ࡱ> q` ;bjbjqPqP .>::W"."#`vvvvQJ """""""K%h'h"]QQ"vvQ#...vv"."..  v  0 d g#0# (2(4  ( 4,.i9""$ #"""$Fd"""F"""  FROM ACADEMIC GUIDELINES TO CLINICAL CARE A WORKING DRAFT ON PRACTICAL GUIDELINES FOR THE MANAGEMENT OF THE METABOLIC SYNDROME: AN INDIAN SCENARIO Section 1 DIAGNOSIS The Metabolic Syndrome is a cluster or collection of risk factors which predispose a person to Type 2 diabetes mellitus (T2DM) and/or cardiovascular disease (ASCVD). The clinical utility of the syndrome for risk assessment lies in its ability to readily identify individuals who are at a relatively high, long-term risk for both ASCVD and T2DM. All such individuals should undergo absolute risk assessment to determine whether they are candidates for preventive drug therapies. But once found to have the metabolic syndrome, they deserve more intensive intervention with lifestyle approaches even in the absence of pharmaceutical interventions. There are two sets of diagnostic criteria which are in general use: the International Diabetes Federation (IDF) criteria and the American heart Association (AHA)/ National Heart, Lung, and Blood Institute (NHLBI) (updated ATP-III) definition. IDF clinical criteria for metabolic syndrome  AHA/NHLBI diagnostic criteria for metabolic syndrome  Measure (central obesity sine qua non plus any two of four other criteria constitute a diagnosis of metabolic syndrome) Categorical cut points Measure (any three of the five criteria below constitute a diagnosis of metabolic syndrome) Categorical cut points  Central obesity Waist circumference ethnic specific ( INCLUDEPICTURE "D:\\MS Grundy\\Diagnosis and Management of the Metabolic Syndrome An American Heart Association-National Heart, Lung, and Blood Institute Scientific Statement -- Grundy et al_ 112 (17) 2735 -- Circulation_files\\ge.gif" \* MERGEFORMATINET 90 cm for men and  INCLUDEPICTURE "D:\\MS Grundy\\Diagnosis and Management of the Metabolic Syndrome An American Heart Association-National Heart, Lung, and Blood Institute Scientific Statement -- Grundy et al_ 112 (17) 2735 -- Circulation_files\\ge.gif" \* MERGEFORMATINET 80 cm for women) for Indian subjects Elevated waist circumference General U.S. population:  INCLUDEPICTURE "http://care.diabetesjournals.org/math/ge.gif" \* MERGEFORMATINET 102 cm ( INCLUDEPICTURE "http://care.diabetesjournals.org/math/ge.gif" \* MERGEFORMATINET 40 in) in men,  INCLUDEPICTURE "http://care.diabetesjournals.org/math/ge.gif" \* MERGEFORMATINET 88 cm ( INCLUDEPICTURE "http://care.diabetesjournals.org/math/ge.gif" \* MERGEFORMATINET 35 in) in women; lower cut points for insulin-resistant individuals or ethnic groups (based on clinical judgment) Raised triglycerides >150 mg/dl (1.7 mmol/l) or on specific treatment for this lipid disorder Elevated triglycerides  INCLUDEPICTURE "http://care.diabetesjournals.org/math/ge.gif" \* MERGEFORMATINET 150 mg/dl (1.7 mmol/l) or on drug treatment for elevated triglycerides Reduced HDL cholesterol <40 mg/dl (1.0 mmol/l) in men, <50 mg/dl (1.3 mmol/l) in women or on specific treatment for reduced HDL-C Reduced HDL cholesterol <40 mg/dl (1.0 mmol/l) in men, <50 mg/dl (1.3 mmol/l) in women or on specific treatment for reduced HDL-C Raised blood pressure  INCLUDEPICTURE "http://care.diabetesjournals.org/math/ge.gif" \* MERGEFORMATINET 130 mmHg systolic blood pressure or  INCLUDEPICTURE "http://care.diabetesjournals.org/math/ge.gif" \* MERGEFORMATINET 85 mmHg diastolic blood pressure or on treatment for previously diagnosed hypertension Elevated blood pressure  INCLUDEPICTURE "http://care.diabetesjournals.org/math/ge.gif" \* MERGEFORMATINET 130 mmHg systolic blood pressure or  INCLUDEPICTURE "http://care.diabetesjournals.org/math/ge.gif" \* MERGEFORMATINET 85 mmHg diastolic blood pressure or on drug treatment for previously diagnosed hypertension Elevated fasting plasma glucose Fasting plasma glucose  INCLUDEPICTURE "http://care.diabetesjournals.org/math/ge.gif" \* MERGEFORMATINET 100 mg/dl (5.6 mmol/l) or on treatment for previously diagnosed type 2 diabetes Elevated fasting plasma glucose  INCLUDEPICTURE "http://care.diabetesjournals.org/math/ge.gif" \* MERGEFORMATINET 100 mg/dl (5.6 mmol/l) or or on treatment for previously diagnosed type 2 diabetes  Table 1. Diagnostic criteria for metabolic syndrome from the International Diabetes Federation (IDF) definition and the American Heart Association (AHA)/National Heart, Lung, and Blood Institute (NHLBI) ( updated ATP-III) definition. It is obvious that the IDF and the AHA/NHLBI (updated ATP-III) definitions are almost similar in most respects. One obvious difference is an essential requirement in the IDF definition for the presence of central obesity as judged by the waist circumference, whilst this is only one of the five criteria in the updated ATP-III definition. The other major difference is the ethnic specific waist circumference in the ATP definition whilst the updated ATP-III definition still asks for a relatively higher waist circumference ( INCLUDEPICTURE "D:\\MS Grundy\\Diagnosis and Management of the Metabolic Syndrome An American Heart Association-National Heart, Lung, and Blood Institute Scientific Statement -- Grundy et al_ 112 (17) 2735 -- Circulation_files\\ge.gif" \* MERGEFORMATINET 102 cm for men and  INCLUDEPICTURE "D:\\MS Grundy\\Diagnosis and Management of the Metabolic Syndrome An American Heart Association-National Heart, Lung, and Blood Institute Scientific Statement -- Grundy et al_ 112 (17) 2735 -- Circulation_files\\ge.gif" \* MERGEFORMATINET 88 cm for women). This is understandable as this definition was essentially U.S. population centric and based on the National Institute of Health Clinical Guidelines. The need for ethnic and nation specific norms has now been accepted by the NHLBI and efforts are on to crease out any differences between the two definitions. Thus, soon one would have a harmonized criteria for the diagnosis of the metabolic syndrome. Section 2 LIFESTYLE MANAGEMENT Presently, no specific drugs are available to manage the metabolic syndrome. Lifestyle changes are the best options to prevent the metabolic syndrome or to manage a person diagnosed as having the metabolic syndrome. Thus, lifestyle changes not only offer the best universal beneficial options for the metabolic syndrome, but they also go a long way in managing and /or reducing the long term consequences of the presence of major risk factors which predispose a person to ASCVD. Although the presence of some of these risk factors may need additional specific drug therapies, lifestyle changes still continue to be central to their treatment. Diet In order to ensure compliance, the prescribed diet should be individualised. It must be realistic, flexible, and take into consideration the patients likes and dislikes, to as large an extent as possible, and must suit the patients life style. It is important to educate the patient about the basic requirements of the diet and judge compliance at regular intervals. BASIC DIET ADVICE Acceptable Body Weight The aim is to attain acceptable body weight with a special emphasis on attaining the desired waist measurement. Other specific changes would be necessary depending on the presence of associated risk factors such as impaired glycemia or diabetes, hypertension, dyslipidemias etc. Aim initially at slow reduction of 7% to 10% from baseline weight over one year of management. Even small amounts of weight loss are associated with significant health benefits. Continue weight loss thereafter to extent possible with goal to ultimately achieve desirable weight Effective weight loss requires a combination of caloric restriction, physical activity, and motivation; effective lifelong maintenance of weight loss essentially requires a balance between caloric intake and physical activity and the maintenance of sufficient skeletal muscle mass/quality. After 6 months, the rate of weight loss usually declines and weight plateaus because of a lesser energy expenditure at the lower weight and the lifestyle prescription may need to be revised. Experience reveals that lost weight usually will be regained unless a weight maintenance program consisting of dietary therapy, physical activity, and behavior therapy is continued indefinitely. CARBOHYDRATES The widespread misconception that carbohydrates (in any form) should not be eaten by people with diabetes should be removed. Carbohydrates in the form of simple sugars need restriction. The carbohydrates should be in the form of complex polysaccharides (starch) and contain adequate amount of digestible fibers. Carbohydrates should constitute around 60-70% of the total calories which is usually found in traditional diets eaten in various parts of India. Very high carbohydrate intakes and/or high glycaemic index foods can exacerbate the dyslipidemia, including hypertriglyceridemia, of the metabolic syndrome, especially if the overall calory intake is very high. In addition, there should be ample intakes of fresh fruits and vegetables, and whole grains; fruits and vegetables are recommended to provide fiber, vitamins, minerals and hydration, and to increase satiety through the volume of food ingested, in order to avoid feelings of deprivation and restriction. PROTEINS Protein intake should be approx. 0.8 gms/kg ideal body weight; this usually comprises around 12-18% of the calorie intake. The requirements for proteins may be increased in catabolic states, pregnancy, lactation and in some elderly patients. This should be preferably taken from natural sources rather than commercially available protein supplements as far as is possible. Protein intake may need to be restricted in patients with nephropathy. FATS Fats should be restricted to around 20-25% of the total calories. If the fat content exceeds 35%, it is difficult to sustain the low intakes of saturated fat required to maintain a low LDL-C. On the other hand, if the total fat content falls below 25%, triglycerides can rise and HDL-C levels can decline; thus, very-low-fat diets may paradoxically exacerbate atherogenic dyslipidemia. It is recommended that the saturated fat be <7% of total calories; reduce trans fat (< 1% based on WHO recommendations); dietary cholesterol <200 mg/dL; total fat 25% to 35% of total calories. Most dietary fat should be unsaturated; simple sugars should be limited. These goals can be achieved by (1) choosing lean meats and vegetable alternatives; (2) selecting fat-free (skim), 1%-fat, and low-fat dairy products; (3) minimizing intake of partially hydrogenated fats i.e. bakery products to decrease trans fatty acids; (4) avoid repeated reusing of the oil for cooking purposes (frying) purposes as this leads to a significant increase in the trans fatty content of the diet. Many foods contains fats; this invisible fat should be taken into account when estimating the total fat intake. On an average 40% of the fat intake is contributed by the invisible fat in a typical Indian diet. It is advisable to restrict the total intake of cooking fats to less than 6% of the total energy intake; in simple terms, food should be cooked in the least amount of oil or ghee; if feasible, food should be preferably be grilled, steamed or broiled, microwaved, rather than fried. The total intake of cholesterol should be restricted to around 300 mg per day. Egg yolks, organ meats, marine invertebrates (including molluscs, crab, shrimps and lobster) have a very high cholesterol content. The fat intake may need to be further modified if associated dyslipidemia is present. ESSENTIAL FATTY ACIDS Recent evidence suggests that attention must be paid to the intake of essential fatty acids (EFAs) such as omega-6 (w6) and omega-3 (w3) fatty acids. These EFAs must be derived from food as they cannot be synthesised in the body. Not only must they be eaten in adequate amounts, but the relative ratio (w6/w3) is around 5-10:1. Indian diets usually contain too much of w6 fatty acids and little, if any, of w3 fatty acids. Indian diets usually give a ratio of around 40:1. The disproportionate ratio is made worse by the use of the so called safe cooking oils such as safflower oil and sunflower oil, in which the ratio is around 150:1! Traditional cooking media like mustard oil, coconut oil and ghee have a poor content of w6 fatty acids allows a more optimal w6/w3 intake, but this has to be balanced with the relatively high saturated fat content. The other alternative is home scale blending of traditional cooking media with oils rich in w6 to lower the ratios, eg. simple blending of sunflower and mustard oil in 1:1 at home would bring down the ratio to approximately 7 as against 163 for sunflower alone The Omega-6 and Omega-3 content of the commonly used edible oils:  Omega - 6 Omega - 3 W6 / W3 Sunflower 49 0.3 163 Safflower 73 0.5 146 Sesame 40 0.5 80 Corn 57 0.8 71 Groundnut 28 0.8 35 Ricebran 33 1.6 34.6 Palm 9 0.3 30 Soyabean 52 5 10.4 Olive oil 7 1 7 Rapeseed 22 10 2.2 Ghee (Cow) 1.6 0.5 3.2 Ghee Buffalo 2 0.9 2.2 Mustard / Rape 13 8.6 1.5 Coconut 1.8 -- -- Flaxseed 16 57  SALT INTAKE Salt restriction is necessary in patients with associated hypertension, cardiac failure and fluid overload. Reduce sodium intake to no more than 100 meq/day (2.4 g of sodium or 6 g of sodium chloride / one teaspoon a day) FRUITS These can be eaten by people with diabetes in moderate amounts. Ripe and very sweet fruits are better avoided. Raw and partially ripe fruits and citrus fruits are preferable. ALCOHOL If consumed, alcohol should be used in moderation. Limit alcohol intake to no more than 1 oz (30 ml) of ethanol (eg, 24 oz [720 ml] of beer, 10 oz [300 ml] of wine, or 2 oz [60 ml] of 100-proof whiskey) per day or 0.5 oz (15 ml) of ethanol per day for women and lighter-weight people. It should be avoided in all diabetics who are severely obese and on a significantly hypocaloric diet, in those who have high triglyceride levels. All other contraindications to alcohol intake also apply to diabetics. INTERESTINGLY, OUR TRADITIONAL INDIAN DIETS, WITH SLIGHT MODIFICATION, ARE CLOSE TO WHAT IS NOW CONSIDERED IDEAL DIETS! PATIENTS DO NOT HAVE TO MAKE ANY MAJOR CHANGES TO THEIR USUAL DIETARY HABITS, WITH THE EXCEPTION OF AVOIDING SIMPLE SUGARS, CUTTING DOWN ON THE SALT AND ADJUSTING THE FAT INTAKE. THIS ALLOWS INCREASING COMPLIANCE WITH THE DIET ADVISE! Section 3 PHYSICAL ACTIVITY AND EXERCISE Increased daily routine physical activity and regular exercise is recommended as an important component of all lifestyle management regimens to prevent and manage the metabolic syndrome as well as all diabetes management regimens. Increasing physical activity assists in weight reduction, reduces insulin resistance, has beneficial effects on metabolic risk factors; and importantly, it reduces overall ASCVD risk beyond that provided by weight reduction alone. It is however being increasingly recognized, that exercise programs carried out without adequate precautions, do carry some risks as well. The potential adverse effects can be on the cardiovascular as well as on the musculoskeletal systems. Incautiously carried out severe exercise, may predispose patients undergoing drug therapy for diabetes to unexpected hypoglycemia, and also, exacerbate existing diabetic complications leading to retinal bleeds and significant increase in renal dysfunction. These risks can be minimised with pre-exercise screening, individualised exercise programme prescription, careful monitoring and patient education. These risks can be minimised with pre-exercise screening, individualised exercise programme prescription, careful monitoring and patient education. PRE-EXERCISE EVALUATION All patients should undergo a complete history and examination to identify cardiac, macro/microvascular and neurologic complications. The extent of investigations would dependent on the risk level of the patient and would need to be individualised. Exercise should not be prescribed to patients with very high blood glucose, and those in ketosis, unless treated adequately. Patients with significantly retinopathy and renal dysfunction may also need to undergo specific treatment before embarking on an exercise program. Patients with foot infections should avoid exercise until adequately treated. Patients with cardiovascular abnormalities and/or uncontrolled hypertension should not undertake exercise unless this is in close consultation with cardiologist. TYPE OF EXERCISE The exercise should be aerobic and isotonic. Although the patient may be allowed to choose his own form of exercise, walking would appear to be the most appropriate, and safe, exercise for most patients. Isometric exercises, such as weight lifting, etc., are not recommended for most patients although they warrant consideration when total skeletal muscle mass needs to be increased. Patients should be encouraged to increase "every day" activities such as taking the stairs instead of the elevator. FREQUENCY AND DURATION Regular moderate-intensity physical activity; at least 30 min of continuous or intermittent (and preferably  INCLUDEPICTURE "http://circ.ahajournals.org/math/ge.gif" \* MERGEFORMATINET 60 min) 5 d/wk, but preferably daily, with a five minute warm up and a five minute cooling off period. The duration and frequency may be adjusted to individual needs. INTENSITY The intensity of the exercise needs to be individualised. For most patients, exercise should be initiated slowly, and the intensity should be increased gradually. The exercise can be done all at one time or intermittently over the day. Initial activities may be walking or swimming at a slow pace. The patient can start by walking 30 minutes for 3 days a week and can build to 60 minutes of more intense walking at least 5 days a week, preferably daily. Before more strenuous exercise, a warm-up period of 5 minutes of stretching and other gentle activity is advised, as is a final cool-down period of progressively decreasing vigor. The intensity of the exercise should be increased gradually. Intensity is usually measured in terms of the percentage of the patients maximum heart rate (MHR). Initial exercise should be at a reduced intensity which should be at a reduced intensity which should then be increased to reach about 60-70% of the MHR. (MHR = 220 age of the patient). Limiting the intensity of the exercise such that the systolic blood pressure does not exceed 180 mm Hg would seem prudent. Any patient undergoing an exercise program, who complains of any signs or symptoms which would have contraindicated such a program initially, should discontinue the program, and have a detailed re-evaluation before restarting the exercise regimen. When the patient does start the exercise program again, the intensity should be such as if the patient were beginning the exercise program anew. The exercise program should never be restarted at the intensity at which it was discontinued. An excellent parameter to judge, is that the patient should be able to carry out a normal conversation whilst exercising, without getting unduly breathless. Table on Calories spent on various activities and sports TABLE ACTIVITY CALORIES Spent per minute.Lying down, sleeping, sitting, Standing, strolling (1 mile per hour) playing cards, knitting, sewing, darning, desk work, car driving, electric typing, using calculators, etc.  1 to 1.25Level walking (2 miles per hour), level bicycling (5 m.p.h.), horse-backriding (walking speed), playing musical instruments like the piano, playing billiards and snooker, golf using a power cart to move around, manual typing, bartending, auto, T.V. and radio repair. 2.5 to 4 Walking at 3 m.p.h., cycling at 6 m.p.h. Volleyball ( 6 man noncompetitive). Horse riding 9 sitting to trot), playing golf with lugging around the golf bag, sailing (handling small boats), badmintion (social doubles), cleaning windows, energetic musician. 4 to 5Walking at 3.5 m.p.h., cycling at 8 m.p.h.. table tennis, golf (carrying clubs), dancing (at a pace of a dance like the foxtrot), Badminton (social singles), tennis (social doubles), any callisthenics, painting walls, light carpentry (hobby); 5 to 6Walking at 4 m.p.h., cycling at 10 m.p.h., roller skating, horse riding (trot), gardening (digging); 6 to 7Walking at 5m.p.h., cycling at 11 m.p.h., badminton (competitive), tennis (social singles), light downhill skiing, water skiing; 7 to 8Logging at 5 m.p.h., cycling at 12 m.p.h., basketball, vigorous downhill skiing, carrying loads of around of 36 kgs; 8 to 10Running at 5.5 m.p.h., cycling at 13 m.p.h., playing squash (social level), handball (social level), vigorous game of basketball; 10 to 11 NOTE: The calories given above are basically for a person weighing around 70 kg. People who weight less than this may spend relatively less calories in carrying out similar activities whilst who are more than this weight spend that much more calories. There may also be a gender difference.  Section 4 OBESITY Obesity, especially central, visceral, "truncal, android (i.e. abdominal) is a major (AHA/NHLBI) or sine qua non (IDF) criteria for the diagnosis of the Metabolic Syndrome. Whilst its presence is an absolute requirement for the diagnosis of the metabolic syndrome as per the IDF guidelines, it is only one out of five criteria, the presence of any three of which leads to a diagnosis of the metabolic syndrome as per the modified ATP-III guidelines. Atherosclerosis is now considered in part to be a consequence of chronic low-grade inflammation and inflammation is an important feature of plaque initiation, progression, and thrombosis. Along with the traditional risk factors, it is these inflammatory adipokines which play a key role in initiating the process and progression of endothelial dysfunction and atheroma formation in the arteries leading to an increased risk and severity of cardiovascular disease. Inflammation is also considered to play an important role in leading to T2DM. Abdominal obesity, due to intra-abdominal adiposity, drives the progression of multiple cardiometabolic risk factors independently of body mass index. This occurs both through altered secretion of adipocyte-derived biologically active substances (adipokines), including free fatty acids, adiponectin, interleukin-6, tumour necrosis factor alpha, and plasminogen activator inhibitor-1, and through exacerbation of insulin resistance and associated cardiometabolic risk factors. Metabolic and Cardiovascular Risk Factors Associated With Visceral Obesity Raised blood pressure ( systolic and /or diatolic) Increased levels of insulin resistance / hyperinsulinemia Atherogenic dyslipidemia Raised levels of LDL-C and apo-B Endothelial dysfunction Increased prothomboitic and procoagulant state Raised pro-inflammatory status Decrease in levels of antiatherogenic levels of adiponectin Premature atherosclerosis ( leading to early onset CHD and stroke) Raised levels of serum uric acid Sleep apnoea syndrome and related Polycystic ovary syndrome Microalbuminuria is an integral component of the cardiometabolic syndrome, and patients with this syndrome have a propensity to develop type 2 diabetes.  At the same time, generalized obesity is also associated with many other disorders and increases to the morbidity as well as even mortality associated with these disorders. Thus, the management strategy has to be a decrease in all obesity, but special attention must be paid to reducing the abdominal obesity. OPTIMAL WEIGHT Generalised obesity is best measured by estimation of the Body Mass Index (BMI) Body Mass Index (BMI) Weight in Kg BMI = ------------------------- Height in meters2 Normal: 20-23; > 23-25 = Overweight; > 25 = Obese Care must be taken that the weight is not decreased below the lower limits, as a BMI of 18.5 signifies low body weight. Waist Measurements Central or visceral obesity is best measured by the waist circumference MEASUREMENT OF THE WAIST CIRCUMFERENCE To measure waist circumference, locate the top of the right iliac crest. Place a measuring tape in a horizontal plane around the abdomen at the level of the iliac crest. Before reading the tape measure, ensure that tape is snug but does not compress the skin and is parallel to the floor. Measurement is made at the end of a normal expiration. A waist measurement of <90cms for men and =23 kg per m2 or significantly increased waist circumference. Avoid use of drugs without accompanying lifestyle modification. Avoid medications which are known to be associated with weight gain. Medications with weight gain as a side effect. These medications should preferably not be used if weight loss is the aim. Moroever, some of these medications lead to lethargy and drowsiness and may make increased physical activity difficult. Some of these medications are given in Table. MedicationsAntidepressantsSerotonin reuptake inhibitors, tricyclic antidepressants, monamine oxidase inhibitors, eg., amitryptiline, imipramine, doxepin, desipramine, trazodone, lithium, etc., Antiepileptics:valproate, carabamazepine, gabapentin, lithium AntipsychoticsAtypical neuroleptic agents: clozapine, olanzapine, risperidone etc., Steroids and other hormonesEstrogens, progesterone, hormonal contraceptives, corticosteroidsDiabetes medicationsInsulin, sulfonylureas, glitazonesAntihypertensive Agents- and -adrenergic receptor blockersSerotonin and histamine inhibitors NOTE: This is not a complete list. Anti-Obesity Drugs The two drugs which are presently available and most commonly used weight reducers are Orlistat and Sibutramine. Characteristics of the Commonly used Antiobesity Medications CharacteristicSibutramineOrlistatIndicated for long-term treatmentYesYesSpecial instructionsBlood pressure monitoring is required before and during therapyPatients must take a multivitamin supplement (2h before a dose). No dose should be taken if a meal is missed or contains no fatAdverse effectsHypertension, tachycardia, dry mouth, anorexia, insomnia, constipationAbdominal pain, oily spotting, fecal urgency, flatulence with discharge, fatty stools, fecal incontinence, increased defecation, increased urinary oxalateContraindications[a]Severe hypertension or poorly controlled hypertension, heart failure, coronary artery disease, arrhythmias, or strokeMalabsorption syndrome and cholestasis. Use with caution in patients with history of nephrolithiasis.Drug-drug interactionsMonoamine oxidase inhibitors, selective serotonin-reuptake inhibitors, drugs that increase blood pressure or heart rate, ketoconazole[b] , erythromycin[b]Fat-soluble vitamins, beta-carotene, and possibly cyclosporineUse with cautionHistory of hypertension, seizures, narrow angle glaucomaHistory of hyperoxaluria or calcium oxalate nephrolithiasisPatient instructionsTake once daily in the mornings. Have blood pressure and pulse checked regularly.Take one capsule t.id. with each meal. If meal is missed or contains no fat, then dose can be skipped. Take a multivitamin daily 2 hr before or after dose. Comply with a low-fat diet. aNone of these medications should be used in patients with a history of anorexia nervosa or bulimia.bInteractions do not appear to be clinically significant. Metformin Metformin was used in the past as a weight reducing agent even in people with normal glucose levels. But its use has decreased with the availability of sibutramine and orlistat. With the increasing awareness of the critical role played by insulin resistance, which leads to many disorders such as Polycystic Ovary Syndrome (PCOS), etc., as well as being a serious risk factor for diabetes and premature cardiovascular disease, its use especially in patients with impaired glucose tolerance, and this is especially so in patients with a family history of diabetes and premature cardiovascular disease. Rimonabant Many trials have shown that a 20 mg dose of rimobanant, which is used in the management of obese diabetics, can lead to an average weight loss of approximately 6 kg over a year when accompanied with lifestyle therapies. Importantly, it leads to a decrease in abdominal obesity and improves cardiovascular risk factors. The most common reported side effects include depression, anxiety, and nausea and should not be used in patients on anti-depressives. It is NOT accepted for use by the U.S. FDA. Incretins GLP-1 analogues have been shown to be associated with weight loss, although the DPP-IV inhibitors are weight neutral. Glitazones The glitazones tend to increase the weight. But it is now being increasingly realized that whilst the glitazones may slightly increase the fat levels in the body, they very significantly decrease the levels of central or visceral obesity. At the same time questions have been raised about the cardiovascular safety of rosiglitazone and it remains to be seen whether this is a class effect and applies to pioglitazone as well. Other drugs including sympathomimetics are now rarely used. Other Drugs Although some other drugs such as bupropion and topiramate are being pushed as agents to use in obesity, but are not widely accepted as antiobesity drugs. Phentermine by itself continues to be occasionally used. Drugs such as fenfluramine, ephedra and phenylpropanolamine should NEVER be used. One has to be very careful as many OTC drugs and herbal products contain them or similar agents and can be dangerous in the long term. Surgery Weight loss surgery is an option in carefully selected patients with clinically severe obesity with comorbid conditions when less invasive methods have failed and the patient is at high risk for obesity-related morbidity and mortality. BMI Charts  INCLUDEPICTURE "http://www.utdol.com/data/images/endo_pix/determ2.gif" \* MERGEFORMATINET   INCLUDEPICTURE "http://www.utdol.com/data/images/endo_pix/determ3.gif" \* MERGEFORMATINET  Section 5 DYSLIPIDEMIAS Dyslipidemias are a key risk factor in people with the metabolic syndrome and contribute significantly towards the long term risk for premature and accelerated atherosclerosis. Lipid disorders are also seen in many people with diabetes and are a major factor in the microvascular and especially in the macrovascular diabetic complications. The dyslipidemias merit rigorous and aggressive correction. The major dyslipidemias are: 1) Increased levels of low density lipoprotein cholesterol (LDL-C) 2) Atherogenic dyslipidaemia describes a combination of Increased serum triglycerides (TG); Increased VLDL particle number; Increased levels of small dense LDL-C particles; Increased levels of apolipoprotein B (ApoB); (The increased number of VLDL and LDL particles accounts for the increased level of total apo B). Decreased levels of HDL-C particles, All of these are atherogenic by themselves, but their atherogenicity is significantly increased when present in combination. Athergenic dyslipidemia is commonly observed in patients with both type 2 diabetes and the metabolic syndrome. A simple strategy for assessing the sum of atherogenic particles is measurement of either LDL+VLDL cholesterol (non-HDL cholesterol) or total apo B. In persons with metabolic syndrome and atherogenic dyslipidemia, both LDL+VLDL cholesterol and total apo B typically are elevated. These measurements should be used increasingly both in risk assessment and as targets of therapy in persons with the metabolic syndrome. A low HDL level is another characteristic of atherogenic dyslipidemia. As a risk predictor, a low HDL rivals an elevated total apo B (or VLDL+LDL cholesterol). Although HDL may be directly antiatherogenic, the presence of a low HDL level carries strong predictive power for development of ASCVD. Target Levels The latest recommendations state that in adults with diabetes, the optimal LDL-C level is less than 100 mg/dl (in patients with additional risks, the target has been brought down to 70mg/dl; High-risk patients are those with established ASCVD, diabetes, or 10-year risk for coronary heart disease >20%. For cerebrovascular disease, high-risk condition includes transient ischemic attack or stroke of carotid origin or >50% carotid stenosis.) and the optimal HDL-C level is more than 40mg/dl in men and 50mg/dl in women; triglyceride levels should be less than 150 mg/dl;. MANAGEMENT According to ATP III, atherogenic dyslipidemia can become a target for lipid-lowering therapy after the goal for LDL-C has been attained. In other words, as long as LDL-C remains above goal level, LDL-C is the primary target of therapy even in the metabolic syndrome. Other lipid risk factors are secondary. The LDL-C goals depend on estimates of absolute risk. In patients with atherogenic dyslipidemia in whom serum triglyceride levels are  INCLUDEPICTURE "http://circ.ahajournals.org/math/ge.gif" \* MERGEFORMATINET 200 mg/dL, non-HDL-C becomes the next target of treatment after the LDL-C goal is reached. If the serum triglyceride levels are significantly raised (>500mg/dl), then lowering these levels should take precedence even over lowering the LDL-C values. Raising HDL-C becomes a tertiary aim. In practice, all the lipid abnormalities are managed together rather than in sequence. Lifestyle Changes Where only lipid levels are abnormal, lifestyle intervention should be undertaken first. Diet Beyond weight control and reduction of total calories, the diet should be low in saturated fats, trans fats, cholesterol, sodium, and simple sugars. HYPERLINK "http://circ.ahajournals.org/cgi/content/full/112/17/2735" \l "R149-169404#R149-169404"  In addition, there should be ample intakes of fruits, vegetables, and whole grains; Very high carbohydrate intakes can exacerbate the dyslipidemia of the metabolic syndrome. Diet therapy is important in optimizing lipid levels. Total fat intake should be restricted to 25-30% of total calorie intake. It is essential to take into account invisible fat in the food. Ensure correct essential fatty acid (EFA) intake, with near optimal omega 6 / omega 3 (w6/w3) ratio (5:1). Cooking oils should be a judicious mix of PUFAs, MUFAS and saturated fats; no one oils is beneficial; cooking oils should contribute <6% total energy intake. Many of these aspects have been discussed in detail in the section dealing with lifestyle changes. Exercise Increases in daily routine activities and a regular exercise regimen is necessary and must be encouraged. Many of these aspects have been discussed in detail in the section dealing with lifestyle changes. Importantly, Rigorous management of other associated disorders such as obesity, hypertension, impaired glycemia and diabetes. Smoking intake to be actively discouraged. Rule out other secondary causes of dyslipidemias DIET AND LIFESTYLE MODIFICATIONS SHOULD BE GIVEN AN ADEQUATE TRIAL BEFORE COMMENCING LIPID LOWERING DRUG THERAPY UNLESS THERE ARE DEFINITE INDICATIONS WHICH NECESSITATE IMMEDIATE STARTING OF THE DRUGS . DRUG THERAPY Drugs Affecting Lipoprotein Metabolism Drug ClassAgents and Daily DosesSide EffectsContraindicationsHMG CoA reductase inhibitors (statins)Lovastatin (20-80 mg), pravastatin (20-40 mg), simvastatin (20-80 mg), fluvastatin (20-80 mg), atorvastatin (10-80 mg) Rosuvastatin (10-40mg)Myopathy Increased liver enzymesAbsolute: Active or chronic liver disease Relative: Concomitant use of certain drugs*Bile acid sequestrantsCholestyramine (4-16 g) Colestipol (5-20 g) Colesevelam (2.6-3.8 g)GI distress Constipation Decreased absorption of other drugsAbsolute: Dysbeta-lipoproteinemia TG > 400 mg/dL Relative: TG > 200 mg/dLNicotinic acidImmediate release (crystalline) nicotinic acid (1.5-3 gm), Extended release nicotinic acid (1-2 g), Sustained-release nicotinic acid (1-2 g)Flushing Hyperglycemia Hyperuricemia (or gout) Upper GI distress HepatotoxicityAbsolute: Chronic liver disease Severe gout Relative: Diabetes Hyperuricemia Peptic ulcer diseaseFibric acidsGemfibrozil (600 mg twice a day) Fenofibrate (200 mg) Clofibrate (1000 mg twice a day)Dyspepsia Gallstones MyopathyAbsolute: Severe renal disease Severe hepatic disease * Some commonly used medications or consumption Fibrates (especially gemfibrozil, but other fibrates too) Nicotinic acid (rarely) Cyclosporine Azole antifungals Itraconazole and ketoconazole Macrolide antibiotics Erythromycin and clarithromycin HIV protease inhibitors Nefazodone (antidepressant) Verapamil Amiodarone Large quantities of grapefruit juice (usually more than 1 quart per day) Alcohol abuse (independently predisposes to myopathy)  NOTE: This does not represent a complete list. A practical approach to the pharmacologic treatment of lipid disorders  Abbreviations: LDL, Low-density lipoprotein; HDL, high-density lipoprotein; TG, triglyceride; TZDs, thiazolidinediones. In general, therapy is started with a statin although when triglycerides are  INCLUDEPICTURE "http://circ.ahajournals.org/math/ge.gif" \* MERGEFORMATINET 500 mg/dL, triglyceride-lowering drugs should be considered alongside to prevent the development of acute pancreatitis. Statins reduce all ApoB-containing lipoproteins and to achieve the LDL-C as well as for non-HDL-C goals. If non-HDL-C remains elevated after the LDL-C goal is reached: Increase the statin dose further. Statins lower both LDL-C and non-HDL-C and in addition, reduce risk for ASCVD events in patients with the metabolic syndrome. Add a fibrate and if necessary nicotinic acid to the statin. Both fibrates and nicotinic acid reduce non-HDL-C and reportedly decrease risk for ASCVD in patients with the metabolic syndrome/type 2 diabetes mellitus. If the Tg levels are relatively high, it may be better to start therapy with a statin and a fibrate. If the HDL-C levels are low,  HYPERLINK "http://circ.ahajournals.org/cgi/content/full/112/17/2735" \l "R163-169404#R163-169404"  HYPERLINK "http://circ.ahajournals.org/cgi/content/full/112/17/2735" \l "R164-169404#R164-169404" combining a fibrate or nicotinic acid with LDL-C-lowering treatment becomes an option.  HYPERLINK "http://circ.ahajournals.org/cgi/content/full/112/17/2735" \l "R166-169404#R166-169404"  Both fibrates and nicotinic acid raise HDL-C as well as reduce triglycerides and small LDL particles. Patients with IFG, IGT, or diabetes who are treated with nicotinic acid deserve careful monitoring for worsening of hyperglycemia. Lower doses of nicotinic acid lessen this risk. If a fibrate or nicotinic acid is used with a statin, higher doses of the statin generally should be avoided to minimize risks for myopathy or hepatic effects. Changes in Serum Lipid Values with Different Classes of lipid lowering drugs Drug class  Total cholesterol levels  LDL levels  HDL levels  Triglycerides  Bile acid binding resins INCLUDEPICTURE "D:\\LIP1\\Management of Dyslipidemia in Adults - May 1, 1998 - American Academy of Family Physicians_files\\down1.gif" \* MERGEFORMATINET 20% INCLUDEPICTURE "D:\\LIP1\\Management of Dyslipidemia in Adults - May 1, 1998 - American Academy of Family Physicians_files\\down1.gif" \* MERGEFORMATINET 10% to 20% INCLUDEPICTURE "D:\\LIP1\\Management of Dyslipidemia in Adults - May 1, 1998 - American Academy of Family Physicians_files\\up1.gif" \* MERGEFORMATINET 3% to 5%Neutral or  INCLUDEPICTURE "D:\\LIP1\\Management of Dyslipidemia in Adults - May 1, 1998 - American Academy of Family Physicians_files\\up1.gif" \* MERGEFORMATINET Nicotinic acid INCLUDEPICTURE "D:\\LIP1\\Management of Dyslipidemia in Adults - May 1, 1998 - American Academy of Family Physicians_files\\down1.gif" \* MERGEFORMATINET 25% INCLUDEPICTURE "D:\\LIP1\\Management of Dyslipidemia in Adults - May 1, 1998 - American Academy of Family Physicians_files\\down1.gif" \* MERGEFORMATINET 10% to 25% INCLUDEPICTURE "D:\\LIP1\\Management of Dyslipidemia in Adults - May 1, 1998 - American Academy of Family Physicians_files\\up1.gif" \* MERGEFORMATINET 15% to 35% INCLUDEPICTURE "D:\\LIP1\\Management of Dyslipidemia in Adults - May 1, 1998 - American Academy of Family Physicians_files\\down1.gif" \* MERGEFORMATINET 20% to 50%Fibric acid analogs  INCLUDEPICTURE "D:\\LIP1\\Management of Dyslipidemia in Adults - May 1, 1998 - American Academy of Family Physicians_files\\down1.gif" \* MERGEFORMATINET 15% INCLUDEPICTURE "D:\\LIP1\\Management of Dyslipidemia in Adults - May 1, 1998 - American Academy of Family Physicians_files\\down1.gif" \* MERGEFORMATINET 5% to 15% INCLUDEPICTURE "D:\\LIP1\\Management of Dyslipidemia in Adults - May 1, 1998 - American Academy of Family Physicians_files\\up1.gif" \* MERGEFORMATINET 14% to 20% INCLUDEPICTURE "D:\\LIP1\\Management of Dyslipidemia in Adults - May 1, 1998 - American Academy of Family Physicians_files\\down1.gif" \* MERGEFORMATINET 20% to 50%HMG-CoA reductase inhibitors INCLUDEPICTURE "D:\\LIP1\\Management of Dyslipidemia in Adults - May 1, 1998 - American Academy of Family Physicians_files\\down1.gif" \* MERGEFORMATINET 15% to 30% INCLUDEPICTURE "D:\\LIP1\\Management of Dyslipidemia in Adults - May 1, 1998 - American Academy of Family Physicians_files\\down1.gif" \* MERGEFORMATINET 20% to 60% INCLUDEPICTURE "D:\\LIP1\\Management of Dyslipidemia in Adults - May 1, 1998 - American Academy of Family Physicians_files\\up1.gif" \* MERGEFORMATINET 5% to 15% INCLUDEPICTURE "D:\\LIP1\\Management of Dyslipidemia in Adults - May 1, 1998 - American Academy of Family Physicians_files\\down1.gif" \* MERGEFORMATINET 10% to 40%Ezetimibe INCLUDEPICTURE "D:\\LIP1\\Management of Dyslipidemia in Adults - May 1, 1998 - American Academy of Family Physicians_files\\down1.gif" \* MERGEFORMATINET  15-20% INCLUDEPICTURE "D:\\LIP1\\Management of Dyslipidemia in Adults - May 1, 1998 - American Academy of Family Physicians_files\\up1.gif" \* MERGEFORMATINET 2-4% INCLUDEPICTURE "D:\\LIP1\\Management of Dyslipidemia in Adults - May 1, 1998 - American Academy of Family Physicians_files\\down1.gif" \* MERGEFORMATINET  3-5%  Although many of the drugs are started as monotherapy, in most patients with the metabolic syndrome or established T2DM it may be necessary to use combination therapies to reach the targeted levels. Section 6 HYPERTENSION Hypertension is a risk parameter in the diagnosis of the metabolic syndrome. A raised systolic blood pressure >/= 135 mm Hg and/or a raised diastolic blood pressure >/=85 mm Hg are the criteria leading to the diagnosis of hypertension. At the same time, it is now accepted that the relationship between BP and risk of cardiovascular disease (ASCVD) events is continuous, consistent, and independent of other risk factors, although the presence of the other risks does significantly increase the ASCVD risk posed by the high blood pressure levels. The classification prehypertension, introduced in the JNC-7 report, recognizes this relationship and introduced a new category of "prehypertension" (120 to 139/80 to 89 mm Hg), in recognition of the fact that underlying risk factors raise blood pressure to ranges that increase risk for CVD. Stages of Hypertension as Recommended by JNC 7 Blood pressure stagesPrehypertension (120 to 139/80 to 89 mm Hg)Stage 1 (140 to 159/90 to 99 mm Hg)Stage 2 (>=160/>=100 mm Hg) JNC = Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure. For individuals aged 40 to 70 years, each increment of 20 mm Hg in systolic BP or 10 mm Hg in diastolic BP doubles the risk of CVD across the entire BP range from 115/75 to 185/115 mm Hg. Benefits of Lowering BP In clinical trials, antihypertensive therapy has been associated with 35% to 40% mean reductions in stroke incidence; 20% to 25% in myocardial infarction; and more than 50% in HF. It is estimated that in patients with stage 1 hypertension (systolic BP, 140-159 mm Hg and/or diastolic BP, 90-99 mm Hg) and additional cardiovascular risk factors, achieving a sustained 12-mm Hg decrease in systolic BP for 10 years will prevent 1 death for every 11 patients treated. In the presence of CVD or target-organ damage, only 9 patients would require this BP reduction to prevent a death. Hypertension is more commonly prevalent in patients with diabetes as compared to people without diabetes. It may or may not be accompanied by renal damage, but is a major risk factor for the development of macro/micro vascular disease in diabetics. TARGET LEVELS When overt hypertension is present without diabetes or chronic kidney disease, the goal for antihypertensive therapy is a blood pressure of 15/10 mm Hg above the goal (<130/80 mm Hg), begin therapy with a combination of an ACEi or ARB and a thiazide diuretic, increasing the dosage of the former, as needed, to the high-dose range to achieve the blood pressure goal. In both the above cases, if blood pressure is still not controlled, add a calcium channel blocker (CCB); a nondihydropyridine CCB is recommended for those with proteinuria of >300 mg/day. Non-dihydropyridine CCBs, verapamil, diltiazem have been shown to reduce both CV mortality, proteinuria and diabetic nephropathy progression independent of an ACE inhibitor. Beta blockers may be substituted for calcium channel blockers if the patient has angina, heart failure, or arrhythmia necessitating their use. The newer highly selective beta blockers with proven efficacy to reduce CV events and the lowest side effect profile are preferred. The use of a beta blocker with a nondihydropyridine CCB should be avoided in the elderly and those with conduction abnormalities. Otherwise, such combinations are safe and particularly effective for lowering blood pressure. If the blood pressure is still not at the optimal level, add a long acting alpha blocker at bedtime Most patients will require multi-drug therapy to achieve and maintain their BP at the optimal levels. Section 7 IMPAIRED GLYCEMIA AND TYPE 2 DIABETES (T2DM) A fasting plasma glucose  INCLUDEPICTURE "http://care.diabetesjournals.org/math/ge.gif" \* MERGEFORMATINET 100 mg/dl (5.6 mmol/l) or previously diagnosed type 2 diabetes are important criteria in either of the two definitions used to diagnose the presence of the metabolic syndrome. The presence of the metabolic syndrome raises the lifetime risk for ASCVD by about two fold, but this risk is significantly more in those people with the metabolic syndrome who already have T2DM. Management Raised Fasting Plasma glucose For patients with a fasting plasma glucose  INCLUDEPICTURE "http://care.diabetesjournals.org/math/ge.gif" \* MERGEFORMATINET 100 mg/dl (5.6 mmol/l), the main goal is to delay the progression to type 2 diabetes mellitus. This progression to type 2 diabetes mellitus can be delayed or prevented by instituting lifestyle changes, especially weight reduction and increased physical activity. Drug therapies to reduce plasma glucose or insulin resistance are not recommended for such patients although recent trials have shown that they may be useful in some category of patients. Diabetes For type 2 diabetes, lifestyle therapy and pharmacotherapy, if necessary, should be used to achieve near-normal HbA1C (<7%). Lifestyle Management DIET should be the mainstay of all diabetes management! In order to ensure compliance, the prescribed diet should be individualised. It must be realistic, flexible, and take into consideration the patients likes and dislikes, to as large an extent as possible, and must suit the patients life style. It is important to educate the patient about the basic requirements of the diet and judge compliance at regular intervals. BASIC DIET ADVICE AVOID simple carbohydrates like sugar, sweets, jaggery, honey, etc., as they tend to cause a sharp rise in the blood glucose levels. Many of these aspects have been discussed in detail in the section dealing with lifestyle changes. ALTERNATIVE SWEETENERS The types of alternative sweeteners that are available are: a) Non-caloric sweeteners like saccharin, cyclamates, sucralose, acesulfame K; b) Aspartame; although this is usually classified as a noncaloric sweetener, it does have a caloric value of 4 calories per gm. c) Non-glucose carbohydrates like fructose, sorbitol, xylitol, lactose, xylitol, isomalt, polydextrose, and maltodextrose. These contain calories and have varying effect on the blood glucose levels. Most of the non-caloric sweeteners and aspartame are safe if taken in small amounts. Many of other aspects have been discussed in detail in the section dealing with lifestyle changes. PHYSICAL ACTIVITY AND EXERCISE A REGULAR EXERCISE PROGRAMME, TAILOR MADE FOR EVERY INDIVIDUAL AND UNDERTAKEN AFTER DUE FITNESS EVALUATION, WITH REGULAR MONITORING, IS AN ESSENTIAL PART OF MODERN DIABETES MANAGEMENT! Increased daily routine physical activity and regular exercise is recommended as an important component of all lifestyle management regimens to prevent and manage the metabolic syndrome as well as all diabetes management regimens. It confers benefits not only on glycemic control, but also on insulin sensitivity, lipid abnormalities, cardiovascular system, physical fitness, psychological well being, optimising body weight and disease prevention. It reduces overall ASCVD risk beyond that provided by weight reduction alone. Many aspects have been discussed in detail in the section dealing with lifestyle changes. DRUG THERAPY ORAL HYPOGLYCEMIC AGENTS (OHAs) If a patient is not optimally controlled by diet and exercise alone, oral hypoglycemic agents (OHAs) are usually the first line of drug therapy in the management of Type 2 diabetes. Drug Of Choice Type 2 diabetes is characterized by three basic abnormalities that contribute to the development of hyperglycemia: A) Impaired insulin secretion by the pancreas; B) Peripheral insulin resistance; and C) Excessive glucose production by the liver; Type 2 patients would have a combination of these three mechanisms which cause the high blood glucose levels. The problem is that the extent and severity of each of these mechanisms varies in different individuals, and the oral agent which would be most optimal for any patient would depend on which of these three mechanism plays a major role in their hyperglycemia. Although there is no hard and fast rule for this, it is widely accepted that in type 2 patients with low body weight, impaired insulin secretion is the predominant defect, while insulin resistance tends to be less severe than in the obese variety. Insulin resistance and hyperinsulinemia are the classic abnormalities of obese individuals with type 2 diabetes. All the oral agents available do not have the same mechanism of action. Thus, one must know how a class of oral agent acts in order to choose the appropriate drug. MAIN GROUPS OF OHAs Oral Agents commonly used in the Treatment of Type 2 Diabetes AgentDoseDuration of actionEfficacyMajor side effectsContraindicationsSulfonylureas Increase insulin secretion by pancreas; Metabolized primarily liver, excreted by kidneyAverage decrease in FPG 60-80 mg% Average decrease in HbA1c: 0.8- 2%Hypoglycemia; abdominal discomfort, nausea in around 1% to 3% patients; hyperacidity, metallic taste or change in taste; weight gain;Significant renal or hepatic dysfunctionGlipizide2.5-20 mg/day8-12 hoursHypoglycemia risk 4-6%Glibenclamide 2.5-20 mg/day 16-24 hoursHypoglycemia risk 4-6%Gliclazide80-240mg/day6-8 hoursHypoglycemia risk < 2%Glimepiride1-8 mg/day24 hoursHypoglycemia risk < 2%Biguanides Decreases hepatic glucose production Not metabolized, eliminated by kidneysAverage decrease in FPG 65-75 mg% Average decrease in HbA1c: 1 - 2%Gastrointestinal discomfort, especially nausea; metallic taste in mouth, loss of appetite; vitamin B12 deficiency, rarely lactic acidosis; weight lossDKA, alcoholism, renal or hepatic dysfunction; congestive heart failure; acute illness; cardiovascular collapse (shock); acute myocardial infarction; septicemia; acute or chronic metabolic acidosis; respiratory insufficiency; Metformin500-1500 mg/ per day with meals8 hoursAlpha-glucosidase inhibitors Delays absorption of complex carbohydrates in intestines Not absorbed systemicallyTo be taken with first bite of the mealAverage decrease in FPG 25-30 mg% Average decrease in HbA1c: 0.5 to1% Abdominal discomfort, bloating, gas formation, nausea and diarrhea;liver disease, bowel or intestinal disease, intestinal obstructionAcarbose25-100 mg with each meal4 HoursMiglitol50-100mg. with each meal4 HoursVoglibose200mg with each mealMeglitinides Increases pancreatic insulin secretion Metabolized in the liverAverage decrease in FPG 30-40 mg% Average decrease in HbA1c: 0.5 to 0.7% Hypoglycemia; gastrointestinal upsets; muscle aches, URTI and flu-like symptoms; body ache;Type 1 DM; diabetic ketoacidosis, hepatic dysfuntionRepaglinide0.5-4 mg with each meal3 hoursNateglinide60-120 mg with each meal3 hoursGlitazones Reduces insulin resistance at cellular level; Metabolized in the liverTaken with or without foodAverage decrease in FPG 70-80 mg% Average decrease in HbA1c: 1.5 2.5 %Weight gain, edema; URTI; toothaches; sore throat; body ache; headaches; Hepatic dysfunction; CHF, increasing edema; Rosiglitazone4-8 mg/day12 hoursPioglitazone15-45 mg/day24 hoursRecently, questions have been raised about cardiovascular safety of rosiglitazone and it should be used with added caution. It should not be used in patients with established cardiovascular disease, elderly patients and along with insulin. Although, it is not clear whether this is a class effect of glitazones, it would appear prudent to be extra cautious even with the use of pioglitazone. If pioglitazone is used along with insulin, the dose should not exceed 30mg/day.  Incretin mimetics PropertyDPP-IV antagonistsGLP-1/agonistsRoute of administrationOralSubcutaneous Mode of actionInhibit peptide hormone metabolism by DPP-IV enzyme, thus a) enhance insulin secretion; b) inhibit glucagon secretion; c) improve -cell function Enhancement of endogenous incretin hormone effects, thus a) enhance insulin secretion; b) inhibit glucagon secretion; c) improve -cell function d) slow gastric emptying e) induce satiety and weight lossSitagliptinExenatideDosing schedule100mg/day can be taken with or without food.Therapy initiated at 5 mcg per dose administered twice daily at any time within the 60-minute period before the morning and evening meals (or before the two main meals of the day, approximately 6 hours or more apart). Not to be administered after a meal. Based on clinical response, the dose can be increased to 10 mcg twice daily after 1 month of therapy. Each dose should be administered as a SC injection in the  HYPERLINK "http://www.medterms.com/script/main/art.asp?articlekey=8759" \t "_blank" thigh,  HYPERLINK "http://www.medterms.com/script/main/art.asp?articlekey=2081" \t "_blank" abdomen, or upper  HYPERLINK "http://www.medterms.com/script/main/art.asp?articlekey=8738" \t "_blank" arm. The pen should be discarded 30 days after first use, even if some drug remains in the pen. Glycemic controlMore dominant effect on postprandial levels, although some effect on fasting levels also seenMost dominant effect appears related to controlling postprandial hyperglycemiaAdverse effectsDiarrhea; gas; headache; indigestion; nausea; sore throat; stomach upset; stuffy or runny nose; vomiting; weakness. anorexia and early satiety are notable;Nausea, vomiting, anorexia, thus not recommended in patients with severe gastrointestinal disease. No hypoglycemia when used as monotherapy; Contra-indicationsNeed for dosage adjustment based upon renal function; Avoid if possible in patients using digoxinNot recommended for use in patients with  HYPERLINK "http://www.medterms.com/script/main/art.asp?articlekey=33640" \t "_blank" end-stage renal disease or severe  HYPERLINK "http://www.medterms.com/script/main/art.asp?articlekey=5298" \t "_blank" renal impairment ( HYPERLINK "http://www.medterms.com/script/main/art.asp?articlekey=12550" \t "_blank" creatinine clearance <30 mL/min) Not recommended in patients with severe gastrointestinal disease.  Protocols for OHA THERAPY OHA THERAPY in a RELATIVELY non-obese Type 2 Diabetes patient Protocol  Recently, questions have been raised about cardiovascular safety of rosiglitazone and it should be used with added caution. Although, it is not clear whether this is a class effect of glitazones, it would appear prudent to be extra cautious even with the use of pioglitazone. In view of this, metformin may the drug of choice as a sensitizer. Managing the Overweight (Obese) Patient Protocol  Recently, questions have been raised about cardiovascular safety of rosiglitazone and it should be used with added caution. Although, it is not clear whether this is a class effect of glitazones, it would appear prudent to be extra cautious even with the use of pioglitazone. In view of this, metformin may the drug of choice to initiate therapy Many trials have shown that a 20 mg dose of rimonabant, which is used in the management of obese diabetics, can lead to an average weight loss of approximately 6 kg over a year when accompanied with lifestyle therapies. Importantly, it leads to a decrease in abdominal obesity and improves cardiovascular risk factors. The most common reported side effects include depression, anxiety, and nausea and should not be used in patients on anti-depressives. It is NOT accepted for use by the U.S. FDA. GENERAL ASPECTS IN OHA THERAPY Theoretically, most Type 2 patients should be given a trial with diet and exercise for an adequate period (usually 4-6 weeks) before using oral hypoglycemic agents. But practically speaking, patients with fasting blood glucose levels more than 200 mg%, or in patients with significant symptoms, OHA therapy can be started along with diet and exercise. This will allow a more rapid relief of symptoms. Sulfonylureas are the drugs of choice in the management of Type 2 diabetics who are not overweight. Sulfonylureas, especially the short acting ones, are to be given 20-30 minutes before food intake, although this needs to be individualised. Long acting sulfonylureas such as glibenclamide and glimepiride can be given as a single daily dose. Meglitinides are much milder in their efficacy, but may be useful in patients with erratic meal timings in that they allow for flexible timing and missed meals. Biguanides are considered the drugs of choice in those overweight Type 2 diabetics. They may be used in lean patients, but care should be taken that patients using biguanides maintain their ideal weight and do not become underweight. Glitazones can be used in obese patients in whom a significant degree of insulin resistance would be expected, but have a significant time lag before showing their full activity. Recently, questions have been raised about cardiovascular safety of rosiglitazone and it should be used with added caution. It should not be used in patients with established cardiovascular disease, elderly patients and along with insulin. Although, it is not clear whether this is a class effect of glitazones, it would appear prudent to be extra cautious even with the use of pioglitazone. If pioglitazone is used along with insulin, the dose should not exceed 30mg/day. If the patient shows a relatively high postprandial levels, then addition of an alpha-glucosidase inhibitors or the newly available DPP-IV inhibitors may be of help. The starting dose should be small, starting with a small dose and giving with meals, if necessary, will help to avoid the gastrointestinal side effects. OHA increments must be made in small amounts (half to one tablet at one time) and gradually (every 1-2 weeks), till optimal control is reached. In many patients, there will be a need to combine two or more oral agents or even insulin therapy with possibly insulin sensitizers. Potential combinations of OHAs for the treatment of type 2 diabetes Sulfonylurea plus Thiazolinediones Metformin Insulin -Glucosidase inhibitor Metformin plus Sulfonylurea Non-sulfonylurea insulin secretagogue Thiazolidinedione -Glucosidase inhibitor Insulin Thiazolidinedione plus Metformin Sulfonylurea Non-sulfonylurea insulin secretagogue Insulin not to be used rosiglitazone ( pioglitazone not more than 30mg/day should be used) -Glucosidase inhibitor -Glucosidase inhibitor plus Metformin Thiazolidinedione Sulfonylurea Non-sulfonylurea insulin secretagogue Insulin Do not combine: Sulfonylurea + non-sulfonylurea insulin secretagogue OR another sulfonylurea Insulin secretagogue + preprandial insulin Insulin + sulfonylureas Insulin with rosiglitazone ( with pioglitazone not more than 30mg/day should be used)  Combinations of submaximal doses of different classes of OHAs may be equally effective as or more effective than maximum dose of monotherapy in improving glucose control with fewer adverse effects. Once Optimal Control Is Achieved Re-enforce importance of diet and exercise; Efforts must be made to reduce the dose slightly to see if the control is maintained; the rationale for this is to try and obtain the optimal target level for the individual with the smallest possible dose. Emphasize need or regular follow-ups. DIRECT EFFECTS OF ORAL ANTIHYPERGLYCEMIC AGENTS ON CARDIOVASCULAR RISK FACTORS IN TYPE 2 DM PATIENTS Agent ClassInsulin ResistanceLipidsBody WeightLipoprotein (a)Prothrombotic state ( PAI-1 levels)SulfonylureasNo effectNo effectIncrease, with small increase in central adiposityNo changeNo changeMeglitinidesNo effectNo effectIncrease, with possible small increase in central adiposityNo changeNo changeBiguanide (Metformin)DecreasedSmall changes;  INCLUDEPICTURE "http://www.endotext.com/diabetes/diabetes16/figures16/arrowdown.gif" \* MERGEFORMATINET TG  INCLUDEPICTURE "http://www.endotext.com/diabetes/diabetes16/figures16/arrowdown.gif" \* MERGEFORMATINET LDL  INCLUDEPICTURE "http://www.endotext.com/diabetes/diabetes16/figures16/arrowup.gif" \* MERGEFORMATINET HDLDecreaseModerate decreaseModerate decreaseThiazolidinediones Pioglitazone RosiglitazoneDecreasedModerate to marked changes;  INCLUDEPICTURE "http://www.endotext.com/diabetes/diabetes16/figures16/arrowdown.gif" \* MERGEFORMATINET TG and FFA  INCLUDEPICTURE "http://www.endotext.com/diabetes/diabetes16/figures16/arrowup.gif" \* MERGEFORMATINET HDL  INCLUDEPICTURE "http://www.endotext.com/diabetes/diabetes16/figures16/arrowup.gif" \* MERGEFORMATINET LDL, but mainly in large less atherogenic buoyant particlesIncrease, but visceral adiposity decreasedModerate decreaseModerate decreaseAlpha-Glucosidase inhibitorsNo effectNo effectNo effectNo changeNo change INSULIN THERAPY A JUDICIOUS USE OF INSULIN THERAPY MAY BE NECESSARY FOR OPTIMAL MANAGEMENT IN MANY PEOPLE WITH TYPE 2 DIABETES! Non dependence does NOT imply that Type 2s may never require insulin in order to obtain optimal control. At the same time, unnecessary insulin therapy should be avoided as there is some evidence that high insulin levels in the blood may contribute to some aspects of the Metabolic Syndrome. In view of this, THE DECISION TO USE INSULIN IN Type 2 patients SHOULD BE TAKEN AFTER CAREFUL, JUDICIOUS CONSIDERATION. DIABETES PATIENTS WHO SHOULD RECEIVE INSULIN Patients not optimally controlled with OHA use. Insulin should be considered in diabetics with significant complications like ischemic heart disease, CVA, peripheral artery disease, significant retinopathy, nephropathy and neuropathy, hepatic complications such as viral hepatitis. Any patient with an acute problem like several infection, injury, any metabolic catastrophe, etc., should receive insulin. Patients with tuberculosis often do better with insulin. Any Type 2 patient who manifests ketosis for whatever reason. Diabetes patients undergoing most surgical procedures, especially those requiring general anesthesia, and where the patient will be on intravenous fluids for any significant period of time should be stabilized on insulin. Pregnant women with diabetes, if not tightly controlled with diet alone, must be managed with insulin. Any patient, even if optimally controlled with OHAs who shows evidence that may contraindicate the use of these oral agents, must be shifted to insulin. Many underweight patients and those with significant symptoms would do better with insulin therapy, possibly in combination with small doses of sensitisers; Patients with INSULIN-REQUIRING diabetes, even though they are not prone to ketosis, should be identified and their management supplemented with insulin to get the best possible control;  Types of INSULINS available for clinical use: Although animal insulins made from beef and pig pancreas may still be found, the vast majority of the insulins used now are of the human variety. Recently there has been an increasing emphasis on the use of the newly available insulin analogs and the clinical question is to place them correctly in the therapeutic armamentarium. It would not be correct to totally replace the use of human insulins with analogs in routine therapy, especially as one has to factor in the costs to the patient and in many cases the use of human insulins would offer good control. Table Showing Commonly used Insulin Preparations: Type of InsulinHumanAnaloguesLong acting Detemir, GlargineIntermediate actingNPH Short actingRegular Human InsulinInsulin Aspart, Lispro, GlulisinePremixedBiphasic Human Insulin (30/70,50/50)Biphasic Insulin Aspart (30/70), Biphasic Insulin Lispro (25/75 and 50/50)  Long acting analogs They exhibit a relatively constant glucose-lowering profile over 24 hours that permits once-daily dosing, although some patients may do better with a twice daily dose of levemir insulin. Clinically, its potency is approximately the same as human insulin and it does not lead to a better glycemic control. Rapid acting analogs Their use in place of the human insulins does not always lead to a better control, but their rapid onset and short duration of action make them of particular use in some clinical situations. PATIENTS WHO SHOULD USE ANALOG INSULINS Rapid acting analogs Their use in place of the human insulins does not always lead to a better control, but their rapid onset and short duration of action make them of particular use in some clinical situations: Patients exhibiting high postprandial glycemia with late hypoglycemia; Brittle diabetes; In the elderly and in children, In those with erratic eating habits; Perioperative period; Sick day therapy; Renal and hepatic dysfunction where one sees low fasting blood glucose levels with high postprandial blood glucose values and the fear of late hypoglycemia; h) People on RT and other tube feeds; i) Significant variations in bioavailability in the same patient on a day to day basis; Long acting analogs These are indicated for the treatment of hyperglycemia in adult and pediatric patients 6 years of age and older with Type 1 or Type 2 diabetes mellitus. It exhibits a relatively constant glucose-lowering profile over 24 hours that permits once-daily dosing, although some patients on levemir may do better with twice daily injections. Clinically, its potency is approximately the same as human insulin and it does not lead to a better glycemic control. But it may have a special role to play in those clinical situations where a steady basal level of insulin is required. TIME-ACTIVITY CHARACTERISTICS Begins WorkingPeaks AtEnds WorkingLows Occur AtInsulin-Lyspro15-20 minutes30-90 min3-4 hours2 to 4 hrInsulin- aspart15-20 minutes40-50 min3-4 hours2 to 4 hrRegular30-60 minutes80-120 min4-6 hours3 to 7 hrNPH2-4 hours6-10 hours14-16 hours6 to 12 hrLente3-4 hours6-12 hours16-18 hours7 to 14 hrUltralente4-6 hours10-16 hours18-20 hours12 to 24 hrInsulin Glargine/Levemir2-3 hoursalmost no peak18-26 hours4 to 24 hr However, each person responds to insulin in his or her own way. That is why onset, peak time, and duration are given as ranges. It is important to have an understanding of the time-activity characteristics of the available insulins. When blood glucose levels are not well controlled at certain times during the day, or if hypoglycemic reactions are occurring, the knowledge of the action and characteristics of each insulin being taken will help to determine where changes need to be made. Fortunately, the picture becomes much more clear, if it is realised that from a practical and clinical viewpoint, human insulins can be divided into two main groups, depending on their time course of action. These are the short-acting (SAI) and the intermediate acting (IAI) insulins. INSULIN TREATMENT SCHEME  * Rosiglitazone should not be used along with insulin and the dose of pioglitazone should not exceed 30mg/day. In most patients with a significant degree of symptoms, or in whom the fasting blood glucose values are higher than 250-300mg%, insulin therapy, if indicated in a particular patient, may be started along with the diet and exercise prescription. Start with a small dose and gradually titrate upwards depending on the time characteristics of the insulins used as well as the individual response of a patient. With increasing use, it would be possible to cut out some of the steps outlined above and start with a twice daily mixture of SAI and IAI insulins, especially in insulin requiring patients. The most commonly used regimen is the Premixed regimen: It is the most convenient and effective insulin regimen for initiation of insulin therapy. In this there is dual coverage as it is a combination of short acting and intermediate acting insulin preparations in fixed ratio like 30:70 or 50:50 respectively (options for different food habits). So the same preparation is able to give both basal and meal related coverage and helps to mimic physiology to a great extent. There for these are considered as the effective and compliant insulin preparations for initiation as well as intensification of insulin therapy.  Rosiglitazone should not be used along with insulin and the dose of pioglitazone should not exceed 30mg/day. Other Regimens Basal Only Regimen: In this patients on OHAs who are not optimally managed are supplemented with just basal insulin. This is done with the help of NPH or the modern insulins. With NPH patients usually require 2 doses per day where as with insulin analogues with one injection per day you can achieve the desired targets in most of the patients, if chosen appropriately. Basal Bolus Regimen: Very rarely required for T2DM patients, but may be necessary in certain clinical scenarios. In this a basal insulin supplementation given with the help of long acting insulins either two or one (with insulin analogues) injections and then three meal related short acting insulin injections. INJECTION SITES INCLUDEPICTURE "../Dr.%20S.M.Sadikot/Desktop/Reddys/Insulin%20and%20Diabetes%20Techniques,%20Types,%20Pumps,%20Reactions,%20Hypoglycemia_files/dm_092.gif" \* MERGEFORMAT  The sites where the injections can be given. Efforts must be made to rotate the site of the injection throughout the permissible areas and not inject only into one region. COMMONLY SEEN SIDE EFFECTS Hypoglycemia Edema Allergy Lipodystrophy and scar formation Section 8 Atherosclerotic Cardiovascular Disease (ASCVD) The Metabolic syndrome is a cluster of metabolic risk factors which is strongly associated with the risk for the development of atherosclerotic cardiovascular disease and Type 2DM. At the same time, the metabolic factors utilized in making the diagnosis of the metabolic syndrome do not take into account all the known risk factors leading especially to ASCVD. Table The risk factors for premature atherosclerotic cardiovascular disease (ASCVD) are: Non-Modifiable Risk factors Genetic factors (family history of premature CAD in first degree relative: male < 55years and female <65 years old) The closeness of the relationships (eg, CHD in a sibling or parent confers greater risk than CHD in an uncle) Age of the patient ( >45 years in men and > 55 years in women) Male Sex Modifiable Risk factors Lifestyle risk factors Obesity, especially central or visceral obesity Atherogenic diet Physical inactivity Smoking Metabolic Risk Factors Atherogenic dyslipidemia (elevations of lipoproteins containing apolipoprotein B, elevated triglycerides, increased small particles of LDL, and low levels of high- density lipoproteins (HDL). Elevated LDL-Cholesterol levels Elevated blood pressure systolic and/or diastolic, Elevated plasma glucose, A prothrombotic state, and A proinflammatory state.  The presence of the metabolic syndrome raises the lifetime risk for both ASCVD and type 2 diabetes (T2DM). Average relative risks are increased about twofold for ASCVD and fivefold for T2DM compared with those for individuals without the metabolic syndrome. The risk for ASCVD is significantly more in those people with the metabolic syndrome who already have T2DM. "BASIC SCREEN" for risk factors: 1) a comprehensive clinical history and examination for the presence of coronary heart disease, or cerebrovascular, or peripheral vascular disease; this includes questions about previous angina. TIAs, intermittent claudication, established myocardial infarction etc. 2) family history for premature coronary artery disease. 3) A complete physical examination for cardiac function, presence or absence of peripheral pulses, presence of bruits, evidence of peripheral and / or cerebral ischemia. 4) Blood pressure recordings. 5) Waist measurements and BMI 6) Lipid profile this profile should include, estimation of serum triglycerides, serum total cholesterol, HDL-cholesterol and calculated LDL cholesterol although preferable to do in a fasting state, may be done with a random sample, and the values confirmed in the fasting stage, if abnormal. 7) Estimation for the presence of microalbuminuria in those who are dipstick (albustix) negative; 8) History of tobacco use. 9) Standard resting 12 lead ECG; sensitivity of the standard 12 lead resting ECG is moderate and cannot rule out the possibility of clinically significant disease. Further investigation would depend on individual circumstances, availability and degree of clinical suspicion. Management The metabolic syndrome is a simple clinical tool to identify people with a particular set of risk factors who are at higher life time risk for both ASCVD and type 2 diabetes. All patients with the metabolic syndrome must be offered 1) lifestyle intervention (weight loss, increased physical activity, and a healthy diet) and 2) more detailed, short-term risk assessment (e.g., Framingham scoring). For management of long-term as well as short-term risk, lifestyle therapies are first-line interventions to reduce the metabolic risk factors. The major lifestyle interventions include weight loss in overweight or obese subjects, increased physical activity, and modification of an atherogenic diet. These changes will produce a reduction in all of the metabolic risk factors simultaneously. In the long run, the greatest benefit for those with the metabolic syndrome will be derived from effective lifestyle intervention. For metabolic syndrome patients without ASCVD or diabetes, Framingham risk (or similar validated risk) scoring should be performed to estimate 10-year risk for coronary heart disease (CHD). This assessment triages patients into 3 risk categories based on 10-year risk for CHD: high risk (10-year risk >20%), moderately high risk(10-year risk 10% to 20%), or lower to moderate risk (10-year risk <10%). Framingham Point Scores NOTE: This system does not take diabetes into its point consideration as all people with diabetes are considered to be in the high risk category.  INCLUDEPICTURE "http://content.nejm.org/content/vol346/issue19/images/large/08f1.jpeg" \* MERGEFORMATINET  People with diabetes and ASCVD are always considered to be in the high risk category. CHD risk is also higher than indicated in the charts for: Those with a family history of premature CHD (male first degree relatives aged <55 years and female first degree relatives aged <65 years) which increases the risk by a factor of approximately 1.5 Those with raised triglyceride levels and other dyslipidemias. Women with premature menopause. Those who are not yet diabetic, but have IFG or IGT, or both. Patients with Type 1 diabetes. Patients with type 2 diabetes Moreover, in ethnic minorities the risk charts should be used with caution because they have not been validated in these populations. For example, in people originating from the Indian subcontinent it is safest to assume that the risk is higher than predicted from the charts.  Management High-risk patients have established atherosclerotic CVD, diabetes, or 10-year risk for CHD >20%. For cerebrovascular disease, high-risk conditions include TIA or stroke of carotid origin or >50% carotid stenosis. All high risk patients merit intensive management of the risk factors as well as T2DM if present. For individuals at high or moderately high 10-year risk, consideration must be given to specific therapies for the metabolic risk factors. A persons 10-year risk status will determine the intensity of therapy for each risk factor and, particularly, whether drug therapy should be employed in addition to lifestyle management. Factors that favor therapeutic option are those that can raise individuals to upper range of moderately high risk: multiple major risk factors, severe and poorly controlled risk factors (especially continued cigarette smoking), metabolic syndrome, and documented advanced subclinical atherosclerotic disease (eg, coronary calcium or carotid intimal-medial thickness >75th percentile for age and sex). No specific drugs are currently recommended for people with the metabolic syndrome independent of those agents most appropriate for specific, abnormal risk factors. The management of most of the traditional risk factors has been dealt with in more detail in separate sections. Prothrombotic State In metabolic syndrome patients who are at high or moderately high risk for ASCVD events, aspirin prophylaxis is an attractive therapeutic option to lower vascular events. Dosage recommendations range from 75 mg to 325 mg per day. The principal risks of aspirin therapy include gastric mucosal injury and gastrointestinal hemorrhage. 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Contraindications to aspirin include allergy, tendency for bleeding, anticoagulant therapy, recent gastrointestinal bleeding and clinically active hepatic disease. Ticlopidine and recently clopidogrel have also been used either by themselves or with aspirin. But most studies still maintain the primacy of aspirin usage. Proinflammatory State Although several drugs used to treat other metabolic risk factors have been reported to reduce CRP levels (eg, statins, nicotinic acid, fibrates, ACE inhibitors, thiazolidinediones), presently,  HYPERLINK "http://circ.ahajournals.org/cgi/content/full/112/17/2735" \l "R187-169404#R187-169404"  HYPERLINK "http://circ.ahajournals.org/cgi/content/full/112/17/2735" \l "R188-169404#R188-169404" these drugs cannot be recommended specifically to reduce a proinflammatory state independent of their indications for other risk factors. 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