Adverse Childhood Experiences and Psychiatric Disorders

 

In my last post, I mentioned that the American Psychiatric Association rejected the diagnosis of Developmental Trauma Disorder in 2011, and refused to acknowledge that “…childhood adverse experiences lead to substantial developmental disruptions” and added that this idea is “more clinical intuition than research-based fact.”

In fact, there have been numerous studies showing a correlation between ACEs and a wide variety of clinical conditions. Below are brief descriptions of the results of four studies, recently published, addressing this contention. One is a review and meta-analysis, which is a research process used to systematically synthesize or merge the findings of, in this case, 39 (!) single, independent studies, using statistical methods to calculate an overall or 'absolute' effect.

Of course, the studies do only show correlations, which means that they do not “prove” that ACE’s actually cause psychiatric disorders or even symptoms. But the correlations are as good as any in the psychiatric research literature, which is pretty much minimal in findings that prove actual causation for almost every psychiatric disorder.

 

Adverse Childhood Experiences Among Adults With Eating Disorders: Comparison To A Nationally Representative Sample And Identification Of Trauma

The primary objectives of the current study were: (1) to examine and compare ACEs between two samples: treatment-seeking adults, and a nationally representative sample of adults, (2) to characterize ACEs items and total scores across demographic and diagnostic information in adults seeking treatment for an ED, (3) to statistically classify ACEs profiles using latent class analysis, and (4) to examine associations between ACEs profiles and diagnosis.  Results: Patients with EDs had significantly higher ACEs scores than the nationally representative sample. Within patients with EDs, four latent classes of ACEs item endorsement were identified. Patients with other specified feeding or eating disorder (OSFED) and binge eating disorder (BED) were more likely to fall into the "Household ACEs" and "Abuse ACEs" groups, respectively, compared to anorexia nervosa-restricting subtype (AN-R). Conclusion: Patients with EDs reported more ACEs than the nationally representative sample, across all ED diagnoses.

“Adverse childhood experiences among adults with eating disorders: comparison to a nationally representative sample and identification of trauma profiles.” Rienecke, Johnson et.al. Journal of Eating Disorders , volume 10, Article number: 72 (2022). 

 

Considerable Mental Health Burden Associated With Childhood Trauma

Trauma is associated with increased odds of anxiety disorders and any psychiatric disorder at age 6 years. There is a considerable mental health burden in association with childhood trauma. 

 “The association between childhood trauma and psychiatric disorders in low-income and middle-income Countries." Alckmin-Carvalho et. al., The Lancet Psychiatry, Oct. 31, 2022.

Association of Neural Connectome With Early Experiences of Abuse in Adults

In this cohort study of 768 participants, individuals with abuse experienced during childhood (but not adolescence) demonstrated an altered connectome [connections between brain neurons] of greater functional connectivity [changes in usual and not pathological connections in various brain areas] associated with somatomotor and dorsal-ventral attention brain networks, irrespective of current diagnosis or symptom state. These findings suggest that a history of child abuse is associated with altered functioning of systems responsible for perceptual processing and attention, and these findings were found in the presence of many different psychiatric conditions.

"Association of Neural Connectome With Early Experiences of Abuse in Adults." Korgaonkar et. al., JAMA Network Open. 2023;6.

 

A  Systematic Review and Meta-Analysis of the Relationship Between Childhood Adversity and Adult Psychiatric Disorder.

A review and analysis of 39 different studies suggests that childhood and adolescence is an important time for risk for later mental illness, and an important period in which to focus intervention strategies for those known to have been exposed to adversity, particularly multiple adversities. There was some evidence of a dose-response relationship with those exposed to multiple forms of maltreatment having more two and a half times odds of developing a mental disorder. 

“A revised and extended systematic review and meta-analysis of the relationship between childhood adversity and adult psychiatric disorder  [Review]." McKay et. al., Journal of Psychiatric Research, 156 (2022).

 

 

Cognitve Behavioral Therapy "Evidence-Base" Grossly Exaggerated

In my post on my Psychology Today blog on November 21, 2011, I discussed how the purveyors of today’s most predominant psychotherapy methodology, cognitive behavioral therapy, grossly exaggerate the strength of their research evidence base in the psychotherapy outcome literature.

My opinion was recently confirmed in a review of meta-analyses of the CBT literature in the Journal of the American Medical Association, published online September 21, 2017 (“Cognitive Behavioral Therapy the Gold Standard for Psychotherapy:  The Need for Plurality in Treatment and Research” by Falk Leichsenring and Christiane Steinert).
 
They reported that a recent meta-analysis using criteria of the Cochrane risk of bias tool reported that only 17% (24 of 144) of randomized clinical trials of CBT for anxiety and depressive disorders were of high quality. The “allegiance factor”—study authors were CBT therapists themselves and often designed the studies to make their treatment look better than it was, and opposing treatments look worse that they were—was rarely controlled for.

Compared with "treatment as usual" —letting subjects get whatever other treatments outside of the study treatment that they chose to have, allowing good therapists and bad therapists, and good therapies and bad therapies, to essentially cancel each other out—the sizes of treatment effects were only small to moderate and might eventually even be found to be due to the allegiance effects.

In panic disorder, CBT was not more effective than treatment as usual but only to being on a waiting list.

Even with these amazing biases, for depressive disorders, response rates of about 50% were reported. This was true for anxiety disorders as well. “Response” just meant there was some significant improvement in symptoms, not that the symptoms of the disorders actually went away. Rates for actual remission from the disorders were even smaller. Conclusion: a considerable proportion of patients do not sufficiently benefit from CBT.

Last but certainly not least, there was no clear evidence that CBT was more effective than other psychotherapies, either for depressive disorders, anxiety disorders, personality disorders or specific eating disorders.

Personally, my biggest beef with CBT and other psychotherapy outcome studies has less to do with symptom relief than with actually changing maladaptive interpersonal behavior. The latter is almost never even looked at, let alone measured in these studies.

CBT’ers seem to think anxiety, depression, and self-destructive behavior are all due to screwed up thinking by individuals rather than being normal reactions to stress-inducing environments. In experimental psychology circles, this is known as the fundamental attribution error. Telling people with these particular symptoms that their problems are basically “all in their heads” in this manner is very invalidating for them.  Ironically, an ‘invalidating environment” is one of the two primary factors these very same therapists cite as the main causes for borderline personality disorder.

Treatment Resistant Depression and Borderline Personality Disorder

On October 18, 2013, John Gunderson, perhaps the most internationally recognized expert on borderline personality disorder (BPD), wrote a piece in the American Psychiatric Association’s newspaper, Psychiatric News. He opined that many if not the majority of cases of treatment resistant depression (TRD - depression that does not respond to antidepressant drugs) may in fact be undiagnosed cases of patients with BPD.  This opinion is totally consistent with my own clinical experience.

John Gunderson, M.D.

Of course, the psychiatric-industrial-Pharma complex immediately went on the offensive. On his Medscape blog, Nassir Ghaemi - a fan of  bipolar m.a. - wrote a two part rebuttal. He expressed the opinion, asserted and not backed by any particular review of the literature, that the DSM criteria for BPD are invalid. In the past, he has also expressed the belief that the DSM duration criteria for manic and hypomanic episodes in bipolar disorder are far too restrictive, and seems to liberally substitute his own personal criteria for these disorders in his arguments

He goes on to assert that the “…bland, broad DSM definition allows Dr Gunderson and other borderline experts to diagnose the condition in a large chunk of persons with mood illness, not just bipolar illness but also simple depression, since depression entails relationship problems, is often associated with irritability and paranoia, frequently involves mood reactivity, often involves suicidal attempts, and can also entail nihilistic thoughts of feeling abandoned or empty.”

Nassir Ghaemi, M.D.

As I shall discuss a little later, these symptoms, when all taken together as a group, are not typical for your average run-of-the-mill case of Major Depressive Disorder (MDD), but are extremely typical of depression in BPD.

Dr. Ghaemi's statement here is misleading, because, while any given patient with major depression and no BPD may indeed have any one or two of these characteristics, they usually do not have almost all of them together. Omitting mention of this pertinent fact is a tactic frequently employed in arguments from the everyone-who-is-moody-is-bipolar crowd.

As a reference for his assertion, Ghaemi cites a study by Angst, who is another bipolar disease monger whose circular pseudo-logic I dissected in a previous post.  

Ghaemi then goes on to focus on one of Gunderson’s statements in his article: Gunderson cited a study that showed that the presence of BPD was a major predictor of persistence of depression over time in a sample of persons who met MDD criteria.

I agree with Dr. Ghaemi that such a study does not prove, in isolation and by itself, that BPD is the most common cause of TRD, as there could very well be very many other even more common causes.

His impeccable logic: “It does not follow that if x makes y worse, then most cases of treatment resistant y are examples of x. Substance abuse makes the course of MDD worse; but it does not follow - it is scientifically incorrect and illogical - to then conclude that most cases of TRD are cases of substance abuse, end of story."

Of course, the fact that Gunderson cited this one particular study did not mean that he thought he was providing a complete literature review, but Ghaemi seems to be implying that Gunderson is saying that this one study is the only evidence he is relying upon - which he didn’t say. There are a host of studies, btw, that show that severe personality disorders are often predictive of a poor response to all sorts of psychiatric medications for all sorts of psychiatric disorders.

Ghaemi himself, on the basis of some highly questionable studies, opines that the most common cause of TRD is “unrecognized bipolarity.” He of course cites references produced by his fellow bipolar m.a. disease mongers in Hagop Akiskal’s incredibly biased Journal of Affective Disorders.

Their logic has always been a one or another version of the following:

Treatment resistant depression is often accompanied by symptoms such as racing thoughts or  hyperactivity

Racing thoughts, hyperactivity, and other such symptoms can look vaguely similar to symptoms of mania

Therefore, such patients must be bipolar

This is every bit as invalid as the logic that Ghaemi is attributing to Gunderson. In fact, anxiety disorders can and do produce, superficially, all of the symptoms that Ghaemi and his buddies attribute to an underlying “bipolarity.” When looked with a more discerning eye, of course, the symptoms of anxiety disorders and mania look very, very different.

A certain type of anxiety mixed with depression, is, as I shall discuss in a bit, one of the major qualitative factors that distinguish depression in BPD from other types of depression. I think the articles that Ghaemi is quoting are not only consistent with what Gunderson is arguing, but could have been used by him as clear evidence for his main thesis!

I have met Professor Gunderson. I think he is more than capable of telling the difference between BPD and bipolar disorder. 

It’s not subtle.

Dr. Ghaemi shows such limited understanding of BPD that I suspect that, in all likelihood, he has never or rarely sat down with such patients in long-term psychotherapy and painstakingly dissected the environmental and interpersonal context in which their depressive symptoms come and go.

Another person who, like myself, has done this with patients is my colleague, academic psychiatrist Ken Silk. He did a far more complete literature search [“The Quality of Depression in BPD and the Diagnostic Process.” Silk, K. Journal of Personality Disorders 24 (1), 2/2010] than was presented in the discussions by either Dr. Ghaemi or Dr. Gunderson.

Kenneth Silk, M.D.

He points out that, rather than restricting the diagnosis of MDD to those who clearly display a biologic depression - the cases that used to respond to tricyclic antidepressants back when they were the dominant drugs - the diagnosis has spread along with the assumption that most presentations of depression are some form of major depression and, even if not MDD, should respond to antidepressants. The term depression is now used in academic discussions to refer to a mood rather than an actual diagnostic construct.

He lists the qualitative difference between the symptoms of MDD and those of depressed BPD’s. Besides the fact that the BPD patients meet criteria for BPD, not to mention that they also exhibit the family dynamics typical of those with the disorder, the quality of their depression is characterized by the following [My comments in italics]:

1.      A“mad-bad” depression closely tied to anger and hostile behavior.

2.      Mood symptoms that are very sensitive to interpersonal situations in which the patient feels abandoned, lonely, or empty in the absense [or in the presence for that matter] of a longed-for important other.

3.      Depressed moods can come on quickly and disappear quickly [the opposite of true MDD] depending on the reactions of an attachment figure.

 

4.      The depression is at times more closely related to chronic self-criticism and a feeling of intrinsic “badness” than in MDD without BPD.

 

5.      It is associated with chronic self destructive behavior [including self-injurious behavior like cutting].

 

6.      It is associated with a loss of gratification and frustration.

 

7.      Recovery from BPD facilitates recovery from MDD when it is co-occurring, rather than the other way around.

 

8.      The depression often comes from exhaustion and demoralization from repeated unsuccessful battles with chronic and overwhelming anxiety. [BPD often is accompanied by panic disorder].

9.      Patients with BPD often exhibit impulsive aggression (a hair trigger leading to rage). [Patients with true major depression, especially of the melancholic variety, tend not to show this characteristic at all. They are usually extremely passive because they do not have the energy to strike out].

Important questions glossed over by Dr. Ghaemi include: in what context do symptoms appear? How attached is the low mood to specific interpersonal events? Is affective dysregulation (high reactivity to interpersonal problems) prominent? 

An important additional point is that these qualitative differences in depression  that Dr. Silk lists are not measured clearly by any of the standard symptom rating scales used in the vast majority of psychiatric studies. Therefore, citing any studies which employ these instruments in this debate is sort of irrelevant to the basic question. 

A few final caveats.  People with BPD can still have depression that does respond to an antidepressant. And even when the depression in BPD does not improve with SSRI antidepressants directly, other symptoms such as panic attacks can improve dramatically with these drugs (especially if the SSRI is combined with certain benzodiazepines).  SSRI’s can also decrease reactivity by raising the bar, so to speak, so that it takes somewhat more extreme behavior by an attachment figure to create a severe emotional reaction. 

In patients in which either or both of these two things happen, their depression may improve indirectly because of the effects of the drug on the other symptoms, as opposed to in MDD, in which the decrease in low mood is a direct effect of the drugs.

Finally, patients can also have both BPD and true bipolar disorder. In fact, patients with bipolar disorder, when not in the midst of a manic or a depressive episode (when they are euthymic), can have just about any psychological or psychiatric reaction or personality issue in addition to bipolar disorder.  That is because, when they are euthymic, they are basically just like anyone else! 

Writers in the Journal of Affective Disorders just love to merely assume that any emotional reaction a patient with bipolar disorder has simply must be due to the underlying bipolar disorder.  What hogwash.

Antipsychotics Are For Psychosis, Not Insomnia Redux



In my post of February 16 of this year, Antipsychotics Are For Psychosis, Not Insomnia, I reported on the increasing off-label (non FDA-approved) prescription of so-called atypical antipsychotic medication for insomnia and anxiety, despite the risk these drugs pose of causing metabolic syndrome (diabetes, obesity, and increased blood cholesterol and triglycerides [blood fats]) as well as an irreversible neurological problem called tardive dyskinesia. 

Somehow doctors - mostly primary practitioners but many psychiatrists as well - have been brainwashed into thinking that this risk is somehow much less than the risks posed by addiction from sedatives and hypnotics  - the old fashioned tranquilizers and sleeping pills. (Tranquilizers and sleeping pills are actually one and the same thing, by the way.  What's the difference?  Marketing.  Some of these drugs are marketed for sleep and some for anxiety, but they all do both of these things).

Anyway, a class of drugs called benzodiazepines are the most commonly used drugs indicated for insomnia and anxiety.  These include drugs like Valium, Librium, Ativan, Klonopin, Dalmane, Restoril, and Xanax.  They replaced the far more addictive and dangerous barbiturates several decades ago.

A newer (and of course much more expensive) group of drugs (Ambien, Lunesta and Sonata) were marketed as being "different" from the other benzodiazepines, so many doctors are much less afraid of prescribing them than the old drugs. 

In truth, these drugs work almost exactly the same way as the older benzo's.  They also cause sleepwalking. And they are every bit as addictive.  In fact, according to my prime source for all things concerning drug abuse, Rolling Stone magazine, the latest fad in D.C. is staying awake while on Ambien. Apparently, you can get really high if you do that. (Now that you know, please don't go out and do it!)

Of course, mild and moderate anxiety and insomnia can often be treated without any medication at all, but don't even get me started on that.

Actually, benzo's (with the possible exception of Xanax, which is very short acting), are not abused by themselves very much at all by addicts.  When was the last time you read a horror story in the news about valium addiction? It is also almost impossible to die from a benzo overdose if no other drugs are taken with them.

The drugs can create trouble, however, when they are combined with opiates - in which case one can overdose on the combination and die.  Unfortunately, this has been happening with increasing frequency lately.  But I digress.

Not only are benzo's by themselves pretty safe, but they have almost no side effects at all except in the elderly.  Compare their risks with the risks of atypical antipsychotics, and it is absolutely no contest at all.  Personally, if I had to choose, I would much prefer to be addicted to a benzo than be addicted to insulin shots!

Despite this obvious discrepancy in the risks, the problem of the misuse of prescriptions for antipsychotics by physicians to treat insomnia and anxiety continues to worsen.  In the September 2, 2011 issue of Psychiatric News, an American Psychiatric Association newspaper, there were two headlines side by side:  "Antipsychotics Increasingly Prescribed for Anxiety" and "Concern Raised Over Antipsychotic Use for Sleep Problems."

Even well known drug company apologist Charles Nemeroff was quoted as bemoaning the use of antipsychotics for anxiety disorders like panic disorder.

For insomnia, the biggest seller is the drug Seroquel (Quetiapine), which is second only to Zyprexa (Olanzepine) in causing metabolic syndrome.  Indeed, Seroquel is probably the most sedating atypical.  The article in the paper pointed out that a lot of physicians who prescribe this medication do not even bother to monitor the patient for increases in weight, blood sugar, and serum fats. 

The article about insomnia was prompted a large increase in prescriptions for this drug for insomnia in military personel.  According to the Department of Defense, in 2001 20-30 soldiers per ten thousand were treated for insomnia.  By 2009, the figure had soared to 226 per ten thousand. 57% of all prescriptions of Seroquel were for insomnia! 

Soldiers reported gaining an average of 6.3 pounds each on the drug.  Only 61% had a check of their blood sugar within six months of starting the medication.  Fortunately, no actual cases of diabetes were found.  The author of the study that generated these statistics agreed with my theory that these drugs were being used by physicians instead of benzo's because of fear of addiction.

That reasoning is a bit like the reasoning of people who will not fly in a commercial airplane for fear of a crash, but refuse to use seatbelts when they ride in a car.  These doctors apparently are completely clueless when it comes to evaluating relative risks.

Practice of Doping up Children to Treat Parental Anxiety Continues to Grow

I have already written several posts about the inappropriate "diagnosing" of bipolar disorder in children and the even more inappropriate use of antipsychotic medications in children.  My main point has been that, rather than having a psychiatric disorder, the vast majority of these children are just acting out.  (For those readers who have difficulty making distinctions - especially those who automatically assume that things that look vaguely alike must be identical - this opinion does NOT apply to those uncommon children who are actually psychotic or to older adolescents who are clearly and obviously manic).



So what proof can I offer?  Well, at the American Psychiatric Association Annual Meeting, John Goethe, MD (director of the Burlingame Center for Psychiatric Research and Education at Hartford Hospital’s Institute of Living), presented the results of a decade-long study of antipsychotic prescribing for children and adolescents in psychiatric hospitals.

The results? Forty-five percent of patients with such behavioral disorders as ADHD or conduct disorder were given antipsychotics and 44% of patients with post-traumatic stress disorder (PTSD) received them. The percentage for other anxiety disorders was 31%!

Forgetting for the moment that an ADHD diagnosis may just be yet another case of acting out, antipsychotic medication is not indicated for ADHD.  In adults, antipsychotic medications are not indicated nor FDA-approved for any anxiety disorder or PTSD.  Not only that, but there is not the slightest evidence from any neurobiological study that the purported mechanism of action of antipsychotic medication has anything to do with anxiety disorders or ADHD. 

And conduct disorder?  This "disorder" was formerly called juvenille delinquincy.  Acting out by any other name. Don't even get me started.

One of the predominant side effects of these medications, is however, sedation.  So one might conclude that the reason the meds seem to both the parents and incompetent doctors to "work" is that the kids quiet down because they are being doped up. (This prescribing practice does not just apply to some psychiatrists but also to many other primary care doctors as well -as to pediatricians, read Claudia Gold's blogpost, Pediatricians Prescribing Psychiatric Medication: A Dose of Reality),

But who's anxiety is really being treated here? 

I submit that it is the anxiety of the parents. Parents who have out-of-control, acting-out children are the real objects of these "treatments."  These parents covertly feel guilty when they are unable to control their children due to inconsistent, neglectful, or abusive parenting practices.  Yet they have great difficulty changing these practices for a variety of reasons - sometimes very understandable reasons.  (One of which is that their doctors make no effort to understand what is really going on in their homes, and take advantage of their insecurities). 

Nonetheless, when the kids are doped up and are therefore less trouble, the parents feel better. And they have the doctors stamp of approval that the problem resides entirely within the child, not with them.

An unsolicited plug


The use of these drugs in kids diagnosed with PTSD is particularly instructive.  Unless you are treating victims of such disasters as the recent outbreak of tornadoes in the South and Midwest, or working with victims of crime like Jaycee Dugard, the most common trauma leading to PTSD in children is child abuse.

Of course, this whole process of sedating acting-out children usually does not end with the first prescription.  For most drugs that have sedation as a side effect, the sedation gradually subsides after  a few weeks on the medication.  Then, of course, the kid starts doing what kids always do - start reverting back to their previous behavior.

The parents then drag him or her back to the incompetent doctor, who starts to take one of the following steps and then another, in no particular order:

1. Increase the dose of the medication.
2. Change to a different medication which also is not indicated for anxiety and conduct disorders.
3. Add a prescription for a second one of those medications, and then perhaps a third or a fourth.
4. Change the diagnosis to something else other than acting out, and begin the whole process all over again.

Since the kid still is not controlled after the sedative side effect subsides, another step the parents can take is to apply for social security disability for the child.  This gives the child the message that the parents think he or she is both sick and incompetent.

Readers of the blog know what I believe happens next.  The child develops a false self that only seems to be sick and incompetent.  Such children hide their abilities as they grow into adults, continue to act in ways that preclude employment, and continue on social security disability. 

When you take the time to actually get to know them, however, it seems that the only thing they can not seem to do that most people can is maintain employment.

And then Robert Whitaker thinks that the medications were the cause of the disability, just like the less-than-thorough doctors thought that the medications caused the initial improvement of the child's "mental illness" when it was just a side effect that temporarily muted acting out behavior. 

It always amazes me how much people who seem to be on opposite sides of a debate think alike.  Basing their conclusions on totally incomplete information seems to be a favorite blind spot of theirs.