Childhood diabetes is about fatty lardbuckets or immigration?

Growing numbers of children and young people are developing type 2 diabetes, a disease usually seen in those aged over 40, in the latest sign of worsening childhood obesity.

The number of people aged up to 25 with the condition in England and Wales increased from 507 in 2013-14 to 715 in 2016-17 – a 41% rise.

The sharp rise has prompted concern among doctors and led to renewed calls for tougher government action to tackle the .

OK, anything is valid, worthwhile, as it’s for the kiddies!

The figures show that people from some ethnic minorities are much more likely than others to develop type 2 diabetes. Almost half of the 715 young people were black or Asian.

Banning immigration, repatriation, would seem to reduce the incidence of Type 2 diabetes in children in England.

Hmm, what’s that? You mean you didn’t actually mean do anything at all to reduce this? Ahhh, so, now we do get to the point that only some things are worthwhile, so which are they?

42 comments on “Childhood diabetes is about fatty lardbuckets or immigration?

  1. Deporting all sick people would improve the health of the British.

    If sick people (Group B) are your issue, why bother to involve any other Group A?

  2. The numbers in the article suggest that less than 1 in 500 of those who are severely obese contract Type 2 Diabetes. 22000 for two years of age are severely obese and the nearly four-fiths of 715 of those <25 gives an average of 22.8 per year of age who are obese including severely obese.
    The Daily Wail says that 1 in 10 children start Primary School obese and 1 in 5 are obese when they finish – say 130,000 so we are looking at 560 of some 2.6m obese young people with Type 2 Diabetes – i.e. 0.02%.
    Either the Grauniad has got its numbers wrong or the journalist doesn't understand them – the other ill-effects of obesity affect hundreds of times as many people.

  3. Deporting sick people who have no business being here in the first place is an excellent plan.

    And taking all your money NiV to pay for their repatriation–and medical care for the short while they are here– is another.

  4. I managed to find the report – it’s worse than you think. Firstly this onlycovers those treated in Paediatric Diabetes Units so the more severe cases, mild cases treated by GPs are excluded.
    Then, looking at the data: of those with “stated ethnicity” only 42.1% were White, 36.3% Asian, 13.5% Black. 5% Mixed and 3.1% [population %ages are said to be 86%, 2.2%., 7.5%, 3.3%, 1% but ONS says that Asians are 7.5%, Black 3.3%]. Prevalence is eight times as frequent among non-Whites.
    47% live in the worst quintile of areas for “deprivation” and 23% in the second worst quintile, only 5% in the best quintile.
    [Incidentally, the much larger number suffering from Type 1 diabetes are pretty representative of the general population by race and class.]
    78.6% of children with Type 2 diabetes were *identified* as obese but 8% of the data was missing so 85% of those measured were obese.
    The media don’t mention that sufferers from Type1 diabetes are more likely to be male, but for Type 2 females outnumber males almost 2:1.

  5. I assume this is yet another case of ‘now we have started looking more extensively for something, we are shocked to discover we are finding more of it.’

  6. Looking around for more information on this, I noted this paper. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2836348/

    It appears (fig 1) that while Mexicans are both fat and inclined to diabetes, that Indians are actually underweight relative to Europeans, but even more inclined to diabetes than the Mexicans. Mmm…

    But among the obese Indians, diabetes is far more common than for other ethnicities. (fig 2)

    Suppose the causal chain is X causes diabetes which (along with other factors, Y, Z, etc.) causes obesity. For indians, X is higher but Y, Z are lower. The reduction in Y, Z, etc. reduces obesity overall, but there are more diabetics there because of X who get diabetes as a result, and therefore a far larger proportion of the Indian obese are diabetic.

    Perhaps the increase in diabetes is because of the increasing global popularity of spicy food?

  7. Childhood obesity in the UK is not worsening. And the definition of it , the measurement which decides who is obese, that’s pretty dodgy. There is a great deal of rabid paternalism and nannying going on.

  8. There are two important causes of increases in cases of Type 2 diabetes. (i) They lowered the threshold used to define it. (ii) They give doctors an incentive payment to diagnose it.

    It’s conceivable that there are also medical causes.

  9. It’s all to do with blood sugar and insulin. The increased intake of sucrose and (in the USA) high fructose corn syrup has not only been a factor in obesity but in insulin resistance and, from there, type 2 diabetes.

    The two conditions have a common cause but are not in themselves directly related. However, burning calories in exercise uses up blood sugar, so couch potatoes do themselves no favour in that respect.

  10. No, Mr. Fuller. The cause of Type 2 diabetes is unknown.

    “The increased intake of sucrose and (in the USA) high fructose corn syrup has not only been a factor in obesity but in insulin resistance and, from there, type 2 diabetes.”

    Absolutely, completely, ridiculously false.

  11. “The cause of Type 2 diabetes is unknown.”

    Yeah, but it’s not though.

    It’s pretty much as Mr Fuller describes.

    Lots of sugar and simple carbs leading to insulin resistance.

    Type 2 diabetes is completely reversible by a change in diet.

  12. There not a single cause behind every case of Type 2 Diabetes – it can hit healthy individuals with a low BMI a sensible balanced diet who keep themselves fit.
    However it has been observed that most cases occur in people with bad diets, who do not take enough exercise, and who are obese. It has also been observed that a significant proportion of these people can free themselves of Type 2 diabetes by adopting a better diet, taking exercise and losing weight.
    There is clearly a genetic pre-disposition as Asians are ten times and blacks eight times as likely as whites to contract type 2 diabetes in their teens – but that cannot explain the near 2:1 ratio of girls to boys whereas the far greater number of obese girls than boys can do so.
    It is a generalisation but not an unfair one to say that *most* (not all, most) cases of Type 2 Diabetes result from a lifestyle choice.

  13. There is no such person as a healthy individual with a low BMI, even the bottom end of the supposedly normal range is not to recommended. Accepting that BMI is not perfect and that there is no single weight that offers optimum protection against all diseases where weight is a possible factor, to have the lowest risk from all cause morbidity and mortality, a BMI of 27 is about right, i.e. supposedly a little over weight by current definitions, but top end of normal in old money.

  14. https://www.mayoclinic.org/diseases-conditions/type-2-diabetes/symptoms-causes/syc-20351193

    ‘Type 2 diabetes develops when the body becomes resistant to insulin or when the pancreas stops producing enough insulin. Exactly why this happens is unknown, although genetics and environmental factors, such as excess weight and inactivity, seem to be contributing factors.’

    Repeat after me:

    “The cause is unknown.”
    “The cause is unknown.”
    “The cause is unknown.”
    “The cause is unknown.”
    “The cause is unknown.”

    Above commenters give speculation as fact. The cause remains unknown, in spite of decades of intense research. Anybody who could pin the tail on Coca Cola would be a rich man. They have been trying for 30 years.

  15. @Gamecock,

    Strong tendency to agree except that overweight combined with dyslipidemia and low exercise is a pretty well-established risk factor. Diabetes (type 2) seems to be more a consequence of disordered fat metabolism than sugar metabolism.

    It’s amazing how some people can (correctly) trash the social theory in one breath only to say it’s because spicy food, more wogs, reasons, etc.

    And yes, part of the reason we see more is we look more closely for it, so marginal cases get diagnosed off routine tests that wouldn’t have been done 30 years ago, and may or may not progress to need pharmacological managment. Sadly, vanishingly few of those routinely diagnosed make the necessary dietary and exercise changes to reduce the risk of progression..

  16. “a pretty well-established risk factor”: so what? “Risk factor” means positive correlate, so unless you believe that correlation = cause, you have to accept that it may be irrelevant.

    A good example is heart attacks – why is a “risk factor” in the UK not a “risk factor” in France? Because these thing are mere correlates.

  17. dearieme, the demonstration of causality in type 2 DM is that when people reverse their weight gain and start moving their lardy arses, it goes away, at least for some years. Almost every early diabetic who makes lifestyle changes sees both regression of the disease and delay of the need to treat it with drugs.

    I’m the last person who needs a lesson in Bradford-Hill’s principles of epidemiology. Some retrospective observations are indeed confirmed by prospectively observing the effectiveness of an intervention, and that is true for the case of fatty lardbucketness -> elevated risk of diabetes.

  18. “Strong tendency to agree except that overweight combined with dyslipidemia and low exercise is a pretty well-established risk factor. Diabetes (type 2) seems to be more a consequence of disordered fat metabolism than sugar metabolism.”

    I don’t know for certain, but I strongly suspect that the causality is reversed. Metabolic failures of the system that regulates weight would be likely to cause obesity. Metabolic failures that caused insulin insensitivity would likely result in people over-indulging in sugar. Desire for foods is controlled by a variety of feedback systems. If those feedback systems break, it deranges the desires and diet.

    The problem is that the socially-based theory – that people of weak and sinful character get fat because they’re greedy and gluttonous and lack self-discipline, and this in turn gives them additional metabolic diseases of the system regulating feeding, and therefore their feeding must be regulated by society for their own good and for the good of society – is well-established as the “everybody knows that…” theory and nobody thinks to question it, or is even allowed to question it. It’s definitely very un-PC to do so. So the observations get bent to fit the theory, rather than being based on the evidence.

    It’s a pity, because there probably are causes that more research could disentangle, but which can’t so easily be researched if it looks like they’re aimed at disproving ‘what everybody knows’. It could completely wreck the media campaign aimed at regulating what everyone eats to hand scienced-backed ammunition like that to opponents!

    “It’s amazing how some people can (correctly) trash the social theory in one breath only to say it’s because spicy food, more wogs, reasons, etc.”

    ‘Spicy food’ was a joke! I suspect Tim’s ‘more wogs’ was, too. He just thought it would get us going.

  19. “Some retrospective observations are indeed confirmed by prospectively observing the effectiveness of an intervention”

    You mean, like malaria is caused by not getting enough quinine in your gin and tonics? 🙂

  20. NiV,

    I prefer the theory that the plasmodium that results in malaria is best combatted by increasing the gin to tonic ratio. We are more at risk of Dengue Fever and Ross River Fever in Mackay, but enthusiastically take our medicine.

  21. BTW, don’t waste your money on “diabetes research.” It was co-opted by CM decades ago.

    CM scum wanted to nail big food companies and big cola. They liked the idea of diabetes caused by magic food. Over 20 years ago, the researchers had all the data they needed: obesity and sugar do NOT cause diabetes.

    Did they shift their focus? NO! Because the objective is not to find the cause of diabetes, but to nail big food and big cola. Research has continued on the disproven line for over 20 years.

  22. Bloke in Germany: ah, so now you have ceased to witter about “risk factors”. That’s an advance, at least.

    As for the lard buckets – how many of their problems have been caused by decades of profoundly dim propaganda by doctors telling them to eat lots of carbohydrates?

    What is your claim? That doctors may not be apologising for their sustained professional stupidity but at least on the quiet are reversing their advice?

  23. @ DocBud
    Sixtiy hears ago my best friend was even skinnier than I and perfectly healthy, the school’s best footballer and cricketer.
    When I was at my fittest I had a BMI of 17.6. When I was running marathons in my middle-age I would prefer to start with a BMI a little over 18 and end with one a little under 18.
    Please, *please* don’t fall for the “one size fits all” dogma of the BMI fanatics.
    I mostly have to argue against people who say that anyone with a BMI after above 25 is overweight.

  24. @ NiV
    I repeat, there is no single cause for Type 2 Diabetes. There are a number of factors which can and, frequently but not always, do contribute to it.
    It has been observed that some individuals can reverse their condition by a change in lifestyle which demonstrates that IN SOME CASES lifestyle is a critical factor.
    Since other individuals with similar lifestyles do not contract Type 2 diabetes, it is not the *sole* factor but it has been shown to be a factor.
    You should broadcast the fact that one in six of cases are not obese, proving that it is not necessary to be a lardbucket to suffer from it.
    If you look at page 67 of the report https://www.rcpch.ac.uk/sites/default/files/2018-07/npda_annual_report_2016_-_2017_april_2018_final_updated_2.pdf you will see that the incidence of obesity among kids with Type 1 diabetes is about 50% higher than the national average – so there is a *some* truth in the claim that obesity is sometimes a consequence of diabetes, but obviously it is *not* an automatic consequence as most of those with Type 1 diabetes are not obese.
    You need to adjust Table 19 on page 69 to exclude “missing data” to get meaningful percentages and then the “obese” %age goes up to 85%, “overweight” to 8% “healthy” to 6% and underweight to about half-a-percent.
    That proves that it is not necessary to be obese to contract type 2 diabetes, just that the kid is playing Russian Roulette

  25. @ Gamecock
    The cause of lung cancer is unknown. That doesn’t stop the world and his wife saying that it is due to smoking.
    The correlation between Type 2 diabetes and obesity is, apparently, higher than that between smoking and lung cancer.
    I know that it isn’t as simple as “obesity causes diabetes” which is why I say that it is a contributing factor. Obesity is A cause, not *the* cause because “The cause” does not exist. It isn’t unknown – it just doesn’t exist because there is no single cause.

  26. @john 77

    Most cancers arise from a mutation in one of our cells that allows it to proliferate outside the normal controls of the human body. There are about (order of magnitude) a trillion cell divisions a day in each of us, so there are likely to be thousands, perhaps millions of such events a day. But the body’s defences mop most of them up without incident, it’s only when one escapes that we can develop cancer.

    What causes the original mutation could be ionising radiation from a cosmic ray or purely random chance. But exposure to carcinogens can greatly increase the likelihood of this happening. If you breath in lots of asbestos fibres, your chances of later developing mesothelioma are much higher than normal. If you breathe in a lot of combustion products (whether from a 40 Marlboro a day habit, or living in a country where most cooking takes place on open fires) your chances of contracting lung cancer will increase.

    We all know anecdotal cases of Uncle Henry who smoked 40 Woodbines a day and lived to be 90. We can never take an individual case of cancer and say “that happened because of cause X”, but we can say “if you have increased exposed to X your chances of contracting cancer Y will also increase”. It’s far from certain, but that’s the way to bet.

  27. @ Chris Miller
    That is roughly what I was trying to say without going on at great length (we do not yet know how the mutation is triggered). But Gamecock is saying that if we cannot be as categorical as “cutting the guy’s head off kills him” then we don’t know anything.

  28. “But Gamecock is saying that if we cannot be as categorical as “cutting the guy’s head off kills him” then we don’t know anything.”

    You are part of the problem, as is Wat. Get off this shit and start looking for the real causes. We have known for over 20 years it is NOT obesity and sugar.

  29. “But Gamecock is saying that if we cannot be as categorical as “cutting the guy’s head off kills him” then we don’t know anything.”

    I don’t know what Gamecock’s saying, and I won’t presume to speak for him. But the issue is more than just the level of certainty. So far as I know (and I’d welcome evidence to the contrary), nobody has ever shown that obesity ever causes diabetes. All they’ve shown is that the two are correlated.

    The correlation is such that it’s obviously not a coincidence. But correlations between A and B can be the result of ‘A causes B’, or ‘B causes A’, or ‘C causes both A and B’. That obesity causes other metabolic illnesses is an assumption.


    Consider an alternative hypothesis. Gut bacteria consist of a number of species, each of which has its own preferences. Some do best on a high protein diet, some on a high-sugar diet, some need various micro-nutrients, and so on. Suppose there is a bacterium that thrives on a high-calorie, high sugar diet. Some mutation causes it to secrete a substance absorbed by the gut, that causes the animal it’s inside to seek out more sugar. That’s going to be a successful mutation – the more sugar the more this bacterium grows, the more substance is released, and the more the host seeks sugar.

    One way it could do that is to block the absorption of glucose into cells, leading the brain to think glucose is low and seek more. That will lead to both high blood sugar (because absorption is blocked) and obesity (because the host overeats).

    If you treat the condition with short-term starvation, you will reduce the population of the mutant gut bacteria, temporarily reducing both blood sugar (because you’re starving), and appetite. But as soon as you return to a normal diet (as opposed to dying of starvation) the bacterium multiplies again and soon you’re back to where you started.

    https://www.bbc.co.uk/news/health-31168511

    https://www.cell.com/cell-metabolism/pdfExtended/S1550-4131(17)30559-4

    https://www.sciencedirect.com/science/article/pii/S1198743X14609769

    It’s a hypothesis. There’s limited evidence, and no reliable treatment developed. But if it was true, and I’m not aware of any evidence that it’s not, it would mean that diabetes isn’t caused by obesity – both are caused by the gut biome.

    And if you can’t eliminate all the alternative hypotheses, you cannot know for sure that obesity causes diabetes, even in the cases where the two are associated. You can cut the head off a corpse – it’s not necessarily what killed him.

  30. John 77,

    Back in my ultra marathon days, my starting BMI was a bit above 24 and my finishing 22 to 23 depending on distance and toughness (56km to 160km). I’ve now ballooned to 28 (much less exercise, maintained same levels of drinking), I could probably do with getting it to 26, but my wife has demanded no lower because she says I look underweight below that.

    Yes it is the quinine, but I like to think you can drown the organisms in gin (and finish them off with red wine and whisky).

  31. @ NiV and Gamecock
    Read the sections on Type 1 Diabetes in the report. That destroys the concept of reverse causality or common causality from a third factor being the explanation for the correlation. To slightly misquote Mr Holmes “When you have eliminated the impossible, the only remaining possibilities must include the truth”.
    Type 1 Diabetes is associated with an above-average frequency of obesity but not significantly so at age 11 (at 4 to 5 the frequency is 34% against a population average of 23% so the argument that failure to burn glucose will lead to a gain in weight *if no action is taken to combat this* would *appear* to apply). If the Diabetes caused obesity then the results for Type 1 and Type 2 would be the same.
    There is a small but statistically significant excess of Asian sufferers for Type 1 Diabetes suggesting that they are more susceptible – but nothing like the excess for Type 2.
    The comparison between Type 1 and Type 2 is the “smoking gun”.
    Incidentally the Mayo Clinic reference is just as wrong as wat dabney – there are some (actually quite a large number) of people who have reversed Type 2 Diabetes by a change in lifestyle. Not everyone who tried succeeded but some did, proving the Mayo Clinic to be wrong.

  32. “If the Diabetes caused obesity then the results for Type 1 and Type 2 would be the same.”

    If Type 1 and Type 2 had the same mechanism, yes. But they have different mechanisms. They’re different conditions, they just happen to have a common symptom.

  33. @ NiV
    All the proposed ways that Diabetes causes obesity of which I have heard would apply equally to Type 1 and Type 2. The causes of the insulin deficiency are different but the impact of insulin deficiency on obesity is going to be the same. If diabetes caused obesity then 100% of diabetics would be obese – but it’s only 85% of type 2 diabetics and 34% of Type 1.
    Equally, if obesity automatically caused diabetes, then all obese people would be diabetic.
    If obesity was not a contributing factor then losing weight and increasing activity would not reverse Type 2 diabetes. In a lot of cases it does. So obesity *is* a contributing factor QED
    As I have already said, some people tried and failed to reverse Type 2 diabetes by losing weight – what I do not know is the reason for the failure because it was not stated, so I do not know whether they would have contracted Type 2 diabetes if they had not let themselves become obese.
    Obese kids will not necessarily contract Type 2 diabetes – the peak incidence is for 15-year-old girls for whom the frequency is less than 2% of those obese and the average for all children is a fraction of 1%. If there *was* a common cause of both then there would not be 99% of obese children without diabetes and 15% of diabetic children without obesity.
    The whole furore is, as I said originally, part of the Grauniad’s innumeracy.

  34. “The causes of the insulin deficiency are different but the impact of insulin deficiency on obesity is going to be the same.”

    Type 2 isn’t insulin deficiency, it’s insulin insensitivity.

    “If obesity was not a contributing factor then losing weight and increasing activity would not reverse Type 2 diabetes. In a lot of cases it does.”

    Crash diets reduce blood sugar (which is how they measure the improvement). That doesn’t imply it reverses the insulin insensitivity (although it may, I don’t know).

    “If there *was* a common cause of both then there would not be 99% of obese children without diabetes and 15% of diabetic children without obesity.”

    It’s complex. There are dozens of biochemical hormones and signals involved in energy regulation. Leptin, Ghrelin, Insulin, Orexin, Glutamate, Melanocortin, Neuropeptide Y, Cholecystokinin, Gastrin, Proglumide, Devazepide, Lorglumide, Adiponectin, and so on – it’s like a big clock with dozens of interlocking cogs and wheels spinning. There are no simple answers, single simple explanations, or straightforward mechanisms here.

    I’m not saying I know the answer, I don’t think anyone does, and I’m not saying that obesity plays no role. I’m just saying that the evidence is insufficient to be able to offer any simple explanations at the moment. We don’t know that obesity promotes diabetes in any cases. Type 1 diabetes seems to be autoimmune – type 2 diabetes we don’t know. And offering advice based on ignorance is potentially as harmful as advising stress reduction to prevent stomach ulcers; with the added disadvantage of justifying the power of the sort of people who want to regulate what other people eat.

    I’m not saying I know and this is the answer. I’m saying it’s complicated and nobody knows, yet.

    “The whole furore is, as I said originally, part of the Grauniad’s innumeracy.”

    Agreed! And not just the Grauniad, either.

  35. @ NiV
    I *never* said it was simple.
    And I am not talking about the short-term effects of “crash diets” – I refer to long-term effects of a change in lifestyle.
    “We don’t know that obesity is factor contributing to diabetes” – just as we don’t *know* that the sun will rise tomorrow. We don’t *know* that training helps Mo Farah to run faster than I.
    You are talking like Woy Jenkind who said there was no proof that abolishing the death penalty increased the rate of murders – using five-figure statistical tables I could not find a non-zero figure for the probability that he wasn’t lying.
    You are welcome to shoot down anyone who says that obesity automatically causes diabetes since 99% of obese children are not diabetic, BUT saying that obesity is not a contributory factor is just ridiculous and will encourage people like wat dabney to ignore all your sensible arguments that it isn’t just a lifestyle choice.

  36. “And I am not talking about the short-term effects of “crash diets” – I refer to long-term effects of a change in lifestyle.”

    I was assuming that people were referring to this study from last year.

    The diet was a formula of 825–853 calories per day for 3 to 5 months, followed by the stepped reintroduction of food over two to eight weeks. The participants were all given support throughout, including cognitive behaviour therapy and were encouraged to exercise.

    They measured progress using the glycated haemoglobin level, which is a measure of average blood glucose level of the past few months. They seemed to think this was quite a new and exciting development.

    Maybe you’re talking about a different study?

    ““We don’t know that obesity is factor contributing to diabetes” – just as we don’t *know* that the sun will rise tomorrow.”

    “We don’t know that obesity is a factor contributing to diabetes” – just as we don’t *know* that global warming will destroy civilisation before 2050.

    Correlation doesn’t imply causation. We don’t know what causes obesity. We don’t know what causes type 2 diabetes. We do know they’re correlated with one another, along with a host of other miscellaneous factors, and because there’s a political campaign for regulating diets that prefers to think obesity is a lifestyle choice rather than a medical condition (or simply normal human biology being misinterpreted and medicalised), that the causality is necessarily and “obviously” in that direction.

    It’s not “obvious” to me.

  37. @ NiV
    I never saw that study and I should *never* base anything, let alone a recommendation, on a crash diet. IMHO they are dangerous, hence foolish, as well as being less effective for losing weight than exercise. I’ve never lost as much weight in one race as DocBud because I never managed (never had enough spare time until I was too old) to get fit enough to do ultra-marathons, but any day that one burns twice as many calories as one consumes will result in greater weight loss than starvation – and it’s not *that* difficult.
    BUT the ability to reverse Type 2 diabetes by becoming less obese demonstrates that obesity is a contributing factor – NB I did point out that 99% of obese kids don’t have Type 2 diabetes so it is not *the cause*, and I never said that it was the cause – I said it is a contributory factor.
    I am pretty confident that it is a much bigger contributory factor to heart disease because it overtaxes the heart muscle.
    The other issue is the idiotic definition of “obesity” which assumes that weight is proportional to cross-sectional area of a human being than his/her volume. It also ignore the wide range of natural shapes – a book I was reading last week referred to a 255lb running back (a star NFL player) whom the NHS would describe as “obese” (and the NHS website asked whether activity level is zero, low or “moderate – it would not allow me to enter “high”), while it is only my middle-aged spread that gets me into the “healthy” category in their view.

  38. “I said it is a contributory factor. I am pretty confident that it is a much bigger contributory factor to heart disease because it overtaxes the heart muscle.”

    Well, that hypothesis at least proposes a specific mechanism, which makes things a bit easier to test. What does it predict in the cases involved in the ‘obesity paradox’?

    https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3920805/

    In terms of ‘overtaxing heart muscle’, why doesn’t it act the same way as routinely doing extra excercise by carrying weights around with you? Doesn’t cardiovascular exercise tax heart muscle too? Is exercise therefore bad for you?

    I’m not criticising here – just asking what I see as obvious questions.

    And please don’t take anything I say as any kind of personal attack on you, or what you say. I’m primarily criticising the prevailing simplistic media story about it as understood by the general public, and the way journalists over-simplify extremely complex medical statistics to generate dramatic health scare stories for public consumption.

    I’ve heard the “overtaxes the heart muscle” story in the media, too. It does sound plausible, at first. But the simple mental picture of “breaking machinery by putting it under excessive strain” it evokes directly contradicts the “exercise is good for you” meme, which suggests there’s more going on.

    Unlike machinery, muscle adapts to the strain it’s subjected to. We make muscle stronger by deliberately subjecting it to excessive strain. So how come the strain involved in carrying an extra 2 stone around with you breaks things, but the strain involved in training for an ultra-marathon doesn’t? And why don’t the general public ask questions like that?

  39. @ NiV
    Lots of good points, but …
    I need my physiopherapist to answer that. He sorts me out after I tear one or other of my leg muscles after I wreck it by doing something stupid. (It’s never my own event, it’s always thinking I can do something else – last time it was a Long Jump). I am not sufficiently expert to understand the detail. I never needed a physio before I was 60 so I haven’t done the homework.
    Of course the analogy of building up muscle by subjecting to modest strain will work for heart muscles as well as leg muscles but when I massively tear a leg muscle I do not drop dead. My physio gradually heals it – when my father, at the age of 60, started heaving paving slabs it damaged his heart muscle to a non-repairable extent.
    Training for an ultra-marathon is gradual and one builds up muscle as one progresses. It is the unexpected strain when someone assumes “I can do this” because he/she found it easy when he/she was a decade or so younger and two or three stone lighter that causes heart attacks.
    I can reassure you that I don’t take *your* criticism as being a personal attack: I am sorry if my responses suggests that I do.

  40. “I can reassure you that I don’t take *your* criticism as being a personal attack: I am sorry if my responses suggests that I do.”

    Thanks. No need to apologise, but I was wondering. I have a tendency to see extended debate just as an interesting debate about how the world works, and miss the emotional import. And to keep arguing long after I ought to let it drop.

    I don’t mind annoying people over things that matter, but I didn’t want to annoy you over something that didn’t. Thanks for the interesting debate.

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