This document discusses the natural history of disease and fetal origins of adult disease. It provides background on how diseases progress over time without treatment and the importance of understanding this progression. It then discusses the theory that nutritional deprivation of the fetus during critical periods of development can force adaptations that become maladaptive when faced with different postnatal nutritional circumstances, potentially leading to adult health disorders. Factors like low birth weight, infant growth, and prenatal exposures are associated with increased risk of adult obesity, cardiovascular disease, and other issues. The document emphasizes that fetal development can permanently affect body structure and function in ways that manifest as disease later in life.

2. 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.

3. 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.

4. 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


5. 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

6. 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

7. 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 (idf.org) 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.

8. 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

9.  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.

10.  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

11. 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

12.  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

13.  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

15. 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

16. 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.

17. 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.

18. 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

19. 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.

20.  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.

21. 
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.

22.  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 .

23. 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.


24. 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 .

25. Insulin Resistance: Associated Conditions

26. 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.

28. 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.

29. Relationship Between Obesity and
Insulin Resistance and Dyslipidemia

31. 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.

33. 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.

34. 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

35. 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

36. Management of obesity

37. 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

38. 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.

40. 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

41. 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 .

42. 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

43. 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.

44. 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.

45. 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.

46. 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

47. 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

48. 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)

49. 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.

50. n Type 2 Diabetes Results From Three Major
Metabolic Defects

52. Indian diabetes risk score

53.  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.

54.  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.

55. 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.

56. LIPI+TENSION

57. 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.

58. 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.

59. 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.

60. 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.

61. 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

62. 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

63. 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

64. 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.

65. 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.

66. 
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.

67. 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.

68. 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

69.  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

70.  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

71. 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.

72. 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)

73.  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.

74. 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

75. 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

76. 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).

77. 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

78. 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

80. 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

81. 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.

82. 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

84. 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

85. 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.

86. 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.

87.  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.

88.  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.

89. 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

90.  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.

91.  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.

92. 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.

93. 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.

94. 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%.

95. 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.

96. 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

97. 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.

99. Only YOU can take care of yourself!
MAKE good choices!
TEACH good choices!

100. Compiled by:
 Dr Neena Mehan (Asstt. Professor)
 Dr Pavneet Kaur (Intern)
( Dr B R Sur Homeopathic medical College, Hospital and
Research Centre)