Depression affects most people at some stage of their lives.
Clinical depression may be defined as a mood disorder which impairs normal function.

Depression is a 'whole-body' disorder affecting many levels of being including the body, nervous system, moods, thoughts, and behaviour. Observable symptoms of depression may include chronic fatigue, sleep disturbances, changes in appetite, headaches, backaches, digestive disorders, restlessness, irritability, loss of interest or pleasure in hobbies, and feelings of worthlessness and inadequacy.

In noting the symptoms of depressed individuals, clinicians often look to the causes and distinguish them between external, environmental variables, and internal physiological variables as depicted in the following table:-

The aspects of self-concept, activity level and body maintenance (or vegetative) functions are altered in these disorders as much if not more than mood.

Clinical experience has shown that understanding of the affective disorders needs to take place at three levels of enquiry:-

1. The experience of the mood disorder, which refers to the conscious feeling of depressive affect or sadness at one end of the continuum or of the elation and euphoria at the other.
2. The outward expression of the affective disorder including changes in the level of activity and neurovegetative functioning
3. The cognitive components of these disorders characterised by the either unduly negative or unduly positive appraisal of internal or external events.

The affective disorders including depression can be characterised by their interference with the emotional tone of the processing of information. The deficits so produced are more by way of a loss of effortful processing rather than intrinsic problems with the actual information processing.

As we can see, depression has multiple possible explanations, and accordingly, there are various schools of thought on the roots of depression, and as is usual, since we are considering a human being's complexity on many levels, - all have their merits and require consideration.

The consistent finding of neuropsycholphysiological studies of depression is that abnormally low levels of neurotransmitters - mainly norepinepherine, dopamine and serotonin - appear to be linked to depression. Other findings correlate with an imbalance of the thalamocortical circuiting and feedback and gating circuits. In the depressed state the overactive circuits represent autonomous and exaggerated activity of prefrontal or basal ganglia circuits that code for negative imagery of self and the larger world^3..

Work as early as 1937 (Papez, 1937) suggested that reverberations through the limbic system were responsible for generating emotional activity. And subsequent studies as well as PET investigations in 1992 by Drevets et.al., found that increased blood flow through the amygdala may be a trait marker for depressive disorders whether depression is manifest or not. Drevets, in comparing his findings to other neurophysiological data available, suggests that the functioning of a prefrontal-amygdala-medial dorsal thalmic circuitry is overactive in a depressed individual's brain^3.. CT studies by Schlegal & Ketzschmar in 1987 cited ventricular enlargement in unipolar as well as bipolar depression ^4..

A study by Starkstein & Robinson in 1997^5., suggests that dysfunction of the frontal lobes (the executive and decision making area of the brain) may produce overinhibition of dorsal brain areas, thus abnormally reducing motor, instinctive, intellectual, and emotional output, and further studies in this area by Mayberg^6., suggest that recovery from depression will involve inhibition of the overactive ventral regions (amygdal/limbic system) and normalisation of the frontodorsal hypofunction.

EEG findings in studies of genetic unipolar depressives show that depressed persons display a disorganised atypical sleep pattern which skips a 'level' of deep sleep and prominent delta and theta waves (which are sleep waves) in the waking state ^7.. So we may conclude that the depressed person's brainwave activity in sleep is invaded by 'waking' waves and the reverse in the waking state.

The Brain-Thyroid axis has also been implicated in the biology of depression and the blunting of the thyroid stimulating hormone (TSH) response to thyrotropin releasing hormone and the elevation of serum T₄ are the most consistent findings^8..

Recent studies suggest that closed head injury of the coup-contra coup type involving axonal shear contribute significantly to depression via reduction of serotonin receptors and disruption of the connections between dorsal and ventral areas of the brain^9..

Many studies have found relationships between the type of food we ingest and depression. One of the most common causes of depression is in fact food allergies, and another is hypoglycemia (low blood/sugar)^11..

Heredity (genetics) is a significant factor which can not be overlooked. In up to 50% of people suffering depression, one or both parents also experienced depression.

Antidepressant therapies began in 1956 when a drug used in the treatment of tuberculosis was found to elevate mood. Two years later, the antidepressant imipramine was marketed.

Today, there is a wide choice of antidepressants available. They are the medically recognised treatment for all forms of moderate and severe depression regardless of cause. About 70 per cent of patients with depression respond to treatment with antidepressants, yet the side effects of these drugs can be a major contributor to depression.

Anti-depressants can be distinguished most commonly by their safety profile or tolerability, although there are indications that efficacy, especially in severe depression, varies between classes of antidepressants

Many drugs which act on the brain have much the same action on people who are unaffected by mental illness or those who have a problem.

Dr D Healy in his book 'Psychiatric Drugs Explained' (Mosby, 1997) explains effects of antidepressants using comparison with coffee or alcohol intake. One cup of coffee may be alerting, two cups more so and three cups makes you really wired up. Similarly the more you drink the greater the effect that alcohol has on the brain. But with antidepressants taking a dose above a certain threshold will not increase the antidepressant effect. The only thing which happens is that you will get more than the usual side effects. And more worrying, some antidepressants can be fatal if taken in relatively small amounts above the recommended maximum dose because of their effects on the heart.

Antidepressants work within the brain to either increase the levels of noradrenaline, serotonin or both. For example, tricyclic antidepressants like amitriptyline increase the levels of both noradrenaline and serotonin in the brain - they consequently have a dual action effect.

However the selective serotonin reuptake inhibitors , SSRIs, work only on the serotonin system. There is a belief among experts that they are not quite as effective as 'dual action' drugs in treating more severe forms of depression.

First you have to be taking an 'adequate' dose of antidepressant regularly for up to six weeks before your doctor will conclude that you have not responded to treatment. If you still haven't improved by this stage, your doctor has a number of alternatives to consider, including raising the dose, switching to another antidepressant or even trying any combination of the available antidepressants.

Following is a brief overview of the main characteristics of the major classes of antidepressants:

Tricyclic antidepressants (TCAs) were introduced over 30 years ago. They are widely regarded as among the most effective antidepressants available. But they have a number of major down sides because their effects in the brain are not only restricted to alleviating depression. They also interact with a number of other brain receptors, thus causing side effects. This means patients are often unable to tolerate them.

TCAs interfere with other receptors in the brain and this means that they tend to be sedative when they are first taken. It's a good idea to take these drugs just before you go to sleep. Curiously in some people, about one in ten, these antidepressants can actually be arousing , making them more alert.

TCAs also interfere with cholinergic receptors in the brain and they are commonly associated with anticholinergic side effects like, dry mouth, blurred vision, constipation, urinary difficulties and tremor. In addition, they tend to lower blood pressure which means that if someone stands up suddenly, they can produce a feeling of faintness and the elderly in particular can fall over, possibly even leading to bone fractures. Other problems include impotence.

Most importantly, TCAs are not safe when taken in overdose. In addition to what is mentioned above, the TCAs also have other effects on the heart inducing tachycardia ( an increase in heart rate) and arrhythmia (abnormal rhythms of heart beat). Cardiotoxicity is the most common cause of fatality following TCA overdose.

The tricyclic antidepressants are usually used in more severe cases of depression, but are also prescribed in general practice.

MAOIs work by inhibiting the action of an enzyme which is responsible for the breakdown of noradrenaline and serotonin in the brain. They are free of the anticholinergic effects described for the TCAs but side effects include insomnia, agitation and headache.

However the most worrying problem associated with these drugs is something called the cheese effect. Cheese and certain other foods contain a substance called tyramine which is normally broken down in the gut. However these antidepressants also inhibit this enzyme so the tyramine enters the body where it can cause a dangerous rise in blood pressure. Tyramine is also found in avocado, bananas, caviar, canned fig, liver and, wines and beers. This effect has severely limited the use of this antidepressant although moclobemide, a newer version of this class of drugs, is not associated with this effect and appears to be safe in this respect.

SSRI antidepressants were introduced in the late Eighties. These drugs are better tolerated and more acceptable to patients than the older TCAs. They have few of the anticholinergic effects, they lack the cardiotoxic effects and are probably safe in overdose.

However they are characterised by a group of side effects which have become known as the serotonergic side effects. One of these that has been the subject of much media coverage in recent years is the fact they can interfere with sexual functioning, usually by causing delayed ejaculation or orgasm. This is a particularly problematic side effect if these antidepressants are used for long term treatment.

Another major group of side effects is gastrointestinal side effects which vary from mild discomfort, nausea, weight loss and in extreme cases vomiting and diarrhoea.

Sleep disturbances are another important problem with the SSRIs particularly because it is a symptom of depression from which people commonly seek relief. In addition varying amounts of nervousness, anxiety and agitation occur in some patients early in treatment although they often subside relatively quickly as the body becomes accustomed to this assault.

There are many more side effects listed in the MIMS - so it is important to ask your prescribing doctor of the possible side effects and interactions with other drugs/foods. If he can't tell you - perhaps he should find out before writing the prescription for you.

A balanced lifestyle is of course a major consideration in the treatment of any disorder. Setting realistic goals, adequate rest, diet and nutrition, and of course adequate exercise, all contribute greatly to a healthy mind and body.

Foods profoundly influence the brain's behaviour. A poor diet - especially one full of junk foods, is a common cause of depression. The neurotransmitters which direct brain function, and regulate our behaviour are closely linked to mood, and are controlled by what we eat.

Recent research into the effects of different foods on the human system indicates that depression can be ameliorated by eating more of certain types of foods, and avoidance of others. Food sensitivities (allergies) are in fact the most common cause of depression - which suggests that susceptibility may be genetically based. Further, it has been demonstrated that genetic expression can be modified through diet and nutrition^12..

Training is similar to stimulation, and constitutes a push that invokes the brain's innate capacity for restoring homeostasis. Over the longer term, this results in a long-term increase in stability. Training at a specific frequency is then a push in a very specific direction, which can be chosen in light of specific arousal disregulation or attentional deficits found in each case.
This brain exercise moves the individual into regions where he or she may not heretofore have been able to reside comfortably or stably. This is made possible not only by increased flexibility of state, but by an increased ability to maintain overall nervous system stability.

Given that hypofusion of the executive areas of the brain (frontal lobes, temporal lobes) is a common trait amongst sufferers of depression it is easy to see the relevance of HEG biofeedback in the amelioration of this disorder.

At Learning Discoveries, our approach looks at guiding and educating the person in their own innate capacities to attain balance and wellbeing in their lives.

After a thorough history and psychometric assessment including a QEEG, an individualised programme will be devised aimed at restoring balance in the autonomic nervous system, and outlook. These include a combination of any of the following:- education and counselling, diet and nutrition, breathwork, biofeedback and/or neurofeedback training, heart rate variability training, meditation and movement exercises.

Consultation is by appointment only, for further information please contact:-

 References:

1. Sternberg, R.J., In Search of the Human Mind, 1995, Harcourt Brace & Co, Orlando, Florida
2. Crowe, S.F., 1998, Neuropsychological Effects of the Psychological Disorders, Harwood Academic Press, Melbourne.
3. Evans, J.R., & Arbarbanel, A., 1999, Quantitative QEEG and Neurofeedback, Academic Press, New York.
4. Schlegal, S. & Kretzschmar, K., 1987, Computed tomography in affective disorder, I. Biological Psychiatry, 22, 4-14.
5. Starkstein, S.E., & Robinson, R.G., 1997, Mechanism of disinhibition after brain lesions, Journal of Nervous and Mental Disease, 185, 108-114.
6. Mayberg, H.S., 1997, Limbic-cortical disregulation: A proposed model of depression, Journal of Neuropsychiatry and Clinical Neurosciences, 9, 471-481.
7. Robbins, J. 2000, A Symphony in The Brain, Atlantic Monthly Press, New York.
8. Bauer, M. S., & Whybrow, P.C., 1988, Biology of depression and mania. Current Opinion in Psychiatry, 6, 75-85.
9. Miller, B.L. & Cummings, J.L., 1999, The Human Frontal Lobes, The Guilford Press, New York.
10. Le Doux, J.E., Romanski, L., Xagoraris, A., 1989, Indelibility of subcortical emotional memories, Journal of Cognitive Neuroscience, 1, 238-243.
11. Balch, P.A., & Balch, J.F., Prescription for Nutritional Healing, 2000, Avery Publisher, New York.
12. Bland, J.S., et al, 1999, Clinical Nutrition: A Functional Approach. Institute For Functional Medicine, Gig Harbour, Washington.
13. Othmer, S., Kaiser, D.A., & Othmer, S.F., 2000, EEG Biofeedback: A Generalised Approach to Neuroregulation, EEG Spectrum July 2000 Training Manual, pp5.1 - 5.57
14. Toomin, H., 2001, Hemoencephlography -(HEG) The Study of Regional Cerebral Blood Flow rCBF & rCBO₂, HEG Workshop, Society For Neuronal Regulation Conference, Monterey, October, 2001.
15. Pelton, R., & LaValle, J.B., 2000, The Nutritional Cost of Prescription Drugs. Morton Publishing Co, Englewood, CO.

References Specific To The Efficacy of Biofeedback as a Treatment for Depression:

Baehr, E., & Baehr, R. (1997). The use of brainwave biofeedback as an adjunctive therapeutic treatment for depression: Three case studies. Biofeedback, 25 (1), 10-11.
Baehr, E., Rosenfeld, J. P., & Baehr, R. (1997). The clinical use of an alpha asymmetry protocol in the neurofeedback treatment of depression: Two case studies. Journal of Neurotherapy, 2 (3), 10-23.
Hammond, D. C. (2001). Neurofeedback treatment of depression with the Roshi. Journal of Neurotherapy, 4 (2), 45-56.
Hardman, E., Gruzelier, L, Chessman, K., Jones, C., Liddiard, D., Schleichert, H., & Birbaumer, N. (1997). Frontal interhemispheric asymmetry: Self-regulation and individual differences in humans. Neuroscience Letters, 221, 117-120.
Jenkins, P., & Moore, W. H. (1985). The effects of visual feedback on hemispheric alpha asymmetries and reported processing strategies: A single-subject experimental design. Brain & Cognition, 4 (1),47-58.
Kotchoubey, B., Schleichert, H., Lutzenberger, W., Anokhin, A. P., & Birbaumer, N. (1996). Self-regulation of interhemispheric asymmetry in humans. Neuroscience Letters, 215, 91-94.
Kumano, H., Horie, H., Shidara, T., Kuboki, T. et al. (1996). Treatment of a depresive disorder patient with EEG-driven photic stimulation. Biofeedback & Self-Regulation, 21 (4), 323-334. 1
Rockstroh, B., Elbert, T., Birbaumer, N. L, & Lutzenberger, W. (1990). Biofeedback-produced hemispheric asymmetry of slow cortical potentials and its behavioral effects. International Journal of Psychophysiology, 9, 151-165.
Rosenfeld, J. P. (1997). EEG biofeedback of frontal alpha asymmetry in affective disorders. Biofeedback, 25 (1), 8-25.
Rosenfeld, J. P., Baehr, E., Baehr, R., Gotlib, 1. H., & Ranganath, C. (1996). Preliminary evidence that daily changes in frontal alpha asymmetry correlate with changes in affect in therapy sessions. International Journal of Psychophysiology, 23,137-141.