Chinese Medicine Times : Keeping You Informed

Chinese Medicine Times : Keeping You Informed

Depression: Towards an Integrated Approach - Part One

by Tony Reid
Abstract

In this paper the author aims to present the current state of knowledge about Depression according to both Western psychiatry and traditional Chinese medicine, with a critical evaluation of the strengths and weaknesses of both approaches. The paper argues for a dramatic shift in the way patients presenting with a depressed mood are assessed and treated. It points the way to an integrated approach involving revised criteria for the diagnosis of a mental disorder as well as the provision of appropriate support for patients using selected methods from TCM as well as Western psychology and psychiatry.

Your joy is your sorrow unmasked.

- Khalil Gibran (from ‘The Prophet’)

Introduction

It seems as if we are in the midst of a ‘depression epidemic’, which has been accompanied by a dramatic increase in the number of prescriptions for the selective serotonin reuptake inhibitor (SSRI) class of antidepressant drugs over the last two decades. (ABC, 2007; Healey, 2003, p.2) The Global Burden of Disease Study has projected that by 2020 Depression will be the leading cause of disease burden in the world. (Murray & Lopez, 1996) and a similar study conducted in Australia has made the same prediction. (Mathers et al., 2000) However, without denying the reality of the extreme suffering experienced by patients with a Depressive disorder, it would seem that in many instances the diagnosis of Depression may not, in fact, be a valid one. (Lee, 1999; Horowitz, A., Wakefield, J. 2007 ) As noted by Arthur Kleinman, a renowned expert in the cross-cultural and anthropological aspects of mental illness: ‘There is no question in my mind that severe clinical depression is a real disease. I could take you all over the world, and you would have no difficulty recognizing severely depressed people in completely different settings. But mild depression is a totally different kettle of fish. It allows us to re-label as depression an enormous number of things’. (Schulz, 2004) This paper explores some of the possible reasons for this by examining the contemporary psychiatric paradigm as well as that of traditional Chinese medicine (TCM) with respect to the diagnosis and treatment of Depression. Subsequently it argues for a complete overhaul of the way depression is diagnosed and treated as well as the ways in which clinical outcomes are assessed. Moreover, it calls for a drastic restriction in the use of SSRI’s because of their dubious risk to benefit ratio.

Depression in Modern Western Psychiatry

Nosology

The generally accepted standard for psychiatric nosology is the Diagnostic & Statistical Manual of Mental Disorders IV– Text Revision, 2000 (DSM-IV-TR). (Reus, 2007; Fawcett, 2005; Bhalla & Aronson, 2006, Lee, 1999) According to the DSM-IV-TR there are five classes of Depressive disorders:
• Dysthymic Disorder
• Major Depressive Disorder (single episode or recurrent)
• Depressive Disorder Not Otherwise Specified (NOS)
• Mood Disorder Due to a General Medical Condition with Depressive Features
• Substance Induced Mood disorders
(APA, 2000)

In addition to the above, the ICD-10 , a diagnostic system developed by the World Health Organization, seeks to harmonize with the DSM. It describes single episode (F32) and recurrent episodes of depression (F33), categorizing them as mild, moderate, severe, and severe with psychotic symptoms. In addition there are ‘other’ and ‘unspecified’ categories for both single episode and recurrent depression. Cyclothymic and dysthymic disorder are classified under ‘Persistent mood [affective] disorders’ (F38). (WHO, 2007) Outside of the USA, the DSM system is generally regarded as a useful tool for research, the ICD system providing a more favoured approach to clinical diagnosis and training. (Mezzich, 2002)

The following discussion is focused on:
• Dysthymic Disorder, Major Depressive Disorder and Depressive Disorder Not Otherwise Specified (NOS) from the DSM-IV
• Mild, Moderate and Severe Episodes of Depression (F32.0, F32.1, F32.2) and Dysthymia (F34.1) from the ICD

Dysthymic Disorder/Dysthymia

Dysthymic Disorder is a depressive mood disorder characterized by a chronic course and an insidious onset. Many people with Dysthymia report that they have been depressed all of their lives and have an outlook coloured by a chronically depressed mood. By definition, Dysthymia is a chronic mood disorder, as distinct from Depressive Disorder (NOS), discussed below. (Reus, 2007; Fawcett, 2005; Bhalla & Aronson, 2006)

Major Depression/Severe Depression

Current scientific opinion views Major Depression is a biological, medical illness. Abnormalities involving the neurotransmitter serotonin are thought to be involved in its pathogenesis. There appears to be a genetic predisposition to Major Depression. Life events, such as the death of a loved one, a major loss or change, chronic stress, and alcohol and drug abuse, may trigger episodes of depression more easily in those with a family history of Major Depression. It is also important to note that a depressive episode may occur spontaneously, i.e. not triggered by a life crisis, physical illness, or other risk factors. (Reus, 2007; Fawcett, 2005; Bhalla & Aronson, 2006)

According to the DSM-IV, TR, the key diagnostic features of Major Depression are as follows:
• At least 5 of the following, during the same 2-week period, representing a change from previous functioning; must include either (a) or (b):
a) Depressed mood
b) Diminished interest or pleasure
c) Significant weight loss or gain
d) Insomnia or hypersomnia
e) Psychomotor agitation or retardation
f) Fatigue or loss of energy
g) Feelings of worthlessness
h) Diminished ability to think or concentrate; indecisiveness
i) Recurrent thoughts of death, suicidal ideation, suicide attempt, or specific plan for suicide
• Symptoms do not meet criteria for a mixed episode (i.e. meets criteria for both manic and depressive episode).
• Symptoms cause clinically significant distress or impairment of functioning.
• Symptoms are not due to the direct physiologic effects of a substance or a general medical condition.
• Symptoms are not better accounted for by bereavement, i.e. the symptoms persist for longer than 2 months or are characterized by marked functional impairment, morbid preoccupation with worthlessness, suicidal ideation, psychotic symptoms, or psychomotor retardation.
(APA, 2000)

Depressive Disorder (NOS)/Minor (or Mild to Moderate) Depression

This is the more controversial category of the depressive disorders, which is included in the DSM-IV, TR as a research category only. (APA, 2000) In comparison with Major Depression, patients with this condition may have fewer vegetative symptoms (appetite, diurnal mood variation) and more subjective symptoms (self-blame, worry, irritability, lethargy). However, they do not have a sufficient number of symptoms (i.e. there are less than five) to be diagnosed with Major Depression; nor has the condition persisted for a sufficient length of time for the disorder to be diagnosed as Dysthymia (i.e. at least 2 years in adults and 1 year in adolescents and children). However, Minor Depressive disorder is more prevalent in primary care than Major Depressive Disorder. (Reus, 2007; Fawcett, 2005; Bhalla & Aronson, 2006) Cognitive-behavioural modes of therapy in conjunction with the administration of SSRI’s have demonstrated efficacy for primary care patients who have Minor Depression. (Banazak, 2000)

Limitations of the DSM-IV

The serious limitations of the DSM approach have been discussed elsewhere. (Satel, 2008; Horowitz & Wakefield, 2007; Lee, 1999; Mosher, 1998; Kaiser, 1996). While a critique of the DSM is beyond the scope of this article there are several points that pertain to our discussion here.

• It is descriptive and not based on aetiology; the idea being that it would be useful for physicians with various theoretical orientations. Because it has a statistical not etiological basis, people sharing the same diagnosis may not have the same aetiology nor require the same treatment.
• A corollary of the above statement is that disorders, such as Major Depressive Disorder, are described without reference to the context in which they occur; the only exceptions, in this case, being bereavement, medical conditions that may cause depression, and substance abuse (APA, 2000)
• It emphasizes reliability over validity. Therefore the validity of a particular diagnosis, i.e. Major Depressive Disorder, is questionable. Thus, when faced with a patient that fulfils the major symptom criteria, described above, any psychiatrist (or general practitioner, for that matter) will invariably make this particular diagnosis. However, as we shall see, the patient may not, in fact, have a psychological disorder. (Lee, 1999; Horowitz & Wakefield, 2007)
• It has been overly influenced by the various multinational pharmaceutical companies, which have a vested interest in ‘widening the net’. Cosgrove et al. found that every psychiatric expert involved in writing the standard diagnostic criteria for disorders such as depression and schizophrenia has had financial ties to drug companies that sell medications for those illnesses. (Cosgrove et al., 2006; Lee, 1999) The ramifications of this are discussed below. The outcome of the above is that the DSM-IV fosters a tendency to both over diagnose Depression as well as to over prescribe SSRI’s. (Horowitz & Wakefield, 2007; Currie, 2005; Healey, 2003; Lee, 1999; Shorter, 1997)

The ‘Phasing’ Out of Neurasthenia

Perhaps one of the more insidious consequences of the hegemony of the DSM is the dropping of Neurasthenia in favour of Depressive and/or Anxiety Disorders. (Lee, 1999) This disorder was first described in 1869 by G. M. Beard, an American neurologist. Subsequently this disorder was commonly diagnosed in the USA and Europe. Neurasthenia arises when a person’s commitments (e.g. work, family, emotional and physical) over-tax the nervous system beyond its capacity to maintain normal functioning. In China and Russia it was the most common psychiatric diagnosis up until the 1980’s, when the impact of modern Western psychiatry, particularly the DSM-III, began to shape the academic and clinical landscapes. Cultural factors aside, it is noteworthy that a disorder, which was mainly treated by non drug methods, should be almost ubiquitously supplanted by disorders that are to be treated primarily with pharmaceutical agents. In practice many clinicians still make this diagnosis, basing treatment strategies on counselling, stress reduction, increased rest, nourishing diet and tonic herbal formulations. This is in keeping with the pathogenesis of this disorder as exhaustion of the nervous system. From the viewpoint of TCM, this is a valid clinical entity, which corresponds with various deficiency- type (xu 虚) syndrome-patterns (Lee, 1999)

The Chinese Classification of Mental Disorders, second edition, revised (CCMD-2-R) defines neurasthenia as follows:
At least 3 symptoms from the following five groups of symptoms
• Weakness (mental or physical fatigue/decreased efficiency)
• Dysphoria (irritable, worrisome, inability to relax)
• Excitement – easily mentally excitable (accompanied by unpleasant feelings)
• Nervous muscular pain (e.g. tension headache, myalgia)
• Sleep disturbances

In addition, the disorder is of at least 3 months duration and there is marked lowering of work, study or social functioning, which causes sufficient mental distress so that the sufferer seeks treatment. (Chinese Medical Association and Nanjing Medical University, 1995, p.85, quoted in Lee, 1999)

In my opinion, this is a valid clinical entity that responds well to TCM treatments. Moreover, such a diagnosis (where appropriate) may help to avoid the stigma as well as the sense of hopelessness that are often associated with receiving a psychiatric diagnosis.

Depression in the Clinical Setting

The rise (and rise) of biopsychiatry

Since the 1980’s research efforts have switched from the psychodynamic model to the biological model, in which psychiatric disorders are to be treated chemically. ‘Biopsychiatry’ is a term that has been coined to denote (and promote) the pharmaceutical industry's preferred view of mental illness as chemical imbalance. It has to a large extent replaced the theoretical base of cognitive therapy within psychiatry using the justification of evidence-based medicine (EBM). Obviously research involving psychoactive drugs lends itself more readily to the ‘gold standard’ randomized clinical trial (RCT) model than the subtle and individual art of human skills based interventions. This transition within psychiatry has not been without its critics and detractors – from within the profession as well as outside. (Kleinman, 2007; Horowitz & Wakefield, 2007, pp. 72-165; Healy, 2003; Lee, 1999; Mosher, 1998; Kaiser, 1996)

As noted by eminent psychiatrist Dr. Loren Mosher in his letter of resignation from the American Psychiatric Association, if all of mental illness is to be regarded as ‘biologically based brain diseases’ then the art and science of psychiatry (such as it is) would become subsumed as a branch of neurology. (Mosher, 1998) This amounts to a denial of the empirically observed ability of one human being’s ability to influence and bring about changes in another through empathetic counsel. In other words this approach has not only dehumanized psychiatry, it also dehumanizes people and their relationships.

In the 1950’s pharmaceutical companies were not interested in developing antidepressant drugs because they did not see much market potential in this area. Indeed, before the 1980’s the prevalence of severe depression, requiring hospitalization, was considered low and experts considered that Depression was one of the psychiatric conditions with the best prognosis, with or without treatment. During the 1980’s through their influence on the development of the DSM as well as through their own promotional activities, multinational pharmaceutical companies gave a different face to Depression. It came to be seen as a chemical ‘deficiency state’, requiring the ingestion of the SSRI’s or similarly acting drugs in order to return serotonin (and/or other neurotransmitters) to normal levels.

Moreover, due to the efforts of these companies to ‘widen the net’ (i.e. to broaden the clinical applications for SSRI’s), what were once regarded as normal – albeit unpleasant – mental states (i.e. our responses to the vicissitudes of daily living) have now come to be relabelled as Depression or some other DSM-IV defined disorder. (Horowitz & Wakefield, 2007, pp. 72-104; Medawar & Hardon, 2004; Healy, 2003, pp.1-40 )

The targets for these activities include not only qualified psychiatrists – who are best equipped to critically evaluate them – but, more significantly, family (or ‘general’) practitioners. The latter have been continually exposed to exhortations to recognize the many depressed patients who would normally go undiagnosed. The implication is that, left to themselves, such patients would deteriorate to the point where suicide becomes a major risk. This campaign is supported with oversimplified diagnostic tests, including a screening questionnaire with only two questions and a four-point depression checklist. (Arroll et al., 2003; Currie, 2005)

In addition to exaggerating the risks of Depression, the adverse effects of SSRI’s have also been minimized. This has been done through selectively drawing on studies that support these views and repressing studies that do not. (Medawar et al., 2004; Whittington et al., 2004; Healy, D., 2003) Indeed, pharmaceutical companies became involved in a concerted campaign to redefine the DSM-IV meaning of ‘prescription drug dependency’ so as to avoid the charge of addiction or withdrawal symptoms being associated with SSRI administration. (Medawar & Hardon, 2004)

Lacasse & Leo have noted that: ‘Contemporary neuroscience research has failed to confirm any serotonergic lesion in any mental disorder, and has in fact provided significant counterevidence to the explanation of a simple neurotransmitter deficiency. Modern neuroscience has instead shown that the brain is vastly complex and poorly understood’. (Lacasse & Leo, 2005) This perspective is affirmed by Charney, who describes the finely orchestrated synergy of eleven different neurochemicals (including serotonin) in the regulation and maintenance of psychological balance. (Charney,2004) Indeed, there are many others share this view. (e.g. Glenmullen, 2000, pp.16-20; Healy, 2003, pp.11-12, 263-266; Breggin, 2001, pp.21-23; 30-32)

Thus, contemporary psychiatry has largely sidestepped the issue of causes in its analysis of Depression by relying on a statistically based diagnostic system. Moreover, the influence of pharmaceutical company interests has shifted the focus to a deficiency of serotonin, reinforcing (or possibly enforcing) an overly simplistic and reductionist perspective on this disorder.

Clinical Depression Redefined

In their recent landmark publication, Horowitz and Wakefield argue convincingly for a return to continuity with the historical roots of Western psychology. In what may seem to be a statement of the ‘blindingly obvious’, they propose that we turn our attention to the issue of depression ‘with cause’ and depression ‘without cause’. If after comprehensive questioning regarding the patient’s current life circumstances the practitioner is able to find one or more reasons why the patient is feeling sad, then the patient is experiencing a normal human response to distressing circumstances (mostly a loss of some kind) and is not suffering from clinical depression. If, on the other hand, the patient is either showing a disproportionate response to such circumstances within the cultural context in which it occurs (i.e. appearing to lose their grip on reality) or in fact no contributing circumstances can be found, then and only then do they become a candidate for the diagnosis of clinical Depression. (Horowitz & Wakefield, 2007) Unfortunately, for the reasons discussed above, this approach has largely been abandoned, particularly in the place where most of the ‘action’ takes place – the surgery of a busy general/family practitioner.

I would like to propose that patients with a depressed mood be classified as follows:
a) Normal healthy response to distressing circumstances
b) Pathological response to distressing circumstances (i.e. exaggerated response or continued response after the circumstances have been resolved)
c) No cause for depressed mood (clinical Depression)

The fact that patients in category a) feel sufficiently distressed to visit a healthcare practitioner would indicate that they require support of some kind, e.g. counselling, stress management, lifestyle change, nutritional supplementation, TCM treatments. Patients in group b) may also benefit from this approach or, in more severe cases Western psychiatric treatment. Those with obvious clinical Depression, in group c), should be referred on to a professional psychiatrist. The use of strong and potentially dangerous drugs (i.e. the SSRI’s) should be reserved for patients with a clear clinical disorder – one in which they exhibit either a severely disproportionate response to external causes or one in which symptoms occur in the absence of external causes.

Selective Serotonin Reuptake Inhibitors (SSRI’s)

Clinical effects

The SSRI class of drugs acts by selectively inhibiting serotonin reuptake and as a result serotonergic neurotransmission is powerfully enhanced. Put simply, serotonin is one of the major (if not THE major) ‘feel good’ neurochemicals in the brain; if there is not enough of it, or if it’s action is curtailed for any reason, a person will feel sad and withdrawn. On the other hand, normal (and possibly enhanced) levels or duration of activity of this chemical result in normal (and possibly enhanced) levels of well being. This is the message that the manufacturers and their advocates have fiercely promulgated from the mid 1990’s to the present day. (Healey, 2003; Glenmullen, 2000, pp.13-15) However, the serotonergic system is widespread throughout the brain as well as the rest of the body and it influences a great variety of activities in addition to its effects on mood. (Glenmullen, 2000, p.16; Breggin, 2001, pp.31-32)

Side effects

The SSRI’s are marketed under the following names: Prozac, Paxil, Zoloft, Celexa, Lexapro, Luvox, Eflexor and Sarafem. The major differences between them are related to the individual side effect profile. (Edwards & Anderson, 1999; Cipriani, Brambilla, Furukawa, Geddes, Gregis, Hotopf, et al., 2005) However, there is evidence that escitalopram is superior to the other drugs of this class in the treatment of Major Depression. (Kennedy et al., 2006) According to the manufacturer’s product information these drugs have around 240 different side effects. Information obtained from the American FDA in 1993 revealed that as of September 16, 1993 (less than six years after the drug had been approved for marketing), 28,623 reports of adverse reactions to Prozac had been received by the FDA. These included: delirium, hallucinations, convulsions, violent hostility, aggression, psychosis, 1,885 suicide attempts and 1,734 deaths - 1,089 by suicide. (Whittle & Wieland, 1994) Moore found that: ‘during a ten year period Prozac was associated with more hospitalizations, deaths or other serious adverse effects reported to the FDA than any other drug in America’. (Moore, 1998, p.9) Spigset found that the following were the most common classes of adverse events associated with SSRI use:
• Neurological (22%)
• Psychiatric (19.5%)
• Gastrointestinal (18%)
• Dermatological (11.4%)
(Spigset, 1999)

In a study on the side effects of various commonly prescribed antidepressants, it was found that 10 – 32% of patients taking Paxil, Zoloft and Eflexor experienced nervousness, agitation, tremor, dizziness, myoclonus, headaches or problems with sleep (Vanderkooy et al., 2002)

Zuckerman et al. examined the incidence of adverse events in a small group of children who were started on SSRI’s at or below 7 years of age and found 28% experienced adverse events, such as gastrointestinal upset and behavioural activation sufficiently severe to cause them to discontinue treatment. (Zuckerman, Vaughan, Whitney, Dodds, Yakhkind, MacMillan, et al., 2007)

Some of these reactions, such as nausea, diarrhoea, headache and agitation are transient and remit after the first 2 – 3 weeks. However, in a number of patients these are severe enough to cause them to discontinue treatment. This is significant because usually, 2 – 6 weeks at a therapeutic dose level are needed to observe a clinical response.

Some of the more significant long term side effects include:
• Increased risk of suicide
• Increased risk of violent behaviour
• Insomnia (15-20%)
• Weight gain (18-50%)
• Sexual dysfunction (generally decreased libido and delayed or absent orgasm)
(Sherman, 1998; Dording et al., 2002; Masand & Gupta, 2002: Csoksa & Shipko, 2006)

SSRI’s and Suicide

There have been several studies on the influence of SSSRI’s on suicide rates. The results are generally conflicting. A systematic review conducted by Fergusson et al. in 2005, found that there was ‘an association between suicide attempts and the use of SSRIs.’ However, the authors noted that their findings were compromised due to ‘several major methodological limitations in the published trials’. (Fergusson et al., 2005). Disingenuously, a recent German meta-analysis of the available randomised, placebo controlled trials on SSRI’s in children and adolescents concluded that the association between SSRI’s and suicide is no more than for depressed patients taking a placebo! (Holtmann et al., 2006) In other words, there is no evidence that SSRI’s have a preventative role on suicide in patients with Depression. A systematic review conducted by Hetrick et al., concluded: ‘While untreated depression is associated with the risk of completed suicide and impacts on functioning, it is unclear whether SSRIs would modify this risk in a clinically meaningful way.’ (Hetrick et al., 2007) It is highly likely that SSRI use is associated with an increased risk of suicide during the early stages of treatment when psychomotor retardation has been alleviated but the mood has not yet improved. Hall recommends that: ‘On the available evidence, it would be prudent for those who prescribe SSRI’s (and newer) antidepressants to monitor suicidal ideation in the first 2 weeks after prescribing them to a depressed patient. (Hall, 2006) Recently the Australian Therapeutic Goods Administration (TGA) regulated to require that sponsors of SSRI’s include warnings to this effect in their product information (Australian Government Department of Health and Ageing, 2004)

Discontinuation, Dependency, Withdrawal and Addiction

As mentioned above, the DSM-IV definition of ‘prescription drug dependency’ was redefined, under the influence of the multinational pharmaceutical companies, so as to avoid the obligation to use the terms ‘dependence’, ‘addiction’ and ‘withdrawal’ in connection with prescribed doses of SSRI’s. However, research now indicates that 35 – 85% of people who abruptly stop taking SSRI’s will develop one or more symptoms of withdrawal. (Fava et al., 1997; Haddad, 1998; Haddad, 2001; Warner et al., 2006; Lader, 2007) These symptoms include dramatic changes in mood (including a worsening of depression), insomnia, appetite changes, agitation and electric shock sensations. Because withdrawal symptoms may mimic the very reason for which the drug was initially prescribed, this gives the appearance of a relapse, leading to the prescribing of additional drugs or higher dosages of the original. (Young & Haddad 2000) Young and Currie found that 70% of physicians involved in a knowledge base survey said that they were unaware of antidepressant discontinuation events; only 17% said that they would caution patients about the possibility of such symptoms. (Young & Currie, 1997)

Efficacy Issues

Although many studies are biased (e.g. through inadequate reporting of adverse events) and many negative ones suppressed (i.e. they are simply not published), the SSRI’s are estimated to be clinically effective in around 50% of cases. (Medawar et al., 2004; Whittington et al., 2004; Healy, D., 2003) A careful analysis of both published and unpublished trails that had been registered with the American Food and Drug Administration (FDA) before 2008 showed that the size of the clinical effect of SSRI’s had been significantly inflated because of inadequate reporting or failure to publish. ‘The increase in effect size ranged from 11 to 69% for individual drugs and was 32% overall.’ (Turner et al., 2008)

The only definite statement that can be made at this stage is that the overall treatment effects of SSRI’s are modest and the burden and costs of harm have never been defined. It is notable that there are neither systematic reviews nor meta-analyses regarding the efficacy of SSRI’s on the Cochrane database at the time of writing. It is also noteworthy that SSRI’s appear to have about the same efficacy as the older tricyclics, which have recently been shown to be only minimally more effective than an ‘active placebo’ (i.e. a placebo that mimics the side effects of the drug in question). (Moncrieff et al, 2004; Cipriani et al., 2005)

Clinical Outcomes of Interest

In addition to the core issues surrounding the diagnosis of Depression, the crucial issue of how to measure the effectiveness of treatments for depression still remains unresolved. Kleinman noted in his 1982 study on Neurasthenia and Depression in China, that in spite of satisfactory symptom relief provided by medication, about one third of patients were no better off in terms of the associated problems that they experienced with work, family, school, marriage, finances, their own personality and other social relations. In fact, a significant percentage (30%) claimed that their situation had become worse. (Kleinman, 1982) Such findings strongly suggest that the sole reliance on symptom relief as an outcome measure is not satisfactory. Additionally, the ‘gold standard’ measurement scales for assessing the severity of the subjective symptoms of depression (e.g. the Hamilton Rating Scale for Depression) have received serious criticism recently and are regarded by many as both flawed and inadequate. (Bagby et al., 2004)

Clearly there is a need for meaningful clinical outcomes in the treatment of Depression to include not only subjective as well as objective measurements of symptom relief, but also a global assessment of quality of life (also both subjectively and objectively determined). Unfortunately these have not been adequately conducted in clinical studies of Depression to date.

Should SSRI’s be confined to Psychiatrists?

While there is some fairly convincing evidence for the efficacy of escitalopram in providing symptom relief for patients with Major Depression, (Kennedy et al., 2006; Montgomery et al., 2007) their use in Minor Depression/Depressive Disorder NOS is questionable. (Fogel, 2006) Perhaps the most telling drawback associated with the clinical application of SSRI’s is the fact that over 80% of them are prescribed by general (or family) practitioners, who have had neither specialized training in psychiatry nor in the specific pharmacology of this class of drugs. (Currie, 2005; Horowitz & Wakefield, 2007) However, there has been a plethora of publicity linking declining suicide rates to increased prescribing of SSRI’s by GP’s (e.g. Mant et al., 2004; Hall et al, 2003). In spite of the fact that much of this ‘evidence’ is bogus (e.g., see: ‘Rapid Responses’ to Hall et al., 2003) it is unlikely that the use of these substances will be restricted to qualified psychiatrists, as, in the author’s opinion, they ought to be.

Non Drug therapies

There is some evidence that the following non-drug therapies may be effective for various types of depression.
• DHEA: (Schmidt et al., 2005).
• St John’s Wort (SJW): (Linde et al., 2005; do Rego et al, 2007)
• 5 Hydroxytryptophan (5-HTP) and tryptophan: (Shaw et al., 2002)
• Music therapy: (Boso et al., 2006; Sliwka et al., 2006; Jones & Field, 1999; Filed et al., 1998)
• Exercise: (Larun, et al., 2006)
• Mindfulness-based cognitive therapy: (Finucane & Mercer, 2006; Smith et al., 2007; Mason & Hargreaves, 2001; Teasdale et al., 2000)

The Role of Nutrition

There is also some evidence that a deficiency of various nutrients may be involved in the development of depressed mood in some cases, e.g. Omega-3 fatty acids (Song & Zhao, 2007; Lin & Su, 2007); B-complex vitamins (either individually or as a group); Folic acid (Fava, 2007; Clement et al., 2007; Young, 2007); Vitamin D (Berk et al., 2007); Magnesium (Eby & Eby, 2006; Siwek et al, 2006); Zinc (Levenson, 2006; Nowak et al., 2005); Iron (Vahdat Shariatpanaahi et al., 2007). (Gariballa & Forster, 2007; Folstein et al., 2007; Sanchez-Villegas et al., 2006). Thus, it would be reasonable to assume that appropriate nutritional supplementation would be likely to benefit patients with depressed mood.

Biography

Tony Reid (MTCM, DTCM, DAc) has been actively involved in Chinese medicine as practitioner, educator, lecturer and author since 1980. Receiving the bulk of his training in Australia, he has also studied and trained in Hangzhou (PRC), where he has contributed to the development of standardized English nomenclature for the interpreters at the Zhejiang TCM Academy and the Zhejiang College of TCM. In recent years, he has authored two clinical reference manuals on prepared Chinese herbal medicines, ‘Essential Formulas’ and ‘Empirical Formulas’. He is a contributor to professional journals such as ‘The Natural Therapist’, ‘NZRA Journal of TCM’, ‘The Lantern’, ‘Australian Journal of Acupuncture and Chinese Medicine’, ‘The Journal of Chinese Medicine’ and ‘Chinese Medicine Times’. Tony conducts annual seminars and workshops throughout Australia and publishes a bi-monthly clinical update, focusing on effective treatment approaches to common health problems.

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End notes

1. In this paper capitalization is used to distinguish a diagnosed disorder or a medical/psychiatric diagnostic category (e.g. ‘Depression’ or ‘Depressive Disorder’) from a symptom (e.g. ‘depression’ or ‘depressive’).
2. An excellent account of the ramifications of the invalid criteria for diagnosing clinical depression is to be found in chapters 4-10, Horowitz & Wakefield (2007). The Loss of Sadness: How Psychiatry Transformed Normal Sorrow into Depressive Disorder. New York, Oxford University Press.
3. International Statistical Classification of Diseases and Related Health Problems, 10th Revision, Version for 2007
4. Readers who are interested in exploring some of the activities of the multinational pharmaceutical companies who produce and market SSRI’s are referred to David Healey’s book: Let Them Eat Prozac. Toronto. James Lorimer and Company, (2003).
5. An in depth discussion of the normal healthy human sadness response is to be found in chapter 2, Horowitz & Wakefield (2007). The Loss of Sadness: How Psychiatry Transformed Normal Sorrow into Depressive Disorder. New York, Oxford University Press (2007).
6. Readers who wish to further explore the dangers of the SSRI’s as well as alternative therapeutic approaches to the problem of depressed mood from the perspective of a practicing clinician are referred to: Glenmullen, J. (2000). Prozac Backlash. New York: Simon & Schuster and Breggin, P. (2001). The Anti-Depressant Fact Book. Cambridge, MA: Da Capo Press.


Depression: Towards an Integrated Approach - Part One

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