Talk Therapy and Antidepressants

Antidepressants are often not enough to alleviate depression and prevent it's recurrence. In many cases, therapy is also beneficial. In fact, it has been shown that in teens, for whom antidepressants are risky and have not proved particularly effective, a combination of antidepressants and cognitive behavioral therapy can be extremely beneficial. Some advantages of therapy are the long term tools which many believe it provides to patients so that they can continue to cope with life even after treatment ends. Also, therapy does not have side effects like antidepressants often do. Is therapy alone as effective as medication in treating depression? One study says that cognitive therapy can match up to the drugs. In this study, those who took medication alone and those who underwent therapy alone both improved at the same rate but those who had therapy had less recurrences than those who took medicine. This is not such a surprisingly result. The chemical imbalance that antidepressants affect is not the sole cause of depression, if a cause at all, it is correlated with it, however, and the treatment of it has shown to help with depression symptoms. It follows though that if you stop treating the imbalance, recurrence is more likely if the patient has not had any therapy because the patient may not have ever dealt with the environmental causes of his or her depression. In my opinion, it seems that the best approach is to find an antidepressant that does not have unbearable side effects and that helps alleviate symptoms while also attending therapy of some kind to learn ways to cope with the causes of depression in the long term.

Sigmund Freud

Psychotherapy, also simply called therapy or talk therapy, has been used as a method to deal with all kinds of psychological phenomena ever since Sigmund Freud began the practice of psychoanalysis in the 19th century. While Freud's ideas still can be found in modern psychology, more types of therapy have developed in time. There is therapy that can be undergone individually, in groups, with family or with significant others. However, what perhaps is most pertinent to the effectiveness of the therapy is the goal of the therapist. In my next post, I will discuss in more detail a few different therapy methods characterized by the different approaches and goals of the therapist as I will not have room to do them justice in this post.


"Cognitive Therapy as Good as Antidepressants, Effects Last Longer." Medical News Today. MediLexicon International, 05 Apr. 2005. Web. 30 Mar. 2012. <http://www.medicalnewstoday.com/releases/22319.php>.

Johns Hopkins Medical Institutions. "Antidepressants Plus 'Talk Therapy' Are Effective Therapy For Teen Depression." ScienceDaily, 18 Aug. 2004. Web. 30 Mar. 2012.

Halberstadt, Max. Sigmund Freud. Digital image. Web. 30 Mar. 2012. <http://en.wikipedia.org/wiki/Sigmund_Freud>.

The Alternative Treatments of Depression (In Pictures)

There are a variety of treatments available for depression. The most well-known, of course, being medication and therapy. While therapy has several approaches and there are a plethora of available prescriptions, perhaps the various alternative treatments are indicative of the prevalence of and the attitude towards depression. The fact that there are so many alternative options would seem to indicate a certain level of dissatisfaction with more conventional methods. Many feel that the side effects of the antidepressants outweigh their therapeutic effects. Another factor in the popularity of alternative treatments is cost; for those with minimal insurance coverage or no insurance coverage, medication can be financially out of reach. Some people simply do not find therapeutic success with antidepressants at all and give up, exploring therapy and other alternatives instead. Some of the alternative options, like St. John's Wort, have actually been around longer than conventional methods. However, this does not automatically mean that they are safer or more effective.

In fact, even herbal remedies like St. John's Wort can have interactions when paired with antidepressants without caution. The bottom line about alternative methods for combating depression is that they are not very well studied and thus, reports of their efficacy vary. In general, credible sources like the Mayo Clinic urge those with depression not to rely on alternative methods alone. Therapy and medication are the mainstays of conventional depression treatment and they are currently accepted by the psychiatric community as the most effective options. However, many people see great potential in alternative methods due to their occasional success in treating mild and moderate depression.

Some of the alternative medicine options are:

St. John's Wort (Returns)

• St. John's Wort is an old herbal remedy that is not approved by the FDA for the treatment of depression but has become increasingly popular in recent decades and brags centuries-long usage in folk medicine. 

 

SAMe structure

• S-adenosylmethionine, known as SAMe (prounounced Sammy), is a chemical naturally produced in the body that is also not approved by the FDA to treat depression. It has similar effects as  antidepressants do on serotonin and epinephrine. SAMe often minimizes side effects but does not interact well with other antidepressants and can cause mania in those with bipolar disorder. 5-hydroxytrptophan (5-HTP) is a similar chemical.

Salmon contains Omega-3

• Omega-3 fatty acids, found in many fish, walnuts and flaxseed, are beneficial to the entire body and seem to be a good dietary supplement in addition to other depression treatment.

Chill

• Relaxation of the mind or body through yoga, meditation, and biofeedback methods designed to help patients control their heart rate can also prove beneficial. This, as with many of theses remedies, is also suggested for anxiety disorders.

Running is aerobic exercise

• Exercise has also been shown to help alleviate depression of all levels and to assist in preventing recurrence. More specifically, aerobic exercise is suggested. However, few, if any, doctors would recommend exercise alone as a treatment. A healthier diet can also help.

• Acupuncture is also lauded as an alternative treatment for depression but has not been studied significantly and much about it's effectiveness remains unclear.

Green leafy vegetables are one place to find folate naturally.

• Folate is a B vitamin that can slow patient's responses to antidepressants, perhaps assisting with side effects and general improvement. This can be taken as a folic acid supplement to antidepressants. Supplements of vitamin B6 and magnesium (both involved in serotonin production) can also be beneficial.

It does not seem that any particular alternative method is sweeping in to replace antidepressants and therapy. In fact, although a select few methods have interactions with antidepressants, most alternative methods are not considered sufficient treatment alone. In my next post, I will describe why therapy is so relevant in the treatment of depression as well as what types of therapy are typically employed.

Also, I'd like to announce that I have found the topic of antidepressant efficacy so complex and intriguing that I have found that I will not be able to cover both antidepressants and anti-anxiety medication, despite the common overlap between the two.

Frazer, Cathy J., Helen Christensen, and Kathleen M. Griffiths. "Effectiveness of Treatments for Depression in Older People." The Medical Journal of Australia. 17 May 2005. Web. 28 Mar. 2012. <https://www.mja.com.au/journal/2005/182/12/effectiveness-treatments-depression-older-people>.


Kessler, Ronald C., Jane Soukup, Roger B. Davis, David F. Foster, Sonja A. Wilkey, Maria I. Van Rompay, and David M. Eisenberg. "The Use of Complementary and Alternative Therapies to Treat Anxiety and Depression in the United States." American Journal of Psychiatry. 1 Feb. 2001. Web. 28 Mar. 2012. <http://ajp.psychiatryonline.org/article.aspx?articleid=174601>.

Davis, Jeanie L. "The Dangers of Alternative Depression Treatment." WebMD. WebMD. Web. 28 Mar. 2012. <http://www.webmd.com/anxiety-panic/features/alternative-depression-treatment-risks>. 


Mayo Clinic Staff. "Alternative Medicine." Mayo Clinic. Web. 28 Mar. 2012. <http://www.mayoclinic.com/health/depression/DS00175/DSECTION=alternative-medicine>.

Wong, Cathy. "Depression Remedies." About.com. 26 Nov. 2011. Web. 28 Mar. 2012. <http://altmedicine.about.com/od/healthconditionsatod/a/Depression1.htm>.

Do These Genes Make My NPY Count Look Big?

How could genetics affect depression? Well, in the study presented in my last post, a specific gene seemed correlated with a monoamine deficiency, which seems to be involved in depression. It has also been supposed that due to the differences in scans of the brains of the depressed and the non-depressed, the development of the brain structures affected could be involved.  Medicine has barely begun to research what genes are involved in depression and for what reason. What is known is that people with a relative with major depression are two to three times as likely to become depressed. This is not a statistic generated by that person's proximity to depression. In separated identical twins, there is a 40-50% risk of one twin developing major depression if the other twin has already done so.

Many studies of genetic predisposition of depression refer to the molecule neuropeptide Y (NPY). Studies have shown that people with less of this molecule have stronger brain responses to stressors. This sort of study identifies a factor that could contribute to the cause of depression that is completely unrelated to the monoamine theory, further convincing me that the cause of depression is multifaceted. This study also pointed out that those lacking NPY were "overrepresented in a population diagnosed with major depressive disorder," indicating a correlation between the two. However, sensitivity to stress can be a risk factor for more than just depression. In fact, this may be a connection between anxiety and depression, two disorders that are treated in similar ways and can coincide. Also, NPY has been shown to induce eating in animals injected with it. The hormone Leptin, which stimulates weight loss, decreases the output of NPY by the hypothalamus. This is especially interesting because depression is sometimes, but not always, accompanied by weight loss.

This article discusses, quite aptly in my opinion, that though the depression gene research is only in it's early stages, the prevalence of this disorder will inevitably lead to more and more research on the subject. An understanding of the genetic factors of depression would yield to a better understanding of the biology of depression generally and perhaps even of some of the environmental factors. The more we know, the better our treatments can become.

Digital image. Mayo Clinic. Web. 22 Mar. 2012. <http://www.mayoclinic.com/health/medical/IM00356>.

"Genetic Factors of Depression." Livestrong. Web. 22 Mar. 2012. <http://www.livestrong.com/article/102769-genetic-factors-depression/>.

"Natural Born Pessimist: Some People Are Genetically Programmed to Be Depressed, Scientists Say." Daily Mail Online. Feb. 2011. Web. 22 Mar. 2012. <http://www.dailymail.co.uk/sciencetech/article-1354811/Some-people-genetically-programmed-depressed-scientists-say.html>.

Zhou, Zhifeng. "Genetic Variation in Human NPY Expression Affects Stress Response and Emotion." Nature.com. Nature Publishing Group. Web. 22 Mar. 2012. <http://www.nature.com/nature/journal/v452/n7187/abs/nature06858.html>.

"Emotion Processing, Major Depression, and Functional Genetic Variation of Neuropeptide Y." Archives of General Psychiatry, a Monthly Peer-reviewed Medical Journal Published by AMA. Feb. 2011. Web. 22 Mar. 2012. <http://archpsyc.ama-assn.org/cgi/content/abstract/68/2/158>.

 "Study Closes In On Genes That May Predispose Some People To Severe Depression." ScienceDaily. ScienceDaily, 01 Feb. 2007. Web. 22 Mar. 2012. <http://www.sciencedaily.com/releases/2007/02/070201082225.htm>.

 "Neuropeptide Y." TheFreeDictionary.com. Web. 22 Mar. 2012. <http://medical-dictionary.thefreedictionary.com/neuropeptide Y>.

More Monoamines Needed

St. John's Wort

From the files of Dr. Jeffrey Meyer comes another monoamine deficiency study; this time around he and his team of colleagues have examined the effectiveness of MAOIs on the enzyme MAO-A Vt, which breaks down monoamines, and the effectiveness of traditional herbal alternative St. John's Wort on the same enzyme. They found that MAOIs were successful and that St. John's Wort did not have a clinically significant effect. This study also discusses how the antidepressant market has shifted to focus on the development of SSRIs, perhaps because they have less drug interactions and possibly less side effects, and has moved away from the development of new MAOIs. It is implied that the development of MAOIs would be useful due to their effects on more monoamines than just serotonin. This study states that SSRIs work for merely half of the depressed patients treated with them. This indicates that in many patients the correction of the lack of serotonin is not enough to help induce recovery if other monoamines remain in deficient quantities.

As you may have guessed, while there is not as much research on the subject of monoamine deficiency as I would like, Dr. Jeffrey Meyer is not the only scientist leading studies on the subject. Another significant study  was conducted to determine whether brain serotonin turnover was greater in depressed patients who were not medicated with SSRIs. This study found this to be true. Patients treated with SSRIs had decrease brain serotonin turnover. This, it seems, is not an uncommon or unexpected finding. After reviewing the work of Dr. Jeffrey Meyer and other scientists, I would venture to say that it is much less than ridiculous to theorize that monoamine deficiency is correlated with depression, and that the antidepressants that are currently on the market do target and positively affect this deficiency. This study also discussed the effects of a particular gene on monoamine deficiency. This finding is significant because it points to a very direct biological way in which some genes can predispose depression.

I have discussed the monoamine theory of depression much in my recent posts. However, I would like to reiterate that I would never go so far as to claim that depression is completely induced by this monoamine deficiency. The effects of the environment cannot be dismissed. I do not think that depression is a simple enough disease to have any one cause. As this malady is complex, so must be the remedy. In my next posts, I will further discuss genetic predisposition, alternative treatments, and talk therapy to illustrate the relation between a comprehensive treatment plan and a successful use of an antidepressant.

Meyer, Jeffrey, and Julia Sacher. "Monoamine Oxidase A Inhibitor Occupancy during Treatment of Major Depressive Episodes with Moclobemide or St. John’s Wort: An [11C]-harmine PET Study." Web. 21 Mar. 2012.

Barton, David A., Murray D. Elser, Tye Dawood, and Elisabeth A. Lambert. "Elevated Brain Serotonin Turnover in Patients With Depression: Effect of Genotype and Therapy." Archives of General Psychiatry, a Monthly Peer-reviewed Medical Journal Published by AMA. Jan. 2008. Web. 21 Mar. 2012. <http://archpsyc.ama-assn.org/cgi/content/full/65/1/38>.

Digital image. Methods of Healing. Web. 21 Mar. 2012. <http://www.methodsofhealing.com/files/2009/07/st-johns-wort.jpg>.

Studying Monoamine Deficiency

So why should antidepressants be allowed to remain on the market despite the occasional occurrence of devastating side effects? Because they may be the first step to understanding the biological symptoms of depression and using that understanding as treatment. When antidepressants were first placed on the market, their efficacy relied on the monoamine deficiency theory, what I have previously called the chemical imbalance theory. In it's simplest form, it states that a deficiency of certain monoamines (neurotransmitters like dopamine, serotonin, etc.) is correlated with major depression.

This simple theory is rejected by many people who reject antidepressants, such as Peter Breggin, Robert Whittaker and Joanna Moncrieff, writers of popular anti-psychiatry literature. Many have pronounced the theory as incorrect. However, I have found some studies that imply that they may have written their verdict too early. While I don't believe that anyone with knowledge on the subject would claim that monoamine deficiency causes depression, I do not think it is ridiculous to believe that the two may coincide. The first study I read with these implications I mentioned in a previous blog post. It was a study lead by Dr. Jeffery Meyer for the Canadian-Based Centre for Addiction and Mental Health that concluded the enzyme that breaks down serotonin was more prevalent in those who had untreated depression. (For more details, see my earlier blog post "Chemical Imbalance Theory: Fact or Fiction?") After reading a press release about this study, I decided I should examine the source so I found the original article in which the results were published. What I discovered was that the sample size was rather small, a comparison of seventeen depressed patients with seventeen control patients. This is a fact that many skeptics use to dismiss the results of this study and studies like it. However, as I continued my research, I found a follow up study by the same Dr. Jeffrey Meyer that focused even more closely on the effects of SSRIs.

In this second study, twenty-eight control subjects were compared with sixteen subjects suffering from major depression and another eighteen subjects in recovery from major depression. Those with major depression were treated with SSRIs and the activity of the enzyme MAO-A VT, whose activity would decrease the number of monoamines. It was shown that the depressed patients had higher enzyme activity than the healthy patients, and that patients in recovery who had more enzyme activity were more likely to experience recurrence. As the study states, this does not only imply the correlation between monoamine deficiency and depression but it also seems to indicate that continued SSRI treatment, even during remission, is advisable in order to prevent recurrence of the depressive episodes. This is a significant positive outcome towards the demonstration of the usefulness of antidepressants, all of which function by increasing the concentration of monoamines in the brain. Studies like these make me hesitant to dismiss antidepressants and convince me that they can be a productive part of a depression patient's treatment plan.

This is a diagram from the first study posted to better under the mechanisms of monoamine deficiency. Figure A demonstrates the enzyme and monoamine activity in a healthy person. Figure B demonstrates the enzyme and monoamine activity in a major depressive episode. Note the higher concentration of enzyme and the lower concentration of monoamines. Figure C demonstrates what occurs when the monoamine transporter that would normally take monoamines away from the site is low, partially balancing out the excess enzyme. Figure D demonstrates what happens when there is both excess enzyme and a high level of monoamine transporter.

I am not one to rely on one doctor's set of studies, so I will examine the two other relevant studies I found in my next blog post.

Nauert, Rick. "Depression's Chemical Imbalance Explained | Psych Central News." Psych Central.com. Web. 02 Mar. 2012. <http://psychcentral.com/news/2006/11/09/depressions-chemical-imbalance-explained/398.html>.

 Meyer, Jeffrey. "Brain Monoamine Oxidase A Binding in Major Depressive Disorder: Relationship to Selective Serotonin Reuptake Inhibitor Treatment, Recovery, and Recurrence." Archives of General Psychiatry, a Monthly Peer-reviewed Medical Journal Published by AMA. Dec. 2009. Web. 15 Mar. 2012. <http://archpsyc.ama-assn.org/cgi/content/full/66/12/1304>.

 Meyer, Jeffrey. "Elevated Monoamine Oxidase A Levels in the Brain: An Explanation for the Monoamine Imbalance of Major Depression." Archives of General Psychiatry, a Monthly Peer-reviewed Medical Journal Published by AMA. Nov. 2006. Web. 15 Mar. 2012. <http://archpsyc.ama-assn.org/cgi/content/full/63/11/1209>.

Medication Madness

This week, to further my knowledge of the accusations made against antidepressants and other psychiatric drugs, I read Medication Madness: A Psychiatrist Exposes the Dangers of Mood-Altering Medications, another product of Peter Breggin. While my critique of his last book may have seemed dismissive, I respect Breggin for his part in many complicated court cases dealing with what he calls "medication madness." I examined this idea in the second book of his. It seems that there are cases in which certain antidepressants and other psychiatric drugs can produce severe adverse reactions. We've all heard the television commercials warning that certain drugs may cause suicidal thoughts, but I doubt many have stopped to imagine the horrific reality that fact is derived from. In the rare occasions that suicidal thoughts are induced they are often severe and accompanied by other side effects like mania, akathisia, and psychosis. Information regarding these symptoms is provided with the prescriptions by the FDA, and the information is available online, however, Breggin laments that this knowledge is not openly acknowledged. I would agree that it is of the utmost importance that the drug companies are forthcoming with the risks of their drugs (the suicidal effects were not recognized until years of the drugs being on the market). Also, it is important that doctors make informed decisions in prescribing these drugs. It seems that the severe suicidal and manic symptoms occur at the beginning of the drug-taking period or after an increase in the dose of the drug. Because I am not as skeptical of the antidepressants' ability to be successful in many cases, I propose that these side effects are made more well known rather than the drugs being taken of the market. The main focus was on the SSRI class of antidepressants. While the disastrous results of these severe side effects are significant, they do not seem to have long-lasting physical damage in the cases where the drugs were prescribed as is clinically proper. For this reason,  I would suggest that the antidepressants serious side effects can be dealt with through a more comprehensive treatment plan. Those beginning to take SSRI antidepressants should be seen by their doctor within the first week of taking the drugs and also after any increases in dosage. Furthermore, I would recommend that the patient notify their loved ones about the warning signs of the severe side effects. Dr. Breggin often speaks about patients being "medication spellbound," in regard to the patient's complete obliviousness to the deterioration of their mental state. With a significant support group of loved ones and doctors, I think that the chances of noticing these more subtle yet serious side effects would be much higher. To emphasize the rarity of these side effects, I recall a study mentioned in Breggin's book that indicates only 8.5% of adults in a clinical trial experienced increased suicidal activity. In my second post this week, I intend to explain why my research has lead me to believe that medicine's antidepressants are on the right track scientifically despite prevalent skepticism and the unavoidable suicide risks. I would like to add that this risk is more profound in children, and the apparent lack of demonstrated efficacy of the drugs in children makes the prescription of SSRI antidepressants to children something I would not endorse.
 

Breggin, Peter Roger. Medication Madness: A Psychiatrist Exposes the Dangers of Mood-altering Medications. New York: St. Martin's, 2008. Print.

Concluding a Review of Breggin's Antidepressant Fact Book

I would like to finish up my review of the claims made by Peter Breggin in The Antidepressant Fact Book.

1."'Antidepressants aren't in any way similar to stimulants like amphetamine and cocaine.'

This claim is irrelevant. Amphetamines and antidepressants are generally accepted to be similar but certainly not the same. This is not a problem. Currently, certain stimulants, such as Adderall, are prescribed for ADHD. Stimulants may sound scary due to their relation to cocaine and methamphetamine but they are not all created equal. Some are more dangerous and some have legitimate medical functions. In fact, in some cases, stimulants have proved effective in treating atypical depressive mood disorders, such as the intense fatigue and anergia of some cancer patients. In these cases, MAOIs are also effective but curiously tricyclic antidepressants are not. The response of certain patients to certain antidepressants is not fully understood at this time, but the similarity to some amphetamines does not make them medically illegitimate. This claim seems to me to hide a critique of all psychiatric drugs, something that I would not stand by, but that Breggin seems to accept as automatically valid.

2."'Antidepressants don't cause cause withdrawal problems; you can stop them without any ill effects.'

Antidepressants are liable to cause withdrawal if a patient abruptly stops consuming them. This is something that I can say from personal experience that doctors are upfront about. When I was prescribed an SSRI for anxiety, I was informed that if I stopped taking it suddenly, I may experience ill effects and that I ought to discuss it with my doctor before I stopped taking the medicine. In general, it is a good policy to discuss it with your doctor before you stop taking any prescribed medicine. Furthermore, the Mayo Clinic lists antidepressant discontinuation syndrome symptoms as "irritability, anxiety, insomnia, headaches, dizziness, fatigue, nausea and continuation of depression symptoms." These are neither life-threatening side effects nor are they particularly surprising. Antidepressant discontinuation syndrome can be combated by having your doctor give you smaller an smaller doses of the medicine rather than abruptly stopping it. The presence of withdrawal effects alone is not sufficient to make antidepressants dangerous or ineffective.

3."'Antidepressants can't make you psychotic unless you have a preexisting mental illness'"

This claim is the most serious of all of these, in my opinion. I have found claims that adverse effects from psychiatric drugs have resulted in mania, murder, violent thought, and commitment to mental institutions. I have read testimonies that people taking antidepressants began to have symptoms of psychosis shortly after they began taking them. And yet no where have I found a reliable source that can make a clear causal connection between the ingestion of an antidepressant and the occurrence of a violent crime. It has been claimed that the shooters in Columbine and a variety of other mass shootings were taking certain antidepressants, mainly SSRIs. However, this is neither confirmed nor does it seem to me very convincing. Is it not possible that those that are highly depressed, if on the wrong antidepressant and not being helped by it, would be more likely to commit a violent crime in the first place? Are the claims that the antidepressants were responsible possibly attempts at rationalizing an evil which people fear and do not want to recognize as originating from a person himself? On this claim, I am not yet sure what to think. I tend to be skeptical that a drug can "make" a person commit a violent crime but I will review this more when I read Breggin's book that focuses more directly on this topic.


Hall-Flavin, Daniel K. "Antidepressant Withdrawal: Is There Such a Thing?" Mayo Clinic. Mayo Foundation for Medical Education and Research, 10 Sept. 2010. Web. 03 Mar. 2012. <http://www.mayoclinic.com/health/antidepressant-withdrawal/AN01425>.

 Ellinwood, Everett H., George King, and Tong H. Lee. "Chronic Amphetamine Use and Abuse." Home. Web. 03 Mar. 2012. <http://www.acnp.org/g4/gn401000166/ch162.htm>.

"Psychiatric Information." Antidepressant Side Effects Cause Psychosis Archive. Web. 03 Mar. 2012. <http://www.psychiatry.info/psychiatrists-in-the-news/antidepressant-side-effects-cause-psychosis/>.

 Take This Antidepressant, and You Too May Have a Violent Psychotic Break. Web. 03 Mar. 2012. <http://www.anh-usa.org/take-this-antidepressant-and-you-too-may-have-a-violent-psychotic-break/>.

Chemical Imbalance Theory: Fact or Fiction?

I would now like to address the next three myths:
"'Antidepressants are not mood-altering, they directly improve the disease of depression.'
'Antidepressants are like insulin for diabetes, they provide essential missing substances.'
'Antidepressants don't cause abnormalities in the brain, they correct biochemical imbalances.'"

I would argue that these three statements are directly connected. Many people believe that a lack of the neurotransmitters that antidepressants affect is one cause of depression. This implies that a chemical imbalance in the brain is involved when people are depressed. Peter Breggin would argue that the chemical imbalance theory is simply false. He says that medicine does not know enough about the brain to determine whether these neurotransmitters are related to depression and thus, that doctors who prescribe antidepressants to combat a chemical imbalance are taking a shot in the dark in fighting depression.

Mood-altering simply means that the drug artificially affects the patient's mood. This is viewed as a negative because it could be argued that this is not treating the disease properly. However, I am of the opinion that facing the grueling cycle of depression to improve the patient's mood, even by artificial means, is treating the disease. The cycle of depression is described many different ways. A good example of the cycle in  practice would be this: John Doe is depressed. Because he is depressed, he does not work as hard and his work is substandard. His work is substandard so he is fired. He is fired so he feels bad about himself and he feels guilt, leading to him being more depressed. Perhaps you are not sympathetic. You may say, John should have used that guilt and self-loathing to find a new job and try harder. That is exactly what a depressed person would have trouble doing. In these cases, a drug that can help elevate mood can result in John doing a better job at work due to him having less depressed feelings. Maybe he would end up getting promoted, at which point, John would begin to feel develop a sense of self worth and pride that might generate a happiness that is not purely deriving from his medication.

What Peter Breggin pictures^^

Breggin's second and third claims are more similar. The first compares depression and diabetes, both diseases that we suppose to cause a chemical imbalance. In this case, the antidepressants, in fixing that imbalance, would clearly be doing a good thing. The third claim states this explicitly. If there is  not chemical imbalance, then Breggin is right, these drugs are being marketed under false pretenses and may not be helpful to depressed patients. However, the research I have read makes me wonder if Breggin's eighteenth book will be a retraction of his attacks. There are studies available that strongly support the chemical imbalance theory. According to a study done by the Canadian-based Centre for Addiction and Mental Health (CAMH), monoamine oxidase A, an enzyme that would break down the neurotransmitters doctors claim to be imbalanced, is more prevalent in people with untreated depression than those who are not depressed. More of this enzyme means less of the neurotransmitters which clearly results in a chemical lack. The study goes on to discuss the significance of monoamine transporters, which are specialized by neurotransmitter. These take the monoamine neurotransmitters away from active sites, creating further imbalance. This would explain the variety and varying severity of depression symptoms. If one had an excess of serotonin transporters, then less serotonin would be in their active sites, while they may have a normal amount of dopamine transporters. These differences would affect symptoms and severity and also which drugs would be effective on which individuals.

This blog post may seem extra long, but this particular topic will most likely be a defining point of my overall project. The validity of the biochemical imbalance theory is extremely significant and I will discuss it's implications in my later posts.


Nauert, Rick. "Depression's Chemical Imbalance Explained | Psych Central News." Psych Central.com. Web. 02 Mar. 2012. <http://psychcentral.com/news/2006/11/09/depressions-chemical-imbalance-explained/398.html>.
 

Breggin, Peter Roger. The Antidepressant Fact Book: What Doctors Won't Tell You about Prozac, Zoloft, Paxil, Celexa, and Luvox. Cambridge, MA: Perseus Pub., 2001. Print.