Friday 27 June 2008

More on 'medical care practitioners'

Following on from my last post moaning about 'medical care practitioners' or 'physician assistants' being introduced to the NHS, I found this fascinating information from the Birmingham PA course about the difference between a PA and a doctor:
"After their internship, PAs can work in general practice, hospital medicine or A&E. Although they will be required to show that they continue postgraduate studies as all clinicians do in terms of keeping up to date, , they are not required to undertake further formal training. PAs who wish to work in other fields (e.g. paediatrics; intensive care) will have to undertake further training. Whether or not they specialise PAs will be assessed periodically to ensure that they retain broad general competence.

The clinical role of the PA is very similar to that of the doctor. Experienced PAs in A&E or general practice may see the same undifferentiated range of patients that the doctor would see; can request the same investigations and initiate management of the patient in the same way. The differences are twofold. Firstly, currently, PAs are not allowed to prescribe. All prescriptions they write must be signed by a doctor. This is expected to change along with registration of the profession. Secondly, throughout their careers, PAs will work as part of a medical team, under the supervision of a doctor and (whatever their previous experience) they cannot work outside the field of competence of their supervisor. Their supervising doctor will have a deeper / more highly developed knowledge base and the PA is able to refer cases to their own supervisor as well as to other specialists."[my emphasis]

Wednesday 25 June 2008

Physician assistants

Apparently American style 'physician assistants' (PAs) are to be introduced to the NHS. This is a rather worrying prospect. A two year course (following a previous degree) and apparently they are ready to do the job of a house officer, senior house officer, or even a registrar (there's a minimum of four years training, for graduate entry to medicine, before becoming a house officer, it makes you wonder why they bother if PAs are so much better) in the primary care and emergency medicine setting (at a rather more generous salary of £39,500 in 2003 compared to an F1 house officer on £21k in 2008*) diagnosing, prescribing, and ordering investigations (although prescriptions or X-rays are supposed to be countersigned by a doctor in the UK at the moment, the experience seems to be that discussion with the doctor are perfunctory at best, and there is likely to be pressure to follow the US model and allow them to prescribe).

Somehow we're supposed to be reassured that a pilot study using US trained PAs (with an average of 11 years experience* as PAs and allied health professionals) found that they worked well. Presumably a study of consultant vascular surgeons would be good evidence for allowing new house officers to carry out AAA repairs unsupervised.

This is absolutely crazy, you cannot create a new paramedical profession de novo and then roll it out across the NHS on the basis of a single study of a highly selected cohort with extensive previous experience. They should at least have evaluated newly qualified US PAs (who, unlike doctors, don't have a probationary year).

Paramedics, nurses, and other allied health professionals jump through a million hoops just to be allowed to do a few extra procedures that doctors can do from day 1. Now we're handing over direct clinical diagnosis and management (and de facto prescribing) to people with minimal knowledge, experience or training. Whatever you think about nurse practitioners, at least they develop their clinical skills in line with their extra responsibilities. The US PAs in this study were a lot closer in experience to UK nurse practitioners than to the newly trained UK PAs that could soon be fucking up our healthcare. Newly qualified junior doctors are scary enough, this is terrifying.


* Hopefully the pay differential is due to the US PAs being highly experienced since otherwise I can see junior doctors going on strike, at this pay rate you could get yourself two newly qualified doctors, or even a single specialist registrar (similar level of training to a GP, likely to have higher qualifications such as membership of the Royal College of Physicians) for this price! According to the Wolverhampton course you can "earn a starting salary of £22,500 - £32,000 at current levels" [my emphasis], brilliant, why go to medical school just to end up earning less and taking legal responsibility for someone else's mistakes, while being told that these people are working at a higher level of competence than you after half the training?

Briffa demented loon: Official

In an apparent effort to ensure that no one is in doubt about his status as a complete nutjob following his comments on MMR and skin cancer, John 'SucroGuard' Briffa is accusing the charity Diabetes UK of deliberately trying to destabilise patients' blood sugar in order to increase the amount of medication they use in order to benefit BigPharma. You couldn't make this deranged shit up:
"Diabetes UK is the UK’s largest and most prominent diabetes charity...However, I’m doubtful that Diabetes UK is fulfilling its brief in this respect, seeing as it continues to suggest that diabetics should include starchy carbohydrates which every meal (see herefor more on this)...Yet, these starchy staples break down into sugar, and some of them can release their sugar quite quickly into the bloodstream too. And if we eat them in quantity, like we often do, that only adds to their disruptive effects. Now, what rationale is there for diabetics to include “at each meal” foods that are disruptive to blood sugar?...However, I reckon there’s another, far more relevant way of interpreting this sentence which goes something like: “The more starchy carbohydrate you eat, the more out-of-control your blood sugar level will be, the more ‘diabetic’ you will be, and the more likely you are to start to take medication for this or to need to increase your medication regime.” Remember the advice to eat generally sugar-disruptive starchy carbs with each meal comes from the UK’s largest diabetes charity which, it says, campaigns for “better standards of care for diabetics”.
What sort of care is it referring to, do you think? Because on the face of it, it doesn’t look like nutritional care is part of its remit. And if that’s the case, maybe what’s being referred to here is medical care including medication...I don’t want to come across unduly cynical, but is it right that a diabetes charity should have a less-than-transparent financial relationship with the drug industry. And is it right that this charity should be giving nutritional advice that, at the end of the day, looks likely to benefit the pharmaceutical industry. And after all of this, should it then go on to partner with that pharmaceutical industry in ‘research’ highlighting the need for people to take their diabetes medication. Or did I miss something?"

Monday 16 June 2008

Briffa on skin cancer

John Briffa's latest post attempts to cast doubt on the association between skin cancer and sun exposure:

"I was therefore interested to read over the weekend an editorial in the British Medical Journal which highlights the importance of sunlight and vitamin D in health...

There are three main forms of skin cancer: what are known as ’squamus cell carcinoma’ and ‘basal cell carcinoma’, and ‘malignant melanoma’. The first two tend to develop on the most sun-exposed parts of the body (e.g. the top of the ear) and are generally very treatable. Malignant melanoma, on the other hand, is generally much less treatable, is quite often deadly, and is usually the major reason cited regarding why we should protect ourselves from the sun...

However, is the relationship between sunlight exposure and risk of malignant melanoma as clear-cut as we are generally led to believe it to be? Michael Holick’s editorial contains information that might cause us to question traditional wisdom on this. He writes: “Notably, non-melanoma skin cancers occur on the most sun exposed areas, such as the face and hands, whereas most melanomas occur on the areas least exposed to the sun [2]. Intermittent and occupational sun exposure has been found to reduce the risk of malignant melanoma [2–5].”

In short, Professor Holick appears to be asking: “If sunlight exposure causes malignant melanoma, how come it tends to develop on parts of the body that are not typically very sun-exposed, and how come there is evidence linking sun-exposure with reduced risk of this condition?” Professor Holick appears to cast considerable doubt on the notion that excessive exposure to sunlight is a major risk factor for malignant melanoma."


Apart from being a little concerned about his attitude to skin cancer (basal cell carcinoma is fairly benign but squamous cell carcinoma has a risk of around 4% of spreading, both need surgical excision, and this isn't always easy or complete) I wondered where he got this view from. The medical consensus is that sun burn (especially in early life) is associated with malignant melanoma (with chronic sun exposure, such as from outdoor jobs, associated with basal cell and squamous carcinoma). Here's what the NHS says:

"There is a definite link between sunbathing (including using a sunbed) and malignant melanoma. Probably the most dangerous type of sunbathing is a short, sharp period of intense exposure, either in a single day or over a short period such as a holiday. The larger the area of skin exposed, the greater the risk. Getting sunburnt increases the risk further. It is the ultraviolet (UV) part of sunlight that does the most damage.
Severe sunburn in childhood can significantly increase your chances of developing malignant melanoma in later life.
It is also possible that you have more chance of developing malignant melanoma if someone in your family has also had one. Family history is most likely to be the cause if you haven't had excessive exposure to the sun. About one in 10 people with a melanoma have family members who have also had at least one.
You may also be at a greater risk if you have a large number of non-cancerous(benign) birthmarks."

The BMJ does indeed contain an editorial by Michael Holick, which mentions in passing that melanomas occur on areas least exposed to the sun:

"Excessive exposure to sunlight causes an estimated annual loss of 1.6 million disability adjusted life years (DALYs)—0.1% of the total global disease burden in the year 2000. This compares with the loss of about 3.3 billion DALYs from bone disease caused by vitamin D deficiency as a result of too little exposure to sunlight.11 These figures do not take into account the other potential health benefits of sun exposure and vitamin D sufficiency in reducing other chronic diseases, which account for 9.4% of total global disease burden. Notably, non-melanoma skin cancers occur on the most sun exposed areas, such as the face and hands, whereas most melanomas occur on the areas least exposed to the sun.12 Intermittent and occupational sun exposure has been found to reduce the risk of malignant melanoma.1 4 5 12"
So does this observation support Briffa's rejection of the melanoma-sun exposure link? Well let's look at the papers Holick links to in his editorial.

Number 1:
"Children and young adults who are exposed to the most sunlight have a 40% reduced risk of non-Hodgkin's lymphoma65 and a reduced risk of death from malignant melanoma once it develops, as compared with those who have the least exposure to sunlight.66"
So, this tells us that once you have developed melanoma sunlight exposure improves prognosis, but has nothing to say on the question of sunlight and malignant melanoma incidence.

Number 4:
"An ecologic study was performed using age-adjusted annual mortality rates for Caucasian Americans for 1950-69 and 1970-94, along with state-averaged values for selected years for alcohol consumption, Hispanic heritage, lung cancer (as a proxy for smoking), poverty, degree of urbanization and UVB in multiple regression analyses. Results: Models were developed that explained much of the variance in cancer mortality rates, with stronger correlations for the earlier period. Fifteen types of cancer were inversely-associated with UVB. In the earlier period, most of the associations of cancer death rates with alcohol consumption (nine), Hispanic heritage (six), the proxy for smoking (ten), urban residence (seven) and poverty (inverse for eight) agreed well with the literature. Conclusion: These results provide additional support for the hypothesis that solar UVB, through photosynthesis of vitamin D, is inversely-associated with cancer mortality rates, and that various other cancer risk-modifying factors do not detract from this link. It is thought that sun avoidance practices after 1980, along with improved cancer treatment, led to reduced associations in the latter period."

Can't get the full text of this - I note it is evil epidemiology, Briffa's not keen on that as we have learned from his views on MMR - there are multiple potential confounds, but assuming that it found a robust correlation between sun exposure and reduced melanoma (can't tell from the abstract), this doesn't really add anything to what we already know, it doesn't separate chronic sun exposure and acute sun burn, and there have been more detailed studies going beyond epidemiology looking at this (see below).

Number 5:

"Because the mortality rates of CMM [cutaneous melanocytic melanoma] are much higher than those of nonmelanoma skin cancer (in some populations, more than a factor of 10 higher), this problem is the most important one to solve regarding the negative consequences of sun exposure. The solution is by no means certain yet. A number of investigators disagree, as we reviewed earlier (12, 13).
The main arguments against the concept that sun exposure causes CMM are that: (i) CMM is more common among persons with indoor work than among those people with outdoor work (14, 15); (ii) in younger generations, more CMMs arise per unit skin area on partly shielded areas (trunk and legs) than on face and neck (16); and(iii) CMMs sometimes arise on totally shielded areas (acral CMM and uveal melanomas). Although the connection between these melanoma types and sun exposure is controversial (1719), their inclusion in the present discussion is justified because of the possible involvement of vitamin D.
However, in our opinion, a significant fraction of CMMs is related to sun exposure (16, 20). The main arguments for this relationship are: (i) the north–south gradients in CMM incidence between Scandinavia and Australia (16), (ii) before the advent of the "top-less" fashion, few women developed CMM on the breast area (13, 16), and (iii) in some animals (Sinclair swine, Monodelphis domestica, the fish Xiphophorus, white horses, angora goats, transgenic mice, etc.) UV exposure leads to CMM (16). The reason that CMM incidence rates decrease with decreasing latitude in Europe is likely because of differences in skin color from region to region."
So we have competing epidemiological observations, none of which is definitive (and I'd argue that their points ii and iii are irrelevant, including the idea that because melanoma more commonly arises on trunk or leg it can't be associated with sun exposure - since these are areas where acute sun burn is common - which could explain the male preponderance for melanoma on the back, and females on the legs).

Number 12:
"Acute and chronic sun exposure may exert different effects in the sequel from common melanocytic nevi, clinically atypical nevi to malignant melanoma (Elwood and Jopson, 1997;Gilchrest et al, 1999). Acute painful sunburns may promote the development of common melanocytic nevi, clinically atypical nevi, and thus, or possibly independently, the development of malignant melanoma. Although there are some contradictory findings regarding the association between chronic lifetime sun exposure and malignant melanoma, most studies found that chronic lifetime sun exposure was associated with a protective effect on the development of malignant melanoma.
This could be explained by the protective mechanisms, which are associated with heavy chronic sun exposure, such as tanning and skin thickening, but this may not be the total explanation (Elwood and Jopson, 1997;Gilchrest et al, 1999). Although it cannot be excluded that sun exposure during adult life promotes the disappearance of nevi, which could be an additional explanation of a decreased risk of malignant melanoma, in our study the disappearance of nevi was completely explained by increasing age of the individuals, and chronic sun exposure had no additional effect."
This case-control study confirmed the consensus that acute sun burn can increase the risk of malignant melanoma. It also supported the view that chronic sun exposure reduces the incidence.

So overall I'd say that this editorial in the BMJ, which really only tangentially mentions a couple of observations about melanoma incidence, far from "[casting] considerable doubt on the notion that excessive exposure to sunlight is a major risk factor for malignant melanoma" adds precisely nothing to what we already know about malignant melanoma and sun exposure, or at least, adds nothing to what well informed clinicians know about the link between malignant melanoma and sun exposure.

Saturday 14 June 2008

The Atheist Thirteen

Via nullifidian, one of those internet 'meme' things to "find out at least a little bit more about each other in the atheist blogging community...If you’d like to take part, copy these questions, and answer them in your own words on your own blog."

Q1. How would you define “atheism”?
The belief that the balance of evidence suggests that the existence of God, gods, or similar supernatural beings is improbable.

Q2. Was your upbringing religious? If so, what tradition?
Marginally. I was brought up in the Anglican tradition (non-evangelical low church), my mother and grandmother are low key believers as are other members of my extended family, and I went to a Catholic school for a few years, but religion was never a big part of my life, although I was more religious than my peers. I continued to be affiliated with the church, getting confirmed in my mid-teens. I increasingly adopted more heterodox positions (partly informed by an interest in church history and comparative religion), rejecting trinitarianism early on, so that I was probably more of a deist by the time I attended university. There I was confronted by the essentially contradictory nature of my continued belief in God (which was by now practically a metaphor for my conscience anyway) yet rejection of the other aspects of Christian belief on the basis of the paucity of evidence. I've self-identified as an atheist ever since.

Q3. How would you describe “Intelligent Design”, using only one word?
Delusion.

Q4. What scientific endeavour really excites you?
Neuroscience is my field of research, and the interface of neuroscience and medicine, particularly psychiatry, is where my interests lie. Fingers crossed we might actually find out something that is of some use to people soon.

Q5. If you could change one thing about the “atheist community”, what would it be and why?
I'd like there to be less smug sneering by certain aspects of the atheist 'community', who can combine a sense of superiority over those unsophisticated atheists who explicitly and unequivocally reject religion, with a patronising defence of the 'opium of the people'. There's a certain strand of studenty contrarianism that likes to say things like 'aah, but isn't science becoming the new religion', to which the answer is 'no, not aah!':



Q6. If your child came up to you and said “I’m joining the clergy”, what would be your first response?
"Shit, when the fuck did I have a child?" Actually, I'd like to think I'd already noticed that my child was religious so I wouldn't be inordinately surprised. I don't think I'd be too worried about my child becoming a protestant priest, in some ways it is a logical and worthy consequence of their beliefs, and many do good work in the community, but I'd be more concerned about them becoming a Catholic priest, because they are rejecting significant and rewarding parts of life. I like to think that if my child were to become religious they would have grown up in an environment where they were able to think about it for themselves, and were not directed one way or the other.

Q7. What’s your favourite theistic argument, and how do you usually refute it?
I'm quite fond of the ontological argument, and the argument from personal experience is always a good way to close down a conversation - but for raw rhetorical chutzpah the bait and switch of changing between a minimally specified deistic god to the God of orthodox Christianity is my favourite. The refutation is obvious.

Q8. What’s your most “controversial” (as far as general attitudes amongst other atheists goes) viewpoint?
I think islamophobia and the demonisation of Muslims is a real problem in the world today.

Q9. Of the “Four Horsemen” (Dawkins, Dennett, Hitchens and Harris) who is your favourite, and why?
I dislike Hitchens because his strand of offensive and arrogant contrarianism really winds me up (see Q5). I don't know much about Harris except that he is supposed to have said something rather Martin Amis-like about torture in the 'War on Terror TM'. I like Dennett as a philosopher, particularly regarding 'qualia', but I find his stuff about religion a bit dry. So Dawkins it is, populariser of evolutionary science, strident and often amusing, if not particularly original, and I think he shot himself in the foot a bit with that line about religion being child abuse.

Q10. If you could convince just one theistic person to abandon their beliefs, who would it be?
Hmm, not sure. Let's say Antony Flew for the moment, not because it would be a great intellectual struggle, but because his late conversion has been a rather sad spectacle.

Now name three other atheist blogs that you’d like to see take up the Atheist Thirteen gauntlet:
Journalology
jdc325
Jean Kazez

Monday 2 June 2008

Briffa's devastating critique

According to John Briffa this is a devastating critique of the Honda et al study that showed there was no relationship between MMR rates and autism in Japan. Basically it claims that even though MMR rates don't correlate with autism rates this is because single measles jabs also cause autism! The data used is not the local single jabs rates for the area studied by Honda et al but the national Japanese rates. I don't know why Briffa thinks this argument supports the MMR-autism link, it looks like a simple post hoc rationalisation to me.

But let's look at this data (plotted top right), vaccination rates (national MMR + single measles, and local MMR) shifted by one year (the Japanese measles vaccines are given at 1-year according to Nakatani et al and Honda et al) plotted against autism rates (cumulative up to seven years) by year of birth - overall autism spectrum and autism with regression are plotted*. Here we can see that there is minimal relationship between overall rates of autism spectrum and combined vaccination rates, and essentially no relationship with autism with regression.

This can be better seen in the figure on the right where the regressions of total measles vaccination rate against autism incidence are plotted - with neither even approaching statistical significance (p>.3), and correlation coefficients .3 and -.2 for autism spectrum and autism with regression respectively. Note that the correlation between MMR vaccination and overall autism spectrum is -.7, so MMR protects against autism!**

*For those interested in these things, autism rates are from Honda et al, and measles vaccine rates are estimated from the figure in Nakatani et al.

**No, obviously I don't think this really.

UPDATE
Here's a bit of fun, let's try another national vaccination rates vs. local autism rate graph. California is apparently a popular target, so how does autism rate (as determined by autism case load - dodgy, but like I say, just a bit of fun) compare with US national vaccination rate (1-year time shift, WHO data)?

Well here it is top right, not very convincing (although r=.7, p<.01). It nicely demonstrates that correlations are fairly common in time series (because all you need for a correlation is a trend for both things to increase with time) but also shows that the relationship is far from a 'dose-response' (sic) since autism keeps climbing while vaccination rates plateau. It accords fairly well with the figure on the left from a study of MMR vaccination rates and autism in California from JAMA which also found little relationship, with a plateau in vaccination rates and a continuing rise in autism.

This is also an interesting figure (below) from a study in the BMJ based on the UK general practice research database. It found that there was no relationship between UK MMR coverage (which remained very high for cohorts from 1988 to 1993) while autism rates continued to climb and nicely reflects the US vaccination plateau.