Guidelines for Diabetes

Transcription

1 Guidelines for Diabetes For healthcare professional use only.

2 Table of Contents Type 1 Diabetes & OPTIFAST VLCD Main points... Review of the evidence... Recommendations for management... Type 1 Diabetes Case study... Type Diabetes & OPTIFAST VLCD Main points... Review of the evidence... Recommendations for management... Type Diabetes Case study...9 Medications used in Type 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, 0 Howleys Road, Notting Hill VIC 1, Australia Nicholls Lane, Parnell, Auckland, New Zealand For more information visit optifast.com.au 1 OPTIFAST VLCD Guidelines for Diabetes

3 Type 1 Diabetes & OPTIFAST VLCD Main points: uu 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.

4 Type 1 Diabetes & OPTIFAST VLCD Review of the evidence: uuthe prevalence of obesity in T1DM is increasing and is associated with a high incidence of vascular (micro and macro) disease and complications. 1 uuthe landmark Diabetes Control and Complications Trial (DCCT) in T1DM showed an average.1kg vs.kg increase in weight with intensive insulin therapy compared to conventional treatment. An 1-year follow-up of this trial found an increase in obesity from.% at baseline to.% possibly due to the community rise in obesity as well as an increase in the intensification of insulin therapy (% at baseline to % at follow-up). uureduction in body weight is associated with an increase in hypoglycaemia 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 uuvlcds 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 0-00g/day. An Intensive Phase OPTIFAST VLCD regimen provides between 0-100g/day carbohydrate. The ketone levels seen in non-t1dm obese subjects consuming VLCDs range between mmol/l and is much lower than the level seen in diabetic ketoacidosis which is generally >_ mmol/l and often much higher. uuthe appetite suppressive capability of VLCDs may be improved with the genesis of a mild ketosis. 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. uualthough previously considered a relative contraindication to VLCDs, under diabetes specialist supervision, VLCDs can be used with appropriate education and patient selection in T1DM. uuwhile there is a paucity of published data showing the efficacy of VLCD in T1DM there is no evidence suggesting harm with a VLCD regimen. 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. 01. 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. 199; 9: 9 9. Purnell JQ et al; DCCT/EDIC Research Group. Circulation. 01 Jan 1;1(): 10-. Circulation. Epub 01 Dec. Jacobsen IB, et al. The effect of metformin in overweight patients with type 1 diabetes and poor metabolic control. Basic Clinical Pharmacology Toxicology. 009:10;1-19. Sumithran and Proietto. Ketogenic diets for weight loss: A review of their principles, safety and efficacy. Obesity Research & Clinical Practice. 00:,1-1. 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. 00:1(1), 1-1. Baker S et al. Effects and clinical potential of very-lowcalorie diets (VLCDs) in type diabetes Scott Baker. Diabetes Research and Clinical Practice. (009):-. OPTIFAST VLCD Guidelines for Diabetes

5 Type 1 Diabetes & OPTIFAST VLCD Recommendations for management: uuan OPTIFAST VLCD Program for weight loss can be considered in selected patients with T1DM if used with close follow up from their diabetes specialist. uuit may be prudent to start with 1 or meal replacements on initiation to work out the bolus (rapid insulin) dose. uuthe OPTIFAST VLCD products contain 1-.g of carbohydrate per serve. In patients who are aware of their carbohydrate to insulin ratio, a suitable dose adjustment should be made. uuone method to estimate the carbohydrate to insulin ratio is the 00 rule where 00 is divided by the total insulin daily dose. For example, if the total insulin daily dose is 100 units Then 00/100= Carbohydrate:Insulin ratio is If taking an OPTIFAST VLCD replacement with 0g of carbohydrate then: 0/= Therefore the dose should be units of rapid acting insulin with the meal. uua reduction in the basal insulin dose should be considered due to the expected reduction in hepatic glucose production. On the Intensive Phase a 0% 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. uuextra care should be taken soon after the diagnosis of T1DM. Patients should be very familiar with all aspects of self-management. uupatients should be familiar with appropriate management of hypoglycaemia. Patients should perform at least 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. uupatients should be counseled to avoid at risk behaviours (e.g. driving, swimming) until they are familiar with the effect of the OPTIFAST VLCD on their glycaemic profile. uumild ketosis may be present while on the Intensive Phase of OPTIFAST VLCD. The expected level is 0.-0.mmol/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. u u 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. OPTIFAST VLCD Guidelines for Diabetes

6 Type 1 Diabetes & OPTIFAST VLCD Case study Tara is a recently married year old woman with T1DM for 10 years complicated by mild non-proliferative retinopathy and microalbuminuria. She weighs 100kg, has a BMI of 0kg/m and has slowly continued to gain weight at about kg per year since adolescence. Her HbA1c is generally between -9% and she is on a basal bolus regimen using around 10 units of insulin daily (0 units long acting and 0 units short acting with each meal). She has moderate hypoglycaemic levels (low s) 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 x 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 00 rule she starts with a ratio of.1. She tries the Berry Crunch Bar, which contains 0.g carbohydrate and takes units of short acting insulin, which is about a ¼ of her usual meal time dose. She does a blood glucose check 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 units of her short acting insulin and has a better post prandial glucose level. She then supplements meals a day while trialling a range of the OPTIFAST VLCD products to see what she likes best. She finds that her dose is - 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 0 to 0 units. After finding that she is stable on this she decides to embark on the Intensive Phase of OPTIFAST VLCD with meal replacements. She reduces her long acting insulin to 0 units (1/ her initial dose) and continues with units of short acting with each supplement. She does additional monitoring before and hrs 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.-10 with no hypoglycaemia. She checks her ketone level for interest and it is 0.mmol/L. Routine blood tests at this time demonstrate normal renal function and no electrolyte disturbance. After weeks she has lost kg and due to borderline hypoglycaemia reduces her insulin dose further. She is able to continue the Intensive Phase for 1 weeks by which time she has lost 0kg. Her ability to do more physical activity increases and she feels happier with her life. Her HbA1c has dropped to.% and she is now normoalbuminuric. Her doses are units long acting, and - units short acting with meals. She relaxes to meal replacements and 1 low carbohydrate meal daily and continues for a further weeks, reducing her weight to kg. 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 0kg she would re-commence the Intensive Phase of the OPTIFAST VLCD Program. OPTIFAST VLCD Guidelines for Diabetes

7 Type Diabetes & OPTIFAST VLCD Main points: u Type Diabetes (TDM) is a common association with obesity. Perpetuating factors common to both of these conditions should be the focus in patients with TDM. 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 TDM. u Use of VLCD, such as OPTIFAST VLCD, is a well established method of weight loss in TDM. 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 TDM 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- 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. OPTIFAST VLCD Guidelines for Diabetes

8 Type Diabetes & OPTIFAST VLCD Review of the evidence: uuin Australia, while other metabolic risks such as blood pressure and total cholesterol have decreased, BMI and mean fasting glucose have increased. In 00 the estimated prevalence of obesity in Australia was over %. Obesity compounds the cardiovascular risk of diabetes and is a major risk factor for TDM, accounting for about 0% of cases of TDM, with about 0% of people with TDM being obese. 9 uuin a recent important trial looking at the impact of lifestyle intervention, the Look AHEAD trial had 000 middle aged participants with TDM and BMI > kg/m. In addition to other lifestyle measures the caloric intake was restricted to approximately kCal/d, which included the option for OPTIFAST VLCD meal replacement to achieve this. Patients were randomised to interventional lifestyle therapy or standard therapy for years and monitored for up to 11 years. After year an % weight loss was associated with better measures of glycaemia and other metabolic risk factors including blood pressure and dyslipidaemia. 10 uuindependent 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. 1 uuin clinical practice it is evident that a large subset of TDM 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 1 otherwise well subjects with TDM showed about 0% responding to a very low caloric intake (<0kCal/d) and achieving a sustained acceptable reduction in blood sugar level (<10mmol/L). A positive response was predicted by a good response on day of the diet. Other predictors of response were a shorter duration of diabetes and higher fasting serum insulin. 1 uua 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 satiety 1. 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. 1 uua number of small studies have shown significant benefits of VLCDs on glycaemic control in TDM. 1 A study using a VLCD for weeks and tapering with a low calorie diet for weeks showed a significant improvement in HbA1c related to the degree of weight loss, with a >1% weight loss contributing to a lowering of HbA1c by about %. 1 uumost international guidelines on diabetes management recommend weight loss with calorie restriction. 1 Recommendation for the use of VLCDs over other diets is limited by the lack of long term efficacy data. 1 However, there are no studies indicating long term safety concerns. uuthe 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 0 day VLCD in 1 TDM patients in which a sustained 1 month improvement in glycaemia and other metabolic parameters was seen, even in those patients who regained body weight. 0 uuthe 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, 1 with cautious use of VLCDs and regular monitoring of renal function, especially initially. Footnotes WHO Noncommunicable Disease Country Profiles whqlibdoc.who.int/publications/011/9910_eng.pdf 9 Obesity & type Diabetes. Maggio CA, Pi-Sunyer FX. Endocrinology and Metabolism Clinics of North America [00, ():0-, viii]. 10 Wing RR. Long-term effects of a life- style intervention on weight and cardio- vascular risk factors in individuals with type diabetes mellitus: four-year results of the Look AHEAD trial. Arch Intern Med. 010;10: Importance of weight management in type diabetes: review with meta-analysis of clinical studies. Anderson et al. Journal of the American College of Nutrition, Vol., No., 1 9 (00). 1 Reversal of type Diabetes: normalisation of beta cell function in association with decreased pancreas and liver triacylglycerol. Lim et al. Diabetologia (011) : Jazet et al. 00 Diabetes UK. Diabetic Medicine,,. 1 Effect of weight loss and ketosis on postprandial cholecystokinin and free fatty acid concentrations. Delbridge et al, Am J Clin Nutr 00;:1-. 1 Baker, S., Jerums, G. & Proietto, J., 009. Effects and clinical potential of very-low-calorie diets (VLCDs) in type diabetes. Diabetes Research and Clinical Practice, (), pp.. 1 Wing, R.R., Effects of a Very-Low-Calorie Diet on Long-term Glycemic Control in Obese Type Diabetic Subjects. Archives of Internal Medicine, 11(), p.1. 1 Diabetes Care. Executive summary Nield et al. Cochrane Review. Dietary advice for treatment of type diabetes mellitus in adults (Review). 19 ACCORD Study Group. 00 Effect of intensive glucose lowering in type diabetes. NEJM ():-9. 0 Jazet, I.M. & de Craen, A.J., Sustained beneficial metabolic effects 1 months after a 0-day very low calorie diet in severely obese, insulin-treated patients with type diabetes. Diabetes research ClinicalTrials.gov identifier: NCT OPTIFAST VLCD Guidelines for Diabetes

9 Type Diabetes & OPTIFAST VLCD Recommendations for management: uuuse of OPTIFAST VLCD Intensive Phase is often initiated prior to bariatric surgery in obese TDM patients (as well as those without TDM) 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. uuobese 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. uumany 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- 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- weeks of initiating OPTIFAST VLCD. uuobese patients with TDM 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. uuobese patients with more severe complications such as proteinuria>1g/d, egfr <0 or risk of fluid balance complications need to be carefully monitored (creatinine, egfr, electrolytes, nutritional markers, nitrogen balance) if considered for VLCD management. uuthe initial approach is to use an Intensive Phase to induce weight loss to a predetermined target. In terms of glycaemic control, -10% weight loss may provide significant benefits. uupatients 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. uuunless 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. uuon 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 meals are replaced with OPTIFAST VLCD, the bolus dose may only need to be reduced or withheld prior to these meals. uupatients 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. uuantihypertensive 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. u u VLCD is not recommended in diabetes with normal or low weight, or diabetes associated with pregnancy or cystic fibrosis related diabetes. OPTIFAST VLCD Guidelines for Diabetes

10 Type Diabetes & OPTIFAST VLCD Case study Erica has had TDM for years with associated obesity, complicated by hypertension, dyslipidaemia, macroalbuminuria (0.g/d) with stage III chronic kidney disease (egfr around ml/min/1.m ) 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 0 units BD. Her HbA1c has improved to.% but she has gained 10 kg and her BMI is now 0kg/m. 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 0 units nocte, and is able to achieve target blood glucose readings. With increasing weight reduction, her glucose levels start to fall to - mmol/l and her insulin dose is progressively reduced so that by the time she has been on the VLCD for weeks she is no longer requiring any insulin. Her blood pressure also falls and she stops the calcium channel blocker. After having been on the VLCD for 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 1 kg so that her BMI is now kg/m. 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- meals daily. 9 OPTIFAST VLCD Guidelines for Diabetes

11 Medications used in Type Diabetes Table 1: Medications used in Type 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 <0 or unstable renal function. Sulphonylureas Increases. Risk of hypoglycaemia if dose not adjusted. Increases insulin secretion (obesogenic). Glitazones Increases. VLCD may potentiate the risk of reduction in bone mineral density with this agent. Acarbose Modest loss or neutral. Unlikely to be additional benefit due to low carbohydrate intake on VLCD. DPP-IV Inhibitors Modest loss or neutral. May exacerbate gastrointestinal discomfort. Avoid if patient at high risk of pancreatitis. GLP-1 Analogues Moderate loss. May exacerbate gastrointestinal discomfort. Avoid if patient at high risk of pancreatitis. May allow control of glycaemia. May allow control of glycaemia. May allow control of glycaemia. May be of benefit in non-replacement meals or maintenance phases. May assist with adherence to VLCD. May assist with adherence to VLCD. INSULIN AGENTS Basal Increases. Risk of hypoglycaemia. Reduction in dose more likely if on Intensive Phase. Mixed Insulin Increases. Risk of hypoglycaemia. Reduce dose if taken with time of supplement. Basal Bolus Increases. Risk of hypoglycaemia. Usually a reduction in dose of both basal and bolus component is required. May allow control of glycaemia. Use of supplement at non insulin meal may allow better glycaemic control. May allow control of glycaemia OPTIFAST VLCD Guidelines for Diabetes 10

12 1pk 1pk CLINICALLY FREE ONLINE SUPPORT BALANCED PROGRAM PROVEN PROGRAM Free Online Support Free Online Support 1pk 1pk CLINICALLY Free Online Support FREE ONLINE SUPPORT BALANCED PROGRAM PROVEN PROGRAM 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. OPTIFAST VLCD is a Food for Special Medical Purposes for the dietary management of obesity and must be used under medical supervision. Reg. Trademark of Société des Produits Nestlé S.A. Nestlé Healthcare Nutrition, a division of Nestlé Australia Ltd, 0 Howleys Road, Notting Hill VIC 1, Australia Nicholls Lane, Parnell, Auckland, New Zealand For more information visit optifast.com.au For healthcare professional use only.