This document discusses metabolic syndrome, which is a combination of medical disorders that increase the risk of cardiovascular disease and diabetes when occurring together. It affects about 20% of the Malaysian population. The core components include hypertension, high triglycerides, low HDL cholesterol, obesity, and impaired glucose tolerance. There are different criteria for diagnosing metabolic syndrome, but central to all definitions is insulin resistance. If left untreated, metabolic syndrome can increase the risk of serious health conditions such as heart disease, stroke, and type 2 diabetes.

1. Metabolic Syndrome
By:
Dr Madhumita Sen

2. Syndrome - X or Metabolic
syndrome
 What is it?
 Is it important?
 How common is it?
 What should be done about it?

3. What is it?
 Metabolic syndrome is a combination
of medical disorders that, when occurring together,
increase the risk of developing cardiovascular
disease and diabetes.
 It affects about 20% of the Malaysian population
and prevalence increases with age.
 There are slight differences in the criteria of
diagnosis - depending on which authority is
quoted.
 Regardless, the concept of a clustering of risks
factors leading to cardiovascular disease is well
accepted.

4. The cluster
 Hypertension
 Hypertriglyceridemia
 Low HDL-cholesterol
 Obesity (central)
 Impaired Glucose Handling
(Insulin Resistance)
 Microalbuninuria
(WHO)

5. How do we define who has metabolic
syndrome?
 International Diabetes Federation
 The IDF consensus worldwide definition of the metabolic syndrome
(2006) is:
 A) Central obesity (defined as waist circumference with ethnicity
specific values)
 AND
 B) any two of the following:
 1. Raised triglycerides: > 150 mg/dL (1.7 mmol/L), or on treatment
for this lipid abnormality.
 2. Reduced HDL cholesterol: < 40 mg/dL (1.03 mmol/L) in males, <
50 mg/dL (1.29 mmol/L) in females, or specific treatment for this
lipid abnormality
 3. Raised blood pressure: systolic BP > 130 or diastolic BP >85 mm
Hg, or treatment of previously diagnosed hypertension.
 4. Raised fasting plasma glucose :(FPG)>100 mg/dL (5.6 mmol/L),
or previously diagnosed type 2 diabetes.
 (If BMI is >30 kg/m², central obesity can be assumed and waist
circumference does not need to be measured)

6.  The World Health Organization criteria (1999)
require presence of one of:
 Diabetes mellitus / Impaired glucose tolerance /
Impaired fasting glucose or Insulin resistance,
 AND
 two of the following:
1.Blood pressure: ≥ 140/90 mmHg
2.Dyslipidemia: triglycerides (TG): ≥ 1.695 mmol/L
and high-density lipoprotein cholesterol (HDL-C) ≤
0.9 mmol/L (male), ≤ 1.0 mmol/L (female)
 3. Central obesity: waist:hip ratio > 0.90 (male); >
0.85 (female), or body mass index > 30 kg/m2
 4. Microalbuminuria: urinary albumin excretion ratio
≥ 20 µg/min or albumin:creatinine ratio ≥ 30 mg/g

7.  The European Group for the Study of Insulin
Resistance (1999) requires :
 A) Insulin resistance - defined as the top 25% of the
fasting insulin values among non-diabetic individuals
,
 AND
 two or more of the following:
 1. central obesity: waist circumference ≥ 94 cm
(male), ≥ 80 cm (female)
 2. dyslipidemia: TG ≥ 2.0 mmol/L and/or HDL-C <
1.0 mmol/L or treated for dyslipidemia
 3. hypertension: blood pressure ≥ 140/90 mmHg or
antihypertensive medication
 4. treatment for diabetes mellitus

8.  The US National Cholesterol Education Program
Adult Treatment Panel III (2001) requires at
least three of the following:
 1. central obesity: waist circumference ≥ 102 cm
or 40 inches (male), ≥ 88 cm or
36 inches(female)
 2. dyslipidemia: TG ≥ 1.7 mmol/L (150 mg/dl)
 3. dyslipidemia: HDL-C < 40 mg/dL (male), <
50 mg/dL (female)
 4. blood pressure ≥ 130/85 mmHg
 5. fasting plasma glucose ≥ 6.1 mmol/L
(110 mg/dl)

9.  American Heart Association
 1. Elevated waist circumference:
◦ Men — greater than 40 inches (102 cm)
◦ Women — greater than 35 inches (88 cm)
 2. Elevated triglycerides: Equal to or greater than
150 mg/dL (1.7 mmol/L)
 3. Reduced HDL (―good‖) cholesterol:
◦ Men — Less than 40 mg/dL (1.03 mmol/L)
◦ Women — Less than 50 mg/dL (1.29 mmol/L)
 4. Elevated blood pressure: Equal to or greater than
130/85 mm Hg or use of medication for hypertension
 5. Elevated fasting glucose: Equal to or greater than
100 mg/dL (5.6 mmol/L) or use of medication for
hyperglycemia

10. Just look at these factors!

11. AND Look at your shape

12. Ethnic specific values for waist
circumference (IDF)
 Europids
 Male ≥ 94 cm Female ≥ 80 cm
 South Asians
 Male ≥ 90 cm Female ≥ 80 cm
 Chinese
 Male ≥ 90 cm Female ≥ 80 cm
 Japanese
 Male ≥ 85 cm Female ≥ 90 cm
(Ethnic South and Central Asians Use South Asian
recommendations).

14. Some other factors
 High-sensitivity C-reactive protein (hs-CRP) has
been developed and used as a marker to predict
coronary vascular diseases in metabolic
syndrome and it was recently used as a
predictor for non-alcoholic fatty liver disease .
 Lahey Clinic Study—
 50-60% of Patients <45 years old, who
suffered MI had Metabolic Syndrome, a mean
BMI of approximately 32.
(The Framingham Risk scores of these patients is typically very
low—because age is low)

15. Other names used
 Syndrome X
 Cardio-metabolic Syndrome
 Cardiovascular Dysmetabolic Syndrome
 Insulin-Resistance Syndrome
 Metabolic Syndrome
 Beer Belly Syndrome
 Reaven‘s Syndrome

16. Note
 ―Until much needed research is completed,
clinicians should evaluate and treat all
CVD risk factors without regard to whether
a patient meets the criteria for diagnosis
of the ‗metabolic syndrome‘.‖
Joint Statement from the American
Diabetes Association and the European
Association for the Study of Diabetes.

17. Other Linked metabolic
abnormalities
 Impaired glucose handling/insulin
resistance
 Atherogenic dyslipidemia
 Endothelial dysfunction
 Prothrombotic state
 Hemodynamic changes
 Proinflammatory state
 Excess ovarian testosterone production
 Sleep-disordered breathing

18. Resulting conditions
 Type 2 diabetes
 Essential hypertension
 Polycystic ovary syndrome (PCOS)
 Nonalcoholic fatty liver disease
 Sleep apnea
 Cardiovascular Disease (MI, PVD,
Stroke)
 Cancer (Breast, Prostate, Colorectal,
Liver)

19. Risk Factors
 Several associated risk factors include:
 1. Genetic Factors: (inherited component):
◦ Family history of type 2 diabetes;
◦ Being Black, Hispanic, American Indian or Asian.
 South Asians in urban and migrant environments
may be at a higher risk of CHD due to the
confluence of
1. genetic factors that predispose to higher
cholesterol levels, and a possible "thrifty gene"
effect, with
2. environmental influences that lead to weight
gain

20.  2. Particular physiological conditions
and environmental factors:
◦ > 40–45 years of age;
◦ obesity
◦ your body storing fat predominantly in
the abdomen, as opposed to storing it in
hips and thighs.
◦ sedentary lifestyle, lack of physical
exercise
◦ hypertension

21. ◦ 3. Pre-diabetes, your sugar levels in
blood have been too high in the past, i.e.
your body has previously shown slight
problems with its production and usage of
insulin ("previous evidence of impaired
glucose homeostasis");
◦ having developed gestational diabetes
during past pregnancies;
◦ giving birth to a baby weighing more than
9 pounds (a bit over 4 kilograms).

22. More risk factors
• Urban populations have higher levels of CVD
risk factors related to diet and physical
activity (overweight, hypertension,
dyslipidaemia and diabetes)
• Tobacco consumption is more widely
prevalent in rural population
• The social gradient will reverse as the
epidemic populations mature. The poor will
become progressively vulnerable to the
ravages of these diseases.

23. History
 The term "metabolic syndrome" dates
back to at least the late 1950s, but came
into common usage in the late 1970s to
describe various associations of risk
factors with diabetes that had been noted
as early as the 1920s.
 The Marseilles physician Dr. Jean Vague,
in 1947, observed that upper body obesity
appeared to predispose to diabetes,
atherosclerosis, gout and renal calculi.

24.  In 1988, in his Banting lecture, Gerald M.
Reaven proposed insulin resistance as the
underlying factor and named the
constellation of abnormalities Syndrome X.

25. INSULIN RESISTANCE IS THE MAIN
PATHOLOGY BEHIND SYNDROME X

26. How Insulin Acts
• Any food or drink containing glucose (or the
digestible carbohydrates that contain it, such
as sucrose, starch, etc.) causes blood glucose
levels to increase.
• In normal metabolism, the elevated blood
glucose level makes beta (β) cells in
the Islets of Langerhans, located in
the pancreas, release insulin into the blood.

27.  Insulin attaches to
glucose-insulin receptors
on cell membranes to
allow glucose to be taken
into the cell.
 GLUT4 is the insulin-
regulated glucose
transporter found
in adipose tissues
and striated
muscle (skeletal and
cardiac) that is responsible
for insulin-regulated
glucose translocation into
the cell.

28. Glucose Transporter 4 Receptor
 The GLUT4 protein is expressed primarily in
muscle and fat cells, the major tissues in the
body that respond to insulin.
 Under conditions of low insulin, GLUT4 is
sequestered in intracellular vesicles in muscle
and fat cells.
 Insulin induces the translocation of GLUT4
from these vesicles to the plasma membrane.
 As the vesicles fuse with the plasma
membrane, GLUT4 transporters are inserted
and become available for transporting
glucose, and glucose absorption increases.

29.  Glucose transporter 4, also known
as GLUT4, is a protein receptor that in
humans is encoded by the GLUT4 gene.

30. • If the cell phospholipid membrane is not ―fluid‖ enough (i.e.
its composition does not have enough PUFA), insulin
receptors are disrupted.
• The insulin cannot act and glucose cannot enter the cells,
and thereby lower the blood glucose level.
• The beta cells reduce insulin output only if the blood
glucose level falls, allowing blood glucose to settle at a
constant of approximately 5 mmol/L (90 mg/dL).
• In IR states, insulin levels remain high, and this promotes
lipogenesis.

31.  When these cells fail to respond adequately to
circulating insulin, blood glucose levels rise.
 Without insulin, the liver is unable to use
glucose, and therefore secretes glucagon,
which further increases blood sugar by
converting liver glycogen (stores) into glucose.
 Glucagon also regulates the rate of glucose
production through lipolysis (breakdown of
stored lipids in adipocytes).
 This raises serum lipid levels.

32. Insulin keeps the blood sugar and cholesterol in
control by influencing their intake and output in
liver, muscle and fat cells.

33. Insulin resistance
 Insulin resistance (IR) is a condition where
the natural hormone insulin becomes less
effective at lowering blood sugars.
 The resulting increase in blood glucose may
cause adverse health effects, depending on
dietary conditions.
 Most cell types, especially fat and
muscle cells require insulin to absorb
glucose.

34. Insulin resistant states
• In an insulin-resistant person, normal levels of
insulin do not have the same effect in
controlling blood glucose levels.
• During the compensated phase, insulin levels
are higher, and blood glucose levels are still
maintained.
• If compensatory insulin secretion fails, then
either fasting (impaired fasting glucose) or
postprandial (impaired glucose tolerance)
glucose concentrations increase.

35. • Eventually, type 2 diabetes occurs when
glucose levels become higher
throughout the day as the resistance
increases and compensatory insulin
secretion fails.
• The elevated insulin levels have
additional effects that cause further
abnormal biological effects throughout
the body.

36. More on insulin resistance
 In IR, reduced muscle glucose uptake, and
increased liver glucose production all
contribute to elevated blood glucose levels.
 Other functions of insulin can also be affected.
 Insulin resistance in fat cells reduces the
normal effects of insulin on lipids and results
in reduced uptake of circulating lipids and
increased hydrolysis of stored triglycerides.

37.  Increased mobilization of stored lipids and reduced
uptake in the cells elevates free fatty acids in
the blood .
 Elevated blood fatty-acid concentrations leads to
atherosclerosis and cardiovascular disease.

38. Factors
influencing
Insulin Resistance

39. Diet
 It is well known that insulin resistance commonly
coexists with obesity.
 Saturated fat appears to be the most effective at
producing IR.
 High-fat diet has the tendency to result in caloric
intake that's far in excess of our energy needs,
resulting in rapid weight gain.
 Being insensitive to insulin is positively correlated
with fat intake, and negatively correlated with dietary
fibre intake.

40. PUFA
 In the long term, diet has the potential to
change the ratio of polyunsaturated to
saturated phospholipids in cell membranes,
correspondingly changing cell membrane
fluidity.
 It is hypothesized that increasing cell
membrane fluidity by increasing PUFA
concentration might result in an enhanced
number of insulin receptors and reduced
insulin resistance.

41. • Recent research is investigating the roles
of adipokines (adiponectin - the inflammatory
substance produced by adipose tissue) in insulin
resistance.
• Obese patients tend to have lower adiponectin
levels probably due to feedback inhibition by fat
accumulation. Adiponectin levels are also lower
in patients with the metabolic syndrome.
 Certain foods can increase adiponectin in the
body, eg. Sweet potato.

42. ADVANCED GLYCATED END
PRODUCTS
 AGE: Elevated blood levels of glucose –
regardless of cause – lead to
increased glycation of proteins with changes
in protein function throughout the body.
 These are called Advanced Glycated End
products and contribute to the end organ
damages of T2DM.

43. Visceral fat
 Unlike subcutaneous adipose
tissue, visceral adipose cells
produce significant amounts
of pro-inflammatory
cytokines such as tumour
necrosis factor-alpha (TNF-
a), Interleukins-1 and -6,
etc.
 In numerous experimental
models, these pro-
inflammatory cytokines
disrupt normal insulin action
in fat and muscle cells.

44. Abdominal obesity increases the
risk of developing type 2 diabetes
<71 71–75.9 76–81 81.1–86 86.1–91 91.1–96.3 >96.3
24
20
16
12
8
4
0
Relativerisk
Waist circumference (cm)

45. Role of leptin
 Yet another problem in metabolic syndrome
involves the phenomenon known
as leptin resistance.
 Leptin is a hormone that regulates long-term
energy balance in many mammals.
 Leptin is secreted by fatty tissue.
 An important role of leptin is long-term inhibition
of appetite in response to formation of body fat.

46.  This mechanism is known to be
disrupted in many obese
individuals: even though their
leptin levels are commonly
elevated, this does not result in
reduction of appetite and caloric
intake.
 Once leptin signalling has been
disrupted, the individual becomes
prone to further overeating,
weight gain, and insulin
resistance.
 Leptin has recently also been
seen to stimulate the genes for
longevity and have anti-aging
properties.

47. Glycemic index
 Integrated blood glucose response to a fixed
quantity of carbohydrates in a meal is known
as glycemic index.
 The rise in blood sugar after a carbohydrate
meal depends on how quickly it is absorbed.
 Complex carbs and foods high in fiber
cause a slower rise in sugar, and reduced
insulin resistance.
 Some diets are based on this concept; they
assume that consumption of low-GI foods is
less likely to result in insulin resistance and
obesity

48. Sedentary lifestyle
 Sedentary lifestyle increases the likelihood of
development of insulin resistance.
 It's been estimated that each 500 kcal/week
increment in physical activity related energy
expenditure reduces the lifetime risk of type 2
diabetes by 6%.
 A different study found that vigorous exercise
at least once a week reduced the risk of type 2
diabetes in women by 33%.

50. Signs and symptoms of insulin
resistance
 These depend on poorly understood variations in
individual biology and consequently may not be
found with all people diagnosed with insulin
resistance.
 1. Fatigue.
 2. Brain fogginess and inability to focus.
 3. High blood sugar.
 4. Intestinal bloating – most intestinal gas is
produced from carbohydrates in the diet, mostly
those that humans cannot digest and absorb.

51.  5. Sleepiness, especially after meals.
 6. Weight gain, fat storage, difficulty losing weight
– for most people, excess weight is from high fat
storage; the fat in IR is generally stored in and
around abdominal organs in both males and
females.
 7. Increased blood triglyceride levels.
 8. Increased blood pressure. Many people with
hypertension are either diabetic or pre-diabetic
and have elevated insulin levels due to insulin
resistance.
 One of insulin's effects is to control arterial wall
tension throughout the body.

52.  9. Increased pro-inflammatory cytokines
associated with cardiovascular disease.
 10. Depression. Due to the deranged metabolism
resulting from insulin resistance, psychological
effects, including depression, are not
uncommon.
 11. Acanthosis nigricans.
 12. Increased hunger.

53. Diagnosis
 Glucose tolerance testing (GTT)
 During a glucose tolerance test, which may be
used to diagnose diabetes mellitus, a fasting
patient takes a 75 gram oral dose of glucose.
 Blood glucose levels are then measured over the
following 2 hours.
 Interpretation is based on WHO guidelines. After 2 hours a
1. Glycemia less than 7.8 mmol/L (140 mg/dl) is considered
normal,
2. a glycemia of between 7.8 to 11.0 mmol/dl (140 to
197 mg/dl) is considered as Impaired Glucose
Tolerance(IGT) and a
3. glycemia of greater than or equal to 11.1 mmol/dl
(200 mg/dl) is considered Diabetes Mellitus

54. MANAGEMENT

55. Multiple risk factor management
 Goals: Minimize Risk of Type 2
Diabetes and Cardiovascular Disease
 Obesity
 Glucose Intolerance
 Insulin Resistance
 Lipid Disorders
 Hypertension

58.  The primary treatment for insulin
resistance is exercise and weight loss.
 Low-glycemic index diet has also been
shown to help.
 Low salt diet helps reduce blood pressure
and improves insulin sensitivity.
 Both metformin and the thiazolidinediones
improve insulin resistance, but are only
approved therapies for type 2 diabetes, not
insulin resistance.

59. Diabetes control
 For every 1% rise in Hgb A1c there is an 18%
rise in risk of cardiovascular events & a 28%
increase in peripheral arterial disease
 Evidence is accumulating to show that tight blood
sugar control in both Type 1 and Type 2 diabetes
reduces risk of CVD
 Goals: FBS - premeal 90-130, postmeal
<180.
 Hgb A1c <7%

60. Hypertension control
BP >130/85 or on Rx for previously
diagnosed hypertension.
 Goal: BP.<130/85
 MRFIT and Framingham Heart Studies:
◦ Conclusively proved the increased risk of CVD
with long-term sustained hypertension
◦ Demonstrated a 10 year risk of cardiovascular
disease in treated patients vs non-treated
patients to be 0.40.
◦ 40% reduction in stroke with control of HTN

61. DYSLIPIDEMIA
 Goals: HDL >40 mg% (>1.1 mmol /l)
 LDL <100 mg/dL (<3.0 mmol /l)
 TG <150 mg% (<1.7 mmol /l)
 Multiple major studies show 24 - 37% reductions
in cardiovascular disease risk with the control of
hyperlipidemia.
 Increased HDL cholesterol can be achieved with
increase in marine omega 3 fats intake.

62. SURGERY?
 Recent research has shown that weight reducing
surgeries like gastric banding and roux-en-y
gastric bypass can cure T2DM and IR,
irrespective of associated weight loss.
 The mechanisms of this effect are still being
studied.

63.  Type 2 diabetes has long been regarded
as inevitably progressive, requiring
increasing numbers of oral hypoglycemic
agents and eventually insulin, but it is
now certain that the disease process can
be halted with restoration of normal
carbohydrate and fat metabolism.
 Type 2 diabetes can be understood as a
potentially reversible metabolic state
precipitated by the single cause of chronic
excess intraorgan fat.

64.  Reversal of type 2 diabetes to normal
metabolic control by either bariatric
surgery or hypocaloric diet allows for the
time sequence of underlying
pathophysiologic mechanisms to be
observed.
 In reverse order, the same mechanisms
are likely to determine the events leading
to the onset of hyperglycemia and permit
insight into the etiology of type 2
diabetes.
 Roy Taylor, MD, FRCP, Diabetes
Care. 2013;36(4):1047-1055.

65.  Within 7 days of instituting a substantial
negative calorie balance by either dietary
intervention or bariatric surgery, fasting
plasma glucose levels can normalize. This
relates to a substantial fall in liver fat
content and return of normal hepatic
insulin sensitivity.
 Over 8 weeks, insulin secretion steadily
return to normal, and this change is in
step with steadily decreasing pancreatic
fat content.

66. New Perspectives on the β-cell Defect
 Chronic exposure of β-cells to triacylglycerol
or fatty acids decreases β-cell capacity to
respond to an acute increase in glucose
levels.
 The cellular process of insulin secretion in
response to an increase in glucose supply
depends on ATP generation by glucose
oxidation. However, in the context of an
oversupply of fatty acids, such chronic
nutrient surfeit prevents further increases in
ATP production.

67.  Fatty acids have been shown to inhibit β-
cell proliferation, and this effect is
magnified by increased glucose
concentration.
 Histological studies of the pancreas in
type 2 diabetes consistently show an
~50% reduction in number of β-cells
compared with normal subjects.
 β-Cell loss appears to increase as
duration of diabetes increases.

68.  In light of new knowledge about β-cell
apoptosis and rates of turnover during
adult life, it is conceivable that removal of
adverse factors could result in restoration
of normal β-cell number, even late in the
disease.
 Regeneration of β-cells is seen after
successful bariatric surgery or Incretin
based therapies.

69. The twin cycle hypothesis of the etiology of
type 2 diabetes.

70. Betatrophin
 Researchers at Harvard University discovered
that the hormone, called betatrophin, promotes
the growth of Beta cells in the pancreas in mice.
 The scientists found the hormone caused mice
to produce these cells at 30 times the normal
rate.
 Rather than having to take daily injections of
insulin to control the amount of sugar in their
blood, patients would need to take this new
hormone just weekly or even monthly,
according to the researchers.
 Dr Melton added, however, that the work was
still in the early stages and it would be several
years before a treatment using the hormone
could be used by humans.
 From the Telegraph, 26 Apr 2013

71. Testostorone
 Testosterone replacement reverses insulin
resistance in hypogonadal men with type 2
diabetes, preliminary data suggest. The
findings, from a randomized trial in 81 men,
were reported by Paresh Dandona, MD, PhD,
head of the division of endocrinology,
diabetes, and metabolism at the University of
Buffalo, State University of New York.
 American Association of Clinical Endocrinologists
2013 Scientific & Clinical Congress Abstract 280,
presented May 2, 2013.

73. Prevention
 There is an urgent need to increase awareness
of the CVD burden, and develop preventive
strategies.
 Prevention and treatment strategies that have
been proven to be effective in developed
countries should be adapted for developing
countries.
 Prevention is the best option as an approach
to reduce CVD burden.

74. Diabetes and CVD – end points
to avoid

75. Screening
 1. Public Education
 2. Screening for at risk individuals:
◦ Blood Sugar/ HbA1c
◦ Lipids
◦ Blood pressure
◦ Tobacco use
◦ Body habitus
◦ Family history

76. Calculating Mortality Risk in T2DM
 Gargano Mortality Risk Score
All-cause 2-year mortality risk score in
patients with type 2 diabetes mellitus.
 Using variables like age, body mass index
(BMI), diastolic blood pressure, LDL
cholesterol, triglycerides, HDL
cholesterol, urine albumin-to-
creatinine ratio, antihypertensive
treatment, and insulin therapy — a
physician can quickly determine whether a
patient has a high risk for death.
 http://www.operapadrepio.it/rcalc/rcalc.php

77. Public education

78. DIET
 Carbohydrates:
1.Eat according to energy requirements and as per
energy expended.
2.Eat complex carbohydrates and fibre.
 Proteins
1.Choose a wide variety of sources, both
Vegetarian and Non-vegetarian over the week
2.Restrict intake to 30 gms per meal (size of a
deck of cards)
 Fats
1.Choose vegetable fats
2.Eat 1 helping of oily fish at least 2 -3 days a
week
3.Snack on nuts

80. Life-Style Modification
 Exercise
◦ Improves CV fitness, weight control,
sensitivity to insulin, reduces incidence of
diabetes
◦ Goal: Brisk walking - 30 min./day
 Weight loss
◦ Improves lipids, insulin sensitivity, BP
levels, reduces incidence of diabetes
◦ Goal: 10% reduction in body wt.

81.  Basic recommendations are
1.3 days a week = aerobics 20 mins +
weight training (anaerobics) 10 mins
2.2 days a week = aerobics 20 mins +
flexibility and core exercises 10 mins.
3.Saturday and Sunday = games or outdoor
activities you enjoy WITH family and
friends , 20 – 30 mins. Even walking will
do!

82.  SMOKING CESSATION
 Both passive and active exposure harmful
 A major risk factor for:
◦ insulin resistance and metabolic
syndrome
◦ Macro-vascular disease (PVD, MI,
Stroke)
◦ Micro-vascular complications of diabetes
◦ pulmonary disease, etc.

83. SLEEP
 People who go to bed late and sleep in late
typically have a greater degree of "circadian
misalignment" between their actual sleep-
wake pattern and their natural body clock.
 Studies have linked such misalignment with a
host of ailments, including coronary artery
disease, metabolic syndrome, and impaired
glucose tolerance.
 The implications of the study are that people
with type 2 diabetes might do well to get to
bed earlier, wake up earlier, and try to keep
as regular a schedule as possible.
 Diabetes Care. Published online May 1, 2013.

84. Key Points
• There is an urgent need to increase
awareness of the CVD and T2DM burden, and
develop preventive strategies.
• Prevention and treatment strategies that
have been proven to be effective in
developed countries should be adapted for
developing countries.
• Prevention is the best option as an approach
to reduce CVD and T2DM burden.

85. Thank you
Any questions?