Open access peer-reviewed chapter

Double Burden of Poverty and Cardiovascular Disease Risk among Low-Resource Communities in South Africa

Written By

Wilna Oldewage-Theron and Christa Grobler

Submitted: 21 December 2020 Reviewed: 13 January 2021 Published: 26 February 2021

DOI: 10.5772/intechopen.95992

From the Edited Volume

Lifestyle and Epidemiology - The Double Burden of Poverty and Cardiovascular Diseases in African Populations

Edited by Kotsedi Daniel Monyeki and Han C.G. Kemper

Chapter metrics overview

351 Chapter Downloads

View Full Metrics


Limited studies evaluating the prevalence of cardiovascular risk (CVR) in resource-poor black communities in South Africa (SA), exist. The objective of this chapter is to evaluate the prevalence of CVR in a cross-sectional studies in randomly selected low income children, adults and elderly in Gauteng, Free State and Eastern Cape, SA. The test panel of CVR markers included: anthropometry, lipid profile, blood pressure, fibrinogen, high sensitive–C–reactive protein (HS–CRP), homocysteine, vitamin B12, folate, glucose and dietary intakes. The main findings indicated high CVR with prevalence of overweight/obesity, Hypertension, hyperhomocysteinaemia, increased fibrinogen and HS-CRP, as well as low intakes of dietary fibre, vitamins B6 and B12, folate and polyunsaturated- and monounsaturated fatty acids, and high intakes of dietary sodium, saturated and trans fatty acids, and added sugars. Multiple CVR factors are present among all the communities. It can thus be concluded that a double burden of poverty and risk of CVD exists across the different age groups and geographical locations in these resource-poor communities.


  • cardiovascular risk
  • poverty
  • South Africa
  • children
  • adults
  • elderly

1. Introduction

South Africa (SA) is a middle-income country that is characterised by contrasting living conditions ranging from wealthy urban suburbs to lower-income, underdeveloped areas. [1] SA has faced many socio-economic challenges such as high levels of poverty, inequality and unemployment [1, 2] despite having the second largest economy on the African continent. Since the country’s transition to democracy in 1994, progress has been made, but unemployment rates and poverty levels remain high. [1] Poverty is the main underlying factor contributing to food insecurity. [3, 4] The food insecure often use strategies to cope with the inability to access food. One of these include reducing the quality and quantity of food consumed, thus consuming poor diversity diets which can have detrimental consequences such as hunger, malnutrition [5, 6] and increased prevalence of metabolic and cardiovascular diseases (CVDs) [7] due to it hindering individuals’ ability to choose the most appropriate foods and beverages for an adequate diet. [8] A disadvantage of food insecurity is thus monotonous diets with consumption of more affordable energy-dense staples and foods that may have detrimental health outcomes such as obesity and its chronic disease comorbidities. [9] Food insecurity thus does not only cause under-nutrition, but also in over-nutrition such as obesity and its comorbidities, especially in low-income communities. [10] SA is a country in health transition and suffers from a quadruple burden of (a) poverty and nutrition-related chronic diseases of lifestyle [CDL], (b) communicable diseases, (c) peri-natal, maternal and injury-related disorders, [11] and (d) a nutrition transition. A recent study has found that this quadruple burden of disease is predominantly present in the black African population. [1] Urbanisation and westernisation of the Black African population of SA is marked not only by demographic transition, but also by increased animal protein, total dietary fat and added sugar intakes [11] and a health transition resulting in an increased prevalence of obesity [6] and CDL such as CVD. [11, 12]


2. Double burden of poverty and cardiovascular disease among black south Africans

The South African population of approximately 59 million people consists of 81% black Africans. [13] In 2017, it was reported that 56% of the SA population lived in poverty [14] with 28% living in extreme poverty, thus not having enough money to purchase enough food to consume around 2,100 calories per day for a month (food poverty). The most vulnerable to food poverty are women, children (66.8%), those with low education (79.2%) and people from the black population group (64.2%). [15, 16]

CVD incidence is increasing rapidly among all population groups in SA. [11] CDLs contribute 51% to the mortality rate, with CVD and diabetes accounting for 19% and 8% of the total deaths. Many people in SA have poor living conditions and limited resources to maintain health and well-being. [15] In spite of cultural background, people that has been subjected to urbanisation, has adopted a more Western lifestyle with lower dietary fibre and higher dietary fat and added sugar intakes, as well as lower physical activity levels. These dietary changes have led to higher prevalence of CDL, [17] specifically an increased risk and susceptibility of CVD among the black population, [18] and not only in adults, but also among children. [19] The face of CVD has thus changed in recent years. Initially it was a disease of the white population group, the affluent and older generations, but since the 2000s, it was also observed that the prevalence of CVD risk factors, such as dyslipidaemia and obesity, has increased among black Africans [20] as well as children and adolescents. [21, 22, 23, 24]

The aim of this chapter was thus to investigate the prevalence of the various cardiovascular risk factors, specifically those that are irreversible, among children (6–18 years old) in peri-urban Free State (FS), [25] rural Eastern Cape (EC), [24, 26, 27, 28] peri-urban [29] and urban [30, 31, 32, 33] Gauteng; adults (19–59 years old) in urban Gauteng [30, 31, 34, 35, 36, 37] and peri-urban FS; [38, 39, 40] and elderly (≥60 years) in urban Gauteng, [41, 42, 43] including both genders, living in poverty in SA. Gauteng was chosen as the authors both resided in Gauteng and it was the focus of the university for funding. No data had been available for the cardiovascular risk factors in the above-mentioned communities and a valuable research opportunity was created to address the paucity of information in these communities. For this reason, the FS and EC provinces were chosen because of funding opportunities and gap in the knowledge base on the areas included in these studies.


3. Methodology

A search of electronic databases focusing on poverty, food insecurity and cardiovascular risk factors was carried out between 2010 and 2020. Databases used included: MEDLINE (PubMed), Web of Science, ScienceDirect, Scopus, EBSCOHost, Springer Link, and Sabinet. The keywords used included: “poverty”, “food security”, “nutrition security”, “food and nutrition security”, “cardiovascular disease”, “CVD”, “cardiovascular risk”, “CVR”, “cholesterol”, “triglycerides”, “HDL”, “LDL”, “C-reactive protein”, “CRP”, “fibrinogen”, “homocysteiene”, “vitamin B6”, “vitamin B9”, “folate”, “folic acid”, “vitamin B12”, “glucose”, “insulin”, “obesity”, “overweight”, “nutritional status”, “hypertension”, “high blood pressure”, “dietary diversity”, “dietary intake”, “children”, “adults”, “elderly”, “older people”, “aged”, “double burden”, and “South Africa”.

The data used for this chapter included all the databases and articles published for the various studies undertaken by the authors between 2000 and 2020 among black children in the EC, FS and Gauteng, [24, 25, 26, 27, 28, 30, 31, 32, 36] adults in Gauteng and the FS [25, 30, 35, 37, 40] and the elderly in Gauteng [37, 41, 43] in various urban, peri-urban and rural areas of SA. For the purpose of this book chapter, urban areas include cities and towns that are developed, thus having a density of human structures such as houses, commercial buildings, roads, and public transport. Peri-urban areas are underdeveloped areas on the outskirts of the towns and cities where people live, but no public transportation or commercial buildings are present. Rural areas refer to areas with low population density and large areas of undeveloped land where people mainly live far apart from their neighbours.

Comparative tables were drawn up using the published articles and, where data were not published, descriptive statistical analyses (frequencies) were calculated using IBM SPSS Statistics, version 26, from the study databases that had not been destroyed. The ethical and scientific procedures for the sampling strategy and data collection methods were the same for the published and unpublished data.


4. Poverty and food insecurity

Poverty and food insecurity were observed in all seven study communities. A large majority of the adults (75.7%–78.0%) [35, 44] and child caregivers (53.0%–94.0%) [27, 29, 30, 44] were unemployed, had either no or only primary education (39.9%–78.8%), [27, 29, 30, 34, 36, 43, 44] and lived in poverty (67.7–100%). [27, 29, 35, 36, 44] The poverty rates of all the communities were more than double the 25.2% national food poverty rate. [15] This may have been due to the high unemployment rate and low education levels found among the adults in all the communities. A chronic money shortage to buy food was also reported in large percentages of the study population.


5. Cardiovascular risk factors

Many risk factors for CVD have been identified in the scientific literature and can be reversible or irreversible (Table 1). In 2016, 20% of the South African adults (15+ years) were smoking. [45] Risk factors present in the South African adult (18+ years) population are obesity (68% women; 31% men) hypertension (46% in women and 44% in men), [46] physical inactivity (37%), high blood pressure (24%) and hyperglycaemia (10%). [45] There is a paucity of national data for other CVD risk factors in adults, and very little CVD national data are available for children, except for the prevalence of overweight and obesity.

5.1 Socio-demographic risk factors

The history of CVD of an individual is directly proportional to the risk of CVD (the earlier the age of onset and the more family members affected the greater is the risk of CVD). [47] It is known that men are at greater risk of developing CVD than women [47, 48] maybe because oestrogen has an inhibiting effect on low density lipoprotein-cholesterol (LDL-C) oxidation and increasing the production of large very low-density lipoproteins (VLDL) and therefore has a protective effect against atherogenesis. [50] Low levels of education in middle-income countries like SA had a significantly higher risk of major CVD events compared to those with high incomes. [49] The majority (>70%) of our communities showed low education (no or primary school education), [29, 31, 34, 35, 43] except for the peri-urban adults in the FS (44.2%); [44] and caregivers of the peri-urban children in Gauteng (39.9%), [29] however, these percentages are still high. High unemployment rates (53.0–94.0%) [29, 30, 31, 35, 44] for the majority of all the communities were also observed. The low education and high unemployment rates of the communities could be some of the main reasons for the high poverty rates in the study communities (67.7–100%). [26, 35, 36, 44] Research has found that people with low education may not have access to health care that may prevent detecting and treating disease and thus compromise their health even further. [50]

5.2 Cigarette smoking

Cigarette smoking doubles the risk of coronary artery disease and contributes seven-fold to the increase in risk for peripheral arterial disease. [51] Cigarette smoking and increases blood pressure and increases the heart’s workload. It deprives the heart muscle of oxygen and damages the platelets that increase coagulation and clot formation. Toxins in cigarettes may also damage the blood vessels and increase atherosclerosis. [48, 52] In SA, the proportion of adult (15+ years) women that smoke (37%) daily is higher than in men (8%). [46] Smoking patterns among children were not measured in our studies, but we previously reported 11.7%, 15.2% and 23.6% smoking among urban elderly, [43] peri-urban adults in Gauteng [31] and rural adults in the FS. [37]

5.3 Obesity

Obesity is considered a multi-factorial condition [20, 53, 54] associated with an increased risk for comorbidities such as type 2 diabetes, insulin resistance, cancer, stroke, [53] hypertension, dyslipidaemia, [53, 55] and hypertriglyceridaemia. [55] Obesity is also considered an independent risk factor for CVD. [40] For every 1% increase above ideal body mass index (BMI), the cardiovascular risk (CVR) increases by 3.3% for females and 3.6% for males. [56] In our studies, the majority of the adults and elderly were overweight/obese. [44, 57] Although we did not report gender differences in this chapter, previous published results confirmed a higher prevalence among women in rural FS [37] and urban elderly [41] than in men. Our results further showed that the urban women in Gauteng had the highest prevalence (82.3%) of overweight/obesity, but cannot be compared to the peri-urban adults and urban elderly that included both men and women. However, the overweight/obesity prevalence among the urban elderly in Gauteng [57] and the peri-urban adults in the FS [44] was consistent with the national prevalence.

There is usually a higher prevalence of overweight/obesity in urban than rural. [20] We did not have any rural adult communities to compare our results, but the urban elderly in Gauteng (61.0%) [57] had lower prevalence of overweight/obesity than the peri-urban adults in the FS (67.9%). [44] This was inconsistent with research from sub-Saharan Africa (SSA) [54] and SA where it was found that age is positively correlated with overweight and obesity. [58, 59] In all three the adult communities, the prevalence of obesity was higher than the prevalence of overweight. (Table 2). The increasing prevalence of childhood overweight/obesity in SA [11] is presenting a major public health problem. Childhood overweight/obesity is associated with early onset of hypertension and hyperglycaemia, both risk factors for CVD, [71] as well as adult obesity, [54] premature death and disability. [54] Similar to adults, a higher prevalence of overweight/obesity among children is found in urban areas. [54, 72, 73] (Table 3) However, our results showed higher prevalence among the rural children (4.3%) [24] compared to the urban children (1.0%). [32] In addition, the rural [28] and urban [32] children had the lowest prevalence of overweight and no obesity prevalence. Both peri-urban areas showed a prevalence of 21.0% in the FS [25] and 18.3% in Gauteng. [32, 33] This was higher than the national prevalence. In our studies among resource-poor communities, the prevalence of obesity was much lower than the prevalence of overweight. Our studies have found significantly higher prevalence of overweight/obesity in girls when compared to the boys. [24, 26] These results were consistent with national data [77] and for SSA, [54] but inconsistent with a recent systematic review and meta-analysis investigating overweight/obesity among 5–19 year old children in 15 countries in Africa where the boys and girls were equally affected by overweight/obesity. [71].

IrreversibleGender (male)
Genetically inherited factors
Potentially reversible factorsCigarette smoking
Hypertension Physical activity
Hyperglycaemia, diabetes
Increased haemostatic factors, decreased fibrinolysis, increased platelet aggregration
Increased levels of homocysteine
Increased inflammatory response (HS-CRP)
Dyslipidaemia (increased cholestrol, LDL, Triglyseride, decreased LDL)
Diet and dietary diversity
PsyschosocialLow socio-economic class
Stressful environment
Personality types
GeographicClimate and season (cold weather increased risk)
Soft drinking water
Environmental pollution

Table 1.

Reversible and irreversible cardiovascular risk factors.

VariableReference valuesUrban women
(n = 628)
Peri-urban adults
Free State
(n = 271)
Urban elderly
(n = 170)
OverweightBMI ≥ 25 < 30 [60]39.3 [37]26.0 [44]29.5 [57]
ObeseBMI ≥ 30 [60]43.0 [37]41.9 [44]31.5 [57]
High serum TC levels≥6.2 mmol/L [61]0.5 [37]16.722.3 [57]
Low HDL-C levels<1 mmol/L (adult men)
<1.3 mmol/L (adult women) [61, 62]
43.0 [37]62.7 [39]76.2 [57]
High LDL-C levels>4.1 mmol/L [60, 63]0.5 [37]16.714.6 [57]
Hypertriglyceridaemia (High TRG levels)≥2.3 mmol/L [60, 63]24.7 [37]12.7 [39]13.8 [57]
High normal BP130–139 mm Hg/85–89 mm Hg
(systolic/diastolic blood pressure) [64]
11.6 [37]12.710.8 [57]
Hypertensive≥140/≥90 mm Hg (systolic/diastolic blood pressure) [64]36.4 [37]53.2 [39]68.0 [57]
Hyperhomocysteienemia>15 umol/L [61](serum homocysteiene)66.4 [57]
Fibrinogen>3.5 g/L [65]68.0 [57]
Inflammation (HS-CRP)≥3 mg/dL [62]56.968.3 [57]
Hyperglycaemia (serum glucose)>5.5 mmol/L [66]16.0 [39]38.5 [57]
Serum vitamin B6<8.6 mcg/L [67]98.0 [57]
Serum vitamin B12<156 pmol/L [68, 69]4.8 [57]
Serum folate<5.9 nmol/dL [70]9.6 [57]

Table 2.

Cardiovascular risk factors in adults and elderly.

VariableReference valuesRural children
Eastern Cape
(n = 232)
Peri-urban children
Free State
(n = 98)
Peri-urban children
(n = 203)
Urban children
(n = 152)
OverweightBMI:A ≥ 2 < 3 [74]4.3 [24]17.0 [25]15.8 [29]1.0 [32]
ObeseBMI:A ≥ 3 [74]0.0 [24]4.0 [25]2.5 [29]0.0 [32]
High serum TC levels≥5.18 mmol/L [75]1.3 [24] [32]
Low HDL-C levels<1.04 mmol/L [75]42.5 [24]30.619.295.9 [32]
High LDL-C levels≤3.37 mmol/L [75]2.12 [24]12.22.528.6 [32]
Hypertriglyceridaemia (High TRG levels)≥1.12 mmol/L (0–9 years old)
≥1.47 mmol/L (10–19 years old)[75]
12.4 [24] [32]
Hyperhomocysteienaemia>15 umol/L [61]1.6
Fibrinogen>3.5 g/L [65]14.8
Inflammation (HS-CRP)≥3 mg/dL [62]19.0 [24]7.8
(serum glucose)
>6.1 mmol/L [76]10.3[24]6.56.9
Serum vitamin B12<156 pmol/L [69]7.6
Serum folate<5.9 nmol/dL [70]4.6

Table 3.

Cardiovascular risk factors of children.

To summarise, overweight/obesity is common among the poor-resource adults and elderly in our study population. The high prevalence observed among the adults, specifically women, and elderly may be due to poor nutrition (Table 2). Although the prevalence of obesity is not yet high among the children in our study communities, the results highlight the increasing burden of overweight among children (Table 3). The high prevalence of overweight and obesity in our study communities is a concern as the comorbidities associated with overweight/obesity have negative effects on health across the life cycle. [71]

5.4 Hypertension

Hypertension (blood pressure ≥ 140/90 mm Hg) [64] is considered one of the most important risk factors for developing CVD [50, 78] due to organ injury to the heart and kidneys. [79] Sharp increases in childhood hypertension have been reported in SA recently. [11] In childhood, hypertension treatment does not reverse the target organ injury and although hypertension treatment will significantly reduce event rates, the burden of CVD event rates will remain high though adulthood. [79] SA has a high hypertension burden with 44% and 41% of adult (≥15 years) black African women and men respectively. [46] In our adult populations the urban women in Gauteng had lower prevalence of 36.4% compared to the peri-urban adults in the FS (53.2%). [39] The elderly in urban Gauteng had the highest prevalence (68.%). [57] (Table 2) This was consistent with the national prevalence (84% among both genders aged ≥65 years), indicating that the hypertension burden increases with age. [46, 80] A recent national survey has found an overall prevalence of 43%, of which 58% were unaware of the condition and thus did not receive treatment. [80] Similar results were observed where only 36.8% of the hypertensive urban elderly in Gauteng used hypertensive medication. [43] No hypertension data were available for the children.

In summary, our results showed high levels of hypertension in adults and the elderly in both urban and peri-urban areas. A recent national survey has found older age, obesity and lower education levels as the main risk factors for hypertension in SA. [80] High prevalence of obesity and poor education levels have been identified in all our adult communities.

5.5 Hyperglycaemia, diabetes and metabolic syndrome

Diabetes mellitus is the most common, but also the most complex CDL. [81, 82] Hyperglycaemia affects multiple organs and can lead to arterial hypertension. [83] It is estimated that the cause of death in 80% of individuals suffering from type 2 diabetes will be due to thrombotic complications of which 75% will result from a cardiovascular event. [84] Data on the incident rates of children with diabetes are available for only 6% of African countries and may be due to lack of screening tests available in the poor and low income communities. [84] Results in Tables 2 and 3 indicated that 38.5% urban elderly (Gauteng), [57] 16.0% peri-urban adults (FS), [39] 10.3% rural children (EC), [24] 6.5% peri-urban children (FS), and 6.9% peri-urban children (Gauteng) had high serum glucose levels. An increased prevalence of diabetes was reported for developing countries, [85] and it can be concluded that the prevalence of hyperglycaemia in all age groups in urban, peri-urban and rural areas in SA is concerning.

5.6 Haemostasis

The development of coronary artery disease and myocardial infarction has both atheromatous and thrombotic components. Haemostasis is a finely balanced system of clot formation and fibrinolysis. [86, 87, 88] Fibrinogen is recognised as an independent risk marker of CVD. Fibrinogen, because of its mass, also has a direct effect on the blood viscosity and a physical functional effect on platelet aggregation. [65, 89] Studies have indicated an increased level of plasma fibrinogen in black South Africans. [12, 57, 90] An increase of one gram per litre in plasma fibrinogen doubles the risk of CVD. [89] The fibrinogen levels were measured in two of the communities. High fibrinogen levels were observed in 68.0% of the elderly [57] (Table 2) and 14.8% of the rural children (Table 3), indicating an increased risk for CVD.

5.7 Homocysteine metabolism

5.7.1 Homocysteine

Several mechanisms have been proposed to clarify the link between homocysteine and pro-thrombotic state. The oxidative damage to the endothelium, combined with inhibition of the vasculo-protective function of nitric oxide, enhances thrombogenecity. [91] Homocysteine is metabolised by (a) the trans-sulphuration pathway which results in the production of cystathionine - a process that requires vitamin B6 and the main route of metabolism is via a methionine-conserving pathway - a process that requires methyltetrahydrofolate (from folic acid) and vitamin B12 as co-factor or alternatively (b) by the remethylation pathway taking place in the kidney and liver (where betaine is utilised instead of folate). [92, 93, 94, 95] An association between elevated plasma homocysteine and the development of atherosclerosis has been confirmed. [96] Studies in animal models have shown that elevated homocysteine promoted atherosclerosis by increased oxidative stress impaired endothelial function and increased thrombogenecity. [92, 93, 95, 96, 97, 98, 99] Epidemiological retrospective and prospective clinical studies established homocysteine as a potent independent risk factor for atherothrombotic vascular disease. [91, 92, 100] Additionally, homocysteine increase superoxide (O2) levels resulting in increased oxidative stress, causing an inflammatory state and increased atherosclerosis and ischemia reperfusion. Oxidative stress in return inhibits the cobalamine metabolism and enhances the cycle. [101, 102] The frequency of hyperhomocysteienaemia as an independent risk factor for atherothrombotic vascular disease [91, 92, 100] was found in 66.4% and 1.6% of the urban elderly [57] and rural children respectively. Thus, although homocysteine measurement did not form part of the objectives in all our communities, prevalence of hyperhomocysteienaemia in the urban elderly (Gauteng) (Table 2) and the rural children (EC) (Table 3) is an additional confirmation of an increased risk for CVD in the low income South African population.

5.7.2 Serum vitamin B6 levels

Vitamin B6 acts as coenzyme in the irreversible trans-sulfuration of homocysteine to cysteine. Higher vitamin B6 level are associated with lower homocysteine levels. Fat metabolism requires carnitine, obtained either directly [103] through diet or via synthesis requiring lysine and vitamin B6. Vitamin B6 deficiency was also found to be associated with decreased plasma PUFAs (n-6 and n-3) which may be associated with elevated cardiovascular risk and a contributing factor to the anti-inflammatory response. [104, 105] Low circulating vitamin B6 levels have been found inversely related to inflammatory markers (HS-CRP, fibrinogen, IL-6 and TNF-α) and are related to the incidence of inflammatory diseases (rheumatoid arthritis, CVD, and diabetes). [106, 107] Vitamin B6 levels were only available for the urban elderly and 98% of the respondents had low serum vitamin B6 levels (Table 2). Vitamin B6 levels were not available for any of the children, but pre-school children in Zambia indicated a suboptimal vitamin B6 in the studied group. [108] It would, therefore, be beneficial to include vitamin B6 serum levels in their analytical profile in future.

5.7.3 Serum folate levels

Low serum folate levels is a cardiovascular risk marker independently from homocysteine level. [109] Folate, as a donor of one-carbon units, is essential for methylation and affects numerous metabolisms involved in CVD [110] and accurate replication of deoxyribonucleic acid (DNA) and its repair. If DNA repair capacity of the cell is exceeded by the rate of damage to the genome, serious defects in cellular and tissue physiology occur, resulting in degenerative diseases including CVD. [111] The four mechanisms by which folate is involved in reducing atherosclerosis are: (1) Optimising methylation cycle and thereby directly reducing the homocysteine levels; (2) Acting directly as an antioxidant; (3) Interacting with enzyme endothelial nitric oxide synthase; (4) Affecting cofactor bioavailability of nitric oxide. Apart from being an independent cardiovascular risk marker, decreased serum folate levels also Indicate a decreased cell regeneration. [112] The serum folate levels were only available for two of the communities and 4.8% and 7.6% had low folate levels in the elderly [57] (Table 2) and rural children (EC) (Table 3) respectively. Study communities included in this study are therefore at risk for CVD and the general effect of ineffective cell recovery.

5.7.4 Serum vitamin B12 levels

The cofactor cobalamin is required for the optimal function of the enzymes methionine synthase and L-methylmalonyl-CoA. [113, 114] During methionine synthase, homocysteine is converted to methionine, when the methyl group is transferred from 5-methylene tetrahydrofolate to cobalamin to form methylcobalamin and tetrahydrofolate while methylcobalamin donates its methyl group that binds to homocysteine to form methionin (required for the synthesis of S-adenosylmethionine [SAM]). [87, 115] SAM is required in many cellular methylation reactions, including the methylation ribonucleic acid (RNA) and DNA. [116, 117] Reduced synthesis of methionine as a result of insufficient cobalamine results in increased homocysteine levels. [104] Vitamin B12 is also the coenzyme required to remove the methyl group from folate, thereby activating folate. [117, 118] Serum vitamin B12 was only available for the elderly in Gauteng (Table 2) and the rural children (EC) (Table 3) and 4.8% [57] and 7.6% had low folate levels respectively, thus at risk of impaired homocysteine metabolism and CVD.

5.8 Inflammation

An inflammatory response is initiated by damage to the vascular cell lining resulting in a series of mechanisms (acute-phase response) including haemodynamic (vasodilatation) activation of endothelial cells (increased adhesion molecule expression), increased permeability (enhanced protein movement) and an increase in acute-phase proteins. [119, 120] Vessel injury can also be caused by high LDL-C, hypertension, cigarette toxins and elevated homocysteine levels. During the inflammatory response that aims to repair the damage to the artery wall, LDL-C becomes trapped in the lesion that is engulfed by the macrophages and the free radicals oxidise the LDL trapped in the macrophage and eventually become plaque. [48] CRP is a β-globulin which is bound strongly to phospholipids and increases twentyfold to thirtyfold during an infectious or inflammatory response and is, therefore, considered a credible marker for systemic inflammation. [47] The prevalence of systemic inflammation was found in 56.9% of the adult respondents (peri-urban FS) and in 68.3% of the elderly, [57] (Table 2) as well as 19% and 7.8% of the rural (EC) [26] and peri-urban children (FS) respectively. (Table 3) Elevated CRP is a strong independent predictor of risk of future cardiovascular events. [121, 122] Thus, the results from our studies indicate an increased risk for CVD.

5.9 Dyslipidaemia

The prevalence of dyslipidaemia varies across the regions in SSA due to increased urbanisation and change of lifestyle factors (epidemiological transition). [123] A similar variation was observed in SA where a significant difference in the prevalence of dyslipidaemia occurs in different ethnic groups. [124] Although, studies indicated that people from an African decent showed an athero-protective lipid profile (lower total cholesterol) compared to their white European or Indian fellow countrymen, widespread low High density Lipoprotein (HDL-C) was present. [125] The use of antiretroviral therapy (ARV) also leads to an increase in dyslipidaemia. With the high prevalence of HIV/AIDS in SA [45, 46], is ARV treatment (the largest health programme internationally) is considered as a contributing factor to dyslipidaemia in SA. [126]. Previous studies indicated that prevalence of dyslipidaemia among black South Africans (independent of rural or urban) varies between 30% and 63%. [125, 127, 128]

The high protein component of high-density lipoprotein-cholesterol (HDL-C) accounts for its metabolic function of removing cholesterol from tissue back to the liver, and is considered as an important anti-atherogenic pathway modulating inflammation. The inverse correlation between serum HDL-C and cardiovascular risk (CVR) is well known and widely accepted. [129] Studies showed that improving poor lifestyle habits to have a positive effect on the HDL-C levels. [130]

With reference to the reported results in Tables 2 and 3, the prevalence of increased total serum cholesterol (TC) with the lowest in the urban adult women in Gauteng where 0.5% of participants had an increased TC. The highest prevalence was observed among the urban elderly population of Gauteng, where 22.3% of participants had an increased TC. The prevalence of low serum HDL-C levels was significantly decreased in all the study communities with the lowest prevalence in the peri-urban children where 19.2% had a HDL-C of less than 130 mg/dl. The highest prevalence was in the urban children where 95.6% had a decreased HDL-C level. The percentage of participants with the highest prevalence of abnormal LDL-C levels was found in the urban children in Gauteng (28.6%) and the lowest prevalence was found in the urban women of Gauteng (0.5%). In contrast, the lowest prevalence of participants with increased serum triglyceride levels were found in the urban children of Gauteng and the highest prevalence was in the urban (Gauteng) women (24.7%). Results obtained from our studies are in line with results obtained from other studies in SA [125, 126, 127, 128], confirming that prevalence of dyslipidaemia (mainly decreased HDL-C) is becoming an increasing concern that needs to be consciously addressed in planning for Health care interventions.

Dyslipidaemia is regarded as an independent CVR marker. [124] As indicated in Figure 1, a total of 4.1% Peri-urban children from the FS had four elevated lipid risk factors, additionally, of the urban elderly from Gauteng 3.8% had four, 13.1% had three, 12.3% had two and 47.7% had one elevated lipid parameter. Interestingly, more than one lipid risk factor were present in almost all the communities (>10% of adults and elderly), even in the children (>5%).

Figure 1.

Dyslipidaemic factors present in study groups.

5.10 Dietary intake factors

Dietary diversity has a significant positive association with health. [34] An inverse relationship between dietary diversity and CVD risk factors, namely hypertension, hypercholesterolaemia and high HDL-C has been observed. [131] Although we did not measure dietary diversity in all the communities, poor to moderate dietary diversity were observed in all of the communities. [26, 29, 33, 35, 38, 57]. This may have been due to their socio-economic status and food insecurity and may be a risk factor for CVD.

5.10.1 Added sugar intakes

An association between higher dietary sugar intakes and overweight/obesity and CDLs such as CVD exists. Increased dietary glycaemic load, caused by high sugar consumption, results in increased hepatic lipogenesis, dyslipidaemia,[132] and CVD. [133] Childhood overweight/obesity risk and morbidity were associated with consumption of sugar-sweetened beverages (SSBs) and highly processed foods and snacks. [54] The World Health Organisation recommends the intake of added sugar to be <10% of total energy intake. [134] More than 20% of the adults, elderly [57] and children in rural EC had high added sugar intakes whereas the children in peri-urban FS and urban Gauteng [33] had no added sugar intakes. Although SSB consumption has not been investigated in our studies, during the past 50 years, SBB consumption has increased [132] and SA is in the top 10 countries with the highest consumption of SSBs globally. [135]

5.10.2 Dietary fibre

Vegetables, legumes, whole grains and fruit all contribute to dietary fibre intake. Dietary fibre is differentiated as soluble (dissolves in water and forms a gel) and insoluble fibres. Good sources of soluble fibre are oats, citrus fruit, barley and legumes. It lowers LDL-C and glucose levels and, therefore, has a protective effect against CVD. [136] Lowering of cholesterol is achieved by the binding of fibre to bile acids, thereby escalating its excretion. This inhibits the production of cholesterol by the liver, resulting in lower blood cholesterol. [137] Food sources of insoluble dietary fibre include whole grains and vegetables. It cannot be fermented and promotes bowel movement and alleviates constipation. [138] A large majority (0–100%) of the children and adults in all our communities had low dietary fibre intakes. [24, 26, 29, 33, 34, 35, 38, 43, 44, 57] This may be due to the mainly refined carbohydrate-rich diet consumed by all these communities.

5.10.3 Dietary fats and fatty acids

Dietary fats consist mainly of cholesterol and fatty acids. Total dietary fat (% of total energy [TE]) intakes were higher than recommended for all the communities, ranging from 13.7% to 32.7% in urban Gauteng women and elderly respectively. [24, 26, 29, 32, 35, 36, 38, 39, 42, 43, 44, 57] High-fat diets cause an increase in postprandial triglyceride levels that are associated with risk of coronary heart disease (CHD). [139, 140] Fatty acids can be either protective against the development of CVD or can be risk factors for CVD. Saturated fatty acids (SFAs) and trans fatty acids (TFAs) have the greatest adverse effect on atherogenic cholesterol levels and are both associated with risk of CVD. [136, 141] Increased SFA intakes increase LDL-C levels. [142] TFAs have a HDL-C lowering effect and also increase LDL-C levels and, therefore, increase the risk of CVD.[47]. The contribution of TFA to CVD is a multiple pathway mechanism affecting lipid metabolism, increased inflammatory response and adiposity, and decreased endothelial function and insulin sensitivity. [143]

Dietary SFA intakes of <10% and TFAs of <1% of total energy intakes are recommended. [144] High TFA intakes were observed in less than 10% of our communities, except for the children in rural EC where the proportion of respondents with high intakes of TFAs was 36.7%. The proportion of the respondents that had high SFA intakes ranged from 18.6% to 42.9%. [24, 26, 32, 34, 37, 38, 42] The elderly (40.0%) [57] and peri-urban children (41.6% in Gauteng and 42.9% in the FS) [25, 29] had the highest prevalence of high TFA intakes (40.0%). Low-cost processed meats such as polony and Russians as well as chicken feet and heads were frequently consumed by our communities and may have contributed to the large intakes. Although there has been controversy about SFA intake and CVD risk, sufficient evidence exists that high SFA intakes cause increased LDL-C level by downregulating LDL receptors. [136]

PUFAs have a protective effect against CVD, specifically omega-6 PUFAs that significantly reduces total cholesterol and LDL-C levels as well as inflammatory markers. [145] High intakes of omega-3 PUFAs lowers the risk for myocardial infarction, CHD and CVD mortality and CVD events. [136] In addition, a diet rich in PUFA reduces the TC:HDL-C ratio and CHD incidence. [146] Linolenic acid (omega-3 fatty acid) and linoleic acid (omega-6 fatty acid) are essential fatty acids that cannot be physiologically produced and, therefore, need to be supplied by food sources. [147] Omega-3 decreases the risk of CVD by preventing thrombus formation, lowering blood pressure and protecting against irregular heart beat. [142] Replacing dietary carbohydrates and SFAs by an increased intake of omega-6 PUFAs lower LDL-C and increase HDL-C levels [148]. A large proportion of all of our communities had low PUFA intakes (33.0–100%), particularly for both omega-3 (93.1–100%) and omega-6 (2.4–29.7%) fatty acids. MUFA intakes were low in a large proportion of the participants (29.0–77.6%), except for the peri-urban children in Gauteng where only 4.8% of the children had low MUFA intakes. The majority of these children also showed high dietary cholesterol intakes (57.6%) whereas the rest of the study communities had relatively low prevalence (<20%) of high dietary cholesterol intakes. Because most of our communities live in poverty, it is questionable if they can afford oily fish, olive oil and the other MUFA and PUFA dietary sources, however, they do consume mostly sunflower oil, but in small quantities. [26, 29, 33, 34, 38, 57]

5.10.4 Dietary vitamin B6, B12 and folate intakes

Dietary sources of vitamin B6 include meat, fish, potatoes and bananas which are good sources. However, it is also present in nuts, whole grain, fortified cereal and leafy vegetables, chicken, legumes, non-citrus fruit, liver and soy products. [149, 150, 151, 152] The bioavailability differs according to food type, with pyridoxine glycoside as the least bioavailable. Vitamin B6 (5–75%) obtained from plant sources is in the form of glycosylated pyridoxine. [153, 154] Owing to the abundance of vitamin B6 in a variety of food sources, deficiency is not very common, however, in our communities, large proportions of the adults (79.1% in peri-urban FS Province and 85.7% urban women in Gauteng) and elderly (91.0%) [57] had low vitamin B6 intakes. Among the children, 36.7% of the rural and 24.8% of the peri-urban children in Gauteng showed low intakes of vitamin B6. Vitamin B6 deficiency often occurs in conjunction with other nutritional disorders and is associated with an increased risk of CVD. [155] Vitamin B6 not only has a homocysteine lowering effect, but is also needed for the metabolism of omega-3 PUFAs. [96]

Folate is the major determinant of homocysteiene [96] and thus has homocysteiene lowering effect. A recent meta-analysis showed that folic acid supplementation resulted in a 4% reduced risk for CVD events and the benefit was even greater among participants without pre-existing CVD or low folate levels. [156] Because folate cannot be physiologically synthesised, concentration depends on consumption. [65] All of our communities showed large proportions of participants (>40.0% ≤ 95.0%) with low dietary folate intakes. Green leafy vegetables, citrus fruit, legumes, yeast, liver and organ meats contain the highest concentration of folate. [155] Low intakes of these food items have been found in our studies. [25, 26, 29, 30, 31, 33, 35, 38, 43, 44, 57] Folate is omnipresent in nature, but heat and oxidation during food preparation and storage have a destructive effect and can destroy up to 50% of the original concentration. [157]

Vitamin B12, together with folate, plays a key role for the enzyme methionine synthase needed for the re-methylation of homocysteine to methionine. [96] Dietary sources of vitamin B12 are animal products (meat, fish, chicken, milk and cheese) and rarely found in plants or yeast. [158] Vitamin B12 is stored in large quantities in the liver and a deficiency is developed over years. [65] The majority of our communities showed large proportions of participants (≥60% ≤ 95.2%) with low intakes of vitamin B12, except for the peri-urban children in Gauteng where 14.4% of the participants had low vitamin B12 intakes. This may be mainly due to the mainly carbohydrate-based diet with low meat and cheese intakes.

5.10.5 Dietary sodium intakes

Sodium is an essential nutrient that is required for many physiological functions. [146] The daily physiological requirement for sodium is estimated at 0.1–1.0 gram. [159] High sodium intakes have been established as the major cause of hypertension in many epidemiological, experimental, controlled clinical and population trials. [160, 161] Sodium is mainly consumed as (a) salt (sodium-chloride) which is added during food preparation and cooking or at meal time, and (b) from sodium used in processed foods in SA. [162] Unfortunately we did not measure dietary sodium intakes in all our communities. Bread was identified as the largest contributor to salt intakes and that 41.0% of the South African population has a high salt intake. [162] Bread also consistently appeared in the top 20 most commonly consumed foods among our study communities [26, 29, 30, 31, 33, 34, 38, 43, 44, 57]. Another contributor to sodium intake in SA is sodium glutamate that is used as a condiment, [163] as well as salt in soup, gravy and spice mixes and powders, margarine and atchar, a spicy condiment, [163] biscuits/cookies, and breakfast cereals [164]. Stock cubes are regularly used for flavouring meat and vegetable dishes in SA [165, 166]. High stock cube consumption has also been observed in these communities by the authors.


6. Conclusions

In the studies reported among various communities, low education and employment status were observed as well as poverty in a large majority of the respondents. The scientific literature shows a strong association between poverty and CVD [163]. Poverty is an underlying factor of food insecurity that often results in poor dietary intakes that were observed in our communities. Many of the dietary CVD risk factors were present in large proportions of the communities. The literature is clear that these dietary factors may be associated with some of the risk factors for CVD, such as obesity, hypertension and the biochemical risk factors for CVD. Irreversible and potentially reversible and physiological (low income) risk markers were found to prevail. A summary of the elevated cardiovascular risk markers in our study is schematically presented in Figure 2. Multiple preventable CVR markers were present among the children, adults and elderly in rural, peri-urban and urban areas. It can thus be concluded that a double burden of poverty and risk of CVD exists across the different age groups and geographical locations in these resource-poor communities. Prevention of CVD can be achieved through nutrition education and awareness programs. It is recommended that policy makers give serious attention to CVR and screening should be done from an early age to identify those at risk and implement appropriate interventions.

Figure 2.

Cardiovascular risk factors prevalent among children, adults and the elderly.



We thank the National Research Foundation (NRF) and Vaal University of Technology (VUT) for financial support. Replamed (Cornel Pretorius) provided technical support, Prof A Egal, Centre of Sustainable Livelihoods (VUT) staff member and team members from the CARE research group for their operational support.


Conflict of interest

The authors have no conflict of interest to declare.


  1. 1. Bradshaw D, Nanna N, Pillay-van Wyk V, Laubscher R, Groenewald P, Dorrington RE. Burden of disease in South Africa: Protracted transitions driven by social pathologies. South African Medical Journal. 2019;109(11 Suppl 1):69-76. DOI: 10.7196/SAMJ.2019.v109illb.14273
  2. 2. Statistics South Africa (Stats SA). Towards measuring the extent of food security in South Africa: an examination of hunger and food adequacy. 2019. Pretoria: Stats SA.
  3. 3. Koch J. The food security policy context in South Africa. International Policy Centre for Inclusive Growth. 2019. Available from: [Accessed 2020-12-10]
  4. 4. Wight V, Kaushal N, Waldfoge, J, Garfinkel I. Understanding the link between poverty and food insecurity among children: Does the definition of poverty matter? Journal of Children and Poverty. 2014;20(1), 1-20. DOI: 10.1080/10796126.2014.891973
  5. 5. Walsh CM, van Rooyen FC. Household FS and Hunger in Rural and Urban Communities in the Free State Province, South Africa. Ecology of Food and Nutrition. 2015;54(2):118-137. DOI: 10.1080/03670244.2014.964230
  6. 6. Tacoli C. Food (in) security in rapidly urbanizing, low-income contexts. International Journal of Environmental Research and Public Health. 2017;14:1554. 8 pages.
  7. 7. United Nation’s Children’s Fund (UNICEF). Improving child nutrition: the achievable imperative for global progress. 2013. Available from: [Accessed 2020-12-14]
  8. 8. Vorster HH, Badham JB, Venter CS. An introduction to the revised food-based dietary guidelines for South Africa. South African Journal of Clinical Nutrition. 2013;26(3)(Suppl):S5-S12.
  9. 9. Naicker N, Mathee A, Teare J. Food insecurity in households in informal settlements in urban South Africa. Issues in public health. 2015;105(4). Available from: [Accessed 2020-12-08]
  10. 10. Global Nutrition Report 2020. Available from: file:///C:/Users/Dr.%20Oldewage/Downloads/Executive_Summary_2020_Global_Nutrition_Report.pdf. [Accessed 2020-12-16]
  11. 11. Wentzel-Viljoen E, Lee S, Laubscher R, Vorster HH. Accelerated nutrition transition in the North West Province of South Africa: results from the Prospective Urban and Rural Epidemiology (PURE-NWP_SA) cohort study, 2005-2010. Public Health Nutrition. 2018;21(14):2630-2641. DOI: 10.1017/S1368980018001118
  12. 12. Hills AP. Exercise: an integral and non-negotiable component of a healthy lifestyle. European Journal of Clinical Nutrition. 2018;72:1320-1322
  13. 13. Republic of South Africa. South African year book 2018-2019. Available from: [Accessed 2020-12-11]
  14. 14. The World Bank. Poverty. Available from:,poverty%20lines%20have%20been%20introduced [Accessed 2020-12-16]
  15. 15. Gooding HC, Gidding SS, Moran AE, Redmond N, Allen NB, Bacha F, Burns TL, Catov JM, Grandner MA, Harris KM, Johnson HM, Kiernan M, Lewis TT, Matthews KA, Monaghan, Robinson JG,Tate D, Bibbins‐Domingo K, Spring B. Challenges and Opportunities for the Prevention and Treatment of Cardiovascular Disease Among Young Adults: Report From a National Heart, Lung, and Blood Institute Working Group. Journal of American Heart Association. 2020. DOI:
  16. 16. Grimaccacia E, Naccarato A. Food insecurity individual experience: A comparison of economic and social characteristics of the most vulnerable groups in the world. Social Indicators Research.02019; 143: 391-410. DOI:
  17. 17. Goryakin Y, Rocco L, Suhrcke M. The contribution of urbanization to non-communicable diseases: Evidence from 173 countries from 1980 to 2008. Economics & Human Biology. 2017; 26:151-163.
  18. 18. Burger A, Pretorius R, Fourie CMT, Schutte AE. The relationship between cardiovascular risk factors and knowledge of cardiovascular disease in African men in North-West Province. Health SA Gesondheid. 2016; 21.
  19. 19. Müller I, Walter C, Du Randt R, et al. Association between physical activity, cardiorespiratory fitness and clustered cardiovascular risk in South African children from disadvantaged communities: results from a cross-sectional study. British Medical Journal Open Sport & Exercise Medicine. 2020; 6:e000823. DOI: 10.1136/bmjsem-2020-000823
  20. 20. Adeboye B, Bermano G, Rolland C. Obesity and its health impact in Africa: a systematic review. Cardiovascular journal of Africa. 2012;22(9):512-521.
  21. 21. Kelishadi R, Pour MH, Zadegan NS, Kahbazi M, Sadry G, Amani A, Ansari R, Alikhassy H, Bashardoust N. Dietary fat intake and lipid profiles of Iranian adolescents: Isfahan Healthy Heart Program – heart health promotion from childhood. Preventive Medicine. 2004;39 760-766.
  22. 22. Boodai SA, Cherry LM, Sattar N & Reilly JJ. Prevalence of cardiometabolic risk factors and metabolic syndrome in obese Kuwaiti adolescents. Diabetes, Metabolic Syndrome and Obesity: targets and therapy. 2014;7:505-511.
  23. 23. Martin L, Oepen J, Reinehr T, Wabitsch M, Glaussnitzer G, Waldeck E, Ingrisch S, Stachow R, Oelert M, Wiegand S & Holle R. Ethnicity and cardiovascular risk factors: evaluation of 40 921 normal-weight, overweight or obese children and adolescents living in Central Europe. International Journal of Obesity. 2015;39:5-51.
  24. 24. Oldewage-Theron, Egal AA, Grobler C. Lipid profile, hyperglycaemia, systemic inflammation and anthropometry as cardiovascular risk factors and their association with dietary intakes in children from rural Cofimvaba, Eastern Cape, South Africa. Journal of Consumer Sciences. 2017;2:1-15.
  25. 25. Egal A, Oldewage-Theron W. Association of micronutrients and child growth in children aged 7-15 years from Qwa-Qwa, South Africa. South African Journal of Clinical Nutrition.2017;4(1):1-5. DOI: 10.1080/16070658.2017.1392743.
  26. 26. Oldewage-Theron W, Kruger R. The association between diet quality and subclinical inflammation among children aged 6-18 years in the Eastern Cape, South Africa. Public Health Nutrition. 2016; 10 pages. DOI: 10.1017/S1368980016001956
  27. 27. Oldewage-Theron WH, Egal AA, Moroka T. Socio-economic factors as determinants of nutrition knowledge of adolescents in Cofimvaba, Eastern Cape of South Africa. African Journal of Physical, Health Education, Recreation and Dance. 2014; 20(3:1):858-869.
  28. 28. Otitoola O, Oldewage-Theron W, Egal A. Prevalence of overweight and obesity among selected schoolchildren and adolescents in Cofimvaba, South Africa. South African Journal of Clinical Nutrition. 2020:6 pages.
  29. 29. Nyathela T. Impact of a school feeding programme on the nutritional status of primary school children in Orange Farms. 2009. MTech dissertation. Vanderbijlpark: Vaal University of Technology (VUT), SA.
  30. 30. Oldewage-Theron WH, Dicks EG, Napier CE. Poverty, household food insecurity and nutrition: Coping strategies in an informal settlement in the Vaal Triangle, South Africa. Public Health. 2006:120:795-804.
  31. 31. Oldewage-Theron WH, Dicks EG, Napier CE, Rutengwe R. Situation analysis of an informal settlement in the Vaal Triangle. Development South Africa. 2005;22(1):13-26.
  32. 32. Oldewage-Theron W, Napier C, Egal A. Dietary fat intake and nutritional status indicators of primary school children in a low-income informal settlement in the Vaal region. South African Journal of Clinical Nutrition. 2011;24(2):99-104.
  33. 33. Napier C. Evaluation of a school feeding programme for primary school children in an informal settlement. 2006. DTech thesis. Vanderbijlpark: Vaal University of Technology (VUT), SA.
  34. 34. Oldewage-Theron WH, Egal AA. A cross-sectional baseline survey investigating the relationship between dietary diversity and cardiovascular risk factors in women from the Vaal Region, South Africa. Journal of Nursing Education and Practice. 2014; 4(1):50-62.
  35. 35. Oldewage-Theron WH, Kruger R, Egal AA. Socio-economic variables and nutrient adequacy of women in the Vaal Region of South Africa. Ecology of Food and Nutrition. 2014;53:514-527. DOI: 10.1080/03670244.2013.873423
  36. 36. Oldewage-Theron W, Slabbert TJC. Depth of poverty in an informal settlement in the Vaal Region, South Africa. Health SA Gesondheid. 2010;15(1):6 pages. DOI: 10.4102/hsag.v15I.456
  37. 37. Oldewage-Theron WH, Egal AA. Prevalence of and contributing factors to dyslipidaemia in low-income women aged 18-90 years in the peri-urban Vaal region. South African Journal of Clinical Nutrition. 2013;26(1):23-28.
  38. 38. Oldewage-Theron W, Kruger R, Egal A. Diet quality in peri-urban settlements: South Africa. In: Preedy VR, Hunter LA, Patel VB, editors. Diet quality. Vol 2. New York: Springer Science + Business Media; 2013. p. 281-297. DOI: 10.1007/978-1-4614-7315-2_20
  39. 39. Oldewage-Theron W, Egal. The effect of consumption of soy foods on metabolic syndrome in women: a case study from peri-urban Qwa-Qwa, South Africa. South African Journal of Clinical Nutrition. 2018;1(1):1-6. DOI: 10.1080/16070658.2018.1438340
  40. 40. Oldewage-Theron W, Egal AA, Grobler C. Is overweight and obesity associated with iron status in low-income men and women? A case study from Qwa-Qwa, South Africa. Integrated Food, Nutrition and Metabolism. 2014;4 pages. DOI: 10.15761/IFNM.1000110
  41. 41. Otitoola O, Oldewage-Theron W, Egal A. Trends in the development of obesity in elderly day care attendees in Sharpeville, South Africa, from 2007-2011. South African Journal of Clinical Nutrition. 2015;28(1):12-17.
  42. 42. Oldewage-Theron WH, Egal AA, Grobler C. Metabolic syndrome of free-living elderly from Sharpeville, South Africa: A prospective cohort study with 10-year follow-up. Journal of Aging Research and Clinical Practice. 2018;7:100-106. DOI: 10.14283/jarcp.2018.18
  43. 43. Oldewage-Theron WH, Salami L, Zotor FB, Venter C. Health status of an elderly population in Sharpeville, South Africa. Health SA Gesondheid. 2008;13(3):3-17.
  44. 44. Oldewage-Theron WH, Duvenage SS, Egal AA. Situation analysis as indicator of food security in low-income rural communities. Journal of Family Ecology and Consumer Sciences. 2012;40:38-58.
  45. 45. World Health Organization (WHO). Country profile: South Africa. 2016. Available from: [Accessed 2020-12-11]
  46. 46. National Department of Health (NDoH), Statistics South Africa (Stats SA), South African Medical Research Council (SAMRC), and ICF. South Africa Demographic and Health Survey 2016. Pretoria: NDoH.
  47. 47. Walli-Attaei M, Joseph P, Rosengren A, Chow CK, Rangorjan S, Lear SA, Habib KFA, Davletov K, Dans A, Lanas F, Yeates K, Poirier P, Teo KK, Bahonar A, Camilo F, Chifamba J, Diaz R, Diolkowska JA, Irazola V, Ismail R, Kour M, Khatib R, Liu X, Mańczuk M, Miranda JJ, Oguz A, Perez-Mmayorga M, zuba A, Tsolekile LP, Varma RP, Yusufali A, Yusuf R, Wei L, Anand SS, Ysug F. Variations between women and men in risk factors, treatments, cardiovascular disease incidence and death in 27 high-income, middle income and low0income countries (PURE): a prospective cohort study. The Lancet. 2020; 396(0244):97-109.
  48. 48. Kristian Thygesen, Joseph S. Alpert, Allan S. Jaffe, Maarten L. Simoons, Bernard R. Chaitman and Harvey D. White. Third Universal Definition of Myocardial Infarction. Circulation. 2012.
  49. 49. Novella S, Laguna-Fernández A, Lázaro-Franco M, Sobrino A, Bueno-Beti C, Tarin JJ, Monsalve E, Sanchis J, Hermenegildo C. Estradiol Acting through estrogen receptor alpha, restores dimethylaminohydrolase activity and nitric oxide production in oxLDL-treated human arterial endothelial cells.Molecular and Cellular Endrocrinology. 2013; 365(1):11-16 DOI:
  50. 50. Rosengren A, Smyth A, Rangarajan S, Ramasundarahettige C, Bangdiwala SI, AlHabib KF, Avezum A, Boström KB, Chifamba J, Hulec S, Gupta R, Igumbor EU, Iqbal R, Ismail N, Joseph P, Kaur M, Khatib R, Kruger IM, Lamelas P, Lanas F, Lear SA, Li W, Wang C, Quiang D, Wang Y, Lopez-Jaramillo, Mohammadifard N, Mohan V, Mony PK, Poirier P, Srilatha S, Szuba A, Tea K, Wielgosz A, Yeates KE, Yusoff K, Yusuf R, Yusufali AH, Attqei MW, McKee M, Yusuf S. Socioeconomic status and risk of cardiovascular disease in 20 low-income, middle-income, and high-income countries: the Prospective Urban Rural Epidemiology (PURE) study. The Lancet. 2019;7:e748-3760.
  51. 51. Egidija Rinkūnienė ,Petrulioniene Z, Dzenkeviciute V, Gimzauskaite S, Mainelis A, Puronaite R, Juceviciene A, Gargalskaite U, Laucevicius A. Trends in Cigarette Smoking among Middle-Aged Lithuanian Subjects Participating in the Primary Prevention Program between 2009 and 2016. Medcina. 2019; 55(5):130. DOI:
  52. 52. Mudau M, Genis M, Lochner A, Strijdom H. Endothelial dysfunction: the early predictor of atherosclerosis. Cardiovascular Journal of Africa. 2012; 23(4): 222-231. DOI: doi: 10.5830/CVJA-2011-068
  53. 53. Otang-Mbeng W, Otunola GA, Afolayan AJ. Lifestyle factors and co-morbidities associated with obesity and overweight in Nkonkobe Municipality of the Eastern Cape, South Africa. Journal of Health, Population ad Nutrition. 2017;36:22. DOI: 10.1186/s41043-017-0098-9
  54. 54. Danquah FI, Ansu-Mensah M, Bawontu V, Yeboah M, Udoh RH, Tahiru M, Kuupiel D. Risk factors and morbidities associated with childhood obesity in sub-Saharan Africa: a systematic scoping review. BMC Nutrition. 2020;6:37. DOI: 10.1186/s40795-020-00364-5
  55. 55. Norris T, Cole TJ, Bann D, Hamer M, Hardy R, Li L, Ong KK, Ploubidis GB, Viner R, Johnson W. Duration of obesity exposure between ages 10 and 0 years and its relationship with cardiometabolic disease risk factors: A cohort study. PLOS Medicine. 2020;17(12):e1003387. DOI: 10.1371/journal.pmed.1003387
  56. 56. Kastorini, C.M., Milionis, H.J., Goudevenos, J.A. and Panagiotakos, D.B. Mediterranean diet and coronary heart disease: Is obesity a link? - A systemic review. Nutrition, Metabolism & Cardiovascular Diseases. 2010. 20: 536-551.
  57. 57. CJ Grobler. Impact of vitamins B12, B6 and folate supplementation on the cardiovascular risk markers in an elderly community of Sharpeville. 2016. D Tech thesis. Durban: Durban University of Technology (DUT), SA.
  58. 58. Craig E, Reilly JJ, Bland R. Risk factors for overweight and overfatness in rural South African children and adolescents. Journal of Public Health. 2016;38(1):24-33. DOI: 10.1093/pubmed/fdv016
  59. 59. Kimani-Murage EW, Kahn K, Pettifor JM, Tollman SM, Klipstein-Grobusch K, Norris SA. Predictors of adolescent weight status and central obesity in rural South Africa. Public Health Nutrition. 2011;14(6):1114-1122.
  60. 60. World Health Organization. Body mass index. Available from: [Accessed 2020-12-16]
  61. 61. NCEP (National Cholesterol Education Program. Expert panel on Detection, Evaluation and Treatment of High blood Cholesterol in Adults. Executive Summary of the Third Report of the National Cholesterol Education Program (NCEP) Adult Treatment Panel (ATP III). 2002
  62. 62. Tahmasebi H, Trajcevski K, Higgins V, Adeli K. Influence of ethnicity on population referencevalues for biochemical markers. Critical Reviews in Clinical Laboratory Science. 2018; 55(5). DOI:
  63. 63. Rouvre, M., Vol, S., Gusto, G., Born, C., Lantieri, O., Tichet, J. and Lecomte, P. Low high density lipoprotein cholesterol: Prevalence and associated risk-factors in a large French population. Annals of Epidemiology. 2011; 21(2): 118-127.
  64. 64. Seedat YK, Rayner BL, Veriava Y. South African hypertension practice guideline 2014. Cardiovascular Journal of South Africa. 2014;25(6):288-294. DOI: 10.5830/CVJA-2014-062
  65. 65. Hoffbrand AV, Moss, PAH. Essential Haematology. 6th ed. Oxford: Blackwell publishing Ltd. 2011.
  66. 66. Ichihara K, Ozarda Y, Barth JH, Klee G, Shimizu Y, Xia L, Hoffman M, Shah S, Matsha T, Wassung J, Smit F, Ruzhanskaya A, Straseski J, Bustos DN, Kimura S, Takahashi A. A global multicenter study on reference values: Exploration of sources of variation across the countries. Clinica Chimica Acta. 2017; 467:83-97. DOI:
  67. 67. Wang Y, Chen W, Hu C, Wen X, Pan J, Xu F, Zhu Y, Shao X, Shangguan X, Fan L, Sha J, Wang Z, Cai Y, Liu Q, Dong B, Xue W. Albumin and Fibrinogen combined prognostic grade predicts prognosis of patients with prostate cancer. Journal of Cancer. 2017; 8(19):3992-4001. DOI:
  68. 68. Babic B, Tagkalos E, Gockel I, Corvinus F, Hadazijusufovic E, Hoppe-Lotichius M, Lang zh, vd Sluis PC, Grimminger PP. C-reactive protein levels after Esopagectomy are associated withincreased surgical trauma and complications. The Annals of Thoracic Surgery. 2020; 109(5): 1574-1583. DOI:
  69. 69. Frithioff-Bojsoe C, Lund MAV, Kloppenborg JT, Nielsen TTH, Fonvig CE, Lausten-Thomsen U, Hedley PL, Hansen T, Pedersen OB, Christiansen M, Baker JL, Hansen T, Holm J-C. Glucose metabolism in children and adolescents: Population based reference values and comparisons to children and adolescents enrolled in obesity treatment. Pediatric Diabetes. 2019;
  70. 70. Strohle A, Richter M, Gonzalez-Gross M, Neuhauser-Berthold M, Wagner K-H, Leschik-Bonnet E, Egert S, The revised D-A-CH-Reference values for the intake of vitaminB12: Preventionof deficiency and beyond. Molecular Nutrition & Food Research. 2019; DOI:
  71. 71. Adom T, Kengne AP, de Villiers A, Puoane T. Prevalence of overweight and obesity among African primary school learners: A systematic review and meta-analysis. Obesity Science & Practice. 2019:487-502. DOI: 0.1002/osp4.355
  72. 72. Pretorius SS, Neophytou N, Watson ED. Anthropometric profiles of 8-11 year old children from a low-income setting in South Africa. BMC Public Health. 2019;19(1):314. DOI: 10.1186/s12889-019-6530-x
  73. 73. Reddy SP, Resnicow K, James S, Funani IN, Kambaran NS, Omardien RG, Masuka P, Sewpaul R, Vaughan RD, Mbewu A.Rapid increases in overweight and obesity among South African adolescents: comparison of data from the South Africa National Youth Risk Behaviour Survey in 2002 and 2008. American Journal of Public Health. 2012;102(2):262-268. DOI: 10.2105/AJPH.2011.300222
  74. 74. Ganji V, Kafai MR. Population reference values for serum Methylmalonic Acid concentration and its relationship with age, sex, race, -ethnicity, supplement use, kidney function and serum vitamin B12 in the post- folic acid fortification period. Nutrients. 2018; 10(1), 74. DOI:
  75. 75. World Health Organization. Training course on child growth assessment. Interpreting growth indicators. 2008. Available from: [Accessed 2020-12-16]
  76. 76. United States Department of Health and Human Services (DHHS), National Institutes of Health (NIH), National Heart, Lung and Blood Institute. Expert Panel on Integrated Guidelines for Cardiovascular Health and Risk Reduction in Children and Adolescents. “Expert panel on integrated guidelines for cardiovascular health and risk reduction in children and adolescents: summary report.” 2012. NIH Publication No.12-7486. Washington DC: NIH.
  77. 77. Shisana O, Labadarios D, Rehle T, Simbayi L, Zuma K, Dhansay A, Reddy P, Parker W, Hoosain E, Naidoo P, Hongoro C, Mchiza Z, Steyn NP, Dwane N, Makoae M, Maluleke T, Ramlagan, S, Zungu N, Evans MG, Jacobs L, Faber M, SANHANES-1 Team, The South African National Health and Nutrition Examination Survey, 2012: SANHANES-1: the health and nutritional status of the nation. 2014. Available from: [Accessed 2020-12-13]
  78. 78. Akpa OM, Made F, Ojo A, Ovbiagele, Adu D, Motala AA, Mayosi BM, Adebamowo SN, Engel ME, Tayo B, Rotimi C, Salako B, Akinyemi R, Gebregziabher M, sarfo F, Wahab K, Agongo G, Alberts M, Ali SA, Asiki G, Boua RP, Gómez-Olivé FX, Mashinya F, Micklesfield L, Mohamed SF, Nonterah EA, Norris SA, Sorgho H, Tollman S, Parekh RS, Chishala C, Ekoru K, Waddy SP, Peprah E, Mensah GA, Wiley K, Troyer J, Ramsay M, Owolabi MO as members of the CVD Working Group of the H3Africa Consortium. Regional patterns and association between obesity and hypertension in Africa. Evidence from the H3Africa CHAIR study. Hypertension. 2020;75:1167-1178. DOI: 10.1161/hypertensionaha.119.14147
  79. 79. Gidding SS, Robinson J. It is now time to focus on risk before age 40. Journal of the American College of Cardiology. 2019;74(3). DOI: 10.1016/j.jacc.2019.04.064
  80. 80. Ware LJ, Chidumwa G, Charlton K, Schutte AE, Kowal P. Predictors of hypertension awareness, treatment and control in South Africa: results from the WHO-SAGE population survey (Wave 2). Journal of Human Hypertension. 2019;33:157-166.
  81. 81. Georgiev AM, Krajnovi D, Kotur-Stevuljevi J, Ignjatovi S, Valentina Marinkovi V. Undiagnosed hyperglycaemia and hypertension as indicators of the various risk factors of future cardiovascular disease among population of Serbian students. Journal of Medical Biochemistry. 2018; 37: 289-298. DOI:
  82. 82. Di Meo S, Lossa S, Venditti P. Improvement of obesity-linked skeletal muscle insulin resistance by strength and endurance training. Journal of Endocrinology. 2017; 234(3):R159-R181. DOI: 10.1530/JOE-17-0186
  83. 83. Grinnan D, Farr G, Fox G, Sweeney. The role of Hyperglycemia and Insulin resistance in the development and progression of pulmonary arterial hypertension. Journal of diabetes research. 2016; DOI:
  84. 84. Karachaliou F, Simatos G, Simatau A. The challenges in the development of diabetes prevention and Care models in low-income settings. Frontiers in Endocrinology. 2020; 11:518. DOI:
  85. 85. Kearney K, Tomlins D, Smith K, Ajjan R. Hypofibrinolysis in diabetes: a therapeutic for the reduction of cardiovascular risk. Cardiovascular Diabetology. 2017;34. DOI: 10.1186/s12933-017-0515-9
  86. 86. Patterson CC, Karuranga S, Salpea P, Saeedi P, Dahlquist G, Soltesz G, Ogle GD. Worldwide estimates of incidence, prevalence and mortality of type 1 diabetes in children and adolescents: Results from the International Diabetes Federation Diabetes Atlas, 9th edition. Diabetes Research and Clinical Practice. 2019.
  87. 87. Animaw W, Seyoum Y. Increasing prevalence of diabetesmellitus in a developing country and its related factors. PLOS ONE. 2017. DOI:
  88. 88. Faxaly L. Imaging Methods for Haemostasis Research. Sweden: LiU- Tryck, Linköping. 2009
  89. 89. Russo, I. The Prothrombotic Tendency in Metabolic Syndrome: Focus on the Potential Mechanisms Involved in Impaired Haemostasis and Fibrinolytic Balance. Scientifica. 2012. 525374:117.
  90. 90. Kaptoge S, White IR, Thompson SG, Wood AM, Lewington S, Lowe GDO, Danesh J, Kostis JB, Wilson AC, Folsom AR, Chambless L, Benderly M, Goldbourt U, Willeit J, Kiechl S, Yarnell JWG, Sweetnam PM, Elwood PC, Cushman M, Psatyr BM, Tracy P, Tybjærg-Hansen, Haverkate F, de Maat MPM, Fowkes FGR, Lee AJ, Smith FB, Salomaa V, Harald K, Rasi V, Vahtera E, Jousilahti P, Pekkanen D’Agostino JR, Kannel WB, Wilson PWF, Tofler G, Levy Marchioli DR, Valagussa F, Rosengren A, Wilhelmsen L, Lappas,. Eriksson H, Cremer P,Nagel D, Curb JB, Rodriguez B, Yano K, The Fibrinogen Studies Collaboration. Associations of plasma fibrinogen levels with established cardiovascular disease risk factors, inflammatory markers, and other characteristics: Individual participants’ meta-analysis of 154 211 adults in 31 prospective studies. American Journal of Epidemiology. 2007. DOI:
  91. 91. Pieters M, Wolkberg AS. Fibrinogen and fibrin: An illustrated review. Research and practice in Thrombosis and Haemostasis. 2019 DOI:
  92. 92. Cronje HT, Nienaber-Rousseau C, Zandberg L, de Lange Z, Green FR, Pieters M. Fibrinogen and clot-related phenotypes determined by fibrinogen polymorphisms: Independent and IL-6 interactive associations. 2017. DOI:
  93. 93. Antoniades, C., Antonopoulos, A.S., Tousoulis, D., Marinou, K. and Stefanadis, C. 2009. Homocysteine and coronary atherosclerosis: from folate fortification to the recent clinical trials. European Heart Journal. 30: 6-15Kaul, S., Zadeh, A.A. and Shah, P.K. 2006. Homocysteine hypothesis for atherothrombotic cardiovascular disease. Journal of the American College of Cardiology. 48(5): 914-923.
  94. 94. Aghayan SS, Farajzadeh A, Bagheri-Hosseinabadi Z, Fadaei H, Yarmohammadi M, Jasarisani M. Elevated homocysteine, as a biomarker of cardiac injury, in panic disorder patients due to oxidative stress. 2020; ODI:
  95. 95. Chouksey D, Ishar HS, Jain R, Athale S, Sodani A. Association between Serum Homocysteine Levels and Methylene‑Tetrahydrofolate‑Reductase Gene Polymorphism in Patients with Stroke: A Study from a Tertiary Care Teaching Hospital from Central India. Journal of Medical Science. 2020; DOI: 10.4103/jmedsci.jmedsci_170_20
  96. 96. Dobrynina LA, Kalashnikova LA, Shabalina AA, Kostyreva MV, Aleksandrova EV, Gafarova ME, Shamtieva KV. Indicators of homeostasis, inflammation, and homocysteine in ischemic stroke in the young age. 2017; 117(12.Vyp.2):25-33. DOI:
  97. 97. Esse R, Barroso M, de Almeida IT, Catro R, Contribution of Homocysteine metabolism disruption to endothelial dysfunction: State-of-the-Art. International Journal of Molecular Science. 2019; 20(4):867. DOI:
  98. 98. McCully, K.S. 1969. Vascular pathology of homocysteinemia: implications for the pathogenesis of arteriosclerosis. The American Journal of Pathology. 56(1):111-128.
  99. 99. Acampa M, Lazzerini PE, Martini G. Postoperative arterial fibrillation and ischemic stroke: The role of homocysteine. European stroke journal. 2017; DOI:
  100. 100. Zhang X, Huang Z, Xie Z, Chien Y, Zheng Z, Wei X, Huang B, Shan Z, Liu J, Fan S, Chen J, Zhao F. Homocysteine induces oxidative stress and ferroptosis of nucleus pulposus via enhancing methylation of GPX4. Free radical Biology and Medicine. 2020; 160:552-565. DOI:
  101. 101. Chen C, Yang W-C, Hsiao Y-H, Huang S-C, Huang Y-C, High homocysteine, low vitamin B-6, and increased oxidative stress are independently associated with the risk of chronic kidney disease. Nutrition. 2016; 32(2):236-241. DOI:
  102. 102. Wang W-M, Jin H-Z. Homocysteine: A potential common route for cardiovascular risk and DNA methylation in Psoriasis. Chinese Medicine Journal. 2017; Aug 20 130(16):1980-1986. DOI: 10.4103/0366-6999.211895
  103. 103. Moreira, E.S., Brasch, N.E. and Yun, J. Vitamin B12 protects against superoxide-induced cell injury in human aortic endothelial cells. Free Radical Biology & Medicine. 2011: 51: 876-883
  104. 104. Bourgonje AR, Abdulle AE, Al-Rawas AM, Al-Maqbali M, Al-Saleh M, Enriquez MB, Al-Siyabi S, Al-Hashmi K, A-Lawati I, Bulthuis MLC, Mulder DJ, Gordijn SJ, van Goor H, Saleh J. Systemic oxidative stress is increased in postmenopausal women and independently associates with homocysteine levels. International Journal of Molecular Science. 2020; 21(1):314. DOI:
  105. 105. Ye, X., Maras, J.E., Bakun, P.J. and Tucker, K.L. Dietary intake of vitamin B6, plasma Pyridoxal 5’-Phosphate, and homocysteine in Puerto Rican adults. Journal of American Dietetic Association. 2010; 110(11):1660-1668.
  106. 106. Adekunle, A.S. and Adedeji, A.L. Anti-atherogenic effects of supplementation with vitamin B6 (Pyridoxine) in albino rats. African Journal of Biochemistry Research. 2011; 5(13):352355.
  107. 107. Zhao, R., Diop-Bove, N., Visentin, M. and Goldman, I.D. Mechanisms of membrane transport of folates into cells and across epithelia. Annual review of nutrition. 2011: 31
  108. 108. Huang, R. S., Hu, G. Q., Lin, B., Lin, Z. Y., and Sun, C.C. MicroRNA-155 silencing enhances inflammatory response and lipid uptake in oxidized low-density lipoprotein-stimulated human THP-1 macrophages. Journal of Investigative Medicine. 2010; 58(8):961-967.
  109. 109. Lotto, V., Choi, S-W. and Friso, S. Vitamin B6: a challenging link between nutrition and inflammation in CVD. British Journal of Nutrition. 2011; 106:183-195.
  110. 110. Titcomb TJ, Schmaelzle ST, Nuss ET, Gregory JF, Tanumihardjo SA. Suboptimal vitamin B intakes of Zambian Preschool children: Evaluation of 24-hour dietary recalls. Food and Nutrition Bulletin. DOI:
  111. 111. Imamura, A., Murakami, R., Takahashi, R., Cheng, X.W., Numaguchi, Y., Murohara T. and Okumura, K. Low folate levels may be an atherogenic factor regardless of homocysteine levels in young health nonsmokers. Metabolism Clinical and Experimental. 2010; 59:728-733.
  112. 112. Abbenhardt, C., Miller, J.W., Song, X., Brown, E.C., Cheng, T.Y., Wener, M.H., Zheng, Y., Toriola, A.T., Neuhouser, M.L., Beresford, S.A.A., Makar, K.W., Baily, L.B., Maneval, D.R., Green, R., Manson, J.E., Van Horn, L. and Ulrich, C.M. Biomarkers of one-carbon metabolism are associated with biomarkers of inflammation in women. The Journal of Nutritional Epidemiology. 2014; 144(5) :714-721
  113. 113. Fenech, M. 2012. Folate (vitamin B9) and vitamin B12 and their function in the maintenance of nuclear and mitochondrial genome integrity. Mutation Research / Fundamentals and Molecular Mechanisms of Mutagenesis. 2012; 733:21-33
  114. 114. Ganeshan, S., Kartihumar, B.A., Viswanath, A., Renjith, A. and Alin, B. Effect of folic acis on serum homocysteine levels in patients with Cardiovacular disease (CVD). Journal of Chemical and Pharmaceutical Research. 2014; 6(3):1141-1148
  115. 115. Riedel, B. M., Molloy, A. M., Meyer, K., Fredriksen, Å., Ulvik, A., Schneede, J., Nexø, E., Hoff, G. and Ueland, P. M. Transcobalamin polymorphism 67A-> G, but not 776C-> G, affects serum holotranscobalamin in a cohort of healthy middle-aged men and women. The Journal of Nutrition. 2011.;141(10):1784-1790.
  116. 116. Lieberman, M. & Marks, A.D. 2013. Marks’ Basic Biochemistry: a Clinical Approach. 4th ed. Baltimore, Maryland: Lippincott Williams & Wilkins.
  117. 117. Jelkmann, W. The disparate roles of cobalt in erythropoiesis, and doping relevance. Open Journal of Hematology. 2012; 3:2-9
  118. 118. Scheitl CPM, Ghaem Maghami M, Lenz AK, et al. Site-specific RNA methylation by a methyltransferase ribozyme. Nature 2020; 587, 663-667.
  119. 119. Pepper, M.R., Black, M.M. B12 in fetal development. Seminars in Cell & Developmental Biology. 2011; 22:619-623.
  120. 120. Froese DS, Fowler B, Baumgartner MR. Vitamin B12, folate, and the methionine remethylation cycle- biochemistry, pathways, and regulation. Journal of Inherited Metabolic Disease. 2018; DOI:
  121. 121. Sedding DG, Boyle EC, Demandt JAF, Sluimer JC, Dutzmann J, Haverich A, Bauersachs J. Vasa Vasorum Angiogenesis: Key player in the initiation and progression of Atherosclerosisand petential target for the treatment of cardiovascular disease. Immunology. 2018; DOI:
  122. 122. Guzik TJ, Touyz RM, Oxidative stress, inflammation, and vascular aging in hypertension. Hypertension. 2017 70(4):660-667. DOI:
  123. 123. Eltoft A, Arntzen KA, Hansen J-B, Wilsgaard T, Mathiesen EB, Johnsen SH. C-Reactive proetein in atherosclerosis- A risk marker but not a causal factor? A 13-year population-based longitudinal study: The Tromso study. Atheroscvlerosis. 2017;263:293-300. DOI:
  124. 124. Elci E, Kaya C, Cim N, Yildizhan R, Elci GG. Evaluation of cardiac risk marker levels in obese and non-obese matients with polycystic ovaries. Gynecological Endocrinology. 2017; 33(1). DOI:
  125. 125. Noubiap JJ, Bigna JJ, Nansseu JR, Nyaga UF, Balti EV, Echouffo-Tcheugui JB, Kengre AP. Prevalence of dyslipidaemia among adults in Africa: a systematic review and meta-analysis. The Lancet. 2018;6(9): E998-E1007. DOI:
  126. 126. Reiger S, Jardim TV, Abrahams-Gessel S, Crowther NJ, Wade A, Gomez F.X, Salomon J, Tollman S, Gaziano TA. Awareness, treatment, and control of dyslipidaemia in South Africa: The HAALSI (Health and Aging in Africa: A Longitudinal Study of an INDEPTH Community in South Africa) study. Plos One. 2017. DOI:
  127. 127. Sliwa K, Lecour S, Carrington MJ, Stewart S, Lyons JG, Stewart S, Marais AD, Raal FJ. Different lipid profiles according to ethnicity in the Heart of Soweto study cohort of de novo presentations of heart disease. Cardiovascular Journal of Africa. 2012 Aug; 23(7): 389-395. DOI:
  128. 128. Levitt, N.S., Steyn, K., Dave, J. and Bradshaw, D. Chronic noncommunicacle diseases and HIV-AIDS on a collision course: relevance for health care deliveray, particularly in lowresource settings-insight from South Africa. American Journal of Clinical Nutrition. 2011.; 94(suppl):1690S-1696S.
  129. 129. Raal, F.J., Blom, D.J., Naidoo, S., Bramlage, P. and Brudi, P. Prevalence of dyslipidaemia in statin-treated patients in South Africa: results of the DYSlipidaemia International Study (DYSIS). Cardiovascular Journal of Africa. 2013; 24(8):330-338
  130. 130. Navab, M., Reddy, S.T., Van Lenten, B.J. and Fogelman, A.M. HDL and cardiovascular disease: atherogenic and atheroprotective mechanisms. Nature Reviews Cardiology. 2011; 8(4):222232.
  131. 131. Azadbakht L, Mirmiran P, Esmaillzadeh A, Azizi F. Dietary diversity score and cardiovascular risk factors in Tehranian adults. Public Health Nutrition. 2005:9(6):728-736. DOI: 10.1079/PHN2005887
  132. 132. De Salvo KB, Olson R, Casavale KO. Dietary guidelines for Americans. Journal of the American Medical Association. 2016;315:457-458.
  133. 133. Te Morenga LA, Howatson AJ, Jones RM, Mann J. Dietary sugars and cardiometabolic risk: systematic review and meta-analyses of randomized controlled trials of the effects on blood pressure and lipids. American Journal of Clinical Nutrition. 2014;100:65-79.
  134. 134. World Health Organization. Guideline: sugar intakes for adults and children. 2015. Available from: [Accessed 2020-12-10]
  135. 135. Vorster HH, Kruger A, Wentzel-Viljoen E, Kruger, HS, Margetts, BM. Added sugar intake in South Africa: findings from the Adult Prospective Urban and Rural Epidemiology cohort study. American Journal of Clinical Nutrition. 2014;99:1479-1486.
  136. 136. Sikand G, Severson T. Top 10 dietary strategies for atherosclerotic cardiovascular risk reduction. American Journal of Preventive Cardiology. 2020;4:100106. DOI: 10.1016/j.ajpc.2020.100106
  137. 137. Yanai, H., Katsuyama, H., Hamasaki, H., Abe, S., Tada, N. and Sako, A. Effects of Carbohydrate and Dietary Fiber Intake, Glycemic Index and Glycemic Load on HDL Metabolism in Asian Populations. Journal of Clinical Medicine Research. 2014; 6(5):321-326.
  138. 138. Kurniawan, I. and Simadibrata, M. Management of chronic constipation in the elderly. The Elderly. 2011. 43(3):195-205
  139. 139. Skeaff CM, Miller J. Dietary fat and coronary heart disease: Summary of evidence from prospective cohort and randomised controlled trials. Annals of Nutrition and Metabolism, 2009;55(1-3):173-201.
  140. 140. Chowdhury R, Warnakula S, Kunutsor S, Crowe F, Ward HA, Johnson L, Franco OH, Butterworth AS, Forouhi NG, Thompson SG, Khaw KT, Mozaffarian D, Danesh J, Di Angelantonio E. Association of dietary, circulating, and supplement fatty acids with coronary risk: A systematic review and meta-analysis. Annals of Internal Medicine. 2014;160(6):398-406.
  141. 141. Steyn N, Eksteen G, Senekal M. Assessment of the dietary intake of schoolchildren in South Africa: 15 years after the First National Study. Nutrients. 2016;8:509. DOI: 10.3390/nu8080509
  142. 142. Vannice, G. and Rasmussen, H. Position of the academy of nutrition and dietetics: dietary fatty acids for healthy adults. Journal of the Academy of Nutrition and Dietetics. 2014; 114(1):136-153.
  143. 143. Drouin-Chartier J-P, Tremblay AJ, Lepine M-C, Lemelin V, Mamarche B, Couture P. Substitution of dietary ω-6 polyunsaturated fatty acids for saturated fatty acids decreases LDL apolipoprotein B-100 production rate in men with dyslipidaemia associated with insulin resistance: a randomised control trial. The American Journal of Clinical Nutrition. 2018; 107(1):26-34. DOI:
  144. 144. Food and Agriculture Organization of the United Nations. Fats and fatty acids in human nutrition. FAO food and nutrition paper 91. Available from: [Accessed 2020-12-01]
  145. 145. Saks FM, Campos H. Editorial: Polyunsaturated fatty acids, inflammation, and cardiovascular disease: Time to widen our view of the mechanisms. The Journal of Clinical Endocrinology and Metabolism. 2006;91(2):398-400. DOI: 10.1210/jc.2005-2459
  146. 146. Anand SS, Hawkes C, de Souza RJ, Mente A, dehgan M, Nugent R, Zulyniak MA, Weis T, Bernstein AM, Krauss RM, Kromhout D, Jenkins DJA, Malik V, Martinez-Gonzalez MA, Mozaffarian D, Yussuf S, Willett WC, Popkin BM. Food consumption and its impact on cardiovascular disease: Importance of solutions focused on the globalized food system. Journal of the American College of Cardiology. 2015;66(14). DOI: 10.1016/j.jacc.2015.07.050
  147. 147. Saini RK, Keum Y-S. Omega -3 and omega-6 polyunsaturated fatty acids: Dietary sources, metabolism, and significance-A review. Life Sciences. 2018; 203:255-267. DOI:
  148. 148. DiNicolantonio JJ, J O’Keefe JH. Omega-6 vegetable oils as a driver of coronary heart disease: the oxidized linoleic acid hypothesis. Open Heart. 2018; DOI:
  149. 149. Dhalla, N.S., Takeda, S. and Elimbam, V. Mechanisms of the beneficial effects of vitamin B6 and pyridoxal 5-phosphate on cardiac performance in ischaemic heart disease. Clinical Chemistry Laboratory Medicine. 2013; 51(3):535-543.
  150. 150. Cellini, B., Montioli, R., Oppici, E., Astegno, A. and Voltattorni, C.B. The chaperone role of the pyridoxal 5’-phosphate and its implications for rare diseases involving B6-dependent enzymes. Clinical Biochemistry. 2014; 47:158-165.
  151. 151. Kim, Y.N. and Cho, Y.O. 2014. Evaluation of vitamin B6 intake and status of 20-to 64-year-old Koreans. Nutrition Research and Practice. 2014. 8(6):688-694.
  152. 152. Friso S, Lotto V, Corrocher R, Choi SW. Vitamin B6 and cardiovascular disease. Subcellular Biochemistry. 2012;56:265-290. DOI: 10.1007/978-94-007-2199-9_14
  153. 153. McNulty H, Pentieva K, Hoey L, Ward M. Homocysteine, B-vitamins and CVD. Proceedings of the Nutrition Society. 2008;67:232-237. DOI: 10.1017/S0029665108007076
  154. 154. Bassett, M.N. and Sammán, N.C. Folate content and retention in selected raw and processed foods. Archivos Latinoamericanos De Nutricion. 2010; 60(3):298-305.
  155. 155. Li Y, Huang T, Zheng Y, Muka T, Troup J, Hu FB. Folic acid supplementation and the risk of cardiovascular diseases: A meta-analysis of randomized controlled trials. Journal of the American Heart Association. 2016;5:e003768. DOI: 10.1161/JAHA.116.003768
  156. 156. Koike, H., Hama, T., Kawagashira, Y., Hashimoto, R., Tomita, M., Lijima, M. and Sobue, G. The significance of folate deficiency in alcoholic and nutritional neuropathies: Analysis of a case. Nutrition. 2012; 28:821-824.
  157. 157. Schwingshackl L, Schwedhelm C, Hoffmann G, Knüppel S, Iqbal K, Andriolo V, Bechthold A, Schlesinger S, Boeing H. Food gropus and risk of hypertension: A systematic review and dose-response meta-analysis of prospective studies. Advances in Nutrition. 2017;8:793-803. DOI: 10.3945/an.1171.017178
  158. 158. Burtis, C.A. and Bruns, D.E. Tietz Fundamentals of Clinical Chemistry and Molecular Diagnostics. 7th ed. St. Louis, Missouri: Elsevier/Saunders. 2015.
  159. 159. Oyebode O, Oti S, Chen YF, Lilford R. Salt intakes in sub-Saharan Africa: a systematic review and meta-regression. Population Health Metrics. 2016;14:1. Available from: [Accessed 2020-09-18]
  160. 160. Psaltopoulou T, Hatzis G, Papageorgiou N, Androulakis E, Briasoulis A, Tousoulis D. Socioeconomic status and risk factors for cardiovascular disease: Impact of dietary mediators. Hellenic Society of Cardiology. 2017;58:38-42. DOI: 10.1016/j.hjc.2017.01.022
  161. 161. Charlton KE, Steyn K, Levitt NS, Zulu J, Jonathan D, Veldman F, Nel JH. Diet and blood pressure in South Africa: Intake of foods containing sodium, potassium, calcium, and magnesium in three ethnic groups. Nutrition. 2005;21(1):39-50.
  162. 162. Charlton K, Ware LJ, Baumgartner J, Cockeran M, Schutte AE, Naidoo N, Kowal P. How will South Africa’s mandatory salt reduction policy affect its salt iodisation programme? A cross-sectional analysis from the WHO-SAGE Wave 2 Salt & Tobacco study. BMJ Open. 2018;8(3):1-9.
  163. 163. World Health Organization. Salt reduction. 2016. Available from: [Accessed 2019-09-18]
  164. 164. Vorster HH, Badham JB, Venter CS. Food-based dietary guidelines for South Africa: an introduction. South African Journal of Clinical Nutrition, 2013;26(3):5-12.
  165. 165. Soto-Ecageda JA, Estañol-vidal B, et al. Does salt addiction exist? Salud Ment. 2016;39(3):175-181.
  166. 166. Chen Z, Oldewage-Theron WH. Household consumption of stock cubes and stock powder in the Vaal Triangle of SA. Nutrition and Food Science. 2004;34(4):174-178.

Written By

Wilna Oldewage-Theron and Christa Grobler

Submitted: 21 December 2020 Reviewed: 13 January 2021 Published: 26 February 2021