Life style and chronic diseases

in population

Prof. MUDr. Hana Rosolov, DrSc., F.E.S.C.

Centrum preventivn kardiologie
2. intern klinika UK-LF v Plzni
 Life style and environment

1. Life style - social sense : living place, dress, eating, cultura,

politics etc..

Medical sense: all factors, that influence health status and the
risk for disease development

2. Environment pollution of watter, air, food etc.

 Life style

nutrition - polysacharides, proteins, fats

physical activity: sedantary life style, activity in leisure
time
habits smoking, alcohol consumption, drugs ...
type of relaxation sleeping, compensation of stress ...
 General source of the disease

Each population civilization brought some

specific life style and specific general sources
of diseases with high prevalence in that
population.
 General source of the disease

Risk factor from the environment

Causal RF = RF which is in the relationship i.s.
casual association with the disease

e.g. High fatty diet - atherosclerosis

 Main risk factors of AS
Smoking
Arterial hypertension
Dyslipidemia (LDL-ch, HDL-ch, TG)
Diabetes mellitus (insulin resistance)
Obesity
Stress
 CV risk factors

1. Modifiable RFs
Factors of life styl: nutrition, smoking, low physical activity

Biochemical and physiological: total chol, LDL-chol.,

HDL-chol, TG, TK, glucose level, IRI, Fg, Hcy aj.

2. Non-modifiable RFs
age (men over 45 y., postmenopausal women)
sex (male)
family history (mother below 65 y. and father below 55 y.)
personal history CVD
 Strategy of CV prevention

High risk approach medical care of the patients

with CVD, high risk individuals
 Strategy of CV prevention

Population approach general population or high

risk population
 Non-pharmacological
management
= modification of life style
Smoking
 Approach to the smoking

1492 - Columbus Indians smoked tabacco, but

they did not inhale smoke
Jean Nicot nicotine - tabacco for local
application (compress)
Cigarettes production in the 60th of the19th
century
 Approach to the smoking

20th century smoking = positive social habit

21th century - nicotine addiction

Tabacco smoking = disease, which is necessary to treat

(2004)
Dg: F17
Why do people smoke ?

Psycho-social motivation in children

Lack of self-confidence
Examples - parents, siblings, friends,
poster advertising etc.
Stress depression
 NICOTINE as a drug

Absorbtion of smoke is very fast in

lungs.

Nicotine goes through arterial blood to

the brain in 10-16 sec.
 NICOTINE as a drug
Stimulation of the nicotinic acetylcholin
receptors in the brain dopamin
catecholamines
} increased activity of SNS

psychomotoric stimulator
development of a tolerance is very quick

(nicotine - amfetamin or cocain)

 Coronary, cardiovascular and total
mortality and heart rate
2-year mortality / 1000 inhabit

60 Coronary mortality
Cardiovascular mortality
50
Total mortality
40

30

20
/ age

10
0
<65 65-74 75-84 85+

Gillman MW: The Framingham Study, Am Heart J 1993;135:1148-54

 Smoking in Europe

30% of men, 15% of women

60-70% smokers would like to stop smoking,

But only 2% of them are successful !
 Impact of smoking ?

Each 5th death is associated with

smoking !
BENEFIT of giving up smoking

In young people below 35 y. life longevity is the same

as in non-smokers.

Risk of lung cancer decreased about 30-50 % after 10 years of giving up

smoking.

1 year ex-smoking decreases risk of CV events about 50% !!!

after 15 y. - CV risk the same as in non-smokers
BENEFIT of giving up smoking
in primary prevention

Giving up smoking is only one life style

modification which is
cost-benefit
in the CVD prevention
 BENEFIT of giving up
smoking in secondary
prevention
Metaanalysis of prognosis after AMI

Giving up smoking reduced risk of death: ORs = 0,54

Standard treatment of AMI reduced risk of death:
ORs = 0,75-0,88
(revascularisation, aspirin, beta-blockers, statins)

Wilson et al., 2000

 Intensive intervention
in stop smoking

Psychosocial and behavioral intervention

Pharmacological treatment - 8-12 weeks
a) Substitution therapy by nicotine
(chewing gum, patch, microtablettes,
inhalator)
b) Antidepressive treatment - bupropion
1-2 weeks before giving up smoking
2x150 mg
 NICOTIN as a drug
What is the safety of nicotine
use?

High risk of side effects :

during pregnancy, child

bearing
in unstable CHD
in adolescents (18 y.)
 Intensive intervention
in stop smoking

Success - 20% smokers

i.e. 10times more than without intensive
intervention

Inervention in a specialized office room

 Control of non-smoking

Measurement of CO in exhaled air

(smokerlyser)

Assessment of cotinine amount in blood, urine,

saline
 Dotaz: Kou? (Uv tabk v jin podob?)

ANO NE (nevykouil nikdy 100 a vce cigaret

nebo 12 a vce msc od posledn cigarety)

Dokumentujte uvn tabku: POCHVALTE

- od kolika let (v ppad bvalho
kuka do kolika let) kouil
- jak tabkov vrobek
- kolik cigaret (jinch tabkovch
vrobk) denn / tdn

Jasn doporute pestat kouit: Motivujte:

Pane/pan XY, pro Vae zdrav je nutn
pestat kouit
CHCE
(cca do msce)
Stanovte zvislost na nikotinu, podle svch
asovch monost aplikujte psychobehaviorln
podporu, u zvislch na nikotinu tak farmakoterapii:
NTN, bupropion nebo kombinaci (rzn formy NTN,
nejlpe nplast + ostatn, nebo bupropion + NTN)
- souvislost s jeho zdravotnm stavem, obtemi,
prognzou, diagnzou, nlezem
- pokuste se najt dal souvislosti (dt/partner
v domcnosti, fyzick kondice)
- pi dal nvtv opt zante dotazem na
NECHCE kuctv, jasnm doporuenm pestat a
motivac (emfaticky: chpu, e pestat kouit
je tk, ale pro Vae zdrav nutn a jsem
pipraven Vm pomoci, a se rozhodnete
pestat)

Pozvte na kontroly,
pedevm v prvnch tdnech

Abstinuje: Kou:
Podpote v nekuctv, Pokuste se opt motivovat, vyut
pi dalch nvtvch zkuenosti (pro i v jak situaci si zaplil,
zdraznte vznam byla farmakoterapie adekvtn?) a podpote
abstinence. v dalm pokusu pestat kouit.

CHCE NECHCE

Opakujte relevantn
intervenci vetn zven
vych dvek a delho
trvn farmakoterapie.
 Sympathetic nervous activity
and risk factors of AS
Smoking increased secretion of catecholamines
F.S. Facchini F.S. Lancet 1992
G. Grassi, Circulation 90, 1994

Sedentary life style - ton of SNS + ton of

parasympathic activity

Overeating - Landsberg theory of obesity prevention

- SNS thermogenesis
Physical activity
Benefits of Physical activity

catecholamines (SNS) hemodynamics

endorphines mood, psyche

insulin resistance metabolism

peristaltic obstipation

bone growth osteoporosis

others
 Physical activity

Aerobic activity, 4-5times per week 30-45 min

Til 60-75% of maximal heart rate.

Better is regular physical activity with less intensity

than irregular and intensive one.
Diet
 Diet - structure

Energy intake
polysacharides 55-65%
proteins 15%
fat 20-30%
Diet energy intake

BMI 24-26 kg/m2

individual !
 Polysacharides-
carbohydrates

Vegetables, fruits, cereals

Potatos, rice, pasta
 Lipids

Vegetable and fish fat more than animal fat

Saturated FA

Un-saturated FA
poly-unsaturated, mono-unsaturated FA
 Lipids

Saturated FA < 7%
cholesterol below 200 mg/24 h
To add omega 3 FA
vegetable sterols
 Relative Priority of Consumption

Essential: High Priority Non-essential: Low Priority

(avoid)

Omega-3 PUFA
Omega-3 PUFA
Some food sources are fatty fish and Omega-6PUFA
Omega-6 PUFA Mono- Saturated FA
Saturated FA
shellfish, flaxseed, walnuts, and Some sources are animal-based
canola oil. Some food sources are unsaturated foods such as cream, butter,
nuts, seeds and
Eicosapentaenoic
Eicosapentaenoicacid
acid(EPA)-fish
(EPA)-fish
vegetable oils such as
FA cheese, and fatty meats.
Lauric acid-coconut, palm oil
Docosahexaenoic
Docosahexaenoicacid
acid(DHA)-fish
(DHA)-fish
sunflower, safflower, corn Some food sources Myristic acid-dairy fat
-Linolenicacid
-Linolenic acid(ALA)-flax
(ALA)-flaxseed,
seed, and soybean oils. are canola oil and Palmitic acid-meat
walnuts
walnuts Stearic acid-meat
Linoleic
Linoleicacid-seeds
acid-seeds olive oil.
Stearidonic
Stearidonicacid
acid(STD)-canola,
(STD)-canola,fish Trans-Saturated FA
Trans-Saturated FA
fish Dihomo-gamma-
Dihomo-gamma- Oleic
Oleicacid-olive,
acid-olive,
Eicosatrienoic acid (ETE)-seafood Some food sources are margarine,
Eicosatrienoic acid (ETE)- linolenic acid-metabolic canolaoiloil
canola
Eicosatetraenoic acid (ETA)-seafood
linolenic acid- fried foods, baked goods and
seafood metabolic product
product Palmitoleic
Palmitoleicacid-
acid- processed foods.
Docosapentaenoic acid (DPA)-
Eicosatetraenoic acid (ETA)- vegetableoiloil
vegetable Elaidic acid-preservative
seafood Arachidonic
Arachidonicacid-
acid-
seafood Partially hyrdogenated plant and
metabolic
metabolic product
product vegetable oils
Docosapentaenoic acid (DPA)-
seafood
Most Harmful
Most Beneficial Promotes: Obesity
Cardioprotective Dyslipidemia
Does not promote obesity American Heart Association Atherosclerosis
 Proteins

Vegetable > animal

(white meat > red meat)
 Healthy diet

reduces wieght
reduces blood pressure
improves lipid profile
improves glucose level
reduces trend to coagulation
 Diet heart hypothesis

Lyon Heart Study (1999) mediterrian diet

reduces risk of CVD about 70%! constant LDL-chol

DASH (Dietary Approaches to Stop Hypertension)

Reduces blood pressure as diuretics!

Etc.
Nine-year multivariable-adjusted hazard
ratios (95% CI) for 3782 cases of metabolic
syndrome
Dietary pattern Quintile 1 Quintile 5 p for
trend
Western diet 1 1.18 (1.031.37) 0.03
Prudent diet 1 1.07 (0.951.20) 0.11
Individual foods
Meat 1 1.26 (1.111.43) <0.001
Dairy 1 0.87 (0.770.98) 0.006
Fruits and 1 1.10 (0.981.24) 0.09
vegetables
Whole grains 1 1.02 (0.921.14) 0.76
Refined grains 1 0.89 (0.781.01) 0.15
Lutsey PL et al. Circulation 2008; available at:
http://circ.ahajournals.org.
Odds ratioa for dyslipidemia indicatorb by % total energy from
added sugar in NHANES analysis

Indicator 5% to <10%, 10% to <17.5% 17.5% to <25% >25% (n=1135)

(n=893) (n=1751) (n=1210)

Low HDL-C 1.0 (0.81.4) 1.5 (1.21.9) 1.9 (1.52.6) 3.1 (2.34.3)c

High 0.8 (0.71.1) 1.1 (0.91.4) 1.3 (1.01.6) 1.2 (0.91.6)c

triglycerides

High LDL-C
a. OR (95% CI) vs reference0.9 (0.71.2)
group 1.1added
(<5% energy from (0.91.3) 1.1
sugar, n=593); (0.91.5)
adjusted for age; sex;1.2 (0.91.7)
race/ethnicity;
poverty; body-mass index; waist circumference; weight change; physical activity; total energy intake; intake of
monounsaturated fatty acids, polyunsaturated fatty acids, saturated fatty acids, cholesterol, fiber, and other
carbohydrates; hypertension; cigarette smoking; and alcohol use
b. low and high levels as defined by NCEP-ATP III guidelines
c. p<0.05 for trend

Welsh JA et al. JAMA 2010; 303:1490-1497.

 Mild consumption of alcohol
reduces risk of CHD
and risk of ischemic stroke

2-4 alcohol drinks per day

ABUSUS
Binge drinking

Mild
consumption
Alcohol beverages

1 l beer
28-33 g alcohol
1 beer = 0,5 l
14 -16 g alcohol
Alcohol beverages

1 l wine
80 -100 g alcohol

2 dl wine
16 -20 g alcohol
Alcohol beverages

1 l destilate = 400 g
alcohol

5 cl = 20 g alcohol
 Alcohol drinking and risk of atherotrombotic
events in primary prevention
CHD morbidity
Ischem. STR

RRR 40-70%

3-9 drinks Alcohol/day

Stampfer MJ et al: A Engl Med J 1988;319:267
Rimm EB et al.: JAMA 1998;279:359
Fuchs CS et al.: A Engl J Med 1995;332:1245
 Mild alcohol consumption reduces
total and CV mortality (n=490 000)

Thun M, Peto R, Lopez A

N Engl J Med 1997;337:
1705
 Cardioprotective effects of
alcohol
Antioxidative fenols, flavonoids
Antithrombotic - plattelets aggregation
- prostacyclin
- fibrinolysis (Fg, PAI,
von Willebrand factor, F VII, t-PA)
Antiflogistic- hs- CRP, IL-6
Others HDL-chol
folates, vitamines B (beer)
Mild consumption
 Alcohol unfavourable effects

More than 50 epidemiological studies

positive association - alcohol (> 3 drinks per day)
and hypertension
reduction of alcohol drinking about 1drink
= decrease of SBP and DBP about 1 mmHg
increase of TG- pancreatitis
liver cirrhosis
Abusus
cardiotoxicity
psycho- social problems
 French paradox

In France lower mortality of CVD than in other countries

Smoking, fatty diet, high chol

Explanation: high consumption of red wine
fenols a flavonoids anti-oxidative and anti-thrombotic effects

Renaud S et a.: Lancet 1992;339:1523

Carnacini A et al.: Alcologia 1994;6:41
 Impact of regular alcohol consumption
on 12-year morbidity a mortality in middle-
aged men
CA all
CA-smokers: RR 1,3 (1,11-1,82)
CMP

IM

Non-fatal CHD: RR 0,76 (0,60-0,97)

Mortality
CVD, total

RR
0,5 0,75 1 1,5

Rosolov H. et al.: Pilsen Longitudinal Study I. Cardiology 1994;85:61-68

 When I read about the
evils of drinking,

I decided

to give up reading

Mild
Mark Twain (1835-1910) consumption

Abusus