“Adder-not-for-all”

(The more scientific name for Adderall)

In my experience, if you fit the criteria for ADD, Ritalin (methylphenidate) is a “slam-dunk” solution about 70% of the time. When I say “slam-dunk,” I mean no significant side-effects at an effectively high dose and fixes or is neutral with respect to any pre-existing sleep problems. About 30% of the time it is not a slam-dunk. If you are in the 30% group, it can take more time to find the right medication. I have not been able to find any valid research that reports the percentages of different medications being used by people for their diagnosis of ADD.

In my experience, there is a large percentage of mis-medication taking place with ADD medications.

In addition, I have not been able to find any scientific literature on the clear downside of Adderall (mixed salts of amphetamine). In my opinion, this medication could be a poster child for “bad science.” What is the clear downside of Adderall, you ask? It is a medication that contains two distinctly different chemicals with very different effects.

Clearly, different medications work for different people. You can read more about that in my book — “Adult ADD Factbook,” at Amazon. Since Adderall is a combination of two very different amphetamines (dextroamphetamine, a short-acting medication, and l-amphetamine, a longer-acting medication), one might be correct for you, and the other might not. In other words, doctors should be asking patients whether or not they are experiencing a period of time with Adderall where it seems optimal and then “turns bad” or was “bad” at the beginning of the duration of the dose, but got better later during the duration of the dose.

If there is a “biphasic” effect of Adderall, where the first three hours or so seem to give more optimal results than the last two or three hours, it should be discontinued and the next trial of medication should be with a single-chemical drug, such as dextroamphetamine. By about three hours into the duration of Adderall, the dextroamphetamine “effect” of the pill is gone and the effects of Adderall during the last couple of hours of its duration are primarily due to the long-acting l-amphetamine in Adderall. [1]

Is it ever true that the long-acting l-amphetamine found in Adderall is actually the correct medication for someone, and the short-acting amphetamine (dextroamphetamine) is not? Yes, it is true, and, that scenario can be problematic.

Generally, if optimal results with no significant side-effects are obtained from the l-amphetamine in Adderall, it will be clearly noticeable in the last two to three hours of the duration of the dose. This may be one of the most controversial aspects of treating ADD with typical ADD medications — the l-amphetamine in Adderall has not existed as a standalone medication since Smith Kline & French discontinued marketing it in 1982 and Lannett Company Inc. ceased marketing it in 1994. Technically, it is still not available, but possibly it has found a home. First, the FDA approved Independence Pharms to manufacture amphetamine sulfate (late 2011) [2] and then Independence never got off the ground. Since August 9, 2012, it appears that Arbor Pharmaceuticals has FDA permission to manufacture. Don’t hold your breath! However, on another note, Arbor Pharmaceuticals is marketing an immediate release dextroamphetamine called Zenzedi, which is manufactured in several dosage sizes between 2.5 mg and 30 mg. [3]

The only currently available medication that comes close to the actions of the l-amphetamine found in Adderall is pharmaceutical methamphetamine (Desoxyn), which is technically dextromethamphetamine. Although FDA guidelines state that it has a shorter half life than both of the amphetamines found in Adderall, anecdotally, patients often report long-acting results.

There seems to be no argument in the scientific community that pharmaceutical methamphetamine is the most powerful dopamine “stimulator” available for the treatment of dopamine dysfunction. However, there is no scientifically-valid research substantiating that conclusion. From my clinical experience, I can tell you this about pharmaceutical methamphetamine: Only about 2% of the ADD population has such severe suboptimal dopamine function that methamphetamine will be helpful without producing above-optimal dopamine side effects.

As you might expect, when a patient is presented with the reality that the only medication out of the currently-available medications that fixes just about everything about their low-working memory, including improving sleep onset and quality of sleep, with no significant side-effects, turns out to be methamphetamine, it can be a psychological challenge due to the constant and widely distributed information about the dangers of illicit methamphetamine.

Unfortunately, the scientific community appears to be rather intimidated about even discussing the use of pharmaceutical methamphetamine for the treatment of ADD. For instance, the most recent, university-leader rich, 326-page compendium of Adult ADHD science published in mid-2011 by Cambridge University Press does not even mention methamphetamine as a treatment medication for ADD, but does mention it as a drug of abuse. [4] Similarly, the National Library of Medicine medication website, MedlinePlus, does not describe its positive, FDA-approved use for the treatment of ADD. Fortunately, at least one national scientific organization, the National Institute of Mental Health, gives appropriate scientific attention to methamphetamine (Desoxyn) for the treatment of ADD. [5]

In my opinion, there are way too many ADDers being treated incorrectly with Adderall who think that the side effects of the Adderall are just part of the treatment protocol. The frequent side effects of the long-acting amphetamine in Adderall are over-stimulation — feeling weird, fuzzy, and experiencing muscle tension, headache, “a crash,” or sleep impairment. Please note: Starting on an extended release form of Adderall is even worse science, since it would be nearly impossible to detect which chemical in the Adderall might be incorrect, since they will be working together or against each other during the exact same period of time. In that regard, if one of the components of Adderall is targeting an already dopamine-optimized part or function in your prefrontal cortex (PFC) and Threat Monitor Center (TMC), it will push such functions to above optimal, which will significantly contribute to side-effects and the production of tolerance and withdrawal.

Side effects are almost always the same if you are taking the incorrect ADD medication or too much of the correct medication — above-optimal dopamine side effects. Although there is no perfect understanding of why one dopamine enhancing medication will work for one person without side effects and make another person quite sick, it appears to be that different medications are targeting different parts of the dopamine-bridge system. If you fit the criteria for the diagnosis of ADD and a dopamine-optimizing medication creates side-effects at average doses, it is likely targeting the dopamine functions in your system that are already working just fine, instead of targeting the parts of the system that may not be working so well. Since we don’t have enough data on what medications work best for what dopamine problems, there is no way to predict which medication may the correct one for any ADDer, even if you knew their dopamine genes profile.

Medications which can make significant differences in an ADD person’s life include Ritalin (methylphenidate), Focalin (dexmethylphenidate), Adderall (mixed salts of dextroamphetamine and amphetamine — two categories and four chemicals in one tablet), Dexedrine (dextroamphetamine), Zenzedi (dextroamphetamine), Desoxyn (methamphetamine), Vyvanse (lisdexamfetamine), Strattera (atomoxetine), Provigil (modafinil), Wellbutrin (bupropion), Catapres (clonidine), Tenex (guanfacine) and, sometimes, a mood stabilizer such as Lamictal (lamotrigine).

ADD medications for optimizing working memory are almost always dopamine enhancers. They have similar final effects of raising extra-cellular levels or increasing cellular synthesis of dopamine but their unique mechanisms for obtaining those results are still not completely understood. [6] [7] [8] [9] [10] [11] [12] [13] [14] [15] [16] [17]

There is some evidence that SPECT scans can help predict correct medication strategies, but the expense of such a scan is far greater than aggressively pursuing appropriate trials of the useful medications and deciding which medication is the most helpful. [18] [19]

“Evidence-based guidelines agree that each patient is unique, and individual treatment strategies should be sought.” [20] ADD medications are clearly not interchangeable, and the scientific community needs to do some serious research to more firmly document this fact. To do otherwise is to doom ADDers to the continuing legacy of “one size fits all” mistreatment.

_______________________________