Placebo effect generally ineffective - 2010 Cochrane review. Your thoughts?

[Octarine]

Psychology is currently dominated by the biopsychosocial ideology and one of the assumptions is that behaviour and cognitions can both cause and relieve somatic symptoms. One of the implications is the hypothesis of the placebo effect - that conditioning can cause biological responses that relieve symptoms. The problem with this model is that the majority of the evidence is subjective in nature. There certainly is a moderate subjective effect after conditioning, that depends on the nature of the conditioning. The problem is that little if any evidence has been shown demonstrating actual biological responses that are well understood enough to explain the relief of symptoms. The subjective response may simply be due to various response biases. The effect has also been questioned due to longer term results where the effect usually reverts to the mean.

The idea of a biological placebo response is controversial as it impacts the validity of the so-called placebo controlled pharmaceutical trials. The argument is that the placebo effect can have a beneficial effect and therefore this comparison reduces the effect size of the treatment. Proposed alternatives include the open treatment results compared to hidden treatment, where the timing of the treatment varies - patients don't actually know when they will receive the actual treatment.

Placebo interventions for all clinical conditions
Placebo interventions are often claimed to substantially improve many clinical conditions. However,most reports on effects of placebos
are based on unreliable studies that have not randomised patients to placebo or no treatment.
We studied the effect of placebo treatments by reviewing 202 trials comparing placebo treatment with no treatment covering 60
healthcare problems. In general, placebo treatments produced no major health benefits, although on average they had a modest effect
on outcomes reported by patients, such as pain. However, the effect on pain varied from large to non-existent, even in well-conducted
trials. Variations in the effect of placebo was partly explained by variations in how trials were conducted, the type of placebo used, and
whether patients were informed that the trial involved placebo.

http://onlinelibrary.wiley.com/o/cochrane/clsysrev/articles/CD003974/pdf_fs.html

Do you think their conclusions are reasonable?
Does this change your view on the placebo effect?
If the outcome effect (the effect that is called the placebo effect by some) is due to biases in subjective reporting, what do you think these specific biases are?
Do you think that the traditional 'randomised placebo controlled study' is still a valid method?

 

[Lark]

This raises questions for me, personally I think that the biopsychosocial thesis in psychology has its basis in sound systemic theorising and holistic/global pictures of patients or individual psychology. I never thought of it as an ideology, perhaps in the instances were it is anathema to cultural theorising, ie what some philosophers attacked as and others supported as sociobiology.

The subjective reporting, all research evidence can be described as subjective reporting, that's why there are problems with correlation and causation conclusions. Are you suggesting that research based on the biopsychosocial thesis should be tighter or have more clear limitations and delimitations in their studies using the placebo effect studay as a case in point?

If a study concluded that placebo effects are not strong I would personally be happier if it indicated that people were less susceptible to suggestion than they once were but there's plenty of counter evidence to that claim from advertising alone, let alone lots of popular stage hypnosis or magician acts like Darren Brown in the UK.

Excellent topical discussion BTW, simply excellent man

 

[Octarine]

I just lost a long reply due to a hard drive freeze up. Bare with me and I might be able to re-type most of it.

Anyway, the biopsychosocial ideology was popularised by Engel, but it basically rose out of the ashes of the old psychology paradigms being combined into one. It is an ideology, because there are no biopsychosocial model. It is just assume to be the correct way of practising psychology.

There are a number of aspects of different sciences that could be considered ideologies and had planned to discuss that in another thread.

I believe that an actual biopsychosocial model actually be devised, lest psychology be relegated to the history books, instead being consumed by biology (and neurology). The fact is that despite the name, the biology and sociology are poorly associated with the psychology. Even when they do try to consider such factors, it is not very rigorous and they measure few variables and always seem to use that data to explain their pre-existing conceptions. Likewise, there is a lot of talk of stress and stress response, but when they actually measure the responses, they find the data doesn't always fit their conceptions. But they seem to ignore this. The fact is that modern computational approaches such as pathway analysis, and more complex sociological models need to be integrated for their thesis to be compelling.

Suggestibility and conditioning are regularly discussed in psychology. Yet they seem to systematically ignore such conditioning when considering the placebo effect, or the efficacy of cognitive behavioural therapy on conditions such as Multiple Sclerosis or Cancer Fatigue.

The question is whether the results of the placebo effect are due to this conditioning of subjective reporting, or whether there are actual biological effects.

The central dogma revolves around pain analgesia in controlled pain tolerance studies (yes, these studies get ethics approval) and the finding that Naloxone a competitive antagonist of opioid receptors seems to 'block' the placebo effect after patients have been conditioned to have a placebo response after morphine administration. The hypothesis seems reasonable. Except that Naloxone is an hyperalgesic that is sometimes precribed for those with neurological defects that drastically reduce their perception of pain. So an alternative explanation for the effect may simply be that the pain is more difficult to ignore.

The case becomes more confusing when slightly different hypothesis are tested. One in particular utilised a few different strategies, but in general compared the conditioned responses after receiving morphine (opioid) or Ketorolac (no opioid). What is interesting is that for those who received Naloxone as a placebo instead of saline and were told that it was either an antibiotic ("conditioning without expectation") or a further dose of the analgesic ("conditioning with expectation"). There was an increased response for those who had previously received Ketorolac but not the Morphine.

They concluded: "These findings show that cognitive factors and conditioning are balanced in different ways in placebo analgesia, and this balance is crucial for the activation of opioid or nonopioid systems. Expectation triggers endogenous opioids, whereas conditioning activates specific subsystems. In fact, if conditioning is performed with opioids, placebo analgesia is mediated via opioid receptors, if conditioning is performed with nonopioid drugs, other nonopioid mechanisms result to be involved."

Does that not seem strange to you? Firstly, the idea that expectation triggers endogenous opioids is not demonstrated at all, merely assumed. They failed to explore the baseline psychological effects of pain tolerance - those receiving Naloxone might have been more conscious of the pain due to its hyperalgesic effect, but still managed to have pain tolerances almost as long as before. The second is more strange - the prior choice of drug determines how the placebo effect works? How does that work when one is not conditioned with a prior drug at all?
I have another explanation. Guess which analgesic has a half life around four times the other and isn't blocked by Naloxone? Why wasn't this mentioned in the study at all?

This is just an example of the types of methodological limitations of these studies.