** Nope. Although antidepressants are associated with increased energy soon after they’re prescribed, their anti-depression properties are not observed until several weeks after treatment begins.
** Prescribing antidepressants to people who desire to kill themselves without watching them carefully IS considered dangerous: the gap between the energy activation and the antidepressant activation can mean that the patients still want to die, and now have enough energy to do so. Sufficiently severely depressed people are actually less of a suicide risk, since they often can’t summon the will to die.
** No, they’re not effective antidepressants at all. There are plenty of ways to keep a more-or-less constant level of cocaine in the body, and plenty of amphetamines that have sufficiently long half-lives.
or if you would like a more scholarly cite wrt to dopamine and norepinephrine -here
I think there are a lot of people who are waiting for some evidence to back up the stuff you are posting here with regard to mental illness. Anyone can pull figures out of the air and pontificate with apparent authority, but no one will take you seriously, unless they have a personal axe to grind themselves, until you produce some evidence for all your assertations.
People have tried using amphetamines and cocaine as antidepressants. They don’t work well – specifically, although they make people feel great, they don’t counteract the symptoms associated with depression. Amphetamines make people more excited and more energetic, but they don’t stop depression at all.
No one is certain how bupropion hydrochlorine actually works, as even the website for the drug itself states. It seems to be a serotonin receptor agonist – as cocaine is a dopamine receptor agonist – but the nature of its effects isn’t understood.
“Antidepressants” are a group of drugs with many different biochemical methods of action. Their one commonality is that they have been observed to reduce depression.
Cocaine is not an antidepressant. Nor are the amphetamines. Not all stimulants are effective antidepressants – most of them aren’t, actually.
The biogenic amine theories were debunked decades ago. Welcome to the 21st century.
Humor me. Give me a cite that shows how biogenic amine theories have been debunked. I’m assuming by biogenic amine theories you mean the theory that depression is related to the function of these amines.
When it became clear that although artifically lowering people’s levels of certain amines did indeed mess with their minds, it didn’t induce depression, schizophrenia, or the anxiety disorders, it necessarily followed that simple deficiencies in those chemicals were not responsible for those conditions.
It’s possible to “induce” simulated thyroid problems, and diabetes, and so on, but the attempts to artificially induce conditions like depression failed miserably.
Although I reached the same general conclusion as Valenstein did long before I read his book, I find that it’s a great resource. Go find Blaming the Brain and actually think about the theses therein. Valenstein isn’t zealous, unthinking, or ideological, and he makes an excellent introduction to the topic.
In reference to The Vorlan Ambassador’s Aide’s claims regarding placebo effects of medication in depression:
I’ve also read otherwise, and would be interested to see that list, or especially if you have access to any on-line professional literature regarding this question. According to the linked article:
**However, I’ve not reviewed the study in question personally, so I can’t vouch for its contents.
Likewise, I would be interested to see some evidential backing for your claims regarding this question, TVAA.
Hmm. All I have at hand are a copy of Valenstein and some of my old psychiatric textbooks. I have some access to online journals – let’s see if I can’t dig up some primary sources for you.
Mr. Svinlesha I can certainly provide you with references to online articles, but you would need to be subscribed to the relevant databases or have access to them via a university library. As you have posted evidence to support TVAA’s position on this from the Washington Post rather than any on-line professional journal, perhaps you don’t.
I suggest you type “psychotherapy” and “pharmacotherapy” into the search engine on the Psycinfo database and you will get ample evidence on the roles of both these therapies compared to placebos. If you are genuinely interested in viewing the references, I believe my email is in my profile here
Well, I don’t have access to online databases, but I do have access to a university library. My problem is the volume of material – I’m juggling quite a few priorities at the moment. I was hoping you could help me out by pointing to a couple general surveys or reviews of the current research results, especially anything pertaining to the effectiveness of anti-depressives vís-a-vís placebo effects, etc. I should be able to find most of the journals at the library.
Also, I’m wondering how you respond to the claims made in the article. I’ve spent some time trying to track down the FDA survey referred to but haven’t found it yet (although I have found some other stuff by Khan). Are you saying that the report misrepresents the scientific literature on this issue?
Finally, thanks for the tip on Psychinfo. I’ll definitely check it out.
Lowering levels of people’s amines resulted in about 20% of them becoming depressed, most of them people who had a history of depression. People with depression are found to have low levels of certain amines. So, according to you my anatomy textbook must be wrong in saying defiencies in certain amines are associated with certain conditions.
And lowering certain amines would never lead to schizophrenia, as it’s caused by a deficiency in GABA, an amino acid, which causes an excess of dopamine, not a deficiency.
Thyroid and diabetes are both problems with hormones, specifically insulin and thyroxin. Hormones are released directly into the blood and perform their actions on cells. The point is an antidepressant is a drug that affects the amount of amines received by target cells, while drugs for diabetes and thyroid problems are either the hormones themselves or an artificial faxsimile.
The main problem is that changes amine levels may not produce psychological effects within the time periods studied. It’s really hard to judge without any idea of the methodology used. If changing amine levels had little to no effect across the board, then there’s clearly something to TVAA’s comments, but if 20% experienced changes, that could be significant enough, especially given a history of depression. Then again, there are potential compounding factors. Speculation is useless.
Arguing about the science of psychiatry really doesn’t further TVAA’s position, because eventually we will have some idea of the causes behind certain behavior, and the question of desirability will still remain as important as ever.
You see, this is exactly the problem TVAA is trying to illustrate (I think).
Excess levels of dopamine are associated with schizophrenia, but as far as I know, no one has thus far succeeded in conclusively demonstrating that “excess dopamine” causes schizophrenia. The theory is merely one of several competing models, and is highly controversial.
Or is that not the case?
In fact, it’s hard to say what schizophrenia really is. From my own anecdotal experience, it’s a grab bag: it’s what psychiatrists call someone who’s really, really crazy, when they don’t know what else to label them. I don’t think I’ve ever met a single example of the “pure types” one finds described in the DSM IV. Every single individual I’ve personally known with that diagnosis (and that’s quite a few, I might add) was uniquely different. In fact, they often possessed several different diagnoses from several different psychiatrists.
The problem is that when stating “dopamine causes schizophrenia,” you assume “schizophrenia” to be a distinct and clear cut syndrome. In the DSM IV this certainly appears to be the case, but in the field it isn’t – at least not in my experience.
ok. What causes diabetes? Who knows, but diabetes causes the body to not produce enough insulin so we use insulin to treat it. How do you know if you have diabetes? There are a range of symptoms, some you may have, others you may not have.
The point is that schizophrenia is the same way. Not all people may exhibit the same symptoms, but all people diagnosed as schizophrenic have one or more of the symptoms. In fact, there are 5 subtypes of schizophrenia. So while the defiency in GABA (or excess levels of dopamine caused by the defiency) may not be the underlying cause of schizophrenia, correcting the levels is how we treat it.
(The cause of schizophrenia is still unknown, but birth factors, genetics, and midpregnancy viruses are known factors)
That being said, when a doctor is attempting to diagnose a mental condition he will usually start off with a diagnosis of schizophrenia, and work from there. That how it was for me. I have probably had about four different diagnosis before they decided I was bi-polar.
If schizophrenia were caused by a global deficit in GABA levels, it would be treatable with alcohol.
Since I’ve never heard even a suggestion that schizophrenia responds to alcohol, I conclude that NeSBiT is either grossly ignorant, lying, or privy to information that will win someone the Nobel Prize. Guess which possibility I think is most likely.
It is understandably hard to know what TVAA’s point is. I agree with you that not all of what he says is nonsense, but his valid points are buried in so much pretentious and arrogant claptrap that it is hard to find them. That and that he can’t seem to apply his own proposed standards and meanings consistently.
Let us take this particular op:
So his bones to pick are:
that mental illnesses implicitly accept that an individual functions (or fails to function) within a particular culture. True 'nuff. If everybody in a society believed that those who heard voices that others failed to hear were prophets or seers, instead of hallucinating, then schizophrenics might be revered instead of treated. It could be a functional, even an advantageous, state for life within that society. To me however this a throwaway point. These individuals are functioning in this society. Unless the option of existing in a society with markedly diffeent standards exists, it is the standards of current culture that need apply.
that the critera are too vague for his taste. True that these terms get fuzzy at the edges. But such is the means by which progress gets made. The DSM is not a final product; rather it is a work in progress. It is the right approach: create a dictionary so that researchers and clinicians are using the same word to mean the same thing. As research and practice comes along such that it is clear that terms need to be defined more precisely or differently, do so. It is far far from perfect either as is or more so as used. But it is the best thing going to allow scientific study of that which is difficult to quantify. (Remember a past discussion about science needing tools to quantify observations? And how the scientific theories and tols mutually drive each others development? The DSM is another example of this process in action.)
And his third point is just untrue for mental disorders in general. The general understanding today is that environment and biological predisposition usually both play roles in the expression of phenotypes, to various degrees depending on the condition discussed. Figuring out how they interact is the key.
Now how does he apply these standards?
Well autism, like schizophrenia and many other labels of the DSM, is indeed based on neurological dysfunction. But it is as subject to his critiques as any other label in the DSM.
It implicitly accepts that individuals function within a culture.
It has critera that are fuzzy at the edges. Qualitatively impaired socialization? Where do you draw the line on that item? Impaired verbal and nonverbal communication? How impaired does it have to be? Restricted patterns of interests and behavior? How restricted? A qualitative judgement.
There is no test for autism. There no single cause of autism: it is associated with multiple genes - some believe at least 10 if not 15.
There is no sharp edge, rather there is a greater appreciation of a broad autism phenotype. Most in the field beleive that the reported rise in incidence is in fact a function of greater use of the label as a result of greater awareness and the availability of less ineffective interventions if and only if it is diagnosed early. Clearly many of those labelled as autistic today would not have been so called 10 or 15 years ago. And the way to intervene is indeed environmental: speech language therapy both formal and home based, developmental therapy, OT, etc. Medications have a minimal role in treating the symptoms for a few.
How about for other mental disorders?
For many the evidence suggests that they are some kind of neurological disorder. Unfortunately, our knowledge of the brain and imaging technology isn’t sufficient to demonstrate exactly what the problem with the brain might be, or how the symptoms of the disorders relate to the problem. For many there are much better leads than for autism, certain alleles definitely associated with increased risk, etc.
Many may indeed end up being not single diseases but collections of phenotypes with commonalities. Some may have been functional in different societies at different times. Or the contributing genes may result in adaptive phenotypes even today but in combination become maladaptive. We have a way to go before we really understand all the neural dynamics involved in these very complex and handicapping conditions. When researchers portray the science as being more advanced than it is, when they imply that they really understand how and why these conditions occur, then they go beyond the knowledge. But when researchers state what is known about biological predisposition and environmental effects, about mechanisms and effective treatments based on label as accurate as today’s understanding allows, then they are being responsible scientists.