feliz

Tuesday, September 14, 2010

SER FELIZ!!!

Ser feliz não é ter um céu sem tempestades, caminhos sem acidentes, trabalhos sem fadigas, relaci

amentos sem decepções.

Ser feliz é encontrar força no perdão, esperança nas batalhas, segurança no palco do medo, amor nos desencontros.

Ser feliz não é apenas valorizar o sorriso, mas refletir sobre a tristeza.

Não é apenas comemorar o sucesso, mas aprender lições nos fracassos. Não é apenas ter júbilo nos aplausos, mas encontrar alegria no anonimato.

Ser feliz é reconhecer que vale a pena viver, apesa

r de todos os desafios, incompreensões e períodos de crise.

Ser feliz não é uma fatalidade do destino, mas uma conquista de quem sabe viajar para dentro do seu próprio ser.

Ser feliz é deixar de ser vítima dos problemas e se tornar autor da própria história. É atravessar desertos fora de si, mas ser capaz de encontrar um oásis no recôndito da sua alma. É agradecer a Deus a cada manhã pelo milagre da vida.

Ser feliz é não ter medo dos próprios sentimentos. É saber falar de si mesmo. É ter coragem para ouvir um "não". É ter segurança para receber uma crítica, mesmo que injusta. É beijar os filhos, curtir os pais e ter momentos poéticos com os amigos, mesmo que eles nos magoem.

Ser feliz é deixar viver a criança livre, alegre e simples que mora dentro de você. É ter maturidade para falar: "Eu Errei". É ter ousadia para dizer: "Me Perdoe". É ter sensibilidade para confessar: "Eu Preciso De Você".

Ser feliz é ter a capacidade de dizer: "Eu Te Amo".

OBRIGADA IRENE- http://mamyrene.blogspot.com/

COMEMORANDO UM ANINHO DE BLOG. PARABÉNS AMIGA.

Acabei de receber esta linda mensagem da minha querida Ana do blog. Pelos caminhos da vida.

Mensagem de Boa Noite

Uma Boa Noite repleta de Carinho..
Uma Boa Noite recheada com muita Fé...
Uma Boa Noite imensa com Afeto...
Uma Boa Noite esplendorosa de Luz...
Uma Boa Noite forte com Energia...
Uma Boa Noite encharcada de Coragem...
Uma Boa Noite embrulhada de Esperança...
E uma Boa Noite cheia de Alegria
desejo a todos esta linda noite para todos...
bjs sandra

Ganhei este lindo presente da minha doce amiga virtual, lá em Portugal Joana Neves..

Amiga querida
Muitos Parabéns
pelo 2º aniversário do seu lindo blog!!:)
É mesmo caso para festejar:)

Desejo muito sucesso
e que venham muitos mais
pois vc já faz falta neste mundinho blogueiro
o qual ilumina com a sua amizade e alegria!

Este é o meu presente para vc!
Espero que goste amiga:)

AMIGOS! SE GOSTARAM DO SELINHO VOU TE OFERECER COM TODO O MEU AMOR E CARINHO. SINTAM-SE A VONTADE PARA LEVAR...

GRADEÇO A SUA COMPANHIA!!!

Poetas-Um Voo Livre-

Sinal de Liberdade-uma expressão de sentimento-

Blog Coletivo-Uma Interação de Amigos- JÁ NOVO TEMA...COMPARTILHE...

MEUS MIMOS . AQUI. OFERECIDOS/RECEBIDOS-

Stopping Antidepressants: Not So Fast

People who quit antidepressants slowly, by gradually decreasing the dose, are much less likely to suffer a relapse, according to Baldessarini et al. in the American Journal of Psychiatry.

They describe a large sample (400) of patients from Sardinia, Italy, who had responded well to antidepressants, and then stopped taking them. The antidepressants had been prescribed for either depression, or panic attacks.

People who quit suddenly (over 1-7 days) were more likely to relapse, and relapsed sooner, than the ones who stopped gradually (over a period of 2 weeks or more).

This graph shows what % of the patients in each group remained well at each time point (in terms of days since their final pill.) As you can see, the two lines separate early, and then remain apart by about the same distance (20%) for the whole 12 months.

What this means is that rapid discontinuation didn't just accelerate relapses that were "going to happen anyway". It actually caused more relapses - about 1 in 5 "extra" people. These "extra" relapses all happened in the first 3 months, because after that, the slope of the lines is identical.

On the other hand, they rarely happened immediately - it's not as if people relapsed within days of their last pill. The pattern was broadly similar for older antidepressants (tricyclics) and newer ones (SSRIs).

The authors note that these data throw up important questions about "relapse prevention" trials comparing people who stay on antidepressants vs. those who are switched - abruptly - to placebo. People who stay on the drug usually do better, but is this because the drug works, or because the people on placebo were withdrawn too fast?

This was an observational study, not an experiment. There was no randomization. People quit antidepressants for various "personal or clinical reasons"; 80% of the time it was their own decision, and only 20% of the time was it due to their doctor's advice.

So it's possible that there was some underlying difference between the two groups, that could explain the differences. Regression analysis revealed that the results weren't due to differences in dose, duration of treatment, diagnosis, age etc., but you can't measure every possible confound.

Only randomized controlled trials could provide a final answer, but there's little chance of anyone doing one. Drug companies are unlikely to fund a study about how to stop using their products. So we have only observational data to go on. These data fit in with previous studies showing that there's a similar story when it comes to quitting lithium and antipsychotics. Gradual is better.

But that's common sense. Tapering medications slowly is a good idea in general, because it gives your system more time to adapt. Of course, sometimes there are overriding medical reasons to quit quickly, but apart from in such cases, I'd always want to come off anything as gradually as possible.

Baldessarini RJ, Tondo L, Ghiani C, & Lepri B (2010). Illness risk following rapid versus gradual discontinuation of antidepressants. The American journal of psychiatry, 167 (8), 934-41 PMID: 20478876

Stopping Antidepressants: Not So Fast

People who quit antidepressants slowly, by gradually decreasing the dose, are much less likely to suffer a relapse, according to Baldessarini et al. in the American Journal of Psychiatry.

Monday, September 13, 2010

CURIOSA RECEBENDO OS PRESENTES....

CURIOSA AGRADECE O CARINHO ESPECIAL DE TODOS. ESTOU MUITO FELIZ COM A SUA COMPANHIA E VISITA. ISSO TUDO TAMBÉM ME FAZ MUITO FELIZ. A SUA COMPANHIA!!!

AGRADEÇO TODOS OS PRESENTES RECEBIDOS DOS AMIGOS VIRTUAIS. ESTE É UM MOMENTO MUITO ESPECIAL. AGRADEÇO AS PESSOAS QUE COMPARTILHARAM COM A ALEGRIA DO BLOG CURIOSA PELA PASSAGEM DE DOIS ANOS. AGRADEÇO AINDA QUEM PARTICIPOU DA COLETIVA. LI TODOS OS TEXTOS. TODOS MUITO ESPECIAIS.
A ALEGRIA DE NOS FAZER FELIZ É CONTAGIANTE. CADA UM TEM SUA FORMA DE SER FELIZ. E DE PODER CONTAR O QUE LHE DEIXA MUITO E MUITO FELIZ.

MUITO OBRIGADA A VOCÊ QUE PARTICIPOU E TAMBÉM A VOCÊ QUE VEIO PRESTIGIAR ESSE MOMENTO LINDO.
AGRADEÇO DE CORAÇÃO.

UM PRESENTE MUITO LINDO!!!
OBRIGADA IRENE

IRENE- http://mamyrene.blogspot.com/

Obrigado a amiga Sandra por nos proporcionar

uma Coletiva com um tema tão FELIZ
*P A R A B É N S*

"Este selinho a M@myrene oferece como lembrança
pelo aniversário da Curiosa"

UM PRESENTE SUPER FOFO RECEBIDO DA PANDORA.

OBRIGADA ROSA MATTOS. AMEI ..LINDO.

https://mail.google.com/mail/?ui=2&ik=8369aea477&view=att&th=12b06fbead50b6df&attid=0.1&disp=inline&zw

DA JOANA
NÃO CONSEGUI POSTAR O PRESENTE DA MINHA DOCE AMIGA JOANA. ASSIM QUE CONSEGUIR POSTAREI.
OBRIGADA AMIGA

OBRIGADA SONIA..AMEI!!

http://coisinhasras.atspace.com/Tags%20Festivas/pagtagsaniversarios/1.gif

MAIS UM MUITO FOFO.OBRIGADA SONIA.

RECEBI DA ANNINHA E REPASSO E VOCÊ QUE TAMBÉM É MEU TOP COMENTARISTA. OBRIGADA MEU(MINHA) QUERIDO(A) AMIGO(A) VIRTUAL.

DEMAIS PRESENTES ABAIXO..
AGRADEÇO O CARINHO DE TODOS.
SANDRA

GRADEÇO A SUA COMPANHIA!!!

Poetas-Um Voo Livre-

Sinal de Liberdade-uma expressão de sentimento-

Blog Coletivo-Uma Interação de Amigos- JÁ NOVO TEMA...COMPARTILHE...

MEUS MIMOS . AQUI. OFERECIDOS/RECEBIDOS-

LEMBRETE: ESTOU COM PROBLEMA NA NET. NÃO ESTOU CONSEGUINDO VISITAR NINGUÉM. MAS AGRADEÇO A SUA VISITA POR AQUI.
NEM MEUS COMENTÁRIOS ESTOU CONSEGUINDO ABRIR.

Shotgun Psychiatry

There's a paradox at the heart of modern psychiatry, according to an important new paper by Dr Charles E. Dean, Psychopharmacology: A house divided.

It's a long and slightly rambling article, but Dean's central point is pretty simple. The medical/biological model of psychiatry assumes that there are such things as psychiatric diseases. Something biological goes wrong, presumably in the brain, and this causes certain symptoms. Different pathologies cause different symptoms - in other words, there is specificity in the relationship between brain dysfunction and mental illness.

Psychiatric diagnosis rests on this assumption. If and only if we can use a given patient's symptoms to infer what kind of underlying illness they have (schizophrenia, bipolar disorder, depression), diagnosis makes sense. This is why we have DSM-IV which consists of a long list of disorders, and the symptoms they cause. Soon we'll have DSM-V.

The medical model has been criticized and defended at great length, but Dean doesn't do either. He simply notes that modern psychiatry has in practice mostly abandoned the medical model, and the irony is, it's done this because of medicines.

If there are distinct psychiatric disorders, there ought to be drugs that treat them specifically. So if depression is a brain disease, say, and schizophrenia is another, there ought to be drugs that only work on depression, and have no effect on schizophrenia (or even make it worse.) And vice versa.

But, increasingly, psychiatric drugs are being prescribed for multiple different disorders. Antidepressants are used in depression, but also all kinds of anxiety disorders (panic, social anxiety, general anxiety), obsessive-compulsive disorder, PTSD, and more. Antipsychotics are also used in mania and hypomania, in kids with behaviour problems, and increasingly in depression, leading some to complain that the term "antipsychotics" is misleading. And so on.

So, Dean argues, in clinical practice, psychiatrists don't respect the medical model - yet that model is their theoretical justification for using psychiatric drugs in the first place.

He looks in detail at one particularly curious case: the use of atypical antipsychotics in depression. Atypicals, like quetiapine (Seroquel) and olanzapine (Zyprexa), were originally developed to treat schizophrenia and other psychotic states. They are reasonably effective, though most of them are no more so than older "typical" antipsychotics.

Recently, atypicals have become very popular for other indications, most of all mood disorders: mania and depression. Their use in mania is perhaps not so surprising, because severe mania has much in common with psychosis. Their use in depression, however, throws up many paradoxes (above and beyond how one drug could treat both mania and its exact opposite, depression.)

Antipsychotics block dopamine D2 receptors. Psychosis is generally considered to be a disorder of "too much dopamine", so that makes sense. The dopamine hypothesis of psychosis and antipsychotic action is 50 years old, and still the best explanation going.

But depression is widely considered to involve too little dopamine, and there is lots of evidence that almost all antidepressants (indirectly) increase dopamine release. Wouldn't that mean that antidepressants could cause psychosis (they don't?). And why, Dean asks, would atypicals, that block dopamine, help treat depression?

Maybe it's because they also act on other systems? On top of being D2 antagonists, atypicals are also serotonin 5HT2A/C receptor blockers. Long-term use of antidepressants reduces 5HT2 levels, and some antidepressants are also 5HT2 antagonists, so this fits. However, it creates a paradox for the many people who believe that 5HT2 antagonism is important for the antipsychotic effect of atypicals as well - if that were true, antidepressants should be antipsychotics as well (they're not.) And so on.

There may be perfectly sensible answers. Maybe atypicals treat depression by some mechanism that we don't understand yet, a mechanism which is not inconsistent with their also treating psychosis. The point is that there are many such questions standing in need of answers, yet psychopharmacologists almost never address them. Dean concludes:

it seems increasingly obvious that clinicians are actually operating from a dimensional paradigm, and not from the classic paradigm based on specificity of disease or drug... the disjunction between those paradigms and our approach to treatment needs to be recognized and investigated... Bench scientists need to be more familiar with current clinical studies, and stop using outmoded clinical research as a basis for drawing conclusions about the relevance of neurochemical processes to drug efficacy. Bench and clinical scientists need to fully address the question of whether the molecular/cellular/anatomical findings, even if interesting and novel, have anything to do with clinical outcome.

Dean CE (2010). Psychopharmacology: A house divided. Progress in neuro-psychopharmacology & biological psychiatry PMID: 20828593

Shotgun Psychiatry

There's a paradox at the heart of modern psychiatry, according to an important new paper by Dr Charles E. Dean, Psychopharmacology: A house divided.

it seems increasingly obvious that clinicians are actually operating from a dimensional paradigm, and not from the classic paradigm based on specificity of disease or drug... the disjunction between those paradigms and our approach to treatment needs to be recognized and investigated... Bench scientists need to be more familiar with current clinical studies, and stop using outmoded clinical research as a basis for drawing conclusions about the relevance of neurochemical processes to drug efficacy. Bench and clinical scientists need to fully address the question of whether the molecular/cellular/anatomical findings, even if interesting and novel, have anything to do with clinical outcome.

Dean CE (2010). Psychopharmacology: A house divided. Progress in neuro-psychopharmacology & biological psychiatry PMID: 20828593

Sunday, September 12, 2010

You're (Brain Is) So Immature

How mature are you? Have you ever wanted to find out, with a 5 minute brain scan? Of course you have. And now you can, thanks to a new Science paper, Prediction of Individual Brain Maturity Using fMRI.

This is another clever application of the support vector machine (SVM) method, which I've written about previously, most recently regarding "the brain scan to diagnose autism". An SVM is a machine learning algorithm: give it a bunch of data, and it'll find patterns in it.

In this case, the input data was brain scans from children, teenagers and adults, and the corresponding ages of each brain. The pattern the SVM was asked to find was the relationship between age and some complex set of parameters about the brain.

The scan was resting state functional connectivity fMRI. This measures the degree to which different areas of the brain tend to activate or deactivate together while you're just lying there (hence "resting"). A high connectivity between two regions means that they're probably "talking to each other", although not necessarily directly.

It worked fairly well:

Out of 238 people aged 7 to 30, the SVM was able to "predict" age pretty nicely on the basis of the resting state scan. This graph shows chronological age against predicted brain age (or "fcMI" as they call it). The correlation is strong: r2=0.55.

The authors then tested it on two other large datasets: one was resting state, but conducted on a less powerful scanner (1.5T vs 3.0T) (n=195), and the other was not designed as a resting state scan at all, but did happen to include some resting state-like data (n=186). Despite the fact that these data were, therefore, very different to the original dataset, the SVM was able to predict age with r2 over 0.5 as well.

What use would this be? Well, good question. It would be all too easy to, say, find a scan of your colleague's brain, run it through the Mature-O-Meter, and announce with glee that they have a neurological age of 12, which explains a lot. For example.

However, while this would be funny, it wouldn't necessarily tell you anything about them. We already know everyone's neurological age. It's... their age. Your brain is an old as you are. These data raise the interesting possibility that people with a higher Maturity Index, for their age, are actually more "mature" people, whatever that means. But that might not be true at all. We'll have to wait and see.

How does this help us to understand the brain? An SVM is an incredibly powerful mathematical tool for detecting non-linear correlations in complex data. But just running an SVM on some data doesn't mean we've learned anything: only the SVM has. It's a machine learning algorithm, that's what it does. There's a risk that we'll get "science without understanding" as I've written a while back.

In fact the authors did make a start on this and the results were pretty neat. They found that as the brain matures, long-range functional connections within the brain become stronger, but short-range interactions between neighbours get weaker and this local disconnection with age is the most reliable change.

You can see this on the pic above: long connections get stronger (orange) while short ones get weaker (green), in general. This is true all across the brain.

It's like how when you're a kid, you play with the kids next door, but when you grow up you spend all your time on the internet talking to people thousands of miles away, and never speak to your neighbours. Kind of.

Link: Also blogged about here.

Dosenbach NU, Nardos B, Cohen AL, Fair DA, Power JD, Church JA, Nelson SM, Wig GS, Vogel AC, Lessov-Schlaggar CN, Barnes KA, Dubis JW, Feczko E, Coalson RS, Pruett JR Jr, Barch DM, Petersen SE, & Schlaggar BL (2010). Prediction of individual brain maturity using fMRI. Science (New York, N.Y.), 329 (5997), 1358-61 PMID: 20829489