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Type 1 Diabetes

Ramadan and Diabetes

27 Jun, 14 | by crichards

Dr Noma Salman is a Senior Tutor for Diabetes Qualifications from BMJ and University of Leicester. She is a GP who practices in Canada, and before that the UAE.

Fasting the holy month of Ramadan is one of the five pillars in the religion of Islam. The adult Muslim is expected to observe this special month by fasting, praying and devoting additional time in service of God. When fasting, Muslims are expected to stop eating, drinking and smoking from dawn till sunset. Ramadan lasts for one lunar month and ends with 3 days feast where Muslims break their fast and enjoy a variety of different social activities and food invitations; sweets constitute a major part of it.

The Muslim population is increasing and expected to rise from the current 1.6 billion to 2.2 billion by the year 2030. Adults and adolescents above the age of 14 are expected to observe Ramadan. They constitute approximately 1.2 billion (1), of which 77 million are estimated to have diabetes (2). Only healthy people are asked to fast. The sick, travelers, debilitated elderly people, and pregnant and lactating women, are exempt from this obligation. Despite this, many persons with diabetes insist on fasting which is sometimes against medical advice.

What is the effect of fasting on the glycemic control of people with diabetes? Who can fast? What are the contraindications of fasting? What kind of medical adjustments must be done before, during and after Ramadan? And how effective is patient education in achieving safe fasting and afterward feasting?

The main concerns and adverse effects of fasting are: Dehydration, Hypo and hyperglycemia attacks, Thrombosis and ketoacidosis.

Health care providers usually categorize patients into main 4 groups (3):
• Low risk group: where patients are well-controlled and treated with diet alone or diet and metformin;
• Moderate risk: Well-controlled patients treated with short-acting insulin secretagogues such as repaglinide or nateglinide, DPP4 inhibitors;
• High risk: Patients with moderate hyperglycemia (average blood glucose between 150 and 300 mg/dl, A1C 7.5–9.0%), renal insufficiency, advanced macrovascular complications, people living alone that are treated with insulin or sulfonylureas, old age or on other medication that affect mental status;
• Very high risk: where patients have experienced severe hypoglycemia or Hyperosmolar hyperglycemic coma or Diabetic Ketoacidosis within the last 3 months prior to Ramadan or have hypoglycemia unawareness, poor glycemic control, acute illness, pregnancy, kidney failure on dialysis.

The current recommendation is to start with a proper counseling 1-2 months before the onset of Ramadan and to do full assessment which includes fasting glucose level, HbA1c, lipids profile, blood pressure and detection of complications. A session of Ramadan-focused education is also mandatory and is found to minimize the risk of hypoglycaemic events and prevents weight gain during this festive period for Muslims, which potentially benefits metabolic control (4). After that, the physicians should work with their patients to prepare an appropriate and individualized life-style, diet and drug plan.

In terms of medication, dose and timing need to be adjusted and blood glucose need to be frequently monitored by SMBG. Metformin alone can be used safely during the fast with minimal possibility of severe hypoglycemia; however, consensus recommendations suggest the dosage can be modified such that two-thirds of the total daily dose is taken with the sunset meal and the other one-third is taken before the pre-dawn meal. Sulfonylureas should be avoided during Ramadan fasting because of the risk of hypoglycemia. When Insulin is involved, always consider intermediate-acting or long-acting insulin preparations plus short-acting insulin before meal (5).

In my clinical practice, every Ramadan I face a major challenge which is the tendency and the deep desire to fast in most of my patients regardless of their risk status. This is mainly to do with patients’ cultural and religious values and usually it is difficult to modify.

The other challenge is having Ramadan in July, the hottest month of the year in most parts of the Middle East. Furthermore in the northern hemisphere, Ramadan day will be the longest and can go up to 19 hours in some countries. These reflect on the possibility of increasing adverse effects and the need for further education.

Eating healthy food during Ramadan and Eid time is a cornerstone as well as doing light physical activity and proper frequent SMBG testing. Education about how to react to low or high readings and staying in close contact with the physician are all essential strategies to reach the goal of safe fasting for people with diabetes.

References:
1- http://www.pewforum.org/2011/01/27/the-future-of-the-global-muslim-population/ (accessed June 24-2104)
2- http://www.idf.org/diabetesatlas (accessed June 24-2014)
3- 1. Al-Arouj M, Bouguerra R, Buse J, Hafez S, Hassanein M, Ibrahim MA, et al. Recommendations for Management of Diabetes During Ramadan. Dia Care. 2005 Sep 1;28(9):2305–11.
4- Bravis V, Hui E, Salih S, Mehar S, Hassanein M, Devendra D. Ramadan Education and Awareness in Diabetes (READ) programme for Muslims with Type 2 diabetes who fast during Ramadan. Diabet Med. 2010 Mar;27(3):327–31.
5- Hui E, Bravis V, Hassanein M, Hanif W, Malik R, Chowdhury TA, et al. Management of people with diabetes wanting to fast during Ramadan. BMJ. 2010;340:c3053

 

 

Dinner with the diabetes team of the year!

6 Jun, 13 | by Dr Dean Jenkins

It was great to meet Dr Julie Edge and the Oxfordshire Paediatric Diabetes Team at the BMJ Awards recently. They were recognised for their work with primary schools overcoming the many barriers to diabetes care. Julie has recently published a review in Practical Diabetes covering some of the issues. (1)

Photo of Diabetes Team of the Year The evening was in central London and a great success as usual. It is good to celebrate good practice – of which there is plenty to choose from – instead of dwelling on the shortcomings of care.

Matthew Billingsley and I managed to record a short interview with the team where they explained what their programme had achieved.

 

1. Edge JA. Diabetes in primary schools: overcoming barriers to good care. Practical Diabetes 2012;29(8):320–323. Available from: http://onlinelibrary.wiley.com/doi/10.1002/pdi.1715/abstract

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 studihttp://commons.wikimedia.org/wiki/File%3APseudomonas_aeruginosa_on_cetrimide_agar.jpged. 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: http://www.endocrine-abstracts.org/ea/0031/ea0031P223.htm

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: http://www.ncbi.nlm.nih.gov/pubmed/16282278

3. Gale, E.A.M. Hygiene hypothesis [internet]. 2012 [cited 2013 Mar 23]; Diapedia 21040851207 rev. no. 30. Available from: http://www.diapedia.org/type-1-diabetes-mellitus/21040851207/hygiene-hypothesis

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: http://diabetes.diabetesjournals.org/content/early/2013/01/30/db12-1113

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: http://www.nejm.org/doi/full/10.1056/NEJMoa1108046

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: http://www.nejm.org/doi/full/10.1056/NEJMoa0802315

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