Old Wine in New Bottles – Remarketing ‘Depression’

Last year, I watched an interview on ABC News 24 informing us about a “new theory on the cause of depression”. This is that it is caused, not by a “chemical imbalance” but by inflammation in the nervous system (notably the brain). This is being presented as an alternative to the “serotonin theory of depression” that was used to justify the presciption of Selective Serotonin Reuptake Inhibitor (SSRI) drugs, beginning with Prozac in 1987.

I have been watching and analysing the changing hype for many years. When I worked as a family doctor, the drug companies were claiming that depression was caused by a chemical imbalance in the neurotransmitter noradrenaline, not the indole amine serotonin (5-hydroxytryptamine). This was because the market leaders in the “depression market” were the toxic and ineffective “tricyclic antidepressants” which were developed in the 1950s and were the mainstay of depression treatment till they were replaced by the SSRIs in the 1990s. Tricyclics were known to affect noradrenaline (norepinephrine) levels in the brain.

The psychiatrist interviewed by the Australian Broadcasting Corporation (ABC) defended the “chemical imbalance theory” that has been such a successful marketing catchphrase for the drug companies but admitted that the SSRI’s don’t work for everyone and that “we don’t know” why some people with depression have disordered serotonin metabolism and others don’t. As usual, she explained that they needed more money for research to get the answers.

Dr Liz Scott, for that was her name, also agreed that the new theory was plausible, pointing to the fact that stress affects the immune system. She didn’t explain how stress, which usually depresses the immune system, is responsible for this inflammation, or why there is no evidence of such inflammation in the brains of depressed people who commit suicide. At the same time it is known that chronic illness of many types causes unhappiness and “depression”, including viral, bacterial and fungal infections, kidney and heart disease, cancer and chronic arthritis. Forced psychiatric treatment (especially incarceration) is an important cause of stress that Dr Liz Scott did not mention, predictably. Many other things cause unhappiness, and unhappiness has long been termed “depression” by the medical treatment industry, rejecting the older term of melancholia (thought to be due to a preponderance of black bile, one of the four humours of Galenic medicine).

In the 1960s American “experimental psychologists” of the “Behaviorist School” did a series of cruel experiments on baby chimpanzees, which demonstrated, as if there was need for it, that primates (as well as cats, dogs and even rats) pine away and become morose and depressed when they are deliberately made lonely and deprived of social activity and the comfort of others. This was heralded as a “discovery”.

Prozac was released with much hype, including a flurry of books in the “popular science” press, especially by Rupert Murdoch’s Harper-Collins publishers. These promoted Prozac for a range of medical and psychiatric conditions beyond depression, and resulted in profits of 3 billion for Eli Lilly. The other major drug companies followed suit, releasing and marketing (including bribing doctors to prescribe) a growing range of alternative SSRIs.

Eli Lilly have a long history of research into psychedelic drugs and psychoactive drugs that affect the serotonin receptors and pathways in the brain. In the 1960s they bought the rights to LSD (or ‘acid’) from the Swiss company (Sandoz) that had developed it. It was known that LSD could cause “schizophrenia-like” psychotic episodes, according to the psychiatric terminology of the time. This terminology dates back to 1909, when the Swiss psychiatrist Eugen Bleuler coined the term “schizophrenia” and promoted its use for what his colleague Emil Kraepelin of the University of Heidelberg in Germany, known as the “Father of Psychiatric Classification”, had termed “dementia praecox” (adolescent dementia).

Bleuler argued that Kraepelin, in Germany was too pessimistic and that a third of his patients in the Swiss Burgholzli asylum recovered and were discharged from hospital. Kraepelin had taught, for many years, that any young person who “heard voices” was eventually destined to die of dementia (terminal mental degeneration) in a lunatic asylum.

German psychiatry became more brutal under the Nazis when patients with “schizophrenia”, “cyclical madness” (manic depression or bipolar disorder) and “personality disorder”, who had been populating the long-term mental asylum wards, were prescribed “euthanasia” – meaning “good” or “mercy killing”. Needless to say this included political enemies of the regime, since it has long been the case that enemies of the state or ruling regime get branded as mad. The same label of schizophrenia was also used in the Soviet Union to justify locking up and drugging, with chemical restraints, social and political dissidents.

In fact, chemicals do have a lot of effect on human thinking and behaviour, as the well-known effects of alcohol and drunkenness demonstates. To understand the hidden crime of “antipsychotic drugs”, and “antidepressants” one needs to know a few basics about catecholamine and indole amine neiurotransmitters and neurohormones.

Neurotransmitters are small molecules that bind to cell membranes of the nerve cells (neurones) in the brain and nervous system, stimulating or inhibiting “action potentials” or electrical impulses that pulse or vibrate in a constant, complex network through the nervous system. There are many different receptors for the same neurotransmitter – for example there are D1, D2, D3, D4 and D5 receptors in different parts of the brain. This results in the same chemical neurotransmitter having different effects depending on the type of receptor on the effector cell.

This science lies behind the efforts, over many decades, to find antipsychotic drugs that did not cause stiffness, dribbling and uncontrollable writhing movements of the face and limbs (Tardive Dyskinesia) which crippled so many of the long-term inmates of mental hospitals in the 1960s, 70s and 80s, when the main drugs that were used were Largactil (Thorazine), Haldol (haloperidol), Stelazine and Modecate. Thousands were crippled and still are, by these horrible drugs – both in the communist and the capitalist nations. The main “indications” were “schizophrenia”, “mania” and “schizoaffective disorder”, though they were also used as chemical restraints in elderly people diagnosed with dementia, a particularly cruel form of elder abuse that was prevalent in the more abusive nursing homes in Australia.

It is important to realise that the neurotransmitters in the brain are in constant dynamic flux. Every emotion or action results in chemical changes. When one listens to music the chemicals in the brain change. When one does for a walk, the chemicals change. When one gets excited, or relaxes, the chemical balance changes. Some neurotransmitters increase and some decrease in activity, made more complex by the fact that different cells have different neurotransmitter receptors, affecting how they respond to them. It been demonstrated that the successful completion of tasks results in measurable increase in serotonin levels.

Chemical imbalance theories make a lot of money for companies selling chemicals (drugs/medications). Millions of dollars are spent on promoting various chemical imbalance theories and the drugs that affect these chemicals. The dopamine theory of schizophrenia and the serotonin theory of depression were used to market dopamine-blocking “antipsychotic drugs” and SSRI “antidepressants” respectively. Despite numerous people demonstrating the fallacy of the different chemical imbalance theories, opponents are up against a multi-billion-dollar industry that is profit-driven and stands to profit from repeating the theories without mentioning the opposition to them.

Don’t believe the hype.

Psychoimmunology, the Nocebo Effect and Psychiatry

In the 5^th century BC, the Athenian general and historian Thucydides wrote about how people who lost hope after contracting the plague were more likely to die from the deadly disease. His was the first description of what is now called psychoimmunology – the effect of the mind on the immune system. Another common manifestation of psychoimmunology is the well-known placebo effect, where belief in a treatment results in greater efficacy of the treatment, even if there is no active ingredient in the said treatment. The nocebo effect is the opposite of the placebo effect – when negative effects of an inert treatment occur due to expectations of harm.

The immune system is always subconsciously active, fighting off potential infections and cancers. It can also be over-active, as in allergic reactions, or become misdirected against the body’s own tissues, causing a wide range of autoimmune diseases. It is a common observation that mental stress can aggravate allergies and autoimmune diseases as well as cause depressed immunity.

The term ‘psychoimmunology’ was coined by George Solomon at UCLA in 1964. In 1975 Robert Ader and Nicholas Cohen coined the term ‘psychoneuroimmunology’ (PNI), emphasising the role of the brain and nervous system (neuro) in the processes by which the mind influences the immune system. This was initially viewed with scepticism since medical orthodoxy taught that the immune system was independent of the nervous system (despite knowledge of the placebo effect). There was less focus on how the immune system affects the brain and mind, although at times it obviously does (such as various types of inflammation of the brain). One of Ader’s interesting experiments was one where he conditioned rats to become immunosuppressed by pairing an immunosuppressive drug with saccharin. He found that he was able to stimulate immunosuppression by merely exposing the rats to saccharin after they had been conditioned to link saccharin with the immunosuppressive effects of the drug Cytoxan.

The placebo effect, and its converse, known as the ‘nocebo effect’ illustrate the effect of the mind on the immune system. How these effects arise and what neurological and physiological processes underpin them are partly unanswered questions, but are likely to involve many parts of the brain, especially those areas that affect emotional reactions (such as the amygdala and nucleus accumbens) and the hypothalamus, which affects the endocrine system via the pituitary and pineal glands as well as the autonomic nervous system. The role of the endocrine system in these effects is emphasised by the new term “psychoneuroendoimmunology” (PNEI).

An interesting thing about the placebo effect is that it operates even when the subject knows that it is a placebo. It has also been found that the colour and size of placebo tablets have a bearing on their effectiveness. Red tablets have been found to be more energising, while blue tablets are more calming. This indicates the role of the visual system on the placebo effect. Effective placebos are not just tablets, however. Injections of saline and ‘sham’ surgery have also been shown to be effective placebos. It has also been found that placebos are effective even when the subject knows that they are placebos and have no active ingredients in them. However, belief that an active drug is in the placebo makes the effect more powerful.

The converse effect, the nocebo effect, is the phenomenon by which a drug or treatment that is expected to cause disease does so. For example people become immunosuppressed, nauseated and lose hair if they think the placebo drug they have been given is a cancer chemotherapy drug (and they have been warned about possible side-effects). This indicates the possible negative, as well as possible positive effects, of suggestions.

Studies have shown that depressed mood is associated with impaired immunity and that a good mood promotes health of the immune system. The problem is that improved mood, especially if sudden and accompanied by insights and reduced need for sleep, is liable to be pathologised as hypomania or mania (and ‘elevated’, rather than improved, mood) and treated by dopamine-blocking drugs and lithium, often after locking the person up (which predictably causes the mood to come down). To complicate matters further, it has been reliably reported that people in a good mood (and those who are mentally relaxed) require less sleep. It is also known that meditation can lead to both insights and less need for sleep.

It is generally accepted that the amygdala, an almond-shaped nucleus located deep in the temporal lobes, plays an important role in the placebo and nocebo effects. The amygdala is activated by fear, alarm and anger responses. These emotions activate the hypothalamus and the sympathetic nervous system causing what the Harvard physiologist Walter Cannon termed the “fight or flight reflex”. Activation of the amygdala causes a cascade of hormonal changes via the hypothalamic-pituitary-adrenal (HPA) axis, causing stimulation of the heart, bronchodilation in the lungs, sweating and diversion of the blood flow away from the gut and towards the muscles (in preparation for fight or flight). Though the sympathetic nervous system is known to be involved in “flight and fight” (fear and anger) responses, this branch of the autonomic nervous system is also involved in positive excitement and healthy activation. As well as this, it innervates the pineal gland, where it regulates the synthesis of melatonin from serotonin (during the night).

The body’s response to stress, both physical and mental, is to secrete the hormone cortisol (from the adrenal glands) under influence of adrenocorticotrophic hormone (ACTH) from the pituitary. The ACTH is secreted in response to corticotrophin-releasing hormone from the hypothalamus, a structure at the base of the brain that is neurally connected with the amygdala and other emotion-related parts of the brain. In addition, neuropeptides such as Substance P, which have pro-inflammatory effects, are secreted by the brain and by immune cells such as macrophages and other white cells. The cortisol affects white cells in complex ways, including increasing some populations and decreasing others, causing apoptosis of some cells and chemotaxis of others. It has a generally suppressive effect on the immune system, for which it is often used therapeutically.

While this stress response is essential for escaping from danger, it is thought that in modern society there is often a chronic overstimulation of the stress pathways, leading to increased illness from a range of stress-related maladies (including heart disease, hypertension, autoimmune disease, headaches, peptic ulceration and irritable bowel syndrome).

The sympathetic nervous system is counterbalanced by the parasympathetic nervous system (associated with “rest and digest” physiology according to Cannon). This branch of the autonomic nervous system is associated with a range of physiological activities associated with healing and regeneration. Many stress-reduction techniques (including biofeedback and meditation) aim to increase parasympathetic activity over sympathetic activity in the autonomic nervous system, with the objective of increasing healing and regeneration.

The possible role of the pineal has not been discussed much, but the pineal’s main hormone, melatonin, is known to have effects on the secretion of pituitary hormones, and is thought to have effects on the immune system. In addition, melatonin is known to be a powerful antioxidant. Antioxidants counter oxidative stress and have positive effects on the immune system (and ageing) as well as beneficial effects on the cardiovascular system and nervous system. It is known that conversion of serotonin to melatonin in the pineal (which occurs mainly at night) occurs under the influence of sympathetic activation and the SNS neurotransmitter noradrenaline (norepinephrine).

There has been considerable study on the effects of neurotransmitters and neurohormones, cytokines and endorphins on the immune system. These studies illustrate the complexity of the brain’s effects on the immune system (especially the activity of white blood cells or leukocytes) and the effects of the immune system on the brain and mind (in such diseases as Multiple Sclerosis, AIDS, Parkinson’s Disease and Alzheimer’s Disease). Though complex and incompletely understood, it is clear that loss of hope and pessimism have negative effects on the immune system, as well as other physiological systems.

Implications for Psychiatry

The detrimental effect of loss of hope, written about by Thucydides 2500 years ago, has serious implications for doctors, especially psychiatrists. Psychiatry is a notoriously pessimistic area of medicine. Hundreds of “mental disorders” have been named, all incurable according to psychiatric orthodoxy. If the signs and symptoms of the “disorder” are no longer evident, the patient is said to have gone into remission, rather than cured. Labels of “personality disorder”, once applied, are never removed and all personality disorders are, according to psychiatric orthodoxy, permanent. This can be expected to depress the mood and the immune system. In addition there is an increasing tendency to regard the normal as abnormal. Excitement, for example, is seen as hypomania and normal sadness as “depression”, while a range of New Age beliefs and alternative science (and political) beliefs are regarded as signs of “schizophrenia”. This leads to self-fulfilling prophesies and partly explains the appalling life expectancy of people once they have been given a label of schizophrenia or bipolar disorder.

In the case of bipolar disorder (manic depression) a single episode of mania or hypomania is taught in psychiatric texts to herald a life-long condition of “mood disorder” requiring long-term mood stabilizing drugs like lithium. These drugs have terrible side-effects and shorten the life, explaining why a diagnosis of bipolar disorder is accompanied by a ten to twenty year shorter lifespan, on average. A diagnosis of schizophrenia shortens the life by 15 to 20 years, on average, and again is treated with long-term antipsychotic drugs that are known to shorten the life and make people lethargic, obese and prone to diabetes and heart disease in addition to causing neurotoxicity in the form of Parkinson’s Syndrome and Tardive Dyskinesia (a permanent condition characterised by involuntary spasms, grimaces and writhing movements that is caused by antipsychotic drugs). Lithium is notorious for causing kidney and thyroid failure.

Though the suicide rate is much higher in people given these diagnoses, most of the morbidity and mortality is not due to suicide. Besides, self-harm and suicide can be partly attributed to the pessimistic diagnosis (resulting in loss of hope), and social stigmatization resulting in loneliness, poverty and other social problems. These commonly lead to loss of motivation and depression, with negative effects on the immune system. The main cause of the shortened life span when on antipsychotic drugs is due the long-term effect of blocking essential neurotransmitters, causing metabolic problems and heart disease. They can also cause irreversible brain damage in the form of cognitive decline, cerebral atrophy and tardive dyskinesia. Though they can be effective in treating hallucinations, they should not be used for behaviour control or as chemical restraints, as they frequently are, especially in the elderly. Delusions are better treated by debate than drugs. The diagnosis of delusions can also be problematic in that the belief system of the interviewer is pitted against, and assumed to be superior, to that of the patient.

To maximise the potential of the body’s own healing mechanisms, and those mediated by the mind, is imperative that people reject labels of incurable mental illness and realise that just because they have been mentally unhealthy in the past does not mean they need to be mentally unhealthy in the future. It is also imperative that doctors and other health workers realise that implanting pessimism in the minds of their patients is a recipe for inducing chronic illness.

My 1995 Theory of Motivation

This is the diagram I drew when I was trying to explain my theory of motivation to Rajan Thomas in March 1995, shortly before I was first “sectioned” (as Thomas called it). BG stands for basal ganglia, and my theory was that satisfaction of instincts for communication, curiosity and play resulted in release of the neurotransmitter dopamine in the midbrain. This is now accepted to be the case in the ‘pleasure circuits’ and dopamine release in the nucleus accumbens.

At the time I had not heard of the nucleus accumbens, but was developing integrative theories about the neurotransmitters dopamine, noradrenaline (NA in the diagram) and serotonin and the function of the reticular activating system (RAS) which is a noradrenergic network involved in sleep and consciousness. I postulated that our motivation is a balance between not just instincts and conditioning as I had learned at medical school, but by free will, which I regarded important both psychologically and legally as well as spiritually. I suggested to Rajan Thomas that free will is influenced by our memories and experiences. I also acknowledged drives for food, shelter and sex, but was more interested in developing theories about the instincts that could be used to promote mental health, like communication, curiosity and play. I subsequently presented my theory of motivation at the physiology department of Monash University (October 1995), Theosophical Society (1996) and the Australian College of Mind-Body Medicine (1998) to a much more receptive response.

Rajan Thomas gathered only that my theory of motivation was that “movement causes improvement in mental health”. The theory evidently went over his head, and I realised this at the time when I asked him what he thought motivated people.

The Lead-up to my First Incarceration

I believe that humans have an instinct to seek freedom. This instinct was called “drapetomania” when expressed by Black slaves in the USA, who tried to escape. The “treatment’ was to catch them, lock them up and whip them. Whipping was a favourite treatment in the early Australian lunatic asylums too, as well as physical restraints and chemical restraints with an increasing range of toxic drugs. When insulin was discovered in 1921, the first thing they tried was to “treat schizophrenics” by sending them into a coma by injecting them with insulin in 1922. Labouring under the delusion that fevers may cure schizophrenia they tried giving people typhoid and malaria – as a treatment – along with injecting turpentine into the abdomen to cause an abscess, which needed to be drained in theatre. This was all on purpose, with a supposedly “scientific” rationale. Prior to that they tried spinning beds and chairs, convinced that mental illness was caused by too much or little blood flow to the brain, and also developed various methods of immobilization of ‘manic’ or ‘excited’ patients.

During the 1930s and 40s the Nazis subjected people labelled with schizophrenia, manic depression and personality disorder to what they called ‘euthanasia’ or mercy killing under the notorious Aktion T4 program. This was before the mass killing of Jews and Gypsies. Prior to that, several American states established eugenics laws prohibiting the marriage of ‘mentally ill’ people and allowing for the castration of mentally ill and “feeble-minded” boys. Eugenics, initially developed at Cambridge in the 1880s, was also embraced in Australia, where it formed the “scientific” basis for the genocide of Aboriginal people and “breeding out the Black” to create a “White Australia”.

They also used to cause convulsions on purpose, using chemical toxins, as an alternative to electrical shocks, which were given without anaesthetic at first. This resulted in fractures, but was declared to be a successful treatment by its enthusiasts, as were the notorious “ice-pick lobotomies” popularised in the 1940s by Walter Freeman and his followers. There were other atrocities committed under the notorious but still rarely mentioned MK programs of the 1950s and 60s , where the CIA enlisted numerous well-known universities in the USA, Canada and UK to assist in brain-washing and mind control programs, supposedly to counter the “Communist menace”. These included “deep-sleep therapy” and insulin comas, combined with such frequent electric shocks to the brain that the victim was rendered incontinent and unable to talk or walk. They were then “reprogrammed” through various methods including playing repeated loops of audio tapes and other such then modern technology.

The age of lobotomies ended in 1950 with the discovery of the first “liquid lobotomy”, the dopamine-blocking drug chlorpromazine in France. This was the first of the phenothiazines, marketed as Thorazine in the USA and Largactil elsewhere (including Australia). Largactil is credited with ending the era of asylums and allowing mentally ill people diagnosed with “schizophrenia” and previously confined for years to be to be discharged from hospital and treated in the “community”. However, Largactil and the other dopamine-blocking “neuroleptics” or “antipsychotics” (also called ‘major tranquillisers’) were found to have serious side-effects, including irreversible brain damage in the form of “tardive dyskinesia” (TD). TD is characterised by uncontrollable facial, tongue and limb movements; it is hard to imagine a more stigmatising condition, since the limbs writhe uncontrollably, the tongue protrudes in and out, with puffing of the cheeks and facial grimaces. A person with TD looks mad, and this is worsened by the uncontrollable urge to pace up and down and inability to sit still known as “akathesia”, which is also caused by these drugs, presumably due to the blockade of dopamine receptors in the basal ganglia of the brain. They also cause anhedonia (lack of pleasure), reduced creativity and flattened emotions. Cruelly, these side-effects are frequently blamed on the “illness” itself.

Wikipedia says:

Chlorpromazine largely replaced electroconvulsive therapy, hydrotherapy,^[40] psychosurgery, and insulin shock therapy.^[36] By 1964, about 50 million people worldwide had taken it.^[41] Chlorpromazine, in widespread use for 50 years, remains a “benchmark” drug in the treatment of schizophrenia, an effective drug although not a perfect one.^[17] The relative strengths or potencies of other antipsychotics are often ranked or measured against chlorpromazine in aliquots of 100 mg, termed chlorpromazine equivalents or CPZE.^[42]

According to Wikipedia, chlorpromazine is a “low potency” antipsychotic and less likely to cause tardive dyskinesia than the “high potency” antipsychotics like haloperidol (Haldol) and fluphenazine (Stelazine). I have never had fluphenzine (notorious for causing the ‘Stelazine shuffle’) forced on me, but I have been forced to take haloperidol by mouth and also been injected with long-acting “depot” preparations of the drug. The side effects I developed traumatised me for years after, and long after the actual effects had worn off. This trauma was because of the memory of the incarceration and drugging.

I haven’t yet developed TD, but the condition may develop many years after treatment starts and increases in likelihood the longer it is continued. It may also worsen despite stopping treatment and is itself untreatable. I dread getting this horrible iatrogenic (treatment-induced) condition. I have experienced the other common neurological problems caused by dopamine blockade, namely akathesia and Parkinsonism, with similar symptoms to Parkinson’s Disease, but caused by dopamine receptor-blocking drugs rather than degeneration of the dopamine-producing nerve cells in the basal ganglia (the known cause of Parkinson’s Disease).

I came to the attention of the psychiatric system because of my family, namely my father Brian Senewiratne, sister Shireen Senewiratne and her boyfriend at the time, Robert Purssey. All were doctors working in the public system and my father also got his friend, Dr Chelvarayan Barr-Kumarakulasinghe, to make another referral, in addition to those of Robert and Shireen. My father then wrote a series of letters to the psychiatrist Rajan Thomas and his registrar Noel Barrett, purporting to provide “collateral history”. I have received these letters and Thomas’s own notes when they were provided as evidence against me at the Queensland Health Practitioner’s Tribunal in 2003, but had already obtained some of them in Freedom of Information (FOI) requests I made myself from the Alfred Hospital and Monash Medical Centre and before that from the Formal Hearing of the Medical Practitioners’ Board of Victoria, held in July and August 1996. These documents have helped me piece together the roles that my various family members played in my initial incarceration and subsequent ones. I have long grappled over their motives.

In his first letter ‘framing letter’ to Rajan Thomas, which was hand-written, long and rambling, my father ended it with the revealing line:

“I hope this long dissertation doesn’t result in someone certifying me!!!!”

He evidently knew that being certified as insane is a traumatic experience, which he didn’t want for himself, but was advocating for his much saner son.

Though my sister made a referral to the Junction Clinic in St Kilda on May 18, 1995, she left it to her boyfriend Robert, who was a psychiatry registrar, to make the phone calls to get me locked up. Robert also went through all my things after I’d been locked up at RPH, looking for evidence to substantiate his claim that I had “mania”. When I escaped the first time from Royal Park it was Robert who tracked me down, a task for which he took “compassionate leave” from work! When I escaped a second time and travelled up to Brisbane, not realising my father’s role in my incarceration, Robert flew up from Melbourne, got a mutual friend, Margie Ruddy to invite me out and then stalked me in a nightclub, all the while refusing to talk with me directly. Instead he followed me around and asked the people I spoke to what I had said, warning them that I was mad and could not be believed.

In response to the initial referral by my family the Junction Clinic sent a psychiatry registrar by the name of Noel Barrett to my flat. I had moved in there in January 1995 after separating from my wife Susan the day she arrived from Brisbane after spending two weeks there with our two-year-old daughter Ruby. Sue was furious after being told by Shireen and Robert that I was having an affair with Sara Di Genova, whom they had invited to mind their house in North Fitzroy while they too holidayed in Brisbane (where our parents live). This was untrue. I was infatuated with Sara, something Shireen knew, but we were not having a romantic relationship, though later we did, and ended up living together and having a daughter, Zoe, many years later. Zoe was born on 30^th August 2009 at the Mater Hospital in Brisbane, by which time Shireen and Robert had two children but had separated, and Robert had remarried. He has since had two more children and is working as a psychiatrist in Brisbane. He refuses contact with me, and has done since he stopped trying to get me locked up. My father has never stopped trying and is trying to get me locked up again right now.

I thought the registrar Noel Barrett was a strange man. I had no rapport with him. He asked me to come to clinic, which was nearby, the next week to see the psychiatrist Rajan Thomas, who my mother had told me was an expert in autism and known to my uncle Chelvarayan Barr Kumarakulasinghe, who was working as a de-facto psychiatrist (his qualification was a surgeon and he had been professor of surgery in Kandy before coming out to Australia after spending some years in the Middle-East) and is married to my mother’s cousin Nirma, who was my piano teacher when I was a child. Rajan Thomas was a strange man too and not an expert in autism at all. This had merely been a ruse to get me to see him. He saw his task not to discuss my evolving theories with me but to see if I could be “sectioned”, meaning certified as mentally ill and involuntarily confined. He wrote in his notes that “the family wants him sectioned” but that he did not think it could be done legally, and sought a second opinion from the director of the clinic, Tobie Sacks, who I was delighted to hear was a nephew of the famous British neurologist and author Oliver Sacks.

I liked Tobie and was able to develop more rapport with him than I could with Rajan Thomas or the registrar Noel Barrett. After interviewing me for an hour he wrote:

“Review”
Thank you for asking me to review Dr Senewiratna. A 30+ yr old separated medical practitioner, he presents with mildly elevated mood, slight grandiosity with pseudophilosophical overvalued ideas regarding mental illness, behaviour and motivation.”…

.
“While it seems very probable, from the recent history, that Dr Senewiratna has been hypomanic, exhibiting elevated mood, grandiosity, flight of ideas and increasingly dysfunctional, uncharacteristic behaviours, and while he is now still mildly elevated in his mood and has several unrealistic, possibly overvalued ideas (his hypothesis) I do not find him to be certifiable/detainable under MHA [Mental Health Act].
There is currently no evidence of flight of ideas, pressure of speech, risk-taking behaviour or impulsivity in his activities. Throughout the interview he remained calm, cooperative and were able to establish good rapport. Affect was reactive and generally appropriate. The overvalued ideas/hypothesis about behaviours/mood etc are fairly firmly held, but not to delusional intensity”.

My hypothesis was that humans have a number of neglected instincts, including communication, curiosity and play, and that these instincts could be used to develop therapeutic strategies individually and as public health programs. I also developed theories about the development of aesthetic appreciation in what we see and hear, that again had practical applications, but the psychiatrists were not interested in my theories other than to determine whether how strongly I held them (and not whether they were justified and rational).

Rajan Thomas has recently been charged with sexually assaulting one of his long-term patients in his rooms and in a Melbourne psychiatric hospital. This came as no surprise to me after his explanation of what motivates people – meaning himself – in March 1995. I asked him, in good faith, what motivated people, something I was developing theories about. His answer is in keeping with the recent charges against him for sexual assault. He said “well, if you see a woman walking down the street (and he put his hands on his chest, simulating breasts) you want to jump on her but you don’t because of the people who are there”. It was a bizarre answer that I was not expecting – my theory was that we are motivated by instincts for communication, curiosity and play!

My Psychiatric Experiences

According to the statistics, at the age of 57 I am getting to the end of my expected life. This is because psychiatric patients in Australia have twenty years less life to expect than the rest of the population that haven’t been branded with the label of “mental illness”.

Before I became a reluctant patient of the Australian psychiatric system, I had graduated and worked as a doctor, specialising in what was called ‘family medicine’, but better known as ‘general practice’. General practice, conducted by General Practitioners (GPs) is contrasted with medical and surgical care provided by specialists, recognised experts in various ‘medical specialties’. The Royal Australian College of General Practitioners (RACGP) established its Family Medicine Program (FMP) to establish general practice as a specialty of its own, devoted to family medicine, an important part of which is preventive medicine. It also includes counselling and a great deal of psychiatry, provided as primary care for people of all ages. I entered the Family Medicine Program as a second year resident, and in 1990 I was granted vocational registration by the RACGP. I was not a member of the college, but received vocational registration when it was introduced because I had already been in general practice for more than 5 years.

I entered the University of Queensland to study medicine in 1978, when I was 17 and straight out of high school. I had attended “Churchie”, a boy’s school that has changed its formal name from “The Church of England Grammar School” to the “Anglican Boy’s Grammar School” and slipped down the comparative academic ranking of Brisbane schools. When I entered the university it was with 17 other boys from Churchie, including the two boys who had shared the Tyrwitt Cup with me for the best academic students in Year 12 (1977). I never actually saw the cup I had won and it was taken home by one of the other victors. I wasn’t much interested in it, to tell the truth, but I was proud of my academic success. It reinforced the belief that my mother had instilled in my sister and I that we came from an “intelligent family”. But intelligence and academic success are not the same; many intelligent people do poorly in the academic system, and many people do well academically by repeating, without questioning it, everything they are told by their teachers. Exams favour people with good memories, and “retentive brains”. It favours students who can apply equations and laws but not necessarily understand how the equations and laws they apply were derived.

From a young age I was expected to “study hard” to “come first in every subject” with the notable exception of Singhala, which I was only expected to pass. This pressure to “come first” came from my father and was transmitted to me by my mother. My father rarely spoke to me, even when I was living in his home. I did, however, have long and varied conversations with my mother and my older sister Shireen, in whom I foolishly confided my innermost thoughts and fears. Foolishly, because she used to knowledge to manipulate, dominate and control me, which she delighted in.

Shireen was also expected to come first in class and the pressure on her continued to her years at university, while my father gave up on my doing well, though he insisted that I sit at my desk and “study”, rather than play the guitar. He was outraged when I first started busking to get around the fact that he tried to control me financially. At the time one of his registrars had seen me and asked if he didn’t give me any money. My father came home furious and demanded that I stop busking. But he didn’t expect me to “win a First Class in Medicine”, which he demanded of my sister. Years later she confessed to me, in tears, that she felt huge pressure to avoid his disapproval.

Though she did well in medicine, and got a First Class, my father and sister had a tumultuous relationship when she was at Uni, mainly because he accused her of “fooling around” with her boyfriend Channa. Channa was the son of Basil and Erangani Seneviratne, who were family friends of my parents and had lived in the same block of flats in England before returning to work as doctors in the hill city of Kandy (Mahanuwara) in Sri Lanka’s central mountainous region. Basil was a cardiologist and Erangani, who had gone to school with my mother, Kamalini, was a pathologist. They moved to Brisbane from Christchurch (New Zealand) in 1978 after sending their oldest children ahead of them, first Arjuna (MIkka) who stayed with us in 1977 till his older brother Channa arrived. Both Mikka and Channa were romantically interested in Shireen, and Mikka was disappointed but not surprised by her decision to go out with Channa, whom she eventually married, but later divorced without children.

Basil and Erangani’s third child and older daughter was Dammi (Damayantha) who I had an adolescent crush on, though I found her hard to communicate with. I took her to the school formal, when Shireen was taken by Mikka, in year 12. I hired a flared white suit for the occasion with no insight into how incongruous I looked, and didn’t have a clue how to start a conversation or sustain one. When, the next year, Dammi invited me to the Somerville House formal as her date, again I didn’t know what to say to her. I was a shy guy.

When I was first locked up, supposedly for an elevated mood and increased talkativeness, Dammi was the only member of her family who visited me, the others having been warned that I had “changed” and was no longer nice. She even offered for me to stay in her flat with her sister Amanda when I was discharged from hospital. This was in the Woden Valley Hospital in Canberra, where I was locked up for three days over Easter, 1995, after escaping from the Royal Park Hospital in Melbourne (RPH). I had been locked up at the RPH on 7^th April, 1995, in an event that disrupted and changed the course of my life. This is when I was transformed from being a respected doctor to being a stigmatised madman, a maniac, a ‘mental patient’.

Welcome to Dr Romesh Senewiratne-Alagaratnam’s Blog

Hi. My name is Romesh, though some others have more unpleasant names for me. This is my blog. I hope you like it. Please feel free to contact me on Facebook or by writing comments. You can also see some of my documentaries and music on YouTube, and my e-books on Scribd. I am a firm believer in free education and health. I hope you find this blog informative, especially about the problems of psychiatry and the psychiatric profession, against which I have battled for many years.

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Implications for Psychiatry

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