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Other older drugs that have been around a surprisingly long time include the recently introduced citalopram which was one of the very first of two or three serotonin reuptake inhibitor antidepressants that was used in Europe from the late 1970s. Fluvoxamine and LuVox has been around a long time even though it came to this country rather recently is paroxetine and sertraline and so on.
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Then among some of the older variable drugs clomipramine or Anafranil is a largely serotonin reuptake inhibitor but again a classic tertiary amine tricyclic that interacts with norepinephrine uptake, is very anticholinergic. Very anticholinergic, produces a lot of sedation, confusional effects, autonomic problems. It’s a tough drug for people to take in the real world in adequate doses and it’s unfortunate because it’s a very effective antidepressant and a marvelous antidepressant, anti-obsessional drug. Perhaps the best but realistically not easy to take.

Venlafaxine is the first, I suppose, along with clomipramine of this new concept of mixing deliberately serotonin and norepinephrine reuptake properties although as I understand it, the in vivo pharmacology of venlafaxine effects are it is mainly a serotonin reuptake inhibitor with a little bit of norepinephrine effect at higher doses. But I wouldn’t make an enormous amount of that and I tend to look on it as basically a serotonin inhibitor. It’s become a very popular agent in this area as an alternative when other antidepressants are failing. Basically this class of drugs tends to be more similar than different in terms of overall efficacy of targets of opportunity. That is among anxiety disorders as well as major depression
and so it’s useful to sort of think of them, at least for overview purposes, as kind of a cluster of drugs that really have many similarities and not terribly major differences.
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There is yet another group of antidepressants we can consider sort of atypical or otherwise unusual compounds. They include the drug bupropion, Wellbutrin which is a mild stimulant. It looks a bit like methamphetamine structurally and shares with the amphetamines a number of stimulant-like properties. It tends to reduce appetite and sleep and it can produce agitation sometimes. It may be useful in attention disorders for some kids although probably not as good as other alternatives.
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Its pharmacology continues to be a bit elusive. It seems to have active metabolites. They seem to interact with both dopamine and norepinephrine systems and the activity of both neurotransmitters.
In the middle there are these complicated named drugs found with piperazine, the triazolones. They include trazodone, nefazodone. These drugs, again, have subtle and complicated pharmacology. Most of it probably involves facilitating serotonin transmission by direct or indirect means. They are both, at least, modest to weak serotonin reuptake inhibitors, nefazodone having the edge on that property and they also interact with autoreceptors in the adrenergic systems which.

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 The group of tricyclic antidepressants fall into two major subcategories. There is a group that chemically have terminal amino groups with three carbons attached – that is, a tertiary amine group – and then there are derivatives that are formed in the body by hepatic oxidative metabolism to P-alkylate – this terminal amino group – to make secondary derivatives that have only two carbons attached. This includes drugs like desipramine, Nortriptyline and then there are still others that are developed primarily as secondary amine antidepressant drugs in their own right that are not necessarily derived from their precursors by body metabolism. This would include drugs like protriptyline.
Amoxapine is a curious drug to put in this category. It’s actually the end of demethylated derivative of loxapine, the classic neuroleptic. It shouldn’t surprise you if I tell you that I have seen cases of tardive dyskinesia in persons maintained for long periods on amoxapine and I think that’s something to be quite concerned about. Amoxapine has some mixed and central antidopamine neuroleptic-like activity as well as blocking norepinephrine uptake and elevating serotonin.
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The reason for splitting the two categories this way is that the tertiary amine group tend to be much dirtier, more complicated drugs pharmacologically. They interact not only with norepinephrine systems but also variably with serotonin reuptake. So they are in a sense mixed norepinephrine serotonin reuptake. Recently there’s the trendy term is now SNRIs or what have you and there are drugs under development and in clinical trials that are deliberately mixing norepinephrine serotonin properties without some of the disadvantages that come from other properties of these drugs that include antihistaminic sedative properties, anticholinergic autonomic side effect producing properties and most ominously, direct cardiac inhibitory effects that slow down the repolarization and conduction parameters in the EKG and on acute overdose can lead to fatal ventricular arrhythmia cardiac arrest. These older drugs and their secondaries have that property as well, have been very popular drugs for self destructive purposes in acute overdoses.
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The secondary amine group are considerably less anticholinergic, much less antihistaminic and are relatively selective for the noradrenergic system in the brain and have much less serotonin activity. In fact, desimformate, for example, was one of the most norepinephrine selective of uptake inhibitors that we have.
More recently, the whole field of depression antidepressant therapeutics has been revolutionized by the introduction of the serotonin reuptake inhibitor group – the SRI or the SSRI group of drugs. The first really successful one clinically and commercially was cheap Prozac or fluoxetine. You’ll notice that fluoxetine is the uricemic mixture of the plus and minus and antimeres.

Theory.
The enforced program of exercise and sweating with niacin-induced cutaneous vasodilation is believed to mobilize fat-soluble “toxic chemicals,” presumably into the circulation, where they are excreted. The oil ingestion is to prevent reabsorption of chemicals through the normal enterohepatic recirculation. The “essential oils” are believed to allow toxic substances mobilized into the gut to be excreted from the colon, but some toxic material is believed to be excreted also through sweat.
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Studies of Effectiveness.
All reports up to now by proponents of this detoxification procedure are anecdotal. Results are measured by the patient’s self-report of symptomatic improvement. Placebo effect, proper diet, elimination of unnecessary medications, exercise, and adequate sleep therefore have not been ruled out as the reason for subjective improvement.
Conclusion.
The form of “detoxification” described above has yet to be proved effective for treatment of allergy, IEI, drug addiction, or any other illness. The ability of the procedure to remove chemicals from fat has not been proved. The theory of immunotoxicity as a cause of allergic disease is contrary to accumulated scientific experimentation. The potential dangers of this program have not yet been adequately evaluated.

Homeopathy is both a philosophy and an alternative medical practice. The theory that “like cures like” is translated into the administration of exceedingly minute quantities of substances believed to cause disease as a method of curing the disease. The substances are called “remedies” and usually consist of dilutions of various natural extracts. The exceedingly small quantities used for treatment are prepared by serial dilution of extracts through the violent shaking of a container of diluted extract. The remedies are given orally. Extracts of plants and of animal organs, particularly endocrine glands such as the adrenal cortex, thyroid, thymus, pancreas, and spleen, are commonly used. Patients will sometimes take as many as 50 different extracts daily. The theory proposes that disease is cured by induction of immunity.
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In common with other practitioners of alternative disease treatment, homeopathists claim to cure numerous diseases, including all forms of allergy.

On theoretical grounds, it is most unlikely that the exceedingly minute quantities of material ingested would have any therapeutic effect. There are no clinical studies showing efficacy for homeopathy in allergy or in any medical disease. Although the materials used for treatment are unstandardized, adverse effects are unlikely because of the small amount of material to which the patient is exposed. The real dangers are psychologic dependence and delay in the institution of effective therapy.
Detoxification
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In recent years numerous “detoxification centers” have been established for treatment of drug addiction. More recently chemical detoxification has been recommended by a small group of practitioners to remove undesirable chemicals from patients believed to have IEI, based on the concept that the sensitivity is caused by toxic effects of low-level synthetic chemicals in the body.

The Procedure
Treatment consists of several steps. Aerobic physical exercise is performed for 20 to 30 minutes, followed immediately by forced sweating in a sauna at 140° to 180° F for 2½ to 5 hours and then physical exercise, a cooling shower, and additional exercise. Niacin is then given in increasing doses to produce a flush. Water and salts of sodium, potassium, calcium, magnesium, and other minerals are prescribed to correct for water and salt depletion from sweating. Polyunsaturated oils (a mixture of soybean, walnut, peanut, and safflower oils, which are said to be essential) are consumed orally. A planned schedule of balanced meals and adequate sleep is recommended, along with avoidance of medications and alcohol. Cialis soft tabs mastercard.
The routine described above is repeated daily, usually for 30 days.

Benzodiazepine tachyphylaxis: that’s a good one. Conventional, classic Board wisdom, the sleep tachyphylaxis happens very quickly, like in 2-6 weeks. First of all, why do we have 25 benzodiazepines, do we really need that many in the American market? In my opinion, the answer is no. You can order prozac 10 mg at our canadian pharmacy shop. They are all very similar. There are differences in how quickly they are absorbed. There are differences in the different sub-units. But by and large, there is a lot of similarity. Some of them though, I will admit, there are some genuine differences in that if they have a rapid onset of action they are better for sleep. A good example is triazolam, Halcion. That drug happens so fast, the onset is so fast, that you really can’t stay awake on it. I think it’s a lot of experiences of people, they will be sitting there drinking a glass of milk with their Halcion and they will fall asleep in their milk. They won’t even make it to bed. Contrast that with something like Clonopin which you can take at 8 o’clock in the morning and not fall asleep.  Why is that? I’ll tell you. With a lot of benzodiazepines what’s happening is this; you are getting a tachyphylaxis to the sleep after 4-6 weeks, but how come you still use it for sleep after three years? I’ll tell you why. Ativan, you take that at 4 o’clock. Do you feel sleepy? No, but you feel very relaxed. What happens if you take it at 12 ‘o clock? It doesn’t put you out like a Mickey Finn, but what happens is this: you are lying awake in bed, you are all wired up. You are thinking about the days events, about tomorrow. Suddenly you take that Ativan and you are very relaxed and sleep takes over naturally. So I think what happens is that it is still useful for sleep, even though the hypnotic effects have tachyphylaxis-ed out, is tolerated out. The sedative effects are still there and as a result people use it for sleep. The sedative and panic attacks seem to stay on long after the hypnotic effects are gone. Now with respect to the muscle relaxing effects, I can’t speak to.
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Ritalin is a very paradoxical drug. Remember the story of how Ritalin was discovered; there was a state hospital where you had all these problem kids, conduct disordered kids. A lot of them had ADD. The director of the hospital said, “All of these kids are going to get very comprehensive medical exams.” And what he did was he gave these kids very comprehensive medical exams, including a lumbar tap. Now neurologists, tell me; what’s one of the side effects of a lumbar tap? Headache. So he was a very humane guy and he said, “These kids are getting headaches, what can we do?” Give them something to speed up their metabolism that will replace the cerebrospinal fluid and that way they won’t have the headaches. Did it work? No. But what happened was that those kids who were taking the Ritalin felt different and what happened is the teacher at the institution said, “What are you giving these kids? This is the first time these kids can actually sit in a seat and learn.” And the kids started calling them “math pills”. Why? Because they had the cognitive ability to do math suddenly? No, it was because the could suddenly concentrate for the first time. Paradoxical discovery. Remember, some things work different in kids. Barbiturates is another classic example. You give those to an adult and you are like, snoring. You give it to a kid and they are bouncing off the ceiling. Same thing with diphenhydramine, Benadryl. Some of you parents have probably seen that in your own kid, the paradoxical reaction.
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Side effects: reduced appetite, insomnia, palpitations, possibly suppressed growth. I don’t know about that one. That’s a controversial one too. Can have withdrawal symptoms, weight gain, fatigue and depression. Pemoline, we talked about liver problems. What else can you use for ADHD? TCA’s, that was the old standard if you didn’t want to give a substance abuse user Ritalin. Bupropion and clonidine have been used with some success. You know, everything in the world has been tried. The SSRI’s, you know canadian Prozac and those drugs, they use those for everything in the world but it doesn’t seem to show much efficacy for ADHD. At the same time, if you ever look in a textbook, what have they tried for ADHD? Everything. I mean there is an open label study supporting everything. And I’ll tell you something. I think a lot of parents out there are giving their kids caffeine. They are giving their kids coffee to try to calm them down. And it does work for some kids. It’s a stimulant.
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Electroconvulsive therapy: let’s just talk for a minute about ECT. Used now generally for depression only. It has been used for mania, it has been used for schizophrenia, but for schizophrenia it takes like 20 treatments and they relapse anyway. Has been used for Parkinson’s. Does anybody have any experience with that? Yeah, so the future is up in the air. Classic absolute contraindication is brain tumor, space-occupying mass. If they ask you, “What is the absolute contraindication to ECT, electroconvulsive therapy?” there are two answers. One is none; there is no absolute contraindication. Another answer is the strongest relative contraindication is brain tumor. What happens is that during a seizure intracranial pressure rises and you’ve got this so-called “brain-in-a-bone-box” and there’s only one escape, which is to herniate. So for that reason you kind of avoid ECT with people with brain tumors. But you can use it if you are careful in people with cardiac problems. They have used it in pregnancy. In the old days when the only alternative was tricyclic antidepressants, it was thought that actually ECT was safer than tricyclics for a developing fetus. Atropine is used in ECT to prevent bradycardia. The anesthesia people also like it because it dries up secretions. I don’t think you really need to know this, but just to look at it. Lithium should be reduced or stopped prior to ECT. This is because, one, it can add to the cognitive side effects of ECT and it can also prolong seizures. And finally, it can prolong the effects of succinylcholine which they use during ECT.
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All right, before we finish up – and I’m going to see how much we can get into the next section – any questions about what we’ve talked about so far?

ADD, to a lot of people’s way of thinking, is simultaneously very over-diagnosed and simultaneously under-diagnosed. There is a lot of thought that kids are over-diagnosed and adults are under-diagnosed. What it is is you start out, you have ADD symptoms by the time you are like three, four, five-years old. And when you are an adolescent you are at a fork in the road. You are either go on to normalcy or you are going to go on to adult ADD. What do you do for those people? It’s probably treated the same way. There’s probably no difference. The exception, for the Boards, is if they are a substance abuser you want to stay away from the stimulants if you can and try something else. Like I say, venlafaxine, Wellbutrin SR online, and probably the TCA’s. I don’t know about the use of clonidine in adults.