I already knew about SJW and SS/SNRIs but not amphetamine. I’ll stop SJW for a while and see if anything changes, thanks.
Was it mainly an energy or focus or motivation problem or something else?
How did your mood change as a result of Adderall? You must have had intrusive/obsessive thoughts during your depression, how did Adderall affect those, if at all?
Did it change how much pleasure you got from things other than food and sleep?
So, my Rx says 20mg/day for 14 days and if that isn’t enough, 30mg for 14 days and if that isn’t enough, 40mg.
I got to two weeks without significant side effects and without enough benefit. Got bumped up to 30mg. I renewed the Rx over the phone and someone picked up the Rx for me. They made a mistake and gave me 30 30mg. My Rx says that in 14 days, it gets possibly bumped up with 14 40mg or if not, 14 30mg.
In your experience, when a drug store makes a mistake like that, what’s likely to happen in 14 days?
In my experience, any error or discrepancy with ADHD meds means you have to deal with insurance companies being a royal pain in your ass. I’m frankly surprised that the pharmacy was able to give you more pills than your prescription specified, due to this hassle.
But also based on my experience, my doctor would probably ask me to hold onto the extra 30 mg pills for the future, and get me another prescription for the 14-day 40 mg. (As you say, it’s 40 mg if 30 mg isn’t enough, which it may well be for you.)
If I were you, I’d call your pharmacy and inform them of the error, and then contact your doctor.
I’m in Canada so perhaps that explains why there were less hassles from the insurance entity. What surprises me is that they would hand out what is essentially speed without making sure they’re giving the right amount. Over here it’s a Schedule I drug, all the way up there with heroine and cocaine.
In your experience, what would happen if no one was informed of the mistake until 14 days from now when I go back to possibly up the dose?
Same here except I’m on Provigil instead of Nuvigil. Back in 1998, Provigil was easy to get but incredibly expensive ($5 per pill). Ritalin was a pain to get, but very cheap. So I stayed away from Provigil for years. It took forever for them to create a generic, but it’s available now. So I find the generic provigil much easier to get filled than the Ritalin.
I find I have a headache after a Provigil dose for an hour or so. But I suppose I can just look at it as a reminder to take the Aleve for my arthritis.
It really isn’t (just) a patent play. Dextro-rotary forms of psychostimulants, including methylphenidate, do seem to do a better job at inhibiting the dopamine and norepinephrine reuptake transporters than their levo-rotary racemic images, such that you can effectively take someone on 10mg of methylphenidate and substitute for 5mg of dexmethylphenidate for about equal results. There are those that claim this results in fewer side effects, though I’ve not come across any head-to-head comparison studies to validate this as anything more than anecdotal.
Adderall (and it’s XR formulation) is more correctly a 3:1 ratio of differing amphetamine salts, with 1 part being a levo-amphetamine salt for every 3 parts of a dextro-amphetamine salt. It likewise is not (mostly) a patent play, as the levo-rotary form of amphetamine has a longer half life (~11-14 hours, iirc, in adults) than it’s dextro-rotary form (~9-12 hours in adults), which may explain why more patients get 6 hours of benefit from it in controlled studies (though these studies are usually based on teacher/parent rated observation scales of a child’s behavior and NOT on how well the patient themselves thinks they are concentrating/doing) versus straight dextroamphetamine sulfate (~4 hours of coverage). It’s also worth noting that several references, including Stahl’s Essential Psychopharmacology, Goodman and Gilman’s Pharmacologic Basis of Therapeutics, and Solanto’s Stimulant Drugs and ADHD: Basic and Clinical Neuroscience all state that levo-rotary amphetamine may have greater peripheral noradrenergic activity (thus greater risk of high blood pressure, heart rate, and muscle tremor) than the dextro-rotary form (which appears to be more balanced in it’s effects on DAT, NET, and VMAT2, the latter of which is not effected by methylphenidate). This, like the difference between dexmethylphenidate and racemic methylphenidate is debated as to how much clinical relevance it may actually play, but there is some basis to suggest a possible difference.
I should also point out that while at one point, it was thought that cleavage of the lysine group from the dextroamphetamine group of Vyvanse was a function of gut enzymes, more recent studies (and now the new labeling, seen here, section 12.3) suggest that this cleavage occurs in red blood cells, which does a much better job of explaining why food alters concentration-versus-time curves of lisdexamfetamine (the parent drug) while not doing so with the metabolite dextroamphetamine it is broken down into.
It’s used, but extremely rarely. It’s one of those we’ve tried every other treatment (or several combinations), so let’s throw this at the wall and see if it sticks sort of drugs.
Depends where you live. Here in Ohio, where Physician Assistants and Nurse Practitioners can write for C-II’s, in addition to the generalist and specialist MD/DO’s, the prescribers have no problems putting people, including those who have several relative or absolute contraindications, on the schedule II psychostimulants in all sorts of crazy doses and interacting combinations, at least where I practice (we try, believe me, to get them to see reason–it usually doesn’t work).
Strattera, on the other hand, has a problem that most of the other ADHD meds don’t face–it takes time to work and it is brand only, so it is wickedly expensive. If it were only as expensive as, say, Vyvanse, or Concerta, it might get more traction, but because it takes weeks for full effect, people (especially those who have already tried the more rapid acting stimulants), tend to write it off too quickly, which is too bad because as a NET-only inhibitor, it’s working where most of the symptomatology of ADHD is suspected to come from (the prefrontal cortex, in which dopamine and norepinephrine reuptake is largely subserved by the Norepinephrine transporter, NOT the dopamine transporter, versus the vental striatum/Nucleus Accumbens, where DAT plays a much larger role in the removal of dopamine from the synaptic space, and this latter region is the region most frequently attached (along with the amygdala) with addiction, which is why Strattera is not controlled–it doesn’t effect the “addiction” part of the brain.
This is mostly true. Individuals with ADHD are believed to have underactive release/function of dopamine and/or norepinephrine in the prefrontal cortex, the part of the brain most often associated with control of executive functions and working memory. Dopamine, by activating D1 receptors on dendrites of cortical pyramidal neurons, results in the opening of HCN-cation channels which shunt the signal out of the neuron before it gets beyond the dendrite, thus reducing noise, if it’s functioning properly. If too little dopamine is being released or too few D1 receptors exist, noise doesn’t get filtered properly. Likewise, norepinephrine, acting on post-synaptic alpha-2a receptors, does the opposite, closing the HCN-cation channels, allowing a signal to propagate. Too little norepinephrine or too few alpha-2a receptors, and you get a weak signal. Combine the two and you get the bottom of what’s been termed the inverted-U for ADHD treatment.
Strattera, guanfacine (specifically by agonizing post-synaptic alpha-2a receptors), clonidine (more generalized alpha-2 receptor agonist than guanfacine), and the psychostimulants all result in an increase in either/both DA and NE in the synaptic (and extrasynaptic) space in parts of the prefrontal cortex which improves noise reduction via D1 while also improving signal propagation via alpha-2a–up to a point. Push too far, however, and you start to move past the top of the inverted U and start to have symptoms of cognitive dysfunction begin to appear again–symptoms which are often mistaken for tolerance and the need for more medication. A savvy prescriber is going to start you relatively low and take you up very slowly to get you to a dose-regimen which keeps you near the top of your inverted U when you need it while interfering as little as possible with sleep and anxiety.
In individuals who are well and truly ADHD, the risk of addiction to the C-II psychostimulants, when taken orally, is functionally nil. Several studies, in fact, show a protective effect on future drug abuse/addiction when kids/adolescents are diagnosed and started on psychostimulants. Unfortunately, the data we have so far does not necessarily extend to adulthood, though I suspect that the risk is still lower as long as the patient in question is using their medication as prescribed and their prescriber isn’t doing something wonky with how they are prescribing the drug. In individuals who are not ADHD but are using them for a “cognitive” advantage (as happens frequently in college but also in the business world), the risk goes up since “normal” people don’t have the underlying pathophysiology that those with ADHD do, and the risk goes even higher when switched from oral to insufflated, to injected/smoked. Basically, if your prescriber knows what they are doing and are sure the diagnosis of ADHD is correct, addiction to psychostimulants should NOT be a patient concern (though we are still at risk for other addictions, per some research).
I’m not aware of methylphenidate absorbing sublingually, though it’s lipophilic enough to be plausible, but if your doctor told you to take it orally, I’d swallow it whole with a small amount of beverage, not dissolve it under your tongue. Faster spikes (assuming methylphenidate does absorb sublingually) are associated with enhancing what we would call phasic dopaminergic transmission in the “addiction” areas of the brain, which isn’t necessarily good (and which is why snorting, smoking, and injecting are more likely to produce addictive behaviors). Slow, oral administration, on the other hand only briefly and mildly (at least per the Stahl and Solanto texts referenced earlier) enhances phasic DA transmission while providing longer lasting tonic DA transmission which appears to be far more beneficial to those of us with ADHD.
As for the preference for Vyvanse, it’s probably because it’s the the most abuse-deterrent form of any C-II psychostimulant we’ve discovered (due to the enzyme-rate-limiting cleavage of l-lysine from the dextroamphetamine molecule) coupled with a very slow and gentle rise to it’s maximum dextroamphetamine concentration (3.5-4 hours roughly), meaning it generally works longer than many other forms of long-acting stimulants, with the long-acting portion of other agents (Adderall XR, Concerta, etc) being easier to break for an intense immediate release rush.
A large part of this is suspected to be because studies done on rats/mice have generally been done using intraperitoneal or intravenous administrations, whereas in humans, oral forms are preferred for a number of reasons. The faster the dopamine rise, the greater the chance of triggering a neurotoxic event, which is unlikely with orally administered agents.
Great info JayRx1981 could you go into more detail about the “symptoms of cognitive dysfunction” that are often mistaken for tolerance?
Also - what’s your opinion of using using Seroquel for the treatment of treatment resistant depression in someone with virtually life long dysthymia with reoccurring bouts of unipolar mdd (of which virtually every class of approved drug for unipolar depression has been tried - as well as adjunctive drugs like ability, lithium, valproate whatchamacallit, etc - and only MAOIs and stimulants have been effective)?
The psychiatrist seems to think there is reason to hope for (and again it is being used for something anyway) possible “repair” (my words not his) of the “damage” - again my words - that tolerance has caused to a dopamine related system in the brain. Says there is nor proof it will work, but there is reason to believe it could.
Does this sound plausible at all?
It would be life changing if I could get Ritalin to work for more than two days every five years or so.
Sorry for the late reply. Worked my first 80 hour week last week. Considering a mistake can potentially maim or kill someone, I figured I should wait to answer.
First, ADHD treatment follows an inverted U pattern (or mountain pattern). Too little drug, and you are easily distracted with poor signal (NE at post-synaptic alpha-2a receptors) and poor noise suppression (weak DA signaling at post synaptic D1 receptors). You’re on one side of the mountain.
Too much and you quiet signals that should probably have gone through (too much D1 signal “shunting”) while rapidly re-assessing what’s important in your enviroment to the point that you again look easily distracted (neurons releasing NE involved in detecting what are known as salient stimuli work too well and…well…almost everything becomes salient, not to mention the effects on alpha-1 and beta receptors which muddle with working memory). You’re on the other side of the mountain (inverted U).
Likwise, too little noise suppression and you have someone wake up in the middle of the night with noisy mental chatter keeping them from sleep (again, plausibly D1 related)–I call them my chattering monkeys. They make noise. Some of it makes sense. None of it makes sense if you put it together, but damned if you can’t get them to shut up. One side of the mountain. On the other hand, too much NE release/in the synapse can fundamentally mess with the sleep/wake cycle, so too much drugs lands you on the other the side of the mountain.
You, I hope, see what I’m getting at. Both sides (too little or too much) cause similar (but not the exact causes for the same) symptoms. Whether it’s being distractable, or insomniatic, or the quest for "New and Shiny™, you can underdo it or overdo it with psychostimulants, particularly with amphetamine. But if your prescriber isn’t savvy enough to ask the right questions, you might already be over the mountain top and further dose increases may only make things worse (particularly in the long run). And going over the the mountain often adds in the fun of rapid heart rate, high blood pressure, and anxiety among other possibilities.
Without giving too much hope, yes there is some plausibility to the use of Quetiapine as an augmenting agent in treatment resistant mdd. Of all of the atypical antipsychotics (not to say you are psychotic, mind), Quetiapine is our drug of choice when we need to least likely to negatively mess with dopamine transmission in certain brain circuits (Parkinson’s Disease and Lewy Body dementia spring to mind). It has partial agonist properties at some serotonin receptors which are thought to enhance dopamine release in certain brain regions, antagonist properties at others which do the same for dopamine and norepinephrine in the prefrontal cortex, and is one of the weaker D2/D3 antagonists in the striatum of the atypicals, so it’s less likely to cause extrapyramidal symptoms or neuroleptic malignant syndrome.
It does come with it’s costs. Being both an H1-antagonist and a 5HT-2c antagonist together seem to increase weight gain and metabolic disturbances. H1 antagonism also tends to beget sedation. Being an alpha-1 antagonist may result in sedation and too low of blood pressure. Being anticholinergic can further contribute to sedation, confusion, falls, and dizziness. It has a relatively short half life, so dosing twice a day is often necessary unless you use the brand only XR form (expensive). However, there is some suggestion that adding on lower doses at bedtime (when you’re out cold anyways) may improve sleep and depression, even at doses much lower than needed for indicated purposes (bipolar I, schizophrenia).
While my current Rx is 30mg of Vyvanse, I did experiment with 60mg and even 90mg. I guess I felt a little better than when I took 30mg.
Whatever the dose, I have noticed a higher heart rate but a lower systolic blood pressure while the diastolic pressure is pretty much the same.
It still cuts my hunger but a lot less than it used to.
I’ve not been feeling badly as a result though, either physically or psychologically.
It’s strange, even after a full night’s rest, I can take 30mg of Vyvanse at 8AM and take a nap at 2PM.
I can take 300mg of Effexor, 30mg of Vyvanse, 2000mg of St John’s Wort and 8 ounces of espresso in a day and I just get a higher heart rate that doesn’t bother me. If anything, it often makes me feel serene and present.
What is ADHD-treatment-related anxiety like? After taking the drug, you just feel anxious for no reason? Something else?
Jay, if you wish to emit an opinion, I understand you’re not a doctor, not my pharmacist, valid where void, for entertainment purposes only etc.
Too fast a dose increase, though not unreasonable (from a patient perspective) if you were started on 30mg capsules. Typically, labeling and guidelines like to see at most an increase of 10-20mg every week. As for feeling better on the higher doses, 30mg may be too low for you. We use it as the starting dose and go from there. 10mg and 20mg capsules now exist to help with this (though, of course, adding these on to a current 30mg prescription may require additional documentation/prior auth with the insurance). One of the most important things to remember with amphetamine based drugs is to titrate slowly. Dextroamphetamine (which Vyvanse converts into) has a half-life of around 9-11 hours in healthy adult individuals with normal urine pH, so it takes some time (~3-5 half-lives–27-55 hours) to reach steady state to give you a good idea of how the drug is going to make you feel at that dose longer term.
How high a heart rate and low a systolic blood pressure? At any rate compensatory responses, would be my guess, but I am not a physician and cardiovascular dynamics is NOT my forte (working nights, I get mostly antibiotics, steroids, and drugs of abuse as prescriptions), so follow up with your doctor if you are concerned. My understanding is that eventually things will usually even out.
Welcome to amphetamines (and phentermine, and bupropion) as weight loss. Lots of weight loss at first, due to increased synaptic DA and NE near the cell bodies of certain POMC (pro-opiomelanocortin) neurons causing them to fire more frequently, but eventually, a feedback loop in these feed/appetite suppressing neurons in part of the brain (the arcuate nucleus of the hypothalamus) results in the appetite suppressing neurons (POMC neurons) feeding back onto themselves in a negative feedback loop, releasing opiates (endorphins) to tune down the activity of the feed suppressing POMC neurons. Thus, you start out losing weight with amphetamine like drugs, but eventually plateau or even gain the weight back. We already have one treatment to get around this, in the form of a combination drug called Contrave, which combines bupropion (pretty weak as far as weight loss goes on it’s own) with naltrexone (to block the negative opiate feedback loop) to slightly enhance weight loss. Of course, said combo could interfere when the patient is/must also use systemic opioid therapy, so not really a great option in pain patients in whom you are trying to get to lose weight. It also doesn’t produce that much weight loss over bupropion alone, iirc.
We do have another option, though, in the form of Qsymia, which combines lower doses of topiramate (a drug used frequently for seizures and migraine prophylaxis among many other uses) with lower doses of phentermine. Like above, phentermine enhances appetite suppressive pathways, but this time, topiramate acts to enhance GABA suppression of appetite promoting neurons (Neuropeptide Y, Agouti-related peptide neurons with cell bodies also originating in the arcuate nucleus) and blunt/block Glutamate excitation of those same neurons. Thus, you block appetite promotion, while enhancing appetite suppression. Win-win, right! Until you consider some of topirimate’s other side effects like blocking glutamate elsewhere in the the brain and some of the cognitive dysfunction and sedation it can bring to the table. Again, lower doses in a controlled release form are used to blunt this, but it still is enough to get many people to stop taking the drug due to side effects (not to mention the ~$300 cost which most insurances don’t cover). It does seem to produce close to (if not the most) weight loss of all weight loss pharmacotherapy. Me? I’ll stick to exercise and trying to control calories in/out. (We’ll ignore a third oral option for weight loss for now, Belviq).
Back when I was on Vyvanse, specifically first put on Vyvanse, I went home, took a pill thinking it would give me a boost of energy, only to find myself waking up 4 hours later. I was so tired from years of poor sleep (the chattering monkeys, mentioned above) that the quieting in my brain finally allowed me to sleep. This was, according to my then psychiatrist, not unusual in his experience, especially in adults, on starting doses.
Your situation might not be exactly the same, but it does sound like the 30mg dose isn’t working long enough for you to get you through the day (~6 hours, when we should ideally be getting 12-14 with Vyvanse). You may want to talk to your doctor at your next visit to see about increasing your dose (rough rule of thumb is for every 10mg increase, you get ~2 more hours of coverage, so eventually, you may titrate to 60mg or even the max labeled 70mg dose). Just do it slowly, giving yourself at least a week, if not 2 to see how you do on each new dose.
As a general point to all ADHD patients: Just remember, the point of this is to move you towards “normal”, not make you cognitively superior (despite what college students, in particular, think, these drugs really aren’t really cognitive enhancers (though yes, they do enhance some aspects of cognitive function in certain controlled studies) without some underlying pathology like ADHD or Narcolepsy or even just terrible sleep habits). Even while on psychostimulants, if you’re not getting enough sleep, eating well enough, or possibly not exercising enough, you might find your meds don’t work as well. This is not an indication you need more meds, it’s an indication you need to take a good hard look at sleep, diet, and exercise. To quote Stahl, “The cure for sleep deprivation is sleep, not drugs.” I’d hold the same to be true for diet and exercise.
I’m with others earlier in the thread. Drop/taper down the St John’s Wort. Very little evidence it does good (if any at all), too many drug interactions, and may be contributing to risk of serotonin syndrome. You’re already getting a pretty decent amount of serotonin reuptake from Venlafaxine (Effexor) at your dosage and it’s primary metabolite (Desvenlafaxine, which also adds a little bit more NET blockage to the mix compared to the parent drug), so that the SJW really shouldn’t be necessary and may in fact be contributing to your elevated heart rate.
Elevated startle reflex, rapid heart rate, excessive sweating, excessive worry, panic attacks, insomnia–basically symptoms of anxiety which didn’t exist prior to starting (or increasing the doses of) psychostimulant drugs. Comorbid ADHD and Anxiety can be tricky to treat, since benzodiazepines are frequently some of the first drugs prescribers reach for (they do work fast and well, at least initially), but psychostimulants don’t fully counter the negative effects of benzodiazepines (and in some areas augment each other) and vice-versa. SSRI/SRNI/TCA’s in combination with psychostimulants can increase risk of elevated heart rate and blood pressure as well as temporarily worsen symptoms of anxiety. Sometimes, a drug like extended-release guanfacine or Strattera are used instead or to augment stimulant therapy to reduce drug-induced anxiety. Stahl, of Essential Psychopharmacology, argues that extreme anxiety or agitation (shchizophrenia or Bipolar mania as two additional examples) is pretty much a contraindication for psychostimulants altogether and that reliance on anti-anxiety antidepressants (SSRI/SNRI/TCA) and ADHD adjuncts (Guanfacine ER and Atomoxetine) may be the treatment of choice in comorbid severe anxiety and ADHD.
Humorously, I am a doctor. Just not an MD or DO or Ph.D. I jokingly refer to my doctorate as the fake one, the Pharm.D. I just really enjoy reading about how psychopharmacology, addiction, and the brain works, and so go way beyond what most of my colleagues do in reading/learning this stuff.
Well, Doc, I recently created a thread in which I asked if the Strattera samples I was given should have started working in the 3.5 hours between taking the first one and the moment my brain went quiet. I still suspect that was self-delusion, but I liked it. Not the chills, shorter temper, and heavy heartbeats that seemed to accompany it, though. Didn’t matter; it was a one-week sample bottle and they are long gone and the effects wore off a couple days later.
What I currently take for depression and OCD is 60mg of Prozac, plus Singulair and an albuteral inhaler for my lungs, OTC sinus pills for my allergic coughing, a large morning-into-noon coffee for my caffeine, and 100mg of Trazodone and a Benadryl to switch me off at night.
In the past I was given Tenuate to lose weight. Worked for three months, but I enjoyed its “false sense of well-being.” Bupropion, either by itself or with Prozac, did nothing. Effexor didn’t work as well as Prozac, which doesn’t work all that well, but keeps me duct taped together. Effexor is also not on the WalMart $4 list, which is a consideration. Neither is 60mg Prozac, but 20mg and 40mg are, so I take two pills.
I’m 61 and very fat. My BP is high-normal and untreated. I have always had balance issues since a series of inner-ear infections as a child, but since cracking my skull in a fall while very drunk (I’m sober now for 3.5 years) it’s worse. I was taking the same drugs before, during, and after my drinking period, so I’m slow to blame them for my current dizziness. I would like to get my ADHD treated, but so many of the drugs have increased BP and dizziness as side effects and that gives me pause, because a stroke or fall may not kill me outright and I don’t want to leave my family with another invalid AND a bigger financial mess.
Because so many of the drugs in this thread are based on amphetamines, should I just skip the middleman and take up crystal meth? I like speed, and I could sell it on the side for extra money. If it didn’t kill me outright, a shoot-out with other dealers should fix that right up. Seems like a win-win!
Okay, the last paragraph wasn’t entirely serious, but I trust pharmacists to know more about meds than MDs do, so I’m interested in your thoughts.
Concerta (slow release Ritalin, as far as I understand it) 36 mg/day here. Just lurking…
I suppose this should probably go without saying but I am not your doctor or pharmacist. Consult with either/both before following any advice listed below. Lawyers, have these warnings ever actually done any good?
Most of my experience with Strattera comes from patient report, Strattera’s labeling, and the experiences of Dr’s like Stahl (lead author of Essential Psychopharmacology) and to a lesser extent from other authors. I probably need to go back on an ADHD med myself (caffeine no longer cutting it, won’t even think about nicotine patches/e-cigs), so once I find a doctor, I might suggest trying it to see how I do (I already know how I responded to Vyvanse and Adderall), if only for the anecdotal experience.
In your other thread you mention a couple of things. One, you said your doctor gave you samples for 60mg of Strattera. You say you’re a big guy, but that shouldn’t matter (so far as currently understood) with adults with ADHD. Starting dose in adults is 40mg for Strattera (pretty much the rule of thumb if we’re doing it correctly with all ADHD medication is to start a low (but usually not the lowest) dose to see if it alleviates all of or most of your symptoms, or titrate up until we get as close to that point as we can or start causing intolerable side effects and/or exceed max studied doses).
Second, yes, it is possible to have a response that quickly. The maximum concentration occurs anywhere between 1-3 hours after taking, depending on if it’s taken with food or not (no food = shorter time to max concentration). It’s somewhat unusual for a single dose to produce a response, IME, but certainly possible.
Meanwhile the labeling for Strattera reports that chills occured in 3% of studied patients vs 0% in placebo, irritability (my interpretation of your “shorter temper”) in 5% vs 3% reported, and generally those go away upon taking the drug for a prolonged period of time.
Atomoxetine is broken down via an enzyme system known as cytochrome 2D6. Fluoxetine is an extensive inhibitor of this system. Put the two together, and you potentially extend it’s half-life, (from 5 hours to 25 hours), AUC (a way we measure how much exposure to a drug you’ve had), and Cmax (max concentration) and Css (concentration at steady state), and many of the side effects you experienced could have been caused by the higher than normal Prozac dose interfering with a higher than normal starting dose of Strattera. The combination can take an extensive metabolizer of strattera and make their blood levels look like those of a poor metabolizer.
The labeling also suggests that while albuterol given systemically may increase heart rate and blood pressure, this does not appear to be the case with inhaled Beta-2 agonists like albuterol, and I couldn’t tell you what if any drug interactions might occur with an “OTC Sinus Pill” so if you can find the active ingredient(s), that might help (hint: if it has phenylephrine in it, my view is that it’s worthless as a decongestent anyways and possibly can make ADHD symptoms worse by working as an alpha-1 agonist in the prefrontal cortex, which for ADHD, is not generally a good thing, as hypothesized/derived from mouse/monkey models).
Finally, Trazodone and Benadryl are largely just duplicating their mechanisms of sedation–they both block Histamine-1 receptors, which produces drowsiness. Trazodone also has some alpha-1 antagonism which may actually be useful were you to continue the Strattera as a small number of men have reported urinary difficulties on Strattera which may be relieved by alpha-1-antagonists, as well as positively affecting (bringing down) blood pressure, while Benadryl has anti-cholinergic side effects which can cause dizziness and cloud thinking. I’d think dropping the benadryl and upping the Trazodone slightly might be a better choice (or switching the benadryl to a second generation antihistamine like Zyrtec, Allegra, or Claritin, if all day allergy relief is needed)
I had to look Tenuate up. I don’t honestly think I’ve ever dispensed it. Essentially, like buproprion, it’s a cathinone–related to a plant called Khat (and is generically named diethylpropion), schedule IV like other weight loss agents (phentermine), and functions by increasing release of serotonin, dopamine, and norepinephrine into the synaptic space–so basically what you are describing is amphetamine-like, just in a slightly different way. Short term weight loss (6-12 weeks) and false sense of well-being (euphoria). Buproprion is a much weaker cathinone, so usually doesn’t produce that much weight loss to begin with and Prozac is a 5HT-2c antagonist, which unfortunately contributes to weight gain, especially in the presence oh H-1 antagonists (or so it has been observed). Between the interaction with the Strattera and the possible weight gain from the Prozac, you may want to consider switching to a different SSRI (Sertraline/Zoloft, for example, functions as an SSRI as well as a very mild dopamine transporter inhibitor, and is officially labelled for both MDD or OCD, and might off label help with ADHD, though again, while not as strong an inhibitor at 2D6 as Prozac, can mess with Strattera levels if that route is pursued.)
While pretty much all of the ADHD meds (except for ER Clonidine and ER Guanfacine, to my knowledge) can increase Heart rate and BP, the reality is that the doses necessary to do so to a clinically appreciable degree tend to run on the high end. If your psych is willing to work with you, low doses of ADHD meds could be tried to see if they have any adverse effects on your BP and very slowly titrated up to effect if you seem to be doing ok. High BP is only a relative concern for psychostimulants, not an absolute no-no, provided we are being very cautious.
I know you’re only joking, but definitely don’t do this (especially the selling or shoot-out part–I’m told they aren’t nearly as lucrative or dramatic as cinema would have us believe). There IS a legal (Schedule II) form of methamphetamine available if other ADHD treatments fail, but most docs, even the well-practiced psychs are generally hesitant to use it. Heck, MAOIs are used more frequently and people are scared half to death of them (even though they actually make for pretty decent antidepressants, as long as one is observant of the food and drug restrictions. If your doc *REALLY *knows what he/she is doing, you can even carefully combine an MAOI with certain tricyclic/tetracyclic agents for an even better response).
I’ll finish with some pharmacists know more than some MD/DO’s do, but the inverse is also true. Finding a good one of either/both can be the trick.
I used “Doc” because traditionally pharmacists were as close to a doctor most people went, so they were traditionally called “Doctor.” It’s a practice I picked up long ago, but a pharmacist I called for work corrected me and said that while new pharmacists in his state needed doctorates, he was grandfathered in. Also, y’all know more about drugs. I’ve had doctors who didn’t know more about some drugs than what they read on WebMD.
I hate Albuteral because it makes my symptoms worse after a while. I preferred Primatine and am thinking of trying that new OTC epinephrine inhaler. Dr warned me against it because of the BP, but I’d like to breathe. Anyway, I let others take fake adrenaline like amphetamines, but I’m hard core and will go to the font of all that’s good and speedy. 
I used to call Tenuate Pretend-you-ate because for that 60-90 days it works real well making you forget to eat. But then stops cold. Weird.
“There IS a legal (Schedule II) form of methamphetamine available if other ADHD treatments fail, but most docs, even the well-practiced psychs are generally hesitant to use it.” Sheee-it, in my day GPs threw speed around like candy. Oh, for the Good Ol’ Days! Nancy Reagan told us to “just say no,” but I’m a member of the “just say yes” generation.
I was actually started on 20mg capsules for 2 weeks. Then 30mg for 2 more weeks. 40mg now.
I was surprised at how easy it was to get the doses increased. I pretty much just had to say over the phone that it wasn’t working enough and that I wasn’t getting major side effects. I could have been gnawing on the bones of my last victim while wearing my favorite clown costume for all they knew.
So it would be wise to wait about half a week between dosage increases? I mean, wise for some hypothetical third person in some hypothetical situation since you aren’t providing medical advice.
I intend to wait a whole week between dose increases anyway. It turns out the drug store really did make a mistake and provided me with 16 capsules of 30mg above what the Rx required. What kind of trouble could the employee/pharmacist/drug store get into for that? As I said upthread, up here in Canada, amphetamine is in the Schedule I club where it hangs out with the bad neighborhood boys like cocaine and heroin.
Normal heart rate: 80s. Heart rate on Vyvanse can go from 100 to 130.
Normal systolic pressure: 120. Systolic pressure on Vyvanse: 100-110
Diastolic stays in the 80s, no major change.
I am also getting paresthesia in the lower legs when I crossed them more than I used to. This may be due to the weather getting colder or my cat taking a liking to lying in my lap while my legs are crossed.
Ooh, please tell about that. Or publish a tell-all book: The seedy underbelly of night pharmacy : )
If someone does have sufficient diet, sleep and exercise and takes this sort of drugs without having an underlying pathology, what can be expected? More of an academic point for me but I’m still curious.
Right. I started tapering down yesterday.
Can you make sense of the following: I take the SNRI and the amphetamine first thing in the morning. Then, for the first 6-8 hours of the day, I feel quite well, I can focus easily, I have high energy and motivation while still feeling calm and posed. After those first 6-8 hours though, I get increasing amounts of intrusive thoughts, sadness and anxiety such that I’m not really able to do much. It’s as difficult to get stuff done, focus, feel motivated or generally enjoy things as it would be while, say, hearing children or animals getting abused.
About meth: While illegal meth is neurotoxic, is this only because of the shoddy production process or is pharmaceutical meth also neurotoxic?
It appears to be a dose-related phenomenom. That street meth is cut with some shady stuff probably doesn’t help, while I imagine a high enough dose of any amphetamine would be capable of killing dopaminergic neurons.
I’m not ignoring your other questions, btw, I’m just going through some shit right now and don’t have the the time to accurately read and answer to the best of my ability.
So, on the 19th, my Rx was upgraded.
300mg Effexor ER, 60mg Vyvanse and some Abilify.
Anyone have experience with Abilify?
Also, Wiki says: (Venlafaxine - Wikipedia)
“At low doses (<150 mg/day), it acts only on serotonergic transmission. At moderate doses (>150 mg/day), it acts on serotonergic and noradrenergic systems, whereas at high doses (>300 mg/day), it also affects dopaminergic neurotransmission.”
How much do the effects on serotonin with dosage? If I understand correctly, norepinephrine is subject to a threshold effect so how do dosage and norepinephrine scale?
It also says “>300mg/day”. What kind of threshold effect are we talking about?
Does that mean that the effect on dopamine is insignificant at 300mg/day? Or was the Wiki badly written and it should read “=>300mg/day”?