Addiction in Society

Well, what I like about what Maria Shriver is doing is at least shedding light on women's lives today. Plus, she has a GREAT platform. And, I'll bet she is open to hearing from the devil's advocates so that version 2 of her report (I sense that might be something she'd be up for) is more inclusive.

So, really good news that Maria, a beautiful, high powered, POSITIVE woman is breaking this new ground. No, her study isn't perfect - no one study or survey ever is. But what is great is that the discussion is occurring.

The problem with highlighting the growing problem (which should be no secret to anyone who knows how many of the people he/she knows are being "treated" for "depression"), is that there does not appear to be any concurrent effort to determine the causes of the increase. That’s probably because most of the research is performed by or at the expense of the pharmaceutical industry, and their interest as businessmen is money, not health. Putting more and more people on a permanent treatment provides a steadily growing income stream (at least until the patent expires), and if the treatment results in long-term injury to the patient, that injury may become a future source of income in the form of another treatment. Cures just aren’t profitable.

Antidepressants are not intended to be cures; they’re treatments. If you feel better taking them, and the cause of the depression hasn’t been corrected, when you stop you will feel depressed. This may be withdrawal, since antidepressants create dependence, but it is not relapse; relapse is when the cause was going away and came back. Antidepressants are intended to change the way people feel, essentially the same way some “recreational drugs” do (by messing with chemicals in the brain); and they’re intended to be taken for life (instructions for use will keep patients on them long enough to create dependence, withdrawal effects tend to be worse than side effects, doses and information appropriate to withdrawal are not readily available, and doctors are afraid to assist in withdrawal because of the danger of suicide).

Why are alcohol and cigarette advertisements no longer permitted on TV, while millions are spent on TV advertising to convince adults and children, that sleeping pills and antidepressants, etc. are not only good for what ails them, but are warm, friendly and nurturing? Drug advertisements feature nature scenes, reassuring voices and gentle butterflies; but the reality is somewhat different. Some people don’t feel better taking them (just as some people don’t like the feeling they get from alcohol or other recreational drugs), and some people feel awful taking them. Search the Internet for groups of words like “[drug name] withdrawal horror stories” or “[drug name] withdrawal hell”. Psychopharmaceuticals may make some patients temporarily feel better, but they also wreck lives and contribute to the ballooning of immediate and future health care costs; while the manufacturers have to laughing all the way to the bank.

I see three fundamental problems with the way we approach depression:

1. The “illness” called “clinical depression” is defined by psychological symptoms only, and being entirely subjective, diagnosis becomes very unreliable. An infection (viral or bacterial) may first be diagnosed from its symptoms, but the infection can be confirmed by identification of the pathogen. For a purely psychological condition, this is not the case. Different people react to life’s events differently, and with different intensity; and unless feeling depressed has a physical cause (e.g., hypoactive thyroid), it is normally accompanied by other feelings such as mourning, sadness, shock, anger, fear, frustration or helplessness. So, unless it has a physical cause, is depression even a feeling in its own right, or is it part of a composite (of possibly yet undefined fundamental feelings) that makes up different feelings (similar to Fritz Riemann’s idea that all fears are really a combination of different degrees of four fundamental fears**). In the absence of a physical cause, where is the cutoff between being justifiably depressed and being mentally ill, when some people take years to get over a serious “traumatic event”, while for others the same event may not even be serious? The result of this lack of clarity is that people who are depressed are being treated for “clinical depression” (a term quite possibly invented so physical interventions could be developed and patented to treat it), and doctors and psychiatrists use “depressed” or “depression” and “clinically depressed” or “clinical depression” interchangeably.

** To my knowledge, Fritz Riemann’s book, Grundformen der Angst: Eine tiefenpsychologische Studie, has not been translated into English. His four fundamental fears are:
fear of loss of individuality, which is experienced as loss of identity and independence
fear of individuation, which is experienced as insecurity and isolation
fear of change, which is experienced as transience and insecurity
fear of compulsion (forced change), which is experienced as finality and bondage

2. The idea that a physical intervention (e.g., a drug) could effectively cure a purely psychological condition (or even reliably eliminate its symptoms) any better than recreational drugs, makes no sense. After all, that’s what recreational drugs are used for; but I don’t think psychology and medicine expect them to work. When talking about causes of depression, some doctors cite changes in brain chemicals and neurological activity that can be measured in depressed individuals, as if those are the causes of the depression. In fact, they may be causes of some physical symptoms of depression, but they are not causes of depression any more than a fever is the cause of a cold; therefore, eliminating them (even if we knew how), could be expected to cure depression about as well as sinking a fever cures a cold. Psychology deals with consciousness; and science has not yet figured out what consciousness is, so medicine and psychology haven’t either. Some firmly believe it’s a purely physical phenomenon, glossing over or ignoring the resulting implication of a collection of presumed unconscious parts (atoms, molecules, etc.) that are constantly being replaced, being conscious of having an identity together, but remaining unconscious of the existence of themselves as distinct parts. If consciousness is not a physical phenomenon, then treating a psychological symptom with a physical intervention is like washing or painting a car if it isn't running properly, or fiddling around with the engine or transmission if it’s looks ugly or dirty.

3. In view of the fact that the newer antidepressants exist no-where in nature, it cannot be expected that the human body has evolved to be able to effectively and safely eliminate them. It is careless to conclude that they are safe for long term use when they have only been tested for, and are only recommended for (read the label) short-term use, and have not been tested for safety on healthy individuals. Manufacturers already claim that the statistically significant relationship between antidepressants and suicide does not prove a causal relationship (which is correct), even though the approvals based on the statistically significant relationship between antidepressants and improvement in (rigged – see below) trials (incorrectly) assume the relationship IS causal. Based on that, if "healthy" trial participants were to commit suicide (if it were suicide), manufacturers could claim the participants weren't healthy after all.

If you understand something about psychology and statistics, you should understand that it is not possible to develop a valid clinical trial for a drug to treat (antidepressants are treatments, not cures) a psychological condition, unless, in each person taking part in the trial; the drug, the control and the placebo would have identical side effects. Even if the people administering the trial don't know who's getting what, the differences caused by side effects cannot be filtered out with statistics, even if active placebos are used.

Also, statistics don't prove anything, they show probabilities. Efficacy is "proved" in a clinical trial by calculating the probability that trial results showing better results from the drug (and control) than from the placebo, are NOT meaningful. What that means is they're calculating the probability that what looks significant is not significant; the underlying assumption being, if what looks significant is significant, it proves the drug works, which is not true. If you were to perform this calculation on a trial to determine if people get more colds when it's cold than when it's warm, you would get a very (depending on the trial design) low value, indicating that people do indeed get more colds when the weather is cold than when it's warm. This does not mean colds are caused by cold; it means that there is a better than 50%-50% chance that there is some connection between people getting colds and cold weather. It says nothing about the connection (people spend more time close together indoors where the virus can spread more easily?), it says nothing about the probability of getting a cold in cold weather (that number would have to be calculated separately, and would depend very much on the design of the trial), and it cannot be applied at all to one particular person getting a cold after being in the cold (which would also depend on many factors that have nothing to do with the design of the trial).

If you look over two Cymbalta "clinical trials" (HMAYa and HMAYb), you'll find that the trials are "rigged" by excluding prospective participants that are expected to not respond to the control (Paxil). Furthermore, if a trial (HMAYb) does not show efficacy, it is called a "failed/negative study" and given little further consideration. In addition, trial participants that drop out of the trials because of unacceptable side effects, “adverse events”, or lack of improvement are also not considered in the trial results. These are not random trials, and because side effects vary from drug to control to placebo, and from patient to patient, they are also not double-blind.

The Cymbalta "clinical trials" do not show efficacy, they show that if you eliminate people from a trial who:
1. Aren't likely to be helped by Paxil,
2. Aren't being helped at all,
3. Are having side effects they consider intolerable,
there is a statistically significant probability of greater temporary improvement in people taking Cymbalta or Paxil over people taking a placebo. It does not say that improvement is due only to the drug; it could also be due to the side effects (directly or due to the placebo effect*).

* As side effects, problems with thinking and memory can make whatever a person is depressed about less present/real; dizziness, anxiety, pain, flu syndrome, insomnia, etc., can distract a person from whatever they are depressed about; and any unpleasant/noticeable side effect (of which the drugs will have more) can convince the patient that he/she is being given the real thing, resulting in improvement due to the placebo effect. By the same token, a lack of side effects, could tell the patient that he/she is getting a placebo, causing some individuals drop out of the trial or to not get better because they feel cheated. These are not the only ways unequal side effects can skew results; cultural, genetic, diet, education and purely subjective differences can also do it.

Something they also don’t show that would be necessary even in a valid trial is how many people must be treated for one person to be helped, and how many people must be treated before one person is harmed. For a treatment of a subjective condition, these things are impossible to determine without making ethically delicate decisions about what constitutes help and what constitutes harm.

...manufacturers have to be laughing all the way to the bank