Untitled Document

The Unified Theory of the Nervous System
and Behavior

Cognitive Philosophy /Brain Theory by Steven Michael Harris

A Test

Which of the following statements are facts and which are conclusions (theories)?

The brain fluid of patients with depressive disorders often show a measure of serotonin level that is lower than the levels in control subjects without depressive disorder. (Measured by sampling cerebral fluid in patients or by examining the brains of cadavers.)
Medications (SRIs, MAO inhibitors, etc. such as Prozac et al) that increase the levels of serotonin available to the receptors have shown beneficial effects on depressive symptoms in a significant number of depression patients better than the controls taking placebo.
Serotonin is a regulator of mood in the brain.
Depression patients are suffering from an insufficient amount of serotonin in the brain that needs to be replaced through medication.

The first two items are facts. Items 3 and 4 are conclusions (theories) but the medical community speaks as if these conclusions can be taken for granted as fact. This is a big mistake and the mistake is so pervasive in the language of medicine and biological science that such assumptions are the basis for almost all research and medication approaches and all theories of the workings of the brain take these conclusions for granted and must build on these conclusions (theories) that a chemical (such as serotonin) can be a regulator of some greater function (such as mood) of the organism and that irregularities in the levels of such chemicals need to be adjusted through the use of medication as the way to a cure.

Our entire society speaks about the advances in the understanding of "brain chemistry" and it is this term as it is understood that is really getting in the way of understanding how the brain really computes.

Yes, the brain has evolved a large number of chemical markers for different regions of the nervous system and these markers can be manipulated by medication or by the body itself in a variety of ways to effect nervous system communication and behavior of systems, but the language of the brain is in the mathematics behind inhibition and excitation as the individual cells influence each other (and in the geography of the wiring).

I’ll now list a variety of facts and arguments that go against the conclusions that serotonin is a regulator of mood and that levels of serotonin are too low in depressed patients and need to be replaced. (This essay is only picking serotonin as an example and such arguments can be applied to a wide variety of different chemicals found in the brain and their associated "functions" as described by the biological community.)

The brain fluid of patients with depressive disorders often do not show a measure of serotonin level that is lower than the levels in control subjects without depressive disorder.
Medications (SRIs, MAO inhibitors, etc. such as Prozac et al) that increase the levels of serotonin available to the receptors do not work for all depressive patients. A successful medication only needs to affect a greater number of people than placebo controls in order to be considered effective. (For instance a medication might be claimed to be helpful to 65% of patients in relieving symptoms but a placebo in those studies might have been helpful to 50%. Another logic would say that only 15% of the people were improved with the medication because there is success with the medication in only 15% more of the patients than with placebo, but no drug company ever markets a product with such honesty.)
If a healthy person takes one of these drugs such as Prozac (the most famous example), that person could develop depression. (The theory is that depressed patients have a lack of serotonin that needs to be replaced, so a lack of serotonin causes depression. The opposite of a lack is too much. The opposite of depression would be excessive happiness, I think.)
When prescribing a medication treatment for depression, the doctors do not promise the depressed patients that the drugs will take them from sad to happy. Success with the drug is described as taking them from sadness to a feeling of being "even" - to a state with a lack of depression but with no promises of happiness. Such a state could possibly be created by chemically effecting the cells that experience or communicate the pain/sadness and stopping them from operating under the same stimulus - effectively putting those cells (or certain groupings of influences on those cells) into a coma. The experience of being "even" could just be a lack of feeling. This could explain why many who are medicated for depression have a kind of amnesia for many of their depressive experiences (a reason why medication gets in the way of psycho-therapy approaches to solving the problems).
Serotonin is also pegged as a regulator for a variety of other types of functioning, besides mood, partly because of the occasional success with using Prozac and other drugs in treating other problems such as obsessive-compulsive disorder. How can one substance be used by the brain as a regulator of more than one type of functioning of an organism? If there is a deficit of serotonin in the brain, shouldn’t all of the various functions attributed to serotonin control then suffer at the same time? The theory is flawed and suspect as long as these questions are not explained.
Once medication treatment is started, the patient is at risk of having a much greater depression than before any medication treatment if treatment is stopped. (This fosters dependence on the drug.)
A percentage of depressive patients who measure lower than average levels of serotonin in their brains will get worse if taking these medications.
These medications have a therapeutic range. If you take too little of the drug you get worse and if you take too much you get worse. If the problem for these people is that they have a deficit of serotonin that needs to be replaced, then logically they should improve with any increase of serotonin in their brain until they have taken too much. This factor alone is enough to throw doubt on the theory that depression is caused by a lack of serotonin. (Click here to see my essay A Very Big Clue that applies to this item.)
There are other ways to explain the lower levels of serotonin in these people’s brains that conflict with the theory that they have a deficit that needs to be addressed with medication that increases the amount of serotonin available to the receptors. (Click here to see my essay A Fatal Flaw in Medical Logic that applies to this item.)
ECT (shock therapy) that significantly stresses the brain can have a beneficial effect on depression even if it can damage the brain in a variety of ways (memory loss, loss of focus, etc.). If a therapy that clearly stresses the brain can relieve the depressive symptoms, who is to say that the medication approaches are not selectively damaging the brain as well? (This does not apply cleanly to this depression/serotonin essay, but many surgical treatments can get the same results as medication treatment for a variety of disorders. But surgery does not improve the brain but selectively kills some part of it.)
Each brain cell and it’s receptor sites make different decisions in response to chemical signals. Exposure to the right chemical will cause changes in the sensitivity to that chemical by changes in the number of receptors and other factors. Some cells need to become more receptive to inhibition and some receptive to more excitation. The clumsy brain-wide application of one particular neuro-transmitter (with medication) will cause all of the cells to move in one direction in their changes of sensitivity in response to increases of that particular chemical, but the processing of information in the brain requires different decisions in different cells and such an application of medication must be interfering with the decisions of cells that need to make a different kind of decision.
If the problem is caused by a simple deficit in a particular chemical in the brain, then replacing the deficit should bring health. The massive number of drug side-effects should not occur in a state of health.

Those who study medicine must first learn biological chemistry. They learn to speak the language of chemistry. They are speaking facts when they show how one carbon-based molecule reacts with another carbon-based molecule (along with another catalyst or two, perhaps) and say that this reaction causes some other carbon-based molecule to be created. This is the language of chemistry and, yes, the body is a construct of a vast array of many different chemicals reacting with each other. But when they make the leap of saying that some particular chemical regulates some particular function of the organism as a whole, and make this statement without being able to explain all the mechanisms by which this is possible, they are speaking theory that is unproved. To constantly state such theory as if it is fact is unscientific and getting in the way of major discoveries of how the system might really work.

It is easy to understand why this inaccurate shorthand is used and why these assumptions are made. Medicine is doing the best it can at the moment. If you are going to prescribe these medications you need to feel that what you are doing is beneficial and this language makes it possible for the doctor to assume the confidence in the approach needed by the patient. (The placebo effect of believing in the doctor is very important. I’ll eventually explain the mechanisms that make placebo effect work in the brain.)

The doctor needs to be able to say that you have a deficit and that he/she will fix the problem by addressing this deficit. The doctor is trained to appear confident and knowing. It is not good style to admit that they don’t really know why some people get better when taking these medications.

But this language is wrought with inaccuracy. The answers will only come from a language that consistently applies to data in all disciplines. The truth can't be found with the current language.

[Click to Go Back to Unified Theory More Essays Page]

[Click to Go Back to Unified Theory Directory Page]