Creepy Crawley: Obesity in adolescents with chronic fatigue syndrome

[Hutan]

There's something a bit weird with the imputation of missing data. If you look at the supplementary material on imputation, it appears that,
for specialist services data at both 13 and 16, only around 15% of the 1680 data points had BMI information;
for ALSPAC data at both 13 and 16, only around 40% of the data points had CFS data and only about 40% had BMI information.

The supplementary material says missing data was imputed using auxiliary variables due to, among other things, 'their strong hypothesised association with CFS/ME'. Auxiliary variables used included
Family Adversity Index
Life Difficulties
School Absences in Year 11
Academic attainment
Anxiety and depression measures

Different variables were used for the imputation in each data source (Alspac and Specialist).

(There was a mention of 99 data points created by imputation for each of data sources, but I'm not sure how that works as they would have had to create a lot more data points than 99 to make up for the missing data.)

But anyway, the supplementary material gives the results from the 'complete case analysis' which presumably is the analysis of the data points that had no missing data. Here's the complete case results (with the results that were reported in the main body of the paper in brackets for comparison).

...............................Alspac No CFS ........... Alspac CFS...............Specialist CFS
13 years
Mean BMI..................20....................................20..............................21...............
% obese....................3.57 (4.18).......................3.92 (3.72).................9.23 (9.28)

16 years
Mean BMI.......... .......21.....................................21..............................22.............
% obese...................3.94 (4.46).........................6.00 (5.46).................6.8 (16.43)

So, the differences between the three groups look a lot less impressive in the un-imputed data. Instead of an upward trend from 9% to 16% obese over three years in the specialist group, there is a downward trend from 9% to 7%.

That makes a big difference - there isn't evidence in the complete data points that the CFS children are growing more massive as each year passes.

The imputation process is not well explained. The raw data however is reported as being available - so that is something.

My conclusion: there may possibly be a very small difference between the BMI's and obesity prevalence of non-CFS and CFS adolescents but there's enough murkiness about what was actually done with the data that I would not be getting excited until someone without an agenda analysed the data afresh.

ETA: There seems to be a few very odd things about this paper, so I may well have misunderstood something. But am too tired to be bothered to look again.

 

[Snow Leopard]

Exercise does not lead to weight loss contrary to popular belief.

It depends on overall behaviour. Most people who exercise then feel hungry and eat more... But if you exercise to excess (several hours per day - simply not possible with severe chronic illness), you can lose weight that way.

I know (regular) marathon runners who lose weight training for marathons, put it back on afterwards and the cycle continues...

My conclusion: there may possibly be a very small difference between the BMI's and obesity prevalence of non-CFS and CFS adolescents but there's enough murkiness about what was actually done with the data that I would not be getting excited until someone without an agenda analysed the data afresh.

So the "effect" was mostly a statistical methodology artifact? Wow...

 

[Woolie]

Lack of activity has nothing to do with obesity in ME/CFS or any other disease. Pushing children into doing GET, which is what Crawley does for a living, is not going to help them lose weight. Exercise does not lead to weight loss contrary to popular belief. Even studies where they made fat people train for a marathon show no weight loss, marginal weight loss of a few lbs or even slight weight gain in individual participants.

Body weight is under homeostatic regulation by many hormones especially leptin which signal to the hypothalamus. If your metabolism is comprehensively busted, as it is in ME/CFS, you can get obese, or alternatively, keep wasting away into oblivion and it has nothing to do with your behaviour.

My own weight trajectory has been all over the place with this illness. When I became mostly housebound several years ago I first maintained my weight for a while. Then I started gaining weight rapidly and put on 40 lbs or more. Then I suddenly stopped being able to eat almost completely and lost almost 70 lbs. My activity levels did not change during that time, I simply went from being in bed almost all the time to sitting in a chair almost all the time.

Yes, @Sidereal, if you're saying that there are a lot of other factors, besides activity, that drive weight gain and weight loss, them I'm in agreement. And sure, its silly to think you can put fat people on an externally imposed exercise regimen and get them to lose weight, that oversimplififes the phenomenon that is obesity.

But if you're saying that suddenly becoming severely limited in your activity is not a huge cause of weight gain in CFS, then that would certainly go against my own personal experience. My caloric requirements now that I'm inactive are so low that its incredibly easy to exceed them. Weight management, which was effortless when I was active, is now a constant concern.

 

[Woolie]

There's something a bit weird with the imputation of missing data. I

Thanks for that perceptive analysis, @Hutan. I have to reluctantly admit that this research makes PACE look really high quality.

 

[Glycon]

This kind of research (provided it's methodologically sound) is actually quite important, since it can be used to help understand the burden ME/CFS places on society and thus help incentivize more investment into research and treatment.

On the other hand, knee-jerk ad hominem attacks on the work of those we don't like may be therapeutic, but mostly they just validate the caricature of ME/CFS activists as extremists not worth taking seriously.

Also, @Hip has made several good posts itt.

 

[Hip]

On the other hand, knee-jerk ad hominem attacks on the work of those we don't like may be therapeutic, but mostly they just validate the caricature of ME/CFS activists as extremists not worth taking seriously.

That's exactly what I have been trying to say, but was not able to express it so clearly as @Glycon has done in one straight-to-the-point sentence.

 

[Glycon]

That's exactly what I have been trying to say, but was not able to express it so clearly as @Glycon has done in one straight-to-the-point sentence.

But you ended up saying a lot of other good things along the way, so don't be too harsh on yourself!

 

[Hip]

To be clear, let me sum up my thoughts: when it comes to published research or articles that imply that ME/CFS is an "all in the mind" psychosocially-caused condition, ME/CFS patients need to strongly criticize.

But when researchers that we know hold a biopsychosocial view on ME/CFS publish ME/CFS works unrelated to this biopsychosocial idea, those works should be examined on their own merits, and if the studies are OK, then let's admit that. It is not a good idea to gratuitously criticize all studies, just because they were produced by researchers that hold biopsychosocial views. That is not a good idea for three reasons:

• First of all, just out of fairplay.

• Secondly, because as @Glycon says, it may make ME/CFS activists look like unreasoning extremists (or if not that, then just a bunch who moan at anything and everything, which will lead to people ignoring us, as nobody listens to chronic moaners).

• Thirdly, we need to encourage these researchers to move away from biopsychosocial notions, and instead direct their energies to other areas of ME/CFS research. It would be a good thing if Prof Esther Crawley were to do more work like this: useful studies that increase the knowledge base of ME/CFS, rather than the BPS stuff.

 

[Hutan]

But when researchers that we know hold a biopsychosocial view on ME/CFS publish ME/CFS works unrelated to this biopsychosocial idea, those works should be examined on their own merits,

Yes

It would be a good thing if Prof Esther Crawley were to do more work like this: useful studies that increase the knowledge base of ME/CFS, rather than the BPS stuff.

But to be clear, based on my understanding of the information given in the paper and supplementary material, this particular study is not useful, it does not increase the knowledge base but instead muddies the waters and the result as reported is strongly impacted by BPS assumptions.

For example, in the specialist data source, there was BMI data for only 14.84% of CFS patients at age 16. That's 250 patients out of the 1685.

However, data (reportedly 99 data points) was created as follows:

Imputation was based on sex, score on the Hospital Anxiety and Depression Scale depression and anxiety subscales, and scores on the EQ5D.

And why did they choose those particular variables to generate BMI data?

The auxiliary variables below were included in the imputation models due to either their strong hypothesised association with CFS/ME,

So, they picked and chose a range of variables in order to create extra BMI data. Somehow this data manipulation increased the rate of obesity in age 16 CFS patients in the specialist data source from 6.8% from the 250 patients with full data to 16.43% when the extra imputed data points were added.

So, no, I don't think it would be a good idea for Prof Esther Crawley to do more work like this.

 

[Chrisb]

You do have to marvel at the unnatural super-powers of observation that some researchers seemingly have:

"For example, it has been observed that those with the CFS-like disorder were also less likely to be physically active (OR: 0.1; 95% CI 0.04 to 0.22).3 This finding of reduced activity levels was also found in a sample of 107 patients with CFS in the north of England, who, although exhibiting no differences in sedentary behaviour, had lower levels of time spent in moderate–vigorous physical activity (>3 METS) compared with controls."

One wonders why these patients might have been diagnosed with CFS. I suppose we should just be grateful that they noticed.

 

[Hutan]

One wonders why these patients might have been diagnosed with CFS. I suppose we should just be grateful that they noticed.

In this study, it's even worse than that. The researchers themselves labelled adolescents in the ALSPAC data source as having CFS on the basis of them having relatively low activity levels as reported by mothers:

In brief, we identified adolescents reported by their mothers to have experienced fatigue lasting >6 months that was associated with absence from full-time school or that had prevented them from taking part in activities ‘quite a lot’ or ‘a great deal’. We excluded those whose mothers thought that the fatigue was caused by playing too much sport, who snored often and who had other illnesses that could cause fatigue.

And then they commented that the ALSPAC CFS kids were less active. Duh.

Compared with healthy adolescents, those classified as CFS/ME in ALSPAC spent a greater proportion of their day, on average, in sedentary activity

It's a lot like saying 'we define 'fruit' as being apples as identified by the orchardist' and then reporting 'we found that almost all 'fruit' are apples'.

(So, the researchers excluded all the young people with fatigue whose mothers thought that it might have been caused by playing 'too much sport' from the Alspac CFS group - even if they were now unable to attend school. We know that very fit very active people can get ME. So excluding them is a bias when it comes to reporting the obesity rates of the CFS group that should have been explored a bit in the report. It would be good to know how many young people were in the 'fatigued due to too much sport' category.)

 

[Sidereal]

But if you're saying that suddenly becoming severely limited in your activity is not a huge cause of weight gain in CFS

Yes, that's exactly what I'm saying. Out of all the people who come down with various illnesses that severely curtail their activity, not everyone (probably not even the majority) will become overweight or obese. The body is not a steam engine into which you passively shove coal (food). Food intake (calories in) and food expenditure (calories out) aren't independent variables. The body senses calorie expenditure and will typically raise appetite to meet the demand which is why if you go to any gym, most of the fat people there stay fat despite working out, whereas the people who were trim to begin with stay trim and attribute this to their virtuous workout habits. Why would one person gain weight, another person lose weight, and another person stay the same when faced with the same activity limitation of ME/CFS, if there isn't some intrinsic metabolic factor driving the feeding behaviour? It's only the subset that gains weight that continues to eat like there's a famine coming even though their metabolism is now burning only, say, 1600 calories a day, while another person's brain/body correctly senses and reduces the hunger drive to adapt to the changed circumstances. It cannot be personality/willpower because as I said above at various stages of my illness I've either gained or lost huge amounts of weight and my personality certainly didn't change to become suddenly gluttonous vs. sensible, my appetite levels simply changed for reasons that are completely biological / outside of my control and have nothing to do with the availability of tasty food or emotional factors or anything like that.

 

[Snow Leopard]

But when researchers that we know hold a biopsychosocial view on ME/CFS publish ME/CFS works unrelated to this biopsychosocial idea, those works should be examined on their own merits, and if the studies are OK, then let's admit that. It is not a good idea to gratuitously criticize all studies, just because they were produced by researchers that hold biopsychosocial views.

If the study has inappropriate methods or conclusions, we're going to criticise it regardless of whether it was biological, psychological or social in focus...

 

[J.G]

This kind of research (provided it's methodologically sound) is actually quite important, since it can be used to help understand the burden ME/CFS places on society and thus help incentivize more investment into research and treatment.

I don't think this article does either. For argument's sake, let's assume the data are valid and that there exists a legitimate, statistically significant correlation between ME/CFS and obesity.

Regarding societal burden: if PWME are indeed at greater risk of developing obesity - which appears the most sensible if still disputable conclusion - is extra body weight really the prism through which ME's societal cost should be viewed? Surely, other indicators thereof are far graver, most notably a reduced - if not entirely absent - capacity to work. Disabling malaise is hugely costly to both society and the individual; any comorbid obesity is a sideshow.

Regarding research funding: the establishment of an obesity-ME correlation would attract funding to extend that line of enquiry. This could conceivably enhance our understanding of obesity, but will do very little for ME/CFS. Moreover, the public perception of obesity is not unequivocally friendly and may undermine rather than rally support. Even if the data are sound, this study merely saddles PWME with yet another controversial label that has little immediate bearing on the central pathology of the illness.

 

[Glycon]

To be clear, let me sum up my thoughts: when it comes to published research or articles that imply that ME/CFS is an "all in the mind" psychosocially-caused condition, ME/CFS patients need to strongly criticize.

But when researchers that we know hold a biopsychosocial view on ME/CFS publish ME/CFS works unrelated to this biopsychosocial idea, those works should be examined on their own merits, and if the studies are OK, then let's admit that.

Indeed, even studies related to BPS should be examined on their own merit. You never know what you may find. Besides, the worst case scenario is that you'll be better equipped to produce brioadly acceptable criticisms.

 

[Hip]

If the study has inappropriate methods or conclusions, we're going to criticise it regardless of whether it was biological, psychological or social in focus...

And so we should, but when, as has happen in this thread, the criticism is married to conspiracy theory ideas that this obesity study is somehow an insidious ploy to promote biopsychosocial ideas on ME/CFS, it does tend to make the criticism look more like extremism.

Indeed, even studies related to BPS should be examined on their own merit. You never know what you may find. Besides, the worst case scenario is that you'll be better equipped to produce brioadly acceptable criticisms

I agree; with biopsychosocial studies, the empirical data should be examined on their own merit.

However, the highly dubious theoretical somatoform ideas behind these biopsychosocial studies (plus the murky disability insurance industry connections to the biopsychosocial model, which help this industry curtail disability support to ME/CFS and other patients) can be independently criticized (as being highly implausible).

In Bayesian methods of ascertaining the truth, it is both the empirical data plus the a priori plausibility of the theoretical model that are taken into account; if the theoretical model seems highly implausible, then your empirical data needs to be even stronger, if you want to prove something (this is sometimes expressed in the phrase: "extraordinary claims require extraordinary evidence").

 

[Glycon]

the highly dubious theoretical somatoform ideas behind these biopsychosocial studies (plus the murky disability insurance industry connections to the biopsychosocial model, which help this industry curtail disability support to ME/CFS and other patients) can be independently criticized (as being highly implausible).

The "murky" stuff can and should be criticized... independently (and with an independent set of standards).

In Bayesian methods of ascertaining the truth, it is both the empirical data plus the a priori plausibility of the theoretical model that are taken into account; if the theoretical model seems highly implausible, then your empirical data needs to be even stronger, if you want to prove something (this is sometimes expressed in the phrase: "extraordinary claims require extraordinary evidence").

You know, unlike most people I actually understand all that. And I know enough to point out many ways in which what you said is disputable and/or imprecise. However, that would be off-topic. But if you want to go there, we certainly can.

 

[Hip]

And I know enough to point out many ways in which what you said is disputable and/or imprecise.

Why don't you start a new thread on this topic? I'd love to see a thread on this. I think many of us would really appreciate a good introductory explanation of Bayesian versus Frequentist statistics, if it is presented in a accessible way, ie, in a brain fog-proof manner (I have a degree in mathematics and physics, but these days with brain fog, I struggle to do the maths that even a 14 year old schoolchild can do).

 

[Kati]

And so we should, but when, as has happen in this thread, the criticism is married to conspiracy theory ideas that this obesity study is somehow an insidious ploy to promote biopsychosocial ideas on ME/CFS, it does tend to make the criticism look more like extremism.





I agree; with biopsychosocial studies, the empirical data should be examined on their own merit.

However, the highly dubious theoretical somatoform ideas behind these biopsychosocial studies (plus the murky disability insurance industry connections to the biopsychosocial model, which help this industry curtail disability support to ME/CFS and other patients) can be independently criticized (as being highly implausible).

In Bayesian methods of ascertaining the truth, it is both the empirical data plus the a priori plausibility of the theoretical model that are taken into account; if the theoretical model seems highly implausible, then your empirical data needs to be even stronger, if you want to prove something (this is sometimes expressed in the phrase: "extraordinary claims require extraordinary evidence").

The problem I have here is obesity can be seen as a psycho-social problem, which can possibly solved with changes of behaviors. I think researchers at the NIH have demonstrated that obesity is a bigger problem than psycho-social. That metabolisms are very difficult to change and if someone loses weight intentionally, the body fights a mighty fight to return to the original body weight. It's quite fascinating unless you're in that situation.

So when Mrs Crawly is attacking the problem, she will likely only take a look at psycho-social interventions and issues like: 'your kid is obese because he's playing video games all day.' And 'your kid should exercise more' . i am sorry but I know her antics.

 

[Glycon]

I'd love to see a thread on this. I think many of us would really appreciate a good introductory explanation of Bayesian versus Frequentist statistics, if it is presented in a accessible way, ie, in a brain fog-proof manner

What do I look like? An expert in special ed?

Not sure this merits a separate thread on these forums, but maybe take a look at this: http://plato.stanford.edu/entries/probability-interpret/