Bad Medicine: Diabetic Medication

by Dr Des Spence

The way we treat diabetes is the poster boy for the idea that our approach to life-style disorders is upside down. Dr Spence’s  succinct and meticulously referenced post makes it clear just how wasteful, ineffective and wrong it is.  In early October a study reported in the BMJ found that exercise was as effective as drug treatments in preventing diabetes. Why not a prescription for serious support in exercising with a low glycaemic diet thrown in? [Editor]

Type 2 diabetes is a modern plague largely brought on by lifestyle and is considered to be a progressive, non-reversible condition. The polypharmacy of chronic disease is the drug industry’s lottery win and no more so than in diabetes, with new drugs and the increasing use of analogue insulin in type 2 diabetes worth tens of billions of pounds worldwide. [1]

The drug industry’s business plan for diabetes follows a familiar pattern:

  • Conduct questionable research and control the original data.
  • Schmooze the politicians, health regulators, and patient groups to suggest undertreatment and need for “urgent action.”
  • Recruit tame diabetologists, massage them with cash and get them to present at marketing events that masquerade as postgraduate education.
  • Pay doctors to switch to newer drugs in dubious international postmarketing “trials.” [2]
  • Seek endorsement from the National Institute for Health and Care Excellence to bully doctors to treat diabetes aggressively with drugs. [3]
  • And so the complexities of diabetes are reduced to simply lowering blood sugar.

What is the annual cost of pursuing this reductionist, drug based approach? In the past decade, spending on insulin in the UK has risen 300%, to £311m4 (€356m; $463m), and on oral diabetic drugs 400%, to £277m. And have you ever wondered why companies generously give away glucose meters? Test strips are a £166m market, the value of which has risen 300% in 15 years. [4] Factor in staff time (when not attending more educational updates sponsored by the drug industry) and the patient and family’s time, and you have a great but expensive business.

But do analogue insulins, new diabetic drugs, and self-monitoring of blood glucose improve outcomes? Does even tight glycaemic control make a difference? No data on mortality or morbidity exist for the new therapeutics. [5] [6] [7] [8] [9] [10] [11] Likewise, intensive glycaemic control is not superior with respect to mortality and cardiovascular disease. [12] So billions of pounds are being spent chasing a ghostly surrogate endpoint: low blood sugar. Worse, there is evidence that these new drugs cause harm. Rosiglitazone has already been withdrawn; pioglitazone has been linked to bladder cancer; and exenatide and sitagliptin double the risk of acute pancreatitis. [13] [14] All these are examples of the scientific illusion that is so-called evidence based medicine, where research is just mechanically reclaimed statistics pulped into junk educational nuggets—mere marketing by another name.

There remains another fundamental question. Can diabetes be reversed or cured by weight loss? A small, well designed study of 11 patients irrefutably showed that it can. [15] And clinical effect is more important than any statistically significant yet clinically undetectable effect that a huge study funded by the drug industry might find. The therapeutic approach in diabetes is upside down. Incredibly, spending on diabetes drugs could employ 40,000 personal trainers. The complicity of doctors and lack of dissent against the drug model of diabetes care is bad medicine.

[1] Cohen D, Carter P. How small changes led to big profits for insulin manufacturers. BMJ2010;341:c7139.FREE Full Text
[2] Gale EA. Post-marketing studies of new insulins: sales or science? BMJ2012;344:e3974. FREE Full Text
[3] National Institute for Health and Care Excellence (NICE). Blood-glucose-lowering therapy for type 2 diabetes. April 2013.
[4] Health and Social Care Information Centre. Prescription Cost Analysis—England, 2012. April 2013.
[5] Davidson MB. Counterpoint: self-monitoring of blood glucose in type 2 diabetic patients not receiving insulin: a waste of money. Diabetes Care2005;28:1531-3.FREE Full Text
[6] Horvath K, Jeitler K, Berghold A, Ebrahim SH, Gratzer TW, Plank J, et al. Long-acting insulin analogues versus NPH insulin (human isophane insulin) for type 2 diabetes mellitus. Cochrane Database Syst Rev2007;2:CD005613.Medline
[7] Van de Laar FA, Lucassen PL, Akkermans RP, Van de Lisdonk EH, Rutten GE, Van Weel C. Alpha-glucosidase inhibitors for type 2 diabetes mellitus. Cochrane Database Syst Rev2005;2:CD003639.Medline
[8] Shyangdan DS, Royle P, Clar C, Sharma P, Waugh N, Snaith A. Glucagon-like peptide analogues for type 2 diabetes mellitus. Cochrane Database Syst Rev2011;10:CD006423.Medline
[9] Black C, Donnelly P, McIntyre L, Royle PL, Shepherd JP, Thomas S. Meglitinide analogues for type 2 diabetes mellitus. Cochrane Database Syst Rev2007;2:CD004654.Medline
[10] Richter B, Bandeira-Echtler E, Bergerhoff K, Clar C, Ebrahim SH. Rosiglitazone for type 2 diabetes mellitus. Cochrane Database Syst Rev2007;3:CD006063.Medline
[11] Ooi CP, Loke SC. Colesevelam for type 2 diabetes mellitus. Cochrane Database Syst Rev2012;12:CD009361.Medline
[12] Hemmingsen B, Lund SS, Gluud C, Vaag A, Almdal T, Hemmingsen C, et al. Targeting intensive glycaemic control versus targeting conventional glycaemic control for type 2 diabetes mellitus. Cochrane Database Syst Rev2011;6:CD008143. Medline
[13] British National Formulary (BNF).
[14] Singh S, Chang HY, Richards TM, Weiner JP, Clark JM, Segal JB. Glucagonlike peptide 1-based therapies and risk of hospitalization for acute pancreatitis in type 2 diabetes mellitus: a population-based matched case-control study. JAMA Intern Med2013;173:534-9.Medline
[15] Lim EL, Hollingsworth KG, Aribisala BS, Chen MJ, Mathers JC, Taylor R. Reversal of type 2 diabetes: normalisation of beta cell function in association with decreased pancreas and liver triacylglycerol. Diabetologia2011;54:2506-14.CrossRefMedlineWeb of Science

This post is reposted here with the permission of the author, and was originally published on 13 May 2013:


Dr Des Spence

Dr Des Spence

Dr Des Spence – is a Glasgow GP and columnist for the British Medical Journal. His description of his blog says precisely what it is about: ‘all the stupid and bad things that medicine does.’
Dr Des Spence

Latest posts by Dr Des Spence (see all)


  • Current pharmaceutical diabetic treatments are not only leading to a poorer quality of life but also killing diabetics.[1]

    The underlying problem with diabetes is insulin resistance (the disease)
    Drugs treat hyperglycemia (the symptom)
    Current Diabetic treatment protocols make things worse, not better.
    Treating INSULIN RESISTANCE (the disease) would stand a better chance of slowing halting progression.
    A lower carbohydrate higher fat diet helps lower insulin resistance.
    Correcting magnesium, Vitamin D3, Omega 3, and melatonin deficiencies also lowers insulin resistance as does regular exercise.
    Even regular blood donation improves insulin resistance
    [1]Diabetes Audit Report Complications and Mortality (pub Dec 2012, pdf
    [2]Iron stores, blood donation, and insulin sensitivity and secretion.

    • Editorial

      Thanks for those specifics, just the kind of material that needs to be part of the mental furniture of anyone involved in treating diabetics.

  • A low carbohydrate diet coupled with magnesium and vitamin D supplements is an even better route. The late Dr Robert Atkins called diabetes the ‘magnesium deficency disease’

  • I ‘ve been diabetic for 17 years, and I tried all possible combinations of drugs,exercise and diets in an attempt to manage my condition. I came to this final conclusion;all diabetic medications made it worse. They try to deal with the symptoms. Diabetes is actually a lipid problem not a carbs problem. It is a manifestation of excessive stored energy. The body tries to stop further deposits of fat by two mechanism s; firstly by dumping glucose in the blood instead of converting it to fat,secondly by avoiding excreting high levels of insulin. This second mechanism is achieved by two ways;by decreasing the efficiency of insulin’ and by excreting it over a longer span of time. This is done by lowering the cellular number of insulin receptors and by allowing the blood glucose to rise thus stimulating the stomach to empty it’s carbs content slowly. The body therfore starts a natural healing process while all medications will only disrupt that process from reaching its end. The best method in my opinion to cure diabetes is to stop all medications and,take this for a surprise,attempt for a zero fat diet. Your body will naturally get rid of excess glucose,and there will be no fat to be stored. This will lead to weight loss and reduction of waist line. Exercise will help and speed things up. Go for fruits and vegetables but it’s okay to have all types of carbs as long as you remain in an energy deficit. Shoot for a waistline that reminds you of yourself before diabetes. You will notice that warmth is returning to your body and all diabetes symptoms are subsiding with time.
    Please spread the word.

    • I too have personal experience of T2DM. The most prominent of my symptoms was severe muscle lethargy.

      My perception (which might be incorrect) trended to think that muscle lethargy is related to muscle tissues becoming overloaded with glycogen. Glycogen is, in effect, glucose polymerised, and it is a useful means to store energy. In healthy people surplus postprandial glucose in the blood is readily converted to glycogen which can be channelled to the liver and muscle tissues for short term storage. Capacity to store glycogen equates to about 700 calories, enough to last around 8 hours. Again, in healthy people, glycogen would be converted back to glucose to fuel cells between meals. All things being equal the logic in this should indicate a healthy person ought not feel hungry and compelled to eat until glycogen stores are running dry. Whereas pooled glycogen in the T2 diabetic seems to be problematical and symptoms such as fatigue and lethargy seem to be cues to go raid the larder.

      Over time I have tried various means to get relief from symptoms. Vigorous work-outs seemed to open the door to mobilisation of glycogen. I used to prepare special food using pulses (beans and lentils) as a mainstay, and the nature of these (supplying much soluble fibre) went to a long way to stabilise BG and HbA1C results. I virtually eradicated margarine and vegetable oils which are rich in polyunsaturated fats, and rich in non-essential omega-6 types especially, and in this n=1 casual trial I found that a beneficial step to take. Something I came to appreciate is that on occasions protein rich food (lean meat) could give me a sugar rush as great as that from fast-carbs. The process at work is gluconeogenesis.

      In the digestive track fats and fibre can help slow the process of digestion and thus help attenuate the postprandial spiking of glucose in the blood. They rank as simple barriers to the process of digestion that can apply the brakes by degree. Plus, when certain fats are present in the digestive track (DT) it is possible they may be involved in feedback signalling and control. While I haven’t verified the following idea fully if agents could trigger attenuation of the supply of bile to the DT then these agents could exercise some control over the rate of digestion when adequate levels of fat are present in chyme. I do not know what these agents might be but my starting point for investigations would be oleoethanolamide and cholecystokinin.
      It is easy to accept that food entering the DT would send signals that digestive agents ought to be supplied to the DT, but it is also worth pondering if overindulgence might have such signals reversed, and for evolutionary reasons it might be fats that potentate this reversal more than anything else.

      Waleed Mahmouds contribution (above) is interesting and there are aspects of the general thrust that I found insightful. The level of thought given over to relating personal experience with physiologic theory is evidently extensive, and I genuinely believe we live in an age where patients attempts to rationalise personal experience with physiologic theory will contribute to cognitive gains at large. Were I to disagree or question it would be over the details and semantics.
      If animals fats were toxic to animals there would be no sense animals laying down fatty reserves for the times when food might become scarce. The supposed angiotoxic (‘heart-stopping’) properties of saturated fats may well be legendary but they are also entirely mythical. And while it was a long-time in the coming I think the most pertinent theory I can relate to personal experience is that life gets so much easier for a T2 diabetic when it is accepted that real fats can be re-included in the diet with complete impunity. Adequate fat in my diet is my route to relief. The effects upon cholesterol seem counter-intuitive, and in any case cholestane-3B,5a,6B-triol and 25-hydroxycholesterol are certain of the 49 possible cholesterol oxides (many of which seem to be expedient to physiology) that can better account for the tissue changes witnessed in experimental atherosclerosis than cholesterol itself can.
      Cholestane-3B,5a,6B-triol has been linked experimentally with necrosis of smooth muscle cells, and 25-hydroxycholesterol has been experimentally linked to the unrestrained bio-synthesis of cholesterol in hepatocytes and macrophages. Cholesterol laden macrophages (termed foam cells) feature prominently in the tissue changes that accompany atherosclerosis. In plain English that basically indicates that oxidative stress afflicting cholesterol leads to heart disease, and not the mere presence or concentration of cholesterol itself.

      More than anything I would say that unnecessary fat-phobia, the low-fat revolution, and a willingness to over-consume polyunsaturated fats in place of long-served saturated fats, has lead to a decline in health, a rise in weight issues and obesity, and much higher incidence of adult onset diabetes (T2DM) but now arising in people of decreasing age and with alarming frequency. But I do not think it is all down to diet and dietary trends.
      I do highly recommend persons read the Earthing book (Ober Sinatra & Zucker) and note that many n=1 accounts reaching the Earthing Institute indicate Earthing improves diabetic control for many diabetics. I also recommend another book, ‘Lights Out’ (auths. Wiley & Formby), which points to the ways the invention of the light bulb may have impact upon salient hormones.

      For Waleed I highly recommend a book by the late Barry Groves, ‘Trick and Treat’, in which, I think, any mistakes or wrongful interpretations are few.
      Most of all I underscore the summary assessment of Edward Hutchinson: “An intermittent exhaustion of the pool of glycogen in the human organism [is] a simple universal health promoting mechanism.”. Furthermore the low fat diet or zero fat diet places a simple universal health promoting mechanism further from peoples reach.
      Details matter mind, and adequate supply of minerals supplying magnesium, chromium, sulphur and others allied to adequate supply of methyl group donating antioxidants (B group vitamins including folate headline) contribute to overall expediency, and help counter levels of homocysteine trending higher in ways that might contribute to (or associate with) levels of oxidative afflicting cholesterol, and thus giving rise to increased prevalence of certain atherogenic cholesterol oxides. (Patrick Holford might underscore this). Nobody should form an opinion (nor promote one) about cholesterol, experimental atherosclerosis, or heart disease, without having read ‘The Biological Effects of Cholesterol Oxides’ (cholesterol sceptics included).

      Illnesses do not come upon us out of the blue. They are developed from small daily sins against Nature. When enough sins have accumulated, illnesses will suddenly appear. [Hippocrates]

      After tabling remarks inspired mainly by comments it’s worth returning to Dr Des Spence’s original themes. There are sins in the modern world that Hippocrates could not have foreseen. The invention of 24 hour light and the trend to a level of electrical isolation from mother Earths entirely natural global electrical field that is now almost total and that cannot be deemed to be natural at all. The accumulation of stress, hormonal stress, and food stress counts as steady attrition that begins to matter in time.
      We are learning how such attrition compromises the life-expectancy of telomeres attached to chromosomes, and we are learning that switches attached to genes matter as much as do genes themselves. What’s more these switches are no more than simple tags. The tags are methyl (CH3) groups. The presence of such a tag mutes a gene and absence permits it to express itself. If we begin to realise genetic predisposition is less of an issue than aberrant methyl switches attached to genes then I think we might be on a wiser track.
      Again Hippocrates did not have such findings at his disposal, so what Hippocrates had to say about Nature and sins seems all the more prophetic. There is no better route to avoiding the complications that follow from sin than avoiding the sin itself.
      Polypharmacy (as treatment) and intervention in the name primary prevention is just another level of sin to impose on top of the first level. Which is tantamount to what Dr Spence says in his post. Medicine will have come of age when it returns to Hippocratic wisdom and discourages people from sinning against Nature, but rather than discouraging sin the dogma of the day is encouraging sins.
      Moreover the intelligence emanating from NICE that guides medical professionals in practice is bordering upon Neanderthal. There exists plenty of scope for the further evolution of NICE and its guidelines. If it doesn’t evolve in the direction that is in keeping with patients best interests, and if instead it continues to kowtow to big pharmas best interests, NICE must face extinction.

  • While of course it’s true what works for you, works for you but it’s also the case what works for you may not work so well for others.
    Perhaps if you watch “Rolf Luft Award 2014, Prize Lecture by Professor Roger Unger” you may understand why it may not just simply be a calorie surplus storage problem.
    Many T2 diabetics may well be able to reduce their medication following the protocol being used by Dr Jason Fung.
    You may also find it interesting to read the abstract here
    An intermittent exhaustion of the pool of glycogen in the human organism as a simple universal health promoting mechanism.

  • Dr Michael Mosley is a journalist and broadcaster whose interests major around diet, lifestyle, and health. He graduated in philosophy, politics and economics, worked in banking, and then elected to venture back to study for a career in medicine, intending to become a psychiatrist. In the event he subsequently joined the BBC to work as a producer, and collaborated on series presented by Professor Robert Winston. So far as I can discern Mosley is not a registered medical practitioner.

    Mosley has trended from producer to presenter, and his style is earnestly transparent. He has fronted some features in the Horizon franchise that have looked at diet and exercise. What marks him out as interesting, is that his opinions have evidently altered over time, and when compared to the general conservatism as prevails within medicine his views seem progressive. It’s interesting, I think, to witness a person shifting long held beliefs upon matters, even to the point of outright reversal. Mosley is a person who has reversed his views upon the role of fat in the diet, amongst other things.

    Your followers might be interested to learn that a BBC Horizon documentary presented by Mosley, The Truth About Exercise, first broadcast on 28 Feb 2012 is again available for on-demand viewing from BBC iPlayer until around 12 Feb 2015. It might also be available from subscription cloud services such as Amazon Prime. It’s worth taking the opportunity to watch or watch again.

    There are ways in which themes raised represent a clash of old school dogma and modern evidence based pragmatism, especially when a young featured doctor discusses blood fats and artery clogging in wholly inadequate old school terms, but other themes are more progressive. Something that was interest to me was mention of an enzyme called liporotein lipase that has bearing upon the metabolism of blood fats. Basically exercise can stimulate production of lipoprotein lipase and more liporptein lipase can significantly alter the % of fat that is in with blood, and this harks to an interesting facet of genetics.

    Every living person ought to have the gene (or genes) that can account for the provenance of lipoprotein lipase, but the genes behind its production can be more or less effective. The clue for ‘how’ comes from the notion of genetic switching. Genes can have simple tags attached and the attachment of a tag effectively turns the switch off. The tag is a methyl (or CH3) group. One consequences of taking exercise is that tags may be added or removed from genes as a consequence of that exercise. Exercise can, it may seem, might remove a tag from the gene(s) behind lipoprotein lipase and therefore permit this enzyme to to do the work nature tasked it with. Inclination to be sedentary might encourage conditions whereby the gene is re-methylated and turned off again.

    Interest in genetic switching was, and is, one of the fastest reappraisals of scientific interpretation ever. Switches that can apply to individual genes are an odd mix of those that seem robust and not easily altered, and those that seem quite transient and dynamic. The more dynamic ones, perhaps, might lend an impression that genes are at fault when really it is these switches that are at fault, and they are at fault because certain of our habits might be.

    Something else of interest was mention of glycogen and muscles, and investigations into insulin sensitivity and the impaired glucose tolerance test. Impaired glucose tolerance and impaired sensitivity to glucose are early steps on route to T2DM, and it seems that factoring simple regular activity into the day can counter the trend to these consequential conditions.

  • Last paragraph: “Impaired glucose tolerance and impaired sensitivity to glucose..”

    Intended: Impaired glucose tolerance and impaired sensitivity to insulin .. ..

  • Here’s some welcome science on diabetes and nutrition to gladden the heart.

    The paper is called ‘Dietary carbohydrate restriction as the first approach in diabetes management: Critical review and evidence base’. The article is dated January 2015.

    There are a number of distinguished authors beginning with Richard D. Feinman and Wendy Pogozelski.

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