).
Thus heritability numbers are an upper bound on the influence of “risk-factor” genes, not a proof of their existence.
Report comment
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?
Report comment
“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.
Report comment
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
Report comment
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.
Report comment
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
Report comment
I’m just going to come straight out with it:
I admit it, it is true…
I AM A GENETIC BEING.
Can “elite” people be genetically proven to exist?
Report comment
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.
Report comment