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Diabetes mellitus-treatment and psychiatric effects

This document provides information on the diagnosis and management of diabetes mellitus. It defines the diagnostic criteria for diabetes as either a random blood glucose of 200 mg/dL or higher, a fasting plasma glucose of 126 mg/dL or higher, an A1C of 6.5% or higher, or a 2-hour plasma glucose of 200 mg/dL or higher during an oral glucose tolerance test. It also outlines treatment goals and management strategies, including lifestyle modifications, oral medications, and insulin therapies.

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Dr Megha Isac Junior resident Dept. of General Medicine Diabetes Mellitus – Management and psychiatric aspects
Criteria for the Diagnosis of Diabetes Mellitus • Symptoms of diabetes plus random blood glucose concentration 200 mg/dL or • Fasting plasma glucose ≥126 mg/dL or • Hemoglobin A1c ≥ 6.5%c or • 2-h plasma glucose ≥200 mg/dL during an oral glucose tolerance test (The test should be performed using a glucose load containing the equivalent of 75 g anhydrous glucose dissolved in water, not recommended for routine clinical use.) Source: Adapted from American Diabetes Association: Diabetes Care 37(Suppl 1):S14,2014
Essentials of diagnosisEssentials of diagnosis Type 1 diabetes  Polyuria, polydypsia and weight loss associated with random plasma glucose >/= 200 mg/dl  Plasma glucose of>/= 126mg/dl after an overnight fast,documented on more than one occasion.  Ketonemia, ketonuria ,or both.  Islet autoantibodies are frequently present.
• Type 2 diabetes • Most patients are over 40 yrs of age and obese. • Polyuria and polydypsia ,ketonuria and weight loss generally are uncommon at the time of diagnosis. candidial vaginitis in women may be an initial manifestation. Many patients have few or no symptoms. • Plasma glucose of >/=126mg/dl after an overnight fast on more than one occasion.2 hrs after 75 mg oral glucose, diagnostic values are >/=200 mg/dl • Hypertension, dyslipidemia and atherosclerosis are often associated
Etiologic Classification of Diabetes Mellitus Type 1 diabetes (beta cell destruction, usually leading to absolute insulin deficiency) •A. Immune-mediated •B. Idiopathic  Type 2 diabetes (may range from predominantly insulin resistance with relative insulin deficiency to a predominantly insulin secretory defect with insulin resistance)
Other specific types of diabetes A.Genetic defects of beta cell development or function B.Genetic defects in insulin action C.Diseases of the exocrine pancreas D.Endocrinopathies E.Drug- or chemical-induced glucocorticoids, vacor (a rodenticide), pentamidine, nicotinic acid, diazoxide, β-adrenergic agonists, thiazides, calcineurin and mTOR inhibitors, hydantoins, asparaginase, α-interferon, protease inhibitors, antipsychotics (atypicals and others), epinephrine F. Infections
G. Uncommon forms of immune-mediated diabetes -anti-insulin receptor antibodies H. Other genetic syndromes sometimes associated with diabetes Down’s syndrome, Klinefelter’s syndrome, Turner’s syndrome, Huntington’s chorea, myotonic dystrophy I. Gestational diabetes mellitus (GDM) Source: Adapted from American Diabetes Association: Diabetes Care 37(Suppl 1)
Worldwide prevalence of diabetes mellitus. Global estimate is 382 million individuals with diabetes. Regional estimates of the number of individuals with diabetes (20–79 yearsof age) are shown (2013). IDF Diabetes Atlas, the International Diabetes Federation, 2013.
Risk Factors for Type 2 Diabetes Mellitus Family history of diabetes (i.e., parent or sibling with type 2 diabetes) Obesity (BMI ≥25 kg/m2 or ethnically relevant definition for overweight) Physical inactivity Race/ethnicity (e.g., African American, Latino, Native American, Asian American, Pacific Islander) Previously identified with IFG, IGT, or an hemoglobin A1c of 5.7–6.4 History of GDM or delivery of baby >4 kg Hypertension (blood pressure ≥140/90 mmHg) HDL cholesterol level <35 mg/dL ) and/or a triglyceride level>250 mg/dL) Polycystic ovary syndrome or acanthosis nigricans History of cardiovascular disease
The goals of therapy (1)eliminate symptoms related to hyperglycemia(RBS<200mg/dl) (2) reduce or eliminate the long-term microvascular and macrovascular complications of DM (3) allow the patient to achieve as normal a lifestyle as possible.
Guidelines for Comprehensive Medical Care for Patients with Diabetes • Optimal and individualized glycemic control • Self-monitoring of blood glucose (individualized frequency) • HbA1c testing (2–4 times/year) • Patient education in diabetes management (annual); diabetes-self management ,education and support • Medical nutrition therapy and education (annual) • Eye examination (annual or biannual) • Foot examination (1–2 times/year by physician; daily by patient) • Screening for diabetic nephropathy (annual) • Blood pressure measurement (quarterly) • Lipid profile and serum creatinine (estimate GFR) (annual) • Influenza/pneumococcal/hepatitis B immunizations • Consider antiplatelet therapy
Treatment Goals for Adults with Diabetes Index Goal Glycemic control HbA1c <7.0%c Preprandial capillary plasma glucose 80–130 mg/dL Peak postprandial capillary plasma glucose <180 mg/dL Blood pressure <140/90 mmHg Lipids Low-density lipoprotein < 100 mg/dL High-density lipoprotein >40 mg/dL in men >50 mg/dL in women Triglycerides <150 mg/dL
Treatment regimenTreatment regimen • A well balanced nutritious diet remains a fundamental element of therapy Limiting the carbohydrate intake and substituting some of the calories with monosaturated fats such as olive oil ,rapeseed (canola) oil can lower TG and increase HDL. Weight reduction by caloric restriction is important goal. High protein intake may cause progression of kidney disease in patients with diabetic nephropathy; reduction in protein intake to 0.8 kg/day (or about 10% of total calories daily)is recommended. Limit cholesterol intake to 300 mg /day ,and in individuals with LDL cholesterol more than 100 mg/day should limit dietary cholesterol to 200 mg daily.
Dietary Fiber ADA recommends food such as oatmeal, cereals and beans with relatively high soluble fiber content as staple components of the diet in diabetics. retards nutrient absorption rates High soluble fibre content in the diet has favourable effect on blood cholesterol levels.
Artificial and other sweeteners Aspartame(aspartic acid and phenylalanine) -180 times as sweet as sucrose, not heat stable Saccharin,sacralose,acesulfame potassium –used for cooking and baking Sugar alcohols eg naturaly occuring in many fruits and vegetables, commercialy made from sucrose, glucose, starch- sorbitol,xylitol ,mannitol,lactitol, isomalt, maltitol and hydrogenated starch hydrolysates  used in “sugar free” food products  if consumed in large quantities will raise blood sugars and can cause bloating and diarrhoea
Weight loss and exercise Multiple positive benefits including • cardiovascular risk reduction, reduced blood pressure • maintenance of muscle mass, reduction in body fat, and weight loss. For individuals with type1 or type 2 DM •lowers plasma glucose (during and following exercise) • increasing insulin sensitivity. Inpatients with diabetes, the ADA recommends 150 min/week (distributed over at least 3 days) of moderate aerobic physical activity withno gaps longer than 2 days. The exercise regimen should also include resistance training.
ORAL HYPOGLYCEMIC AGENTS Biguanides • ↓ Hepatic glucose production • Metformin α-Glucosidase inhibitors •↓ GI glucose absorption •Acarbose, miglitol, voglibose Dipeptidyl peptidase IV inhibitors •Prolong endogenous GLP-1 action •Alogliptin, Anagliptin, Gemigliptin, linagliptin, saxagliptin,sitagliptin, teneligliptin, vildagliptin
Insulin secretagogues:Sulfonylureas ↑ Insulin secretion Glibornuride, gliclazide, glimepiride, glipizide, gliquidone, glyburide, Glyclopyramide Insulin secretagogues:Nonsulfonylureas ↑ Insulin secretion Nateglinide, repaglinide, mitiglinide Sodium-glucose cotransporter 2 inhibitor ↑ Urinary glucose excretion Canagliflozin, dapagliflozin,empagliflozin Thiazolidinediones ↓ Insulin resistance, glucose utilization↑ Rosiglitazone, pioglitazone
Properties of Insulin Preparations Time of Action(Hrs) Preparation Onset Peak EffectiveDuration Short-acting Aspart <0.25 0.5–1.5 2–4 Glulisine <0.25 0.5–1.5 2–4 Lispro <0.25 0.5–1.5 2–4 Regular 0.5–1.0 2–3 3–6 Long-acting Detemir 1–4 12-24 Glargine 2–4 20-24 NPH 2–4 4–10 10–16
Insulin combinations 75/25 75% protamine lispro, 25% lispro <0.25 10–16 70/30 70% protamine aspart, 30% aspart <0.25 15-18 50/50 50% protamine lispro, 50% lispro <0.25 10–16 70/30 70% NPH, 30% regular 0.5–1 10–16
Type 1 Diabetes Mellitus The goal is to design and implement insulin regimens that mimic physiologic insulin secretion. In all regimens  long-acting insulins (NPH, glargine, or detemir) supply basal insulin regular, insulin aspart, glulisine, or lispro insulin provides prandial insulin
HOW??HOW MUCH??? Short-acting insulin analogues should be injected just before (<10 min) or just after a meal; regular insulin is given 30–45 min prior to a meal. Sometimes short-acting insulin analogues are injected just after a meal (gastroparesis, unpredictable food intake). In general, individuals with type 1 DM require 0.5–1 U/kg per day of insulin divided into multiple doses, with ~50% of the insulin given as basal insulin
HOW TO ADJUST DOSES???? The insulin dose in such regimens should be adjusted based on SMBG results with the following general assumptions: (1) the fasting glucose is primarily determined by the prior evening long- acting insulin (2) the pre-lunch glucose is a function of the morning short-acting insulin (3) the pre-supper glucose is a function of the morning long-acting insulin (4) the bedtime glucose is a function of the pre-supper, short-acting insulin. This is not an optimal regimen for the patient with type 1 DM, but is sometimes used for patients with type 2 DM.
Amylin •A 37-amino-acid peptide co-secreted with insulin from pancreatic beta cells, in normal glucose homeostasis is uncertain. However, based on the rationale that patients who are insulin deficient are also amylin deficient, an analogue of amylin (pramlintide) was created and found to reduce postprandial glycemic excursions in type 1 and type 2 diabetic patients taking insulin. •Pramlintide injected just before a meal slows gastric emptying and suppresses glucagon but does not alter insulin levels. Addition of pramlintide produces a modest reduction in the HbA1c and seems to dampen meal-related glucose excursions. In type 1 DM, pramlintide is started as a 15- g SC injection before eachμ meal and titrated up to a maximum of 30–60 g as tolerated.μ In type 2 DM, pramlintide is started as a 60- g SC injection before eachμ meal and may be titrated up to a maximum of 120 g.μ
Management of Type 2 Diabetes Individualized glycemic control • Diet/lifestyle • Exercise • Medication Treat associated conditions • Dyslipidemia • Hypertension • Obesity • Coronary heart disease Screen for/manage complications of diabetes • Retinopathy • Cardiovascular disease • Nephropathy • Neuropathy • Other complications
Biguanides  Metformin, representative of this class of agents • reduces hepatic glucose production • improves peripheral glucose utilization •Mild increase in insulin sensitivity Metformin activates AMP-dependent protein kinase and enters cells through organic cation transporters (polymorphisms of these may influence the response to metformin). Recent evidence indicates that metformin’s mechanism for reducing hepatic glucose production is to antagonize glucagon’s ability to generate cAMP in hepatocytes. • reduces fasting plasma glucose (FPG) and insulin levels • improves the lipid profile •Promotes modest weight loss.
An extended-release form is available and may have fewer gastrointestinal side effects (diarrhea, anorexia, nausea, metallic taste). Because of its relatively slow onset of action and gastrointestinal symptoms with higher doses, the initial dose should be low and then escalated every 2–3 weeks based on SMBG measurements. Metformin is effective as monotherapy and can be used in combination with other oral agents or with insulin. The major toxicity of metformin, lactic acidosis, is very rare and can be prevented by careful patient selection. Vitamin B12 levels are ~30% lower during metformin treatment.
Metformin should not be used in patients with 1. renal insufficiency (glomerular filtration rate [GFR] <60 mL/min) 2.any form of acidosis 3.unstable congestive heart failure (CHF) 4. liver disease 5.severe hypoxemia. Metformin should be discontinued in hospitalized patients, in patients who can take nothing orally, and in those receiving radiographic contrast material. Insulin should be used until metformin can be restarted.
Insulin secretagogues stimulate insulin secretion by interacting with the ATP-sensitive potassium channel on the beta cell These drugs are most effective in individuals with type 2 DM of relatively recent onset (<5 years) who have residual endogenous insulin production. First-generation sulfonylureas (chlorpropamide, tolazamide, tolbutamide) have a longer half-life, a greater incidence of hypoglycemia and more frequent drug interactions, and are no longer used. Second-generation sulfonylureas have a more rapid onset of action and better coverage of the postprandial glucose rise, but the shorter half-life of some agents may require more than once-a-day dosing
Sulfonylureas reduce both fasting and postprandial glucose and should be initiated at low doses and increased at 1- to 2- week intervals based on SMBG. In general, sulfonylureas increase insulin acutely and thus should be taken shortly before a meal; with chronic therapy, though, the insulin release is more sustained. Glimepiride and glipizide can be given in a single daily dose and are preferred over glyburide, especially in the elderly
Repaglinide, nateglinide, and mitiglinide are not sulfonylureas but also interact with the ATP-sensitive potassium channel. Because of their short half-life, these agents are given with each meal or immediately before to reduce meal-related glucose excursions.
Insulin secretagogues, especially the longer acting ones, have the potential to cause hypoglycemia, especially in elderly individuals. Most sulfonylureas are metabolized in the liver to compounds (some of which are active) that are cleared by the kidney. Thus, their use in individuals with significant hepatic or renal dysfunction is not advisable. Weight gain, a common side effect of sulfonylurea therapy, results from the increased insulin levels and improvement in glycemic control. Some sulfonylureas have significant drug interactions with alcohol and some medications including warfarin, aspirin, ketoconazole, α- glucosidase inhibitors, and fluconazole
DPP-IV inhibitors inhibit degradation of native GLP-1 and thus enhance the incretin effect. Incretins” amplify glucose-stimulated insulin secretion. DPP-IV, which is widely expressed on the cell surface of endothelial cells and some lymphocytes, degrades a wide range of peptides (not GLP-1 specific). Exenatide is an analogue of GLP-1. Unlike native GLP-1, which has a half-life of >5 min, differences in the exenatide amino acid sequence render it resistant to the enzyme that degrades GLP-1 (dipeptidyl peptidase IV [DPP-IV]). Thus, exenatide has prolonged GLP-1-like action and binds to GLP-1 receptors found in islets, the gastrointestinal tract, and the brain. GLP-1 receptor agonists increase glucose-stimulated insulin secretion, suppress glucagon, and slow gastric emptying
DPP-IV inhibitors promote insulin secretion in the absence of hypoglycemia (unless there is concomitant use of an agent that can lead to hypoglycemia—sulfonylureas, etc.) or weight gain and appear to have a preferential effect on postprandial blood glucose. The levels of GLP-1 action in the patient are greater with the GLP-1 receptor agonists than with DPP-IV inhibitors. Reduced doses should be given to patients with renal insufficiency . Initial concerns about the pancreatic side effects of GLP-1 receptor agonists and DPP-IV inhibitors (pancreatitis, possible premalignant lesions) appear to be unfounded.
These agents do not promote weight gain; in fact, most patients experience modest weight loss and appetite suppression. Treatment with these agents should start at a low dose to minimize initial side effects (nausea being the limiting one). The major side effects are nausea, vomiting, and diarrhea Some patients taking insulin secretagogues may require a reduction in those agents to prevent hypoglycemia.
 α-Glucosidase inhibitor • reduce postprandial hyperglycemia by delaying glucose absorption Postprandial hyperglycemia, secondary to impaired hepatic and peripheral glucose disposal, contributes significantly to the hyperglycemic state in type 2 DM. These drugs, taken just before each meal, reduce glucose absorption by inhibiting the enzyme that cleaves oligosaccharides into simple sugars in the intestinal lumen. The major side effects (diarrhea, flatulence, abdominal distention) are related to increased delivery of oligosaccharides to he large bowel and can be reduced somewhat by gradual upward dose titration
Simultaneous treatment with bile acid resins and antacids should be avoided. These agents should not be used in individuals with • inflammatory bowel disease • gastroparesis •serum creatinine >2 mg/dL This class of agents is not as potent as other oral agents in lowering the HbA1c but is unique because it reduces the postprandial glucose rise even in individuals with type 1 DM
Thiazolidinediones   reduce insulin resistance by binding to the PPAR- (peroxisomeγ proliferator–activated receptor ) nuclear receptor (which forms aγ heterodimer with the retinoid X receptor). Agonists of this receptor regulate a large number of genes •promote adipocyte differentiation •reduce hepatic fat accumulation • promote fatty acid storage. • redistribution of fat from central to peripheral locations. •Circulating insulin levels decrease indicating a reduction in insulin resistance.
Thiazolidinediones are associated with: • weight gain (2–3 kg) •small reduction in the hematocrit •a mild increase in plasma volume • Peripheral edema and CHF are more common in individuals treated with these agents. •Changes in lipid profile •(Rosiglitazone raises low-density lipoprotein (LDL), high-density lipoprotein (HDL), and triglycerides slightly. Pioglitazone raises HDL to a greater degree and LDL a lesser degree but lowers triglycerides.) •worsening of diabetic macular edema. •increased risk of fractures has been noted in women •induce ovulation in premenopausal women with polycystic ovary syndrome. These agents are contraindicated in patients with liver disease or CHF (class III or IV).
Concerns about increased cardiovascular risk associated with rosiglitazone led to considerable restrictions on its use and to the FDA issuing a “black box” warning in 2007. However, based on new information, the FDA has revised its guidelines and categorizes rosiglitazone similar to other drugs for type 2 DM. Because of a possible increased risk of bladder cancer, pioglitazone is part of an ongoing FDA safety review.
Sodium-Glucose Co-Transporter 2 Inhibitors (SLGT2) These agents lower the blood glucose by selectively inhibiting this co- transporter, which is expressed almost exclusively in them proximal, convoluted tubule in the kidney . This inhibits glucose reabsorption, lowers the renal threshold for glucose, and leads to increased urinary glucose excretion. Thus, the glucose-lowering effect is insulin independent and not related to changes in insulin sensitivity or secretion. Adverse effects •urinary or vaginal infections are more common •the diuretic effect can lead to reduced intravascular volume. • increased incidence of hyperkalemia
Insulin therapy in type 2 DM. As the initial therapy in type 2 DM •in lean individuals or those with severe weight loss • in individuals with underlying renal or hepatic disease •in individuals who are hospitalized or acutely ill. Insulin therapy is ultimately required by a substantial number of individuals with type 2 DM because of the progressive nature of the disorder and the relative insulin deficiency that develops in patients with long-standing diabetes. Both physician and patient reluctance often delay the initiation of insulin therapy, but glucose control and patient well-being are improved by insulin therapy in patients who have not reached the glycemic target.
Choice of initial glucose-lowering agent : The level of hyperglycemia and the patient’s individualized goal should influence the initial choice of therapy. Assuming that maximal benefit of MNT and increased physical activity has been realized, patients with mild to moderate hyperglycemia (FPG 200– 250 mg/dL) often respond well to a single, oral glucose-lowering agent. Patients with more severe hyperglycemia (FPG >250 mg/dL) may respond partially but are unlikely to achieve normoglycemia with oral monotherapy.
A stepwise approach that starts with a single agent and adds a second agent to achieve the glycemic target can be used Insulin can be used as initial therapy in individuals with severe hyperglycemia (FPG < [250–300 mg/dL]) or in those who are symptomatic from the hyperglycemia. This approach is based on the rationale that more rapid glycemic control will reduce “glucose toxicity” to the islet cells, improve endogenous insulin secretion, and possibly allow oral glucose-lowering agents to be more effective. If this occurs, the insulin may be discontinued
Patient with type 2 diabetes Individualized glycemic goal Medical nutrition therapy, increased physical activity, weight loss + metformin Reassess HbA1c Combination therapy -metformin + second agent Reassess HbA1c Combination therapy -metformin + two other agents Insulin + metforminReassess HbA1c
Metformin’s advantages are that it • promotes mild weight loss • lowers insulin levels •improves the lipid profile slightly Based on SMBG results and the HbA1c, the dose of metformin should be increased until the glycemic target is achieved or maximum dose is reached. If metformin is not tolerated, then initial therapy with an insulin secretagogue or DPP-IV inhibitor is reasonable.
In clinical practice it is clear that a diabetic who is poorly endowed or emotionally unstable can pose a considerable therapeautic problem- Cooperation in treatment is essential There is indications that psychological stresses can be important in aggravating the disorder or precipitating episodes of loss of control, and even suggestions that emotional factors may sometimes bring the disorder in to being. -Wilkinson D.G.(1981) Psychiatric aspects of diabetes mellitus .British Journal of psychiatry 138,1-9. -Tattersall R.B (1981) Psychiatric aspects of diabetes – a physician ‘s view.British Journal of Psychiatry 139,485-493.
Emotional influences on the course of diabetes Emotionally stressful experiences can produce fluctuations in levels of blood glucose and ketone bodies,both in diabetic and non diabetic persons. -Hinkle L.E and Wolf S. (1952b)A summary of experimental evidence relating life stress to Diabetes Mellitus.Journal of the Mount Sinai Hospital 19,537-570. It has proved difficult,however to define the extent to which such factors may be operative in the actual disease.
Diabetes is a disorder of adaptation and that persons showing it have reacted to various life stresses with a physiological response that is appropriate to starvation.The pathway for such emotional origin would be via hypothalamic autonomic or pituitary endocrine relationships. -Treuting. T.F (1962) The role of emotional factors in the etiology and course of diabetes mellitus:a review of the recent literature.American journal of medical sciences 244,93-109 However no increase in incidence among battle casualities from 1st and 2nd world war. Stress may sometimes change a latent case of diabetes into an active one.
In long term studies by Hinkle & Wolf (1952) extending over several years, periods of exacerbation and remission were correlated with events in the life situation. Events which were consciously or unconsciously interpreted by the patients as threatening to their security appeared to be particularly liable to lead to loss of control. ?extend of direct metabolic consequences ?effect of abandoning dietary regimes or medicines ?effect of alcohol ?deliberately induced coma to secure attention
Insulin dependent Diabetes – ”the manipulators delight” Tattersall R.B (1981) Psychiatric aspects of diabetes – a physician ‘s view.British Journal of Psychiatry 139,485-493.
Baker and Barcai(1970) – a small number of juvenile diabetics in whom the emotional arousal led directly to ketoacidosis mediated by an increased ketone response to endogenous catecholamines. -Baker L. & Barcai A.(1970)Psychosomatic aspects of Diabetes Mellitus.Ch 7. in Modern trends of psychosomatic medicine.Vol 2,ed Hill.O.W. Butterworths:London -Treuting. T.F (1962) The role of emotional factors in the etiology and course of diabetes mellitus:a review of the recent literature.American journal of medical sciences 244,93-10
Psychological problems in Diabetes Juvenile Diabetics: Neurotic developments or disturbed family relationships,and hypochondriacal attitudes may be established Eating disorders including bulimia, anorexia nervosa more common. Difficulty in adhering to treatment especialy during loneliness, depression or tension. Explosive rebellion and wilful neglect of treatment. The anxiety of mother may be transferred to the child or a perfectionist mother may gain control over the illness at the cost of behaviour difficulties Child may utilise illness to manipulate home environment
• Minor abnormalities in measures of dependence/independence, self perception, manifest and latent anxiety and sexual identification. -Sterky G.(1963) Diabetic school children .Acta Pediatrica Scandinavica ,Suppl.144,1-39. -Swift C.R .,Seidman F & Stein h.(1967)Adjustment problems in juvenile diabetics .Psychosomatic Medicine 29, .555-571.
In adult life Employment or marriage prospects affected. Pruritis and decreased sexual interest, impotence and amenorrhoea,ocular problems may contribute to emotional complications and family life. Delayed psychosexual development when diabetes sets in an early age. -Surridge et al(1984) psychiatric aspects of Diabetes Mellitus. British journal of psychiatry 145,269-276. .
Increased frequency of impotence in men and anorgasmia in women. -Kolodny R.C 1971 .Sexual dysfunctions in diabetic females.Diabetes 20,557-559 Disturbances in ejaculation. -Fairburn et al(1982) The clinical features of diabetic impotence : A preliminary study .British journal of Psychiatry 140,447-452
Hypoglycemia Fear of attack May cause lassitude, depression, undue difficulty in waking, early morning headaches ,nocturnal fits. Affected appeared pale, apathetic, torpid and demoralised, others complained of lethargy, depression and difficulty in concentration -Gale E.A.M and Tattersall R.B. (1979) unrecognised nocturnal hypoglycemia in insulin treated diabetes. Lancet I,1049-1052
Diabetics chronically overtreated with insulin; their symptoms included excessive appetite , polydipsia, vertigo, mood swings ,irritability and chronic fatigue. -Schwandt P.,Richter W &Wilkening J.(1979) Chronic insulin overtreatment,Lancet 2,261-262 In management of manic depressive illness in diabetics it may sometimes be necessary to consider the possibility that insulin requirements increase during markedly depressive phases: -Crammer and Gillies(1981) -Kronfol et al. (1981)Psychiatric aspects of Diabetes Mellitus:diabetes and depression .British Journal of Psychiatry 139,172-173
The causal roles are unclear, although impaired central nervous system glucose metabolism, sedentary lifestyle, diet and smoking may all contribute. A recent study has shown that leptin, originally studied in relation to adipose tissue, has receptors in the limbic system and could have a potential role in emotional processes. Increasing the leptin signals in brain may be a new approach to treat depressive disorders. -Haupt D, Newcomer J. Depression is associated with hyperglycemia and other metabolic abnormalities. Diabetes Spectr 2004; 17 : 154-5. - Lu XY, Kim CS, Frazer A, Zhang W. Leptin: a potential novel antidepressant. Proc Natl Acad Sci USA 2006; 103 : 1593-8.
Persons with diabetes were twice as likely to have depression compared to those without diabetes. The odds of depression occurring in women were higher than in men
Brain damage in diabetics Episodes of hypoglycemia or diabetic coma may have contributed to brain damage, or associated atherosclerosis may be responsible. Study reflected some degree of brain damage or merely the psychological impact of a chronic disease at young age(<5yrs) -Act et al(1961) Intelligence in children with diabetes mellitus.Pediatrics 28,764-770
Ives(1963) surveyed 380 adult diabetics in the general hospital and found that 45 were mentally abnormal. 18- organic brain syndromes 9- personality disorders 4- psychotic -cerebral atherosclerosis was probably the responsible factor Similar studies by Bale(1973) It is possible that the association between impaired cognitive capacity and hypoglycemic episodes may merely reflect the fact that patients with poor endowement manage their diabetes less well
Incidence of brain parenchymal changes secondary to vascular changes are more in diabetics -Dandona et al(1978), Reske Neilsen and Lundback(1963),Grunnet (1963), Alex et al (1962).
Co-existence of diabetes and psychiatric illness Diabetes is difficult to manage as such, but patients with mental health disorders receive even less intensive medical care for diabetes - Desai MM, Rosenheck RA, Druss B, Perlin JB. Mental disorders and quality of diabetes care in the Veterans Health Administration. Am J Psychiatry 2002; 159 : 1584-90. - Frayne SM, Halanych JH, Miller DR, Wang F, Lin H, Pogach L, et al. Disparities in diabetes care: impact of mental illness. Arch Intern Med 2005; 165 : 2631-8. Self care behaviour in diabetes was adversely affected by the occurrence of natural calamities -Ramachandran A. Experiences of the WHO Collaborating Centre for Diabetes in India in managing tsunami victims with diabetes. Pract Diabetes Int 2005; 22 : 98-9.
Lesser degree of psychological distress not amounting to psychiatric morbidity is more common. Sridhar GR, Madhu K. Psychosocial and cultural issues in diabetes mellitus. Curr Sci 2002; 83 : 1556-64 There is recent intriguing evidence that maternal pre- and peri-natal depression can adversely impact the health of their infants, leading to poorer growth. Rahman A, Iqbal Z, Bunn J, Lovel H, Harrington R. Impact of maternal depression on infant nutritional status and illness: a cohort study. Arch Gen Psychiatry 2004; 61 : 946-52.
At the next step, a variety of psychological distress can occur when diabetes mellitus is first diagnosed: denial, anger, guilt, reactive depression and finally acceptance. Physicians must be aware of these reactions which are anticipated with chronic conditions. They must be trained to manage these, which may take months to resolve
In clinical practice, identification of depression in diabetes is often overlooked for a variety of reasons: •societal disapproval of depression •complicity between physicians and patients not to discuss depressive symptoms • wrongly considering depression as a ‘normal consequence of difficult medical illness’ The potential benefits of treatment are thereby missed. Lustman PJ, Clouse RE. Practical considerations in the management of depression in diabetes. Diabetes Spectr 2004; 17 : 160-6.
Use of antidepressant medications can disturb glycaemic control: •tricyclic antidepressants stimulate appetite •selective serotonin reuptake inhibitors suppress appetite, enhance insulin sensitivity and lead to hypoglycaemia if diet is not regulated. Besides, once depression is treated eating habits exercise and drug compliance may change, leading to unstable metabolic control. In the presence of autonomic neuropathy tricyclic antidepressants may worsen orthostatic hypotension, induce constipation and urinary retention Sridhar GR, Madhu K. Depression and psychosocial stress in diabetes mellitus. In: Kapur A, Joshi JK, editors. Novo nordisk diabetes update proc. Mumbai: Business Networ Inc; 2002 p. 87-92.
Psychotic disorders, obesity, metabolic syndrome and type 2 diabetes mellitus Schizophrenia was believed to be a predisposing factor to diabetes Patients with severe mental illness had higher prevalence of metabolic syndrome Outpatients with bipolar disorder had greater severity of illness with increasing number of co-morbid conditions including diabetes mellitus. There is evidence for type 2 diabetes and Alzheimer’s to occur together, because of common underlying pathogenetic mechanisms.
Atypical antipsychotic drugs have a propensity to induce weight gain in the following order: clozapine > olanzapine > thioridazine > quetiapine > chlorpromazine > risperidone > haloperidol > fluphenazine > ziprasidone The average short-term weight gain varies from a mean of 0.43 to 4.45 kg, with its attendant effects on carbohydrate and lipid metabolism. Clozapine and olanzapine, with a greater propensity to induce weight gain seem to be frequently associated with type 2 diabetes mellitus Consensus development conference on antipsychotic drugs and obesity and diabetes. Diabetes Care 2004; 27 : 596-601. .
A similar hierarchy exists for hyperlipidaemia: high for clozapine and olanzapine; low for risperidone. However a recent study from India which compared the use of olanzapine and haloperidol/trifluoperazine for 12 wk did not find a change in glycaemic status, weight or body mass index among the three drugs Guha P, Roy K, Sanyal D, Dasgupta T, Bhattacharya K. Olanzapine-induced obesity and diabetes in Indian patients: a prospective trial comparing olanzapine with typical antipsychotics. J Indian Med Assoc 2005; 103 : 660-4.
Mechanism -direct stimulation of appetite via feeding areas of the brain Indirectly by endocrine effects such as hyperprolactinaemia, decreased gonadal levels and hypercortisolism Environmental factors also contribute Even though definite conclusions cannot yet be drawn leptin and ghrelin levels are also being evaluated. Drug-induced insulin resistance, either directly or via stimulation of cytokine production, and interference with glucose transport across membranes. Tighe S, Dinan T. An overview of the central control of weight regulation and the effect of antipsychotic medication. J Psychopharmacology 2005; 19 (Suppl) : 36-46.
Conclusions Atypical Antipsychotic drugs Diabetes mellitus Cooperation in treatment is essential There is indications that psychological stresses can be important in aggravating the disorder or precipitating episodes of loss of control, and even suggestions that emotional factors may sometimes bring the disorder in to being. Increased incidence of DM with psychiatric illness
Diabetes mellitus-treatment and psychiatric effects

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In this document
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Dr. Megha Isac introduces diabetes mellitus management focusing on medical and psychiatric aspects.

Diagnosis criteria include blood glucose levels and A1C for diabetes. Adapted from ADA guidelines.

Type 1 diabetes diagnostic essentials: symptoms like polyuria, weight loss, and blood glucose levels.

Essentials of diagnosing Type 2 diabetes, highlighting symptoms common in diagnosed cases and complications.

Classification into Type 1 and Type 2 diabetes, along with details on causes such as autoimmune and idiopathic.

Other specific diabetes types include genetic defects, infections, and drug-induced causes.

Other uncommon diabetes forms and conditions associated with diabetes like gestational diabetes.

Global diabetes prevalence in 2013 is estimated at 382 million individuals aged 20-79.

Lists various risk factors for Type 2 diabetes, including obesity, family history, and hypertension.

Therapy goals: eliminate hyperglycemic symptoms, reduce complications, and support normal lifestyle.

Guidelines for comprehensive diabetes care focusing on glycemic control, screening, and patient education.

Specific treatment goals for adults with diabetes including HbA1c and glucose levels.

Balanced diets, carbohydrate limits, weight management, and cholesterol intake recommendations.

ADA recommendations for high soluble fiber foods in diabetic diets to regulate blood glucose.

Description of artificial sweeteners and their effects on blood sugar levels.

Emphasizes exercise benefits, guidelines for activity duration, and types of exercise recommended.

Overview of oral hypoglycemic agents used in diabetes treatment and their functions.

Details on insulin secretagogues and their action in increasing insulin secretion.

Properties of different insulin preparations, including duration and onset of action.

Overview of various insulin combinations for effective diabetes management.

Key components for insulin regimens that mimic physiological insulin secretion in Type 1.

Guidelines for adjusting insulin doses based on self-monitoring blood glucose (SMBG) results.

Amylin's role in glucose control and its benefits in treatment of diabetes.

Comprehensive approach to manage Type 2 diabetes, including lifestyle, diet, and medication.

Metformin's role in lowering glucose production, improving insulin sensitivity, and weight.

Metformin's dosing adjustments, side effects, and contraindications.

Explains insulin secretagogues' role in stimulating insulin release.

Prescription guidelines for sulfonylureas and their mechanism of increasing insulin.

Short-acting insulin agents' application to manage post-meal glucose spikes.

Potential hypoglycemia risks associated with sulfonylureas and management strategies.

DPP-IV inhibitors' mechanism to enhance GLP-1 action and insulin response.

Benefits of GLP-1 agonists in diabetes treatment and effects on weight loss.

Weight loss aspects of DPP-IV inhibitors and their side effects.

Effects of α-glucosidase inhibitors on postprandial hyperglycemia.

Guidelines for using α-glucosidase inhibitors and contraindications.

Thiazolidinediones' mechanism in reducing insulin resistance and potential side effects.

Monitoring and side effects associated with thiazolidinediones.

FDA updates regarding cardiovascular safety issues related to rosiglitazone.

Mechanism of SGLT2 inhibitors in diabetes management and associated risks.

Indications for initiating insulin therapy in Type 2 diabetes patients.

Factors influencing the choice of initial glucose-lowering agents based on hyperglycemia.

A structured, stepwise approach to manage diabetes and medications.

Combination therapy steps including metformin and other agents.

Metformin's benefits in weight control, insulin reduction, and tolerability.

Discusses the importance of psychological aspects in managing diabetes effectively.

Effect of emotional stress on blood glucose control in diabetes.

Describes diabetes as a response to life stresses and physiological impacts.

Longitudinal studies correlating diabetes control with life stress events.

Explores the emotional adjustment challenges faced by diabetes patients.

Psychosocial challenges experienced in juvenile diabetes management.

Impact of diabetes on adult life, intimacy, and emotional well-being.

Fear and psychological effects associated with hypoglycemia in diabetics.

Condition effects of chronic over-treatment and manic depressive illness in diabetics.

Research linking diabetes with depression and potential biochemical links.

Statistical data on higher incidence of depression among diabetes patients.

Exploring links between diabetic events and potential brain damage.

Findings from surveys concerning mental health disorders among diabetics.

Examines the coexistence of psychiatric disorders and diabetes management.

Impact of psychological factors on diabetes management in healthcare.

Reactions to diabetes diagnosis including denial and acceptance phases.

Barriers to identifying and treating depression in diabetic patients.

Effects of antidepressant medications on diabetes management and glycemic control.

Discusses antipsychotic medications' effects on diabetes and weight management.

Effects of atypical antipsychotics on weight gain and diabetes risk.

Exploration of leptin's role in appetite regulation and implications for diabetes.

Summarizes the importance of psychological well-being in diabetes management.

Diabetes mellitus-treatment and psychiatric effects

  • 1.
    Dr Megha Isac Juniorresident Dept. of General Medicine Diabetes Mellitus – Management and psychiatric aspects
  • 2.
    Criteria for theDiagnosis of Diabetes Mellitus • Symptoms of diabetes plus random blood glucose concentration 200 mg/dL or • Fasting plasma glucose ≥126 mg/dL or • Hemoglobin A1c ≥ 6.5%c or • 2-h plasma glucose ≥200 mg/dL during an oral glucose tolerance test (The test should be performed using a glucose load containing the equivalent of 75 g anhydrous glucose dissolved in water, not recommended for routine clinical use.) Source: Adapted from American Diabetes Association: Diabetes Care 37(Suppl 1):S14,2014
  • 3.
    Essentials of diagnosisEssentialsof diagnosis Type 1 diabetes  Polyuria, polydypsia and weight loss associated with random plasma glucose >/= 200 mg/dl  Plasma glucose of>/= 126mg/dl after an overnight fast,documented on more than one occasion.  Ketonemia, ketonuria ,or both.  Islet autoantibodies are frequently present.
  • 4.
    • Type 2diabetes • Most patients are over 40 yrs of age and obese. • Polyuria and polydypsia ,ketonuria and weight loss generally are uncommon at the time of diagnosis. candidial vaginitis in women may be an initial manifestation. Many patients have few or no symptoms. • Plasma glucose of >/=126mg/dl after an overnight fast on more than one occasion.2 hrs after 75 mg oral glucose, diagnostic values are >/=200 mg/dl • Hypertension, dyslipidemia and atherosclerosis are often associated
  • 5.
    Etiologic Classification ofDiabetes Mellitus Type 1 diabetes (beta cell destruction, usually leading to absolute insulin deficiency) •A. Immune-mediated •B. Idiopathic  Type 2 diabetes (may range from predominantly insulin resistance with relative insulin deficiency to a predominantly insulin secretory defect with insulin resistance)
  • 6.
    Other specific typesof diabetes A.Genetic defects of beta cell development or function B.Genetic defects in insulin action C.Diseases of the exocrine pancreas D.Endocrinopathies E.Drug- or chemical-induced glucocorticoids, vacor (a rodenticide), pentamidine, nicotinic acid, diazoxide, β-adrenergic agonists, thiazides, calcineurin and mTOR inhibitors, hydantoins, asparaginase, α-interferon, protease inhibitors, antipsychotics (atypicals and others), epinephrine F. Infections
  • 7.
    G. Uncommon formsof immune-mediated diabetes -anti-insulin receptor antibodies H. Other genetic syndromes sometimes associated with diabetes Down’s syndrome, Klinefelter’s syndrome, Turner’s syndrome, Huntington’s chorea, myotonic dystrophy I. Gestational diabetes mellitus (GDM) Source: Adapted from American Diabetes Association: Diabetes Care 37(Suppl 1)
  • 8.
    Worldwide prevalence ofdiabetes mellitus. Global estimate is 382 million individuals with diabetes. Regional estimates of the number of individuals with diabetes (20–79 yearsof age) are shown (2013). IDF Diabetes Atlas, the International Diabetes Federation, 2013.
  • 9.
    Risk Factors forType 2 Diabetes Mellitus Family history of diabetes (i.e., parent or sibling with type 2 diabetes) Obesity (BMI ≥25 kg/m2 or ethnically relevant definition for overweight) Physical inactivity Race/ethnicity (e.g., African American, Latino, Native American, Asian American, Pacific Islander) Previously identified with IFG, IGT, or an hemoglobin A1c of 5.7–6.4 History of GDM or delivery of baby >4 kg Hypertension (blood pressure ≥140/90 mmHg) HDL cholesterol level <35 mg/dL ) and/or a triglyceride level>250 mg/dL) Polycystic ovary syndrome or acanthosis nigricans History of cardiovascular disease
  • 11.
    The goals oftherapy (1)eliminate symptoms related to hyperglycemia(RBS<200mg/dl) (2) reduce or eliminate the long-term microvascular and macrovascular complications of DM (3) allow the patient to achieve as normal a lifestyle as possible.
  • 12.
    Guidelines for ComprehensiveMedical Care for Patients with Diabetes • Optimal and individualized glycemic control • Self-monitoring of blood glucose (individualized frequency) • HbA1c testing (2–4 times/year) • Patient education in diabetes management (annual); diabetes-self management ,education and support • Medical nutrition therapy and education (annual) • Eye examination (annual or biannual) • Foot examination (1–2 times/year by physician; daily by patient) • Screening for diabetic nephropathy (annual) • Blood pressure measurement (quarterly) • Lipid profile and serum creatinine (estimate GFR) (annual) • Influenza/pneumococcal/hepatitis B immunizations • Consider antiplatelet therapy
  • 13.
    Treatment Goals forAdults with Diabetes Index Goal Glycemic control HbA1c <7.0%c Preprandial capillary plasma glucose 80–130 mg/dL Peak postprandial capillary plasma glucose <180 mg/dL Blood pressure <140/90 mmHg Lipids Low-density lipoprotein < 100 mg/dL High-density lipoprotein >40 mg/dL in men >50 mg/dL in women Triglycerides <150 mg/dL
  • 14.
    Treatment regimenTreatment regimen •A well balanced nutritious diet remains a fundamental element of therapy Limiting the carbohydrate intake and substituting some of the calories with monosaturated fats such as olive oil ,rapeseed (canola) oil can lower TG and increase HDL. Weight reduction by caloric restriction is important goal. High protein intake may cause progression of kidney disease in patients with diabetic nephropathy; reduction in protein intake to 0.8 kg/day (or about 10% of total calories daily)is recommended. Limit cholesterol intake to 300 mg /day ,and in individuals with LDL cholesterol more than 100 mg/day should limit dietary cholesterol to 200 mg daily.
  • 15.
    Dietary Fiber ADA recommendsfood such as oatmeal, cereals and beans with relatively high soluble fiber content as staple components of the diet in diabetics. retards nutrient absorption rates High soluble fibre content in the diet has favourable effect on blood cholesterol levels.
  • 16.
    Artificial and othersweeteners Aspartame(aspartic acid and phenylalanine) -180 times as sweet as sucrose, not heat stable Saccharin,sacralose,acesulfame potassium –used for cooking and baking Sugar alcohols eg naturaly occuring in many fruits and vegetables, commercialy made from sucrose, glucose, starch- sorbitol,xylitol ,mannitol,lactitol, isomalt, maltitol and hydrogenated starch hydrolysates  used in “sugar free” food products  if consumed in large quantities will raise blood sugars and can cause bloating and diarrhoea
  • 17.
    Weight loss andexercise Multiple positive benefits including • cardiovascular risk reduction, reduced blood pressure • maintenance of muscle mass, reduction in body fat, and weight loss. For individuals with type1 or type 2 DM •lowers plasma glucose (during and following exercise) • increasing insulin sensitivity. Inpatients with diabetes, the ADA recommends 150 min/week (distributed over at least 3 days) of moderate aerobic physical activity withno gaps longer than 2 days. The exercise regimen should also include resistance training.
  • 19.
    ORAL HYPOGLYCEMIC AGENTS Biguanides •↓ Hepatic glucose production • Metformin α-Glucosidase inhibitors •↓ GI glucose absorption •Acarbose, miglitol, voglibose Dipeptidyl peptidase IV inhibitors •Prolong endogenous GLP-1 action •Alogliptin, Anagliptin, Gemigliptin, linagliptin, saxagliptin,sitagliptin, teneligliptin, vildagliptin
  • 20.
    Insulin secretagogues:Sulfonylureas ↑ Insulinsecretion Glibornuride, gliclazide, glimepiride, glipizide, gliquidone, glyburide, Glyclopyramide Insulin secretagogues:Nonsulfonylureas ↑ Insulin secretion Nateglinide, repaglinide, mitiglinide Sodium-glucose cotransporter 2 inhibitor ↑ Urinary glucose excretion Canagliflozin, dapagliflozin,empagliflozin Thiazolidinediones ↓ Insulin resistance, glucose utilization↑ Rosiglitazone, pioglitazone
  • 21.
    Properties of InsulinPreparations Time of Action(Hrs) Preparation Onset Peak EffectiveDuration Short-acting Aspart <0.25 0.5–1.5 2–4 Glulisine <0.25 0.5–1.5 2–4 Lispro <0.25 0.5–1.5 2–4 Regular 0.5–1.0 2–3 3–6 Long-acting Detemir 1–4 12-24 Glargine 2–4 20-24 NPH 2–4 4–10 10–16
  • 22.
    Insulin combinations 75/25 75% protaminelispro, 25% lispro <0.25 10–16 70/30 70% protamine aspart, 30% aspart <0.25 15-18 50/50 50% protamine lispro, 50% lispro <0.25 10–16 70/30 70% NPH, 30% regular 0.5–1 10–16
  • 23.
    Type 1 DiabetesMellitus The goal is to design and implement insulin regimens that mimic physiologic insulin secretion. In all regimens  long-acting insulins (NPH, glargine, or detemir) supply basal insulin regular, insulin aspart, glulisine, or lispro insulin provides prandial insulin
  • 24.
    HOW??HOW MUCH??? Short-acting insulinanalogues should be injected just before (<10 min) or just after a meal; regular insulin is given 30–45 min prior to a meal. Sometimes short-acting insulin analogues are injected just after a meal (gastroparesis, unpredictable food intake). In general, individuals with type 1 DM require 0.5–1 U/kg per day of insulin divided into multiple doses, with ~50% of the insulin given as basal insulin
  • 25.
    HOW TO ADJUSTDOSES???? The insulin dose in such regimens should be adjusted based on SMBG results with the following general assumptions: (1) the fasting glucose is primarily determined by the prior evening long- acting insulin (2) the pre-lunch glucose is a function of the morning short-acting insulin (3) the pre-supper glucose is a function of the morning long-acting insulin (4) the bedtime glucose is a function of the pre-supper, short-acting insulin. This is not an optimal regimen for the patient with type 1 DM, but is sometimes used for patients with type 2 DM.
  • 26.
    Amylin •A 37-amino-acid peptideco-secreted with insulin from pancreatic beta cells, in normal glucose homeostasis is uncertain. However, based on the rationale that patients who are insulin deficient are also amylin deficient, an analogue of amylin (pramlintide) was created and found to reduce postprandial glycemic excursions in type 1 and type 2 diabetic patients taking insulin. •Pramlintide injected just before a meal slows gastric emptying and suppresses glucagon but does not alter insulin levels. Addition of pramlintide produces a modest reduction in the HbA1c and seems to dampen meal-related glucose excursions. In type 1 DM, pramlintide is started as a 15- g SC injection before eachμ meal and titrated up to a maximum of 30–60 g as tolerated.μ In type 2 DM, pramlintide is started as a 60- g SC injection before eachμ meal and may be titrated up to a maximum of 120 g.μ
  • 27.
    Management of Type2 Diabetes Individualized glycemic control • Diet/lifestyle • Exercise • Medication Treat associated conditions • Dyslipidemia • Hypertension • Obesity • Coronary heart disease Screen for/manage complications of diabetes • Retinopathy • Cardiovascular disease • Nephropathy • Neuropathy • Other complications
  • 28.
    Biguanides  Metformin, representative ofthis class of agents • reduces hepatic glucose production • improves peripheral glucose utilization •Mild increase in insulin sensitivity Metformin activates AMP-dependent protein kinase and enters cells through organic cation transporters (polymorphisms of these may influence the response to metformin). Recent evidence indicates that metformin’s mechanism for reducing hepatic glucose production is to antagonize glucagon’s ability to generate cAMP in hepatocytes. • reduces fasting plasma glucose (FPG) and insulin levels • improves the lipid profile •Promotes modest weight loss.
  • 29.
    An extended-release formis available and may have fewer gastrointestinal side effects (diarrhea, anorexia, nausea, metallic taste). Because of its relatively slow onset of action and gastrointestinal symptoms with higher doses, the initial dose should be low and then escalated every 2–3 weeks based on SMBG measurements. Metformin is effective as monotherapy and can be used in combination with other oral agents or with insulin. The major toxicity of metformin, lactic acidosis, is very rare and can be prevented by careful patient selection. Vitamin B12 levels are ~30% lower during metformin treatment.
  • 30.
    Metformin should notbe used in patients with 1. renal insufficiency (glomerular filtration rate [GFR] <60 mL/min) 2.any form of acidosis 3.unstable congestive heart failure (CHF) 4. liver disease 5.severe hypoxemia. Metformin should be discontinued in hospitalized patients, in patients who can take nothing orally, and in those receiving radiographic contrast material. Insulin should be used until metformin can be restarted.
  • 31.
    Insulin secretagogues stimulateinsulin secretion by interacting with the ATP-sensitive potassium channel on the beta cell These drugs are most effective in individuals with type 2 DM of relatively recent onset (<5 years) who have residual endogenous insulin production. First-generation sulfonylureas (chlorpropamide, tolazamide, tolbutamide) have a longer half-life, a greater incidence of hypoglycemia and more frequent drug interactions, and are no longer used. Second-generation sulfonylureas have a more rapid onset of action and better coverage of the postprandial glucose rise, but the shorter half-life of some agents may require more than once-a-day dosing
  • 32.
    Sulfonylureas reduce bothfasting and postprandial glucose and should be initiated at low doses and increased at 1- to 2- week intervals based on SMBG. In general, sulfonylureas increase insulin acutely and thus should be taken shortly before a meal; with chronic therapy, though, the insulin release is more sustained. Glimepiride and glipizide can be given in a single daily dose and are preferred over glyburide, especially in the elderly
  • 33.
    Repaglinide, nateglinide, andmitiglinide are not sulfonylureas but also interact with the ATP-sensitive potassium channel. Because of their short half-life, these agents are given with each meal or immediately before to reduce meal-related glucose excursions.
  • 34.
    Insulin secretagogues, especiallythe longer acting ones, have the potential to cause hypoglycemia, especially in elderly individuals. Most sulfonylureas are metabolized in the liver to compounds (some of which are active) that are cleared by the kidney. Thus, their use in individuals with significant hepatic or renal dysfunction is not advisable. Weight gain, a common side effect of sulfonylurea therapy, results from the increased insulin levels and improvement in glycemic control. Some sulfonylureas have significant drug interactions with alcohol and some medications including warfarin, aspirin, ketoconazole, α- glucosidase inhibitors, and fluconazole
  • 35.
    DPP-IV inhibitors inhibitdegradation of native GLP-1 and thus enhance the incretin effect. Incretins” amplify glucose-stimulated insulin secretion. DPP-IV, which is widely expressed on the cell surface of endothelial cells and some lymphocytes, degrades a wide range of peptides (not GLP-1 specific). Exenatide is an analogue of GLP-1. Unlike native GLP-1, which has a half-life of >5 min, differences in the exenatide amino acid sequence render it resistant to the enzyme that degrades GLP-1 (dipeptidyl peptidase IV [DPP-IV]). Thus, exenatide has prolonged GLP-1-like action and binds to GLP-1 receptors found in islets, the gastrointestinal tract, and the brain. GLP-1 receptor agonists increase glucose-stimulated insulin secretion, suppress glucagon, and slow gastric emptying
  • 36.
    DPP-IV inhibitors promoteinsulin secretion in the absence of hypoglycemia (unless there is concomitant use of an agent that can lead to hypoglycemia—sulfonylureas, etc.) or weight gain and appear to have a preferential effect on postprandial blood glucose. The levels of GLP-1 action in the patient are greater with the GLP-1 receptor agonists than with DPP-IV inhibitors. Reduced doses should be given to patients with renal insufficiency . Initial concerns about the pancreatic side effects of GLP-1 receptor agonists and DPP-IV inhibitors (pancreatitis, possible premalignant lesions) appear to be unfounded.
  • 37.
    These agents donot promote weight gain; in fact, most patients experience modest weight loss and appetite suppression. Treatment with these agents should start at a low dose to minimize initial side effects (nausea being the limiting one). The major side effects are nausea, vomiting, and diarrhea Some patients taking insulin secretagogues may require a reduction in those agents to prevent hypoglycemia.
  • 38.
     α-Glucosidase inhibitor • reducepostprandial hyperglycemia by delaying glucose absorption Postprandial hyperglycemia, secondary to impaired hepatic and peripheral glucose disposal, contributes significantly to the hyperglycemic state in type 2 DM. These drugs, taken just before each meal, reduce glucose absorption by inhibiting the enzyme that cleaves oligosaccharides into simple sugars in the intestinal lumen. The major side effects (diarrhea, flatulence, abdominal distention) are related to increased delivery of oligosaccharides to he large bowel and can be reduced somewhat by gradual upward dose titration
  • 39.
    Simultaneous treatment withbile acid resins and antacids should be avoided. These agents should not be used in individuals with • inflammatory bowel disease • gastroparesis •serum creatinine >2 mg/dL This class of agents is not as potent as other oral agents in lowering the HbA1c but is unique because it reduces the postprandial glucose rise even in individuals with type 1 DM
  • 40.
    Thiazolidinediones   reduce insulin resistanceby binding to the PPAR- (peroxisomeγ proliferator–activated receptor ) nuclear receptor (which forms aγ heterodimer with the retinoid X receptor). Agonists of this receptor regulate a large number of genes •promote adipocyte differentiation •reduce hepatic fat accumulation • promote fatty acid storage. • redistribution of fat from central to peripheral locations. •Circulating insulin levels decrease indicating a reduction in insulin resistance.
  • 41.
    Thiazolidinediones are associatedwith: • weight gain (2–3 kg) •small reduction in the hematocrit •a mild increase in plasma volume • Peripheral edema and CHF are more common in individuals treated with these agents. •Changes in lipid profile •(Rosiglitazone raises low-density lipoprotein (LDL), high-density lipoprotein (HDL), and triglycerides slightly. Pioglitazone raises HDL to a greater degree and LDL a lesser degree but lowers triglycerides.) •worsening of diabetic macular edema. •increased risk of fractures has been noted in women •induce ovulation in premenopausal women with polycystic ovary syndrome. These agents are contraindicated in patients with liver disease or CHF (class III or IV).
  • 42.
    Concerns about increasedcardiovascular risk associated with rosiglitazone led to considerable restrictions on its use and to the FDA issuing a “black box” warning in 2007. However, based on new information, the FDA has revised its guidelines and categorizes rosiglitazone similar to other drugs for type 2 DM. Because of a possible increased risk of bladder cancer, pioglitazone is part of an ongoing FDA safety review.
  • 43.
    Sodium-Glucose Co-Transporter 2Inhibitors (SLGT2) These agents lower the blood glucose by selectively inhibiting this co- transporter, which is expressed almost exclusively in them proximal, convoluted tubule in the kidney . This inhibits glucose reabsorption, lowers the renal threshold for glucose, and leads to increased urinary glucose excretion. Thus, the glucose-lowering effect is insulin independent and not related to changes in insulin sensitivity or secretion. Adverse effects •urinary or vaginal infections are more common •the diuretic effect can lead to reduced intravascular volume. • increased incidence of hyperkalemia
  • 44.
    Insulin therapy intype 2 DM. As the initial therapy in type 2 DM •in lean individuals or those with severe weight loss • in individuals with underlying renal or hepatic disease •in individuals who are hospitalized or acutely ill. Insulin therapy is ultimately required by a substantial number of individuals with type 2 DM because of the progressive nature of the disorder and the relative insulin deficiency that develops in patients with long-standing diabetes. Both physician and patient reluctance often delay the initiation of insulin therapy, but glucose control and patient well-being are improved by insulin therapy in patients who have not reached the glycemic target.
  • 45.
    Choice of initialglucose-lowering agent : The level of hyperglycemia and the patient’s individualized goal should influence the initial choice of therapy. Assuming that maximal benefit of MNT and increased physical activity has been realized, patients with mild to moderate hyperglycemia (FPG 200– 250 mg/dL) often respond well to a single, oral glucose-lowering agent. Patients with more severe hyperglycemia (FPG >250 mg/dL) may respond partially but are unlikely to achieve normoglycemia with oral monotherapy.
  • 46.
    A stepwise approachthat starts with a single agent and adds a second agent to achieve the glycemic target can be used Insulin can be used as initial therapy in individuals with severe hyperglycemia (FPG < [250–300 mg/dL]) or in those who are symptomatic from the hyperglycemia. This approach is based on the rationale that more rapid glycemic control will reduce “glucose toxicity” to the islet cells, improve endogenous insulin secretion, and possibly allow oral glucose-lowering agents to be more effective. If this occurs, the insulin may be discontinued
  • 47.
    Patient with type2 diabetes Individualized glycemic goal Medical nutrition therapy, increased physical activity, weight loss + metformin Reassess HbA1c Combination therapy -metformin + second agent Reassess HbA1c Combination therapy -metformin + two other agents Insulin + metforminReassess HbA1c
  • 48.
    Metformin’s advantages arethat it • promotes mild weight loss • lowers insulin levels •improves the lipid profile slightly Based on SMBG results and the HbA1c, the dose of metformin should be increased until the glycemic target is achieved or maximum dose is reached. If metformin is not tolerated, then initial therapy with an insulin secretagogue or DPP-IV inhibitor is reasonable.
  • 50.
    In clinical practiceit is clear that a diabetic who is poorly endowed or emotionally unstable can pose a considerable therapeautic problem- Cooperation in treatment is essential There is indications that psychological stresses can be important in aggravating the disorder or precipitating episodes of loss of control, and even suggestions that emotional factors may sometimes bring the disorder in to being. -Wilkinson D.G.(1981) Psychiatric aspects of diabetes mellitus .British Journal of psychiatry 138,1-9. -Tattersall R.B (1981) Psychiatric aspects of diabetes – a physician ‘s view.British Journal of Psychiatry 139,485-493.
  • 51.
    Emotional influences onthe course of diabetes Emotionally stressful experiences can produce fluctuations in levels of blood glucose and ketone bodies,both in diabetic and non diabetic persons. -Hinkle L.E and Wolf S. (1952b)A summary of experimental evidence relating life stress to Diabetes Mellitus.Journal of the Mount Sinai Hospital 19,537-570. It has proved difficult,however to define the extent to which such factors may be operative in the actual disease.
  • 52.
    Diabetes is adisorder of adaptation and that persons showing it have reacted to various life stresses with a physiological response that is appropriate to starvation.The pathway for such emotional origin would be via hypothalamic autonomic or pituitary endocrine relationships. -Treuting. T.F (1962) The role of emotional factors in the etiology and course of diabetes mellitus:a review of the recent literature.American journal of medical sciences 244,93-109 However no increase in incidence among battle casualities from 1st and 2nd world war. Stress may sometimes change a latent case of diabetes into an active one.
  • 53.
    In long termstudies by Hinkle & Wolf (1952) extending over several years, periods of exacerbation and remission were correlated with events in the life situation. Events which were consciously or unconsciously interpreted by the patients as threatening to their security appeared to be particularly liable to lead to loss of control. ?extend of direct metabolic consequences ?effect of abandoning dietary regimes or medicines ?effect of alcohol ?deliberately induced coma to secure attention
  • 54.
    Insulin dependent Diabetes –”the manipulators delight” Tattersall R.B (1981) Psychiatric aspects of diabetes – a physician ‘s view.British Journal of Psychiatry 139,485-493.
  • 55.
    Baker and Barcai(1970)– a small number of juvenile diabetics in whom the emotional arousal led directly to ketoacidosis mediated by an increased ketone response to endogenous catecholamines. -Baker L. & Barcai A.(1970)Psychosomatic aspects of Diabetes Mellitus.Ch 7. in Modern trends of psychosomatic medicine.Vol 2,ed Hill.O.W. Butterworths:London -Treuting. T.F (1962) The role of emotional factors in the etiology and course of diabetes mellitus:a review of the recent literature.American journal of medical sciences 244,93-10
  • 56.
    Psychological problems inDiabetes Juvenile Diabetics: Neurotic developments or disturbed family relationships,and hypochondriacal attitudes may be established Eating disorders including bulimia, anorexia nervosa more common. Difficulty in adhering to treatment especialy during loneliness, depression or tension. Explosive rebellion and wilful neglect of treatment. The anxiety of mother may be transferred to the child or a perfectionist mother may gain control over the illness at the cost of behaviour difficulties Child may utilise illness to manipulate home environment
  • 57.
    • Minor abnormalitiesin measures of dependence/independence, self perception, manifest and latent anxiety and sexual identification. -Sterky G.(1963) Diabetic school children .Acta Pediatrica Scandinavica ,Suppl.144,1-39. -Swift C.R .,Seidman F & Stein h.(1967)Adjustment problems in juvenile diabetics .Psychosomatic Medicine 29, .555-571.
  • 58.
    In adult life Employmentor marriage prospects affected. Pruritis and decreased sexual interest, impotence and amenorrhoea,ocular problems may contribute to emotional complications and family life. Delayed psychosexual development when diabetes sets in an early age. -Surridge et al(1984) psychiatric aspects of Diabetes Mellitus. British journal of psychiatry 145,269-276. .
  • 59.
    Increased frequency ofimpotence in men and anorgasmia in women. -Kolodny R.C 1971 .Sexual dysfunctions in diabetic females.Diabetes 20,557-559 Disturbances in ejaculation. -Fairburn et al(1982) The clinical features of diabetic impotence : A preliminary study .British journal of Psychiatry 140,447-452
  • 60.
    Hypoglycemia Fear of attack Maycause lassitude, depression, undue difficulty in waking, early morning headaches ,nocturnal fits. Affected appeared pale, apathetic, torpid and demoralised, others complained of lethargy, depression and difficulty in concentration -Gale E.A.M and Tattersall R.B. (1979) unrecognised nocturnal hypoglycemia in insulin treated diabetes. Lancet I,1049-1052
  • 61.
    Diabetics chronically overtreatedwith insulin; their symptoms included excessive appetite , polydipsia, vertigo, mood swings ,irritability and chronic fatigue. -Schwandt P.,Richter W &Wilkening J.(1979) Chronic insulin overtreatment,Lancet 2,261-262 In management of manic depressive illness in diabetics it may sometimes be necessary to consider the possibility that insulin requirements increase during markedly depressive phases: -Crammer and Gillies(1981) -Kronfol et al. (1981)Psychiatric aspects of Diabetes Mellitus:diabetes and depression .British Journal of Psychiatry 139,172-173
  • 62.
    The causal rolesare unclear, although impaired central nervous system glucose metabolism, sedentary lifestyle, diet and smoking may all contribute. A recent study has shown that leptin, originally studied in relation to adipose tissue, has receptors in the limbic system and could have a potential role in emotional processes. Increasing the leptin signals in brain may be a new approach to treat depressive disorders. -Haupt D, Newcomer J. Depression is associated with hyperglycemia and other metabolic abnormalities. Diabetes Spectr 2004; 17 : 154-5. - Lu XY, Kim CS, Frazer A, Zhang W. Leptin: a potential novel antidepressant. Proc Natl Acad Sci USA 2006; 103 : 1593-8.
  • 63.
    Persons with diabeteswere twice as likely to have depression compared to those without diabetes. The odds of depression occurring in women were higher than in men
  • 64.
    Brain damage indiabetics Episodes of hypoglycemia or diabetic coma may have contributed to brain damage, or associated atherosclerosis may be responsible. Study reflected some degree of brain damage or merely the psychological impact of a chronic disease at young age(<5yrs) -Act et al(1961) Intelligence in children with diabetes mellitus.Pediatrics 28,764-770
  • 65.
    Ives(1963) surveyed 380adult diabetics in the general hospital and found that 45 were mentally abnormal. 18- organic brain syndromes 9- personality disorders 4- psychotic -cerebral atherosclerosis was probably the responsible factor Similar studies by Bale(1973) It is possible that the association between impaired cognitive capacity and hypoglycemic episodes may merely reflect the fact that patients with poor endowement manage their diabetes less well
  • 66.
    Incidence of brainparenchymal changes secondary to vascular changes are more in diabetics -Dandona et al(1978), Reske Neilsen and Lundback(1963),Grunnet (1963), Alex et al (1962).
  • 67.
    Co-existence of diabetesand psychiatric illness Diabetes is difficult to manage as such, but patients with mental health disorders receive even less intensive medical care for diabetes - Desai MM, Rosenheck RA, Druss B, Perlin JB. Mental disorders and quality of diabetes care in the Veterans Health Administration. Am J Psychiatry 2002; 159 : 1584-90. - Frayne SM, Halanych JH, Miller DR, Wang F, Lin H, Pogach L, et al. Disparities in diabetes care: impact of mental illness. Arch Intern Med 2005; 165 : 2631-8. Self care behaviour in diabetes was adversely affected by the occurrence of natural calamities -Ramachandran A. Experiences of the WHO Collaborating Centre for Diabetes in India in managing tsunami victims with diabetes. Pract Diabetes Int 2005; 22 : 98-9.
  • 68.
    Lesser degree ofpsychological distress not amounting to psychiatric morbidity is more common. Sridhar GR, Madhu K. Psychosocial and cultural issues in diabetes mellitus. Curr Sci 2002; 83 : 1556-64 There is recent intriguing evidence that maternal pre- and peri-natal depression can adversely impact the health of their infants, leading to poorer growth. Rahman A, Iqbal Z, Bunn J, Lovel H, Harrington R. Impact of maternal depression on infant nutritional status and illness: a cohort study. Arch Gen Psychiatry 2004; 61 : 946-52.
  • 69.
    At the nextstep, a variety of psychological distress can occur when diabetes mellitus is first diagnosed: denial, anger, guilt, reactive depression and finally acceptance. Physicians must be aware of these reactions which are anticipated with chronic conditions. They must be trained to manage these, which may take months to resolve
  • 70.
    In clinical practice,identification of depression in diabetes is often overlooked for a variety of reasons: •societal disapproval of depression •complicity between physicians and patients not to discuss depressive symptoms • wrongly considering depression as a ‘normal consequence of difficult medical illness’ The potential benefits of treatment are thereby missed. Lustman PJ, Clouse RE. Practical considerations in the management of depression in diabetes. Diabetes Spectr 2004; 17 : 160-6.
  • 71.
    Use of antidepressantmedications can disturb glycaemic control: •tricyclic antidepressants stimulate appetite •selective serotonin reuptake inhibitors suppress appetite, enhance insulin sensitivity and lead to hypoglycaemia if diet is not regulated. Besides, once depression is treated eating habits exercise and drug compliance may change, leading to unstable metabolic control. In the presence of autonomic neuropathy tricyclic antidepressants may worsen orthostatic hypotension, induce constipation and urinary retention Sridhar GR, Madhu K. Depression and psychosocial stress in diabetes mellitus. In: Kapur A, Joshi JK, editors. Novo nordisk diabetes update proc. Mumbai: Business Networ Inc; 2002 p. 87-92.
  • 72.
    Psychotic disorders, obesity,metabolic syndrome and type 2 diabetes mellitus Schizophrenia was believed to be a predisposing factor to diabetes Patients with severe mental illness had higher prevalence of metabolic syndrome Outpatients with bipolar disorder had greater severity of illness with increasing number of co-morbid conditions including diabetes mellitus. There is evidence for type 2 diabetes and Alzheimer’s to occur together, because of common underlying pathogenetic mechanisms.
  • 73.
    Atypical antipsychotic drugshave a propensity to induce weight gain in the following order: clozapine > olanzapine > thioridazine > quetiapine > chlorpromazine > risperidone > haloperidol > fluphenazine > ziprasidone The average short-term weight gain varies from a mean of 0.43 to 4.45 kg, with its attendant effects on carbohydrate and lipid metabolism. Clozapine and olanzapine, with a greater propensity to induce weight gain seem to be frequently associated with type 2 diabetes mellitus Consensus development conference on antipsychotic drugs and obesity and diabetes. Diabetes Care 2004; 27 : 596-601. .
  • 74.
    A similar hierarchyexists for hyperlipidaemia: high for clozapine and olanzapine; low for risperidone. However a recent study from India which compared the use of olanzapine and haloperidol/trifluoperazine for 12 wk did not find a change in glycaemic status, weight or body mass index among the three drugs Guha P, Roy K, Sanyal D, Dasgupta T, Bhattacharya K. Olanzapine-induced obesity and diabetes in Indian patients: a prospective trial comparing olanzapine with typical antipsychotics. J Indian Med Assoc 2005; 103 : 660-4.
  • 75.
    Mechanism -direct stimulation ofappetite via feeding areas of the brain Indirectly by endocrine effects such as hyperprolactinaemia, decreased gonadal levels and hypercortisolism Environmental factors also contribute Even though definite conclusions cannot yet be drawn leptin and ghrelin levels are also being evaluated. Drug-induced insulin resistance, either directly or via stimulation of cytokine production, and interference with glucose transport across membranes. Tighe S, Dinan T. An overview of the central control of weight regulation and the effect of antipsychotic medication. J Psychopharmacology 2005; 19 (Suppl) : 36-46.
  • 76.
    Conclusions Atypical Antipsychotic drugsDiabetes mellitus Cooperation in treatment is essential There is indications that psychological stresses can be important in aggravating the disorder or precipitating episodes of loss of control, and even suggestions that emotional factors may sometimes bring the disorder in to being. Increased incidence of DM with psychiatric illness