21.11.2019.

Medical Nutrition therapy for

Anemia

Anemia-key terms
ANEMIA: a deficiency in the size or
number of red blood cells or the THE MOST
amount of hemoglobin they contain
that limits the exchange of oxygen COMMON
and carbon dioxyde between NUTRITIONAL
theblood and tissue cells
ANEMIAS

CLASSIFICATION: based on cell size:

macrocytic, normocytic, microcytic;
and based on Hb content: Iron defficiency
hypochromic, normocromic anemia

CAUSES: nutritional defficiencies

(inadequate intake of iron, protein,
copper and vitamins (B12, folate,
pyridoxine and ascorbic acid);
Folic acid deficiency
hemorrhage, genetic abnormalities, anemia
chronic disease states, drug toxicity

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 21.11.2019.

Iron deficiency anemia

diarrhea, achlorhydria, intestinal
excessive menstrual blood, Increased disease, drug interactions
Inadequate
hemorrhage, chronic blood loss (antacids, cholestyramine,
absorption
blood loss or excretion cimetidine, tetracycline...

Chronic inflamation Defects in

Inadequate
or other chronic release from
utilization
disorder stores

infancy,
Inadequate Iron Increased adolescence,
poor diet ingestion deficiency requirement pregnancy,
lactation

CHARACTERISTICS:
• microcytic erythrocytes
• diminshed level of circulating hemoglobin

Iron deficiency anemia

Clinical findings iron
Stages of deficiency deficiency

• Moderate depletion of iron • Inadequate muscle function

Stage 1 stores
• No disfunctions
•
•
Growth abnormalities
Epithelial disorders
early
• Reduced immuno-
competence
• Severe depletion of iron
Stage 2 stores
• No disfunctions
• fatigue

• Defects in epithelial tissues

late • gastritis
Stage 3 • Iron deficiency
• Disfunction • Cardiac failure

INDICATORS OF IRON STATUS:

Stage 4 • Iron deficiency
• Disfunction and anemia
• serrum ferritin levels
• total iron-binding capacity

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 21.11.2019.

Iron deficiency anemia

• the most common symptoms: headache, fatigue,

dyspnea, difficulty concentrating

Iron deficiency anemia-diagnosis

The most sensitive parameter Preferbly used for definite diagnosis

Quantity of serum or Quantity of serum or Quantity of total

plasma ferritin plasma iron circulating transferrin

Percent saturation of
Quantity of soluble
circulating transferrin Percent saturatuion
serum transferrin
(cal. serum of ferritin with iron
receptors
iron/TIBC); >16%

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Iron deficiency anemia-management

Medical management Nutrition management

Assess for underlying
disease and treat
• Include
Oral iron salts
vitamin C at
every meal
Increase
Oral iron chelated with absorbable • Include meat,
fish or poultry
amino-acids iron in the at every meal
diet
Oral sustained-release • Decrease tea
iron and coffee
consumption
Iron-dextran by
parenteral administration

Iron supplementation
Chief treatment: oral administration of inorganic
iron in the ferrous form

At dose of 30 mg, absorption of ferrous iron is

3×greater in comparisson to ferric form

Dose is calculated in terms of the amount of

elemental iron provided

Available iron salts; all absorbed to about the same degree

Ferrous Ferrous
Ferrous sulfate fumarate glutamate

Ferrous Ferrous Ferrous

lactate glycine sulfate gluconate

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Iron supplementation

dosage goals

 Generally prescribed for at least 3  To ensure the absorption of 10-20 mg of

months, 3 times daily iron per day which permits red blood
cells production to increase to three
 Daily dose of elemental iron depends times the normal rate and induces the
on the severity of anemia: 50-200 mg rise of hemogolobin concentration to
for adults and 6 mg/kg of body weight rise at a rate of 0.2 g/dL daily
for children
 Increased number of young red blood
 It is best absorbed when the stomach cells is seen within 2-3 days after iron
is empty; it tends to cause gastric administration, Hb levels begin to rise by
irritation. In that case patient is told to day 4 of treatment
take supplements with meal; it sharply  Clinical symptoms are start to decrease
reduces the absorption within 2 days after iron administration
 Ascorbic acid keeps iron in reduced  Supplementation should be continued
state and therefore increases iron for 4-5 months, even after restoration of
absorption but also iron gastric normal Hb levels in order to allow the
irritation repletion of body iron reserves

What if iron supplementation fails to correct

anemia?
The patient is not taking the
medication as prescribed Absence of results of oral
(because of unpleasant side iron administration
effects)

Bleeding may be continuing at

the faster rate than the Parenteral administration of
erythroid marow can replace iron-dextran may be
the blood cells necessary

The supplemental iron may

Replanishment of iron stores
not be absorbed by this route is faster, but it
(malapsorbtion, -steatorrhea, is more expensive and not as
celiac disease, hemodialysis) safe as oral administration

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Medical nutrition therapy of iron deficiency

anemia- proper nutrition

1.8 mg 6 mg 30 %

of iron must be Bioavailability of iron

/1000 kcal is the
absorbed every day in the diet is clearly
average content of
to meet daily needs more important
the iron in the
of 80-90 % of than the total
typical Western diet
women amount

Absorption of iron depends on:

• The lower iron stores, the greater will be the rate of absorption.
Iron status of
• Individuals with iron deficiency anemia absorb 20-30% of dietary
the individual iron; others 5-10 %.

The form of • Heme iron (15% absorbable) is present in meat, fish, and poultry
iron in the (MFP)
diet • Non-heme iron is present in MFP, eggs, grains, vegetables and fruits

• Iron absorbtion can be inhibited to varying degreesby a number

of factors (carbonates, oxalates, phosphates, phytates)
The • Taken meals with tea and coffee can reduce iron absorption by
composition 50% through the formation of insoluble iron compounds with
of the diet tannins.
• Iron in egg yolk is poorly absorbed because of the presence of
phosytin

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General approaches to maximize iron

absorption from foods

Improve food
Include sources of
choices to increase
viamin C to every
total dietary iron
meal
intake

Avoid drinking
Include heme-
large mounts of
containing MFP at
tee and/or coffee
every meal
with meals

Megaloblastic anemias
Normal body folate stores are
Disturbed depleted within 2-4 months in
synthesis of individuals consuming folate
DNA deficient diet

Morphologic and
functional changes Vitamin B12 stores are
in erythrocytes, depleted only after several
leukocytes, years of vitamin B12-deficient
platelets diet

It is usually caused
In persons with vitamin B12
by folate or deficiency supplementation
vitamin B12 with folate can mask B12
deficiency deficiency

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Absorption of vitamin B12

The principal source of vitamin B12 is animal proteins. The preliminary step in the
metabolism of vitamin B12 involves its release from animal sources, a process
mediated by the action of pepsin and gastric acid. After the release, dietary vitamin
B12 binds to the R-protein secreted by the salivary glands. In the duodenum, in the
presence of an alkaline medium and pancreatic proteases, the R- protein is
hydrolysed to release vitamin B12 which later binds with the intrinsic factor (IF)
secreted by the gastric parietal cells.
The vitamin B12 –IF complex is highly resistant to proteolytic degradation. The
complex attaches at its specific receptors on the mucosa of the terminal ileum, a site
where its absorption occurs. This stage of vitamin B12 absorption is calcium
mediated.
The intracellular vitamin B12 is released following IF degradation. This free vitamin
B12 attaches to another protein carrier, transcobalamin –II (TC-II) and is later
released into the circulation. This vitamin B12 – TC-II complex, also referred to as
holo TC-II is then actively taken up by the liver, bone marrow and other vital body
cells. The liver serves as the principal storage site of up to 90% of the body’s total
vitamin B12

Pernicious and other vitamin B12 deficiency

anemias
 Most commonly, B1 defficiency is
secondary to a lack of intrinsic factor (IF),
a glycoprotein in the gastric juice that is
necessary for the absorption of the
dietary vitamin B12
 After absorption vitamin B12 complexes
wit binding proteins: holotranscobalamin
II (holo TCII) (25%), TC I (75%) and TC III
 Holo TC II is important in delivery of B12
to cells – patients lacking TCII develop
anemia; those with TC I disturbances have
no symptoms
 Rearly, B12 defficiency anemia develops in
strict vegetarians who do not take B12
supplements. It is the result of
enterohepatic cyrculation and efficient
reapsorbtion of B12

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Clinical sings of pernicious anemia

 Blood: low TCII levels, low b12 on
TC II and haptcorrin, , low red
Folate deficiency Pernicious blood cell folate,
anemia anemia
hypersegmentation of
erythrocytes, macroovalocytic
errythrocytes, elevated MCV,
elevated TCII levels, increased
homocysteine and methylmalonic
acid
 Nervous system: subtle
neuropsychiatric damage: impaired
short term and recent memory,
myelin damage: paresthesia
(numbness and tingling in hands
and feet), diminution of the senses
of vibration and position, poor
muscular coordination,
poormemory, and hallucination

B12 deficiency and Helicobacter pylori

infection
 10-15 % of men and women older than 65 are B12
deficient
 58 % of them have Helicobacter pylori infection (clinical
study, 138 patients with B12 deficiency)
 Treating the infection corrected the anemia and
normalized B12 levels in 40 % of affected patients
 Can H. pylori infection cause B12 deficiency?
 Atrophic gastritis (H. pylori infection) reduces the release
of B12 from protein and decreases total absorption
 Due to decreased acidity of the stomach overgrowth of
normal bacterial flora occurs; this bacterial flora utilizes
B12 for their own purposes further contributing to
deficiency.

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Management of pernicious anemia

Medical management Medical nutrition therapy

 Intramuscular or subcutaneous High protein diet (1.5 g/kg
injection of 100 mcg or more of body mass): improves
of vitamin B12 once per weak. liver functiona and blood
 After an intial responce, the regeneration
frequency of responce is
reduced Liver should be included
 Very large oral doses (1000 frequently: good supply of
mcg) can be effective even iron, vitamin B12, folic acid.
without IF since 1% of B12 is Include meats, eggs and milk
absorbed under these
conditions
 Responce to treatment: Increase intake of green
improved appetite, alertness, leafy vegetables: they contain
improved hematologic results
both iron and folic acid

Does metformin induce vitamin B12

deficiency?

It may take 10-15 years of

30 % of the patients develop
Metformin is one of the therapy to develop vitamin
vitamin B12 deficiency after
most commonly used B12 deficiency and
long-term therapy with
antidiabetics experience the first
metformin
symptoms

In many cases it remains

B12 deficiency can cause undetected (and untreated) Patients taking metformin
nerve damage that may bi since the symptoms may be should test their B12 levels
irreversible mistaken for diabetic once a year!
neuropathy

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Folic acid deficiency anemia

sources absorption

Protein • Liver, beans,

Enzyme conjugase hydrolyze the
group soybeans polyglutamates to monoglutamates
and reduce them to dihydrofolate
and tetrahydrofolate

Fruit • Orange, orange

group juice, banana From the enterocytes, these forms
are transported to circulation
where they are bound to protein
and transported as methyl THFA
Vegetable • Spinach, broccoli, into the cells of the body
group endibe, potato

In the absence of vitamin B12, 5-

methyl THFA, the major circulating
Grain • Fortified cereals, form, is metabolically inactive
wheat germ, whole
group wheat bread
because 5-methyl group can not be
removed

Methylfolate trap-masking of B12 deficiency

Deoxyuridylate

DNA synthesis Thymidylate

5,10-methylTHFA
(coenzyme form)

Methionine
THFA accumulates
THFA (active a methyl form from
B12 form) reactions with
other compounds

Homocysteine
Methyl

B6
5-methyl THFA
(inactive form)
Cysteine

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Folic acid deficiency anemia

Causes of folate deficiency

INCREASED REQUIREMENT: extra tissue

INADEQUATE INGESTION ( poor diet: lack of
demand (pregnancy, lactation, by malignant
unprocessed, fresh, food or fruity juices) chronic
tissue), infancy, increased hematopoiesis,
alcocholism
increased metabolic activity, drugs

INADEQUATE ABSORPTION: different types

of malabsorption syndromes (celiac disease, INCREASED EXCRETION: vitamin B12
idiopatic steatorrhea), drug therapy deficiency, liver disease, kidney dialysis, chronic
(anticonvulsants, barbiturates, cycloserine, exfoliative dermatitis
ethanol, metformin, cholestiramine, sulfasalazine
INADEQUATE USE (METABOLIC BLOCK):
folic acid antagonists, enzyme deficiency
(congenital or aquired due to liver disease), INCREASED DESTRUCTION: oxydants in diet
vitamin B12 deficiency, , ascorbic acid deficiency,
alcohol

Folic acid deficiency anemia

Clinical findings Diagnosis

 Deficiency of either vitamin B12  Folate stores are depleted after 2-
or folic acid will result in the same 4 months of folate deficient diet
clinical sign: megaloblastic anemia resultin in macrocytic
 The immature nuclei do not megaloblastic anemia
mature properly and large  Low serum folate (<3 ng/mL), low
(macrocytic) and immature red blood cell (RBC) folate levels
(megaloblastic) red blood cells are (<140-160 ng/mL) – it reflects
the result actual body folate stores and
 The common clinical signs of folic therefore is superior measurment
acid deficiency include: fatigue, of for determining folate nutriture
dyspnea, sore tongue, diarrhea.  To differentiate foalte deficiency
Irritability, forgetfulness, anorexia, and B12 deficiency radioassay kits
flossitis and weight loss are available that measure
stimultaneously serum folate, RCF,
serum B12 and TCII bound B12

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Folic acid deficiency anemia

Medical nutrition therapy
Medical management

 After anemia is corrected patients

Correct diagnosis of are instructed to eat at least one
megaloblastosis fresh uncooked fruit or vegetable
or drink fruit juice daily
 One cup of orange juice supplies
about 135 mcg of folic acid
1 mg of folate is take orally  Fresh uncooked fruit and vegetables
every day for two or three are the most important food
weeks. Minimum oral intake sources of folate since folic acid can
for the maintainance of folate easily be destroyed during thermal
stores is 50-100 mcg/day processing
 Women in childbearing age or
pregnant women (during the first
If folate deficiency is trimester) are adviced to take 400
complicated by alcoholism or mcg of folic acid daily in the form of
other conditions, therapy supplement
should remain at 500-1000
mcg/day

Medical nutrition therapy for

cardiocvascular disease

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Epidemiology of CVD – Croatia, 2011

 Cardiovascular mortality currently
accounts for almost half of all
deaths in the country in 2011 ischemic heart disease cerebro-vascular diseases
 In total population, the ten leading heart failure hypertensive diseases
causes of death in 2011were:
atheroschlerosis
ischemic heart disease (21,30%),
cerebro-vascular diseases (14,72%),
neoplasms of trachea, bronchus and 21.3
lung (5,56%), malignant neoplasms
of colon, rectum and anus (3,94%),
heart failure (3,61%), hypertensive 14.72
diseases (2,93%), diabetes mellitus
(2,34%), athero-sclerosis (2,21%),
and chronic liver diseases, fibrosis
and cirrhosis (2,19%).
3.61 2.93
 According to hospital morbidity 2.21
and structure of admissions, the
leading cause of hospitalization in
Croatia were diseases of the mortality (%)
circulatory system (14,2%).

Pathophysiology of atheroschlerosis
1. ENDOTHELIAL DISFUNCTION:
reversible – the endpoint that can be
modified by diet and other lifestyle
changes. Decreased NO production and
vasoconstirction, increased permeability

Endothelial disfunction is caused by

dyslipidemia, hypertension, cigarette
smoking, diabetes, obesity,
hyperhomocystinemia and high-saturated
fat diet

2. ACCUMULATION OF PLAQUE
(cholesterol from LDL, calcium and fibrine)
in large and medium arteries. It can grow
and produce ischemia (formation of
thrombus or high oxygen demand)

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Patophysiology of atheroschlerosis
 Artherial changes
begin in infancy and
progress
asymptomatically
throughout adulthood
if the person has risk
factors, is suspectible
to arterial thrombosis
or has genetic
suspectibility to
getting
atherosclerosis
 A silent disease
because many
individuals are
asymptomatic until
the first MI which is
often fatal

Clinical outcome-depends on the location of

artheroschlerotic changes
Strokes,
transient
ischemic attacks
(cerebral
arteries)
angina, MI, Intermittent
sudden death claudication, limb
(coronary ischemia,
arteries) gangrene

Impaired
arterial
function

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Modifiable cardiovasular risk factors

Modifiable cardiovasular risk factors
Markers in blood
Prevention of CHD and stroke
Lipoprotein profile
•low density lipoprotein cholesterol
•total triglycerides Primary prevention of CVD involves altering
•high density lipoprotein cholesterol risk factor stoward a healthy patient profile
Inflamatory markers
•Fibrinogen
•C-Reactive protein It is necessary to achieve optimal lipid levels;
LDL has been set as the target lipoprotein
Lifestyle risk factors
•tobacco
•physical inactivity
• poor diet As more is known about the disease, other
•stress risk factors are becoming more important
•excessive alcohol consumption
Related diseases/syndrome
Future goals of prevention could include
•hypertension how to maintain endhothelial function, how
•diabetes to stabilize plaque and prevent inflammation
•obesity
•metabolic syndrome

Assesing risk of CVD

Risk category LDL-C goal initiate TLC consider drug
therapy
High risk < 100 mg/dL > 100 mg/dL > 100 mg/dL
(10-year risk > 20%) (optional goal <70 mg/dL)
Moderately high risk < 130 mg/dL > 130 mg/dL > 130 mg/dL
(10-year risk: 10%-20%)
Moderate risk < 130 mg/dL >130 mg/dL >160 mg/dL
(10-year risk < 10%)

LIPOPROTEIN PROFILE:
DESIRABLE LIPOPROTEIN
PROFILE:
TC< 200 mg/dL
Total cholesterol, Should be
Friedwald formula LDL<130 mg/dL
LDL cholesterol, measured after a
(estimation of LDL LDL<100 mg/dL: patients with high
HDL cholesterol, person has fasted
cholesterol) risk; LDL< 70: patients with very
total TG 8-12 hours
high risk
HDL> 40 mg/dL
TG< 150 mg/dL

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Blood lipids and lipoproteins

 blood lipids are transported in the blood bound to

proteins
cholesterol  these compounds (lipproteins) vary in composition, size
and density
 clinical practice: VLDL, LDL, HDL, chylomicrons
 density is determined by ratio of proteins to fat (HDL
have more protein than fat)
 Total cholesterol measurement captures cholesterol
Blood lipids triglycerides captured in all three fractions (60-70% in LDL, 20-30% in
HDL, 10-20% in VLDL)
 High serum cholesterol, especially high LDLcholesterol is
one of the key causes of CHD, stroke and mortality
(cross population studies, within-population studies,
clinical studies)
phospholipids
 diets high in saturated fat cause hypercholesterolemia,
CHD incidence and mortality

Total triglyceride

< 150 mg/dl: normal fasting TG

Total TG-rich particles
150-199 mg/dl: borderline high
TGs

200-499 m/dl: high TGs

Remnants of
VLDL Chylomicrons intermediary
products > 500 mg/dl: very high TGs

atherogenic • elevated TGs: familial dyslipidemias, patients

lacking LPL (hydrolizes TGs before they enter
Activate platelets and coagulation the cell
cascade •TGs at very high range: risk for panceatitis,
low fat diets (10-15% of energy intake,
Lead to plot formation pharmacotherapy

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Total triglyceride

It is inversly related to TG FACTORS THAT INCREASE

levels (due to their roles TG LEVELS
in metabolism)
INFLAMMATION
(acute phase responce – effect of
cytokines)

Large biologic variability DIET

It has been recognized as in TG measurements: excesivelly low fat high, refined
an independed risk factor single sample analyzed carbohydrates
for CHD may not reflect true
values ESTROGENS
ALCOHOL
OBESITY
DIABETES, UNTREATED
HYPERTRIGLYCERIDEMIA HYPOTHYROIDISM, CHRONIC
RENAL DISEASE, LIVER DISEASE

Lipoproteins and metabolism-chylomicrons

Dietary fat and

cholesterol from small  Apolipoproteins carry lipids in the
intestines blood but also controlthe metabolism
of the lipoprotein molecule
 When about 90% of chylomicron is
hidrolized the particle is released back
to the blood as remnant
 Remnant is hydrolized by the liver;
chylomicrons
some of the remnants deliver
ApoC cholesterol to the arterial wall and
-II Fatty acids thus is considered atherogenic
LPL  Consumption of high-fat meals
produces more chylomicrons and
remnants
Liver and periphery

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Treatment of hypertriglyceridemia

Consumption of a Decreased intake of

Weight loss for
low saturated-fat- refined
obese patients
low-cholesterol diet carbohydrates

Increased physical Management of

Smoking cessation
activity diabetes if present

DRUG THERAPY: when it co-exists with established

Restricted alcohol
use CHD, positive family history, concurrent high
cholesterol and low HDL, genetic form

Lipoproteins and metabolism- VLDL

VLDL (60% of TGs): sintethized by the liver to transport

of endogenous triglyceride and cholesterol

Large VLDL particles Smaler VLDL (after TG hydrolisis

(vegetarians) by LPL)

nonatherogenic VLDL remnants or IDLs:

atherogenic, taken up by
receptors on the liver or are
converted to LDL

Clinical measurement of total TG

levels (fasting): triglycerides from Some of the smaler LDL particles
VLDL, IDL and remnants remain in the blood, are oxidized
and taken int the arterial wall

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Lipoproteins and metabolism- HDL

Apo E and ApoC are transfered to

More proteins than chylomicrons from HDL
any other lipoprotein:
reservoir of
lipoproteins
Apo E is transfered to chylomicrons; it
metabolizes its remnants and supresses hunger
Apo A-I: the main
lipoprotein in HDL:
antiinflammatory,
antioxidant:removes Ch
from arterial wall High HDL: low levels of chylomicrons, VLDL
remnants and small dense LDLs: lower risk for
arteroschlerosis

ApoB/ApoA-I: the lower

the ratio the lower • exception: familiar hyper-
would be the risk for cholesterolemia (FH) when patients may
getting CHD have triglyceride enriched HDL wich is
considered proatherogenic

Lipoproteins and
metabolism- HDL Major factors increasing HDL
exogenous estrogen
Inflammation and HDL intensive excercise
loss of excess body weight

Inflamation decreases moderate consumption of alcohol

HDL levels

Decreased reversed Major factors decreasing HDL

cholesterol transport, inflammation
changes in
obesity
apolipoproteins
resulting in increased inactivity
blood TGs, reduced cigarette smoking
antioxidant role
anabolic steroids, progesterone-dominant oral
contraceptives

ATHEROSCLEROSIS β-blockers
hypertriglyceridemia
genetic factors

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Lipoproteins and metabolism- LDL

metabolism
Primary cholesterol carrier in blood and  The number and activity of LDL
is formed by VLDL brakedown
receptors are major determinants of
LDL cholesterol levels in the blood
 95% of apolipoproteins in LDL
particles apo B 100 (apoB)
 apoB is also present in small amounts
LDL formation
in VLDLs and IDLs of hepatic origin
 Persons with high triglyceride levels
usually have high apoB levels
 That gives these particles longer time
60% is taken up by The remainder is to deposit into the arterial wall
the LDL receptors metabolized via
on the liver, adrenals nonreceptor The main focus of dislipidemia therapy is
and other tissues pathway tu lower LDL levels in the blood

Lipoproteins and metabolism- LDL

FACTORS THAT INCREASE LDL
CHOLESTEROL
ageing
genetics
LDL diet
reduced estrogen levels (postmenopausal
women)
The
primary progestins
target for diabetes
intervention A decrease of
1mg/dL in LDL: hypothyroidism
1-2% nephrotic syndrome
decreased risk
for CHD obstructuve liver disease
obesity
some steroid and antihypertensive drugs

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Inflammatory markers of CVD

Several markers have been

It is credible to use inflammatory suggested.
Increasing knowledge about the markers to indicate the presence
role of inflammation of CVD of A in asymptomatic individuals What is the impact of diet on
these markers?

potential inflammatory markers for cardiovascular risk

oxidized LDL cholesterol

• adhesion molecules The most widely studied
• selectins inflammatory biomarkers
Cytokines
• interleukin-1
• tumor necrosis factor-α
Fibrinogen (marker of
vascular damage)
Acute-phase reactants
• fibrinogen
•C-reactive protein CRP (risk factor and causal
• serum amyloid A (SAA) agent for atherothrombosis)
White blood cell count
Erythrocyte sedimentation rate

Is elevated homocysteine a risk factor for

CVD?
Numerous studies with large numer
methionine of patients report small or weak
Genetic relationship between homcystein
deficiency
levels and atherotthrombotic CVD

homocysteine

cystathionine B
synthase Randomized control trials of
vitamin supplementationcausal
relationship was not proven

.
Accumulation of
. homocysteine and
premature
. atheroschlerosis in sick
children Homocystein screening or vitamin B
supplementation is not
recommended in CVD on the basis
of evidence to date

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Atheroschlerosis- etiology
smoking genes Decreased HDL C

High/saturated fat
obesity aging
/cholesterol diet

hypertension Elevated serum TGs hyperhomocystinemia

Elevated LDL C inactivity Endothelial disfunction

diabetes

Accumulation of plaque
Production of less nitric oxide
Oxidized LDL C taken up by macrophages
Formation of foam cells and fatty streaks

Atheroschlerosis- pathophysiology
Accumulation of plaque
Production of less nitric oxide
Oxidized LDL C taken up by macrophages
Formation of foam cells and fatty streaks

Clinical findings Nutrition assessment

 Elevated serum total  BMI evaluation

cholesterol  Waist circumference;
 Elevated LDL cholesterol  Waist to hip ratio
 Dietary assessment for: SFA,
 Elevated serum triglycerides trans fatty acids, omega -3-
 Elevated C-reactive protein fatty acids, fiber, sodium,
alcohol, refined carbohydrates
 Low HDL cholesterol

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Atheroschlerosis- management

Medical management Nutrition management

 Bile acid sequestrants  TLC dietary pattern – 7% kcal from SFA
 AHA dietary pattern - 7% kcal from SFA
 HMG-COA reductase inhibitors
 DASH dietary pattern
 Nicotinic acid  All low-fat diets that will significantly
 Triglyceride lowering medications reduce LDL cholesterol levels
 Weight reduction (if needed)
 Blood pressure lowering medications
 Increase dietary fibre (25-30 g/day)
 Medication for glucose management  Add stanols and sterols in multiple doses
 Percutaneous coronary intervention (2-3-g/day)
 Baloon
 Add omega-3 fats
 Add soy proteins
 Stent
 Add fruits and vegetables for
antioxidants
 Reduce dietary cholesterol (<200
mg/day)

Steps in therapeutic lifestyle changes (TLC)

Visit II: evaluate

Visit III: evaluate
6 wk LDL responce 6 wk 4-6 mo
LDL responce Follow-up visit
Visit 1 begin If LDL goal not
lifestyle therapy If LDL goal not Monitor
achieved intensify
achievedconsider adherence to TLC
LDL lowering
drug therapy Tx
treatment

• emphasize • reinforce
reduction in reduction in high
saturated fat and saturated fat, Initiate Tx for
cholesterol trans fat or high metabolic
• encourage cholesterol diet syndrome
moderate physical • consider adding Intensify weight
activity plant management and
physical activity
sterols/stanols to
diet
•Increase fiber
intake

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TLC/ADA: recommendation for fat intake

Monounsaturated
fatty acids

Saturated fatty Polyunsaturated

acids fatty acids

Total fat intake

Fat Dietary

intake cholesterol

TLC/ADA: recommendation for fat intake

Total fat intake Saturated fatty acids (SFAs)

Major sources: animal foods (meat and diary).
Palmytic (C16:0), myristic (C14:=0 and lauric acid
(C12:0)
 Low-fat diets are indicated
 <25% of kcals from fat
 They rise TG levels and decrease They need to be restricted since they have the
most potent effect on LDL cholesterol
HDL levles????
 Those changes are not asociated with
CHD risk because
General mean consumption of SFAs is 11% of
 LDL cholesterol is low kcal intake; intake
 Large non-atherogenic VLDLs are
produced
For CVD prevention/treatment it should be
reduced to 7% of the total kcal

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TLC/ADA: recommendation for fat intake

Monounsaturated fatty
acids (MUFAs) Trans fatty acids

There are no recommendations for the intake  Stereoisomers of the naturally

of the cis-forms of MUFAs occuring cis-linoleic acid
 They are produced by the
hydrogenation process used in the
The most prevalent MUFA is oleic acid food industry to increase shelf-life of
(C18:1). Substituting MUFA for carbs has no foods and to make margarines
beneficial efect  Maximally 1-3 g/day (<1% of
calories) should be from trans fat
SFAs should be replaced with MUFAs (i.e.  They raise LDL cholesterol
Replace butter with olive oil): it lower total  they may have proinflammatory effects
cholesterol, LDL and TGs to the same level as (results of clinical studies are still
substitution with PUFA conflicting)
 The majority of trans fat come from
Additional effect of oleic acid: it has been partially hydrogenated vegetable oils
shown to possess antioxidant properties as a
part of Mediterranian diet

TLC/ADA: recommendation for fat intake

Polyunsaturated fatty acids
(PUFAs) Omega-3-fatty acids
The predominant PUFA is The main omega-3 fatty acids are EPA and
linoleic acid (LA) – intake DHA high in fish oils, fish oil capsules, and
negativelly correlates with
CHD incidence. Should we fatty fish
increase PUFA to lower
LDL?
Eating fish is associated with decreased CVD
LA decreases both LDL and risk. Recommendations: increase salmon,
HDL; effect on HDL is very tuna and sardine consumption. 1g/day is
significant in the case of high recommended if not from fish than from
total fat intake. Monitor omega supplements
6:omega 3 ratio!

Eliminating SFA from diet

is twice as effective in 2-4 g of EPA and DHA per day are effective
lowering LDL as increasing in decreasing TG levels by ingibiting VLDL
PUFA and Apob-100 synthesis. ALA (omega -3
Low omega-6:omega 3 ratio from vegetables) has antiinflammatory effects
should be maintained and reduces serum CRP levels

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TLC/ADA: recommendation for fat intake

Dietary cholesterol Stanols and sterols

It raises total  Isolated from pine tree oil and
To lesser extent
cholesterol and
LDL
than SFAs soybean oil
 They lower blood cholesterol
 Recently they have been
esterified and made into
Cholesterol
respondivenes
AHA/TLC: <200
mg of
margarines
varies among
individuals:
cholesterol/day  2-3 g/day lowers cholesterol by
9-20% by inhibiting its
absorption from the diet
Hyperresponders:
apo E 4 allele and
Normal responce:  They can adversely affect the
poor rate of
only after 500 mg/day
intake blood levels of
absorption of fat soluble
conversion to bile
acids
LDL slightly increase vitamins and antioxidants

TLC/ADA: recommendation for fat intake

Soluble fibre: gums, pectines, some

Dietary fibre intake hemicelluloses, algal polysaccharides
lower LDL cholesterol

Proposed mechanisms: fiber bound bile

acid which repletes the bile acid pool
and decreases serum cholesterol
5 or more
servings of
Supplements are
25-30 g /day; 6-10 fruit/day not
soluble fibre 6 or more recommended Bacteria in the colon ferment dietary
servings of grain fibre to produce SCFA (acetate,
propionate, butirate) that inhibit
cholesterol synthesis

Insoluble fiber have no effect on serum

cholesterol levels

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Practical dietary tips

Food choices and
Lifestyle preparation
 Monitor the caloric value of food  Read nutrition facts labels
and your caloric intake. Adjust it  Eat fruits and vegetables, fresh or frozen,
to maintain healthy body weight. without added sugar and salt. Replace high-
calorie foods with fruits and vegetables
Track weight, physical activity and
calorie intake  Eat beans, whole-grain products, fruits and
vegetables to increase fiber intake
 Prepare and eat smaller portionts  Drink water instead of juices
 Track and decrease screen-time  Reduce intake of bakeries: eat whole grain
products
 Do not smoke, consume alcohol in
moderation  Use low-fat diary products, use lean cuts of
meat, remove skin from poultry before
 Incorporate physical activity into eating. Limit processed meat. Grill, bake or
habitual activityies (i.e. use stairs broil
instead of an elevator)  Reduce salt intake (best results – limitation
of processed food intake)

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