Metabolic syndrome is one of the most common risk factor for Cardiovascular disease. Greek, unani, ayurvedic Herbal medicine shows great potential in helping fight the condition. in these presentation an attempt made to understand the pathophysiology in detail, and How Unani system of medicine address this whole syndrome along with the details of potent herbs which can be used for the Metabolic syndrome.

1. Metabolic Syndrome:
CONCEPT AND MANAGEMENT IN UNANI
MEDICINE
Presented by
Dr Mohd Shaheryar
PG scholar dept of Medicine (Moalajat)
National institute of Unani Medicine

2. Contents:
• Introduction
• Definition
• Epidemiology
• Pathophysiology
• Clinical presentation
• Investigations
• Management
• Unani correlation

3. Introduction & Epidemiology
• Metabolic syndrome (MetS) is a cluster of metabolic abnormalities that includes
hypertension, central obesity, insulin resistance, and atherogenic dyslipidemia.
• It is also known as ‘insulin resistance syndrome’, ‘syndrome X’, hyper
triglyceridemic waist’, and ‘the deadly quartet’, is increasingly being recognized
as an important cardiovascular risk factor.
• Metabolic syndrome has become a truly global problem number of individuals
with MetS is increasing, and its worldwide prevalence is estimated to be
approximately 20% - 25%. The incidence of metabolic syndrome often parallels
the incidence of obesity and incidence of type 2 diabetes according to which
about one third of US adults have metabolic syndrome while the prevalence of
MetS in China is about would be about 15.5%. In India, almost one in three
adults suffer from MetS. Females and people living in urban areas and in the
northeast region had a higher prevalence of MetS.

4. 0
5
10
15
20
25
30
35
Percentage
of
population
Prevelence Of MetS in USA INDIA And CHINA

5. Metabolic
Syndrome
Normal
PREVELANCE IN AFRICAN-AMERICAN
WOMEN
Normal
Metablic
Male
PREVELANCE IN AFRICAN-
AMERICAN MEN

7. Definition (Criteria)
The World Health Organization (WHO)first developed its definition in 1998,
Because insulin resistance was felt to be central to the pathophysiology of metabolic
syndrome, evidence for insulin resistance is an absolute requirement in the WHO
definition.
National Cholesterol Education Program (NCEP) Adult Treatment Panel III (NCEP
ATP III) is The widely Used definition for MetS which does not compulsory any
specific criteria rather if a person fulfills any three criteria out of five, will be
considered having metabolic syndrome.
the International Diabetes Foundation (IDF) compulsory central obesity criteria
whereas the European Group for the Study of Insulin Resistance (EGIR)
compulsory Hyperinsolinemia ( fasting plasma insulin > 75th percentile)

10. Pathophysiology
• MetS is a state of Chronic low-grade inflammation as a
consequence of the complex interplay between genetic and
environmental factors.
• Visceral adiposity, insulin resistance, dyslipidemia,
endothelial dysfunction, genetic susceptibility, elevated
blood pressure, hypercoagulable state, and chronic stress are
the several factors that constitute the syndrome.

11. Visceral Obesity
• Increased consumption of calorie-dense food, and a sedentary lifestyle
leads to alteration in nutrient excess which causes hypertrophy and
hyperplasia of adipocytes
• With adipocytes enlargement blood supply to adipose tissue gets
reduced causing hypoxia leads to many necrosis and macrophage
infiltration into adipose tissue causing overproduction of biologically
active metabolites known as adipocytokines
• Adipocytokines include free fatty acids (FFA), pro-inflammatory
mediators (TNFα, IL-6, Plasminogen activator inhibitor PAI-1, CRP
And Resistin) causing localised inflammation in adipose tissue that
propagates an overall systemic inflammation,

13. Free fatty Acids (FFA)
• FFA increases insulin resistance and leads to multiple consequences
like increase Gluconeogenesis, lipogenesis, and triglycerides.
• FFA reduces glucose uptake in muscles and decreases the antilipolytic
activity of insulin resulting in more FFA.
• FFA is lipotoxic to beta cells of the pancreas causing a decrease in
insulin secretion
• Increase in FFAs leads to increased triglyceride synthesis and the
production of apolipoprotein B containing triglyceride-rich very low-
density lipoprotein (LDL) in the liver.

14. TNF-α, IL-6, PAI-1 And Resistin
• Macrophages within the adipose tissue secrete TNF-α, which causes
phosphorylation and inactivation of insulin receptors in the adipose tissue as well
as in smooth muscle cells leading to more FFA load and Inhibit Adiponectin
release (Anti-Inflammatory anti-atherogenic protective agent).
• Interleukin 6 (IL-6) is a cytokine produced by adipocytes and immune cells and
has complex regulatory mechanisms, with an increase in body fat and insulin
resistance, It acts on the liver, bone marrow, and endothelium, leading to
increased production of acute phase reactants in the liver, including C-reactive
protein (CRP) causing inflammatory state it increases fibrinogen levels in
resulting in the prothrombic state.
• Adipocytes also secrete Plasminogen activator inhibitor (PAI-1) causing a
prothrombic state.
• Resistin is a cystine-rich hormone secreted from white adipocytes involved in
Insulin resistance

15. Adipokines and Renin-Angiotensin System
• Adipose tissue secretes Leptin and Adiponectin. In visceral obesity Level of
leptin Increases while adiponectin decreases.
• Leptin through the TH-1 pathway releases Cytokines that give rise to a
proinflammatory state.
• Whereas Adiponectin has anti-atherogenic properties which counters the
effect of leptin. It decreases both vascular reactivity and smooth muscle
proliferation, and improves plaque stability Adiponectin has been
considered a protective factor against the development of diabetes,
hypertension, and acute myocardial infarction.
• Adipose tissue Produces ACE leads to high Angiotensin 2 levels.
• Ang II, through activation of the type 1 receptor, activates nicotinamide
adenine dinucleotide phosphate oxidase leading to the generation of reactive
oxygen species (ROS)

16. • ROS precipitate a multitude of effects including oxidation of
LDL, endothelial injury, platelet aggregation, and expression of
lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1)
on the endothelium and vascular smooth muscle cells.
• RAS, ROS, and LOX-1 have an interrelated positive feedback
loop that initiates a vicious cycle of inflammation, endothelial
damage, and fibroblast proliferation that contributes to the
development of hypertension, dyslipidaemia, diabetes, cardiac
hypertrophy, and CVD.
RAS ROS LOX-1
Inflammation
Endothelial
damage
Fibroblast
proliferation

18. • In the skeletal muscle and adipose tissue, insulin stimulates
glucose uptake by translocation of the GLUT4 glucose
transporter to the cell surface. In the skeletal muscle and
liver, insulin stimulates the synthesis of glycogen from
glucose and inhibits glycogenolysis.
• In the liver, insulin also decreases hepatic gluconeogenesis,
preventing an influx of more glucose into the bloodstream.
• In adipose tissue, insulin inhibits fat breakdown, or lipolysis,
and stimulates glucose uptake. The net effect of all of these
changes is to increase glucose uptake, reduce circulating
glucose levels and increase the conversion of glucose into
the storage molecules, glycogen or fat.
• In Insulin resistance there is increase in gluconeogenesis,
glycogenolysis and lipolysis giving rise to more FFA leading
to Dyslipidaemia risk factor of atherosclerosis.
• Binding of insulin to Tyrosine kinase results in activation of
two parallel pathways: the phosphoinositide 3-kinase (PI3K)
pathway and the mitogen activated protein (MAP) kinase
pathway.

19. • (PI3K) pathway Activates endothelial nitric oxide synthase (eNOS) which causes
vasodilation and increases insulin sensitivity
• The MAP kinase pathway mediates endothelin-1 (ET-1) production, leading to
vasoconstriction; expression of the vascular cell adhesion molecules VCAM-1 and E-
selectin, leading to more leukocyte-endothelial interactions; and growth and mitogenesis
effects on vascular smooth muscle cells.
• In insulin resistance, the PI3K-Akt pathway is affected, whereas the MAP
kinase pathway is not leads to imbalance. Inhibition of the PI3K-Akt
pathway leads to a reduction in endothelial nitric oxide (eNO) production,
resulting in endothelial dysfunction, and a reduction in GLUT4
translocation, leading to decreased skeletal muscle and fat glucose uptake.
• By contrast, the MAP kinase pathway is unaffected, so there is continued
ET-1 production, expression of vascular cell adhesion molecules and
mitogenic stimulus to vascular smooth muscle cells. In these ways, insulin
resistance leads to vascular abnormalities that predispose to
vasoconstriction Inflammation, HTN and atherosclerosis.

21. Dyslipidemia
• Insulin resistance leads to atherogenic dyslipidemia in several ways. First, insulin normally
suppresses lipolysis in adipocytes, so impaired insulin signaling increases lipolysis, resulting
in increased FFA levels. In the liver, FFAs serve as a substrate for synthesis of TGs. FFAs
also stabilize the production of apoB, the major lipoprotein of very-low-density lipoprotein
(VLDL) particles, resulting in more VLDL production.
• Insulin normally degrades apoB through PI3K-dependent pathways, so insulin resistance
directly increases VLDL production. Third, insulin regulates the activity of lipoprotein
lipase, the rate-limiting and major mediator of VLDL clearance.
• Thus, hypertriglyceridemia in insulin resistance is the result of both an increase in VLDL
production and a decrease in VLDL clearance. VLDL metablises to Small dense LDL which
can promote atheroma formation.

23. Hypertension
• Essential HTN is frequently associated with obesity, glucose intolerance and
dyslipidaemia.
• Adipocytes increase secretion of ACE leading to RAS activation playing
important role in HTN
• hyperglycemia and hyperinsulinemia stimulate the Renin-angiotensin system
• (RAS) by increasing the expression of angiotensinogen, angiotensin II (AT II), and
the AT1 receptor, which may contribute to the development of hypertension in
insulin resistance patients it also contributes to SNS activation and, as a result, the
kidneys increase sodium reabsorption, the heart increases cardiac output, and the
arteries respond with hypertension causing vasoconstrictions

24. Clinical Features
• The Metabolic syndrome typically does not associate with any specific signs and
symptoms, some clinical features which may be associated with risk factors or
components of metabolic syndrome are as follows
• Increased waist circumference
• Raised blood pressure
• Weight gain
• PCOS
• Fatigue
• Depression
• Peripheral polyneuropathy
• Acanthosis nigricans
• Xanthomas

25. Investigation
• Lipid profile ( total cholesterol, LDL, HDL And Triglycerides)
• Fasting blood Glucose
• Other tests to signify insulin resistance, complications like CRP,
Fibrinogen.

26. Management
• Therapeutic Lifestyle changes (TLC) aka TLC diet
• Weight reduction
• Pharmacological Approach
• Bariatric surgery

27. NCEP ATP III recognizes MetS as a Secondary treatment target after LDL
cholesterol is controlled.

28. Weight Reduction
• Weight reduction helps with improvement in all components of MetS. Exercise
increases calorie consumption, aiding weight loss and reducing overall CVD risk:
around 30–60 min of moderate-intensity exercise and conscious efforts to alter a
sedentary lifestyle can be beneficial for the management of MetS.
• The goal of weight reduction is a loss of 7–10% in body weight over a period of 6-
12 months as well as a reduction of caloric intake by 500–1000 calories/day.

29. Pharmacological Approach
• Statins (atorvastatin) are the drug of choice for elevated LDL cholesterol.
• Oral Hypoglycaemic agents (metformin, glimepiride) are used to control
Hyperglycemia.
• Antihypertensive Drugs(Thiazides, CCB, ACE inhibitors)
• Appetite Suppressant (phentermine, sibutramine) and inhibitor of nutrient
absorption (Orlistat)
• Aspirin is given to prevent clotting.

30. Unani Correlation
• Metabolic syndrome may correspond to Sue Mizāj Bārid Māddῑ as in classical literature of Unānῑ
medicine and obesity is the driving force behind the metabolic syndrome. Obesity occurs as a result
of decreased harārat-i-gharῑzia (innate heat), generally by birth, and as a result of bārid Mizāj found in
obesity.
• To understand MetS in unani context we need to understand the Process of digestion in unani
Huzoom Arbaa
• 1. Huzoom-e-maedi 2. Huzoom -e-Kabdi 3. Huzoom-e-Urooqi 4. Huzoom-e-Uzw
• Hazm-e-medi: in the stomach, mainly breakdown of the nutriment or we can say Ghiza and mixes it
with Ratubat (Digestive juices) to form in semi-solid substance called Chylous.
• In Hazm-e-kabdi this Chylous go to the Liver where metabolic processes take place to form Akhlat
(humors)
• Hazm urooqui: In the vessels, humours undergo transformation that is referred to as Hazm urooqui
• Hazm Uzwi: In Hazm Uzwi Unani scholars have described the changes occurring in the blood that
have entered the organs for nutrition. This is the fourth stage of digestion. It can be inferred chemical
changes that nutrients undergo in the cells and tissues for the sustenance of life. In this process,
several chemical compounds and even wastes are produced in the cells and tissues. When Huzoom
Arbaa functions normally it produces saleh akhlat (Normal Humor) And Hararat Ghariziya.

31. Excessive Diet and Sedentary lifestyle (sukoon)
Increase In rutūbat and Madda
Decrease in Hararat Ghariziya and Tehlallul
Increases moisture and cold in liver
Produces Ghaleez and luzj akhlat
Shaham (Fat) Obesity
Unani Pathophysiology

32. • Ibn Rushd stated that vascular diseases are under control of the liver Because of
burudat (Cold) of liver, the kaymus (Chyme) is not processed well therefore,
akhlat Kham (Immature humours) increases in the body. If there is
lazoojat(Adhesiveness), they become attached to the walls of cavities and vessels,
narrowing them; it decreases the supply of blood and ruh haywani (Vital pneuma),
causing a variety of complications/disorders.
• Sheikh stated that obesity causes such narrowing of vessels that circulation of ruh
(Pneuma) gets hindered/ affected and proper oxygen levels do not reach the organs
due to which there is alteration of mizaj of organs and when blood circulates
through these narrowed vessels, forcefully rupture of vessels may occur.
• Due to lack of hararat ghariziya, other quwwat also become weak. Quwwat
Tabiyya (Vegetative faculty) is affected more by burudat (Cold) which impairs the
process of digestion and assimilation which leads to compositional deterioration of
humours and the proportion of undigested and unprocessed components in blood
increases increase Dasumat e dam which can be correlate to dyslipidaemia,
hypercholesterolaemia and hypertriglyceridemia.

33. Metabolic Syndrome Sue Mizaj Barid maddi
Causes: mainly surplus energy intake,
sedentary habits, Genetic environmental factor
Causes: kasrat e giza, ifraat naum w sukoon,
qillat harkat badni, khalqi mizaj e burūdat
Obesity it leads to excessive shaham and saman e
mufarrat
Hypertension Saman mufarrat causes narrowing of vessels,
burūdat make them constrict.
Dyslipidemia Zofe hazm kabdi Burudat Jigar
Dasumat dam
Fatigue Susti Kahli, Zof, Girani
PCOS Farba (Obese) women finds difficult to
conceive and kasrat Isqat (repeated abortion) is
seen – Zakhera Khwarzamshahi
People with MetS have 50% high CVD risk
than others
Acc to Buqrat life span of obese people is less
as compared to thin people. It is due to the fat
which clogs the body veins and hararat
ghariziya (Innate heat) travels through the

34. • Ilaj: umoomi
• Correction of the sù-'i-mizaj, Istigfrag madda
• Taqleel-e-ghidha (Dietary restrictions)
• Use of Muarrique Advia (diaphoretics)
• Hammam yabis
• Use of harr-yabis foods
• Use of hārr wa mohallil (Resolvent) drugs
• Saree(Rapid) Kaseer wa Qawi Riyazat
• Stay in hot and dry places
• Reduce sleeping hours.

35. Ilaj bil Giza
• Use of Khusk Yabis Ghiza (dry diet) like wheat (Khusk roti), Barley,
use of vinegar and vinegar containing food keep away from fatty
(roghani), fried diet.
• all those ghiza (food) which promote the formation of Dam (blood)
should be reduced and hot spices should be added in ghiza(food) e.g.
Darchini (Cinnamomum zeylanicum), Jaiphal (Myristica fragrance),
Filfil daraz (Piper longum), Zeera (Cuminum cyminum), Lehsun
(Allium sativum), Rai(Brassica nigra) with Sirka, because they have
mulattif property intake of ghiza once a day in winter season and daily
use of hot water and avoid too cold drink items.

36. Ilaj bid Dawa
• Following principle of ilaj biz zid Drug which are Haar-yabis in
temperament are used.
• Mufradat like Ajwain, Badyan, Bikh Ajmod, Bikh Khatmi, Bora
Armani, Fitra saliyoon, Gudmar Booti, Halela, Lehsun, Luk Maghsul,
Marzanjosh, Methi, Sandrus, Saad kofi, tukhm karafs, tukhm suddab,
sumbuluttib.
• Murakkabat like Arq zeerah, jawarish kamoni, majoon flafli, sufoof
Muhazzil, itrifal sagheer, sirka, jawarish falafali, habbe muqil,
jawarish bisbasa, sufoof darchini.
• Ajwain Desi, badyan, zeerah 1,1 part. Dunamarwa, Borah Armani one
fourth part and laakh 2 parts Take 4gm everyday

37. Source Active ingredient Actions
Turmeric haldi
(Curcuma longa)
Curcumin Anti-inflammatory, antioxidant
↑ Insulin sensitivity
↓ Obesity
↓ Leptin and ↑ adiponectin
Garlic -Seer
(Allium sativum)
Allicin Anti-inflammatory
Antioxidant
↑ Insulin sensitivity
↓ Total cholesterol and triglycerides
↑ Adiponectin levels
Cinnamon darchini
(Cinnamomum verum)
Polyphenols Antithrombotic
Anti-inflammatory
↑ Insulin sensitivity
Improves fasting blood glucose, blood
pressure, and body composition
Oregano marzanjosh
(Oreganum Vulgare)
(Quercetin, luteolin, rosmarinic acid, and
diosmetin)
ACE inhibiting - Antihpertensive
Alpha glucosidase inhibitor-
Hypoglycemic
Antihyperlipidemic
Actions of Unani Medicine Shown in Experiments

38. Source Active ingredient Action
Ginger Zanjabeel
(Zingiber officinale)
Gingerols, shogaols,
parasols
Anti-inflammatory
↓ Cyclooxygenase-2, ↓ 5-lipoxygenase
↓ Systolic blood pressure
Grapes (Vitus vinifera) Resveratrol,
3,5,4′-trihydroxy-transstilbene
↓ Adipogenesis
↑ Lipolysis
↓ Insulin resistance
↓ Body mass index
Neem
(Azadirachta indica)
Neem oil ↑ Insulin secretion
↓ Postprandial hyperglycemia