OPTIFAST VLCD™ Program Guidelines for Diabetes ® OPTIFAST® VLCD™ is a food for special medical purposes for the dietary management of obesity. Must be used under medical supervision. For healthcare professional use only. Table of Contents Type 1 Diabetes & OPTIFAST® VLCD™ Main points................................................................................................................................................................................ 2 Review of the evidence............................................................................................................................................................. 3 Recommendations for management....................................................................................................................................... 4 Type 1 Diabetes Case study..................................................................................................................................................... 5 Type 2 Diabetes & OPTIFAST® VLCD™ Main points................................................................................................................................................................................ 6 Review of the evidence............................................................................................................................................................. 7 Recommendations for management....................................................................................................................................... 8 Type 2 Diabetes Case study..................................................................................................................................................... 9 Medications used in Type 2 Diabetes.................................................................................................................................... 10 This evidence-based guideline has been prepared by Dr. Daniel Fineberg BMedSci MBBS FRACP We would also like to thank the following experts for their contribution, feedback and review: Clinical Associate Professor Tania Markovic MBBS PhD FRACP Director, Metabolism & Obesity Services, Royal Prince Alfred Hospital Dr. Sharon J Marks MBBS(Hons), FRACP Consultant Physician in Clinical Nutrition, Monash Medical Centre This Guideline document is a work in progress and will continue to evolve over time. We would appreciate any feedback or comments you may have on how to improve the Guideline and make it more relevant to you and your clinical practice. The GI Symbol is your trusted guide to healthier food choices. Foods that carry the GI Symbol meet strict nutrient criteria and the GI value is certified as accurate. For more information go to gisymbol.com Further information is available on request at: Nestlé Healthcare Nutrition, a division of Nestlé Australia Ltd, 20–24 Howleys Road, Notting Hill VIC 3168, Australia 1800 671 628. 12–16 Nicholls Lane, Parnell, Auckland, New Zealand 0800 607 662. For more information visit optifast.com.au 1 OPTIFAST® VLCD™ Guidelines for Diabetes Type 1 Diabetes & OPTIFAST® VLCD™ Main points: Care needs to be taken if using OPTIFAST® VLCD™ in patients with Type 1 Diabetes (T1DM). uu The issue of obesity in T1DM is important for the clinician to consider with the increasing number of patients with T1DM and obesity. uu The risk of hypoglycaemia and ketosis needs to be carefully monitored but, with appropriate insulin adjustment, there may be less hypoglycaemia while on a VLCD because of the reduced likelihood of insulin to carbohydrate mismatch. uu Glycaemic control is critical to reducing the risk of diabetic complications. Reduction of insulin dose needs to be matched to the change in carbohydrate and energy intake. The established targets of glycaemia, with avoidance of hypoglycaemia, and management of other established cardiovascular risk factors should be priority issues in the management of T1DM. uu 2 Type 1 Diabetes & OPTIFAST® VLCD™ Review of the evidence: The prevalence of obesity in T1DM is increasing and is associated with a high incidence of vascular (micro and macro) disease and complications.1 uu The landmark Diabetes Control and Complications Trial (DCCT) in T1DM showed an average 5.1kg vs 3.7kg increase in weight with intensive insulin therapy compared to conventional treatment.2 An 18-year follow-up of this trial found an increase in obesity from 3.4% at baseline to 22.7% possibly due to the community rise in obesity as well as an increase in the intensification of insulin therapy (7% at baseline to 82% at follow-up).3 uu Reduction in body weight is associated with an increase in hypoglycaemia4 that may be due to a number of factors including reduced carbohydrate intake, increased insulin sensitivity and change in physical activity. Although, a study on people with T1DM who were fasted showed a transient increase in insulin resistance due to reduced glucose oxidation.1 uu The appetite suppressive capability of VLCDs may be improved with the genesis of a mild ketosis.6 Adjustment of insulin dosing can be associated with a mild ketosis with avoidance of ketoacidosis.1 Thus the ketosis seen with a VLCD should not pose any problems for subjects with T1DM. uu Although previously considered a relative contraindication to VLCDs, under diabetes specialist supervision, VLCDs can be used with appropriate education and patient selection in T1DM.7 uu While there is a paucity of published data showing the efficacy of VLCD in T1DM there is no evidence suggesting harm with a VLCD regimen. uu VLCDs are associated with ketosis via the production of acetoacetate and beta-hydroxybutyrate from breakdown of fatty acids. The total amount of carbohydrate where ketosis is likely to occur is between 50-200g/day. An Intensive Phase OPTIFAST® VLCD™ regimen provides between 50-100g/day carbohydrate. The ketone levels seen in non-T1DM obese subjects consuming VLCDs range between 0.33-0.72 mmol/L and is much lower than the level seen in diabetic ketoacidosis which is _ 3mmol/L and often much higher.5 generally > uu Footnotes 1 Musil F, et al. Effect of low calorie diet and controlled fasting on insulin sensitivity and glucose metabolism in obese patients with type 1 diabetes mellitus. Physiological Research. 2013. 2 The effect of intensive treatment of diabetes on the development and progression of long-term complications in insulin-dependent diabetes mellitus: the Diabetes Control and Complications Trial Research Group. N Engl J Med. 1993; 329: 977–986. 3 OPTIFAST® VLCD™ Guidelines for Diabetes 3 Purnell JQ et al; DCCT/EDIC Research Group. Circulation. 2013 Jan 15;127(2): 180-7. Circulation. Epub 2012 Dec 4. 4 Jacobsen IB, et al. The effect of metformin in overweight patients with type 1 diabetes and poor metabolic control. Basic Clinical Pharmacology Toxicology. 2009:105;145-149. 5 Sumithran and Proietto. Ketogenic diets for weight loss: A review of their principles, safety and efficacy. Obesity Research & Clinical Practice. 2008:2,1-13. 6 McClernon et al. The Effects of a Low-Carbohydrate Ketogenic Diet and a Low-Fat Diet on Mood, Hunger, and Other Self-Reported Symptoms. Obesity. 2007:15(1), 182-187. 7 Baker S et al. Effects and clinical potential of very-low-calorie diets (VLCDs) in type 2 diabetes Scott Baker. Diabetes Research and Clinical Practice. (2009)85:235-242. Type 1 Diabetes & OPTIFAST® VLCD™ Recommendations for management: An OPTIFAST® VLCD™ Program for weight loss can be considered in selected patients with T1DM if used with close follow up from their diabetes specialist. uu It may be prudent to start with 1 or 2 meal replacements on initiation to work out the bolus (rapid insulin) dose. uu The OPTIFAST® VLCD™ products contain 13-22.5g of carbohydrate per serve. In patients who are aware of their carbohydrate to insulin ratio, a suitable dose adjustment should be made. uu One method to estimate the carbohydrate to insulin ratio is the 500 rule where 500 is divided by the total insulin daily dose. uu – For example, if the total insulin daily dose is 100 units – Then 500/100=5 – Carbohydrate:Insulin ratio is 5 – If taking an OPTIFAST® VLCD™ replacement with 20g of carbohydrate then: – 20/5=4 – Therefore the dose should be 4 units of rapid acting insulin with the meal. A reduction in the basal insulin dose should be considered due to the expected reduction in hepatic glucose production. On the Intensive Phase a 50% reduction in the basal dose is a suggested starting point. Further adjustment may be required, especially if there is overnight or pre-meal hypoglycaemia. Patients should not withhold or significantly reduce the basal insulin dose without discussion with their diabetes specialist. uu Patients should be familiar with appropriate management of hypoglycaemia. Patients should perform at least 4 finger prick glucose checks a day with additional monitoring depending on the context. If the predominant form of hypoglycaemia is a mismatch between insulin and carbohydrate intake then a VLCD may actually improve the situation. Patients prone to severe hypoglycaemia due to exercise or other physiological changes are likely to still have difficulty with their control. uu Patients should be counselled to avoid at risk behaviours (e.g. driving, swimming) until they are familiar with the effect of the OPTIFAST® VLCD™ on their glycaemic profile. uu Mild ketosis may be present while on the Intensive Phase of OPTIFAST® VLCD™. uu – The expected level is 0.3-0.7mmol/l and this is likely to persist while the individual remains on the VLCD. It is unlikely that there would be an increased risk of ketoacidosis especially if the blood glucose remains acceptable and the insulin is taken regularly. – If monitoring, a fingerprick ketone level > 1.0mmol/l should be discussed with a diabetes professional. Health professionals should be aware of the possibility that patients may significantly reduce or withhold insulin as a weight management strategy. The risks of this practice may need to be discussed with your patient. uu Extra care should be taken soon after the diagnosis of T1DM. Patients should be very familiar with all aspects of self-management. uu OPTIFAST® VLCD™ Guidelines for Diabetes 4 Type 1 Diabetes & OPTIFAST® VLCD™ Case study Tara is a recently married 26 year old woman with T1DM for 10 years complicated by mild non-proliferative retinopathy and microalbuminuria. She weighs 100kg, has a BMI of 40kg/m2 and has slowly continued to gain weight at about 2kg per year since adolescence. Her HbA1c is generally between 8-9% and she is on a basal bolus regimen using around 120 units of insulin daily (60 units long acting and 20 units short acting with each meal). She has moderate hypoglycaemic levels (low 3s) associated with symptoms. She has tried metformin but is unable to tolerate the gastrointestinal side effects. She finds it frustrating that the pattern of meal-time insulin and BGL monitoring (at least 4x daily) appears to not follow a particular pattern in that sometimes her glucose levels are very high but at other times she has unexplained hypoglycaemic episodes. She has seen dietitians over the past 10 years and implemented recommended dietary behaviour but her weight has not reduced. She is screened for other associated conditions including hypothyroidism and has no other medical cause for insulin resistance or weight gain. Her diabetes specialist suggests a trial of closely monitored OPTIFAST® VLCD™ with a goal to reduce her weight to see if it helps with controlling her average blood glucose, avoiding mismatch in dosing causing hypoglycaemia and achieving weight reduction. She starts with one OPTIFAST® VLCD™ meal replacement a day to see how to adjust her short acting insulin dose. She has not previously determined an insulin to carbohydrate ratio but using the 500 rule she starts with a ratio of 4.17. She tries the Berry Crunch Bar, which contains 20.8g carbohydrate and takes 5 units of short acting insulin, which is about a ¼ of her usual meal time dose. She does a blood glucose check 2 hours after the supplement to see the effect of the dose which is higher than her recommended post prandial target. When she next has a Berry Crunch Bar she takes 6 units of her short acting insulin and has a better post prandial glucose level. She then supplements 2 meals a day while trialling a range of the OPTIFAST® VLCD™ products to see what she likes best. She finds that her dose is 6-7 units of rapid acting insulin with each supplement depending on the carbohydrate content. She starts to have some overnight and early morning borderline low glucose levels and reduces her long acting insulin from 60 to 40 units. After finding that she is stable on this she decides to embark on the Intensive Phase of OPTIFAST® VLCD™ with 3 meal replacements. She reduces her long acting insulin to 30 units (1/2 her initial dose) and continues with 6 units of short acting with each supplement. She does additional monitoring before and 2hrs after each replacement meal. She continues this for 10 days and finds that she feels quite well on the program. Her blood glucose levels range between 4.5-10 with no hypoglycaemia. She checks her ketone level for interest and it is 0.6mmol/L. Routine blood tests at this time demonstrate normal renal function and no electrolyte disturbance. After 3 weeks she has lost 6kg and due to borderline hypoglycaemia reduces her insulin dose further. She is able to continue the Intensive Phase for 12 weeks by which time she has lost 20kg. Her ability to do more physical activity increases and she feels happier with her life. Her HbA1c has dropped to 6.2% and she is now normoalbuminuric. Her doses are 24 units long acting, and 4-5 units short acting with meals. She relaxes to 2 meal replacements and 1 low carbohydrate meal daily and continues for a further 6 weeks, reducing her weight to 72kg. She then starts a healthy normal diet with the occasional OPTIFAST® VLCD™ supplement, usually at lunch time. She tries to exercise regularly and usually manages to swim or walk 1 hour daily, as she is very keen to maintain her current weight. She decides that if her weight increased up to 80kg she would re-commence the Intensive Phase of the OPTIFAST® VLCD™ Program. 5 OPTIFAST® VLCD™ Guidelines for Diabetes Type 2 Diabetes & OPTIFAST® VLCD™ Main points: Type 2 Diabetes (T2DM) is a common association with obesity. Perpetuating factors common to both of these conditions should be the focus in patients with T2DM. Tackling obesity will help to achieve health targets, reduce further complications and improve long term quality of life. u Weight loss has been shown to be directly related to improvements in glycaemia in patients with T2DM. u Use of VLCD, such as OPTIFAST® VLCD™, is a well established method of weight loss in T2DM. u Improvement in beta cell function and glycaemia can occur in some patients early in the course of a VLCD, which may be independent to weight loss, but rather related to the reduction in energy intake. u Methods to improve glycaemia and reduce obesity should be implemented as soon as possible in the course of T2DM as it is likely to have the greatest impact on avoiding cardiovascular and microvascular complications. u Transition to less obesogenic agents is recommended by avoiding insulin or sulphonylurea therapy and adding metformin, DPP-IV inhibitor or GLP-1 agonist therapy. With normal eating, acarbose may be of benefit. The emerging SGLT-2 inhibitors may also be of benefit to both glycaemic and weight control. u Agents that appear to promote satiety such as the DPP-IV inhibitors and, even moreso, GLP-1 agonists may have an additional benefit of improving compliance with a VLCD, or limiting intake when on a healthy regular diet. u OPTIFAST® VLCD™ Guidelines for Diabetes 6 Type 2 Diabetes & OPTIFAST® VLCD™ Review of the evidence: In Australia, while other metabolic risks such as blood pressure and total cholesterol have decreased, BMI and mean fasting glucose have increased. In 2008 the estimated prevalence of obesity in Australia was over 25%.8 Obesity compounds the cardiovascular risk of diabetes and is a major risk factor for T2DM, accounting for about 80% of cases of T2DM, with about 80% of people with T2DM being obese.9 uu In a recent important trial looking at the impact of lifestyle intervention, the Look AHEAD trial had 5000 middle aged participants with T2DM and BMI >25 kg/m2. In addition to other lifestyle measures the caloric intake was restricted to approximately 1200-1500kCal/d, which included the option for OPTIFAST® VLCD™ meal replacement to achieve this. Patients were randomised to interventional lifestyle therapy or standard therapy for 4 years and monitored for up to 11 years. After 4 year an 8% weight loss was associated with better measures of glycaemia and other metabolic risk factors including blood pressure and dyslipidaemia.10 uu Independent of weight loss, in selected patients, early initiation of a VLCD can lead to significant improvements in glycaemic control.11 Beta cell function improvements can be seen with improvement in dynamic insulin secretion, insulin production, modulation of pulsatility and improved synchrony.12 uu In clinical practice it is evident that a large subset of T2DM patients who appear to have a requirement for exogenous insulin, when exposed to inpatient care and periods of fasting due to procedures or diagnostic tests, often require much less insulin or manage with their endogenous insulin function alone. The concept of pancreatic beta cell rest for uncontrolled hyperglycaemia is increasingly popular and often involves the use of early insulin therapy. An additional method of islet rest can be achieved with a VLCD. A study of 14 otherwise well subjects with T2DM showed about 50% responding to a very low caloric intake (<450kCal/d) and achieving a sustained acceptable reduction in blood sugar level (<10mmol/L). A positive response was predicted by a good response on day 2 of the diet. Other predictors of response were a shorter duration of diabetes and higher fasting serum insulin.13 uu A proposed mechanism for glycaemic control is that caloric restriction leads to glycogen depletion in muscle and liver. Restriction of carbohydrate leads to lipolysis and the formation of ketone bodies by the liver. Together these responses lead to reductions in hepatic glucose output via inhibition of gluconeogenesis and reduced glycogenolysis. High protein stimulates insulin secretion and increases satiety. Circulating ketone bodies have also been shown to increase satiety14. Weight loss and reduction of fat deposits in the liver, muscle, pancreas and perivisceral space lead to reductions in insulin resistance. Improved insulin sensitivity, dynamic insulin secretion and reduced hepatic glucose output lead to reductions in blood glucose levels.15 uu A number of small studies have shown significant benefits of VLCDs on glycaemic control in T2DM.15 A study using a VLCD for 8 weeks and tapering with a low calorie diet for 4 weeks showed a significant improvement in HbA1c related to the degree of weight loss, with a >15% weight loss contributing to a lowering of HbA1c by about 2%.16 uu Most international guidelines on diabetes management recommend weight loss with calorie restriction.17 Recommendation for the use of VLCDs over other diets is limited by the lack of long term efficacy data.18 However, there are no studies indicating long term safety concerns. uu The concept of metabolic memory, whereby improvement of glucose for a period leads to sustained improvement in outcomes, even if glycaemic control is later relaxed, has been demonstrated in the follow-up of some of the large landmark studies (ACCORD)19. This phenomenon was shown in a 30 day VLCD in 18 T2DM patients in which a sustained 18 month improvement in glycaemia and other metabolic parameters was seen, even in those patients who regained body weight.20 uu The use of VLCD in the management of diabetic complications is not clear. Future studies are looking at the use of VLCDs in patients with complications such as microalbuminuria,21 with cautious use of VLCDs and regular monitoring of renal function, especially initially. uu Footnotes WHO Noncommunicable Disease Country Profiles 2011. http:// whqlibdoc.who.int/publications/2011/9789241502283_eng.pdf 8 Obesity & type 2 Diabetes. Maggio CA, Pi-Sunyer FX. Endocrinology and Metabolism Clinics of North America [2003, 32(4):805-22, viii]. 9 Wing RR. Long-term effects of a life- style intervention on weight and cardio- vascular risk factors in individuals with type 2 diabetes mellitus: four-year results of the Look AHEAD trial. Arch Intern Med. 2010;170:1566-1575. Reversal of type 2 Diabetes: normalisation of beta cell function in association with decreased pancreas and liver triacylglycerol. Lim et al. Diabetologia (2011) 54:2506–2514. 12 OPTIFAST® VLCD™ Guidelines for Diabetes Nield et al. Cochrane Review. Dietary advice for treatment of type 2 diabetes mellitus in adults (Review). ACCORD Study Group. 2008 Effect of intensive glucose lowering in type 2 diabetes. NEJM 358(24):2545-59. Jazet et al. 2004 Diabetes UK. Diabetic Medicine, 22, 52–55. 19 14 Effect of weight loss and ketosis on postprandial cholecystokinin and free fatty acid concentrations. Delbridge et al, Am J Clin Nutr 2008;87:1238-46. 20 Jazet, I.M. & de Craen, A.J., Sustained beneficial metabolic effects 18 months after a 30-day very low calorie diet in severely obese, insulin-treated patients with type 2 diabetes. Diabetes research 2007. 21 ClinicalTrials.gov identifier: NCT01671969. 15 Baker, S., Jerums, G. & Proietto, J., 2009. Effects and clinical potential of very-low-calorie diets (VLCDs) in type 2 diabetes. Diabetes Research and Clinical Practice, 85(3), pp.235–242. 16 Wing, R.R., 1991. Effects of a Very-Low-Calorie Diet on Long-term Glycemic Control in Obese Type 2 Diabetic Subjects. Archives of Internal Medicine, 151(7), p.1334. 11 7 18 13 10 Importance of weight management in type 2 diabetes: review with meta-analysis of clinical studies. Anderson et al. Journal of the American College of Nutrition, Vol. 22, No. 5, 331–339 (2003). Diabetes Care. Executive summary 2013. 17 Type 2 Diabetes & OPTIFAST® VLCD™ Recommendations for management: Use of OPTIFAST® VLCD™ Intensive Phase is often initiated prior to bariatric surgery in obese T2DM patients (as well as those without T2DM) to reduce the liver size and so improve accessibility and visibility for laparoscopic procedures. It is likely that other metabolic markers improve preoperatively with OPTIFAST® VLCD™ and may assist with reduction of perioperative complications. uu Obese or overweight patients with poor glycaemic control may benefit from OPTIFAST® VLCD™ as a result of improved insulin sensitivity (due to weight loss) and possibly ‘islet cell rest’, resulting in improved endogenous insulin production and action so that patients may achieve target glucose levels alone or in conjunction with other hypoglycaemic agents. uu Many patients are reluctant to initiate insulin management despite having high blood glucose. If OPTIFAST® VLCD™ Intensive Phase is used in this setting a considerable improvement in glycaemic control usually occurs within 1-2 weeks. If not, other hypoglycaemic measures should be instituted. Thus, patients with poor glycaemic control who are starting a full OPTIFAST® VLCD™ Program should monitor their blood glucose levels regularly and be reviewed within 1-2 weeks of initiating OPTIFAST® VLCD™. uu Obese patients with T2DM and associated diabetic complications such as microalbuminuria, nonproliferative retinopathy, obstructive sleep apnoea, non-alcoholic fatty liver disease and diastolic cardiac dysfunction are suitable for OPTIFAST® VLCD™ management. uu Obese patients with more severe complications such as proteinuria>1g/d, eGFR <60 or risk of fluid balance complications need to be carefully monitored (creatinine, eGFR, electrolytes, nutritional markers, nitrogen balance) if considered for VLCD management. uu The initial approach is to use an Intensive Phase to induce weight loss to a predetermined target. In terms of glycaemic control, 5-10% weight loss may provide significant benefits. uu Patients on insulin or sulphonylureas need to be careful to avoid hypoglycaemia and if possible, simplifying the insulin regimen or changing to an oral agent that does not increase basal insulin secretion would be preferable. uu Unless glycaemic control has been poor, the insulin or sulphonylurea dose should usually be reduced on commencement of a VLCD and glucose levels should be closely monitored. uu On the full VLCD, patients on basal bolus insulin usually do not need pre meal insulin bolus doses and require a reduction in the basal dose. A practical recommendation is to initially halve the dose and review frequently with self blood glucose monitoring. When only 1 or 2 meals are replaced with OPTIFAST® VLCD,™ the bolus dose may only need to be reduced or withheld prior to these meals. uu Patients on twice daily mixed insulin (breakfast and dinner) who are starting the Intensive Phase of the OPTIFAST® VLCD™ Program are often best managed by changing their insulin regimen to a single basal insulin injection at half the dose of their usual total insulin dose. uu Antihypertensive treatment may need to be adjusted while on a VLCD as often the blood pressure falls. Thus in these patients blood pressure should be regularly monitored. Lipids often improve markedly following weight loss so it may be possible to reduce doses of lipid lowering medications following a VLCD. uu VLCD is not recommended in diabetes with normal or low weight, or diabetes associated with pregnancy or cystic fibrosis related diabetes. uu OPTIFAST® VLCD™ Guidelines for Diabetes 8 Type 2 Diabetes & OPTIFAST® VLCD™ Case study Erica has had T2DM for 7 years with associated obesity, complicated by hypertension, dyslipidaemia, macroalbuminuria (0.6g/d) with stage III chronic kidney disease (eGFR around 55ml/min/1.73m2) and sleep apnoea (on CPAP). She is on metformin, a sulphonylurea, maximum dose ACE-Inhibitor, a calcium channel blocker and a statin. Six months ago her HbA1c was 9% and she was commenced on twice daily mixed insulin. She is now on 60 units BD. Her HbA1c has improved to 7.6% but she has gained 10 kg and her BMI is now 40kg/m2. She has now developed gastro oesophageal reflux and is finding physical activity very difficult largely because of her weight. She decides to go on OPTIFAST® VLCD™. In anticipation of a fall in her glucose levels she is changed to a basal insulin at a dose of 30 units nocte, and is able to achieve target blood glucose readings. With increasing weight reduction, her glucose levels start to fall to 4-5 mmol/L and her insulin dose is progressively reduced so that by the time she has been on the VLCD for 6 weeks she is no longer requiring any insulin. Her blood pressure also falls and she stops the calcium channel blocker. 9 OPTIFAST® VLCD™ Guidelines for Diabetes After having been on the VLCD for 3 months she starts having 1 regular healthy evening meal and replaces breakfast and lunch with an OPTIFAST® VLCD™ meal. She gradually weans off the OPTIFAST® VLCD™ products over the next month and is extremely happy with her progress. She has managed to reduce her weight by 14 kg so that her BMI is now 35kg/m2. She no longer requires insulin and her dose of sulphonylurea has been halved. Her ability to exercise is much improved and she is intent on maintaining her weight by walking regularly and eating a healthier diet. She realises that she will need to monitor her weight regularly and if she finds it increasing, she would consider recommencing OPTIFAST® VLCD™ either to replace all meals or 1-2 meals daily. Medications used in Type 2 Diabetes Table 1: Medications used in Type 2 Diabetes - considerations and potential benefits with the OPTIFAST® VLCD™ Program. Medication Effect on weight Important considerations with OPTIFAST® VLCD™ Potential benefits with OPTIFAST® VLCD™ NON INSULIN AGENTS Metformin Modest loss or neutral. Monitor renal function – cease if eGFR <50 or unstable renal function. May allow control of glycaemia. Sulphonylureas Increases. Risk of hypoglycaemia if dose not adjusted. May allow control of glycaemia. Increases insulin secretion (obesogenic). Glitazones Increases. VLCD may potentiate the risk of reduction in bone mineral density with this agent. May allow control of glycaemia. Acarbose Modest loss or neutral. Unlikely to be additional benefit due to low carbohydrate intake on VLCD. May be of benefit in non-replacement meals or maintenance phases. DPP-IV Inhibitors Modest loss or neutral. May exacerbate gastrointestinal discomfort. Avoid if patient at high risk of pancreatitis. May assist with adherence to VLCD. GLP-1 Analogues Moderate loss. May exacerbate gastrointestinal discomfort. Avoid if patient at high risk of pancreatitis. May assist with adherence to VLCD. INSULIN AGENTS Basal Increases. Risk of hypoglycaemia. Reduction in dose more likely if on Intensive Phase. May allow control of glycaemia. Mixed Insulin Increases. Risk of hypoglycaemia. Reduce dose if taken with time of supplement. Use of supplement at non insulin meal may allow better glycaemic control. Basal Bolus Increases. Risk of hypoglycaemia. Usually a reduction in dose of both basal and bolus component is required. May allow control of glycaemia. OPTIFAST® VLCD™ Guidelines for Diabetes 10 Bars Soups Desserts Shakes 12pk 21pk FREE ONLINE SUPPORT CLINICALLY PROVEN PROGRAM BALANCED PROGRAM Free Online Support www.optifast.com.au Free Online Support www.optifast.com.au 12pk Free Online Support 21pk FREE ONLINE SUPPORT BALANCED PROGRAM www.optifast.com.au Nestlé Healthcare Nutrition is a member of the Weight Management Council of Australia This means that the OPTIFAST® VLCD™ Program and materials must comply with the Weight Management Code of Practice. Healthcare professionals can therefore recommend the OPTIFAST® VLCD™ Program to their patients with confidence. The GI is a ranking of carbohydrates according to their effect on blood glucose levels. ®© & ™ of GI Symbol, University of Sydney, used under licence. OPTIFAST® VLCD™ is a food for special medical purposes for the dietary management of obesity. Must be used under medical supervision. ® Reg. Trademark of Société des Produits Nestlé S.A. Nestlé Healthcare Nutrition, a division of Nestlé Australia Ltd, 20–24 Howleys Road, Notting Hill VIC 3168, Australia 1800 671 628. 12–16 Nicholls Lane, Parnell, Auckland, New Zealand 0800 607 662. For more information visit optifast.com.au For healthcare professional use only. CLINICALLY PROVEN PROGRAM