Hi Dr. Aftab: Thank you for posting this. I am hesitant to go too far back in a writer's archives, since commenting on older posts seems to invite very few, if any, responses or further discussion. I am reposting similar comments I made earlier with edits appropriate for here.
I am assuming, maybe incorrectly, that the P.S. part of the post is speaking directly to my wanting to be clear about certain aspects of one of your recent posts. I think you made it clear in the PS section for sure.
I think this post hits all the right notes. I went back and read your earlier post on Treatment Related Suicidality. I will comment on it there, and copy to notes so that it may be noticed, since it was a much older post. From my first scan of it, it looks like it significantly speaks to the right concerns, mostly because you are clearly able to formulate the right questions, among other things. In addition, it would unforgivable of me not to say "Your analysis and writing is easily in the top five of any writing by a psychiatrist that I have ever read."
My conclusions as noted below come from over 15 years of an intense dive into diagnosing and treating ADHD in adults who were trying to figure out what the heck was going on with them. A large majority of them were unevaluated for, or even apprised of, ADHD when put on SSRIs for panic, anxiety, agoraphobia, OCD, and depression, among other things.
My early observations led me to doing 3 hour evaluations of new clients, utilizing my own diagnostic evaluation checklists and insisting that new clients bring along someone who would be willing to corroborate or clarify the self reporting of the person being evaluated (a child, sibling, parent, good friend or several members of a family). I have an observational and recorded database that includes more than 300 clients. I also used a standardized method for testing working memory at baseline and during treatment, which consisted of what the literature says is the most useful, cost-effective way to assess working memory capacity -- a reverse digit span protocol.
From all of my observations, research and reading, it seems that working memory at baseline (meaning non-threat scenario) is a valid proxy for understanding what I would call the main vulnerability indicator for possible manifestation of ADHD characteristics. I use the term "free roaming dopamine" to stand for "tonic dopamine," as opposed to synaptic or phasic dopamine. Although phasic may contribute a bit to working memory capabilities, the literature is more than clear about the connection between "tonic" and working memory operations.
Threat scenarios increase tonic dopamine, and, thus, you could say "threats treat poor working memory," and thus, treats the major variable in the manifestation of ADHD characteristics. A large part of my 2013 book discusses my findings related to the "upside" of the ADHD brainset – threat response capabilities. Non-ADHDers (good working memory) aren't so good at threat response due to tonic dopamine quickly accelerating to above optimal, which degrades working memory (the upside-down U shaped curve), among other non-helpful actions.
My data showed that 90% of about 35 TRD diagnosed patients fit or did fit the criteria for the diagnosis of ADHD, but had not been evaluated or diagnosed for ADHD. Twelve of those had received a course of treatment that included a series of increasing dosages of an SSRI, then an "augmentation" medication (usually olanzepine, but also aripiprazole) and then ECT. They clearly fit the criteria for ADHD, but had never been evaluated, or even apprised of the possibility.
A similar set of percentages of undiagnosed ADHD was also found to be true with respect to patients who had been diagnosed with panic and anxiety disorders. Much larger percentages existed for undiagnosed ADHD in OCD, hoarding, AUD, SUD, binge drinking or eating, bulemia, tobacco use disorder, fibromyalgia, etc. In my book, I set out a table showing 25 different disorder types which have been studied for the co-existence of, or the missed diagnosis, of ADHD.
My experience and ongoing studies of the best ways to assess and treat adult ADHD clearly shows TRD and other "sickening" effects of missed diagnosis and mistreatment of such undiagnosed ADHD with SSRIs happens all of the time.
There are few published studies about the prevalence of undiagnosed and untreated ADHD among diagnosed anxiety disorders (including panic disorders and PTSD in a couple of studies) is around 38%. Interestingly, that is close to the same percentage of undiagnosed ADHD found in a more recent TRD study.
Biases are so programmed that docs learn to find ways around even attempting an evaluation which could lead to first line treatment with a so-called "stimulant." Clearly, the influence of what constitutes first line treatment for ADHD, a "stimulant," is a huge obstacle to considering the diagnosis. I call it "comfort-zone prescribing." Being diagnosed with ADHD carries almost no stigma these days. It has been normalized to the extent that it is now "okay." However, the first line treatments have been demonized and carry more stigma than the diagnosis, by far.
You have covered that issue in this post.
The language needs to change before docs will ever get scientific about ADHD and its treatment, rather than engage in emotional responses based on repeated misinformation based on even more biased statements from past, outdated, science. Such a nomenclature using "stimulant" (a side effect) is tantamount to categorizing ibuprofen as a "kidney damage pill."
Until the terminology changes to, let's say, "dopamine enhancers" or "norepinephrine enhancers" or "combined DA/NE enhancers," the clearly almost unalterable highly-programmed response to the term "stimulant" will rule. Not to mention how calling a category of medications "stimulant" is great advertising for encouraging diversion. I mean, come on….
Enough data exists, but clearly more studies are needed on the downside of SSRIs that decrease dopamine dependent working memory functionality. The studies exist. The observations are huge. And, why is it not being studied more intensely?
Suboptimal working memory at baseline (non-threat scenarios) is the common denominator to 90% of the downside characteristics of what we currently call ADHD.
Decreasing working memory below an already low baseline dopamine dependent working memory with an SSRI will create the perfect storm for an ongoing depression with ever more cognitive downsides as the SSRIs and antipsychotics continue the downward spiral, until? Until the patient with the undiagnosed ADHD finally receives a dopamine enhancer (TMS, ECT, ketamine).
This same perfect storm can increase suicidality in those undiagnosed for ADHD presenting as anxiety or depressive disorders. By depressing working memory and other cognitive corollaries with SSRIs, what do you get? Less able to think twice, more forgetful, distracted, more impulsive, impatient, frustrated, fuzzy, less fearful (more risk capable), in addition to likely feeling weird and sickly, not to mention the resulting loss of hope.
I am hoping that you will read my book to get most of the full story. It is still ahead of its time. I will bet good money that you will find it more than a little interesting.
Thank you again for your excellent work and best wishes. Hope we can continue to discuss.
Thank you for sharing this; this is all so fascinating! (Please, call me Awais). I just downloaded your book and look forward to reading these ideas in some detail in the coming weeks.
Do you have any thoughts on how ADHD is current conceptualized and diagnosed à la
DSM? Should we be moving towards a dimensional neuropsychological assessment of attention, working memory, and executive functioning?
On the conceptualization question. Yes. Yes. Yes. It took a book to explain what I have concluded is the correct conceptualization of what we currently call ADHD. So, will get the whole story there. For now, here's a few thoughts on your questions.
I do.
Not likely to ever happen but hoping for "disorder" to be ditched. Prefer condition or, even better, "vulnerability" so one type might be "Distractibility Vulnerability, High, with Sensory Amplification-High, Working Memory-Low, IQ-average, and WHODAS 36-item score or GAF score."
In my world, what it has boiled down to is that the actual clinically relevant variables for creating the typical characteristics of ADHD are: (1) low working memory (using reverse digit span testing and data related to reading, forgetfulness, etc.), (2) IQ (in my world WM is comparable to RAM and IQ is comparable to CPU power (speed)), thus there are folks who have very low reverse digit span but high IQ and that allows them to look like they have good working memory since they can process information fast and thus, do more with a low working memory space than an average IQ; (3) sensory sensitivity -- I call it sensory amplification. High amplification can, in and of itself, look like ADHD in terms of distractibility and staying on task, since, those folks even with good working memory get overwhelmed with above average data loads due to how much they notice stuff.
Without assessing, for instance, working memory and the characteristics of lower working memory capabilities (forgetfulness, etc.) there are folks who may have other stuff creating the perfect storm for them to exhibit ADHD characteristics, but not really fit the working memory deficit. If you try to assist such a person with dopamine enhancers, it is not going to work. I feel it is not a good idea, since working memory is a valid proxy for tonic dopamine functions.
You don't want to push dopamine to above optimal, since that has significant side effects and long term down regulation, etc.
Sensory amp needs to be assessed because dopamine enhancers and SNRIs will have effects on amplification, and thus will make it worse and then it looks like no dopamine enhancer is going to work. Increase tonic dopamine it increases tonic NE due to first step breakdown by enzymes to norepinephrine. NE, in my world is highly relevant to amplification of all sensory input. Those signals can be amplified by actions of the locus coeruleus, which, for me, turns out to be modifiable with alpha blockers. Too many vacant receptors that can become triggers when the NE becomes even more available with the enhancers. Bad enough to have more receptors triggering amplification (genetic) without adding to it.
Sensory signal amplification is much higher in some folks than others and I feel I have more than enough data to conclude that those who amplify are dealing with more alpha receptors than the next person and when more receptors get occupied either tonically or phasically, the gain goes up. High baseline gain with even higher gain when dealing with higher levels of sensory data. I discovered it is possible to change that with clonidine or guanfacine at bedtime and about 10 am, low dose for most folks... it is a longer story. But, it is very important for me, since I learned that the side effects of all dopamine enhancers and even worse for bupropion and SNRIs (Strattera) are clearly related to increased NE secondary to increased breakdown of the increased tonic dopamine from dopamine enhancers. Thus, they all give NE excess side effects in sensory sensitive folks. I found that with a co-administration of the appropriate dose of an alpha blocker changed everything, by actually turning down the volume, so to speak. Blocking the NE from triggering the surplus vacant and available receptors.
I get a little carried away discussing these things. So, I would say that in my experience, yes, assessing WM with reverse digit span (it has to be consistent and thorough, but it is simple and short) is well studied. WM, of course, is complex, so there is no perfect assessment tool, but there are effective ones that give a good enough assessment along with assessment of daily activities impacted by forgetfulness (in one ear and out the other, out of sight out of mind, lose stuff, all that).
Further testing via formalized testing seems to be over-kill and just discourages everyone since it can be expensive and time consuming for everyone involved.
IQ is easy enough to observe and test if there is a question. WM can look okay in high IQ folks, but it actually isn't, so you have to pay attention to that. How someone does in high school is not a measure of WM, but can be a measure of IQ. Some high IQ folks are stunned when they get to college and can't perform the tasks required there which are intense reading, note taking, review of notes, complex multiple choice, etc. Studies have consistently shown that good working memory is more important for post high school academic success than high IQ.
I try to not talk much about executive function. It seems to confuse rather than clarify. I think EF correlates highly to WM, including time estimation, etc. If you think of time estimation and noticing the passage of time, as dependent on working memory, you don't need a separate explanation. If you cannot mark a beginning and an end (duration) due to very little cache to hold or slow down data, you can't actually mark time, thus time sensitivity, in a very real way, depends on good working memory function. Self-regulation, for instance, is heavily tied to being able to think twice (reappraisal mechanisms) before acting. You need a place to hold a thought, if you are ever going to do important on the fly reappraisal. It doesn't matter what your training is. It is interesting to note that there is a ton of research looking at self-regulation and the DAT1 9R/9R and DRD4 4R/4R, and the 4R/7R. The DAT1 9R/9R has been called the "straight arrow" gene.
Hopefully, I am making sense. Thank you for the chance to dive deeper into these worlds.
This is another problem with medically assisted suicide.
I used to be all for it. I even thought it was obvious that we should have it. But it's because I used to buy into the lie that the value of human life is SOOOOO deeply entrenched in modern society that we naturally have a VERY strong resistance towards deliberate killing (at least in the kind of calm, cool-head atmosphere in which medical decisions are allegedly made).
But look at how much medically assisted suicide tends to expand once it's introduced. Look at all the testimonies coming from Canada, of people who's faced pressure from clinicians and care workers to "choose" death. Of people who's received the message, in no uncertain terms, that their lives aren't worth living, they should just die already.
I still think there's a strong case to be made that people should be allowed to choose, e.g., death by meds instead of death by suffocation if they have something like ALS. And I understand the argument that death by meds is better for depressed people than suicide BUT.
BUT.
Even though it's logically possible to do all we can to treat people, while also allowing them medically assisted suicide, this is not how real life works. Once a condition has been placed in the box of "if you have this, it's only rational to want to die", once clinicians regard this condition as something for which we DO have ONE treatment, namely death, that's gonna make a big difference to whether people still think it's worth the time and effort and money to find an actual treatment.
(I'm not sure what I think of Alexandre Bareil's radical ideas, but they're very different from looking at a bunch of specific conditions and go "when you've got one of THESE - and in particular if you're also poor and marginalized - it's only rational to die, would be kinda weird for you to stay alive".)
Hi Dr. Aftab: Thank you for posting this. I am hesitant to go too far back in a writer's archives, since commenting on older posts seems to invite very few, if any, responses or further discussion. I am reposting similar comments I made earlier with edits appropriate for here.
I am assuming, maybe incorrectly, that the P.S. part of the post is speaking directly to my wanting to be clear about certain aspects of one of your recent posts. I think you made it clear in the PS section for sure.
I think this post hits all the right notes. I went back and read your earlier post on Treatment Related Suicidality. I will comment on it there, and copy to notes so that it may be noticed, since it was a much older post. From my first scan of it, it looks like it significantly speaks to the right concerns, mostly because you are clearly able to formulate the right questions, among other things. In addition, it would unforgivable of me not to say "Your analysis and writing is easily in the top five of any writing by a psychiatrist that I have ever read."
My conclusions as noted below come from over 15 years of an intense dive into diagnosing and treating ADHD in adults who were trying to figure out what the heck was going on with them. A large majority of them were unevaluated for, or even apprised of, ADHD when put on SSRIs for panic, anxiety, agoraphobia, OCD, and depression, among other things.
My early observations led me to doing 3 hour evaluations of new clients, utilizing my own diagnostic evaluation checklists and insisting that new clients bring along someone who would be willing to corroborate or clarify the self reporting of the person being evaluated (a child, sibling, parent, good friend or several members of a family). I have an observational and recorded database that includes more than 300 clients. I also used a standardized method for testing working memory at baseline and during treatment, which consisted of what the literature says is the most useful, cost-effective way to assess working memory capacity -- a reverse digit span protocol.
From all of my observations, research and reading, it seems that working memory at baseline (meaning non-threat scenario) is a valid proxy for understanding what I would call the main vulnerability indicator for possible manifestation of ADHD characteristics. I use the term "free roaming dopamine" to stand for "tonic dopamine," as opposed to synaptic or phasic dopamine. Although phasic may contribute a bit to working memory capabilities, the literature is more than clear about the connection between "tonic" and working memory operations.
Threat scenarios increase tonic dopamine, and, thus, you could say "threats treat poor working memory," and thus, treats the major variable in the manifestation of ADHD characteristics. A large part of my 2013 book discusses my findings related to the "upside" of the ADHD brainset – threat response capabilities. Non-ADHDers (good working memory) aren't so good at threat response due to tonic dopamine quickly accelerating to above optimal, which degrades working memory (the upside-down U shaped curve), among other non-helpful actions.
My data showed that 90% of about 35 TRD diagnosed patients fit or did fit the criteria for the diagnosis of ADHD, but had not been evaluated or diagnosed for ADHD. Twelve of those had received a course of treatment that included a series of increasing dosages of an SSRI, then an "augmentation" medication (usually olanzepine, but also aripiprazole) and then ECT. They clearly fit the criteria for ADHD, but had never been evaluated, or even apprised of the possibility.
A similar set of percentages of undiagnosed ADHD was also found to be true with respect to patients who had been diagnosed with panic and anxiety disorders. Much larger percentages existed for undiagnosed ADHD in OCD, hoarding, AUD, SUD, binge drinking or eating, bulemia, tobacco use disorder, fibromyalgia, etc. In my book, I set out a table showing 25 different disorder types which have been studied for the co-existence of, or the missed diagnosis, of ADHD.
My experience and ongoing studies of the best ways to assess and treat adult ADHD clearly shows TRD and other "sickening" effects of missed diagnosis and mistreatment of such undiagnosed ADHD with SSRIs happens all of the time.
There are few published studies about the prevalence of undiagnosed and untreated ADHD among diagnosed anxiety disorders (including panic disorders and PTSD in a couple of studies) is around 38%. Interestingly, that is close to the same percentage of undiagnosed ADHD found in a more recent TRD study.
Biases are so programmed that docs learn to find ways around even attempting an evaluation which could lead to first line treatment with a so-called "stimulant." Clearly, the influence of what constitutes first line treatment for ADHD, a "stimulant," is a huge obstacle to considering the diagnosis. I call it "comfort-zone prescribing." Being diagnosed with ADHD carries almost no stigma these days. It has been normalized to the extent that it is now "okay." However, the first line treatments have been demonized and carry more stigma than the diagnosis, by far.
You have covered that issue in this post.
The language needs to change before docs will ever get scientific about ADHD and its treatment, rather than engage in emotional responses based on repeated misinformation based on even more biased statements from past, outdated, science. Such a nomenclature using "stimulant" (a side effect) is tantamount to categorizing ibuprofen as a "kidney damage pill."
Until the terminology changes to, let's say, "dopamine enhancers" or "norepinephrine enhancers" or "combined DA/NE enhancers," the clearly almost unalterable highly-programmed response to the term "stimulant" will rule. Not to mention how calling a category of medications "stimulant" is great advertising for encouraging diversion. I mean, come on….
Enough data exists, but clearly more studies are needed on the downside of SSRIs that decrease dopamine dependent working memory functionality. The studies exist. The observations are huge. And, why is it not being studied more intensely?
Suboptimal working memory at baseline (non-threat scenarios) is the common denominator to 90% of the downside characteristics of what we currently call ADHD.
Decreasing working memory below an already low baseline dopamine dependent working memory with an SSRI will create the perfect storm for an ongoing depression with ever more cognitive downsides as the SSRIs and antipsychotics continue the downward spiral, until? Until the patient with the undiagnosed ADHD finally receives a dopamine enhancer (TMS, ECT, ketamine).
This same perfect storm can increase suicidality in those undiagnosed for ADHD presenting as anxiety or depressive disorders. By depressing working memory and other cognitive corollaries with SSRIs, what do you get? Less able to think twice, more forgetful, distracted, more impulsive, impatient, frustrated, fuzzy, less fearful (more risk capable), in addition to likely feeling weird and sickly, not to mention the resulting loss of hope.
I am hoping that you will read my book to get most of the full story. It is still ahead of its time. I will bet good money that you will find it more than a little interesting.
Thank you again for your excellent work and best wishes. Hope we can continue to discuss.
Thank you for sharing this; this is all so fascinating! (Please, call me Awais). I just downloaded your book and look forward to reading these ideas in some detail in the coming weeks.
Do you have any thoughts on how ADHD is current conceptualized and diagnosed à la
DSM? Should we be moving towards a dimensional neuropsychological assessment of attention, working memory, and executive functioning?
Hi Awais!
On the conceptualization question. Yes. Yes. Yes. It took a book to explain what I have concluded is the correct conceptualization of what we currently call ADHD. So, will get the whole story there. For now, here's a few thoughts on your questions.
I do.
Not likely to ever happen but hoping for "disorder" to be ditched. Prefer condition or, even better, "vulnerability" so one type might be "Distractibility Vulnerability, High, with Sensory Amplification-High, Working Memory-Low, IQ-average, and WHODAS 36-item score or GAF score."
In my world, what it has boiled down to is that the actual clinically relevant variables for creating the typical characteristics of ADHD are: (1) low working memory (using reverse digit span testing and data related to reading, forgetfulness, etc.), (2) IQ (in my world WM is comparable to RAM and IQ is comparable to CPU power (speed)), thus there are folks who have very low reverse digit span but high IQ and that allows them to look like they have good working memory since they can process information fast and thus, do more with a low working memory space than an average IQ; (3) sensory sensitivity -- I call it sensory amplification. High amplification can, in and of itself, look like ADHD in terms of distractibility and staying on task, since, those folks even with good working memory get overwhelmed with above average data loads due to how much they notice stuff.
Without assessing, for instance, working memory and the characteristics of lower working memory capabilities (forgetfulness, etc.) there are folks who may have other stuff creating the perfect storm for them to exhibit ADHD characteristics, but not really fit the working memory deficit. If you try to assist such a person with dopamine enhancers, it is not going to work. I feel it is not a good idea, since working memory is a valid proxy for tonic dopamine functions.
You don't want to push dopamine to above optimal, since that has significant side effects and long term down regulation, etc.
Sensory amp needs to be assessed because dopamine enhancers and SNRIs will have effects on amplification, and thus will make it worse and then it looks like no dopamine enhancer is going to work. Increase tonic dopamine it increases tonic NE due to first step breakdown by enzymes to norepinephrine. NE, in my world is highly relevant to amplification of all sensory input. Those signals can be amplified by actions of the locus coeruleus, which, for me, turns out to be modifiable with alpha blockers. Too many vacant receptors that can become triggers when the NE becomes even more available with the enhancers. Bad enough to have more receptors triggering amplification (genetic) without adding to it.
Sensory signal amplification is much higher in some folks than others and I feel I have more than enough data to conclude that those who amplify are dealing with more alpha receptors than the next person and when more receptors get occupied either tonically or phasically, the gain goes up. High baseline gain with even higher gain when dealing with higher levels of sensory data. I discovered it is possible to change that with clonidine or guanfacine at bedtime and about 10 am, low dose for most folks... it is a longer story. But, it is very important for me, since I learned that the side effects of all dopamine enhancers and even worse for bupropion and SNRIs (Strattera) are clearly related to increased NE secondary to increased breakdown of the increased tonic dopamine from dopamine enhancers. Thus, they all give NE excess side effects in sensory sensitive folks. I found that with a co-administration of the appropriate dose of an alpha blocker changed everything, by actually turning down the volume, so to speak. Blocking the NE from triggering the surplus vacant and available receptors.
I get a little carried away discussing these things. So, I would say that in my experience, yes, assessing WM with reverse digit span (it has to be consistent and thorough, but it is simple and short) is well studied. WM, of course, is complex, so there is no perfect assessment tool, but there are effective ones that give a good enough assessment along with assessment of daily activities impacted by forgetfulness (in one ear and out the other, out of sight out of mind, lose stuff, all that).
Further testing via formalized testing seems to be over-kill and just discourages everyone since it can be expensive and time consuming for everyone involved.
IQ is easy enough to observe and test if there is a question. WM can look okay in high IQ folks, but it actually isn't, so you have to pay attention to that. How someone does in high school is not a measure of WM, but can be a measure of IQ. Some high IQ folks are stunned when they get to college and can't perform the tasks required there which are intense reading, note taking, review of notes, complex multiple choice, etc. Studies have consistently shown that good working memory is more important for post high school academic success than high IQ.
I try to not talk much about executive function. It seems to confuse rather than clarify. I think EF correlates highly to WM, including time estimation, etc. If you think of time estimation and noticing the passage of time, as dependent on working memory, you don't need a separate explanation. If you cannot mark a beginning and an end (duration) due to very little cache to hold or slow down data, you can't actually mark time, thus time sensitivity, in a very real way, depends on good working memory function. Self-regulation, for instance, is heavily tied to being able to think twice (reappraisal mechanisms) before acting. You need a place to hold a thought, if you are ever going to do important on the fly reappraisal. It doesn't matter what your training is. It is interesting to note that there is a ton of research looking at self-regulation and the DAT1 9R/9R and DRD4 4R/4R, and the 4R/7R. The DAT1 9R/9R has been called the "straight arrow" gene.
Hopefully, I am making sense. Thank you for the chance to dive deeper into these worlds.
This is another problem with medically assisted suicide.
I used to be all for it. I even thought it was obvious that we should have it. But it's because I used to buy into the lie that the value of human life is SOOOOO deeply entrenched in modern society that we naturally have a VERY strong resistance towards deliberate killing (at least in the kind of calm, cool-head atmosphere in which medical decisions are allegedly made).
But look at how much medically assisted suicide tends to expand once it's introduced. Look at all the testimonies coming from Canada, of people who's faced pressure from clinicians and care workers to "choose" death. Of people who's received the message, in no uncertain terms, that their lives aren't worth living, they should just die already.
I still think there's a strong case to be made that people should be allowed to choose, e.g., death by meds instead of death by suffocation if they have something like ALS. And I understand the argument that death by meds is better for depressed people than suicide BUT.
BUT.
Even though it's logically possible to do all we can to treat people, while also allowing them medically assisted suicide, this is not how real life works. Once a condition has been placed in the box of "if you have this, it's only rational to want to die", once clinicians regard this condition as something for which we DO have ONE treatment, namely death, that's gonna make a big difference to whether people still think it's worth the time and effort and money to find an actual treatment.
(I'm not sure what I think of Alexandre Bareil's radical ideas, but they're very different from looking at a bunch of specific conditions and go "when you've got one of THESE - and in particular if you're also poor and marginalized - it's only rational to die, would be kinda weird for you to stay alive".)