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Taking diabetes prevention out of the clinic seems to work

1 Apr, 13 | by Dr Dean Jenkins

We know from a number of studies – including the Diabetes Prevention Programme (DPP) [1] and the Finnish Diabetes Prevention Study [2] – that lifestyle advice to people with abnormal glucose metabolism greatly reduces the risk of diabetes. However, the interventions are expensive.

Researchers from the Wake Forest University School of Medicine in the US have therefore looked at the use of community-based programmes to achieve the same results. They report the two year results [3] of their Healthy Living Partnership to Prevent Diabetes (HELP-PD) programme that uses community health workers leading groups in parks and recreation centres rather than clinics. They claim their results are comparable with those at a similar stage in the DPP but at a third of the cost.

help-pd-logo“The lifestyle weight-loss group in HELP PD cost $850 in direct medical costs for 2 years, compared to $2631 in direct medical costs for the first 2 years of DPP.”  [4]

This is a well documented randomised controlled trial that demonstrates efficacy and cost-effectiveness but only in one county in the US. Local policies and culture (strong pre-existing community networks and motivation) could have affected the results. Community prevention strategies if they can be deployed successfully could feasibly be more cost-effective than more traditional, clinic-focussed services.


1. Knowler WC, Barrett-Connor E, Fowler SE, Hamman RF, Lachin JM, Walker EA, Nathan DM. Reduction in the incidence of type 2 diabetes with lifestyle intervention or metformin. N. Engl. J. Med 2002 Feb;346(6):393–403. Available from:
2. Lindström J, Eriksson JG, Valle TT, Aunola S, Cepaitis Z, Hakumäki M, Hämäläinen H, Ilanne-Parikka P, Keinänen-Kiukaanniemi S, Laakso M, Louheranta A, Mannelin M, Martikkala V, Moltchanov V, Rastas M, Salminen V, Sundvall J, Uusitupa M, Tuomilehto J. Prevention of diabetes mellitus in subjects with impaired glucose tolerance in the Finnish Diabetes Prevention Study: results from a randomized clinical trial. J. Am. Soc. Nephrol. 2003 Jul;14(7 Suppl 2):S108–113. Available from:
3. Katula JA, Vitolins MZ, Morgan TM, Lawlor MS, Blackwell CS, Isom SP, Pedley CF, Goff DC. The Healthy Living Partnerships to Prevent Diabetes Study: 2-Year Outcomes of a Randomized Controlled Trial. American Journal of Preventive Medicine 2013 Apr;44(4):S324–S332. Available from:
4. Lawlor MS, Blackwell CS, Isom SP, Katula JA, Vitolins MZ, Morgan TM, Goff Jr. DC. Cost of a Group Translation of the Diabetes Prevention Program: Healthy Living Partnerships to Prevent Diabetes. American Journal of Preventive Medicine 2013 Apr;44(4, Supplement 4):S381–S389. Available from:

Is Type 1 diabetes linked to lower exposure to bacteria in early life?

23 Mar, 13 | by Dr Dean Jenkins

One of the posters at the Society for Endocrinology 2013 conference in Harrogate was from a team in Malta who claimed Type 1 diabetes is related to reduced exposure to bacteria in early life [1]. They pulled together three sources of data the WHO DiaMond Project (reported cases of Type 1 diabetes), the WHO estimates of mortality, and the Alexander Project [2] (antimicrobial susceptibility). The Society for Endocrinology also published a press release from the conference.

In their abstract the authors concluded:

“We found a negative correlation between country incidence of T1DM and its mortality from infectious diseases. Mortality from infectious diseases is a strong marker of the total infective burden. Incidence of T1DM was found to be positively correlated with the susceptibility of S. pneumoniae to all antibiotics studi Increased antibiotic susceptibility of a given organism may be an indirect marker of a low degree of exposure of the community to it. Our results provide support for the hygiene hypothesis, namely that diminished bacterial exposure in early post-natal life results in increased risk of developing T1DM.”

Whilst there is not a great deal that can be extrapolated from this abstract – which has the potential of compounding the errors of observation within the three different surveys – it is, perhaps, a signal worthy of further study. The hygiene hypothesis has a long history and seeks to explain the higher incidence of Type 1 diabetes where societies have lost their ‘old friends’ – co-evolutionary organisms – and their immune systems develop abnormal responses. [3]


1. Abela A-G, Fava S. Association of the incidence of type 1 diabetes with markers of infection and antibiotic susceptibility at country level. Presented at Society for Endocrinology BES 2013, Harrogate, UK. Endocrine Abstracts (2013) 31 P223 | DOI:10.1530/endoabs.31.P223. Available from:

2. Felmingham D, White AR, Jacobs MR, Appelbaum PC, Poupard J, Miller LA, Grüneberg RN. The Alexander Project: the benefits from a decade of surveillance. J. Antimicrob. Chemother. 2005 Oct;56 Suppl 2:ii3–ii21. Available from:

3. Gale, E.A.M. Hygiene hypothesis [internet]. 2012 [cited 2013 Mar 23]; Diapedia 21040851207 rev. no. 30. Available from:

Filtering the diabetes noise

20 Mar, 13 | by Dr Dean Jenkins

I’ve always been interested in how to keep up to date. Staying abreast of developments in a specialty is an important aspect of the role of a physician. You can share this knowledge with others. I came across these three papers today and I’ll explain how in a moment.

“Soft drink consumption is significantly linked to overweight, obesity, and diabetes worldwide, including in low- and middle-income countries.”

Basu S, McKee M, Galea G, Stuckler D. Relationship of Soft Drink Consumption to Global Overweight, Obesity, and Diabetes: A Cross-National Analysis of 75 Countries. Am J Public Health 2013 Mar;

“Low self-rated health was associated with a higher risk of type 2 diabetes. The association could be only partly explained by other health-related variables, of which obesity was the strongest.”

Wennberg P, Rolandsson O, Van der A DL, Spijkerman AMW, Kaaks R, Boeing H, Feller S, Bergmann MM, Langenberg C, Sharp SJ, Forouhi N, Riboli E, Wareham N. Self-rated health and type 2 diabetes risk in the European Prospective Investigation into Cancer and Nutrition-InterAct study: a case-cohort study. BMJ Open 2013;3(3)

“long-term BPA exposure [a compound in plastic bottles] at a dose three times higher than the tolerable daily intake of 50 µg/kg, appeared to accelerate spontaneous insulitis and diabetes development in NOD mice.”

Bodin J, Bølling AK, Samuelsen M, Becher R, Løvik M, Nygaard UC. Long-term bisphenol A exposure accelerates insulitis development in diabetes-prone NOD mice. Immunopharmacol Immunotoxicol 2013 Mar;

If I were presented with these papers as someone with a keen interest in the clinical care of diabetes then I think I’d find them rather interesting. Apart from the plastic bottles and NOD mice – which I know less about – the papers would seem to shape my understanding of the causes of diabetes. The first paper would raise my awareness of the importance of soft drinks (which has been in the news recently as well so patients might visit with questions). The second would highlight the psychological factors behind the risks for Type 2 Diabetes and obesity.

So, where did they come from?

From the library? No.

From a news agency on a website or email spam? No.

A PubMed search and crawl? No.

From my mates on Twitter? Not exactly.

From collecting all 40,000 tweets in the past 48 hours mentioning ‘diabetes’ and analysing them using various algorithms. Well yes.

Is this another way of filtering the diabetes noise? By tapping into the collaborative work of others. I think we’ll see more of it … perhaps, in the 21st Century, we already do.

Diabetes in chronic liver disease

27 Feb, 13 | by pratapjethwani

Researchers in Vienna have made a breakthrough with synthetic bile acids in the treatment of primary sclerosing cholangitis. These compounds could feasibly be of use in fatty liver and diabetes – but would require further study.

“Bile acids are not only involved in the secretion of bile fluids and fat digestion, but also have hormone-like effects, particularly on the regulation of fat and glucose metabolism in the liver. Researchers at the MedUni Vienna are currently also investigating what role these effects of Nor-Urso [norursodeoxycholic acid] and other bile acid derivatives play in the treatment of fatty liver, diabetes, fat metabolism problems and arteriosclerosis and how they could replace current conventional treatment methods and drugs.”[tt_news]=3258&cHash=35e4b2cd38

This news is interesting and it reminds us of the strong link between diabetes and the liver. What is this relationship and what are the implications for clinical practice?

The liver plays an important role in the regulation of glucose homeostasis. This helps explain why glucose intolerance is a feature or complication of chronic liver disease and cirrhosis.

Liver disease associated with diabetes mellitus can be divided into three groups as shown below [1]:

1. Liver disease occurring as a consequence of diabetes mellitus
• Glycogen deposition
• Steatosis and nonalcoholic steatohepatitis (NASH)
• Fibrosis and cirrhosis
• Biliary disease, cholelithiasis, cholecystitis
• Complications of therapy of diabetes (cholestatic and necroinflammatory)

2 . Diabetes mellitus and abnormalities of glucose homeostasis occurring as a complication of liver disease
• Hepatitis
• Cirrhosis
• Hepatocellular carcinoma
• Fulminant hepatic failure
• Postorthotopic liver transplantation

3 . Liver disease occurring coincidentally with diabetes mellitus and abnormalities of glucose homeostasis
• Hemochromatosis
• Glycogen storage diseases
• Autoimmunebiliary disease

Hickman et al. have used the term “hepatogenous diabetes” to describe the association between cirrhosis and impaired glucose metabolism [2]. Up to 96% of patients with cirrhosis have diabetes or glucose intolerance in one report – and this diabetes is different from type 2 diabetes because it occurs in the absence of standard risk factors of type 2 diabetes such as age, body mass index and family history of diabetes [2,3]. This is the reason for the need for new terminology for form of diabetes. In one study, prevalence of diabetes was much higher in Hepatitis C virus-related cirrhosis and alcoholic liver disease, but not in cholestatic liver disease suggesting the important role of underlying cause in the development of diabetes in these patients [4].

Exact mechanisms of development of diabetes in cirrhosis are still unclear but porto-systemic shunting of insulin resulting in systemic hyperinsulinemia with subsequent down regulation of insulin receptors causing insulin resistance. Chronic inflammation also plays a role in development of insulin resistance [2].

Chronic hepatitis C virus infection (HCV) is associated with an increased risk of type 2 diabetes, risk being 3 fold higher in patients above 40 years of age in NHANES [1]. There is conflicting evidence of increased risk of type 2 diabetes in patients with chronic hepatitis B infection (HBV). Grimbert et al. had shown that type 2 diabetes development was 2.7 times more common in patients with HCV as compared to patients with HBV and alcoholic liver disease [1,5]. There may be a direct causative role of HCV in glucose intolerance and proposed mechanisms are direct interference with insulin signaling by some genotypes like type 1 and direct or autoimmune damage to beta cells by the virus [1]. Also antiviral therapy such as pegylated interferon alpha used in treatment of chronic hepatitis may predispose to the development of hyperglycemia and type 1 diabetes [6].

This raises some important questions:

Would you screen every patient with cirrhosis for glucose intolerance and by which method?

Does management of diabetes in patients with chronic liver disease or cirrhosis have any impact on survival or the course of cirrhosis?

Management of hyperglycemia in people with cirrhosis is also challenging because many oral drugs are contraindicated in such patients and insulin will be associated with higher risk of hypoglycemia [6]. Similarly monitoring by glycated hemoglobin HbA1c will not be reliable in these patients and much emphasis will be laid on self monitoring of blood glucose in patients with cirrhosis and chronic liver disease [7].


1. Levinthal GN, Tavill AS. Liver Disease and Diabetes Mellitus. Clinical Diabetes 1999, 17(2), accessed online on 27/02/2013.
2. Hickman IJ, Macdonald GA. Impact of Diabetes on the Severity of Liver Disease. The American Journal of Medicine, 2007;120 :829-834.
3. Holstein A, Hinze S, Thiessen E, Plaschke A, Egberts EH. Clinical implications of hepatogenous diabetes in liver cirrhosis. J Gastroenterol Hepatol. 2002;17:677-681.
4. Zein NN, Abdulkarim AS, Wiesner RH, Egan KS, Persing DH. Prevalence of diabetes mellitus in patients with end-stage liver cirrhosis due to hepatitis C, alcohol, or cholestatic disease. J Hepatol. 2000;32:209-217.
5. Grimbert S, Valensi P, Lévy-Marchal C, Perret G, Richardet JP, Raffoux C, Trinchet JC, Beaugrand M. High prevalence of diabetes mellitus in patients with chronic hepatitic C: a case-control study. Gastroenterol Clin Biol 1996;20:544-48.
6. Khan R, Foster GR, Chowdhury TA. Managing Diabetes in Patients with Chronic Liver Disease. Postgraduate Medicine 2012;124(4):130-137.
7. Blendea MC, Thompson MJ, Malkani S. Diabetes and chronic liver disease: Etiology and Pitfalls in monitoring. Clinical Diabetes, 2010;28(4):139-144.

Gene transfer for Type 1 Diabetes proof-of-concept works in dogs.

16 Feb, 13 | by Dr Dean Jenkins

Researchers from Barcelona have just published a paper detailing their more than 4-year experience of treating Type 1 Diabetes with a single intramuscular injection. The technique transfers the glucokinase (GCK) and insulin (INS) genes to the host using a viral vector.

“We previously demonstrated that it is possible to generate a “glucose sensor” in skeletal muscle through co-expression of glucokinase (Gck) and insulin (Ins), increasing glucose uptake and correcting hyperglycemia in diabetic mice. Here, we demonstrate long-term efficacy of this approach in a large animal model of diabetes. A one-time intramuscular administration of adeno- associated viral vectors of serotype 1 (AAV1) encoding for Gck and Ins in diabetic dogs resulted in normalization of fasting glycemia, accelerated disposal of glucose after oral challenge, and no episodes of hypoglycemia during exercise for >4 years after gene transfer. This was associated with recovery of body weight, reduced glycosylated plasma proteins levels, and long-term  survival without secondary complications.” [1]

In this study the dogs did not have autoimmune Type 1 Diabetes. Instead they had been given drugs toxic to their pancreatic beta-cells to induce diabetes. The gene transfer creates a ‘glucose sensor’ in skeletal muscle.Picture of team with dogs

“The therapy is minimally invasive. It consists of a single session of various injections in the animal’s rear legs using simple needles that are commonly used in cosmetic treatments. These injections introduce gene therapy vectors, with a dual objective: to express the insulin gene, on the one hand, and that of glucokinase, on the other. Glucokinase is an enzyme that regulates the uptake of glucose from the blood. When both genes act simultaneously they function as a “glucose sensor”, which automatically regulates the uptake of glucose from the blood, thus reducing diabetic hyperglycemia (the excess of blood sugar associated with the disease).”  UAB press release Feb 2013.

The researchers now propose an experiment on pet dogs with Type 1 Diabetes.

They also point out the historical similarities with the discovery of insulin in 1922 by Banting and Best and the recent success of viral vector technologies in humans (in haemophillia B [2] and Leber’s Congenital Amaurosis [3]) all of which followed work on dogs.


1. Callejas D, Mann CJ, Ayuso E, Lage R, Grifoll I, Roca C, Andaluz A, Gopegui RR, Montane J, Muńoz S, Ferre T, Haurigot V, Zhou S, Ruberte J, Mingozzi F, High K, Garcia F, Bosch F. Treatment of Diabetes and Long-term Survival Following Insulin and Glucokinase Gene Therapy. Diabetes 2013 Feb; Available from:

2. Nathwani AC, Tuddenham EGD, Rangarajan S, Rosales C, McIntosh J, Linch DC, Chowdary P, Riddell A, Pie AJ, Harrington C, O’Beirne J, Smith K, Pasi J, Glader B, Rustagi P, Ng CYC, Kay MA, Zhou J, Spence Y, Morton CL, Allay J, Coleman J, Sleep S, Cunningham JM, Srivastava D, Basner-Tschakarjan E, Mingozzi F, High KA, Gray JT, Reiss UM, Nienhuis AW, Davidoff AM. Adenovirus-Associated Virus Vector–Mediated Gene Transfer in Hemophilia B. New England Journal of Medicine 2011;365(25):2357–2365. Available from:

3. Maguire AM, Simonelli F, Pierce EA, Pugh EN, Mingozzi F, Bennicelli J, Banfi S, Marshall KA, Testa F, Surace EM, Rossi S, Lyubarsky A, Arruda VR, Konkle B, Stone E, Sun J, Jacobs J, Dell’Osso L, Hertle R, Ma J, Redmond TM, Zhu X, Hauck B, Zelenaia O, Shindler KS, Maguire MG, Wright JF, Volpe NJ, McDonnell JW, Auricchio A, High KA, Bennett J. Safety and Efficacy of Gene Transfer for Leber’s Congenital Amaurosis. New England Journal of Medicine 2008;358(21):2240–2248. Available from:

Gliptins – where are we now?

30 Jan, 13 | by sghosal

Insulin resistance and beta cell dysfunction has traditionally been held responsible for the development and progression of diabetes. However, with time we have identified many more pathophysiological defects popularly termed “The Ominous octet” [1]. One of the most important determinants of post-meal hyperglycemia is the pattern of insulin secretion with the first phase (0-10 minutes after an intravenous glucose challenge) playing a very important part [2]. In type 2 diabetes this response is blunted resulting in post-meal hyperglycemia [2].

Alogliptin molecular structure



GLP-1 is a gut hormone, which has an influence on the pancreatic beta cells influencing the first phase insulin release as well as the alpha cells reducing release of glucagon [3]. In type 2 diabetes GLP-1 activity is blunted resulting in hyperglycemia [3]. Systemic GLP-1 has a very short half life (t½ ~ 1-2 min) being degraded by the enzyme Dipeptidyl peptidase-4 (DPP-4) [4]. Gliptins are agents, which inhibits the enzyme DPP-4 thereby increasing the circulatory time of GLP-1 and hence restoring its actions.

We have come a long way in managing hyperglycemia. Yet the goal of reducing CVD outcomes remains elusive. Although the follow-up data from two landmark trials (UKPDS 10-year follow up & DCCT/EDIC) demonstrated CVD outcomes benefit, it was not documented in the trial period per se. [5,6]. It took 23 years in DCCT & 20 years in UKPDS to demonstrate cardiovascular benefits of tight glycemic control. Later on other randomized trials (ACCORD, ADVANCE & VADT)  failed to demonstrate a reduction in CV events in spite of stringent A1C control [7]. Increased incidence of hypoglycemia and weight gain was the two major barriers not only in achieving the stringent glucose targets but also nullifying the CVD benefits.

This is where the incretins (Gliptins & GLP-1 analogs) comes into the picture. The advantages with these agents are the glucose-dependent release of insulin negating the hypoglycemic episodes and also weight loss with GLP-1 analogs & weight neutrality with DPP-4 inhibitors. Recent data suggests when a DPP-4 inhibitor is added to metformin its A1C reducing capacity is equivalent to that of a sulfonylurea [8]. As a result achieving the new composite target in diabetes (A1C reduction without hypoglycemia and weight gain) looks more attractive with a combination including the incretins [9]. In addition to the advantages enlisted above the renal and hepatic safety profile also makes gliptins an attractive choice. Since the introduction of sitagliptin in 2006  and subsequently vildagliptin in 2008 (EU) there has been a lot of changes noticeable not only in the prescribing pattern of the physicians but also the guidelines and recommendations. Saxagliptin was the next to get FDA approval [10] followed by linagliptin and adding to the recent list is Alogliptin, which has received FDA approval this year. Linagliptin can be used in full dose at any stage of renal impairment adding to the already existing list of advantages with DPP-4 inhibitors.

Alogliptin’s FDA approval was put up as a FDA news release on the 25th of January 2013 [11]. Three formulations were given approval – Nesina (alogliptin), Kazano (alogliptin & metformin hydrochloride),and Oseni (alogliptin & pioglitazone). As monotherapy the A1C reduction from baseline was 0.4-0.6%, an additional 1.1% with Kazano & 0.4-0.9% with Oseni (10). However dose alteration is probably required in moderate (50% dose reduction) & severe (25% dose reduction) CKD in line with most gliptins except linagliptin [11].

A few questions:

  • What does alogliptin add to the existing anti-hyperglycemic armamentarium? Is it just another gliptin or does it have something more to offer? Alogliptin has the highest DPP-4 selectivity versus DPP-8,9 & fibroblast activator protein [11] the clinical significance of which is still unknown [12].
  • The other noticeable fact about this new drug is that it got approval (the first of its kind) in all 3 formulations – monotherapy as well as in combination with metformin & pioglitazone. With all the recent controversies surrounding pioglitazone how popular is Oseni going to be?


1. Ralph A. DeFronzo. From the Triumvirate to the Ominous Octet: A New Paradigm for the Treatment of Type 2 Diabetes Mellitus. Diabetes 2009;58: 773-795.

2. Del Prato S and Tiengo A. The importance of first-phase insulin secretion: implications for the therapy of type 2 diabetes mellitus. Diabetes Metab Res Rev 2001; 17(3): 164-74.

3. Garber A.J. Incretin Effects on ß-Cell Function, Replication, and Mass. Diabetes Care 2011; 34(Suppl 2): S258-S263.

4. Andre´ J Scheen. A review of gliptins in 2011. Expert Opin. Pharmacother. 2012; 13(1):81-99.

5. Rury R. Holman, Sanjoy K. Paul, M. Angelyn Bethel, et al. 10-Year Follow-up of Intensive Glucose Control in Type 2 Diabetes. N Engl J Med 2008; 359:1577-89.

6. The Diabetes Control and Complications Trial/Epidemiology of Diabetes Interventions and Complications (DCCT/EDIC) Study Research Group. Intensive Diabetes Treatment and Cardiovascular Disease in Patients with Type 1 Diabetes. N Engl J Med 2005; 353:2643-53.

7. Faramarz Ismail-Beigi, Etie Moghissi, Margaret Tiktin, et al. Individualizing Glycemic Targets in Type 2 Diabetes Mellitus: Implications of Recent Clinical Trials. Ann Intern Med. 2011; 154:554-559.

8. M. A. Nauck, G. Meininger, D. Sheng, et al. Efficacy and safety of the dipeptidyl peptidase-4 inhibitor, sitagliptin, compared with the sulfonylurea, glipizide, in patients with type 2 diabetes inadequately controlled on metformin alone: a randomized, double-blind, non-inferiority trial. Diabetes, Obesity and Metabolism, 2007; 9: 194–205.

9. Bernard Zinman, Wolfgang E. Schmidt, Alan Moses, et al. Achieving a clinically relevant composite outcome of an HbA1c of <7% without weight gain or hypoglycaemia in type 2 diabetes: a meta-analysis of the liraglutide clinical trial programme. Diabetes Obes Metab. 2012; 14(1): 77-82.

10. FDA News Release. FDA approves new drug treatment for type 2 diabetes. 2009. Available at:

11. FDA News Release. FDA approves three new drug treatments for type 2 diabetes. 2013. Available at: [Accessed on:28th January 2013]

12. C. F. Deacon. Dipeptidyl peptidase-4 inhibitors in the treatment of type 2 diabetes: a comparative review. Diabetes, Obesity and Metabolism, 2011; 13: 7–18.

Avandia compensation claims in the UK

30 Jan, 13 | by Dr Dean Jenkins

The Guardian is today running with a story about the difference in compensation claims for families in the UK and US whose relatives may have suffered harm from rosiglitazone (Avandia) which was a drug for Type 2 Diabetes until its license was revoked in 2010.

“The manufacturer, GlaxoSmithKline, has admitted concealing data about the damaging side-effects of the drug, and there is evidence of the drug’s harmful effects. But, despite this, GSK is not prepared to settle claims in the UK without a court fight.

The history of drug litigation in the UK suggests that families might not easily get  compensation.”

Rosiglitazone seemed to be a useful drug in Type 2 diabetes which worked very well in only a small proportion of people with Type 2 diabetes. In others it increased the risk of fluid retention, heart failure and myocardial infarction. GSK hid the data and it took a meta-analysis of published data from the FDA and GSK itself to highlight the risk [1]. In 2012 the company paid a multi-billion dollar fine for Avandia and several other drugs which some have suggested could be written off as a business cost.

How court cases are settled in the UK and US obviously differ but it is hard to explain that to families who feel they are affected when there has been such international corporate wrongdoing. Expect to see more news of the ongoing Avandia saga for some time yet.

1. Nissen SE, Wolski K. Effect of Rosiglitazone on the Risk of Myocardial Infarction and Death from Cardiovascular Causes. New England Journal of Medicine 2007;356(24):2457–2471. Available from:

Diabulimia – what’s in a name?

25 Jan, 13 | by Dr Dean Jenkins

The charity DWED (Diabetes with Eating Disorders) is “campaigning to have omitting insulin to lose weight officially recognised as a mental illness“.

Image of a roseIt is alarming that as many as 30% of adolescent Type 1 females may have altered their insulin doses to lose weight [1]. Reducing insulin causes glucose to rise, many calories are ‘excreted’ in the urine and there is a risk of ketosis and dehydration. In the longer term the poor control increases the risk of microvascular complications of diabetes. Adding binge-eating with vomiting or anorexia to this insulin manipulation makes for a dangerous venture in weight control.

A patient perspective case report [2] gives a good account of how a young person with diabetes started using insulin manipulation and vomiting to control her weight after diagnosis:

“I developed a fear that my weight would continue increasing and never stop. I began cutting back on my insulin to lose a few pounds. When I moved away to college, I started using insulin manipulation again to lose weight. This time, my body was more fragile. One night, I was nauseated, throwing up, and on the verge of diabetic ketoacidosis. I realized I no longer needed to wait until my blood sugar became dangerously high to throw up; I could just make myself do it. It was then that I came to believe that, between insulin manipulation and bulimia, I had found the perfect ‘diet’.”

Giving some ‘condition’ a name is a very useful way of increasing its recognition. The more academic and descriptive ‘disordered eating behaviour in people with type 1 diabetes’ is nowhere near as succinct as the combination of two terms ‘diabetes’ and ‘bulimia’ into a single word ‘diabulimia’. What is in a name? What matters most is what something is, not what it is called.

Is there sufficient reason for labelling this condition as a mental illness? For those that have an eating disorder there is already a classification system and an evidence base for management [3]. I think the additional manipulation of insulin does not necessarily represent another diagnosis; instead, it should be a marker of increased risk and urgency for management under existing guidelines.


1. Rydall AC, Rodin GM, Olmsted MP, Devenyi RG, Daneman D. Disordered Eating Behavior and Microvascular Complications in Young Women with Insulin-Dependent Diabetes Mellitus. New England Journal of Medicine 1997;336(26):1849–1854. Available from:

2. A battle to overcome ‘diabulimia’. Am Fam Physician 2009 Feb;79(4):263; discussion 263.

3. NICE Eating disorders (CG9): Core interventions in the treatment and management of anorexia nervosa, bulimia nervosa and related eating disorders. 2004.

New formula suggested for BMI

24 Jan, 13 | by Dr Dean Jenkins

In 1832, whilst trying to define ‘normal’, Adolphe Quetelet, Belgian polymath, defined an index – the Quetelet Index – which later became known as the Body Mass Index (BMI) and is used as an indicator of obesity which has become recognised as an important marker of early mortality. [1] Typical BMI chart

The formula is well known to us though rather cumbersome to calculate. It is weight in kilograms divided by the square of height in metres. We are all familiar with the swathes of colour that map out underweight, normal, overweight and obese. We may very well say to people in our clinics that ‘according to your BMI you seem to be obese!’.

However, there is a problem with the index in that it doesn’t quite catch the nature of obesity and human growth. Those who tend to be below average height score slightly lower on this index than perhaps they should. The opposite is true of people who are taller than average. Clearly we can’t change our height but when certain recommendations [2] have explicit levels of BMI we need to be sure it is representing what we feel it should. The problem is mainly to do with the power that the height is raised to and Quetelet seems to have recognised that too (though he wasn’t so concerned with obesity). Babies seem to require a power of 3 to correctly recognise their growth in all dimensions and children would probably benefit from a figure of 2 since they grow more vertically. Adults fall in between and 2.5 seems to fit better.

So, Professor Nick Trefethen of Oxford University, made all these points and has suggested a refined formula following a letter to The Economist where he said:

“millions of short people think they are thinner than they are, and millions of tall people think they are fatter”

His formula is:

BMI = 1.3*weight(kg)/height(m)2.5

In the diabetes literature there is concern over the suitability of BMI in those with short-stature [3] and its usefulness when compared with other measures [4].

So, will you be using the new (slightly more cumbersome) formula in your clinic?


1. Garabed Eknoyan. Adolphe Quetelet (1796–1874)—the average man and indices of obesity.  Nephrol. Dial. Transplant. (2008) 23 (1): 47-51. doi: 10.1093/ndt/gfm517

2. NICE Clinical Guideline 43. Obesity.

3. Lara-Esqueda A, Aguilar-Salinas CA, Velazquez-Monroy O, Gómez-Pérez FJ, Rosas-Peralta M, Mehta R, Tapia-Conyer R. The body mass index is a less-sensitive tool for detecting cases with obesity-associated co-morbidities in short stature subjects. Int J Obes Relat Metab Disord. 2004 Nov;28(11):1443-50.

4. Lee CM, Huxley RR, Wildman RP, Woodward M. Indices of abdominal obesity are better discriminators of cardiovascular risk factors than BMI: a meta-analysis. J Clin Epidemiol. 2008 Jul;61(7):646-53. doi: 10.1016/j.jclinepi.2007.08.012.


8 Jan, 13 | by Dr Dean Jenkins

Welcome to the BMJ Group Diabetes Blog which has now launched!

This Blog will be maintained by a team of writers mostly made up of the faculty of the Postgraduate Diploma in Diabetes programme run by BMJ Learning and validated by the University of Leicester.

We hope to bring comments and opinions about diabetes, the different perspectives, latest scientific discoveries, reports of conferences, and the views of people with diabetes.

Looking forward to a much wider discussion and hoping to share some of the enthusiasm and advocacy for diabetes that we see on the Diploma programme.

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