Life Style disorder


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Life Style disorder

  1. 1. Natural history of disease  The phrase natural history of disease signifies the way in which a disease evolves over time from the earliest phase to its termination, i.e., in recovery, disability or death, without treatment or prevention. The importance of study of natural history of disease lies in the control of disease stages and prevention of complications.  All preventive measures are based on the knowledge of its natural history which depends on 2 sets of condition; pre-pathogenic phase and pathogenic phase.
  2. 2. Foetal origin of adult onset disease The theory of fetal origins of disease is that nutritional deprivation of the fetus during critical periods of development forces the baby to resort to adaptive survival strategies, which entail a resetting of the normal course of metabolic, physiological, and anatomical development. These adaptations become maladaptive if the organism encounters contrasting nutritional circumstances in later life. It has also become clear that maternal constraint must have a central role in fetal programming. Under such circumstances, maternal uterine constraint becomes a dominant regulator of fetal growth. Shortness and fatness are thought to be the result of maternal hyperglycaemia, with consequent imbalance in the supply of glucose Andother nutrients to the fetus.
  3. 3. Over the past two decades, it has been increasingly recognized that the risk of adult health disorders, particularly metabolic syndrome, can be markedly influenced by prenatal and infant environmental exposures (i.e., developmental programming). Low birth weight, together with infant catch-up growth, is associated with a significant risk of adult obesity and cardiovascular disease, as well as adverse effects on pulmonary, renal, and cerebral function. Conversely, exposure to maternal obesity or high birth weight also represents an increased risk for childhood and adult obesity. In addition, fetal exposure to select chemicals (eg, phytoestrogens) or environmental pollutants (eg, tobacco smoke) may affect the predisposition to adult disease. Under nutrition change the structure and function of the body etc . Prenatal care is transitioning to incorporate goals of optimizing maternal, fetal, and neonatal health to prevent or reduce adult-onset diseases. Guidelines regarding optimal pregnancy nutrition and weight gain, management of low- and high-fetal-weight pregnancies, use of maternal glucocorticoids, and newborn feeding strategies, among others, have yet to fully integrate long-term consequences on adult health.  Studies in southern India have shown that babies who are short and fat tend to become insulin deficient and have high rates of non-insulin dependent diabetes.  The basic premise of the thrifty gene hypothesis is that certain populations may have genes that determine increased fat storage, which in times of famine represent a survival advantage, but in a modern environment result in obesity and type 2 diabetes. The fetal origins theory is of greatest relevance to the developing world 
  4. 4. Barker‟s Hypothesis FOAD  Fetal origins of adult-onset diseases (FOAD)  Under nutrition and unfavorable intrauterine environment at critical periods in early life can cause permanent changes (in both structure and function) in developing systems of the fetus (i.e. programming).  May manifest as disease over a period of time due to `dysadaptation‘ with changed environmental circumstances 1986
  5. 5. Developmental origins of adult disease: hypothesis Maternal malnutrition Placental transfer Fetal genome FETAL UNDERNUTRITION (Nutrient demand exceeds supply) Altered body composition Early maturation Down regulation of growth Muscle mass Fat mass  HYPERLIPIDAEMI A HYPERTENSION Cortisol  Brain sparing Impaired development (Liver, Pancreas, Blood vessels) CENTRAL OBESITY INSULIN RESISTANCE Type 2 Diabetes and CHD
  6. 6. Assessment Panels 1. JNC7( Joint National Committee for Detection, Evaluation and Treatment of High Blood Pressure) by the U.S. DEPARTMENT OF HEALTH AND HUMAN SERVICES, supported by National Institutes of Health, National Heart, Lung, and Blood Institute, National High Blood Pressure Education Program in August 2004. 2. NCEP ATP (National Cholesterol Education Program (NCEP) Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III) by National Heart, Lung, and Blood Institute, National Institutes of Health in September 2002, updated in 2004. 3. International Diabetes Federation ( The International Diabetes Federation (IDF) is a worldwide alliance of some 200 diabetes associations in more than 160 countries, who have come together to enhance the lives of people with diabetes everywhere. The Federation is committed to raising global awareness of diabetes, promoting appropriate diabetes care and prevention, and encouraging activities towards finding a cure for the different types of diabetes, released in 2006. 4. IHS ( Indian Health Services) Guidelines for Care of Adults with Prediabetes and/or the Metabolic Syndrome in Clinical Settings (April 2006).The purpose of these guidelines is to help provide consistent, quality care to adults with Prediabetes and the Metabolic Syndrome and prevent diabetes and cardiovascular disease.
  7. 7. Latent stage Pre-clinical stage Early secondary clinical presentation Late Terminal secondary clinical clinical presentation presentation Individual with latent miasm Individual with risk factors 9miasmatc markers present0, suitable exciting stimulus; precipitates the syndrome Early signs, symptoms and pathology, which is mostly reversible Pathological changes are established, and become obstruction to recovery Chronic state with disability and defect9compli cations0 Primordial prevention Primary prevention Early secondary prevention Late secondary prevention Tertiary prevention Health promotion Specific protection Early diagnosis and treatment Effective control of disease Disability limitation and rehabilitation Miasmatic treatment Constitutional with intercurrent miasmatic treatment Constitutional and symptomatic Symptomatic and organospecific treatment Conservative palliative treatment
  8. 8.  Pre-pathogenic phase (dynamic)- in this all intrinsic and extrinsic factors interact to shift the equilibrium of health preparing the ground for disequilibrium i.e., the disease.  Pathogenic phase (organic) - in this the patient shifts from stage of no signs to early signs of disease again depends whether such signs can be elicited by clinical or laboratory methods. Levels of prevention  Primordial prevention -at this stage prevention is not directed against any particular disease, it aims to improve the general health and well being of the person.  Primary prevention- it is specific disease prevention and signifies intervention in pre pathogenesis phase of a disease.  Secondary prevention (early and late secondary)- early secondary prevention involves early diagnosis (which can be determined by conducting screening tests and giving prompt and appropriate treatment to restore the illness before any pathological changes takes place.  Late secondary prevention attempts to arrest disease process; to provide the symptomatic relief and to minimise the complications.
  9. 9.  Tertiary prevention- It is an intervention in late pathogenesis phase. Patient has already developed some of the complications. Modes of interventions  Health promotion- It is the practise of enabling people to increase control and to improve health. its main thrust is to strengthen the individual through: 1.Health education 2.Environmental modification 3.Nutritional intervention 4.Lifestyle intervention 5.Behavioural changes  Specific protection- Prophylaxis , use of specific nutrients, protection against occupational hazards, protection against accidents, protection against carcinogens, avoidance of allergens, control of consumer quality products.  Early detection and treatment- It involves early detection of disturbances in homeostatic and compensatory mechanism while biochemical, morphological, and functional changes are still reversible.  Disability limitations and rehabilitations
  10. 10. Constitution, diathesis and susceptibility  Constitution is defined as the aggregate of hereditary characters  1. 2.    influenced by environment, which determines the individual‘s reaction, successful or unsuccessful to the stress of the environment. The constitution of the person depends on the two basic factors: Endogenous factor- which are acquired at the time of birth and are called genotype. Exogenous factor- different environmental factors. Both theses endogenous and exogenous factors become intimately intermingles resulting in the expression of what is called phenotype. Classical eg isAsian Indian Phenotype (Thin-Fat Asian Indian) At any body mass index (BMI) and age, Asian Indians have higher body fat, visceral fat and waist circumference (WC); lower skeletal muscle mass; thinner hips; short legs; profoundly higher rates of insulin resistance, metabolic syndrome, diabetes, dyslipidemia hypoadiponectinemia, and increased cardiovascular risk than Europids.1-8 These unique clinical and biochemical characteristics that are commonly found among Asian Indians in particular and South Asians in general are collectively referred to as the ―Asian Indian Phenotype‖ or thin –fat phenotype. At comparable levels of total body fat, intra abdominal fat and subcutaneous abdominal fat, Asian Indians have significantly larger adipocytes compared to Europids and is correlated with insulin resistance
  11. 11.  Diathesis can be defined as a constitutional weakness which leads to a morbid disposition for specific pathological process in evolution of a disease.  Psoric diathesis Sycotic diathesis- gout, rheumatic conditions, inflammatory conditions involving the urogenital system, liver and gall bladder diseases, and renal stone formation. Metabolic disorders, diabetes, hyperlipidemia, atherosclerosis and coronary artery disease.  Syphilitic diathesis- carcinoma, and other malignant growths, dementia, hypertensive stroke, hypertensive nephropathy and retinopathy
  12. 12.  Susceptibility is defined as a quality of the living organism to react  1. 2. 3. 4. 5. against any stimulus. It is more in those : Who have delicate physical build. Intellectual persons Impulsive, jealous and temperamental Intellectual occupations, with sedentary lifestyle People with effeminate trait  It is less in: 1. Dull subjects 2. Those who are slow to act and comprehensive 3. Those who are coarse in physical build 4. People who are engaged in physical labour 5. Mentally retarded persons
  13. 13. Abstract  South Asia is home to one of the largest population of people with metabolic syndrome (MetS). The prevalence of MetS in South Asians varies according to region, extent of urbanization, lifestyle patterns, and socioeconomic/cultural factors. Recent data show that about one-third of the urban population in large cities in India has the MetS. All classical risk factors comprising the MetS are prevalent in Asian Indians residing in India. The higher risk in this ethnic population necessitated a lowering of the cut-off values of the risk factors to identify and intervene for the MetS to prevent diabetes and cardiovascular disease. Some homoeopathic (pharmacological) and life style modifications (non-pharmacological) interventions are underway in MetS to assess the efficacy in preventing the diabetes and cardiovascular disease in this ethnic population.  Keywords: South Asians, prediabetes, prehypertension, hyperlipidemia, obesity
  14. 14. INTRODUCTION  The ―metabolic syndrome‖ (MetS) is a clustering of components that reflect over nutrition, sedentary lifestyles, and resultant excess adiposity. The MetS includes the clustering of abdominal obesity, insulin resistance, dyslipidemia, and elevated blood pressure and is associated with other co morbidities including the prothrombotic state, proinflammatory state, non-alcoholic fatty liver disease, and reproductive disorders. Because the MetS is a cluster of different conditions, and not a single disease, the development of multiple concurrent definitions has resulted. The prevalence of the MetS is increasing to epidemic proportions not only in the United States and the remainder of the urbanized world but also in developing nations. Most studies show that the MetS is associated with an approximate doubling of cardiovascular disease risk and a 5-fold increased risk for incident type 2 diabetes mellitus. Although it is unclear whether there is a unifying path physiological mechanism resulting in the MetS, abdominal adiposity and insulin resistance appear to be central to the MetS and its individual components. Lifestyle modification and weight loss should, therefore, be at the core of treating or preventing the MetS and its components. In addition, there is a general consensus that other cardiac risk factors should be aggressively managed in individuals with the MetS.
  15. 15. Definition as per IDF ( for Asian Indians) o According to the new IDF definition, for a person to be defined as having the metabolic syndrome they must have: o Central obesity (defined as waist circumference ≥ 90cm for Indian men and ≥ 80cm for Indian women, with ethnicity specific values for other groups) plus any two of the following four factors: o raised TG level: ≥ 150 mg/dL (1.7 mmol/L), or specific treatment for this lipid abnormality o reduced HDL cholesterol: < 40 mg/dL (1.03 mmol/L*) in males and < 50 mg/dL (1.29 mmol/L) in females, or specific treatment for this lipid abnormality o raised blood pressure: systolic BP ≥ 130 or diastolic BP ≥ 85 mm Hg, or treatment of previously diagnosed hypertension o raised fasting plasma glucose (FPG) ≥ 100 mg/dL (5.6 mmol/L), or previously diagnosed type 2 diabetes If above 5.6 mmol/L or 100 mg/dL, OGTT is strongly recommended but is not necessary to define presence of the syndrome.
  16. 16. NCEP ATP III Definition  Definition and Associations The term ―metabolic syndrome‖ describes a constellation of cardiovascular risk factors related to hypertension, abdominal obesity, dyslipidemia, and insulin resistance.  According to this definition, a subject has the MS if he or she has three or more of the following criteria:  Abdominal obesity: WC ≥102 cm in men and ≥88 cm in women  Hypertriglyceridemia: ≥150 mg/dl (1.695 mmol/l)  Low HDL-C: <40 mg/dl in men and <50 mg/dl in women  High blood pressure (BP): >130/85 mmHg  High fasting glucose: >110 mg/dl
  17. 17. Extended definition  Desirable with less risk factors LDL cholesterol goal is < 100 mg.dl. In people     with CHD or CHD equivalent (e.g., diabetes, peripheral arterial disease, abdominal aortic aneurysm, or symptomatic carotid artery disease), the LDL cholesterol goal is < 70 mg/dl. Non-HDL cholesterol is a strong predictor of CHD risk, and is the total cholesterol minus the HDL cholesterol. The non-HDL cholesterol target value is generally 30 mg/dl higher than the LDL cholesterol target values. Non-HDL cholesterol is particularly useful when LDL cholesterol cannot be calculated due to elevated TG or when lipid specimens are collected in the non-fasting state. If the TG level is 500 mg/dl, the patient is at risk for pancreatitis and treatments should be instituted. LDL level cannot be measured by the formula LDL= total cholesterol – (HDL + triglycerides/5), it has to be measured directly. When the TG level is 200–499 mg/dl, the non-HDL cholesterol value should be determined. Small dense LDL particles should be evaluated. Treatment of TG, including use of pharmacologic agents, should be done until the non-HDL cholesterol target has been achieved. When the TG level is borderline high (150–199 mg/dl), lifestyle modification should be emphasized. Calculation of the non-HDL cholesterol value is not required, but may be useful.
  18. 18.  Post parandial lipemia i.e. decreased exogenous and endogenous      triglycerides clearance. Albuminuria A I subclinical stage - < 30 mg in 24 hrs, < 20 ug/min, Albumin Creatinine ratio < 30ug/mg of creatinine. A II clinical stage – 30-300 mg in 24 hrs, 20-200 ug/min, ACR 30-300 ug/mg creatinine A III clinical stage- > 300mg in 24 hrs, > 200 ug/min ACR > 300 ug/mg creatinine. The presence of albuminuria is an indicator for screening for possible vascular disease and aggressive intervention to reduce all cardiovascular risk factors—elevated LDL, hypertension, smoking, and physical inactivity. Several factors are known to slow the rate of albumin excretion or to prevent its development. They are control of hypertension, glycaemic control and lipid lowering.
  19. 19.  WC be replaced by ICO (index of central obesity) in all definitions of MS. With the use of ICO, the need for various race- and gender-specific cutoffs for WC can be obviated. Although a number of studies have proposed ICO cutoffs ranging between 0.45 and 0.55, we propose the use of a simple cutoff of 0.5 across both genders and all races. MS is a screening tool, and we believe that it should be used to identify people at high risk of metabolic complications and cardiovascular disease so that further detailed investigations can be performed. This definition translates into a very simple message to the community 'If your waist size is more than half of your height, you should consult your doctor.' Thus, all patients with ICO >0.5 should be evaluated for high blood pressure, prediabetes, and dyslipidemia.  In view of the role of central obesity and dyslipidemia in atherosclerotic process, an alternative continuous index of lipid overaccumulation, the lipid accumulation product (LAP), has been proposed. LAP is computed using WC and fasting triglycerides level (in mmol/l): (WC − 65) × TG (men) and (WC − 58) × TG (women). This parameter has been found to be better than BMI for predicting diabetes and has also been suggested for use in the identification MS. It has been shown to be a good predictor of cardiovascular disease ] though one study has shown that it may not be better than ICO or WHR for predicting cardiovascular disease.
  20. 20.  Waist circumference is unable to distinguish between visceral adipose tissue and subcutaneous adipose tissue. Visceral adiposity is more strongly associated with cardiometabolic risks compared with subcutaneous adipose tissue . Visceral adipose tissue adipocytes have a higher rate of lipolysis (metabolically more active) and also produce more adipocytokines, such as interleukin-6,IL-6,  hsCRP, and plasminogen activator inhibitor-1 . Therefore, it is important to include a routinely applicable indicator for evaluation of visceral adiposity. Triglyceride has been reported as a significant correlate of visceral adipose tissue in healthy men, even after controlling for abdominal subcutaneous adipose tissue . Furthermore, the use of triglyceride levels in combination with waist circumference, termed hypertriglyceridemic waist, has been shown to be able to identify individuals with the greatest amount of visceral fat and to be associated with increased risk of MS , diabetes , and coronary artery disease .
  21. 21. PATHOPHYSIOLOGY  Insulin resistance occurs when cells in the body (liver, skeletal muscle and adipose/fat tissue) become less sensitive and eventually resistant to insulin, the hormone which is produced by the beta cells in the pancreas to facilitate glucose absorption. Glucose can no longer be absorbed by the cells but remains in the blood, triggering the need for more and more insulin (hyperinsulinaemia) to be produced in an attempt to process the glucose.  The production of ever-increasing amounts of insulin weakens and may eventually wear out the beta cells. Once the pancreas is no longer able to produce enough insulin then a person becomes hyperglycaemic (too much glucose in the blood) and will be diagnosed with type 2 diabetes. Even before this happens, damage is occurring to the body, including a build-up of triglycerides which further impairs insulin sensitivity.  plasma concentration of adipose tissue metabolites, leptin and non-esterified fatty acids are higher and adiponectin levels are lower in insulin resistant Asian Indians as compared to more insulin sensitive Caucasians and could contribute to insulin resistance and atherogenic dyslipidemia. 
  22. 22. A. Insulin resistance: a conceptual prologue  Insulin is a pleiotropic molecule that has effects on amino acid uptake, protein synthesis, proteolysis, adipose tissue triglyceride lipolysis, lipoprotein lipase activity, very low-density lipoprotein (VLDL) triglyceride secretion, muscle and adipose tissue glucose uptake, muscle and liver glycogen synthesis, and endogenous glucose production. Individuals are generally defined as insulin sensitive or insulin resistant by their response to an oral or iv glucose or insulin stimulus . Characteristics of the insulinsensitive phenotype include a normal body weight without abdominal or visceral obesity , being moderately active , and consuming a diet low in saturated fats . Alternatively, insulin-resistant individuals demonstrate impaired glucose metabolism or tolerance by an abnormal response to a glucose challenge, elevated fasting glucose levels and/or overt hyperglycemia, or reductions in insulin action after iv administration of insulin (euglycemic clamp technique) with decreased insulin-mediated glucose clearance and/or reductions in the suppression of endogenous glucose production. In general, the characteristics of this phenotype are more likely to include being overweight or obese , being sedentary , and consuming a diet high in total or saturated fats .
  23. 23. Insulin Resistance: Associated Conditions
  24. 24. B. Obesity as a “driving force” in the prevalence of insulin resistance  The worldwide increase in the prevalence of obesity in the recent decades is startling and is likely a cause of the rising incidence of insulin resistance and the MetS , as well as CVD and T2D . Although not all overweight or obese individuals are metabolically unhealthy, the majority are insulin resistant . Indeed, many experts assert that the MetS would never have been put forth if the obesity epidemic had not become the public health concern that it is today . In particular, the combination of obesity, physical inactivity, and consumption of an atherogenic diet is believed to lead to insulin resistance . In this state of insulin resistance, normoglycemia is initially maintained by a modest increase in β-cell mass and/or an increase in insulin secretory capacity. Although the mechanism for this compensation is unclear, there is recent evidence supporting glucose signaling as a dominant force in this process ; it is also acknowledged that genetic factors may be involved . However, the loss of insulin secretory capacity in the natural history of T2D is likely an admixture of β-cell dysfunction in addition to reductions in β-cell mass . If the increasing β-cell function and/or mass is successful long-term as a compensatory mechanism to obesity and insulin resistance, T2D could be prevented for an undetermined amount of time, despite hyperinsulinemia as a consequence.
  25. 25. C. Insulin resistance in adipose tissue  Adipose tissue insulin resistance appears to be important to the pathophysiology of the MetS . Specifically, a larger, expanded adipose tissue mass often results in an increased turnover of free fatty acids (FFAs) . In the setting of insulin resistance and expanded adipose tissue triglyceride stores, the process of FFA mobilization (lipolysis) from stored adipose tissue triglyceride is accelerated. Under normal conditions, insulin inhibits adipose tissue lipolysis; however, in the setting of insulin resistance, insulin is unable to properly suppress lipolysis, resulting in relatively more FFA being liberated into the plasma . Although it is well accepted that this process is mediated by hormone-sensitive lipase (HSL) , recent evidence points to adipose triglyceride lipase as playing an additional role; and collectively these two hormones account for 95% of triglyceride hydrolysis. In obese subjects, insulin resistance and hyperinsulinemia are strongly associated with decreased adipose triglyceride lipase.
  26. 26. Relationship Between Obesity and Insulin Resistance and Dyslipidemia
  27. 27. Who should be tested ?  • Body mass index (BMI) > 23 kg/m2. Waist circumference >90cms in           males and 80cms in females. • Hypertension. • High-density lipoprotein (HDL) < 40 mg/dl in men or < 50 mg/dl in women. • Triglycerides (TG) > 150 mg/dl. • Women with a history of gestational diabetes or birth weight > 9 lbs (4.0 kg). • Offspring of a pregnancy complicated by diabetes, gestational diabetes, high birth weight (> 9lbs or 4.0 kg) or low birth weight (< 2.5 kg or 5.5 lbs). • Women with polycystic ovarian syndrome (or hyper androgenic chronic an ovulation). • A family history of type 2 diabetes. Impaired glucose tolerance (IGT) or impaired (IFG) on previous testing. Other clinical conditions associated with insulin resistance (e.g. acanthosis nigricans). Male gender.
  28. 28. Obesity is defined as an abnormal growth of the adipose tissue due to an enlargement of fat cell size(hypertrophic obesity)or an increase in fat cell number(hyperplast ic obesity)or a combination of both. Central obesity is defined as waist circumference ≥ 90 cm in males and ≥ 80 cm in females. + Any two of the following -Increased triglycerides ≥ 150 mg/dl (1.70 mmol/L) -reduced HDL cholesterol <40 mg/dl in males and < 50 mg/dl in females. -raised blood pressure systolic bp ≥ 130 mm Hg and diastolic bp ≥ 85mm Hg. -raised fasting plasma glucose ≥ 100 mg/dl. Or treatment for previously diagnosed any of the above condition.
  29. 29. Classification BMI Risk of Co-morbidities (kg/m2 ) Underweight <18.5 Low (Risks are increased in other areas) Desirable 18.522.9 Average Overweight 22.929.9 Mildly Increased Obese >30.0 Class I Obesity 30.034.9 Moderate Class II Obesity 35.039.9 Severe Class III (morbid obesity) >40.0 Very severe
  30. 30. Factors responsible Changes in Life Style (Urbanization) •Unhealthy eating patterns •Wrong choices of food, increased portions •Increased oil consumption •Snacks, colas, rewards…… Sedentary pursuits • Long school hours, tuitions, Reduced physical activity  vehicles, reduced play areas TV, telephones Other factors High glycemic index of foods Genetic / Constitutional predisposition „Early life origins‟ -programmed to accumulate fat Silent genes unmasked? Thrifty genotype Gestational diabetes – intergenerational effects7
  31. 31. Management of obesity
  32. 32. Desirable 18.5-22.9 WC- in males-< 90cm Females < 80 Overweight 22.9-29.9 WC- in males 90100cm In females 80-90cms Obese stage I 30-34.9 WC –in males- 100110cms In females 90-100cms Obesity stage II 35-39.9 WC –in males -110120 In females 100-110 Obesity stage III >40 WC in males >120 In females >110 No treatment required Constitutional or antimiasmatic treatment to maintain this desirable range. Lifestyle modification. MNT Constitutional or antimiasmatic to reach the desirable range. Lifestyle modification and homeopathic intervention (constitutional ) with organopathic medicines. Lifestyle modification and homoeopathic intervention along with organopathic treatment and conventional treatment Bariatric surgery liposuction
  33. 33. SOCIO-CULTURAL ISSUES AND CHILDHOOD OBESITY IN INDIA  1. There is a general misconception in parents in India and other developing     countries that an obese child is a healthy child. And that if the child is fat, ―baby fat‖ will go away with time. In an effort to keep child ―healthy‖, he/she is fed in excess. Many of these children remain obese for life. 2. High burden of school work and academic competitiveness have led to decreased participation in sports and any other form of physical activity. This is particularly true for girls who are sedentary from school years. Many of the studies from India show that females have more obesity and the metabolic syndrome as compared to males. 3. The lack of appropriate play area and limited open space around home makes it difficult for children to stay physically active. 4. Parents are often overworked and find it easy to let children order ―fast foods‖ and hardly have any time to oversee balanced nutrition for children. 5. Lastly, children spend more time in front of television and computers at the expense of sports and physical activity.
  34. 34. How do we define type II Diabetes  T2DM is a non-autoimmune, complex, heterogeneous and polygenic metabolic disease condition in which the body fails to produce enough insulin, characterized by abnormal glucose homeostasis.  T2DM occurs when impaired insulin effectiveness (insulin resistance) is accompanied by the failure to produce sufficient β-cell insulin
  35. 35. DETERMINANTS Physical inactivity Sedentary life style compounded with the change in the nutritional in South Asians makes them more vulnerable to NCDs . The change occupations, advent of newer technologies, and rapid pace of urban have increasingly resulted in more sedentary work and less energy expenditure; however, this needs more research in context of South Asians. In one such study, lower levels of physical activity in Asian I Pakistanis and Bangladeshis was seen to be inversely correlated wit WC, systolic blood pressure, plasma glucose and insulin levels. genetics A few studies show genetic association of obesity, insulin resistance dyslipidemia in South Asians . In a recent study, variants of Myosta gene was shown to predispose to obesity, abdominal obesity and low body mass in Asian Indians in north India . In another important st LMNA 1908T/T and C/T genotypes emerged as independent geneti factors for generalized obesity in non-diabetic Asian Indians in nort . Association of AMD1 variant with obesity has been shown in Asian children. Further, there is recent evidence for genetic associations o NAFLD with SREBP-2 1784 G>C genotype and peroxisome prolifer activated receptor-γ (Pro12Ala and C161T) polymorphisms in Asian Indians. A recent study has shown DOK5 as a susceptibility gene for obesity and T2DM in Asian Indians in north India .
  36. 36. Nutritio South Asians are becoming increasingly more affluent. Further, nal with economic liberalization, there is a widespread presence of transitio transnational food company outlets and availability of packaged n foods in 24 h supermarkets. With better purchasing power, South Asians are increasingly consuming diets high in saturated fats, cholesterol, and refined carbohydrates and low in polyunsaturated fatty acids and fibres. Availability of edible vegetable oils for consumption has nearly tripled in developing countries in the last few years. Importantly, while processed nontraditional “fast-foods” contribute to faulty diets, some of the locally made “fast foods” sold by street vendors in several developing countries are equally unhealthy. These food items contain high amount of trans fatty acids (TFA) due to deep-frying using low cost and widely available partially hydrogenated vegetable oils Urbanizat ion, Demogra phic Transitio n and Rural-toUrban Migration In South Asia, urbanization is increasing rapidly and is now nearly 38%, but is expected to be 50% by 2020. Urbanization exposes people to a number of challenges, imbalanced diets, physical inactivity, long working hours and other urban stress making them vulnerable to NCDs. The average life expectancy of Indian population at birth now is 67.14 years, as compared to 31 years in 1947 Similarly, life expectancy is going up in the other countries of the region as well. This has resulted in the rise of elderly population in the region, again leading to rise in NCDs. Migration, whether inter-country or rural-to-urban within country, is a risk factor for T2DM
  37. 37. In a review, South Asian migrants showed nearly four times high prevalence rates of T2DM than those of rural populations. Similar observations were also reported in intracountry migrants and resettled indigenous populations. Migration results in increasing physical inactivity, faulty nutrition and exposure to stress. We have previously shown that migrant postmenopausal women settled in urban slums have high prevalence of multiple CVD risk factors. In a recent study, we have shown a gradient in NCDs between rural, ruralurban migrants and urban residents . Nutrients 2013, 5 2720 Importantly, there was a significant correlation of duration of migration with waist size and high fat content in the diets SocioEconomic and Cultural Factors The prevalence of obesity, dyslipidemia, T2DM and CVD in South Asia is more in the people belonging to the upper socio-economic strata unlike in the developed nations . However, with new found wealth and a number of dietary choices and ―western foods‖ available at relatively low prices, people belonging to middle and low socio-economic strata are being increasingly afflicted with NCDs . Socio-cultural and psychological factors and prevalent misconceptions are important in modifying diet and lifestyle habits of women and children in South Asia. In this region, there is a prevalent misconception that an ―obese child is a healthy child‖ and, hence should be fed in excess.
  38. 38. Mothers often have traditional belief that feeding excess ghee (clarified butter) and butter to child would be beneficial to growth and impart them strength. In a cross-sectional study of 1800 children aged 9 to 18 years and their mothers, using qualitative (focus group) and quantitative (semi-structured survey) data, widely prevalent myths, and correlation between obesity and dietary habits of children and their mothers has been shown . Other social factors as a cause of physical inactivity are: priority for Nutrients 2013, academics at the cost of playing time in children, increasing use of television and computers, lack of playfields and open spaces, and security concerns in the outdoors, especially for women . In particular, cultural and social restrictions for outdoor physical activity in women in South Asian countries may be an important reason for increasing obesity and the metabolic syndrome.
  39. 39. Phenotype of Obesity in South Asians 1. Body Fat  Several studies have shown that at similar level of BMI, body fat level is higher in Asians, particularly South Asians, as compared to white Caucasians . This feature has been documented in other Asian ethnicities as well; Indonesians, Chinese, and Malays in Singapore . In a study conducted in Singapore, at any given percentage of body fat, BMI value of Chinese, Malays and Asian Indians was 3 kg/m2 lower than that in white Caucasians. This can be partly explained by ethnicity, body frame (trunk-to-leg-length ratio and lean body), muscularity and adaptation to chronic calorie deprivation 2. Truncal and Abdominal Adiposity  The truncal fat includes fat over chest and abdomen both subcutaneous abdominal adipose tissue (SCAT) and intra-abdominal adipose tissue (IAAT), all of which are more in Asian Indians than in white Caucasians . The metabolic perturbations and adverse cardiovascular risk may be associated more with fat deposition in specific location over trunk and abdomen.
  40. 40. 3. For Body Fat Depots  The simplest equation for predicting %BF derived from DEXA included age, sex, BMI, triceps skinfold and WC. 4. Deposition of Fat at “Ectopic” Sites  Insulin sensitivity can be affected by fat accumulation in tissues other than where it is usually deposited (―ectopic fat‖); for example, liver, muscle and heart. It appears that South Asians have tendency for deposition of fat in some of these sites. 5. Hepatic Fat  It is now recognized that NAFLD an important component of the metabolic syndrome . Hepatic steatosis accompanied with portal inflammation in advanced stages is termed as non-alcoholic steato-hepatitis (NASH) and may progress to hepatic fibrosis and even cirrhosis. 6.Skeletal Muscle Triglycerides  Intra-myocellular lipids (IMCL) are located in the mitochondria, along with enzymes involved in fatty acid esterification, hydrolysis, ion transport and cellular oxidation. Combined effect of high concentration of serum insulin and free fatty acids can cause enhanced storage of IMCL. These lipids are believed to be important in the pathogenesis of insulin resistance
  41. 41. 7. Other Ectopic Sites of Fat Deposition  There are few other ectopic sites of fat deposition; over the neck (―buffalo hump‖) frequently observed in Cushing‟s syndrome and HIV-associated lipodystrophy, and excess fat under the chin (―double chin‖) seen in familial partial lipodystrophy . These ectopic fat depositions are frequently associated with insulin resistance and other features of the metabolic syndrome . Extending research on these signs to obese people in whom these signs are frequently seen, we showed that mild ―buffalo hump‖, and ―double chin‖ signify the heightened risk of metabolic syndrome in urban Asian Indians. 8. Adipocyte Size  Large subcutaneous abdominal adipocyte size predicts insulin resistance and T2DM independent of obesity . In this study, done on Pima Indians, mean subcutaneous abdominal adipocyte size was 19% and 11% higher in subjects with T2DM and impaired glucose tolerance (IGT), respectively as compared to persons with normal glucose tolerance (p < 0.001). In this context, it is important to note that adipocyte cell size was significantly higher in South Asians (3491 ± 1393 µm2 ) as compared to white Caucasians in USA (1648 ± 864 µm2; p-value = 0.0001) . These findings need to be further researched for clinical implications
  42. 42. Classifications of impaired glucose homeostasis. Classification Impaired glucose tolerance (IGT) Prediabetes Diabetes Impaired fasting glucose (IFG) Prediabetes Diabetes Tests used diagnostic values 75 gram oral glucose tolerance test (OGTT) 2-hour plasma glucose 140–199 mg/dl <7.0 (<126) >=7.8 (>=140) and <11.1 (<200) Fasting plasma glucose (FPG) after 8hour fast Fasting plasma glucose 100–125mg/dl >=6.1 (>=110) and <7.0 (<126) .8 (<140)
  43. 43. Natural History of Type 2 Diabetes There are five stages in the progression of diabetes, each of which is characterized by different changes in beta-cell mass, phenotype, and function. Stage 1 is compensation: insulin secretion increases to maintain normoglycemia in the face of insulin resistance and/or decreasing beta-cell mass. This stage is characterized by maintenance of differentiated function with intact acute glucose-stimulated insulin secretion (GSIS). Stage 2 occurs when glucose levels start to rise, reaching approximately 5.0-6.5 mmol/l; this is a stable state of beta-cell adaptation with loss of beta-cell mass and disruption of function as evidenced by diminished GSIS and beta-cell dedifferentiation. Stage 3 is a transient unstable period of early decompensation in which glucose levels rise relatively rapidly to the frank diabetes of stage 4, which is characterized as stable decompensation with more severe betacell dedifferentiation. Finally, stage 5 is characterized by severe decompensation representing a profound reduction in beta-cell mass with progression to ketosis. Movement across stages 1-4 can be in either direction. For example, individuals with treated type 2 diabetes can move from stage 4 to stage 1 or stage 2.
  44. 44. n Type 2 Diabetes Results From Three Major Metabolic Defects
  45. 45. Indian diabetes risk score
  46. 46.  Subjects with IDRS score ≥60 at baseline also had the highest proportion of conversion to diabetes (27.8%) followed by those with medium risk score of IDRS (16.9%) and was lowest in those with low IDRS (<30), (5.6%, P < 0.001). Moreover, 38.4% of 'converters' to either diabetes or pre-diabetes had high IDRS scores at baseline. IDRS had the highest relative risk (RR) for predicting incident diabetes. Even after adjusting for age and gender, the RR for incident diabetes remained significant (IDRS ≥ 60: RR 3.1, P = 0.035, IDRS 30-50: RR 2.7, P = 0.032). Thus a high IDRS can be useful to identify those who are likely to develop diabetes or pre-diabetes in the future, even if they have normal glucose tolerance now.  With the prevalence of diabetes on the rise, the complications of T2DM, such as retinopathy, nephropathy, neuropathy, peripheral vascular disease (PVD) and coronary artery disease (CAD) are also rising in India and this could have devastating results. Asian Indian T2DM subjects may be at greater lifetime risk for these complications due to the earlier onset of their disease.
  47. 47.  Prevalence of several diabetic complications was higher among subjects in the high-risk category of IDRS ≥60. Thus, CAD [9.2% vs. 5.4%, P = 0.043], diabetic peripheral neuropathy [29.2% vs. 8.8%, P < 0.001] and PVD [4.8% vs. 1.9%, P= 0.038] were all significantly higher among subjects in the highrisk category [IDRS ≥ 60] compared to those with IDRS score <60. In the regression analysis, the odds ratio (OR) for neuropathy was 4.27 (95% CI: 2.74-6.67, P < 0.001), for PVD it was 2.57 (95% CI: 1.02-6.46, P = 0.045) and for CAD it was 1.79 (95% CI: 1.01-3.18, P = 0.046) in subjects with IDRS ≥ 60. Even after adjusting for the duration of diabetes, neuropathy [OR: 4.03, 95% CI: 2.55-6.37, P < 0.001); and PVD [OR: 2.54, 95% CI: 1.016.41, P = 0.049] were associated with IDRS ≥60. However, IDRS did not show any significant association with diabetic retinopathy or macroalbuminuria.  Use of IDRS for targeted screening in T2DM patients could help pick up those who are likely to have CAD, PVD and neuropathy.  With increasing IDRS scores, <30, 30-50, and ≥60, the prevalence of hypertension: 9.4, 22.1 and 38.2% (P for trend: <0.001), hypertriglyceridemia: 8.8, 19.9 and 25.3% (P for trend: <0.001) and hypercholesterolemia: 7.2, 20.3 and 34.9% (P for trend: <0.001) also increased.
  48. 48. Treatment Low risk Moderate risk High risk Lifestyle modification Medical nutrition therapy Constitutional medicine to prevent. Lifestyle modification with medical nutritional therapy with constitutional homoeopathic medicine and organopathic medicine. Oral hypoglycaemic drugs. Lifestyle modification with organopathic medicines, symptomatic treatment with oral hypoglycaemic drugs and insulin if required.
  49. 49. LIPI+TENSION
  50. 50. Dyslipidemia  Dyslipidemia refers to the derangements of one or many of the lipoproteins; elevations of total cholesterol, low-density lipoprotein (LDL) cholesterol and/or triglycerides, or low levels of high-density lipoprotein (HDL) cholesterol.  The term ‗atherogenic dyslipidemia‘ denotes a combination of elevated triglycerides and small-dense LDL particles, and low levels of HDL- cholesterol.  A primary dyslipidemia (e.g. familial hypercholesterolemia) typically refers to a genetic defect in the lipid metabolism that causes abnormal lipid levels. A secondary dyslipidemia may be due to a variety of reasons; environmental factors (diet rich in saturated fat or a sedentary lifestyle), diseases (type 2 diabetes, hypothyroidism, obstructive jaundice etc.), and medications (thiazide diuretics progestins, anabolic steroids etc.).  Individuals with abnormal fat distribution, characterized by a high waist-to-hip circumference ratio or high truncal subcutaneous fat appear to be predisposed to developing insulin resistance and dyslipidemia. Such a body composition is commonly seen in Asian Indians.
  51. 51. ATP III Classification of Total Cholesterol and LDL Cholesterol Total cholesterol (mg/dl) < 200 desirable Lifestyle modification with MNT with Constitutional medicine to maintain this desirable range 200-239- borderline high LSM with MNT with constitutional medicine with organopathic medicine. ≥240 high This above regime along with conventional cholesterol lowering drugs.
  52. 52. LDL cholesterol (mg/dl) < 100 optimal LSM, MNT with constitutional drugs to maintain the desired range. 100-129 near optimal/above optimal AHA Step I diet, constitutional med, LSM 130-159 borderline high AHA step II diet, constitutional medicine with organo pathic medicine. 160-189 high LSM, MNT with constitutional medicines and conventional treatment. ≥240 very high Conventional treatment.
  53. 53. ATP III Classification of HDL Cholesterol Serum HDL cholesterol (mg/dl) <40 ≥60 Total cholesterol HDL ratio Low HDL Cholesterol Normal- 4.5-11 High HDL Cholesterol LSM,MNT with constitutional medicine to maintain the desired range. If ratio more than 11 above treatment with conventional treatment.
  54. 54. ATP III Classification of serum Triglycerides Serum Triglycerides (mg/dL) <150 150-199 normal Constitutional to maintain the desired range, LSM, MNT borderline high Above treatment with glycaemic control. At this level LSM needs to be emphasized. Above treatment with organopathic medicines 200-499 500 high very high Conventional treatment
  55. 55. ATP III non-lipid risk factors for CHD Modifiable risk factors Non-modifiable risk factors Modifiable Risk Factors Hypertension Cigarette Smoking Thrombogenic/Haemostatic State Diabetes Obesity Physical Inactivity Atherogenic Diet Age Male Gender Family History of Premature CHD
  56. 56. Approach to the Patient with Hyperlipidemia for Evaluating Risk for CHD and for Implementing Therapy  Rule out secondary dyslipidemia (Diabetes, hypothyroidism,  obstructive liver disease, chronic renal failure, drug-induced)  Perform risk assessment  Encourage smoking cessation  Control hypertension and diabetes  Implement therapeutic lifestyle changes (improved diet, weight loss,  increased physical activity)  Achieve LDL-cholesterol goal with statin therapy  Achieve other lipid (HDL, triglycerides, Lp[a]) and non-lipid  (homocysteine) goals with niacin or Niaspan.  Monitor response and adherence to therapy every 4 to 6 months
  57. 57. The broad guidelines are as follows-  Total fat intake should be less than 30% of total calories.  Saturated fat intake should be less than 10%.  Monounsaturated fats should replace polyunsaturated fats.  To consume at least five portion of fresh fruits and vegetables daily.  Total cholesterol intake to be kept less than 300mg/day.  Fish oils which contain omega three fatty acids should be consumed.  Calorie intake should not be more than energy expenditure to prevent the endogenous production of lipoproteins.  Salt intake should be 1600-2400 mg in 24 hrs depending upon the stage of the cardiovascular disease.
  58. 58. Cardioprotection by Nutraceuticals  With the ever increasing epidemic of obesity, diabetes and hypertension among young adults, the risk of mortality and morbidity due to atherosclerotic heart disease is gradually increasing. Dyslipidemia is an additional risk factor for cardiovascular disease. Nutraceutical supplements can provide valid alternate to patients who are intolerant to statins or patients preferring alternative treatments. The combination of a lipid lowering diet and scientifically proven nutraceutical supplements can significantly reduce low density lipoprotein (LDL) cholesterol, increase LDL particle size, decreased LDL particle number decreased triglycerides and increased high density lipoprotein (HDL) particles. In addition, they address lipid induced vascular damage by suppressing inflammation, oxidative stress and immune response leading to additional antihypertension, antidiabetic properties. The current article reviews the evidence in support of different dietary supplements and their lipid lowering beneficial effects.
  59. 59.  With 1% hike in cholesterol and LDL cholesterol (LDL-C), there is increase in risk for coronary heart disease (CHD) to the tune of 2-3% and 1.2-2.0%, respectively. Similarly with 1% fall in HDL-C there is 3% increase in CHD risk. Lifestyle changes and diet reduce CHD risk by 82%; nutritional practices alone reduce the risk by 60%.  Institution of high-carbohydrate/high-fiber diet leads to reduction of total cholesterol and LDL-C by 30% and >40%, respectively, over 4-6 weeks and 18% after 1 year. The American diabetes association (ADA) step 1 diet with saturated fat (<10% of energy) and cholesterol (<300 mg/ day) is associated with >8% decrease in LDL-C. The dietary approach to stop hypertension (DASH) diet that limits consumption of saturated fats and cholesterol with increased intake of fruits and vegetables, is associated with 9% decrease in LDL-C after 8 weeks. Vegetarian diets are related to 19-29% LDL-C reduction at 4 weeks and 15% at 1 year, respectively, leading to 20-40% CAD risk reduction. Refined carbohydrate intake is more important in changing serum lipids than saturated fats through effects on insulin resistance, atherogenic LDL, LDL particle number, very low density lipoprotein (VLDL), TGs, and total HDL and thus contributes more to CHD risk.
  60. 60. MECHANISM OF ACTION  Studies have highlighted the role of nutraceuticals in dyslipidemia. Others have reported reductions in vascular markers (carotid intima-media thickness [IMT] and obstruction, plaque progression, coronary artery calcium score by electron beam tomography [EBT], generalized atherosclerosis.  Decrease endothelial permeability, gap junctions, and endothelial dysfunction and improve endothelial repair, endothelial nitric oxide synthase and nitric oxide. Decrease cholesterol crystals, low-density lipoprotein (LDL) phospholipids, oxidized LDL.Decrease LDL burden Reduce cholesterol absorption Increase cholesterol bile excretion Decrease LDL particle number,LDL sizeModify.
  61. 61. Action of various neutraciticals  Inhibition of LDL oxidation      Niacin Green tea extract Monounsaturated fats Garlic Sesame  Inhibition of low density lipoprotein glycation   Histidin Pomegranate  Lower low-density lipoprotein     Niacin Sesame Green tea extract and green tea Omega 3 fatty acids
  62. 62.  Convert dense low density lipoprotein B to large low density lipoprotein A   Niacin Omega 3 fatty acids  Reduce intestinal cholestrol absorption   Soy Green tea extract and green tea  Lower lipoprotein A    Niacin Omega 3 fatty acids Vitamin C  Lower triglycerides   Niacin Omega 3 fatty acids  Increase reverse cholestrol transport   Plant sterols Glutathiobe  Decrease low density lipoprotein particle number   Niacin Omega 3 fatty acids
  63. 63.  Reduce inflammation    Niacin Omega 3 fatty acids Monounsaturated fats  Reduce apolipoprotein B lipoprotein    Niacin Omega 3 fatty acids Green tea extract and green tea  Decrease low density lipoprotein particle number   Niacin Omega 3 fatty acids  Upregulate the low density lipoprotein receptor   Green tea extract and green tea Sesame  Increase bile acid secretion     Citrus bergamot Fiber Sesame probiotics
  64. 64. HYPERTENSION  Jnc 7 STATES beginning at 115/75mmHg CVD doubles for each 20mmHg rise in SBP and 10 mmHg in DBP and this risk becomes 4 times if patient has type II diabetes mellitus  Goal of blood pressure- 140/90 mm Hg  Goal of blood pressure inpatients with diabetes is 130/80mmHg.
  65. 65. Category Systolic blood Diastolic pressure blood (mm of hg) pressure (mm of hg) Follow up recommended Normal < 130 < 85 Recheck in 2 yrs Prehypertension 130-139 85-90 Recheck in 1 yr Stage 1 (mild) 140-159 90-99 Confirm within 2 months Stage II ( moderate) 160-179 100-109 Evaluate or refer to source of care within 1 month >180 >110 evaluate and treat immediately or within 1 week depending on clinical situation and complications. Hypertension Stage III (severe)
  66. 66.  Importance of systemic blood pressure  The rise of SBP continues throughout life in contrast tp DBP which rises until 50yrs of age, later tends to remain same or fall. Diastolic hypertension predominates before 50yrs of age and systolic hypertension increases with age and is potent CVD risk factor after 50yrs called Isolated Systolic hypertension.  Ambulatory BP monitoring- is a gold standard.
  67. 67. Classification of hypertension by extent of organ damage Stage I No manifestations of organic change Stage II At least one of the following manifestations of organ involvement. Left ventricular hypertrophy (detected by radiogram, electrocardiogram, echocardiogram) Generalized and focal narrowing of the retinal arteries Microalbumiurea, proteinuria, and/or slight elevtaion of plasma creatinine conc. Ultrasound or radiological evidence of atherosclerotic plaque( in the aorta, or carotid, iliac or femoral arteries) Stage III Both symptoms and signs have appeared as a result of organ damage. These include: Heart Anigina pectoris Myocardial infarction Heart failure
  68. 68. Brain Stroke Transient ischemic attack Hypertensive encephalopathy Vascular dementia Optic fundi Retinal haemorrhages and exudates with or without papilloedema( these features are pathognomic of the malignant or acclereated phase) Kidney Plasma creatinine concentration > 2.0mg/dl Renal failure Vessel Dissecting aneurysm Symptomatic arterial occlusive disease
  69. 69. Modification Recommendation Approximate SBP Reduction (Range)† Weight reduction Maintain normal body weight (body mass index 18.5–24.9 kg/m2). 5–20 mm Hg/10 kg92,93 Adopt DASH eating plans Consume a diet rich in fruits, vegetables, and low-fat dairy products with a reduced content of saturated and total fat. 8-14mmhg Dietary sodium Reduce dietary sodium intake to no reduction more than 100 mmol per day (2.4 g sodium or 6 g sodium chloride). 2-8mmhg Physical activity 4-9mmhg Engage in regular aerobic physical activity such as brisk walking (at least 30 minutes per day, most days of the week).
  70. 70. Moderation of alcohol consumption Limit consumption to no more than 2 drinks (eg, 24 oz beer, 10 oz wine, or 3 oz 80-proof whiskey) per day in most men and to no more than 1 drink per day in women and lighterweight persons. 2-4mmHg
  71. 71. HYPERTENSION Category Treatment and intervention Normal Recheck in 2 yrs Pre-hypertension Lifestyle modification, medical nutrition therapy alonwith constitutional drug in order to maintain the BP in desirable range. Hypertension Stage 1(mild) Stage II( moderate) Stage III (severe) LSM, MNT with constitutional drug and organopathic drugs Lifestyle modification, MNT, constitutional drug, organopathic treatment conventional treatment with lifestyle modification
  72. 72. Recommended care for individuals with metabolic syndrome Typical recommendations Suggested lifestyle changes Moderate weight loss (7–10% reduction in starting weight or, on average, 20–25 pound weight loss over 6 months) Caloric intake should be reduced by 250–1,000 calories per day to produce the recommended goal of –2 pounds weight loss per week. Calorie reduction should be realistic and achievable and based on an individualized assessment, weight history, dietary intake, physical activity, and weight loss goals. The National Heart, Lung, and Blood Institute recommends the following daily calorie intake: • For men: 1,200–1,600 kcal/day. (Also for women who exercise and who weigh > 165 pounds). • For women: 1,000–1,200 kcal/day (most women). • If client is hungry, you may want to increase calories by 100–200/day. • Activity/Exercise: 30–60 minutes/day most days of the week. Weight loss and maintenance is difficult to achieve without exercise and activity
  73. 73. Reduce calorie and modify fat intake (Less saturated fats) Establish mutually agreed upon goals: • Eat smaller portions. • Drink more water and little or no sugar-containing beverages each day. • Choose leaner cuts of beef and pork. • Eat white meat of turkey, chicken, and wild game more often. • Eat fish high in omega-3 fatty acids, no more than 12 ounces per week. Increase intake of whole fruits and vegetables. • Choose whole grains like rolled oats, barley, bran, and 100% whole grain bread instead of refined, processed carbohydrates like baked products made with white flour Choose low-fat or no-fat dairy products. • Use unsaturated vegetable oils that are liquid at room temperature like olive, canola, peanut, safflower, sunflower, corn, soybean, and cottonseed oils, and use soft-tub, squeeze, or spray margarine. • Eat at regular mealtimes. • Use low-fat food preparation (grilling, broiling, boiling, steaming, etc.). • Eat breakfast. • Reduce frequency of eating out, especially in fast food restaurants.
  74. 74. Patient “selfmonitoring” records Document food intake, physical activity, and feelings. Awareness is a key step in changing behaviour. Food and activity diaries help a person become more aware of current lifestyle habits to identify small changes to make toward achieving healthier lifestyle habits. Education Education topics focusing on, but not limited to: Healthy Food Choices: • Choosing meals and snacks from a variety of foods. • Types of fats (less saturated fat). • Types of carbohydrates (more whole grains and fibre). Healthy Food Preparation: • Appropriate portion sizes. • Understanding the food label. • Recipe modification. Psychology of Eating Habits: • Understanding physical cues of hunger and fullness. • Setting goals. • Enlisting support. • Rewarding yourself
  75. 75. Primary intervention  IDF recommends that primary management for the metabolic syndrome is a healthy lifestyle. This includes: moderate calorie restriction (to achieve a 5–10 per cent loss of body weight in the first year) moderate increase in physical activity change in dietary composition.  The results of Finnish and American prevention of diabetes studies have shown the marked clinical benefits associated with a small weight loss (as well as increased physical activity) in terms of preventing (or at least delaying by several years) the conversion to type 2 diabetes among high-risk individuals with glucose intolerance who were, generally, obese
  76. 76. Secondary intervention In people for whom lifestyle change is not enough and who are considered to be at high risk for CVD, drug therapy may be required to treat the metabolic syndrome. There is a definite need for a treatment that could modulate the underlying mechanisms of the metabolic syndrome as a whole and thereby reduce the impact of all the risk factors and the long term metabolic and cardiovascular consequences. However, these mechanisms are currently unknown and specific pharmacological agents are therefore not yet available. It is currently necessary instead to treat the individual components of the syndrome in order that a lower individual risk associated with each component will reduce the overall impact on CVD and diabetes risk.
  77. 77. Lifestyle modification rationale  It is also realized that overweight and obese patients if cannot reach to the normal body mass index a weight reduction of even a 2-5% of basal weight in overweight, 5-7% in obese grade I and 10% in obese grade II have beneficial effects. This is because visceral fat is metabolically more active, and a weight loss of even few percent is associated with significant loss of visceral fat and thus reducing abdominal obesity. On the basis of these observations, medical nutrition therapy and exercises is now recommended to all overweight and obese patients with metabolic syndrome.  The long lasting effectiveness of non drug interventions to prevent the incidence of hypertension is low outside the controlled conditions of randomized clinical trials. In the absence of high risk factors in the young individuals the use of BP agents can reduce the incidence of hypertension by more than 60% and these subjects are suitable candidates to treatment with an aim to prevent the development of hypertension. Clinical trials testing the efficacy of BP agents to prevent the hypertension in population based perspective are required. In the meantime it is worthy to present the option to start BP lowering or constitutional drugs (modifying drugs) for individuals with pre-hypertension and without any co-morbidities who do not respond to prescription of non drug intervention (lifestyle modification).  Pre-diabetes is not a benign condition. The data showing increased risk for glycemic progression and micro vascular complications strengthen the rationale for intervention in prediabetic individual. there is now abundant evidence that progression to type 2 diabetes can be delayed or prevented through lifestyle and pharmacological interventions.
  78. 78.  Reduces and control blood pressure and type 2 diabetes.  Prevents and delays the incidence of hypertension and type 2 diabetes.  Controls blood pressure in desirable range.  Weight management.  Enhances the efficacy of drugs.  Decreases the risk of CVD, diabetes, hypertension and severity of complications.  For example: reduction of salt to 1600mg (low risk) and 2400mg (high risk), has a similar effects of single drug therapy in reducing and controlling B.P, so combination of 2 or more modalities of LSM can achieve even better results.
  79. 79.  In conclusion LSM ( modest calorie restriction and moderate intensity physical activity) in prediabetic individual have shown remarkable efficacy in preventing the development of type 2 diabetes.favorable effects on glycaemia in conjunction with other metabolic and cardiovascular beefits makes the implementation of lifestyle interventions a public health imperative. several medications have also been reported to decrease the rate of progression from prediabeets to diabetes. However, drug based diabetes prevention approach is fraught with inherent drawbacks, including toxicity, tolerability, cost and lower efficacy than lifestyle intervention, among others. For the millions of people with prediabetes, lifestyle modification is the ideal initial option because of its minimal toxicity and excellent efficacy compared with medication. Therefore, pharmacologic interventions for diabetes prevention should be individualized as a second line adjunct to lifestyle modification.
  80. 80. Exercise guidelines  The goal is to exercise 150 minutes a week (e.g., a 30-minute walk, 5 days a       week) Frequency: Beginning: 3–5 days/week Goal: 5–7 days/week Intensity: Beginning: Low–moderate Goal: Moderate Time: Beginning: 30 minutes intermittent or continuous, as tolerated Goal: 30–60 minutes continuous Type: Aerobic: Walking, bicycling, swimming, rowing, cross-country skiing Target heart rate- 50%-85%of maximum heart rate according to the condition of the patient. HEART RATE = 220- age of the patient
  81. 81.  Incorporate 5–10 minutes of warm-up and cool-down during the exercise session:  • Warm-up by performing the aerobic exercise at low intensity (i.e., walking slowly and gradually increasing pace over 5–10 minutes).  • Cool-down by reducing the pace of exercise over 5–10 minutes, followed by easy stretching. To avoid injury, stretching should be done after the muscles have warmed up. Generally, stretching is best saved for the cool-down period.  • After establishing an aerobic program, consider adding resistance exercises (e.g., weight-lifting, therabands, etc.) for those without CVD, following provider approval and under the direction of a qualified individual. To minimize risk for injury, a weight lifting program should be individualized and under the direction of a qualified person.  Tobacco cessation counselling, if needed  Avoiding or quitting smoking may be the single most important intervention to reduce risk for CVD. In a recent large multinational study, smoking and abnormal lipids were the two most important risk factors for acute myocardial infarctions worldwide (Yusuf et al., 2004). Oral tobacco use also increases risk for CVD by increasing blood pressure and lipid abnormalities.
  82. 82.  Losing 5-7%of basal body weight can reduce the chances of type II diabetes by      58% Decrease time in sedentary behaviours such as television watching, video game play, or spending time online Increase physical activity such as walking, biking, aerobic dancing, tennis, soccer, basketball, etc In addition, physical activity is critical to the maintenance of weight loss and is important for overall reduction in cardiovascular risk; 60 to 90 minutes per week of walking can reduce CHD mortality by about 50%. The CVD benefits of slow walking appear to be comparable to those of walking more quickly, suggesting that the most important predictor of benefit was walking time, not speed. Weight loss of as little as 10 lbs (4.5 kg) reduces BP and/or prevents hypertension in a large proportion of overweight persons, although the ideal is to maintain normal body weight.
  83. 83. Medical nutrition therapy  The intervention model was the ‗Therapeutic Lifestyle Change (TLC) diet consisting     of carbohydrate 50-60% of total calories, protein 1 gm/kg body weight or 15-20% of total calories; saturated fat less than 5-7% of total calories, polyunsaturated fat up to 10% of total calories, monounsaturated fat up to 20% of total calories, cholesterol less than 200 gm/day, fiber 20-30 gm/day, viscous/soluble fibres 10-25 gm/day, total calories to balance energy intake and expenditure to maintain desirable body weight and/or to prevent weight gain. American heart association (AHA) has recommended step I diet consisting of total fat calories 25-35%, saturated fat 7-10% ,< 300 mg of cholesterol for LDL level 100130mg/dl. AHA step II diet consist of total fat calories 15-20% to obtain optimum possible results and to prevent endogenous production of lipoproteins and < 200 mg of cholesterol, saturated fat 5-7% for the LDL level > 130 mg/dl. Trans fatty acids < 1%. Carbohydrates were derived predominantly from foods rich in complex carbohydrates and foods with low glycaemic index including grains, especially whole grains, fruit and vegetables.
  84. 84. Detection and treatment efforts will:      Identify undiagnosed diabetes in some patients. Delay the onset of diabetes in others. Assist in the earlier detection of those patients who progress to diabetes. Identify undiagnosed hypertension and undiagnosed dyslipidemia in some patients. Help lay the groundwork for healthy lifestyle choices.
  85. 85. HBA1C  The term HbA1c refers to glycated haemoglobin. It develops when     haemoglobin, a protein within red blood cells that carries oxygen throughout your body, joins with glucose in the blood, becoming 'glycated‗. By measuring glycated haemoglobin (HbA1c), clinicians are able to get an overall picture of what our average blood sugar levels have been over a period of weeks/months. For people with diabetes this is important as the higher the HbA1c, the greater the risk of developing diabetes-related complications. elevated HbA1c values increase the likelihood of the microvascular complications of diabetes. HbA1C is a screening marker, can‘t predict diabetes complications. Improving HbA1C by 1% or 11mmol/mol cuts the risk of microvascular complications by 25% cataract complications by 19% CVD by 16% peripheral vascular disease by 43%.
  86. 86. Target of HbA1C  An HbA1c of 6.5% is recommended as the cut point for diagnosing diabetes.  Prediabetes- 5.4-6.5% and it requires LSM,MNT with constitutional drug in order to maintain the value in the desirable range.  HbA1C should be less than < 7%, constitutional medicine and LSM and MNT.  If HbA1C is 7-8 than it requires constitutional medicine, LSM, MNT , organopathic medicines and if required monotherapy with single hypoglycaemic drug and insulin sensitizer.
  87. 87. HbA1c Blood glucose in mmol/l Average blood glucose mg% 5% 5 97 6% 7 126 7% 8 154 8% 10 183 9% 12 212 10% 13 240
  88. 88. SUMMARY  Obesity and dyslipidemia are emerging as major public health challenges in South Asian countries. The prevalence of obesity is more in urban areas than rural, and women are more affected than men. Further, obesity in childhood and adolescents is rising rapidly. Obesity in South Asians has characteristic features: high prevalence of abdominal obesity, with more intra-abdominal and truncal subcutaneous adiposity than white Caucasians. In addition, there is greater accumulation of fat at ―ectopic‖ sites, namely the liver and skeletal muscles. All these features lead to higher magnitude of insulin resistance, and its concomitant metabolic disorders (the metabolic syndrome) including atherogenic dyslipidemia. Because of the occurrence of type 2 diabetes, dyslipidemia and other cardiovascular morbidities at a lower range of body mass index (BMI) and waist circumference (WC), it is proposed that cutoffs for both measures of obesity should be lower (BMI 23–24.9 kg/m2 for overweight and ≥25 kg/m2 for obesity, WC ≥80 cm for women and ≥90 cm for men for abdominal obesity) for South Asians, and a consensus guideline for these revised measures has been developed for Asian Indians. Increasing obesity and dyslipidemia in South Asians is primarily driven by nutrition, lifestyle and demographic transitions, increasingly faulty diets and physical inactivity, in the background of genetic predisposition. Dietary guidelines for prevention of obesity and diabetes, and physical activity guidelines for Asian Indians are now available. Intervention programs with emphasis on improving knowledge, attitude and practices regarding healthy nutrition, physical activity and stress management need to be implemented. Evidence for successful intervention program for prevention of childhood obesity and for prevention of diabetes is available for Asian Indians, and could be applied to all South Asian countries with similar cultural and lifestyle profiles. Finally, more research on pathophysiology, guidelines for cut-offs, and culturally-specific lifestyle management of obesity, dyslipidemia and the metabolic syndrome are needed for South Asians.
  89. 89. Only YOU can take care of yourself! MAKE good choices! TEACH good choices!
  90. 90. Compiled by:  Dr Neena Mehan (Asstt. Professor)  Dr Pavneet Kaur (Intern) ( Dr B R Sur Homeopathic medical College, Hospital and Research Centre)