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Nutrition in Metabolic Syndrome

dr. Luh Eka Purwani, M.Kes, Sp. GK


Definition
 The metabolic syndrome is a constellation of interrelated
abnormalities (namely obesity, dyslipidaemia,
hyperglycaemia, and hypertension) that increase the risk
for cardiovascular disease and type 2 diabetes.
ATP III criteria for identification of metabolic
syndrome
WHO working definition of metabolic
syndrome
Pathogenesis
 As discussed earlier, insulin resistance is the link between the
different components of metabolic syndrome.
 It has strong association with obesity especially its central or
visceral component.
 The present epidemic of obesity is primarily environmental
in origin
Role of lipotoxicity and inflammation on
obesity
Obesity
 Definition : Fat accumulation >>>

Body Mass Index ≥ 25 kg/m2


Overweight : 23-24,9 kg/mm2
Obese I : 25-29,9 kg/m2
Obese II :30-39,9 kg/m2
Obese III : ≥ 40 kg/m2
Etiology
 Medical Disorders, Pharmacological Treatments, and Smoking
Cessation
 Disordered Eating Patterns (night eating
syndrome consume as much as 50% of their total energy intake)
 Genetics (appetite, taste preferences, energy
intake, resting energy expenditure, the thermic effect of food,
nonexercise activity thermogenesis (NEAT), and the body’s
efficiencyin storing energy.)
 Obesigenic Environment
 Changes in Physical Activity
Pharmacological Treatments
Pharmacological Treatments
Etiology

Energy
intake

Energy
expenditure
Etiology
Disease and obesity
Disease and obesity
Management
 Lifestyle modification including diet, exercise, and behavior
therapy

 Pharmacotherapy may be helpful when compliance to


lifestyle modification begins to waver or physical hunger
becomes an issue during dieting
 Surgery
Management Obesity
Nutrition therapy
 Moderate calorie diet (1500-1800)
 Low calorie diet (800-1500)
 Very low calorie diet (<800 kcal)
Nutrition therapy
Popular Diet
Blood type Diet
Paleo Diet
Mayo diet
Dr Atkin’s Diet

VLCD,
Temporer
Medical therapy
 Anorrectic agent
 Lipase inhibitor
Surgery
 (a) Adjustable gastric banding;
 (b) vertical sleeve gastrectomy;
 (c) Roux-en-Y gastric bypass;
 (d) biliopancreatic diversion with duodenal switch
Surgery
Diabetes Mellitus
Patophysiology
Management
 Education
 Medical nutrition therapy
 Exercise
 Pharmacotherapy
Management
Medical management
 Alpha-glucosidaseinhibitors (AGIs)
 Amylinanalogs
 Biguanides
 Incretin mimetics
 Meglitinides
 Sulfonylurea agents
 Thiazolidinediones
Goals of nutrition therapy
PHYSICAL ACTIVITY
 Physical activity improves blood glucose levels by enhancing
muscle blood glucose uptake during or shortly after activity
and by improving insulin sensitivity.

 Furthermore, it enhances weight loss eff orts, which in turn


improve insulin sensitivity and glycemic control.

 Thirty to forty-five minutes of moderate-intensity physical


activity three to five days a week is recommended to improve
glycemic control
Nutrition therapy
 Because the total amount of dietary carbohydrate is a strong
predictor of glycemic response, monitoring total grams of
carbohydrate
 Low-carbohydrate diets are not suggested
 Carbohydrate recomendation 4565% of total kcal
 PROTEIN Intake of dietary protein exceeding 20% ofenergy
 intake may be a risk factor for development of nephropathy.
 Protein intake for individuals with diabetes who have
nephropathy shouldnot exceed0.8 g/kg or ~10% oftotal
kcal.
Nutrition therapy
 Total fat intake shouldnot exceed 25% to 35% of total
kcal,and saturated fat intake should not exceed7%.
 Intake of trans fat should be minimal.
 Th e U.S. Dietary Guidelines recommendconsuming 14
grams of fi ber for every 1000 kcal,
 while the Food and Nutrition Board recommends that men
under 50 consume 38 grams of fiber/day and women
consume 25 grams of fiber/day.
 A varietyof fiber-containing foods such as legumes and fiber-
rich cereals (≥5 g fiber/serving), as well as fruits, vegetables,
and whole-grain products, are recommended.
Nutrition therapy
Dyslipidemia
Dyslipidemia is a condition in whichLDL levels are elevated and
high-density lipoprotein (HDL) levels are low.
A variety of other dyslipidemic conditions can also exist,such
as the combination of normal LDL and high triglyceride
levels.

Etiology :
 primary hyperlipoproteinemia
 Secondary hyperlipoproteinemia
(Obesitas, diabetes, hipotiroid, ESRD, liver disease, cushing’s
syndrome)
Dyslipidemmia
Lipoprotein
 Because lipid is not water soluble, it is carried in the blood
bound to protein.

 These complex particles, called lipoproteins, vary in


composition, size, and density.

 Lipoproteins measured in clinical practice-chylomicrons,


verylow-density lipoprotein (VLDL) , low-density
lipoproteins (LDL), and high-density lipoproteins (HDL)-
consist of varying amounts of triglyceride, cholesterol,
phospholipid, and protein
Chylomicrons
 Chylomicrons, transport dietary fat and cholesterol from the small
intestine to the liver and periphery.
 Once in the bloodstream, the triglycerides within the
chylomicrons are hydrolyzed by lipoprotein lipase (LPL), located
on the endothelial cell surface in muscle and adipose tissue
 When approximately 90% of the triglyceride is hydrolyzed, the
particle is released back into the blood as a remnant.
 The liver metabolizes these chylomicron remnants, but some
deliver cholesterol to the arterial wall and thus are considered
atherogenic.
 Consumption of high-fat meals produces more chylomicrons and
remnants.
VLDL
 Synthesized in the liver to transport endogenous triglyceride
and cholesterol.
 Triglyceride accounts for 60% of the VLDL particle.
 The large, buoyant VLDL particle  nonatherogenic.
 Smaller VLDL particles (i.e., remnants) are formed from
triglyceride hydrolysis by LPL.
 Normally these remnants, called intermediate-density
lipoproteins (IDLs), are atherogenic
 IDL and are taken up by receptors on the liver or converted
to LDLs.
LDL
 Some of the smaller LDL in blood are oxidized, and are
then taken into the arterial wall
 LDL is the primary cholesterol carrier in blood, formed by
the breakdown of VLDL.
 After LDL formation, 60% is taken up by LDL receptors on
the liver, adrenals, and other tissues.
 The remainder is metabolized via nonreceptor pathways.
 Both the number and activity of these LDL receptors are
major determinants of LDL cholesterol levels in the blood.
 High LDL cholesterol is specifically associated with
atherosclerosis.
HDL
 HDL particles contain more protein than any of the
other lipoproteins, which accounts for their metabolic role as
a reservoir of the apolipoproteins that direct lipid
metabolism.

 Apo A-I, the main apolipoprotein in HDL, is an


antiinflammatory, antioxidant protein that also helps to
remove cholesterol from the arterial wall to the liver
Lipoprotein
 The triglyceride-rich lipoproteins include chylomicrons,
VLDLs, and any remnants or intermediary products formed
in metabolism.

 Of these triglyceride-rich lipoproteins, chylomicrons and


VLDL remnants, and LDL are known to be atherogenic
because they activate platelets, the coagulation cascade, and
clot formation
Dyslipidemia
The following values have been classified as abnormal and are
associated with increased CHD risk:
1. Total cholesterol higher than 240 mg/dL
2. Triglycerides higher than 150 mg/dL
3. Non–HDL-C (total cholesterol HDL-C) higher than
190 mg/dL
4. LDL-C higher than 160 mg/dL
5. HDL-C lower than 40 mg/dL in men and lower than
50 mg/dL in women
Lipid transport
Reverse cholesterol transport
Diagnosis
Management
Non Pharmacology
 Nutrition management
 Weight loss and exercise

Pharmacology
 Statin
 Bile acid sequestrant
 Fibric acid derivate
Nutrition Management
Nutrition Management
Nutrition Management
Hypertension
 Though its cause is unknown, primary hypertension may be a
result of a variety of factors.
 Lifestyle factors such as diet (including excessive sodium
intake, low potassium intake, excessive alcohol intake),
 lack of exercise, smoking, stress
 Resistance is dependent upon the radius of all arterioles,
length of the vessel, and the blood viscosity.
Patophysiology of hypertension
Diagnosis
Medical management
 Diuretics
 ACE Inhibitors
 Beta-1-Blocker
 Alpha Adrenergic Blockers
 Calcium Channel Blockers
 Aldosterone Antagonists
 Angiotensin II Receptor Blockers
 Nitrate
 Digitalis
Nutrition Management
DASH diet
FOOD GROUP DAILY SERVINGS SIGNIFICANCE

grains and grain product 7-8 Major sources energy and fiber
vegetables 4-5 Rich sources potassium, Mg, and
fiber
fruits 4-5 Rich sources potassium, Mg, and
fiber

low fat or fat free dairy food 2-3 Ca, protein

meats, poultry, fish 2 OR LESS Protein, Mg


nuts, seeds and dry beans 4-5/WK Energy, prot, Mg, K, fiber

fats and oil 2-3 Lows fat


sweets 5/WK Low fat
Tips reducing sodium intake
 Avoid fast-food restaurants, because these food choices are
prepared with large amounts of salt.
 Ask how foods are prepared. Request that they be prepared
without added salt, monosodium glutamate (MSG), or salt
containingingredients.
 Know the terms that indicate high sodium content: pickled,
soysauce
 Do not use any added salt in food preparation or at the table.
 Limit condiments, such as mustard, pickles, and sauces with
salt-containing ingredients.
 Choose fruits or vegetables instead of salty snack foods.

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