Lifestyle and obesity and how it impacts on health. The pathology of obesity.

1. Obesity & Metabolic
Syndrome
By:
Dr Madhumita Sen

2. Learning Objectives
After this lesson, the audience are expected to
know
- The causes of obesity
- The prevalence of obesity worldwide and in
Malaysia
- Pathophysiology of Obesity
- Regional fat distribution and its relationship to the
obesity health consequences
- Appetite regulation
- The role of gut hormones in obesity
- The endocrine function of the adipose tissue
- Clinical complications of obesity

3. Factors affecting Health

4. Rise of obesity
 The recent rise in obesity and type 2 diabetes
rates has reached disturbing levels.
 This has occurred despite the fact that our
knowledge about the importance and effects of
diet and exercise are at an all time high.
 Overweight and obesity lead to adverse
metabolic effects on blood pressure, cholesterol,
triglycerides and insulin resistance.
 Risks of coronary heart disease, ischemic stroke
and type 2 diabetes mellitus increase steadily.

5. Raised body mass index also
increases the risk of cancer of
the breast, colon, prostate,
endometrium, kidney and gall
bladder.

6.  http://www.healthworks.my/malaysians
 “Malaysia is ranked sixth in the Asia-Pacific region
for obesity and tops the list in South-East Asia for
both obesity and diabetes,” stated Prof Dr. Mohd Ismail
Noor, the president of Malaysian Society for the Study of
Obesity.
 Malaysians diagnosed with diabetes has increased by
two folds, from 1.5 million in 2006 to about three million
in 2011.

7. What causes obesity?
The thrifty gene hypothesis
The central premise of this theory is that through
natural selection we evolved to be efficient at
food storage and utilization.

8. Feast and Famine
Paleolithic Era > 25,000 years ago
 The thrifty gene hypothesis theorizes that if a
person was more efficient at storing energy during
the feasting portion of the cycle, he would be
more likely to survive during the famine portion.
 Physical activity-rest cycle is just as important
as the feast-famine cycle.
 In the hunter-gatherer society, food was obtained
largely through physical activity.
 Men hunted 1 to 4 non-consecutive days per
week, while women gathered food 2 to 3 days per
week.

9. Combining exercise into the thrifty gene
hypothesis means that we likely did not evolve
just to survive feast or famine, but also to be
able to have enough fitness to survive the
procurement of food.
This brings us to our current environment which
consists of low activity levels, high calorie
diets, and positive energy balance.
How does obesity occur? The formula is simple:
Food eaten – Exercise = Weight Gained

10. Other Causes:
Social factors
Social factors play a major role in weight gain.
 adolescence,
 pregnancy,
 mid-life in women, and
 following marriage in men.
 Persons who emigrate to a more urbanized culture
tend to gain weight.
 Behavioural or environmental changes in life, such
as smoking cessation, are associated with weight
gain.
 Weight gained during holiday periods and festivals
is more than at other times of the year and tends
not to be lost.

11. Family Matters
 Among pairs of adult siblings, if one sibling
becomes obese, the chance that the other
becomes obese increases by 40%.
 If one spouse becomes obese, the likelihood
that the other spouse becomes obese increases
by 37%.

12. Sitting for Too Long
 At one time or another, we all end up spending
too much time at our desk staring at the
computer screen.
 Research shows that extended periods of sitting
can increase our risk of heart disease, diabetes,
depression, and certain types of cancer.
 What we may not know is that even an
adequate amount of exercise cannot reverse
the unhealthy effects of sitting for eight hours.

13.  Drinking Sugary Soft
Drinks
 People who drink a can of
soda a day increase their risk
of suffering a heart attack by
20 percent according to a
recent Harvard University
study.
 The amount of sugar in a
single can of soda, 10
teaspoons, or 100 percent of
our daily recommended
intake, can also increase our
risk of pulmonary
complications such as asthma
and chronic obstructive
pulmonary disorder (COPD).

14. Appetite Regulation

15. Appetite
 Appetite is the amount of food one eats, felt
as hunger.
 Appetite exists in all higher life-forms, and
serves to regulate adequate energy intake to
maintain metabolic needs.
 It is regulated by a close interplay between
the digestive tract, adipose tissue and
the brain.

16. The Main Hormones of Appetite Regulation
OREXIGENIC MOLECUES ANOREXIGENIC MOLECULES
Neuropeptide Y
Agouti Related Peptide
Melanin Concentrating Hormone
(MCH)
Orexins 1 & 2
Galanin
Ghrelin
Insulin
Endocannabinoids
Glutamate
Endorphins
Catecholamines (adrenaline,
noradrenaline, dopamine)
Alpha MSH
Cocaine and Amphetamine related
Transcript (CART)
Corticotrophin releasing hormone
(CRH)
Leptin
Serotonin
Peptide YY
GABA
Glucagon Like Peptide 1 (GLP1)
Cholecystokinin
Estrogen
Neurotensin

17. Hormones in Appetite Regulation
Amylin  A partner hormone to insulin, released
after meals
 Secreted by the pancreas
 It slows the emptying of our stomach
and suppresses glucagon

18. GLP-1  Released when blood glucose levels are
above the norm
 Secreted by cells of the gut in
proportion to the amount of energy
ingested
 Stimulates insulin secretion, may assist
in signalling the brain to stop eating
 GLP-1 is secreted from L cells in the
gastrointestinal tract and is induced by
sugars, amino acids, and long-chain
fatty acids. Short-chain fatty acids also
increase GLP-1 secretion

19. Leptin  Released with low calorie intake and low
body fat levels. Secreted by fat cells
 Low leptin means a slower metabolism
and drive to increase food consumption.
 Administering leptin analogs in humans
is ineffective for appetite suppression.
 Leptin exists to prevent starvation, not
to lose weight.

20. Gastrin  Released when food enters stomach,
protein dense foods are the
most potent stimulator of gastrin
 Secreted by cells in
stomach/small intestine
 Initiates the digestion process

21. Secretin  Released when acids reach small
intestine
 Secreted by cells in small intestine
 Produces pancreatic fluid, inhibits
gastrin release, and enhances effects
of cholescystokinin

22. Cholecysto
kinin
(CCK)
 Released when protein and fat enter
the small intestine
 Secreted by cells in small intestine
 Signals pancreas to produce
enzymes, inhibits gastrin, stimulates
gallbladder contraction, and triggers
satiety in the brain

23. Gastric
inhibitory
polypeptide
(GIP)
 Released when food enters small intestine
 Secreted by cells in small intestine
 Enhances insulin release, inhibits gastric
secretions and motility
Motilin  Released when bicarbonate is dumped into
the small intestine and between
meals/when fasting
 Secreted by cells in small intestine
 Promotes muscle contraction of GI tract,
and when released between meals,
borborygmus (growling stomach)

24. Ghrelin  Released in response to low food
intake/fasting
 Secreted by cells of the stomach,
pancreas, placenta, kidney, pituitary
and hypothalamus
 Stimulates release of growth hormone
to encourage eating and acts to
regulate energy balance.

26.  Adiponectin
 Adiponectin, is a 244-amino acid protein
secreted from adipose tissue.
 The plasma concentration of adiponectin is
inversely correlated with adiposity in humans.
 Studies show that treatment with adiponectin
can reduce body weight gain, increase insulin
sensitivity, and decrease lipid levels.
 Thus adiponectin, as well as increasing energy
expenditure, may also provide protection
against insulin resistance and atherogenesis.

28.  Recent data have suggested that brain reward
pathways that are involved in alcohol and drug
addiction are also essential elements of the ghrelin
responsive circuit. And ghrelin has been shown to
both signal hunger and increase food intake.
 A subgroup of obese patients indeed show
'addictive-like' properties with regard to
overeating.
 Binge eating disorder (BED) is part of the
recently published fifth edition of the Diagnostic
and Statistical Manual of Mental Disorders (DSM-
5)Oct 2013

29. Hypothalamic Lipid Metabolism
and Energy Homeostasis
 Within the central nervous system the
metabolism of fatty acids is primarily for the
purposes of membrane function and the
central regulation of energy metabolism.
 Fats do not serve as a major source of energy
within the brain.
 Fatty acids, specifically long-chain fatty acids
via the formation of long-chain fatty acyl-CoAs,
have very recently been shown to exert
anorexigenic effects via the hypothalamus.

30.  Zinc:
 Leptin levels decrease in
response to zinc depletion
and increases after zinc
supplementation.
 Importantly, the
magnitude of leptin level
changes were proportional
to the changes of cellular
zinc.
 Adequate zinc levels
reduce appetite,
possibly by increasing
brain sensitivity to leptin.

31. Probiotics:
 Recently, a potential link between gut microbiota
and obesity has emerged.
 The study by Cani et al. [2011] evaluated the
effect of prebiotics on plasma levels of gut
hormones in healthy subjects.
 After two weeks of probiotic treatment, they
observed increased gut microbiota fermentation,
decreased appetite, and improved
postprandial glucose responses.
 Furthermore plasma levels of GLP-1 was increased
in subjects following probiotic treatment.

32.  Estrogen deficiency might result in a higher energy
intake and increased body weight. Food intake varies
across the menstrual cycle. Women tend to eat more in
the luteal phase (the premenstrual period) compared
with the follicular phase.
 Testosterone (directly) seems to have little effect on
food intake, although many people supplementing
anabolic doses of testosterone (e.g. bodybuilders) do
report increased appetite.
 Including a balanced intake of omega-6:omega-3 fats
can help with appetite regulation.
 A high protein diet can reduce appetite.

33.  Fibre seem to help control appetite.
 Refined carbohydrates, on the other hand,
appear to increase appetite.
 Dietary fat has mixed results; when combined
with refined carbohydrate it seems to increase
appetite while on its own or combined with
protein, it typically decreases appetite.
 Elderly people have less appetite than young
people from not only decreased energy
expenditure but also from mechanisms
potentially involving sex–steroid balance as well
as altered CNS signalling to and from peripheral
organs.

34. Don’t forget sleep!

35.  Appetite regulation has so many
factors!!!!
 Dietary changes can manage weight
as well as appetite.

36. Pathology of fats

37. Adipose Tissue as an Endocrine Organ
 Adipose tissue is an important endocrine organ
that secretes numerous protein hormones,
collectively called Adipokines.
 These hormones generally influence energy
metabolism, which is of great interest to the
understanding and treatment of type 2
diabetes and obesity.
 Their relative roles in modifying appetite, insulin
resistance and atherosclerosis are the subjects
of intense research.

38. Obesity and Inflammation
 Obesity is associated with a state of chronic,
low-grade inflammation.
 There is associated chronic inflammatory response
characterized by abnormal cytokine production,
increased acute-phase reactants, and activation of
inflammatory signalling pathways.
 A feature of this inflammatory response is that it
appears to be triggered, and to reside
predominantly, in abdominal adipose tissue, and
not in subcutaneous fat.

39.  Growth and angiogenic factors: Fibroblast growth
factors (FGFs), insulin-like growth factor-1 (IGF-1),
hepatocyte growth factor (HGF), nerve growth factor
(NGF), vascular endothelial cell growth factor (VEGF),
transforming growth factor-β (TGFβ), angiopoietin-1,
angiopoietin-2, tissue factor (TF, factor 3).
 Cytokines: IL-1β, IL-4, IL-6, IL-8, IL-10, IL-18, TNFα,
macrophage migration inhibitory factor (MIF)
 Complement-like factors: adipsin, adiponectin,
acylation stimulating protein (ASP)

40.  Adhesion molecules and ECM components: α2-
macroglobulin, vascular cell adhesion molecule-1 (VCAM-1),
intercellular adhesion molecule-1 (ICAM-1), fibronectin, lysyl
oxidase.
 Acute phase proteins: C-reactive protein (CRP), serum
amyloid A3 (SAA3), plasminogen activator inhibitor-1 (PAI-1),
haptoglobin
 Chemokines: chemerin, monocyte chemotactic protein-1
(MCP-1), macrophage inhibitory protein-1 alpha (MIP-1α)-
regulated upon activation, normally T cell expressed and
secreted (RANTES)

41.  Metabolic processes: adipocyte fatty acid binding
protein (aP2), apolipoprotein E (apoE), resistin,
omentin, vaspin, apelin, retinol binding protein 4
(RBP4), visfatin, leptin
 Other processes: COX pathway products PGE2 and
PGI2 (prostacyclin), nitric oxide synthase pathway,
renin-angiotensin system

42.  The proinflammatory state in the adipose tissue
also leads to a local insulin resistance including an
impaired inhibitory effect of insulin on FFA release.
 The insulin resistance further supports the pro-
inflammatory state because insulin, by itself, is
antilipolytic.
 Although energy restriction leading to weight loss is
the primary dietary intervention to reverse these
obesity-associated metabolic disorders, other
interventions targeted at alleviating adipose tissue
inflammation have not been explored in detail.

43. Omega-3 Fatty Acids Alleviate Adipose Tissue
Inflammation and Insulin Resistance
 There are studies showing that adipose
tissue inflammation can be reduced
without changing adipose mass.
 EPA reverses high-fat–induced metabolic
disorders and adipose inflammation.
 In one study, EPA supplementation
reversed high-saturated fat diet-induced
insulin resistance and hepatic steatosis.
 Omega 3 fatty acids are known to
increase fatty acid oxidation in liver,
adipose tissue, and small intestine

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

46. 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.

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

48. 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

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

51. 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

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

53. 3. Pre-diabetes:
 sugar levels in the blood have been too high in
the past, i.e. the 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).

54. More risk factors
• Urban populations have higher levels of 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.

55. Environmental toxins
Xenobiotic and dietary compounds with hormone-
like activity (obesogens) can disrupt endocrine
signaling pathways that play important roles
during perinatal differentiation and result in
alterations that are not apparent until later in life.
Environmental obesogens: organotins and endocrine disruption via
nuclear receptor signaling. Grün F, Blumberg B Endocrinology. 2006
Jun; 147(6 Suppl):S50-5.

56. History
 The term "metabolic syndrome"
dates back to at least the late
1950s.
 The Marseilles physician Dr. Jean
Vague, in 1947, observed that
upper body obesity appeared to
predispose to diabetes,
atherosclerosis, gout and renal
calculi.
 In 1988, in his Banting lecture,
Gerald M. Reaven
proposed insulin resistance as the
underlying factor and named the
constellation of abnormalities
Syndrome X.

57. INSULIN RESISTANCE IS THE MAIN
PATHOLOGY BEHIND SYNDROME X

58. How Insulin Acts
• Any food or drink containing glucose (or any
digestible carbohydrates) causes blood
glucose levels to increase.
• In normal metabolism, the elevated blood
glucose level and intestinal incretin makes
beta (β) cells in the Islets of Langerhans,
release insulin into the blood.

59.  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 that is
responsible for
insulin-regulated
glucose translocation
into the cell.

60. 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.

61. • 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.

62. • Without insulin, the liver is unable to use glucose,
and therefore secretes glucagon, which further
increases blood sugar by converting liver glycogen
into glucose.
• The beta cells reduce insulin output only if the
blood glucose level falls.
• In IR states, insulin levels remain high, and this
promotes lipogenesis.

63. Factors
influencing
Insulin Resistance

64. Diet
 It is well known that insulin
resistance commonly
coexists with obesity.
 Saturated fat appears to be
the most effective at
producing IR.
 Being insensitive to insulin is
positively correlated with fat
intake, and negatively
correlated with dietary fibre
intake.

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

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

67. 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.
 These pro-inflammatory
cytokines disrupt normal
insulin action in fat and
muscle cells.

68. Role of leptin
 Yet another problem
in metabolic
syndrome involves
the phenomenon
known as leptin
resistance.
 An important role of
leptin is long-term
inhibition of appetite
in response to
formation of body
fat.

69.  Once leptin
signalling
has been
disrupted,
the
individual
becomes
prone to
further
overeating,
weight gain,
and insulin
resistance.

70. Glycemic index
 Integrated blood
glucose response to a
fixed quantity of
carbohydrates in a meal
is known as glycemic
index.
 Complex carbs and
foods high in fiber
cause a slower rise in
sugar, and reduced
insulin resistance.

72. 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 simple carbohydrates in the diet.

73.  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. One of insulin's
effects is to control arterial wall tension
throughout the body.

74.  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.

75. MANAGEMENT

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

77. Treating Insulin Resistance
 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.

78. Diabetes control
 For every 1% rise in Hb A1c there is an 18% rise in risk of
cardiovascular events & a 28% increase in peripheral
arterial disease.
 Goals: FBS = premeal 90-130,
postmeal <180.
 Hgb A1c = 6.5 - 7%

79. Hypertension control
BP >130/85 or on Rx for previously
diagnosed hypertension.
 Goal: B.P.<130/85

80. 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.

81. 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 (? Incretin effect).

82.  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
intra-organ fat.
 Roy Taylor, MD, FRCP, Diabetes Care.
2013;36(4):1047-1055.

83. Betatrophin
 Researchers at Harvard University discovered that
a hormone, called betatrophin, promotes the
growth of Beta cells in the pancreas of mice.
 Rather than having to take daily injections of
insulin, 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.
 Cell. 2013 May 9;153(4):747-58.
doi:10.1016/j.cell.2013.04.008. Epub 2013 Apr 25.

84. 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.

86. 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.

87. Diabetes and CVD – end points
to avoid

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

89. Public education

90. 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

92. Life-Style Modification
 Exercise
◦ Improves CV fitness, weight control, sensitivity
to insulin, reduces incidence of diabetes
◦ Goal: Brisk walking - 30 min./day/5 days a
week
 Weight loss
◦ Improves lipids, insulin sensitivity, BP levels,
reduces incidence of diabetes
◦ Goal: 10% reduction in body wt.

93. 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.
◦ Cancers

94. 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.
Diabetes Care. Published online May 1, 2013.

95. Note: Obesity Paradox
 The original description of the obesity paradox
was published in 1999 using data from >1300
patients with chronic kidney disease undergoing
haemodialysis.
 The obesity paradox suggests that a BMI of
~25–35 kg/m2 carries benefit in patients with
chronic disease possibly because excess fat
serves as an energy depot in times of need.

96.  The available studies, together with previously
published study data, permit the conclusion that
weight loss in patients with chronic illness and a
BMI <40 kg/m2 is bad, and in fact not a single
study exists to suggest that weight loss in chronic
illness makes patients live longer.
 This statement, however, should not be
extrapolated to healthy individuals.
 In summary, the most obvious seems to be most
confusing in understanding the obesity paradox:
healthy people and patients with chronic diseases
are quite different.

97.  Obesity may carry
benefit up to a certain
degree, and it should
be recognized that
obesity is not
necessarily associated
with abnormal
metabolic function.
Eur Heart J. 2013;34(5):330-
332. © 2013 Oxford
University Press

98. Key Points
• There is an urgent need to increase awareness of the
obesity, 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.

99. Thank you
Any questions?
Ref: http://www.medscape.com/viewarticle/851929?src=wnl_edit_tpal&uac=130781BG