Modelo social versus Modelo Médico da deficiência

O modelo médico, ainda hoje hegemônico para as políticas de bem-estar  voltadas para os deficientes, afirmava que a experiência de segregação, desemprego e baixa escolaridade, entre tantas outras variações da opressão, era causada pela inabilidade do corpo lesado para o trabalho produtivo.

Se para o modelo médico o problema estava na lesão, para o modelo social, a deficiência era o resultado do ordenamento político e econômico capitalista, que pressupunha um tipo ideal de sujeito produtivo. Houve, portanto, uma inversão na lógica da causalidade da deficiência entre o modelo médico e o social: para o primeiro, a deficiência era resultado da lesão, ao passo que, para o segundo, ela decorria dos arranjos sociais opressivos às pessoas com lesão. Para o modelo médico, lesão levava à deficiência; para o modelo social, sistemas sociais opressivos levavam pessoas com lesões a experimentarem a deficiência.

Diniz, D. O que é deficiência?

Freud responsabilidade e liberdade

"A maioria das pessoas não quer realmente a liberdade, porque liberdade envolve em responsabilidade, e a maioria das pessoas tem medo da resposabilidade" Sigmund Freud

Frase Voltaire Dominação

"Para saber quem governa sobre você , simplesmente procure quem você não pode criticar" Voltaire

http://chriskresser.com/the-chemical-imbalance-myth

The "chemical imbalance" myth

by CHRIS KRESSER 179 comments

“A theory that is wrong is considered preferable to admitting our ignorance.” – Elliot Vallenstein, Ph.D.

The idea that depression and other mental health conditions are caused by an imbalance of chemicals in the brain is so deeply ingrained in our psyche that it seems almost sacrilegious to question it.

Direct-to-consumer-advertising (DCTA) campaigns, which have expanded the size of the antidepressant market (Donohue et al., 2004), revolve around the claim that SSRIs (the most popular class of antidepressants) alleviate depression by correcting a deficiency of serotonin in the brain.

For example, Pfizer’s television advertisement for Zoloft states that “depression is a serious medical condition that may be due to a chemical imbalance”, and that “Zoloft works to correct this imbalance.”

Other SSRI advertising campaigns make similar claims. The Effexor website even has a slick video explaining that “research suggests an important link between depression and an imbalance in some of the brain’s chemical messengers. Two neurotransmitters believed to be involved in depression are serotonin and norepinephrine.” The video goes on to explain that Effexor works by increasing serotonin levels in the synapse, which is “believed to relieve symptoms of depression over time.”

These days serotonin is widely promoted as the way to achieve just about every personality trait that is desirable, including self-confidence, creativity, emotional resilience, success, achievement, sociability and high energy. And the converse is also true. Low serotonin levels have been implicated in almost every undesirable mental state and behavioral pattern, such as depression, aggressiveness, suicide, stress, lack of self-confidence, failure, low impulse control, binge eating and other forms of substance abuse.

In fact, the idea that low levels of serotonin cause depression has become so widespread that it’s not uncommon to hear people speak of the need to “boost their serotonin levels” through exercise, herbal supplements or even sexual activity. The “chemical imbalance” theory is so well established that it is now part of the popular lexicon.

It is, after all, a neat theory. It takes a complex and heterogeneous condition (depression) and boils it down to a simple imbalance of two to three neurotransmitters (out of more than 100 that have been identified), which, as it happens, can be “corrected” by long-term drug treatment. This clear and easy-to-follow theory is the driving force behind the $12 billion worth of antidepressant drugs sold each year.

However, there is one (rather large) problem with this theory: there is absolutely no evidence to support it. Recent reviews of the research have demonstrated no linkbetween depression, or any other mental disorder, and an imbalance of chemicals in the brain (Lacasse & Leo, 2005; (Valenstein, 1998).

The ineffectiveness of antidepressant drugs when compared to placebo cast even more doubt on the “chemical imbalance” theory. (See my recent articles Placebos as effective as antidepressants and A closer look at the evidence for more on this.)

Folks, at this point you might want to grab a cup of tea. It’s going to take a while to explain the history of this theory, why it is flawed, and how continues to persist in light of the complete lack of evidence to support it. I will try to be as concise as possible, but there’s a lot of material to cover and a lot of propaganda I need to disabuse you of.

Ready? Let’s start with a bit of history.

The history of the “chemical imbalance” theory

The first antidepressant, iproniazid, was discovered by accident in 1952 after it was observed that some tubercular patients became euphoric when treated with this drug. A bacteriologist named Albert Zeller found that iproniazid was effective in inhibiting the enzyme monoamine oxydase. As its name implies, monoamine oxydase plays an essential role in inactivating monoamines such as epinephrine and norepinephrine. Thus, iproniazid raised levels of epinephrine and norepinephrine which in turn led to stimulation of the sympathetic nervous system – an effect thought to be responsible for the antidepressant action of the drug.

At around the same time, an extract from the plant Rauwolfia serpentina was introduced into western psychiatry. This extract had been used medicinally in India for more than a thousand years and was thought to have a calming effect useful to quite babies, treat insomnia, high blood pressure, insanity and much more. In 1953 chemists at Ciba, a pharmaceutical company, isolated the active compound from this herb and called it reserpine.

In 1955 researchers at the National Institutes of Health reported that reserpine reduces the levels of serotonin in the brains of animals. It was later established that all three of the major biogenic amines in the brain, norepinephrine, serotonin, and dopamine, were all decreased by reserpine (again, in animals).

In animal studies conducted at around the same time, it was found that animals administered reserpine showed a short period of increased excitement and motor activity, followed by a prolonged period of inactivity. The animals often had a hunched posture and an immobility that was thought to resemble catatonia (Valenstein, 1998). Since reserpine lowered levels of serotonin, norepinephrine and dopamine, and caused the effects observed in animals, it was concluded that depression was a result of low levels of biogenic amines. Hence, the “chemical imbalance” theory is born.

However, it was later found that reserpine only rarely produces a true clinical depression. Despite high doses and many months of treatment with reserpine, only 6 percent of the patients developed symptoms even suggestive of depression. In addition, an examination of these 6 percent of patients revealed that all of them had a previous history of depression. (Mendels & Frazer, 1974) There were even reports from a few studies that reserpine could have an antidepressant effect (in spite ofreducing levels of serotonin, norepinephrine and dopanmine).

As it turns out, that is only the tip of the iceberg when it comes to revealing the inadequacies of the “chemical imbalance” theory.

The fatal flaws of “chemical imbalance” theory

As Elliot Valenstein Ph.D., Professor Emeritus of psychology and neuroscience at Michigan University, points out in his seminal book Blaming the Brain, “Contrary to what is often claimed, no biochemical, anatomical or functional signs have been found that reliably distinguish the brains of mental patients.” (p. 125)

In his book, Valenstein clearly and systematically dismantles the chemical imbalance theory:

1. Reducing levels of norepinephrine, serotonin and dopamine does not actually produce depression in humans, even though it appeared to do so in animals.
2. The theory cannot explain why there are drugs that alleviate depression despite the fact that they have little or no effect on either serotonin or norepinephrine.
3. Drugs that raise serotonin and norepinephrine levels, such as amphetamine and cocaine, do not alleviate depression.
4. No one has explained why it takes a relatively long time before antidepressant drugs produce any elevation of mood. Antidepressants produce their maximum elevation of serotonin and norepinephrine in only a day or two, but it often takes several weeks before any improvement in mood occurs.
5. Although some depressed patients have low levels of serotonin and norepinephrine, the majority do not. Estimates vary, but a reasonable average from several studies indicates that only about 25 percent of depressed patients actually have low levels of these metabolites.
6. Some depressed patients actually have abnormally high levels of serotonin and norepinephrine, and some patients with no history of depression at all have low levels of these amines.
7. Although there have been claims that depression may be caused by excessive levels of monoamine oxydase (the enzyme that breaks down serotonin and norepinephrine), this is only true in some depressed patients and not in others.
8. Antidepressants produce a number of different effects other than increasing norepinephrine and serotonin activity that have not been accounted for when considering their activity on depression.

Another problem is that it is not now possible to measure serotonin and norepinephrine in the brains of patients. Estimates of brain neurotransmitters can only be inferred by measuring the biogenic amine breakdown products (metabolites) in the urine and cerebrospinal fluid. The assumption underlying this measurement is that the level of biogenic amine metabolites in the urine and cerebrospinal fluid reflects the amount of neurotransmitters in the brain. However, less than one-half of the serotonin and norepinephrine metabolites in the urine or cerebrospinal fluid come from the brain. The other half come from various organs in the body. Thus, there are serious problems with what is actually being measured.

Finally, there is not a single peer-reviewed article that can be accurately cited to support claims of serotonin deficiency in any mental disorder, while there are many articles that present counterevidence. Furthermore, the Diagnostic and Statistical Manual of Mental Disorders (DSM) does not list serotonin as the cause of any mental disorder. The American Psychiatric Press Textbook of Clinical Psychiatryaddresses serotonin deficiency as an unconfirmed hypothesis, stating “Additional experience has not confirmed the monoamine depletion hypothesis” (Lacasse & Leo, 2005).

When all of this evidence is taken in full, it should be abundantly clear thatdepression is not caused by a chemical imbalance.

But, as Valenstein shrewdly observes, “there are few rewards waiting for the person who claims that “the emperor is really nude” or who claims that we really do not know what causes depression or why an antidepressant sometimes helps to relieve this condition.”

How have we been fooled?

There are several reasons the idea that mental disorders are caused by a chemical imbalance has become so widespread (and none of them have anything to do with the actual scientific evidence, as we have seen).

It is known that people suffering from mental disorders and especially their families prefer a diagnosis of “physical disease” because it does not convey the stigma and blame commonly associated with “psychological problems”. A “physical disease” may suggest a more optimistic prognosis, and mental patients are often more amenable to drug treatment when they are told they have a physical disease.

Patients are highly susceptible to Direct-to-Consumer-Advertising (DCTA). It has been reported that patients are now presenting to their doctors with a self-described “chemical imbalance” (Kramer, 2002). This is important because studies show that patients who are convinced they are suffering from a neurotransmitter defect are likely to request a prescription for antidepressants, and may be skeptical of physicians who suggest other interventions such as cognitive behavioral therapy (DeRubeis et al., 2005). It has also been shown that anxious and depressed patients “are probably more susceptible to the controlling influence of advertisements (Hollon MF, 2004).

The benefit of the chemical imbalance theory for insurance companies and the pharmaceutical industry is primarily economic. Medical insurers are primarily concerned with cost, and they want to discourage treatments (such as psychotherapy) that may involve many contact hours and considerable expense. Their control over payment schedules enables insurance companies to shift treatment toward drugs and away from psychotherapy.

The motivation of the pharmaceutical companies should be fairly obvious. As mentioned previously, the market for antidepressant drugs is now $12 billion. All publicly traded for-profit companies are required by law to increase the value of their investor’s stock. Perhaps it goes without saying, but it is a simple fact that pharmaceutical companies will do anything they legally (and sometimes illegally) can to maximize revenues.

Studies have shown that the advertisements placed by drug companies in professional journals or distributed directly to physicians are often exaggerated or misleading and do not accurately reflect scientific evidence (Lacasse & Leo, 2005). While physicians deny they are being influenced, it has been shown repeatedly that their prescription preferences are heavily affected by promotional material from drug companies (Moynihan, 2003). Research also suggests that doctors exposed to company reps are more likely to favor drugs over non-drug therapy, and more likely to prescribe expensive medications when equally effective but less costly ones are available (Lexchin, 1989). Some studies have even shown an association between the dose and response: in other words, the more contact between doctors and sales reps the more doctors latch on to the “commercial” messages as opposed to the “scientific” view of a product’s value (Wazana, 2000).

The motivation of psychiatrists to accept the chemical imbalance theory is somewhat more subtle. Starting around 1930, psychiatrists became increasingly aware of growing competition from nonmedical therapists such as psychologists, social workers and counselors. Because of this, psychiatrists have been attracted to physical treatments like drugs and electroshock therapy that differentiate them from nonmedical practitioners. Psychiatry may be the least respected medical specialty (U.S. General Accounting Office report). Many Americans rejected Fruedian talk therapy as quackery, and the whole field of psychiatry lacks the quality of research (randomized, placebo-controlled, double-blind experiments) that serves as the gold-standard in other branches of medicine.

Dr. Colin Ross, a psychiatrist, describes it this way:

“I also saw how badly biological psychiatrists want to be regarded as doctors and accepted by the rest of the medical profession. In their desire to be accepted as real clinical scientists, these psychiatrists were building far too dogmatic an edifice… pushing their certainty far beyond what the data could support.”

Of course there are also many “benefits” to going along with the conventional “chemical imbalance” theory, such as free dinners, symphony tickets, and trips to the Caribbean; consultancy fees, honoraria and stock options from the pharmaceutical companies; and a much larger, growing private practice as the $20 billion spent by drug companies on advertising brings patients to the office. Psychiatrists are just human, like the rest of us, and not many of them can resist all of these benefits.

In sum, the idea that depression is caused by a chemical imbalance is a myth. Pharmaceutical ads for antidepressants assert that depression is a physical diseases because that serves as a natural and easy segue to promoting drug treatment. There may well be biological factors which predispose some individuals toward depression, but predisposition is not a cause. The theory that mental disorders are physical diseases ignores the relevance of psychosocial factors and implies by omission that such factors are of little importance.

Stay tuned for future articles on the psychosocial factors of depression, the loss of sadness as a normal response to life, and the branding of new psychological conditions as a means of increasing drug sales.

Recommended resources

• Blaming the Brain, by Elliot Valenstein Ph.D.
• Rethinking Psychiatric Drugs, by Grace Jackson M.D.
• America Fooled: The truth about antidepressants, antipsychotics and how we’ve been deceived, by Timothy Scott Ph.D.
• The Loss of Sadness, by Alan Horwitz and Jerome Wakefield
• The Myth of the Chemical Cure, by Joanna Moncrieff

Intolerância

A intolerância seria uma for-

ma de imputar culpa aos que não souberam controlar

os riscos que os tornaram diferentes. Ora, como exis-

te um valor para um padrão de beleza, saúde, quali-

dade de vida, autocontrole, entre outros, os que se

distanciam desses alvos devem ser punidos por tal

negligência. A intolerância torna-se uma agressividade

irracional contra formas de ser e estilos de vida con-

trários aos que se convencionou, por escolha ou

(pseudo)formação, como absolutamente verdadeiros.

Nesse sentido, as diferenças tornam-se

desigualdades nas quais os indivíduos são negados

entre os que se consideram iguais. É pertinente con-

siderar a produção social dessa diferença, que resulta

em atitudes, preconceitos, estereótipos e estigmatiza-

ção, posicionando socialmente aqueles considerados

diferentes como cidadãos de segunda categoria.

Texto: Silva, L. O estranhamento causado
pela deficiência: preconceito e experiência

Negação social da fragilidade

O preconceito às pessoas com deficiência configura-se como um mecanismo de negação social, uma vez que suas diferenças são ressaltadas como uma falta, carência ou impossibilidade. A deficiência inscreve no próprio corpo do indivíduo seu caráter particular. O corpo deficiente é insuficiente para uma sociedade que demanda dele o uso intensivo que leva ao desgaste físico, resultado do trabalho subserviente; ou para a construção de uma corporeidade que objetiva meramente o controle e a correção, em função de uma estética corporal hegemônica, com interesses econômicos, cuja matéria-prima/corpo é comparável a qualquer mercadoria que gera lucro. A estrutura funcional da sociedade demanda pessoas fortes, que tenham um corpo "saudável", que sejam eficientes para competir no mercado de trabalho. O corpo fora de ordem, a sensibilidade dos fracos, é um obstáculo para a produção. Os considerados fortes sentem-se ameaçados pela lembrança da fragilidade, factível, conquanto se é humano.

O estranhamento causado pela deficiência: preconceito e experiência

Luciene M. da Silva

Universidade do Estado da Bahia, Programa de Pós-Graduação Educação e Contemporaneidade

http://www.scielo.br/scielo.php?pid=S1413-24782006000300004&script=sci_arttext

Opressão da ordem estabelecida e "doença mental"

O preconceito, que é uma disposição individual, mas não apenas, deriva do objeto e é, ao mesmo tempo, independente dele, não admitindo uma conceituação universal, pois tem "aspectos constantes e aspectos variáveis", que se relacionam mais com aquilo que é de interesse do preconceituoso, dentre as diversas representações que lhes são atribuídas (Crochik, 1997). O indivíduo preconceituoso fecha-se dogmaticamente em determinadas opiniões, sendo assim impedido de ter algum conhecimento sobre o objeto que o faria rever suas posições e, assim, ultrapassar o juízo provisório. O diferente estigmatizado evoca lembranças que quer negar, e mesmo nos momentos em que se torna possível a convivência é convencido da inconveniência de mostrar o que pode parecer identificação com "um outro". Esse sentimento ambíguo, de que nos fala Crochik (1997), é que determina o afastamento, o que impede o contato pelo medo de que, com a identificação, sejamos analogamente humilhados. Vem também do medo do diferente, do que não é conhecido, podendo ser transformado em inferioridade, desigualdade e exclusão. O preconceituoso afasta esse "outro", porque ele põe em perigo sua estabilidade psíquica. Assim, o preconceito cumpre também uma função social: construir o diferente como culpado pelos males e inseguranças daqueles que são iguais.

A ação irrefletida, a "economia do esforço intelectual" (Crochik, 1997), são as características do preconceito como predisposição para a ação de discriminação. A agressão é encaminhada para o alvo errado, por não se ter a consciência de que são os princípios sociais impregnados nas relações entre os homens e nas formas de trabalho que devem ser combatidos e não suas vítimas. O preconceito é, portanto, contrário às diferenças, levando o preconceituoso a uma outra identificação, como esclarecem Horkheimer e Adorno (1973, p. 179): "Para que se sintam alguém, essas pessoas têm necessidade de se identificar com a ordem estabelecida e essa identificação faz-se com tanto mais agrado quanto mais inflexível e poderosa for essa ordem. E dessa forma as particularidades são destroçadas em função da totalidade".

No ensaio "Educação após Auschwitz", Adorno (1995b, p. 122) afirma que "a violência contra os fracos se dirige, principalmente, contra os que são considerados fracos". A lembrança da fragilidade humana, da diferença compreendida como obstáculo à inserção funcional na sociedade, determina a prática da negação social. Por outro lado, a renúncia de autonomia por parte dos adaptados é algo que fica internalizado, retornando na forma de agressão e discriminação àqueles que demonstram algum tipo de resistência. É o caso dos alunos que são tipificados como indisciplinados ou com distúrbios de comportamento. A esse respeito, diz Adorno: "A pressão do geral dominante, sobre tudo que é particular, os homens individualmente e as instituições singulares, tem uma tendência a destroçar o particular e o individual, juntamente com seu potencial de resistência" (idem, ibidem).

O estranhamento causado pela deficiência: preconceito e experiência

Luciene M. da Silva

Universidade do Estado da Bahia, Programa de Pós-Graduação Educação e Contemporaneidade

http://www.scielo.br/scielo.php?pid=S1413-24782006000300004&script=sci_arttext

Consumo de Ritalina no Brasil cresce 775% em dez anos

Consumo de Ritalina no Brasil cresce 775% em dez anos

Droga é usada no tratamento do transtorno de déficit de atenção e hiperatividade.

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Na última década, a importação e a produção do medicamento também cresceram 373% no PaísFoto: Emílio Pedroso / Agencia RBS

Em dez anos, a importação e a produção de metilfenidato - mais conhecido como Ritalina, um de seus nomes comerciais - cresceram 373% no País. A maior disponibilidade do medicamento no mercado nacional impulsionou um aumento de 775% no consumo da droga, usada no tratamento do transtorno de déficit de atenção e hiperatividade (TDAH). Os dados são de pesquisa do Instituto de Medicina Social da Universidade Estadual do Rio de Janeiro (UERJ).

O remédio é usado sobretudo em crianças e adolescentes, os mais afetados pelo transtorno. Para especialistas, a alta no uso do medicamento reflete maior conhecimento da doença e aumento de diagnósticos, mas também levanta o alerta de uso indevido da substância, até por pessoas saudáveis que buscam aumentar o rendimento em atividades intelectuais.

Em sua tese de doutorado pela UERJ, defendida em maio, a psicóloga Denise Barros compilou os dados dos relatórios anuais sobre substâncias psicotrópicas da Junta Internacional de Controle de Narcóticos, órgão vinculado às Nações Unidas. De acordo com o levantamento, o volume de metilfenidato importado pelo Brasil ou produzido em território nacional passou de 122 kg em 2003 para 578 kg em 2012, alta de 373%. A pesquisadora cruzou os dados da produção e importação e do estoque acumulado em cada ano, dado também disponível nos relatórios, para chegar aos prováveis índices anuais de consumo. De acordo com o levantamento, foram 94 kg consumidos em 2003 contra 875 kg em 2012, crescimento de 775%.

Dados mais recentes obtidos pelo jornal O Estado de S. Paulo na Agência Nacional de Vigilância Sanitária (Anvisa) confirmam a tendência de alta. Segundo o órgão, o número de caixas de metilfenidato vendidas no Brasil passou de 2,1 milhões em 2010 para 2,6 milhões em 2013.

— Houve um aumento da divulgação da doença e do número de pessoas que passaram a ter acesso ao tratamento, mas há outro fator importante, que é uma maior exigência social de administrar a atenção — afirma a especialista

Ela lembra ainda que há casos de adultos sem o transtorno que tomam o metilfenidato para melhorar a concentração e o foco nos estudos.

—Isso é comum entre concurseiros, vestibulandos, estudantes de Medicina. Pouco se fala sobre isso no Brasil, mas nos Estados Unidos e em algumas partes da Europa, esse uso inadequado já é tratado como um problema de saúde pública — declara.

Diagnóstico

Para o psiquiatra infantil Rossano Cabral Lima, professor da UERJ, a alta no consumo é motivo de alerta porque o diagnóstico de TDAH nem sempre é acompanhado de uma investigação aprofundada das possíveis causas do comportamento incomum da criança.

— Apesar de a medicação ser importante em alguns casos, o diagnóstico rápido de TDAH e o tratamento medicamentoso parecem ter se tornado a solução mais rápida e fácil de vários problemas, sem que a origem deles seja analisada a fundo. Não se questiona se a inquietude da criança pode estar relacionada a alguma questão da escola, se é uma resposta a algo que ela não está sabendo lidar — diz o especialista.

Presidente da Associação Brasileira de Psiquiatria (ABP), Antônio Geraldo da Silva, afirma que, apesar da alta no consumo, ainda há milhares de brasileiros com TDAH sem tratamento.

— Com o crescimento do acesso à medicação, estamos talvez começando a adequar a proporção de pessoas com o transtorno e pacientes tratados. Mas hoje, infelizmente, ainda temos subtratamento de TDAH — declarou o presidente da ABP

O especialista cita também um estudo publicado em 2012 na Revista Brasileira de Psiquiatria que apontou que apenas 19% dos brasileiros com TDAH fazem o tratamento com medicação.

As Empresas hospitalares - A medicina e a realidade brasileira

As Empresas hospitalares - A medicina e a realidade brasileira 

"Comprovou-se a presença de fraudes em escala intolerável, acima de 90%, nos documentos examinados, escolhidos aleatoriamente. As irregularidades mais frequentes foram: 1. Pacientes fanstasmas (que nunca haviam existido ou que já haviam falecido). 2. Falso Diagnóstico (formulado para efeito de cobrança. conforme havia sido verificado, anteriormente pela professora da USP (Maria Lúcia Lebrão). 3. Complicações inexistentes. 4. Cobrança de diárias de período em que o paciente não esteve internado. 5. Cobrança de exames não realizados. 6. Desmembramento de contas (a mesma conta apresentada mais de uma vez). 7. Internações desnecessárias. 8. Exames desnecessários. 9. Cobrança de medicamentos não utilizados. 10. Cobrança de taxas irregulares (Centro de tratamento intensivo, Centro Cirúrgico). 11. Cobrança indevida de honorários médicos. 12. Cobrança de exames não realizados (radiografias, laboratório)."

Autor: Carlos Gentile de Mello 

A Medicina e a Realidade Brasileira. Rio de Janeiro: Achiamé; 1983 (Série Saúde e Realidade Nacional, vol. 4

Associações Médicas - A medicina e a realidade brasileira

"Não explicitou que a livre escolha, tese programática da AMB, tem sido, ampla e abusivamente, utilizada como um biombo para escamotear o sistema de remuneração médica em função da quantidade de tarefas executadas, conhecido como "pagamento por unidades de serviço", fator incontrolável de corrupção".

"Em nome da liberdade a AMB tem defendido um sistema altamente corruptor, responsável pela deterioração da imagem do médico e do conceito da medicina. Quem melhor e mais detalhadamente definiu esse sistema de pagamento foi um dos mais destacados estudiosos do problema, Murillo Villela Bastos, que disse:

"O pagamento por tratamento realizado induz o médico a buscar, no paciente, algo que resulte em lucro. Os doentes crônicos passam a ser cultivados e, de certo modo, asseguram uma renda previsível. As pessoas que tem amídalas e apêndices são instadas a removê-los. Os casos graves são evitados porque a remuneração que propiciam não correspondem ao trabalho que dão. O parto tende a se transformar de ato fisiológico em ato operatório. O exagero de exames complementares e de aplicações terapêuticas passa a ser confundido com a boa qualidade da medicina. A assistência domiciliar tende a desaparecer por ser menos lucrativa em comparação com as facilidades do lucro no atendimento em consultório ou hospital. O médico é levado, quase inconscientemente, a fragmentar o tratamento em uma série de atos médicos, de acordo com a tabela de honorários, e, para finalizar, o diagnóstico passa a ser aquele que justifique maior remuneração, anulando o valor das estatísticas de morbidade que tenham por base esse registro".

Autor: Carlos Gentile de Mello 

A Medicina e a Realidade Brasileira. Rio de Janeiro: Achiamé; 1983 (Série Saúde e Realidade Nacional, vol. 4

Ética médica - A medicina e a realidade brasileira

"Quando o novo texto se reporta aos pacientes crônicos e irrecuperáveis entra em detalhes da maior importância. Por exemplo: "O médico não pode abandonar o paciente por ser este portador de moléstica crônica ou incurável, mas deve continuar a assisti-lo, ainda que somente para mitigar o sofrimento físico ou psíquico, ajudar ou confortar"".

Autor: Carlos Gentile de Mello 

A Medicina e a Realidade Brasileira. Rio de Janeiro: Achiamé; 1983 (Série Saúde e Realidade Nacional, vol. 4

PRESIDENTE ABRASME FALA DA PORTARIA DA SMS-SP SOBRE RITALINA

Recentemente, a Secretaria Municipal de Saúde de São Paulo (SMS/SP) publicou portaria regulamentando o uso do medicamento metilfenidato no tratamento de crianças e adolescentes diagnosticadas com Transtorno de Déficit de Atenção com Hiperatividade (TDAH). A doença é caracterizada por sintomas como desatenção, inquietude e impulsividade e, de acordo com dados da Associação Braisleira do Déficit (ABDA), ocorre em 3 a 5% das crianças de diferentes regiões do mundo em que já foi pesquisada.

A utilização de psicofármacos é uma das formas de tratamento mais adotadas atualmente. O uso do medicamento metilfenidato em crianças menores de idade é cada vez mais frequente e os efeitos prejudiciais desse fenômeno vem sendo analisados e denunciados por cientistas de diversas áreas relacionadas à saúde pública.

Para entender melhor a questão, a ENSP TV conversou com o coordenador do Laboratório de Estudos e Pesquisa em Saúde Mental e Atenção Psicossocial da Escola (Laps/ENSP), e presidente da Associação Brasileira de Saúde Mental (Abrasme), Paulo Amarante, que falou sobre algumas características do TDAH, as formas de diagnóstico e a medicalização, além da regulamentação do uso do metilfenidado no tratamento infantil.

Confira a entrevista em vídeo!

YouTube: http://youtu.be/crFwLJvx8D8

 Informe ENSP: http://www.ensp.fiocruz.br/portal-ensp/informe/site/materia/detalhe/35934

On Investigating the Psychiatric-Pharmaceutical Complex

http://www.madinamerica.com/2014/08/taking-entry-point-investigating-psychiatric-pharmaceutical-complex/

Taking an Entry Point: On Investigating the Psychiatric-Pharmaceutical Complex

• 

Bonnie Burstow, Ph.D.

August 4, 2014

There are various ways to analyze an institution like psychiatry. One of the most common is by mining examples. You might, for example, talk to few survivors who seem to embody what befalls most folk subject to psychiatric rule (a common research sampling strategy called by the unfortunate name “typical cases”; see Patton, 2000). Or you might pen a stirring phenomenological account based on your own experiences. All, without question, highly worthwhile.

A very different approach that I wish to demonstrate and would encourage other critics to consider employing now and then is choosing a single entry point—a moment where something feels wrong and which, for reasons that you may not yet fathom, appears to hold the promise of helping you open up the institution—and then seeing where it can lead you. This is a part of a method known as institutional ethnography (see Smith, 2006 and Smith and Turner, 2014). For the purposes of this article, I will give a simplified version and will introduce you to the bare beginnings of an inquiry—one that I found myself falling into but a couple of weeks back. The entry point is the arrival of a letter. I choose it partly because it is helpful as a demonstration, albeit also because it indeed unlocks a direction and modus operandi that it behooves us to be aware of.

In short, I arrived at my office to find a letter from the Centre for Addiction and Mental Health (CAMH)—a huge psychiatric hospital/research institute in the centre of Toronto.  I was perplexed, for as a well known critic of CAMH and as someone who had recently forced an investigation into one of their research projects, I would have thought that I was the last person that they would want to interact with. I proceeded to open the letter. It was from the coordinator of a research project. The project was investigating the use of a “new treatment” for people “with anorexia” (You can see the letter in its entirely here). To quote some of the key passages, it states,

“I am writing you on behave [their typo] of Dr. Allan Kaplan regarding a treatment study for anorexia nervosa. We hope that this study could be a great referral source for you and offer an important supplement to the therapy you provide.”

It proceeds to say,

“We offer (1) weekly visits with a psychiatrist/study physician for participants; (2) a commitment to find appropriate follow up care for participants at the completion of the study…(3) a commitment to follow up with referring clinicians to ensure continuity of care.” It ends with contact information.

Even as I started to read, I was perplexed. My immediate concern was: Why is a psychiatric research institute turning to me — a feminist therapist utterly unconnected with psychiatry, moreover, famous/infamous for organizing against it? A plausible explanation is that they had no idea who I was but had simply cobbled together a list of all therapists in the city known to work with people thought of as having “eating disorders.”

As I continued reading, my perplex turned into a kind of alarm, for the words, “We hope that this study would be a great referral source for you” signals that they are hoping to use therapists as a means of recruiting people into their study. The point is, it is bad enough that studies that place people in jeopardy are being advertised on buses, on the internet, in the main media. Now they are hoping to hook people’s own counselors or therapists into “referring” them. In essence, my first discovery.

As I pondered this, as a feminist, I began to catch a whiff of a possibly formidable new assault on women – overwhelmingly, the gender diagnosed as “anorexic.” The pressing question now was: What “treatment” were they researching? My hunch was one of the psychopharmaceutical substances. I was likewise eager to know what they were actually telling people about the product being tested.

In the interests of finding out more, I proceeded to call the coordinator. She confirmed that I had been contacted because I was on a list of therapists they had developed and clarified that this was a study on the use of olanzapine (better known by the brand name “Zyprexa”). “Would you like me to send you study material?” she offered. Shortly thereafter she emailed me an article about the use of olanzapine for anorexia as well as some general advertisements for the study (not one of which mentioned olanzapine).

What I did not receive, though I had explicitly asked for it, is the written information on olanzapine that they would be providing to prospective “participants.” I accordingly renewed my request. Her response was, “Generally [the doctor] discusses the details of the medication with the people in person if they are interested in finding out more.” (personal email, July 22, 2014) Which left me wondering if any written information is provided, and if so: a) what it says and b) why they are reluctant to share it with the very people they are theorizing as a prospective referral source and, if not, why nothing is being put in writing.

My own suspicion here? A couple of years ago, I forced an investigation into an ECT trial at CAMH, using as the basis for the complaint the very material that the principal investigator made public or handed to prospective participants. Now to be clear, the investigation in question, as expected, concluded that nothing wrong had happened. Given that the complaint caused the organization considerable consternation, however, one obvious possibility is that it is now policy to put as little as possible in writing. Be that as it may, of course, this much is clear: If little or nothing is put in writing, it is very hard to prove what is being told participants—that is, whether risks are greatly minimized or indeed mentioned at all and whether the claims being made have any credibility. What goes along with this, even if judged by less critical standards, under such circumstances, the likelihood that what consent participants give will be “informed” is negligible.

Which brings us to the nature of olanzapine itself. For those unfamiliar with it, olanzapine is an atypical antipsychotic. It is approved for use with “schizophrenia” and has never been approved for use with “anorexia.” Unfortunately, nor need it be so approved, for off-label prescribing (prescribing for purposes other than those for which a drug has been approved) is legal. Now olanzapine is a particularly risky substance known to cause all the problems that typically attend antipsychotics, but in addition causes hypoglycemia, diabetes, and hormonal imbalance, the last of which, in turn, leads to pathological weight gain—likewise well documented (see Breggin, 2008; also postings HERE and HERE.

The question that immediately presents itself is this: How many, if any, of these untoward effects do prospective participants hear about? And why do these researchers consider olanzapine effective for “anorexia” in the first place? And why in the larger scheme of things is this new “treatment approach” being pursued?

The first question remains unanswered largely because the process is not transparent. I leave you to conjecture in whose interest that lack of transparency is. In an attempt to answer the last two, I proceeded to hunt for earlier studies. I also investigated what the principal investigator himself had written.

Some salient findings? In 2007, there was a pilot study on the use of olanzapine for “anorexia.” It was funded in part by Eli Lilly—the manufacturer of Zyprexa. There were also a few other small studies. This larger study itself (the topic of the letter) is predicated on those earlier studies and it is taking place at CAMH in collaboration with Columbia University and three other U.S. sites. Correspondingly, what is being tested is precisely the proposition that olanzapine is efficacious with “anorexia.”

Question: What makes the earlier studies sufficiently promising to warrant such a study? It is here where what is essentially fancy footwork takes place. While anxiety relief is being hypothesized, the main and only convincing finding, as seen in Attia et al., (2011, p. 5), is that “in a small group of outpatients with AN, olanzapine was associated with greater increase in BMI [Body Mass Index] than was placebo.” To put this in layman’s terms, the participants on olanzapine gained more weight than the participants on placebo.

What is going on here? Quite simply, pathological weight gain caused by hormonal imbalance which in turn is caused by olanzapine is being repositioned as indicative of effectiveness for “anorexia.” In other words, not “normal” but pathological weight gain is itself being re-packaged as successful treatment. Something not hard to do, given the worry that people naturally have about the weight loss of women diagnosed with “anorexia.”

Put aside our understandable worry about women in these circumstances—and I am in no way denying that women deemed anorexic are often in very serious trouble with themselves (see Burstow, 1992)—what we have here, in effect, is the patriarchal control and harming of women, made to look palatable.

Exactly how far this new direction will go remains to be seen. That depends on what happens with other research studies on anorexia (note; there is more than one new “approach to anorexia” being researched at CAMH and around the world).

It likewise  depends on how coopted therapists become, what propaganda is churned out, with what “before and after” pictures, how much money is pumped into the marketing, and what distraught family members can be brought onside. However, it is not hard to imagine a substantial chemical onslaught on young women with eating problems ensuing.

As for the participants themselves, what is the likely fate of the women once the trial  ends? The answer is latent in the letter. The investigators promise to find “appropriate follow-up care at the completion of the study” and commit to ensuring “the continuity of care.” Translation? They will refer the women to doctors likely to keep them on the olanzapine, using, among other things, the pathological weight gain (repackaged as benign) as the reason why the women should continue on the “med.”

If it is now fairly clear what is going on, also why it is a win-win for the pharmaceutical industry. Further clarity arose as I unearthed and scrutinized one other publication. In an article called “Drug Rescue and Repurposing,” Kaplan, the principal investigator of the CAMH research in question states that olanzapine is being studied for “its repurposing potential.” He goes on to explain:

“Many pharmaceutical companies are moving away from developing new central nervous system drugs and psychiatric drugs in particular, due to the high costs of drug development, the absence of good animal models for psychiatric disorders, and low success rates in phase 3 clinical trials. As a result the CNS line is drying up and drug repurposing ends up an important and valuable research approach to able to develop new drugs in a cost-effective manner.” (Kaplan, 2013)

Despite the use of the term “develop new drugs” the companies, in point of fact, are not in these instances “developing new drugs” but rather, as Kaplan puts it, “repurposing.”  The very words inserted into the title of his article “Drug Rescue,” correspondingly, is an answer to my final question. The pharmaceutical companies are experiencing what they see as a challenge to their bottom line — that is, purportedly they are in need of “rescue.” Stringent “repurposing” for drugs, whatever the type and whatever population can be theorized in relation to it, is the solution. The sacrifice of people for the greater good of the drug companies, I would add, is astonishingly close to being acknowledged.

To return to the beginning of this article and retrace our steps, we began with a letter offering what sounded like a benefit to the therapist. However, besides that as an antipsychiatry activist, I have no connection with psychiatry and so such communication is minimally an annoyance, in this instance something in particular did not “sit right.” And so instead of throwing away the letter or commenting on its “errors” or using it as an example of the type of letter that I receive from time to time, I approached it as a possibly useful entry point that could be employed to shed light on psychiatric processes. That is, I followed the different institutional threads that presented themselves.

What I found initially is a lack of transparency, combined with the use of a highly dangerous drug − olanzapine. Probing further, I discovered that what recommended this off-label use of the drug was nothing less injurious than the pathological weight gain arising from hormonal disturbance. And in the process I found what may well be the beginning of a new frontal pharmaceutical assault on women diagnosed with anorexia.

Finally, while of course the prevalence of “off-label” prescribing − and that its purpose is to increase industry profit − is well known, one related finding surfaced that is minimally less theorized: The immediate reason for the “repurposing” note is to get around not only the problem that stage 3 trials (the huge trials mandatory when attempting to bring a new drug to market) are expensive, but the at least as serious problem that they typically yield dismal results.

Hence the need for what is euphemistically being termed “repurposing,” and hence for studies that use whatever evidence can be mustered (including ones that can reasonably be put down to harm, pure and simple) to declare effectiveness. In essence, not only is this cost-effective, it has the added advantage of sidestepping the entire approval process, while creating the appearance of acting responsibly. A further direction that appears to have been uncovered is the use of people’s own therapists—including private feminist therapists—to secure research participants and the practice of guaranteeing repeat customers by guaranteeing “continuity of care.”

All these findings are important to make known. Moreover—and this takes us back to the beginning of this article—a modest demonstration of the value of employing an “entry point” approach.

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A final methodological comment in conclusion: I stated at the outset that there was a relationship between what I was doing and institutional ethnography (IE). So was this an institutional ethnography study? No. What I did is to take a few IE elements and fashion an easily accessible method available to anyone. Should this intrigue you about IE itself and should you want to know what could be done if one were actually using real IE in all its dimensions and complexity, keep reading BizOMadness and Mad in America. I am in the process of training a veritable army of antipsychiatry critics in IE, so you will be hearing more about this serviceable methodology in the months and years to come.

* * * * *

This blog is a slightly revised version of one that appeared first on
BizOMadness, Bonnie Burstow’s personal website

References

Attia, Ec. et al. (2011). Olanzapine versus placebo for anorexia nervosa. Pathological Medicine, p. 1.

Breggin, P. (2008). Brain-disabling treatments in psychiatry. New York: Springer.

Burstow, B. (1992). Radical feminist therapy: Working in the context of violence. Newbury Park: Sage.

Kaplan, A. (2013). Drug rescue and repurposing. IMS Magazine. Downloaded July 30 2014 fromhttp://www.imsmagazine.com/drug-rescue-and-repurposing-allan-s-kaplan/.

Patton, M. (2000). Qualitative evaluation and research methods (2nd ed.). Newbury Park: Sage.

Smith, D. (Ed.) (2006). Institutional ethnography as practice. New York: Rowan and Littlefield,

Smith, D. and Turner, S. (Eds.) (2014). Incorporating texts into institutional ethnography. Toronto: University of Toronto Press.

Bonnie Burstow, Ph.D.

Deconstructing the Institution: Dr. Burstow is a faculty member at U. of Toronto, and an antipsychiatry activist. She writes about language, institutional ruling, resistance, and social change. Works include Radical Feminist Therapy and Psychiatry Disrupted. For more information, see bizomadness.blogspot.ca