Treatment of Bipolar Disorder Goes Psychotic

 

Ever since I did my psychiatric residency training way back in 1974-1977, bipolar disorder (then called manic-depressive illness) was the easiest of the major psychiatric disorders to treat medically. There was (and is) absolutely no evidence the craziness of the patient during a manic episode or a bipolar depressive episode is amenable to any psychotherapy technique, although therapy might be important when the patient is euthymic (that is, not in a manic or depressive episode – which is most of the time) to deal with the aftermath of their having been psychotic or for other co-morbid psychological problems. Euthymic bipolar patients can have co-occurring personality disorders and anxiety disorders and anything else just like anyone. Since, when euthymic, they are in fact just like everyone else.

If you want to see what a manic patient looks like, look at this video of Charlie Sheen (https://www.youtube.com/watch?v=pipTwjwrQYQ). He actually took a show on the road but had no act. Now, cocaine can mimic mania, but he’d taken cocaine before and he never acted like this. See videos of him when he was back to his usual self to see the difference. Sheen denies he was manic, but I’m not sure I believe that.

Anyway, about 80% of these patients could tolerate and were responsive to lithium for prevention of manic episodes. The longer they took it, the more likely it would be to also prevent depressive episodes as well. If the patient got depressed while taking lithium, antidepressants worked just great. Journal articles saying they do not were full of crap – the most important of these is discussed in this post.  Most of my patients on lithium were basically symptom free for decades, no matter if I saw them in a public clinic, an academic clinic, or a private practice environment.

 

When patients first got manic, we used antipsychotic medications to bring them down, usually in inpatient settings, because lithium takes a couple of weeks to kick in. Once lithium was on board, we discontinued the antipsychotic medication because they didn’t need it any more. The only other time we used antipsychotic medication in bipolar patients was during depressive episodes in which the patient also had delusions and hallucinations (psychotic depression). Again, the antipsychotic meds could often be discontinued after the episode was over.

 

When a patient couldn’t tolerate or was not responsive to lithium, we would then use antipsychotic medications as the only alternative back then, but always had to worry about them causing a neurological disorder (tardive dyskinesia [TD]). Until it was found that the anticonvulsants Tegretol and Depakote were good for mood stabilization – so then they became the second line drugs.

 

When the new, “second generation” antipsychotics came out, which can cause huge weight gain and diabetes in addition to TD, the drug companies started to push them. The use of lithium started to plummet. After it was found that some of them had some antidepressant effects – although usually only to augment an antidepressant – Pharma started to push them even more. Despite the major risks, use of them increased from 12% of cases to 53% of cases between 1997 and 2008.

 

Not only that, but the number of patients diagnosed with bipolar disorder inflated by more than double since 2000. Everybody and their brother who had any mood symptoms at all were misdiagnosed with it, most due to the insane idea known as “bipolar spectrum,” or as I call it, B.S. Another study in the Journal of Clinical Psychiatry that I wrote about previously  showed that 40% of patients in their sample who met clear DSM criteria for borderline personality and not for bipolar had been misdiagnosed as bipolar by a prior mental health professional, as well as 10% of all of the other patients.

Caveat emptor, which in this case means, let the patient beware!

Book Review: The Kevin Show by Mary Pilon

In this impressively well written book – I may have to steal a few of her cool phrases, like when she discusses situations in which people walking on eggshells start to feel more like they are walking on landmines – Mary Pilon tells the story of Kevin Hall and his family. Kevin Hall was a championship sailor who on one occasion made the Olympic Team, although he did not win a medal. At the same time, he struggled with Bipolar Disorder. The real illness, not what passes for bipolar disorder these days.

The author’s discussions of what went on inside of Hall’s head during a manic episode are some of the best I’ve ever seen. After reading them, readers will know that this has absolutely nothing in common with normal human thinking. After coming down off of a manic high, a sufferer knows that. Although they may question themselves about the “reality” of what they had experienced during an episode, it still seems to them to be bizarre and alien.

The book also does a great job of describing the traumatic effects on parents, spouses, and siblings in having to deal with a family member with a major mental illness – especially one who is not always cooperative with treatment but doesn’t let them know when he goes off his meds.

Hall’s delusion when manic was that he was some part of a larger “Show,” run by some all-knowing “Director”  - sort of like the movie “Truman Show,’ which indeed is mentioned several times in the book -  in which he is meant to save the world by interpreting various “signs” in the environment. The signs could be things he happened to see in the environment, unusual coincidences like his having been a college classmate of one of the doctors who treated him, song lyrics, or passages in various books he liked to read.

Unfortunately the author, who seems only to have a limited  familiarity with mental illness and, in particular, the treatment of manic-depressive illness, falls a bit into the trap of starting to wonder if it may just be some variation of normal. After all, with the rise of Instagram, selfies, and social media, everyone is seemingly thinking of themselves as in some sort of show and as having an almost national presence in the minds of others.

Mary Pilon

Not only that, but the author adds that certain delusions are more common in certain cultures than others, and some only seem to exist in a single culture.

In fact, the difference between psychotic delusions and false beliefs that are due to groupthink, everyday human foibles, wishful thinking, and just plain kidding oneself is colossal and not in the least bit subtle. Of note is that the author spends almost no time describing Hall’s thinking during periods of bipolar depression. She only mentions one episode in which he maintained that he was depressed but not delusional - but we do not know if he ever experienced a psychotic depression.

Either way, when depressed, it is mentioned almost in passing, he believed the exact opposite of what he felt while manic – that he was a born loser, loony-bin screw-up who was worth absolutely nothing despite his fairly spectacular accomplishments in love and work while euthymic (neither manic or depressed – in other words, normal).

Hall kept going off his medication because he felt that it was drugging the real him, which is why he kept having recurrences. While I obviously can’t say for certain anything about his reasons for stopping his treatment, the frequent reason bipolar patients discontinue their meds is that mania feels so good in so many ways that normal feels like down to many sufferers, and they want the high back.

Another possibility is that he was taken off lithium -  which generally does not make people taking it feel drugged – not because it was ineffective but because the doctors thought it was ineffective when in actuality he had stopped taking it or his blood level was too low. Good doctors monitor lithium blood levels.

He was apparently put on the antipsychotic Haldol at one point, which definitely does make people feel drugged. Antipsychotics, while they do prevent mania, should only be give in acute mania (because it takes time for lithium or depakote to kick in) – and then discontinued after the other drugs start working. Or used indefinitely only if all other options fail or are not tolerated. The author does not really tell us any details about Hall's treatment.

And what about the cultural aspects of delusions? Well of course delusions concern things that people with the disorder are familiar with. You can’t think the CIA is following you around with ray guns if you have never heard of the CIA or ray guns. And just like with Alzheimer’s disease, in which underlying personality traits affect the expression of impaired memory issues and cognitive confusion, they affect the content of delusions as well. 

Pointing out the cultural differences as a possible reason that bipolar is not a real brain disease is a bit like doing the same by pointing out that the delusions of Japanese people are expressed and thought about in the Japanese language, while the delusions of Spanish people are expressed and thought about in Spanish.

Bipolar versus Borderline: Disease Mongering Pill Pushers Stack the Deck

In my Psychology Today blogpost of 12/11/11, Bipolar or Borderline, I described how disease mongering, pill-pushing psychiatrists have done their utmost best to blur the distinction between the mood (affective) instability seen in borderline personality disorder (BPD) with the mood episodes characteristic of true bipolar disorder. 

This distinction is important because BPD is clearly a disorder of interpersonal relationships and behavior mixed in with a history of trauma and family dysfunction, while true bipolar disorder is a serious biogenic brain disease. BPD, while some of its symptoms do respond quite well to the right medications, should be treated primarily with psychotherapy, while bipolar disorder should be treated primarily with medication.

In the prior post I discussed the use of invalid symptom checklists in studies to exaggerate the incidence of bipolar disorder. They are also used by some incompetent psychiatrists to make diagnoses that justify snowing every patient who walks in the door with potentially toxic antipsychotic medication. In the June 2016 issue of the Journal of Personality Disorders, researcher Mark Zimmerman goes into some detail about exactly how corrupt researchers use slight of hand to distort their data (Improving the Recognition of Borderline Personality Disorder in a Bipolar World, pp. 320-335).

They are very good at it. And it matters. Zimmerman states: "Although BPD is as frequent as (if not more frequent than) bipolar disorder, as impairing as (if not more impairing than), and as lethal as (if not more lethal than) bipolar disorder, it has received less than one tenth [emphasis mine] the level of funding from the NIH [the National Institutes of Health] and has been the focus of many fewer publications in the most prestigious psychiatric journals."

And, Zimmerman points out, the difference is not due to just the fact that there were more drug studies for bipolar disorder. In fact, the amount of funding for the drug treatment of bipolar disorder was just a little more than 10% of the total.

As I have mentioned several times in this blog, self-report symptom checklists are meant to be screening devises. This means that if you are positive for bipolar disorder on the screen, it does not mean you have bipolar disorder. It means you should be evaluated further! Screening tests are designed to have a lot of false positives - people who come out as positive on the test but who do not actually have the disorder. In fact, the majority of people who screen positively do not have bipolar disorder.

Zimmerman specifically brings up the Mood Disorders Questionnaire (MDQ) that I discussed in the previous post. Get this: in one study by Frye and others in the journal Psychiatric Services in 2005, the authors found that one half of the patients who were positive for bipolar disorder on the MDQ were not diagnosed with bipolar disorder by the treating clinician.  

Their conclusion? They said the clinicians "failed to detect" or "misdiagnosed" bipolar disorder in these patients! Actually, the exact opposite is far more likely: it sounds like the clinicians' judgments tended to be correct.

Frye and others then went on to state that these patients were "inappropriately treated because they were given antidepressants instead of mood stabilizers." Again, exactly the wrong conclusion to draw from the authors' own data. Yet they went on to say that this completely false conclusion was "worrisome." Some of us would call this real chutzpah.

Bipolar, my ass researchers love to talk about the bipolar "spectrum," based on the crazy logic that if a given symptom appears slightly similarly in two people, they must both have a version of the same syndromic psychiatric disorder. Zimmerman asks why no one talks of a borderline spectrum, when clinically, many patients are diagnosed as having borderline traits. This means that out of the nine criteria, of which you are required to meet any 5,6,7, 8, or all nine to qualify for the diagnosis, the patients may only have three or four. 

In fact, as reported in the July issue of the American Journal of Psychiatry (Vol. 173, pp. 688-694), Zanarini and others followed 290 patients with BPD closely over 2 years. They found that "...the symptoms of borderline personality disorder are quite fluid..." This means that they come and go over time. This was particularly true for acute symptoms like self-mutilation. Therefore, people with the disorder may frequently go from 5 symptoms to 4, and suddenly they don't "have" it anymore - unless and until the 5th symptom recurs!

In actual reality, he said redundantly, those people who exhibit three or four of the nine symptoms look a lot more like those folks who have five or more than they do like those folks who have none of them. Now that sounds like a "spectrum" to me.

Latuda and Bipolar Depression

Have you seen them? The brand new, direct to consumer (DTC), ads touting the drug Latuda for bipolar depression? The drug company just received the indication for this purpose from the FDA a very short time ago, but the drug company, Sunovion Pharmaceuticals Inc., was ready to roll.

Latuda is a dopamine blocking drug, which makes it an antipsychotic medication and not an antidepressant.  We have known since the 1950’s that all antipsychotic medications have some effectiveness in bipolar disorder, although primarily for the prevention of the manic phase of the illness. We have known that they also may augment an antidepressant for those who only get a partial response to the antidepressant in both unipolar and bipolar depression. A colleague of mine routinely used the antipsychotic Navane to augment the old tricyclic antidepressants in the 1970's.

Only two other antipsychotic medications have official FDA indications for bipolar depression, probably because the other drug companies did not spend the money to get it.  If doctors know one member of a class works, they’ll know that the others probably will too, so why bother?  One of these two drugs that has the bipolar indication is actually a combination drug containing an antipsychotic medication (Olanzepine [Zyprexa]) AND the antidepressant Prozac. The other is Quetiapine [Seroquel].

The main problem with using an antipsychotic instead of an antidepressant in this condition – aside from the unequivocal fact that antidepressants are way more effective – is that antipsychotics have much more potential toxicity. Latuda is probably one of the safer ones in this regard, having a low incidence of the two biggest concerns, metabolic syndrome (weight gain, higher cholesterol, diabetes - horrible and very common problems with Zyprexa and Seroquel) and the long-term neurological side effect, tardive dyskinesia.  Interestingly, the FDA won’t let Sunovion make that claim despite the fact that it’s true!  Go figure.

Almost simultaneously with the start of Latuda's DTC ad campaign, two research studies of the drug’s use in bipolar depression were published in the February 2014 issue of the flagship psychiatry journal, the American Journal of Psychiatry (AJP). The studies showed that the drug was effective by itself for the disorder, and also effective as an adjunct treatment when combined with either of the two major anti-manic drugs, lithium and valproate.  Weirdly, the  “effect size” of the improvement in patients, a measure of how much better patients got, was less (0.34) with combination therapy than it was in the case of the drug by itself (0.51). Both of these effect sizes are moderate at best, btw.

That difference is particularly odd in the case of valproate, since there is zero evidence that it is effective for the depressed stage of bipolar disorder (lithium sometimes is, but not usually). Does valproate somehow make Latuda less effective than it would be otherwise?

There is a big issue here:  the question of whether antidepressants alone are the better choice for treatment of bipolar depression.

The last author of the first AJP Latuda  study is Gary Sachs, someone I have discussed previously in this blog [ 10/31/11].  He is the author of a major study that claimed to show that antidepressants were completely ineffective – worse than placebo – in the treatment of the depressed phase of bipolar disorder.  

He conveniently neglected to point out in the earlier paper that the sample of patients he used in this study had already proved to be resistant to antidepressant medication in the first place, and continued to dissemble about this omission when I had the opportunity to confront him about it. Some subjects of his had even failed a trial of a combined antidepressant and antipsychotic. The conclusion of the study as presented in the study was bogus as hell.

A defender of Dr. Sachs made this point: Dr Sachs and colleagues in the abstract did not say that they had proven that antidepressants were ineffective in bipolar depression. They reported their finding and immediately called for additional long-term well designed studies - what I have called plausible deniability.

The more recent Latuda article which Sachs co-authored did in fact state the following: “There is limited evidence of the use of standard antidepressants for the treatment of bipolar depression.”  I guess that isn’t exactly the same as saying they don’t work, is it?  Might as well be, though! It's not what you say, it's what people hear.

Furthermore, I learned from the article that Dr. Sachs is a paid consultant for Sunovion pharmaceuticals!  

The article’s reference for the statement about antidepressants not being effective was one study that was a meta-analysis of existing studies of antidepressants in bipolar depression (a study which combines the statistics from several other studies). In an editorial in the same AJP issue publishing the Latuda studies, one R.H. Belmaker restates the opinion that “the evidence that antidepressants can be useful seems less and less convincing.”  

His reference for this statement? It is an editorial he himself wrote in the same journal as the original bogus Sachs article appeared [New England Journal of Medicine 356 (17), 4/26/07 (NEJM)]!  I went and got a copy of it.  These folks seem to all run in the same circles, as well as in the same circular reasoning.

In that editorial, he mentions the same meta-analysis that was mentioned in the AJP Sachs article.  But he also mentions that there are two other meta-analytic studies, both totally ignored in the AJP Latuda articles, that showed that antidepressants could be “highly beneficial” in bipolar depression.

There is fairly subtle obfuscation of the evidence going on here, since the other two meta-analyses never seem to be mentioned in articles touting antipsychotics for bipolar depression any more.  I wonder why that is?

In Belmaker’s original NEJM editorial, he opines that maybe the condition is heterogeneous and that subjects in studies outside of the United States may be different than they are here. The two positive metastudies were by authors from outside the USA.

Aside from the fact that there is absolutely no clinical evidence for that whatsoever, Belmaker neglects to mention that at least one of the two meta-analyses showing that antidepressants were effective did not limit itself to studies done overseas, but included studies done in the States! (I could not get a hold of the second, but this is probably also true of that one as well).

Of course, the issue of antidepressants causing bipolar patients to switch into mania is also brought up again and again ad nauseum all over the place, even though everyone agrees – even the original Sachs article in NEJM - that the anti-manic drugs like lithium and divalproate prevent this.  Since true bipolar patients should be on one of those drugs to begin with, this is a superfluous issue.

I also have my doubts that all of the subjects in the Latuda studies were even diagnosed correctly, since one of the diagnostic tools used was the Bipolarity Index, which includes the items, “Episodes with characteristic symptoms of hypomania, but symptoms, duration or intensity are subthreshold for hypomania or cyclothymia” and “baseline hyperthymic personality when not manic or depressed. " 

For a discussion of the significance of that nonsense, see my posts about treatment resistant depression and bipolar disease mongering.

These folks are doing nothing but trying to sell expensive and potentially toxic drugs to both doctors and the public when more effective and safer alternatives already exist.

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.

More Surprising Findings from the Psychiatry Literature

As we did on my posts of November 30, 2011 and October 2, 2012, it’s once again time to look over the highlights of the latest issues of my two favorite medical journals, Duh! and No Sh*t, Sherlock. 

As I pointed out in those posts, research dollars are very limited and therefore precious. Why waste good money trying to study new, cutting edge or controversial ideas that might turn out to be wrong, when we can study things that that are already thought to be true but have yet to be "proven"?  Such an approach increases the success rate of studies almost astronomically. And studies with positive results are far more likely to be published than those that come up negative.

So, we have a lot of academics weighing in with studies on the obvious. Literally weighing in. Since academic promotions are often based on the quantity of papers, rather than their quality, schools might measure faculty members' progress towards tenure by calculating the physical weight of the paper on which their authored articles have been written. 

If Albert Einstein had only published his two papers on relativity - which literally changed the entire field of physics forever - that obviously would not have been anywhere near enough for him to get tenure at most universities these days.

So here we go with more fantastic additions to our knowledge base.

 

Early Drinking Associated With Problem Drinking Later

MedPage Today (8/16, Petrochko) reports, "Students who started drinking and getting drunk at an early age were more likely to engage in frequent heavy drinking and associated problems by senior year of college," according to a study published online Aug. 15 in the journal Alcoholism: Clinical and Experimental Research. "A longitudinal analysis of incoming college freshmen showed a significant association not only between younger drinking age and heavy drinking, but also with difficulties in work and school, blackouts, vomiting, and other problems by senior year (P<0.001 for all)," researchers reported.

So self destructive behavior has its roots in childhood experiences, eh?  Someone please tell the psychoanalysts.

And on a related note:

Youth With Conduct Disorder More Likely to Abuse Substances

5/15/13.   A longitudinal study of youth with and without conduct disorder (CD) finds that the former are significantly more likely to abuse substances. The findings are published in the May Journal of the American Academy of Child and Adolescent Psychiatry. Researchers from the University of Colorado prospectively followed 1,165 community-dwelling adolescents without CD, 194 youth in the community with CD, and 268 youth who were in treatment for CD. They were re-interviewed during young adulthood, and self-reports on age of substance initiation for 10 substance classes were analyzed.

Gee, I wonder if family problems and adverse childhood environments lead to both antisocial behavior AND substance abuse? That just never occurred to me before. 

Depression, Mania In Bipolar Disorder Have Differential Social Adjustment Effects

1/23/12.  Medwire (1/23, Cowen) reports, "Results from a UK study show that depression and mania symptoms have specific and differential effects on social adjustment in patients with bipolar disorder (BD). Richard Morriss (University of Nottingham) and team found that depression symptoms have a negative effect on performance and interpersonal behavior, while mania symptoms increase interpersonal friction."

And to think that I used to be under the impression that other people would react to hyperactive, impulsive, hypersexual people in exactly the same way as they would to someone who doesn’t even want to get out of bed or have sex with someone lying naked in the bed next to them.

High Doses of Opioids May Impair Driving

Drivers taking 20 mg of morphine or more per day, or the equivalent, are up to 42% more likely to be involved in road trauma than drivers taking the lowest doses of opioids, according to a new study from the Keenan Research Center of the Li Ka Shing Knowledge Institute, St. Michael's Hospital, Toronto, Ontario, Canada.

Higher doses of intoxicants lead to more impairment than lower doses?  Who knew?

Anger Due To Delusions May Explain Violent Behavior In Patients With Psychosis

In print and in its "Well" blog, the New York Times (3/11/13) reports that "a new study finds that anger, coupled with psychotic delusions, may be the most significant factor in violence committed by people with mental illness." Medwire (3/12, Piper) reports, "Anger due to delusions appears to be a key factor explaining violent behavior in patients with acute psychosis," according to the results of the 458-patient East London First Episode Psychosis Study published online March 6 in JAMA Psychiatry.  

So people with paranoid delusions that make them feel angry or threatened are more likely to become violent than when they are not experiencing those reactions. So are such people actually psychotic if they act just like everyone else would?

Handling Stress Poorly May Increase Long-Term Risk For Anxiety/Mood Disorders

USA Today (4/4/13) reports that handling "stress poorly...may put you at greater risk for anxiety disorders and other mental health issues 10 years later," according to a study published online in the journal Psychological Science. Researchers from the University of California-Irvine "analyzed data on 711 men and women, ages 25 to 74, who were interviewed two times 10 years apart." Investigators found that "people who responded to stress with more anxiety and sadness than the average person were much more likely to have self-reported anxiety/mood disorders and psychological distress 10 years later."

Oh I get it now! Anxiety is caused by stress. That’s a remarkable insight.

And on a related note:

Association Between Mood and Alcoholism

The Los Angeles Times (5/2/13) A study that was published May 1 in JAMA Psychiatry, found that individuals "who drank 'to alleviate mood symptoms' were three times more likely to become dependent on alcohol than were those who did not use alcohol to calm themselves down or improve their mood."

And mood symptoms are also related to stress, leading to abuse of a psychoactive substance!?!  Even more remarkable.

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And we also just learned that actively trying to solve problems rather than just ignoring them is the better way to go. Now that’s counter-intuitive:

Small Study: Way Of Dealing With Emotions Linked To Anxiety Levels

The Time (5/13/14) "Healthland" blog reports, "When faced with a challenge, whether you deny the problems it poses or dive in to solve them in a positive way may determine how much anxiety you feel overall," according to research published in Emotion. The investigators "found that the participants who regularly reframed what was happening to them to view their situation in a better light reported less severe anxiety than the participants who suppressed their emotions in trying situations."

And finally, the question of whether or not the prospect of dying or of someone you love dying leads to psychological distress has at long last been settled by two recent studies.

Parents of Children with Cancer Show High Psychological Distress

5/17/13. A group of researchers associated with several pediatric oncology treatment facilities has published one of the first studies to describe the experience of distress in parents of children with advanced cancer. The researchers found that psycho­logical distress was associated with par­ent perceptions of prognosis, goals of therapy, their child's symptoms/suffer­ing, and financial hardship.

 

   Anxiety May Be Common Among Cancer Patients, Spouses

7/12/13.  The New York Times (7/12, Hoffman) “Well” blog reports that an analysis published in the Lancet Oncology indicates that “within two years of a cancer diagnosis, the pervasiveness of depression in patients and their spouses tends to drop back to roughly the same levels as in the general population, only to be replaced by another mind-demon: anxiety, which can even intensify as time passes.”