Hi: Thank you for the comments and questions! Dopamine enhancers available through prescriptions are effective for changing working memory. They are advantageous and longer acting than non-prescription dopamine enhancers (alcohol, tobacco, marijuana, cocaine, lab meth, opioids, MDMA, ketamine, eating, fidgeting, exercise, and any threat related activity, etc. My book goes deeper.)
It is unfortunate that they have been classified as stimulants when, in fact, that is almost an ancient term that took place before dopamine was well understood. Stimulation is not the intended effect. It is a side-effect of too much dopamine enhancement which can happen easily in those already have an optimal baseline working memory (optimal dopamine processes and presence).
As for "So is it really true that effectiveness greatly varies for ADHDers, or does low/no effectiveness mean that the person doesn't really have ADHD, just a condition with similar or related symptoms?
There is a ton of misunderstanding about dopamine enhancers. Prescription enhancers are, as noted, longer acting than non-prescription enhancers, and thus produce a more consistent working memory result. When no effectiveness and no side effects are taking place with what could be called "average" doses, AND a person fits the criteria for low working memory (not just the ADHD characteristics), then, yes, it may just be they require a higher dose or a different dopamine enhancer.
Here's the thing about "dopamine deficiency." It is misleading. It's is easier to say than "dopamine processes and presence." It is not a deficiency per se. Dopamine processes include manufacturing of it, storage, release, destruction (enzymes), and the distribution, density, and functionality of at least five different receptor types. That means at least 10 to the 10th variations of dopamine profiles. That's 10 billion. We have about 8 billion folks on earth.
Such a huge variation in profiles means there are those whose working memory is not affected significantly and, then, there are those whose working memory is affected. There is no really good, consistent data where certain dopamine profiles have been found that respond to specific dopamine enhancers. Thus, it is highly individual and can vary from below average to above average dosing. The most important thing is not to adjust to side effects. If side effects take place it is either the wrong medication or too much of the right one.
Metabolic dysfunction is a tricky phrase. Metabolism can means so many things. Not sure if you are talking about a particular kind of nutritional issue or not. Some of the things I mention above that are part of the dopamine system could be called metabolic (manufacturing, storage, break down).
I might expand on this later. Hope that helps. Take care, Ron
I've been wondering about a topic related to that:
They say that the effectiveness of ADHD meds greatly varies depending on the individual.
But if SAS, for example, can be a standalone condition, but often get's you diagnosed as having ADHD, it's obvious why the meds don't work in that case (as you've so clearly explained in your post).
So is it really true that effectiveness greatly varies for ADHDers, or does low/no effectiveness mean that the person doesn't really have ADHD, just a condition with similar or related symptoms?
On another note, I also heard that ADHD appears to be closely related to some kind of metabolic dysfunction, and some theorize this might not be a symptom, but a cause of disregulations in the ADHD brain...
Though I have no clue whether that's a realistic hypothesis or just alternative bs, as I'm just an inofficially diagnosed ADHDer without any scientific background.
Thank you Ruminations! I am impressed, honestly, that you already adopted the lingo SAS. It helps for me to know that my language choices fit the data. Depending on how sensory amplified things are, sometimes the dopamine enhancer, alone, may be just fine. The individuality of all brains, including those with only slightly poor working memory or those with excellent working memory is the thing to keep in mind. Given the major dopamine gene variables (at least 10) means 10 to the 10th different brainsets. That's more than the current population of earth. And, obviously, there are way more than 10 controlling variables involved in thousands of organic brain operations.
The key to diagnosing and differentiating whether a dopamine enhancer (called stimulants, unfortunately) is whether it improves working memory capacity (the key). If working memory gets worse on meds, even if there are no side-effects, that likely means other dopamine enhancers would not be helpful and further investigation is not warranted.
One important problematic myth is "if methylphenidate is not helpful, it means you don't fit the criteria for ADHD." That is very misleading. If you show poor working memory and it affects reading, staying on task, distractible, impulsive, forgetful, etc. then it is very rare that a correct dopamine enhancer cannot be found. However, that means your doc and you have to be patient and thorough.
In my clinical practice, quite often we would be down to the last test of a dopamine enhancer before we found the right one. Methylphenidate seems to be the right one for about 70% of those who fit the criteria for ADHD. The remaining 30% will end up utilizing one of the other enhancers.
And, yes, that means that Adderall and Vyvanse may often be misprescribed due to miseducation on the proper protocols for finding the right medication. It doesn't take long to find the right one, even you have to go through the whole list. However, all of this is in an ideal world. A correct treatment world. Unfortunately, some meds are stigmatized and controlled so much that they become unavailable or very expensive. This situation means that suboptimal treatment is being forced on folks due to factors beyond the docs control. It is fortunate that methylphenidate is not so stigmatized or unavailable. International guidelines suggest methylphenidate as first line choice for seeking the correct medication.
One way to keep this in mind is say "Adderral is Not-For-All." It is a significant problem that such a practice protocol would still be around suggesting an amphetamine as a first line med choice. It boils down to about 15% using Adderall and 10% using Vyvanse, 5% using dexmethylphenidate, etc., and 60 to 70% using methylphenidate. I can't give you all details in this one reply, but, I will be spotlighting the proper protocols for finding, maintaining, and tracking the effects of medications.
As for SAS, it is imperative that you do a proper inventory of sensory sensitivities. There are detailed questionnaires for that and I will be writing about the questionnaire I developed very soon. More than you might expect, in my clinical practice we had to address the SAS before the ADHD dopamine enhancer trials, since it became clear that those with SAS were not going to even be able to find the right dopamine enhancer due to how much all dopamine enhancers can create increased sensory problems.
I developed a protocol for that which I will write about soon which turned out to be slam-dunk. It is too complicated to explain here, but I will give you a hint. SAS can be altered by "turning down amplification" of sensory input by the locus coeruleus. The LC is not talked about in the mainstream as much as it is published about in the medical literature. Its amplification of signals relates to norepinephrine processes that are both phasic and tonic (baseline neutral to baseline overamped).
All dopamine enhancers will affect norepinephrine functions. It just so happens that two well-known norepinephrine modifiers, clonidine and guanfacine, can turn down the amplification allowing for less noise, more noise tolerance, less distractions, better (less fragmented) sleep, less touch and texture sensitive, etc. Once that amplification (loudness of all sensory systems - sound, vision (light, certain patterns), etc., touch, pain, vibration, smell, taste, was deamplified the norepinephrine side effects of dopamine enhancers would be minimized so that the correct medication could be discovered and utilized. I hope that makes sense. It is a lot of information that needs to be communicated. Please hang around for more details as I get this substack up to speed.
Hi: Thank you for the comments and questions! Dopamine enhancers available through prescriptions are effective for changing working memory. They are advantageous and longer acting than non-prescription dopamine enhancers (alcohol, tobacco, marijuana, cocaine, lab meth, opioids, MDMA, ketamine, eating, fidgeting, exercise, and any threat related activity, etc. My book goes deeper.)
It is unfortunate that they have been classified as stimulants when, in fact, that is almost an ancient term that took place before dopamine was well understood. Stimulation is not the intended effect. It is a side-effect of too much dopamine enhancement which can happen easily in those already have an optimal baseline working memory (optimal dopamine processes and presence).
As for "So is it really true that effectiveness greatly varies for ADHDers, or does low/no effectiveness mean that the person doesn't really have ADHD, just a condition with similar or related symptoms?
There is a ton of misunderstanding about dopamine enhancers. Prescription enhancers are, as noted, longer acting than non-prescription enhancers, and thus produce a more consistent working memory result. When no effectiveness and no side effects are taking place with what could be called "average" doses, AND a person fits the criteria for low working memory (not just the ADHD characteristics), then, yes, it may just be they require a higher dose or a different dopamine enhancer.
Here's the thing about "dopamine deficiency." It is misleading. It's is easier to say than "dopamine processes and presence." It is not a deficiency per se. Dopamine processes include manufacturing of it, storage, release, destruction (enzymes), and the distribution, density, and functionality of at least five different receptor types. That means at least 10 to the 10th variations of dopamine profiles. That's 10 billion. We have about 8 billion folks on earth.
Such a huge variation in profiles means there are those whose working memory is not affected significantly and, then, there are those whose working memory is affected. There is no really good, consistent data where certain dopamine profiles have been found that respond to specific dopamine enhancers. Thus, it is highly individual and can vary from below average to above average dosing. The most important thing is not to adjust to side effects. If side effects take place it is either the wrong medication or too much of the right one.
Metabolic dysfunction is a tricky phrase. Metabolism can means so many things. Not sure if you are talking about a particular kind of nutritional issue or not. Some of the things I mention above that are part of the dopamine system could be called metabolic (manufacturing, storage, break down).
I might expand on this later. Hope that helps. Take care, Ron
I've been wondering about a topic related to that:
They say that the effectiveness of ADHD meds greatly varies depending on the individual.
But if SAS, for example, can be a standalone condition, but often get's you diagnosed as having ADHD, it's obvious why the meds don't work in that case (as you've so clearly explained in your post).
So is it really true that effectiveness greatly varies for ADHDers, or does low/no effectiveness mean that the person doesn't really have ADHD, just a condition with similar or related symptoms?
On another note, I also heard that ADHD appears to be closely related to some kind of metabolic dysfunction, and some theorize this might not be a symptom, but a cause of disregulations in the ADHD brain...
Though I have no clue whether that's a realistic hypothesis or just alternative bs, as I'm just an inofficially diagnosed ADHDer without any scientific background.
Thank you Ruminations! I am impressed, honestly, that you already adopted the lingo SAS. It helps for me to know that my language choices fit the data. Depending on how sensory amplified things are, sometimes the dopamine enhancer, alone, may be just fine. The individuality of all brains, including those with only slightly poor working memory or those with excellent working memory is the thing to keep in mind. Given the major dopamine gene variables (at least 10) means 10 to the 10th different brainsets. That's more than the current population of earth. And, obviously, there are way more than 10 controlling variables involved in thousands of organic brain operations.
The key to diagnosing and differentiating whether a dopamine enhancer (called stimulants, unfortunately) is whether it improves working memory capacity (the key). If working memory gets worse on meds, even if there are no side-effects, that likely means other dopamine enhancers would not be helpful and further investigation is not warranted.
One important problematic myth is "if methylphenidate is not helpful, it means you don't fit the criteria for ADHD." That is very misleading. If you show poor working memory and it affects reading, staying on task, distractible, impulsive, forgetful, etc. then it is very rare that a correct dopamine enhancer cannot be found. However, that means your doc and you have to be patient and thorough.
In my clinical practice, quite often we would be down to the last test of a dopamine enhancer before we found the right one. Methylphenidate seems to be the right one for about 70% of those who fit the criteria for ADHD. The remaining 30% will end up utilizing one of the other enhancers.
And, yes, that means that Adderall and Vyvanse may often be misprescribed due to miseducation on the proper protocols for finding the right medication. It doesn't take long to find the right one, even you have to go through the whole list. However, all of this is in an ideal world. A correct treatment world. Unfortunately, some meds are stigmatized and controlled so much that they become unavailable or very expensive. This situation means that suboptimal treatment is being forced on folks due to factors beyond the docs control. It is fortunate that methylphenidate is not so stigmatized or unavailable. International guidelines suggest methylphenidate as first line choice for seeking the correct medication.
One way to keep this in mind is say "Adderral is Not-For-All." It is a significant problem that such a practice protocol would still be around suggesting an amphetamine as a first line med choice. It boils down to about 15% using Adderall and 10% using Vyvanse, 5% using dexmethylphenidate, etc., and 60 to 70% using methylphenidate. I can't give you all details in this one reply, but, I will be spotlighting the proper protocols for finding, maintaining, and tracking the effects of medications.
As for SAS, it is imperative that you do a proper inventory of sensory sensitivities. There are detailed questionnaires for that and I will be writing about the questionnaire I developed very soon. More than you might expect, in my clinical practice we had to address the SAS before the ADHD dopamine enhancer trials, since it became clear that those with SAS were not going to even be able to find the right dopamine enhancer due to how much all dopamine enhancers can create increased sensory problems.
I developed a protocol for that which I will write about soon which turned out to be slam-dunk. It is too complicated to explain here, but I will give you a hint. SAS can be altered by "turning down amplification" of sensory input by the locus coeruleus. The LC is not talked about in the mainstream as much as it is published about in the medical literature. Its amplification of signals relates to norepinephrine processes that are both phasic and tonic (baseline neutral to baseline overamped).
All dopamine enhancers will affect norepinephrine functions. It just so happens that two well-known norepinephrine modifiers, clonidine and guanfacine, can turn down the amplification allowing for less noise, more noise tolerance, less distractions, better (less fragmented) sleep, less touch and texture sensitive, etc. Once that amplification (loudness of all sensory systems - sound, vision (light, certain patterns), etc., touch, pain, vibration, smell, taste, was deamplified the norepinephrine side effects of dopamine enhancers would be minimized so that the correct medication could be discovered and utilized. I hope that makes sense. It is a lot of information that needs to be communicated. Please hang around for more details as I get this substack up to speed.