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 Diet and cardiovascular disease risk factors in Botswana

Lemogang Daniel Kwape

BS. Dietetics, Texas Southern University (Houston, Texas USA)

MSc. Nutrition & Health (Public Health & Epidemiology) Wageningen, The
Netherlands.

A thesis presented for the degree of

Doctor of Philosophy

in the Public Health Nutrition Research Group, Institute of Applied Health

Sciences, University of Aberdeen

June 2012
 Declaration

Declaration
I declare that the work in this thesis has been undertaken by myself, and has not been

submitted in support for a degree from any other university. All work was carried out

by myself with assistance from individuals and organisations acknowledged here.

Bantle Modibedi and Tapologo Ramotswaiso were involved in recruitment and

measurement of participants along with myself. Blood samples were collected and

analysed by staff at Diagnofirm Medical Laboratories in Gaborone Botswana. The Food

Frequency Questionnaire was analysed by Dr Maria Jackson, University of Jamaica at

Mona. All quotation marks and all sources of information have been acknowledged.

...............................................

Lemogang Daniel Kwape

June, 2012

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 Table of Contents

Table of Contents
Declaration i

Abstract vi

Acknow ledgements vii

List of abbreviations viii

List of figures ix

List of tables x

Summary xiii

1 Chapter 1 2

1.1 Introduction 2
1.1.1 Definitions 2
1.1.2 Morbidity and mortality 4

1.2 Risk factors fo r cardiovascular disease 6

1.2.1 Sex 8
1.2.2 Blood pressure 9
1.2.3 Diabetes mellitus 11
1.2.4 Blood lipids 13
1.2.5 Physical activity 16
1.2.6 Obesity 17
1.2.7 Alcohol 19
1.2.8 Smoking 22

1.3 Nutrition transition 23

1.4 Diet and risk of CVD 23

1.4.1 Dietary fat 24
1.4.2 Dietary fibre 27
1.4.3 Sodium and potassium 29
1.4.4 Antioxidant nutrients 30
1.4.5 Fruit and vegetable consumption 31
1.4.6 Dietary patterns 32

1.5 Antiretroviral medication and ca rdiovascular diseases 33

1.6 Diet and CVD in Botswana 34

1.7 Aims and objectives 40

2 Methodology 42

2.1 Introduction to Bo tswana 42

2.2 Roles in the study 44

2.3 Ethical considerations 45

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 Table of Contents
2.4 Recruitment centres 45

2.5 Study participants 46

2.6 Sample size 47

2.7 Questionnaire 48
2.7.1 Socioeconomic status 48
2.7.2 Education 48
2.7.3 History of cardiovascular diseases 49
2.7.4 Smoking 49
2.7.5 Physical activity questionnaire 51
2.7.6 Use of hormone replacements or birth control 52
2.7.7 Food frequency questionnaire (FFQ) 53

2.8 Biophysical measurements 54

2.8.1 Body weight and height 54
2.8.2 Waist and hip circumference 55
2.8.3 Body composition 56
2.8.4 Blood pressure and pulse rate 58

2.9 Collection of biological samples and initial bio chemistry 58

2.9.1 Quality control 59

2.10 Statistical Analyses 61

2.10.1 Descriptive statistics 61

3 Diet and CVD risk factors 64

3.1 Introduction 64

3.2 Statistical methods 65

3.2.1 Descriptive statistics 65
3.2.2 Dietary patterns 68

3.3 Socio-demographic characteristics 70

3.3.1 Socio-demographic characteristics by sex 70
3.3.2 Socio-demographic characteristics by age group 75

3.4 Anthropometric and physical chara cteristics of participants 79

3.5 Lipids, Lipoproteins and glucose measurements of participants 87

3.6 Dietary Data 91

3.6.1 Under and over reporting 91
3.6.2 Macronutrient intake 93
3.6.3 Proportion of individuals commonly consuming specific foods 99
3.6.4 Intakes of commonly consumed foods 110
3.6.5 Dietary pattern analyse 120

3.7 Discussion 126

3.7.1 Obesity 126
3.7.2 Hypertension 131
3.7.3 Dyslipidaemia 132
3.7.4 Diet and dietary patterns 134

4 Associations between diet and CVD risk factors 138

4.1 Statistical methods 139

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 Table of Contents
4.2 Correla tions between diet and CVD risk factors 141

4.3 Association between total fa t intake and CVD risk factors 143

4.4 Association between SFA intake and CVD risk fa cto rs 149

4.5 Association between PUFA intake and CVD risk factors 155

4.6 Association between PUFA:SFA ratio and CVD risk fa cto rs 160

4.7 Association between dietary fibre intake and CVD risk factors 165

4.8 Association between alcohol intake and CVD risk factors 170

4.9 Association between dietary patterns and CVD risk factors 176
4.9.1 Association between dietary patterns and CVD risk factors in women 176
4.9.2 Association between dietary patterns and CVD risk factors in men 181

4.10 Association between frui t and vegetables intake and blood pressu re 193

4.11 Discussion 198

4.11.1 Saturated fat intake and CVD risk factors 198
4.11.2 Polyunsaturated fatty acids intake and CVD risk factors 200
4.11.3 Fibre intake and CVD risk factors 201
4.11.4 Alcohol intake and CVD risk factors 202
4.11.5 Dietary patterns and CVD risk factors 204
4.11.6 Fruit and vegetable intake and blood pressure 205

5 Diet and risk of CVD/diabetes/hypertension 208

5.1 Introduction 208

5.2 Statistical methods 211

5.3 Comparison between participants with CVD, hypertension or diabetes 214

5.4 Characteristics of “healthy” and “diseased ” participants 219

5.4.1 Socio-demographic characteristics 219
5.4.2 Physical and anthropometric measurements 221
5.4.3 Macronutrient intake 223
5.4.4 Lipids, lipoproteins and glucose 224

5.5 Risk of CVD/diabetes/hypertension by dietary factors 226

5.5.1 Carbohydrate intake 226
5.5.2 Fibre intake 226
5.5.3 Total fat intake 227
5.5.4 Saturated fatty acid intake 227
5.5.5 Polyunsaturated fatty acids intake 227
5.5.6 Polyunsaturated fatty acids and saturated fatty acid ratio (PUFA:SFA ratio) 227
5.5.7 Alcohol use 227

5.6 Discussion 236

6 Discussion 241

6.1 Strengths 242

6.2 Limitations 243

6.3 Major findings 245

6.3.1 CVD risk factors 245
6.3.2 Association between diet and CVD risk factors 248
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 Table of Contents
6.3.3 Diet and disease 254

6.4 Future research wo rk focus 257

6.5 Public health perspective 261

6.6 Conclusion 263

Appendix 1 Ethics permit i

Appendix 2 Information sheet (English) i

Appendix 2 Information sheet (Setswana) ii

Appendix 3 Questionnaire iii

Appendix 4 Description of food items listed in the FFQ xxviii

Appendix 5 Publication xxxii

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 Abstract

Abstract
Kwape LD: Diet and cardiovascular disease risk factors in Botswana
Cardiovascular disease (CVD) is the leading cause of mortality and morbidity wo rldwide.
In Sub-Saharan Africa, rates of CVD are increasing rapidly, but there is little evidence
about the potential determinants of CVD risk in this population.

This thesis investigated CVD risk factors in Gaborone, capital city of Botswana, by (i)
documenting CVD risk factors in this population, (ii) investigating the association between
diet and CVD risk factors and (iii) assessing the association between diet and risk of CVD.
787 adults were recruited. Of these 566 were generally “healthy” with no his tory of CVD,
while 221 (“diseased”) had at least one reported CVD condition, hypertension or
diabetes. The median (interquartile range) age was 27 (23, 32) and 52 (42, 62) years for
healthy and diseased participants respectively. All participants completed an interview
administered questionnaire, including a food frequency questionnaire. Height, weight,
waist circumference and blood pressure were measured, and a non-fasting blood sample
was obtained for analysis of lipids, lipoproteins and glucose.

A high prevalence of overweight and obesity (36.8%), particularly in women (50.0%), and
low HDL cholesterol (<1.0 mmol/L men and <1.3 mmol/L women) (62.6%) was found.
High levels of triglycerides, LDL cholesterol, glucose and high blood pressure were also
found in this population of young adults in Gaborone.

Total fat and/or saturated fat intake (as percentage energy) was significantly linearly
associated with increased LDL cholesterol (p=0.017), triglycerides (p=0.048), glucose
(p=0.044) and with decreased HDL cholesterol (p=0.021). However, fibre, polyunsaturated
fatty acids and dietary patterns were not independently associated with CVD risk factors.

Carbohydrates intake was significantly associated with increased risk of disease.

Unexpectedly, saturated fat intake was associated with reduced disease risk, but
weakened after nutrients adjustment.

CVD risk factors are relatively high in this population. These results suggest a need for
further research on CVD in Botswana.

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 Acknowledgements

Acknowledgements
Many people contributed in many ways to the success of the research work described
in this thesis.

First I would like to thank the participants who volunteered their time and blood in the
advancement of science.

I am grateful to Professor Geraldine McNeill for her guidance and encouragement

throughout my PhD. Thank you for always seeing the glass half full.

Dr Lindsey Masson, thank you for your attention to details and for your guidance and
encouragement.

Dr Nadeem Sarwar, many thanks for your guidance and invaluable contribution in the
formulation and initiation of the study.

Dr Lorna Aucott, thank you for your advice on analysis of the data.

Thank you to Professor Kiran Bhagat and the staff at Heart Foundation of Botswana for
your support during planning and data collection of this study.

Phlebotomists at DML, thank for your services during the data collection. It was not
easy but we made it.

Thank you to the nurses and support staff at Cardiac, Extension 2 and Nkoyaphiri
clinics.

Bantle Modibedi and Tapologo Ramotswaiso thank you for your assistance during the
data collection.

I am immensely grateful to the Department of Research Science and Technology,

University of Aberdeen, Diagnofirm Medical Laboratory & the Dennis Burkitt fellowship
for providing funding for my PhD.

Staff and fellow PhD students (past and present) in the Public Health Nutrition
Research Group, thank you for your assistance during my PhD. You shared, you cared
and the group will remain close to my heart.

Finally to my family, thank you for your immeasurable support. I owe my success to
you and with this thesis I humbly thank you.

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 Abbreviations

List of abbreviations
AIDS Acquired Immune Deficiency Syndrome
ANOVA Analysis of Variance
ARV Anti-Retro Viral
BFHS Botswana Family Health Survey
BIA Bio-Impedance Analysis
BMI Body Mass Index
BMR Basal Metabolic Rate
BWP Botswana Pula (1 BWP~ £0.11)
CDE Carbohydrates-Deficiency Transferrin
CHD Coronary Heart Disease
CSO Central Statistics Office
CVD Cardiovascular disease
DBP Diastolic Blood Pressure
DM Diabetes Mellitus
DALY Disability Adjusted Life Years
DML Diagnofirm Medical Laboratories
FBG Fasting Blood Glucose
FFQ Food Frequency Questionnaire
GGT Gamma-Glutamyl Transferase
GLM General Linear Model
HC Hip Circumference
HDL High Density Lipoprotein
HIV Human Immuno Virus
IHD Ischaemic Heart Disease
IQR Inter Quartile Range
LDL Low-Density Lipoprotein
LMIC Low Middle Income Countries
MI Myocardial Infarction
MRC Medical Research Council
MRFIT Multi Risk Factors Intervention Trial
MUFA Monounsaturated Fatty Acids
OR Odds Ratio
PAI Physical Activity Index
PAL Physical Activity Level
PURE Prospective Urban and Rural Epidemiology
RCT Randomised Controlled Trials
RR Relative Risk
SACN Scientific Advisory Committee on Nutrition
SBP Systolic Blood Pressure
SD Standard Deviation
SFA Saturated Fatty Acids
SPSS Statistical Package for Social Sciences
PCA Principal Component Analysis
P:S ratio PUFA:SFA ratio
PUFA Polyunsaturated Fatty Acids
THUSA Transition and Health during Urbanisation in South Africa
WHO World Health Organisation
WHR Waist-to-Hip ratio

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 Abbreviations

List of figures

Figure 1.1 Complex lesion and thrombosis in atherosclerosis 3

Figure 1.2 CVD mortality trends for males and females (United States 1979-2007) 4
Figure 1.3 Global mortality and risk factors 6
Figure 1.4 Conceptual framework of development of CVD 7
Figure 1.5 CVD mortality for men and women in the USA 8
Figure 1.6 Prevalence of CVD risk factors by gender in Tanzania. 9
Figure 1.7 Prevalence of hypertension (≥ 140/90mmHg) in Sub-Saharan Africa 10
Figure 1.8 Age- and sex-adjusted prevalence of hypertension (HTN), smoking, elevated
cholesterol, obesity, and diabetes among CVD cases in the early versus the later ti me
period of the Framingham study. 12
Figure 2.1 Map of Botswana showing population distribution 43
Figure 2.2 Sample of smoking history questionnaire 50
Figure 2.3 Sample of the FFQ 53
Figure 2.4 Measuring waist and hip circumference 56
Figure 2.5 Measuring body composition with bio-impedance analysis 57
Figure 3.1 Age distribution of participants 71
Figure 3.2 Income categories of participants by sex 74
Figure 3.3 Income of participants by age group 78
Figure 3.4 Prevalence of underweight, overweight and obesity by BMI 81
Figure 3.5 Prevalence of abdominal obesity 82
Figure 3.6 Prevalence of hypertension 85
Figure 3.7 Proportion of physical activity levels of participants 86
Figure 3.8 Prevalence of low HDL & high atherogenic index 89
Figure 3.9 Proportion of commonly consumed food items 100
Figure 3.10 Fat and oils used in food preparation 119
Figure 5.1 Distribution of participants by disease status 208
Figure 5.2 Age distribution of participants by disease status 210
Figure 5.3 Proportion of participants with overweight and obesity 222
Figure 5.4 Proportion of participants with hypertension 222
Figure 5.5 Proportion of participants with high lipids, lipoproteins and glucose 225

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 List of tables

List of tables
Table 1.1 BMI categories (WHO, 2000) 18
Table 1.2 WC categories for risk of metabolic complications (WHO, 2000) 18
Table 1.3 Description of Mediterranean, prudent western dietary and oriental patterns
32
Table 1.4 Literature search strategy for diet and CVD in Botswana 35
Table 1.5 Studies measuring CVD risk factors and diet in Botswana 37
Table 2.1 Physical activity status and weight factors 51
Table 2.2 Physical activity levels for different lifestyles 52
Table 3.1 Socio-demographic characteristics by sex: n (%) 71
Table 3.2 Lifestyle characteristics of participants by sex: n (%) 73
Table 3.3 Socio-demographic characteristics of participants by age group: n (%) 76
Table 3.4 Lifestyle characteristics of participants by age group: n (%) 77
Table 3.5 Mean (SD) anthropometric measurements by age and sex 80
Table 3.6 Mean (SD) of physical measurements 84
Table 3.7 Mean (SD) of lipids, lipoproteins and glucose (mmol/L) 88
Table 3.8 Number (%) of participants classed as under and over reporters 92
Table 3.9 Variation of selected variables by energy cut-off points: Mean (SD) 93
Table 3.10 Daily energy, carbohydrate, fibre and protein intake: Median (P25, P75) 95
Table 3.11 Daily fat and alcohol intake (grams) of participants: Median (P25, P75) 96
Table 3.12 Mean (SD) percentage contribution of macronutrients daily to energy 98
Table 3.13 Proportion n (%) of individuals who commonly consumed cereals and
starches by age group and sex 103
Table 3.14 Proportion (%) of individuals who commonly consumed meat and dairy
products by age group and sex 105
Table 3.15 Proportion n(%) of individuals who commonly consumed fruit and
vegetables by age group and sex 107
Table 3.16 Proportion n (%) of individuals who commonly consumed sugar sweets and
condiments by age group and sex 109
Table 3.17 Median (P25, P75) intake of commonly consumed cereals and starchy
foods (g/day) by sex and age group 111
Table 3.18 Median (P25, P75) intake of commonly consumed dairy and meat products
(g/day) by sex and age group 112
Table 3.19 Median (P25, P75) intake of commonly consumed vegetables (g/day) by
sex and age group 114
Table 3.20 Median (P25, P75) intake of commonly consumed fruit (g/day) by sex and
age group 115
Table 3.21 Median (P25, P75) intake of commonly consumed sugar, sweets,
condiments (g/day) by sex and age group 117
Table 3.22 Median (P25, P75) intake of commonly consumed beverages (ml/day) by
sex and age group 118
Table 3.23 Dietary patterns for all participants 121
Table 3.24 Dietary patterns for all women 122
Table 3.25 Dietary pattern for all men 123
Table 3.26 Results from WHO steps survey in selected sub-Saharan countries 127
Table 3.27 Participants characteristics by BMI classification 130
Table 4.1 Correlations between diet and CVD risk factors 142
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 List of tables
Table 4.2 Association between lipid, lipoprotein and glucose levels mean (SE) and total
fat intake (%E) in all participants 144
Table 4.3 Association between lipid, lipoprotein and glucose levels mean (SE) with
total fat intake (%E) in men and women 145
Table 4.4 Association between physical measurements mean (SE) and total fat intake
(%E) in all participants 147
Table 4.5 Association between physical measurements mean (SE) and total fat intake
(%E) in men and women 148
Table 4.6 Association between lipid lipoprotein and glucose levels mean (SE) and SFA
intake (%E) in all participants 150
Table 4.7 Association between lipid lipoprotein and glucose levels mean (SE) and SFA
intake (%E) in men and women 151
Table 4.8 Association between physical measurements mean (SE) and SFA (%E) in all
participants 153
Table 4.9 Association between physical measurements mean (SE) and SFA (%E) in men
and women 154
Table 4.10 Association between lipid lipoprotein and glucose levels mean (SE) and
PUFA (%E) for all participants 156
Table 4.11 Association between lipid lipoprotein and glucose levels mean (SE) and
PUFA (%E) for men and women 157
Table 4.12 Association between physical measurements mean (SE) and PUFA (%E) in all
participants 158
Table 4.13 Association between physical measurements mean (SE) and PUFA (%E) in
men and women 159
Table 4.14 Association between lipid lipoprotein and glucose levels mean (SE) and
PUFA:SFA ratio in all participants 161
Table 4.15 Association between lipid lipoprotein and glucose levels mean (SE) and
PUFA:SFA ratio in men and women 162
Table 4.16 Association between physical measurements mean (SE) and PUFA:SFA ratio
in all participants 163
Table 4.17 Association between physical measurements mean (SE) and PUFA:SFA ratio
in men and women 164
Table 4.18 Association between lipid lipoprotein and glucose levels mean (SE) and
dietary fibre (g/1000kcal) in all participants 166
Table 4.19 Association between lipid lipoprotein and glucose levels mean (SE) and
dietary fibre (g/1000kcal) in men and women 167
Table 4.20 Association between physical measurements mean (SE) and dietary fibre
(g)/1000kcal in all participants 168
Table 4.21 Association between physical measurements mean (SE) and dietary fibre
(g)/1000kcal in men and women 169
Table 4.22 Association between lipids, lipoproteins and glucose mean (SE) and alcohol
use (g) in all participants 171
Table 4.23 Association between lipids, lipoproteins and glucose mean (SE) and alcohol
use (g) in men and women 172
Table 4.24 Association between physical measurements mean (SE) and alcohol use (g)
in all participants 174
Table 4.25 Association between physical measurements mean (SE) and alcohol use (g)
in men and women 175

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 List of tables
Table 4.26 Association between lipids, lipoproteins and glucose and the “high sweets”
pattern 177
Table 4.27 Association between physical measurements and the “high sweets” pattern
178
Table 4.28 Association between lipids lipoproteins and glucose and the “high fruit”
pattern 179
Table 4.29 Association between physical measurements and the “high fruit” pattern
180
Table 4.30 Association between lipids, lipoproteins and glucose and the “mixed”
pattern 182
Table 4.31 Association between physical measurements and the “mixed” pattern 183
Table 4.32 Association between lipids, lipoproteins and glucose and the “convenience”
pattern 185
Table 4.33 Association between physical measurements and the “convenience”
pattern 186
Table 4.34 Association between physical measurements and the “traditional” pattern
188
Table 4.35 Association between physical measurements and the “traditional” pattern
189
Table 4.36 Association between lipids, lipoproteins and glucose and the “high
vegetable” pattern 191
Table 4.37 Association between physical measurements and the “high vegetable”
pattern 192
Table 4.38 Association between fruit and vegetables and blood pressure 194
Table 4.39 Association between fruit and vegetables and blood pressure 195
Table 5.1 Pearson correlation coefficient for nutrients, physical and biochemical
measurements 213
Table 5.2 Socio-demographic characteristics of participants by disease status: n (%) 216
Table 5.3 Mean (SD) physical and anthropometric measurements by disease status 217
Table 5.4 Daily mean (SD) macronutrient intake (%E) of participants by disease status
217
Table 5.5 Mean (SD) biochemical indicators (mmol/L) by disease status 218
Table 5.6 Socio-demographic characteristics of participants by disease status: n (%) 220
Table 5.7 Mean (SD) physical and anthropometric measurements by disease status 221
Table 5.8 Daily mean (SD) nutrient intake (%E) of participants by disease status 223
Table 5.9 Median (P25, P75) biochemical indicators (mmol/L) by disease status 224
Table 5.10 OR (95% CI) for risk of CVD/diabetes/hypertension according to
carbohydrate (%E) intake 228
Table 5.11 OR (95% CI) for risk of CVD/diabetes/hypertension according to fibre
(g/1000kcal) intake 229
Table 5.12 OR (95% CI) for risk of CVD/diabetes/hypertension according to total fat
(%E) intake 230
Table 5.13 OR (95% CI) for risk of CVD/diabetes/hypertension by SFA (%E) intake 231
Table 5.14 OR (95% CI) for risk of CVD/diabetes/hypertension by PUFA (%E) intake 232
Table 5.15 OR (95% CI) for risk of CVD/diabetes/hypertension by PUFA:SFA ratio 233
Table 5.16 OR (95% CI) for the likelihood of having CVD/diabetes/hypertension by
alcohol use 234

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 Summary

Summary
Cardiovascular disease (CVD) is the leading cause of mortality and morbidity

worldwide. In Sub-Saharan Africa, rates of CVD appear to be increasing rapidly, yet

there is little evidence about the potential determinants of CVD risk in the region. This

thesis therefore sought to investigate CVD risk factors in Gaborone, capital city of

Botswana, by (i) documenting CVD risk factors in the population, (ii) investigating the

association between diet and CVD risk factors and (iii) assessing the association

between diet and CVD.

In this study 787 individuals aged ≥18 years were recruited. Of these, 566 were

generally “healthy” with no history of CVD, while 221 had at least one CVD condition,

hypertension or diabetes. All participants completed an interview administered

questionnaire, including a food frequency questionnaire, measurement of height,

weight, waist circumference and blood pressure, and a non-fasting blood sample was

obtained for analysis of lipids, lipoproteins and glucose.

In chapter 3 CVD risk factors in healthy 566 “healthy” participants were described.

Obesity measured by defined by BMI≥30 was high in women (6.9% in < 25 years old,

20.6% in 25-35 years old and 46.7% in >35 years). In men the prevalence of obesity

was <6% across all age groups and was lowest at 1% in men aged <25 years. At least 1

in 5 women aged >25 years had abdominal obesity and for those women aged >35

years almost 1 in 2 had abdominal obesity, while only 1 in 10 men aged 25-35 years

had abdominal obesity. Conversely, at least 15% of men 35 years or younger were

underweight (BMI <18.5 kg/m2). The prevalence of overweight and obesity was

significantly higher in older and married participants as well as in participants with a

xiii | P a g e
 Summary
primary education or less, but was not significantly different by income or physical

activity level although physical activity level was significantly lower in women than in

men (p ≤ 0.001). About 1 in 4 men and women aged >35 years had high blood pressure

(SBP ≥ 140 mmHg or DBP ≥ 90 mmHg). Men had higher SBP compared to women (p ≤

0.001) and both SBP and DBP increased significantly with age.

Sixty-three percent of participants had a low HDL cholesterol level (< 1.0 mmol/L men

& < 1.3 mmol/L women), and more women than men had low HDL cholesterol (74.4%

versus 44.7%, p<0.001). The proportion of participants with low HDL cholesterol

increased with age in both sexes. Around 29% of men and women in the oldest age

group had a high atherogenic index (total cholesterol/HDL cholesterol > 5) and more

women than men had a high atherogenic index (11.3% versus 7.5%, p<0.001).

The proportion of participants with a high triglyceride level (≥1.7 mmol/L) was 7.4%,

and was significantly higher in men than women (12.1% versus 5.0%, p<0.001).

Conversely, the percentage of participants with high LDL cholesterol level (≥3.8

mmol/L) was significantly higher in women than me n (7.6% versus 6.5%, p<0.001). The

percentage of participants with high a random glucose level (≥6.1 mmol/L) was 4.6%

and was similar for both sexes. The relatively high prevalence of CVD risk factors in this

population are similar to those reported in other Sub-Saharan countries.

Reported energy intake (as measured by FFQ) was unexpectedly high in this

population, possibly due to overestimation. However the percentage contribution to

energy from the macro-nutrients was within recommended levels.

xiv | P a g e
 Summary
In chapter 4 the association between diet and CVD risk factors in “healthy”

participants was investigated. SFA (%E) intake was associated with increased LDL

cholesterol (p for trend = 0.017), triglycerides (p for trend = 0.048), glucose (p for trend

= 0.044) and was also associated with decreased HDL cholesterol (p for trend = 0.021)

after adjustment for potential confounders (age, sex, physical activity level, education,

income, tobacco use and alcohol use). PUFA intake was not associated with CVD risk

factors. Dietary fibre was inversely associated with random glucose only in men (p for

trend = 0.046), while alcohol intake was significantly positively associated HDL

cholesterol (p for trend <0.001) and inversely associated with BMI (p for trend = 0.020)

only in women.

In Chapter 5 the effect of diet on risk of disease (CVD/hypertension/diabetes) was

investigated. Individuals in the highest tertile of carbohydrate intake had increased risk

of disease compared to those in the lowest tertile of intake (OR 3.53 95% CI 1.45-8.60),

but the OR was no longer significant after adjustment for fibre and total fat.

Unexpectedly, high total fat and SFA intakes were associated with reduced risk of

disease but the association also weakened after adjustment for other nutrients. PUFA,

fibre and alcohol were not associated with disease risk. In this study however

“diseased” participants were older, their time of diagnosis of disease was not

verifiable, and they had a significantly lower intake of energy and fat, but a higher

carbohydrate intake compared to “healthy” participants. Therefore it is likely that

following diagnosis the “diseased” participants were advised on dietary changes (e.g.

replacing fat with carbohydrates) and weight loss.

In summary, this study found a relatively high prevalence of overweight and obesity

and of low levels of HDL cholesterol in young adults in Gaborone. High levels of

xv | P a g e
 Summary
triglycerides, LDL cholesterol, glucose and high blood pressure were also found. The

results from the FFQ support literature suggesting that dietary patterns are shifting

from traditional diet to diets high in sugar, refined starches and meat. It is therefore

necessary for government to intensify CVD prevention strategies by promotion of

healthy eating and physical activity, and to monitor CVD risk factors through research

and surveillance.

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 Chapter 1: Introduction

Chapter 1

Introduction

“If we knew what it was we were doing, it wouldn’t be called resea rch, would it?” Albert Einstein

1 |P age
 Chapter 1: Introduction

1 Chapter 1

1.1 Introduction

1.1.1 Definitions

Cardiovascular disease (CVD) covers a number of disorders, amongst them diseases of

the cardiac muscles and the vascular system supplying the heart, brain and other vital

organs (Mendis et al., 2011).

CVD morbidity and mortality is predominantly due to coronary heart disease (CHD) and

cerebrovascular diseases (stroke). CHD is clinically manifested as ischemic heart

disease (IHD). It develops when the arteries supplying the blood to the heart become

partially or wholly blocked. This is usually caused by fatty deposits building up inside of

the arteries. Symptoms of CHD are chest pain which is temporary and treatable;

however, if blood supply to the heart is interrupted for a long time it is characterised

by severe chest pain (angina) and damage to the heart muscles resulting in a heart

attack (myocardial infarction). Stroke is caused by a disruption in the flow of blood to

part of the brain either because of narrowing of blood vessel (ischemic stroke) or

rupture of a blood vessel (Hemorrhagic stroke) (Sanders & Emery, 2003).

CVD is usually associated with atherosclerosis, an inflammatory disease characterised

by the accumulation of lipids and fibrous elements in the intima of the large to

medium arteries (Lusis, 2000). Atherosclerosis is primarily initiated by the

accumulation of low density lipoprotein (LDL) in the sub-endothelial matrix. Oxidation

of LDL is the most significant modification that gives rise to pro-inflammatory activity.

The accumulation of oxidised LDL triggers the recruitment of monocytes and

lymphocytes to the arterial wall and stimulates endothelial cells to produce pro-

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 Chapter 1: Introduction
inflammatory factors (adhesion molecules and growth factors), and at the same time

LDL can inhibit nitric oxide production which has anti-atherogenic properties. Highly

oxidised LDL is then taken up by macrophages to form foam cells.

Accumulations of these cholesterol-engorged macrophages or foam cells are

described as a fatty streak: the first visible sign of atherosclerosis. In humans, such

'fatty streak' lesions can usually be found in the aorta in the first deca de of life, the

coronary arteries in the second decade, and the cerebral arteries in the third or fourth

decades. Because of differences in blood flow dynamics, there are preferred sites of

lesion formation within the arteries such as branches and curvatures. Several risk

factors contribute to the damage of the endothelium and pro-inflammation including

hypertension, haemodynamic factors, sex hormones, diabetes, infections, elevated

homocysteine and hyperlipidaemia (Ross, 1999; Lusis, 2000).

Accumulation of lipids and smooth muscle cells and monocyte derived

macrophages lead to the formation of a fibrous plaque. Although a fibrous

plague can grow sufficiently large to block blood flow, the most important clinical

complication is an acute occlusion due to the formation of a thrombus or blood

clot (figure 1.1), resulting in myocardial infarction or stroke (Lusis, 2000).

Figure 1.1 Complex lesion and thrombosis in atherosclerosis (Lusis, 2000)

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1.1.2 Morbidity and mortality

In 2002, almost one third (16.7 million) of global deaths were due to CVD, with low

income and middle income countries (LMIC) accounting for more than 86% of the

global CVD disease burden (WHO, 2002). In 2008 17.3 million people died from

CVD, and more than 17% of the deaths occurred in people younger than 60 years

(WHO, 2010). Over the last 20 years, deaths from CVD have been declining in high

income countries (WHO, 2010). In the United States of America, for example, the

death rate from CVD has been steadily declining for both men and women (figure

1.2). However, 80% of CVD mortality occurs in LMIC countries and continues to

increase rapidly; this disparity in CVD mortality has been largely attributed to better

combination of treatment regimes and a reduction in risk factors in developed

countries (WHO, 2010).

Figure 1.2 CVD mortality trends for males and females (United States 1979-2007),

(Roger et al., 2011)

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 Chapter 1: Introduction
In sub-Saharan Africa an estimated US$84 billion national income of some LMIC

countries will be lost due to CVD diseases (Abegunde et al., 2007). CVD is the major

contributor to the global burden of disease among the non-communicable diseases,

and it is projected that it will remain amongst the world’s leading killers until at

least 2030. Consequently, CVD is also projected to rank in the top 10 leading causes

of disability adjusted life years (DALY) in the same time period (Mathers & Loncar,

2006).

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 Chapter 1: Introduction

1.2 Risk factors for cardiovascular disease

Major risk factors for CVD are behavioural (tobacco use, physical inactivity,

unhealthy diets and harmful use of alcohol) and metabolic (hypertension, diabetes,

obesity and raised blood lipids), and other risk factors include age, gender poverty,

genetic predisposition and psychological factors (Mendis et al., 2011). In 2009 WHO

published a global health risk report which attributed more than 15 million (~60%)

deaths in middle income countries to CVD risk factors such as hypertension,

tobacco, alcohol use, overweight and obesity, low fruit and vegetable intake and

low physical activity (figure 1.3). (WHO, 2009).

Figure 1.3 Global mortality and risk factors (WHO, 2009)

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 Chapter 1: Introduction
Some of the risk factors described in figure 1.4 leading to atherosclerosis and

ultimately CVD include; elevated and modified low density lipoproteins (LDL), free

radicals caused by smoking, hypertension, genetic predisposition, infectious micro

organisms, obesity, low high density lipoprotein (HDL), and a combination of these

and other factors (Berse et al.,1992; Ross, 1999).

Lifestyle risk factors such a smoking, diet, physical inactivity and heavy alcohol

consumption are modifiable through lifestyle change whereas sex, age, race and

familial history (genetic and shared environment) are non-modifiable. Antiretroviral

medication used to treat human immune-deficiency virus (HIV) have also been

reported to increase risk of myocardial infarction (DAD study group, 2003).

Modifiable risk factors/lifestyle

risk factors:
Non modifiable risk
factors:
 Smoking
 Heavy alcohol
o Sex
consumption
o Age
 Physical inactivity
o Race
 Diet o Familial
o Saturated fat history
o Salt
o Cholesterol
o Energy
Intermediate conditions:

o Hypertension
o Obesity
o High low density cholesterol
o Low high density cholesterol
Anti- o Diabetes
retrov iral
treatment

Cardiovascular
disease

o CHD
o Stroke

Figure 1.4 Conceptual framework of development of CVD (modified from Wong,

Black & Gardin, 2005)

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