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Really though, I'm only focusing on your statement that there is are "large structural brain differences" in people with ADHD. I do not believe you are correct. I find no evidence for that in the primary literature, and what I've found basically says that any structural differences, if it does exist, must be small. Your responses also suggest that you haven't read the primary literature, nor understand the difficulties in interpreting the primary literature. (Which is entirely reasonable - it's not an easy skill to learn.)

As I pointed out in my earlier response, science journalism does a poor job of communicating science. Even the primary journals are subject to publication bias and other factors, which has lead to articles like "Why Most Published Research Findings Are False" http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1182327/ . If your information comes primarily filtered through science journalism and an occasional primary reference, then you may have an overly skewed view of the research results.

Based in what you've just written, you confirm by implication that there aren't large brain differences. If there were large differences, then ADHD would have a well characterized physical diagnosis. As you point out, it doesn't. It depends on psychological tests. You mention those tests take "multiple days and cost thousands of dollars to administer." But NMR or MRI scans do not take that much time nor cost that much, and would pick out "large structural brain differences", which tells me that there are no large structural brain differences that can be used as a diagnostic test for ADHD.

Then you mention 'the entire "ADHD isn't real" crowd'. I empathize with your frustrations, but that is a different topic. I am not a member of that crowd, nor was the primary reference which started this HN discussion saying that ADHD isn't real. Its argument is that ADHD is very likely overdiagnosed:

> Only one significant study has ever been done to try to determine how many kids have been misdiagnosed with ADHD, and it was done more than twenty years ago. It was led by Peter Jensen, now the vice-chair for psychiatry and psychology research at the Mayo Clinic, but at the time a researcher for the National Institute of Mental Health. After a study of 1,285 children, Jensen estimated that even way back then—...—between 20 and 25 percent were misdiagnosed. They had been told they had the disorder when in fact they did not.

It agrees with your statement that there are "variety of diagnostic criteria", and emphatically agrees with your earlier statement that "a 30 minute patient interview should not be the sole determining factor." It's horrible if someone isn't diagnosed as ADHD who would do better under ADHD treatment. It point is that it's also horrible if someone is misdiagnosed as ADHD and gets ADHD treatment even if it that treatment doesn't help, likely makes things worse by not getting the right treatment.

BTW, I looked for information about your [0]. See http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3028268/ , "Bipolar and ADHD Comorbidity: Both Artifact and Outgrowth of Shared Mechanisms" (2010).

> Published rates of comorbidity between pediatric bipolar disorder (PBD) and attention-deficit/hyperactivity disorder (ADHD) have been higher than would be expected if they were independent conditions, but also dramatically different across different studies. This review examines processes that could artificially create the appearance of comorbidity or substantially bias estimates of the ADHD-BPD comorbidity rate ...

(The point is that if there are dramatically different results, then that may be because of artificial biases, rather than real ones.)

See also http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3201827/ , "Pediatric bipolar spectrum disorder and ADHD: comparison and comorbidity in the LAMS clinical sample" (2012)

> "Of 707 children, 538 had ADHD, 162 had BPSD, 117 had both ADHD and BPSD, and 124 had neither. Comorbidity (16.5%) was slightly less than expected by chance (17.5%). ... The high rate of BPSD in ADHD reported by some authors may be better explained as a high rate of both disorders in child outpatient settings rather than ADHD being a risk factor for BPSD." (italics are mine)

The limited search I did of the primary literature does not seem to give the same conclusion as what you have stated. While I don't know the literature, nor the field, I will be so bold as to suggest that things you believe to be true about ADHD are actually not so well understood as you believe them to be.



> The limited search I did of the primary literature does not seem to give the same conclusion as what you have stated. While I don't know the literature, nor the field, I will be so bold as to suggest that things you believe to be true about ADHD are actually not so well understood as you believe them to be.

Again I'd encourage you to watch the linked to video. ADHD has many subtypes, co-morbidity differs based on subtype. There are some important genetic links as well.


I am asking you to tell me how you came to your conclusions, specifically that:

1) there are "large structural brain differences" between those with and without ADHD, and

2) there is a 'tragically' high co-morbidity between bipolar disorder and ADHD

The literature, as best as I could determine, says that there are no large structural differences, and there isn't a tragically high co-morbidity. I pointed you to relevant research articles which say that. It seems that you are trying to change the topic. My tentative hypothesis is that your knowledge of ADHD helps you cope with the disease, and you don't want to evaluate the possibility that some of your knowledge may be incorrect.

Rather than point to research which confirms you point (2), you now say that there are "many subtypes, co-morbidity differs based on subtype." That's a perfectly reasonable argument, but it's a different argument than your previous one. You previously wrote "ADHD's co-morbidity with bi-polar disorder is tragically high" not "co-morbitity between some subtypes of ADHD and bi-polar disorder is tragically high."

That's okay - this is HN, not peer-reviewed literature and I don't expect you do put in all of the details when you first write something. My question is only, how do you know that what you wrote is true?

You pointed me to a video. I stopped after 23 minutes into it because it was low-information content and I didn't like the speaker's style. There are no links to the primary research, no qualifiers or evidence as to the certainty of the speaker's statements, and some terms used (like "psychopathy" at 18:03) have no basis in the DSM and are only used for general public lectures. This sounded very much like someone who has a specific model of ADHD and is looking for evidence which confirms that model, rather than for evidence which break the model.

As an example, 20:45 ("just a milder variant of the combined type") combined with the further ("it's simply a group where parents confuse oppositional behavior with ADHD"). This is odd because ADHD is not diagnosed by the parents. In addition, in his paper at http://www.ncbi.nlm.nih.gov/pubmed/22179974 he uses parental input in his own research uses parental input to design a 3-part model. How does he determine when the parents are "confused" and when they are not?

I had to stop at 23:24 because the presentation was too information-poor to be interesting. I couldn't tell which were his views and which were conclusions drawn from research, and more importantly, I couldn't tell if he understood the difficulties in that research.

For example, he says sluggish cognitive tempo is an ADHD subtype (actually, in http://www.ncbi.nlm.nih.gov/pubmed/24394633 he "conjecture[s] that SCT is probably distinct from ADHD rather than being an ADHD subtype, although there is notable overlap with the ADHD predominantly inattentive and combined presentations." That detail isn't relevant for the rest of this post, but I will point out that it's equivalent to saying that ADHD is likely overdiagnosed.)

Further, at 17:17 he says that identification of co-morbitity is a simple linear test.

This goes back to your point (2) and your modification that there are several subtypes.

Did you read the http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3028268/ link I pointed out earlier? It lists 5 different ways to get false co-morbitity. Since you emphasis that "co-morbidity differs based on subtype", I refer specifically to its point (3).

> (3) Over-Splitting: Artificial Subdivision of Syndromes

> There is a long and fruitful debate between “lumpers” who favor diagnostic parsimony versus “splitters” who prefer carefully nuanced clinical description. Over-splitting would create a falsely inflated rate of comorbidity by treating multiple components of the same larger diagnostic entity as separate conditions that frequently co-occur. High rates of comorbidity thus invite questions about whether a nosological system is over-splitting.

In other words, if you add more subtypes then you would expect to see higher co-morbidity even if it were due to over-splitting, and not based on actual subtype differences.

Thus, increased co-morbitity alone can't be used to tell if a subtype exists.

But neither you nor the presenter have provided the evidence that that increased co-morbitity is anything other than a false signal. (I would also like to see evidence of the increased co-morbitity vs. subtype, but am willing to accept your word on it, because that's what I expect.)

Actually, the speaker's elision of the difficult details reminds me of this quote from http://www.madinamerica.com/2014/03/psychiatry-admits-wrong-... :

> By doing so, psychiatry allowed a “little white lie” to take hold in the public mind, which helped sell drugs and of course made it seem that psychiatry had magic bullets for psychiatric disorders. That is an astonishing betrayal of the trust that the public puts in a medical discipline; we don’t expect to be misled in such a basic way.

Is the speaker misleading me by telling a "little white lie"? I looked at the presenter's research literature. Most deals with adult ADHD, sluggish cognitive tempo, and executive function. Based on the abstracts, I see he prefers "theoretically driven .. approaches" (http://www.ncbi.nlm.nih.gov/pubmed/18295154 ), which fits my idea that prefers to fits things to a model rather than test the validity of the model first. (Models are useful, because they allow you to make predictions. Models are terrible, because they don't fit reality. This is an old debate.)

What I don't see in his research is anything about how there are "large structural brain differences" nor how there is a 'tragically' high co-morbidity between bipolar disorder and ADHD, which are the two statements you said are true about ADHD.

Again I ask that you tell me how you came to your two conclusions, since the literature seems to disagree with you and nothing you've referenced seems to actually address those points.




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