Artifacts in Nuclear Medicine with Identifying and resolving artifacts.
National NCD Programmes: Challenge and the Way Forward - Experience in the industrialized countries
1. National NCD Programmes:
Challenge and the Way Forward -
Experience in the industrialized
countries
Prof. Jaakko Tuomilehto
Department of Public Health,
University of Helsinki, Finland
and
Center for Vascular Prevention,
Danube-University Krems, Krems, Austria
2. Core Public Health Functions
to prevent and control NCDs
Evidence
Action – Health protection and
assurance
Action – Health promotion
Research
Financing
Training
3. Factors Contributing to Death
Worldwide
10 global risk factors account for more than one
third of deaths worldwide
Small number of risk factors cause high number
of premature deaths and large share of global
burden of disease
Risk factors causing premature deaths include:
high cholesterol - 4.4 million deaths (7.9% of
total)
tobacco - about 4.9 million deaths
elevated blood pressure - 7.1 million deaths
The World Health Report 2002.
4. Risk Factors for CVD and NCDs
Modifiable Non-modifiable
Smoking Personal history
Dyslipidaemia of CVD
• Raised LDL-C Family history
• Low HDL-C of CVD
Age
• Raised triglycerides
Gender
Raised blood pressure
Diabetes mellitus
Obesity
Dietary factors
Thrombogenic factors
Lack of exercise
Excess alcohol consumption
5. Relationship Between Cholesterol and
CHD Risk: Framingham Study
150
125
CHD incidence per 1000
100
75
50
25
0
<204 205–234 235–264 265–294 >295
(<5.3) (5.3–6.1) (6.1–6.8) (6.8–7.6) (>7.6)
Serum total cholesterol, mg/dL (mmol/L)
Castelli WP. Am J Med. 1984;76:4–12.
6. Most of the people dying from coronary heart
disease have ”intermediate” level of a risk factor
7.
8. SOUND COMBINATION OF THE
POPULATION STRATEGY WITH
HIGH RISK STRATEGY
1. Population strategy:
- Greatest public health gains
- Cost effective
- Results also in other health benefits
1. High risk strategy:
- Great benefits to the persons concerned
- Effective use of health services
16
12.09.12
9. Relationship of Serum Cholesterol to
Mortality: Seven Countries Study
35
Northern Europe
Death rate from CHD/1000 men
30
25
United States
20
15
10 Southern Europe, inland
Serbia
Southern Europe, Mediterranean
5
Japan
0
2.60 3.25 3.90 4.50 5.15 5.80 6.45 7.10 7.75 8.40 9.05
(100) (125) (150) (175) (200) (225) (250) (275) (300) (325) (350)
Serum total cholesterol, mmol/L (mg/dL)
Verschuren WM et al. JAMA 1995;274(2):131–136.
10. Levels of Risk Associated with Smoking,
Hypertension and Hypercholesterolaemia
Hypertension
(SBP 195 mmHg)
x3
x4.5 x9
x16
x1.6 x6 x4
Smoking
Serum cholesterol level
(8.5 mmol/L, 330 mg/dL)
11. Prospective Studies Collaboration
Lancet 2007; 370: 1829-39
Established chiefly to investigate associations of
blood pressure and cholesterol with cause-specific
mortality
Individual data on 900 000 participants without any
previous history of vascular disease from 61
prospective cohort studies
> 55 000 vascular deaths (34 000 ischaemic heart
disease [IHD], 12 000 stroke, 10 000 other)
150 000 participants from 23 studies also had HDL
cholesterol (5000 vascular deaths)
12. IHD mortality (33 744 deaths) versus usual total cholesterol
IHD mortality (33 744 deaths) versus usual total cholesterol
Age at 1 mmol/L ↓
risk total cholesterol
80-89 15% ↓ risk
70-79 18% ↓ risk
Usual total cholesterol (mmol/L)
60-69 28% ↓ risk
50-59 42% ↓ risk
4·0 5·0 6·0 7·0 8·0
40-49 56% ↓ risk
256
128
0·5
64
32
16
8
4
2
1
CI)
(floating absolute risks & 95%
Hazard ratio
13. IHD mortality (33 744 deaths) versus usual total cholesterol
IHD mortality (33 744 deaths) versus usual total cholesterol
by BMI
by BMI
Age at BMI No. of
risk (kg/m2) deaths
70-89 30+ 2369 0·77 (0·73-0·81)
25-29 7198 0·78 (0·75-0·80)
<25 6736 0·79 (0·76-0·81)
60-69 30+ 1518 0·74 (0·70-0·79)
25-29 4679 0·72 (0·69-0·74)
<25 4123 0·70 (0·68-0·73)
40-59 30+ 827 0·62 (0·57-0·67)
25-29 3105 0·56 (0·54-0·59)
<25 2881 0·55 (0·53-0·58)
0·4 0·6 0·81·0
Hazard ratio (& 95% CI) for
1 mmol/L lower usual total cholesterol
17. St
u
1950
di e
s:
to
b ac
co
To ca
1960
b us
ac
c e sc
oc an
on
su c er
W mp
or t
1970
kin ion
gg pe
TO ro ak
BA up s
•A CC to
POLICY
re
1976
•S dver O A du
pu
mo tis CT ce
bli king in g sm
•S b ok
ale c pla ban an ing
ba ce s:
Mid
80’s
St nt s pu
ud op bli
ies er ct
:p so ra
as ns ns
siv un po
de rt
es an
Gu mo r1 d
1985
ide kin 6y
lin gc ea
es au r s.
for se
•B sm sc
•W an o ok an
ce
1995
efr
•S ork f ind ee r
ale pla ire wo
ba ces ct a rk
nt sm dve pla
•S om ce
ok rti s
2000
mo ino el si n
•E ke rs fr e
TS fr es g
ca e e
rci ar
no eas
2001 ge
n i c i n th
by e r
law est
au
ra
Pla nt
n s
2003
re n
sta ing
ur s
an t ag
ts eo
FC ns
m
2005
TC
ra ok
tif efr
ica ee
tio
n
Sm
2007
ok
efr
eer
All es
•li re tau
ce st a ra
•R n
2009
nt
es sing uran s(
tri gr
cti of r ats ad
on eta sm ua
so lly
nt
il s oke )
ra ale free
ve
lle
2010:
r’s
17
all
ow
•Enlargement of smokefree places
•Ban on tobacco displays
•Objective: to end tobacco consumption
•Smokefree Finland by 2040
•Restrictions related to snus
an
ce
s
THE HISTORY OF THE FINNISH TOBACCO
18. THE HISTORY OF THE FINNISH TOBACCO
POLICY
s
nt
s
)
ce
ra
lly
ing
ee
an
au
ua
ok
er
ow
law est
efr
ad
sm
c
s
ra ale free
gr
an
all
ak
by e r
ok
TOBACCO ACT
s(
ce
sc
pe
m
n i c i n th
r’s
il s oke
•Advertising ban
du
nt
ns
e
lle
ion
us
ra
eta sm
re
18
ve
no eas
•Smoking bans: public
ts ge o
ca
tau
t
to
mp
cti of r ats
ge
n
co
rci ar
transport and public
es
up
nt
tio
ur g sta
su
ac
es sing uran
er
ca e e
ro
so
ica
on
places
b
an
e
gg
TS efr
to
oc
re nnin
on
tif
efr
st a
•Sale ban to persons
s:
• E ok
kin
ra
c
ok
re
di e
s ta
ac
m
la
TC
tri
or
n
Sm
under 16 years.
All
b
•S
ce
u
P
W
FC
To
St
•li
•R
1950 1960 1970 Mid 1985 2000 2001 2003 2005 2009
80’s
1976 1995 2007 2010:
•Ban on tobacco displays
•Restrictions related to snus
•Enlargement of smokefree places
•Objective: to end tobacco consumption
•Smokefree Finland by 2040
19. St
u
1950
di e
s:
to
b ac
co
To ca
1960
b us
ac
c e sc
oc an
on
su c er
W mp
or t
1970
kin ion
gg pe
TO ro ak
BA up s
•A CC to
POLICY
re
1976
•S dver O A du
pu
mo tis CT ce
bli king in g sm
•S b ok
ale c pla ban an ing
ba ce s:
Mid
80’s
St nt s pu
ud op bli
ies er ct
:p so ra
as ns ns
siv un po
de rt
es an
Gu mo r1 d
1985
ide kin 6y
lin gc ea
es au r s.
for se
sm sc
ok an
ce
1995
efr
ee r
wo
rk
pla
ce
s
•Sale ban to minors
2000
•Workplaces smokelfree
2001
•Ban of indirect advertising
Pla
2003
re nnin
s ta
ur g sta
an
ts ge o
FC ns
m
2005
TC
ra ok
tif efr
ica ee
tio
n
Sm
2007
ok
efr
ere
All es
•li re tau
ce st a ra
•R n
2009
nt
es sing uran s(
tri gr
cti of r ats ad
on eta sm ua
so lly
nt
il s oke )
ra ale free
ve
lle
2010:
r’s 19
all
ow
•Enlargement of smokefree places
•Ban on tobacco displays
•Objective: to end tobacco consumption
•Smokefree Finland by 2040
•Restrictions related to snus
an
ce
s
THE HISTORY OF THE FINNISH TOBACCO
20. St
u
1950
di e
s:
to
b ac
co
To ca
1960
b us
ac
c e sc
oc an
on
su c er
W mp
or t
1970
kin ion
gg pe
TO ro ak
BA up s
•A CC to
POLICY
re
1976
•S dver O A du
pu
mo tis CT ce
bli king in g sm
•S b ok
ale c pla ban an ing
ba ce s:
Mid
80’s
St nt s pu
ud op bli
ies er ct
:p so ra
as ns ns
siv un po
de rt
es an
Gu mo r1 d
1985
ide kin 6y
lin gc ea
es au r s.
for se
•B sm sc
•W an o ok an
ce
1995
efr
•S ork f ind ee r
ale pla ire wo
ba ces ct a rk
nt sm dve pla
•S om ce
ok rti s
2000
mo ino el si n
•E ke rs fr e
TS fr es g
ca e e
rci ar
no eas
2001 ge
n i c i n th
by e r
law est
au
ra
nt
s
2003
2005
Smokefree
(gradually)
restaurants
2007
A
•li ll re
c s
2009
• R e n s t au
es ing ran
tri
cti of r ats
on e s
s o tail mok
n t sal efr
ra e ee
ve
lle
2010:
r’s20
all
ow
•Enlargement of smokefree places
•Ban on tobacco displays
•Objective: to end tobacco consumption
•Smokefree Finland by 2040
•Restrictions related to snus
an
ce
s
THE HISTORY OF THE FINNISH TOBACCO
21. St
u
1950
di e
s:
to
b ac
co
To ca
1960
b us
ac
c e sc
oc an
on
su c er
W mp
or t
1970
kin ion
gg pe
TO ro ak
BA up s
•A CC to
POLICY
re
1976
•S dver O A du
pu
mo tis CT ce
bli king in g sm
•S b ok
ale c pla ban an ing
ba ce s:
Mid
80’s
St nt s pu
ud op bli
ies er ct
:p so ra
as ns ns
siv un po
de rt
es an
Gu mo r1 d
1985
ide kin 6y
lin gc ea
es au r s.
for se
•B sm sc
•W an o ok an
ce
1995
efr
•S ork f ind ee r
ale pla ire wo
ba ces ct a rk
nt sm dve pla
•S om ce
ok rti s
2000
mo ino el si n
•E ke rs fr e
TS fr es g
ca e e
rci ar
no eas
2001 ge
n i c i n th
by e r
law est
au
ra
Pla nt
n s
2003
re n
sta ing
ur s
an t ag
ts eo
FC ns
m
2005
TC
ra ok
tif efr
ica ee
tio
n
Sm
2007
ok
efr
eer
All es
•li re tau
ce st a ra
•R n
2009
nt
es sing uran s(
tri gr
cti of r ats ad
on eta sm ua
so lly
nt
il s oke )
ra ale free
ve
lle
2010:
r’s
21
all
•Enlargement of smokefree places
•Ban on tobacco displays
ow
•Smokefree Finland by 2040
•Objective: to end tobacco consumption
•Restrictions related to snus
an
ce
s
THE HISTORY OF THE FINNISH TOBACCO
22. Proportion of daily smokers (%)
1950-2011, age 15-64
80
70
60
50
Men
40
%
Women
30
20
10
0
50 60 70 80 90 00 5 6 7 8 9 11
Year
Sources: * Years -50, -60 and -70: Finnish Gallup
The National Institute for Health and Welfare (THL). Health Behaviour and Health among the
Finnish Adult Population, Spring 2011. Report 45/2012.
23. Exposure to environmental tobacco smoke
in Finland 1983 - 2011
40
35 Home
30 Workplace
25
20
%
15
10
5
0
83 86 89 91 93 95 96 97 98 99 00 01 02 03 04 05 06 7 8 11
year
The National Institute for Health and Welfare (THL). Health Behaviour and Health among the
Finnish Adult Population, Spring 2011. Report 45/2012.
32. CVD PREVENTION WORKS
Start of the
North
Karelia Nationwide
Project CVD
Age-adjusted 700
prevention
CHD mortality activity
600
in North Karelia
and the whole 500
North Karelia
of Finland 400
Men 35-64 yrs 300
Finland -82%
1969 to 2001 200
Mortality
per 100
100
000
population
-75%
70 75 80 85 90 95 20
Year
M Paimensaari 2.9.2005 32
33. IMPACT Model: CHD mortality
fall in Finland 1982 – 1997
0
Risk Factors -71%
-100 Cholesterol - 53%
Smoking - 11%
Blood pressure - 7%
-200
Treatments -24%
-300 AMI treatments - 4%
373 fewer deaths Secondary prevention - 8%
Heart failure - 2%
-400 Angina:CABG & PTCA - 8%
1982 1997 Angina: Aspirin etc - 2%
Laatikainen et al Am J Epid 2005 162 764
34. Trends in salt intake in Finland
based on dietary surveys and
24-h urinary sodium excretion
35. Salt intake distributions following different food
choices and cooking practices among Finnish men
Ideal target
Present situation
36. International CHD mortality trends
in men, 1968-2003
Per 100,000
800
Finland
600
400
Ireland
Netherlands
UK
200
USA
France Italy
0
0
3
6
9
2
5
8
1
4
7
0
7
7
7
8
8
9
9
0
7
8
9
9
9
9
9
9
9
9
9
9
9
0
1
1
1
1
1
1
1
1
1
1
2
Source:WHO statistics 2005 Men aged 35 - 74,
40. Change in 9-year Mortality (%) (from Cohort 1 to
Cohort 2) for US Men and Women
With and Without Diabetes
Cohort 1: 1973-75; Cohort 2: 1983-85
41.
42. Finnish Diabetes Prevention Study: lifestyle goals
Weight reduction > 5%
Fat intake < 30 Energy-%
Saturated fat intake < 10 Energy-%
Fibre intake ≥ 15 g/1000 kcal
Physical activity > 30 min/day
Intervention group
• Individually tailored diet based on 3-day food diaries
• 7 dietary counselling sessions during the first year, every 3 months
thereafter
• Free-of-charge gym
Control group
• General advice about healthy diet and exercise habits
• No individualised counselling
Tuomilehto et al. 2001
43. Reduction of the Incidence of Diabetes
During the Lifestyle Intervention – DPS
Risk reduction: 58%
44. DPS: Diabetes Incidence is Sustained
During the Extended Follow-Up without a
further Intervention
50
Log-rank test: p=0.0001
Control
Cumulative incidence of T2D, %
Hazard ratio = 0.57 (95% CI 0.43-0.76)
40
30
20
Intervention
10
Intervention ceased
0
0 1 2 3 4 5 6 7 8
Follow-up time, years
Lindström J et al. Lancet 2006; 368(9548):1673-79.
45. Prevention of Type 2 Diabetes by
Lifestyle Management: The Evidence
DPS - Finland DPP - USA SLIM - Netherlands
Risk 58% ↓
Risk 58% ↓
Risk 58% ↓
EDIPS Newcastle - UK Da Qing - China
IDPP - India
Control
Risk 55% ↓ Risk 43% ↓
Risk 28,5% ↓
Metformin
Lifestyle
46. Protection against diabetes
when achieving the intervention targets
at the one-year examination - DPS
%
SUCCESS SCORE Tuomilehto et al. N Engl J Med 2001; 344:1343
47.
48.
49.
50. Combined effect of midlife vascular risk
factors on late-life dementia
OR (95% CI) 10
9
8
BMI 2.1 (1.2 - 3.8) 6.21
7
>30 kg/m2 6
5
4
SBP >140mmHg 2.0 (1.0 - 3.8) 3.03
3
1.37
2
1
Cholesterol 1.9 (1.0 - 3.5) 1 0 1 2 3
0
>6.5 mmol/l
Number of risk factors present
Adjusted for sociodemographic
factors. Kivipelto et al., Arch Neurol 2005
51. ApoE4 Magnifies Effects of Lifestyle for the Risk of Dementia
APOE ε4 non-carriers
Active
Sedentary APOE ε4 carriers
Physical activity
Active
Sedentary 5.5
IV
III
II
I
PUFA intake- IV
quartiles III
II
4
I 5
I
II
III
SFA intake - quartiles IV
I
II 7.1
III
IV 7.1
Non-drinkers
Infrequent
Frequent
Alcohol
Non-drinkers
drinking Infrequent
Frequent
3.8
Non-smokers
Smokers
Smoking Non-smokers ORs for dementia
Smokers 3.2
Greeting: Good afternoon and thank you for coming to this presentation! Today I would like to talk about our research project titled … Before starting my presentation I would like to thank Simon and Julia for their valuable scientific and social support. Guven araliklarini koyarsan iyi olur results tablosuna CHD icin akis semasini koy Degiskenlerin tanimlarini koy
The World Health Report 2002 1 reported that the top 10 global risk factors for premature death are: childhood and maternal underweight; unsafe sex; high blood pressure; tobacco; alcohol; unsafe water, sanitation and hygiene; high cholesterol; indoor smoke from solid fuels; iron deficiency and overweight/obesity. Together, they account for one-third of global loss of healthy life years (DALY; disability-adjusted life years) annually and about 40 per cent of the 56 million deaths that occur worldwide. The burden from many of the risks is borne almost exclusively by the developing world, while other risks have already become global. The report predicts that unless action is taken, by the year 2020 there will be nine million deaths caused by tobacco, compared to almost five million a year now; five million deaths attributable to overweight and obesity, compared to three million now; that the number of healthy life years lost by underweight children will be 110 million, which, although lower than 130 million now, is still unacceptably high. High cholesterol is estimated to cause about 4.4 million deaths (7.9% of total) and a loss of 40.4 million DALYs (2.8% of total), although its effects often overlap with high blood pressure. This amounts to 18% of strokes and 56% of global ischaemic heart disease. Reference 1. World Health Organization. The World Health Report 2002.
Some of the risk factors that predispose an individual to the development or progression of CVD are outlined above. Evidence has shown that lifestyles associated with a ‘western’ culture such as a diet rich in saturated fats and high in calories, smoking and physical inactivity, are some of the modifiable risk factors leading to an increase in the prevalence of CVD. Of these, three are considered to be of prime importance: 1 Smoking is responsible for 50% of all avoidable deaths, of which half are due to CVD. Raised blood pressure has been found to be an important risk factor for the development of CVD, cardiac failure and cerebrovascular disease. The greater the increase in blood pressure, the higher the risk. Greatest benefit of blood pressure lowering is seen in those at higher risk. Even modest reductions produce substantial benefits in those with multiple risk factors. Dyslipidaemia, in particular, raised low-density lipoprotein (LDL) cholesterol and triglyceride levels, and low high-density lipoprotein (HDL) cholesterol are associated with increased risk of CVD. Reference 1. Pyörälä K et al. Eur Heart J 1994; 15 :1300–1331.
Cardiovascular disease is associated with increased levels of total cholesterol. 1 Other risk factors include an increase in total to HDL-C ratio, hypertension, cigarette smoking, excess weight, elevated blood sugar levels, lack of exercise, stress, and electrocardiographic abnormalities. Intervention trials have shown that identifying and lowering these risk factors may help to reduce the subsequent rate of coronary heart disease, stroke, and other cardiovascular disease. Reference Castelli WP. Am J Med. 1984; 76 :4–12. Adapted from Am J Med 1984; 76 :4–12, with permission from Excerpta Medica Inc.
Twenty-five year follow-up data from the Seven Countries study 1 show that serum total cholesterol levels are linearly related to CHD mortality across cultures. The relative increase in CHD mortality rates with a given increase in cholesterol are similar. However, the large between-country difference in CHD mortality rates at a given cholesterol level indicates that other factors, such as diet, also play a role in the development of CVD. The link between high cholesterol levels and increased incidence of CVD has also been shown in the prospective part of the Multiple Risk Intervention study. 2 In epidemiological studies, measurements of serum cholesterol have been routinely used. The relationship between cholesterol levels and the incidence of CVD is almost entirely dependent on low-density lipoprotein (LDL) cholesterol, the main carrier of cholesterol and a major atherogenic lipoprotein. 3 Results from the Framingham study 4 during 26 years of observation show that men have twice the incidence of CHD mortality and morbidity of women. This difference tends to diminish during the later years, after the menopause. Other factors that influence susceptibility to CHD include ethnic background and social class. 5-7 References 1. Verschuren WM et al. JAMA 1995; 274 (2):131–136. 2. Martin MJ et al. Lancet 1986; ii :933–936. 3. Kannel WB et al. In Proceeding of Golden Jubilee International Congress, Minnesota, 1980. Eds Loan MS, Holman RT.Oxford, Pergamon Press 1982;339–348. 4. Lerner DJ, Kannel WB. Am Heart J 1986; 11 (2):383–390. 5. Rosamond WD et al. N Engl J Med 1998; 339 :861–867. 6. Goff DC et al. Circulation 1997; 95 :1433–1440. 7. Poulter N. In Cardiovascular Disease: Risk Factors and Intervention. Eds: Poulter N, Sever P, Thom S. Radcliffe Medical Press, Oxford, 1993. Adapted from JAMA 1995; 274 :131–136, with permission from American Medical Association. All rights reserved.
Multiple risk factors for CVD are usually present in an individual; rarely do they occur in isolation. When risk factors co-exist the effect is often exponential; their combined effect is greater than the sum of their individual effects. 1 Multiple risk factors are also associated with the metabolic syndrome which is characterised by dyslipidaemia, hypertension, insulin resistance, visceral distribution of body fat, and a prothrombotic state. 2 References 1. Poulter N. In Cardiovascular Disease: Risk Factors and Intervention. Eds: Poulter N, Sever P, Thom S. Radcliffe Medical Press, Oxford, 1993. 2. Deedwania PC. Am J Med 1998; 105 (1A);1S–3S. Reproduced with permission from Radcliffe Medical Press.
The Prospective Studies Collaboration is a collaborative meta-analysis combining data from existing prospective observational studies that recorded both blood pressure and blood cholesterol at baseline and that followed participants for cause-specific mortality. Investigators from around the world have collaborated to combine data from 61 existing prospective studies involving a total of one million participants from Europe, North America, Australia, Israel, China and Japan. During 12.7 million person-years of follow-up there were 120 000 deaths involving more than 55 000 vascular deaths (12 000 stroke, 34 000 ischaemic heart disease [IHD], 10 000 other vascular) and more than 65 000 other deaths.
Figure 1(a): IHD mortality (33 744 deaths) versus usual total cholesterol. Age-specific associations The hazard ratios are plotted on a floating absolute scale of risk (so each log hazard ratio has an appropriate variance assigned to it. NOTES: 1 mmol/L lower total cholesterol was associated with about a half , a third and a sixth lower IHD mortality in both sexes at ages 40-49, 50-69 & 70-89, respectively, throughout the main range of cholesterol in most developed countries, with no apparent threshold. Although the proportional differences in risk decrease with age, the absolute effects of cholesterol on annual IHD mortality rates are much greater at older than at younger ages. For example, the absolute difference in the annual risk of IHD death for a 1 mmol/L difference in total cholesterol was about 10 times greater at 80-89 than at 40-49 years of age.
Figure 2(c). IHD mortality (33 744 deaths) versus usual total cholesterol by body mass index (BMI). Conventions as in figure 1(b). (The BMI analysis involved just 33 436 deaths because of missing BMI values for 308 people who died of IHD.) NOTES: Similarly, BMI was of little relevance to the proportional effects of cholesterol on IHD mortality within each age group, so the absolute difference in IHD mortality (for a given difference in total cholesterol) was somewhat greater for more obese.
Biggest changes will be in Africa, followed very closely by MENA. NAC and Europe will change the least.
In a recent study we investigated the combined effect of several midlife vascular risk factors. We were interested in seeing whether the vascular risk factors were independent of each other, or whether ne factor could explain the associations observed for another factor. When bmi, sbp, and cholesterol were all put simultaneously into the same model, they all independently increased the risk of dementia and AD. The Or for each factor was around 2. We know, that risk factors tend to cluster together, and the same person can have several risk factors. This clustering increased the risk of dementia in an additive manner. The more there were risk factors, the higher was the risk, so that those who had all three factors – high sbp, high bmi and high cholesterol had an or of 6 for dementia when compared to persons with none of the risk factors.