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Both iron and omega-3 (n-3) polyunsaturated fatty acids may play an important role in bone development. The aim of this study was to investigate the effects of pre- and post-natal iron and n-3 fatty acid deficiency (FAD), alone and in combination, on bone development in rats, and to determine whether effects are reversible when a sufficient diet is provided post-weaning. Using a 2×2-factorial design, 56 female Wistar rats were allocated to one of four diets: (1) control, (2) iron deficient (ID), (3) n-3 FAD or (4) ID and n-3 FAD, and were maintained on the respective diets throughout gestation and lactation. At weaning (post-natal day [PND] 21), offspring (n = 24/group; male:female=1:1) were randomly allocated to either continue with their respective diets or to switch to the control diet until PND 42-45. Bone mineral density (BMD) and bone strength were determined using dual X-ray absorptiometry and three-point bending tests, respectively. Pre- and post-natal ID resulted in significantly lower BMD in the spine and bone strength in the left femur. Both ID and n-3 FAD resulted in lower BMD in the right femur, with an additive reduction in the combined ID and n-3 FAD group vs. controls. While negative effects of pre- and post-natal ID alone were reversed in offspring switched to a control diet post-weaning, lower BMD and bone strength persisted in offspring with combined ID and n-3 FAD during the prenatal and early post-natal period. Effects were not sex-specific. These results indicate that ID during early life may negatively influence bone development, with potential additive effects of n-3 FAD. While the effects of ID alone seem reversible, a combined ID and n-3 FAD may result in irreversible deficits in bone development., Frontiers in Nutrition, 8, ISSN:2296-861X

PhD (Biochemistry), North-West University, Potchefstroom Campus, 2016 Urinary 3-hydroxyisovaleric acid and 3-methylcrotonylglycine are usually indicative of the possibility of 3-methylcrotonyl-CoA carboxylase (MCC) deficiency. In this study a South African family which presented with these metabolites was investigated. A standard metabolic work-up, analyses of relevant enzyme activity and in vivo loading tests indicated that two of the males in the family might have marginal MCC-deficiency of unknown genetic origin. The standard workup was extended with transcriptome analyses. Affymetrix HuExST1.0 arrays were used to generate the transcriptome from cultured skin fibroblasts of two affected males of the family and then the underlying molecular interactions and functional network analyses were explored. Transcriptomes were also generated from immortalised skin fibroblast cultures of well-documented clinically severe MCC-deficient patients as well as healthy controls. Subsequently, the three transcriptomes (from the South African family, the clinically severe MCC-deficient patients and controls) were compared to further characterise and identify similarities and differences between clinically severe and marginal MCC deficiency. The biochemical phenotype indicative of MCC-deficiency in this South African family suggested an X-linked association. The transcriptomic and functional analyses identified possible candidate genes to further investigate this apparent X-linked association of some MCC-deficient patients, especially the FAAH2 gene. The clinically severe 3-methylcrotonyl-CoA carboxylase deficient skin fibroblast transcriptome had a footprint indicative of mitochondrial dysfunction. The comparison of the transcriptomes and functional analyses from clinically severe and marginal 3-methylcrotonyl-CoA carboxylase deficiency further suggested the presence of aberrant pro-inflammatory cytokine signalling and associated impaired membrane integrity. The data presented in this thesis supports the notion that secondary factors other than the MCC loci might contribute to the presentation of the biochemical phenotype which is usually indicative of MCC-deficiency. The data also suggested that the long-term impact of a 3-methylcrotonyl-CoA carboxylase deficient biochemical phenotype should not be underestimated, especially since aberrant regulation of reactive oxygen species seems to play an intricate role in MCC-deficiency. It is evident that MCC-deficiency is far more complex than what was thought. However, despite the complexity of the functional analyses and the secondary signalling responses observed in the transcriptomes, interesting relationships were revealed that contribute to a better insight into the molecular impact of MCC-deficiency. In summary, it is clear that this dataset has potential to be mined even more. It is however important to keep in mind that the current state of the data is of an explorative nature and any specific implications thereof must be confirmed experimentally. A vast amount of options for possible follow-up experiments are available and should be carefully explored. Doctoral

Thesis (M.Sc. (Biochemistry))--North-West University, Potchefstroom Campus, 2007. The perception is that inborn errors of metabolism (IEM) are rare, but the reality is that more than 600 lEMs are now recognized. The organic aciduria, 3-methylcrotonyl-CoA carboxylase (MCC) deficiency arises when 3-methylcrotonyl-Coenzyme A (CoA) carboxylase that participates in the fourth step of the leucine catabolism is defective. Tandem mass spectrometry (MS/MS) based screening programmes in North America, Europe and Australia, showed that MCC deficiency is the most frequent organic aciduria detected, with an average frequency of 1:50 000. Therefore MCC deficiency is considered an emerging disease in these regions. The incidence of MCC deficiency in the Republic of South Africa (RSA) is not yet known. However, one 48 year old male Caucasian individual (HGS) was diagnosed suffering from mild MCC deficiency, since elevated levels of 3-hydroxyisovaleric acid, 3- hydroxyisovalerylcarnitine, 3-methylcrotonylglycine was present in his urine. Several groups are currently working on various aspects of this emerging disease with the focus on the molecular characterisation of MCC deficiency. In the RSA no molecular based diagnostic method which complements MS/MS screening programmes have yet been implemented. Therefore, the aim of this study was to implement the necessary techniques for the molecular characterisation of MCC deficiency, the determination of the sequence of the open reading frame (ORF) of mccA and mccB subunits to determine which mutation(s) are present in the South African MCC deficient patient. For the implementation of the molecular characterisation, a two-pronged approached was used to characterize MCC of a MCC non-deficient individual (CFC). This approach included the reverse transcriptase polymerase chain reaction (RT-PCR) amplification of the ORFs of the associated genes [mccA (19 exons) and mccB (17 exons] and the PCR amplification of selected (genomic deoxyribonucleic acid (gDNA) regions (exons mccA8, mccA11 , mccB5, mccB6 and mccB5-intron 5-6 exon 6 (mccB5-6) which have been found to have mutations associated with MCC deficiency in Caucasians. The sequence analyses produced surprising results of the amplified ORFs (CFCmccA and CFCmccB) of the MCC non-deficient individual CFC. A non-synonymous single nucleotide polymorphism (SNP) (1391C→A, H464P) associated with MCC deficiency (Gallardo et al., 2001) was identified in the CFCmccA subunit. Another SNP (1368G→A, A456A) recently listed in GenBank was observed in the amplified CFCmccB ORF. No significant novel variations or described mutations were identified in the amplified genomic regions mccA8, mccA11 ,mccB5, mccB6 and mccB5-6. The implemented molecular approach was used to characterise MCC of our MCC deficient patient (HGS). The patient did not have any mutation in the four selected exons mccA8, mccA11, mccB5, mccB6 or the genomic region mccB5-6. The RT-PCR amplification of both ORFs (HGSmccA and HGSmccB) resulted in multiple amplicons. Gel extracted amplicons of the expected size were sequenced. Of the 36 exons, 34 exons were sequenced. This includes all 19 exons of HGSmccA and 15 of 17 exons of HGSmccB (exons 1-6 and exons 9-17). The non-synonymous SNP (1391C→A, H464P) detected in CFCmccA (MCC non-deficient individual), seems to be present in the HGSmccA subunit of the MCC deficient individual, HGS. The HGSmccB amplicons could not be entirely sequenced. However, the region exon 1-6 and 9-17 was sequenced but no described or novel mutations were identified. The lack of sequence data of region exon 7-8 led to an incomplete molecular characterisation of the MCC deficiency in HGS. In conclusion, the basic methods and techniques for the molecular characterisation of MCC deficient patients have been implemented locally. A few additional sequencing primers need to be designed to cover mccB7 and mccB8 as well as the entire coding and non-coding strands of each MCC gene (mccA and mccB). The primers for RT-PCR of both mccA and mccB need to be further refined to ensure better specificity. Masters

MSc (Dietetics), North-West University, Potchefstroom Campus Introduction and aim - Globally, dietary habits have shifted over the years from a traditional rural diet to a more Westernised diet. This has caused a drastic change in the intake ratio of n-6:n-3 polyunsaturated fatty acids (PUFA) from 1:1 to 20:1. Biosynthesis of long-chain polyunsaturated fatty acids (LCPUFA) is associated with genetic variation within the fatty acid desaturase (FADS) gene cluster. The FADS1/2 genes encode for the rate-limiting desaturation enzymes in the LCPUFA biosynthesis pathway. Thus far, genetic variations in the FADS1/2 gene cluster and their effect on LCPUFA metabolism have been investigated in the United States and in Europe, but limited research exists for the African population. The aim of this study was to characterise the genetic variations of the FADS1/2 genes and their effect on delta -5 and -6 desaturase (D5D and D6D) activity and study the associations with n-3 LCPUFA status at early pregnancy in women of African descent. Methods - In this cross-sectional study, a total of 250 apparently healthy pregnant women of African descent were enrolled and 243 of these women gave consent for genetic testing. Participants were divided into two groups depending on their n-6:n-3 LCPUFA ratio: a higher and lower n-3 LCPUFA status group. Nine variants, located in the FADS1/2 gene cluster, were investigated, and genotyping of these selected variants was done using the iPLEX® MassARRAY system from Agena Bioscience™. The genetic variants were investigated for association with D5D and D6D activity, estimating PUFA ratios and n-6:n-3 LCPUFA ratio. To determine D5D and D6D enzymatic activities, LCPUFA product to precursor ratios were determined. Univariate analyses were performed to assess differences between genotypes, adjusting for gestational age, age of the mother, and dietary FA intakes. Results - The alternative allele carriers of FADS1-rs174546(C/T) and FADS2-rs112425493(G/A) associated with both lower AA:DGLA and higher DGLA:LA ratios that are respectively indicative of lower D5D and higher D6D activities. Alternative allele carriers for FADS-rs174547(C/T), FADS1-rs174549(A/G), FADS1-rs174555(C/T) and FADS2-rs73489307(T/C), were all associated with higher DGLA:LA and therefore were associated with higher estimated D6D activity in comparison to the homozygous ancestral alleles. Alternative allele carriers of FADS2-rs78678033(G/A) were associated with higher AA:DGLA ratio, estimated D5D activity as well as lower DGLA:LA ratio and D6D activity. Alternative allele carriers of FADS2- rs174606(T/G) and FADS2-rs174616(G/A) associated with both lower AA:LA and lower DGLA:LA ratios, lower combined D5D and D6D activity, and lower individual D6D activity. The carriers for the G allele for FADS2-rs112425493(G/A), T allele for FADS1-rs174546(C/T), T allele for FADS1-rs174547(C/T), and the G allele for FADS1-rs174549(A/G) all associated or tended to associate with a lower n-6:n-3 LCPUFA ratio and therefore with a higher n-3 LCPUFA status (P=0.033, P=0059, P=0.062 P=0.071, respectively). All associations were unaffected when adjusting for dietary intake of the individual n-6 or n-3 essential PUFA or LCPUFA. Conclusion - This mini-dissertation sheds light on the unique and noteworthy African genome and the importance of conducting genetic research in a population of African descent. The current study contributes to the investigation of the FADS1/2 gene cluster and the associations with LCPUFA metabolism in an African population. Nine genetic variants influenced estimated desaturase activities and four variants related to both increased desaturase activities and an improved n-3 LCPUFA status, and may thus be advantageous to improve n-3 LCPUFA status in pregnant women of African descent even in the context of low functional LCPUFA such as EPA and DHA dietary intake. This information may create an opportunity to alter the n-3 LCPUFA status of South Africans through dietary intervention which could in turn result in a decline in inflammatory diseases and an increase in optimal birth outcomes for the South Masters

MSc (Nutrition), North-West University, Potchefstroom Campus Introduction - Globally, hypertensive disorders affect 10% of pregnancies and are the most common risk factors for maternal and perinatal morbidity and mortality. Between 2011 and 2013, 14.8 % of maternal mortalities were associated with hypertensive disorders in South Africa. Adequate intake and status of n-3 long chain polyunsaturated fatty acids (LCPUFA) have been linked to improved endothelial function and reduced blood pressure. However, the South African longitudinal Prospective Urban Rural Epidemiology (PURE) study has shown a positive association between plasma n-3 LCPUFA and hypertension and a negative association between n-6 LCPUFA and hypertension. In addition, in South Africa, pregnant women are supplemented routinely with 60 mg/d of elemental iron to prevent iron deficiency. This supplementation programme may lead to oxidative stress and increased inflammation, especially in women with sufficient iron status, increasing their risk to develop gestational hypertension. This study assessed the relationship of n-3 and n-6 LCPUFA status with blood pressure in pregnant African women receiving routine iron supplementation. Methods - This was a longitudinal analysis where 250 pregnant women were recruited at

MSc (Dietetics), North-West University, Potchefstroom Campus Background: It has been shown that poor nutrition during early development has a causal relationship with adverse pregnancy outcomes, morbidity, mortality and the increased risk of short- and long-term adverse health outcomes for the child and future generations. Furthermore, a mother’s nutritional status has an impact on the unborn baby, possibly through epigenetic mechanisms. In developing countries, women are reliant on poor-quality diets. In these circumstances, nutrient deficiencies do not occur in isolation, and it is likely that in pregnant women, iron deficiency (ID) and inadequate omega-3 polyunsaturated fatty acid (n-3 PUFA) status coexist. Both deficiencies play a role in the development of colon inflammation. Inflammation in the gut and colon can lead to dysbiosis of the microbiota, compromised tight junctions, increased gut permeability, and pathogens to enter the bloodstream. The result is low-grade systemic inflammation contributing to the development of gastrointestinal diseases such as irritable bowel syndrome and also to the development of adult diseases such as diabetes, obesity, cancer, and neuro-pathologies. Therefore, optimum nutrition before and during pregnancy is crucial for the gut development and future health of the offspring. Apart from being reliant on nutrients from the mother’s diet during gestation, offspring in the human situation will most likely also continue consuming a similar diet to that of their mother. Data on the combined ID and n-3 PUFA deficiency ((n-3)FAD), specifically in relation to gut inflammation, is scarce. Aim: Therefore, in this study, the pre-and postnatal effects of ID and (n-3)FAD, alone and in combination, on colon lining lipid mediator concentrations, which indicates colon inflammation, will be investigated in rats. Methods: Fifty-six female Wistar rats were allocated to one of four diets: 1) Control, 2) ID, 3) (n- 3)FAD, or 4) ID + (n-3)FAD and were maintained on the respective diets throughout pregnancy and lactation. Offspring (n=96) continued on the respective diets after weaning until postnatal day 42-45. Concentrations of lipid mediators were analysed in homogenized colon lining tissue from the offspring, with liquid chromatography-tandem mass spectrometry (LCMSMS). Pro-inflammatory lipid mediators, 5-, 8-, 11-, 12- and 15-hydroxyeicosatetraenoic acid (HETE), and pro-resolving lipid mediators, 17-hydroxydocosahexaenoic acid (HDHA); and 11-, 12-, 15- and 18 hydroxyeicosapentaenoic acid (HEPE) were measured. Results: ID resulted in higher colonic pro-inflammatory lipid mediator concentrations in offspring derived from arachidonic acid (ARA), including 5-, 12-, 15- and 8-HETE (all p

MSc (Nutrition), North-West University, Potchefstroom Campus Background: Resistance exercise can cause inflammation and it is known that inflammation is closely related to oxidative stress. Oxidative stress can be defined as an imbalance between free radicals and anti-oxidative mechanisms, or the excess of reactive oxygen species (ROS). The body reacts to injury or infection, as well as to excessive ROS production during exercise, with an inflammatory response. A complex network of lipid mediators regulates the inflammatory response. Lipid mediators are also known as eicosanoids and can regulate inflammation by eliciting either a pro-inflammatory or anti-inflammatory response. There is still little evidence to the question as to whether there is a difference in pro-inflammatory lipid mediator status between recreational runners and untrained individuals, and which factors can modulate this response. Objectives: The aim of the study is to compare exercise-induced lipid mediator inflammatory signalling in male recreational runners with untrained males considering potential modulating factors such as fatty acid and antioxidant status, as well as antioxidant nutrient intake. Study design: This was a cross-sectional study on healthy, male, untrained individuals (n=20) and recreational runners (n=20). A medical screening was done (blood pressure, heart rate, temperature and fingerprick blood glucose). The participants’ height and weight were measured, and a three-day dietary record was administer red. Blood samples were collected before both groups participated in resistance exercises at 80% of their 1 repetition max and immediately on completion of that exercise challenge, as well as 1, 2, 24 and 72 hours after cessation of the exercise. Results: The runners were taller and heavier than the non-runners (P = 0.018 and P = 0.04, respectively). Runners did significantly more running exercise than non-runners (P < 0.001). Eicosapentaenoic acid (EPA), monounsaturated fatty acids (MUFA), n-3 polyunsaturated fatty acids (PUFA) and n-3 long chain (LC) PUFA were higher in the runner group compared to the non-runner group (P = 0.001, P = 0.045, P = 0.040 and P = 0.041). On the other hand, the total n-6:n-3 PUFA and the n-6:n-3 LCPUFA ratios were higher in the non-runner group compared to the runner group (P = 0.032 and P = 0.031) . The runners’ linoleic acid, vitamin C and Vitamin E intake were higher than the intake of the non-runners (P = 0.035; P = 0.028 and P = 0.013), respectively. There was a significant difference in response over time in the runners compared to the non-runners for 5-HETE and 12-HEPE (P = 0.005 and 0.008). When adjusted for BMI and diet, 5-HETE, 15-HETE and 8-HETE showed a significantly different response over time between the two groups (P = 0.012, P = 0.033, P = 0.016), respectively. There was also a significant different response for 8-HETE, 12-HEPE and 18-HEPE adjusted for BMI and oxidative stress (P = 0.041, P = 0.059 and P = 0.085), respectively. When adjusting for BMI, diet and oxidative stress this resulted in a significant difference between the groups for 5-HETE (P = 0.016) and 8-HETE (P = 0.043). Conclusion: This study showed that pro- and anti-inflammatory lipid mediator responses are different among runners and non-runners and are influenced by BMI, vitamin C and E intake, the n6:n3 LCPUFA status ratio and endogenous oxidative stress adaptation. Masters

The double burden of malnutrition, an emerging concern in developing countries, can exist at various levels: individual, household, and population. Here, we explore the nutritional status of Tajik women (15–49 years) and children (5–59 months) focusing on overweight/obesity along with undernutrition (underweight, stunting, and micronutrient deficiencies). For this, nutritional markers (haemoglobin (Hb), transferrin receptor (TfR), serum ferritin (Sf), retinol binding protein (RBP), vitamin D, serum folate, and urinary iodine), height, and weight were assessed from 2,145 women and 2,149 children. Dietary intake, weaning, and breastfeeding habits were recorded using a 24‐hr recall and a questionnaire. Overweight (24.5%) and obesity (13.0%) are increasing among Tajik women compared with previous national surveys (2003 and 2009). Prevalence of iron deficiency and anaemia was 38.0% and 25.8%, respectively; 64.5% of women were iodine deficient, 46.5% vitamin A deficient, and 20.5% had insufficient folate levels. Women in rural areas had significantly lower iron status and body mass index and higher iodine intake compared with urban areas; 20.9% of children were stunted, 2.8% wasted, 6.2% underweight, 52.4% iron deficient, and 25.8% anaemic; all more prominent in rural areas. Dietary diversity was higher among urban women. Intraindividual or household double burden was not seen. In summary, double burden of malnutrition constituted an increase in overweight among women, especially in urban areas, and persisting levels of undernutrition (stunting, iron, and vitamin A deficiency), predominately in rural areas. A holistic, innovative approach is needed to improve infant and young children feeding and advise mothers to maintain an adequate diet., Rituximab was digested with immobilized pepsin and papain to yield F(ab')2 and Fab' fragments respectively. Fragments were conjugated with p‐SCN‐Bn‐NOTA and immunoconjugates labeled with Ga‐68. Specificity of radioimmunoconjugates was ascertained by cell binding and inhibition assays with unlabeled antibody.

MSc (Nutrition), North-West University, Potchefstroom Campus Background: Globally, iron deficiency is the most common nutrient deficiency and can lead to various adverse health consequences. Iron absorption, circulation and storage are regulated by the hormone hepcidin, which is expressed by the HAMP gene in the liver. Iron cannot be actively excreted by the human body, thus hepcidin is released to decrease iron absorption and recycling to prevent iron overload. Hepcidin expression is activated by high iron stores and by inflammation via the inflammatory cytokine interleukin-6 (IL-6). This occurs via two main pathways known as the bone morphogenetic protein–small mothers against decapentaplegic (BMP/SMAD) pathway (induced by iron levels) and the JAK/STAT3 pathway (induced by IL-6). Long chain omega-3 (n-3) fatty acids can resolve inflammation by acting as a precursor for the synthesis of anti-inflammatory and pro-resolving lipid mediators. Low n-3 fatty acid status can lead to a decreased ability by the host to resolve inflammation and sets off pro-inflammatory signalling and increased IL-6 levels. Multiple nutrient deficiencies, such as a combined iron and n-3 fatty acid deficiency, often co-exist in populations and individuals. The presence of a combined iron deficiency with a low n-3 fatty acid status may lead to an inability to effectively resolve inflammation and increased circulating IL-6 levels, therefore potentially leading to the upregulation of hepcidin in an already iron deficient state, further hindering mechanisms to improve iron status. Aim and Objectives: Therefore, the aim of this study was to determine the effects of n-3 fatty acid and iron deficiency, alone and in combination, on hepcidin regulation and lipid mediator (docosahexaenoic acid (DHA)-, eicosapentaenoic acid (EPA)- and arachidonic acid (ARA)- derived) signalling in rats. The objectives of this study were to investigate the effects of n-3 fatty acid and iron deficiency, alone and in combination, on (A) Expression of the hepcidin regulatory pathway genes HAMP, BMP2 and TFR2 in rat liver. (B) ARA-derived 5-, 8-, 11-, 12- and 15- hydroxyeicosatetraenoic acid (HETE); EPA-derived 12-hydroxyeicosapentaenoic acid (HEPE) and DHA-derived 17-hydroxydocosahexaenoic acid (HDHA) lipid mediators in rat plasma. (C) To determine the correlations of HAMP, BMP2 and TFR2 expression with plasma lipid mediator concentrations in rats. Design: Female Wistar rats were fed a standard or n-3 fatty acid deficient (FAD) diet. The female rats were mated, and 39 male rats were included in the study with a 2x2 factorial. At weaning (postnatal day 21), the male rats were fed either a 1) control, 2) iron deficient (ID), 3) n-3 FAD or 4) ID + n-3 FAD diet for five weeks. Expression of HAMP and the HAMP regulatory genes BMP2 and TFR2 was analysed in hepatic tissue using quantified real time polymerase chain reaction (RT-qPCR). Peripheral lipid mediators such as ARA-derived pro-inflammatory lipid mediators, 5-, 8-, 11-, 12- and 15-hydroxyeicosatetraenoic acid (HETE), EPA-derived anti-inflammatory 12-hydroxyeicosapentaenoic acid (HEPE), and DHA-derived pro-resolving lipid mediator 17-hydroxydocosahexaenoic acid (HDHA) were measured in plasma using liquid chromatography-tandem mass spectrometry (LCMSMS). Results: HAMP expression was significantly upregulated by ID, whilst BMP2 and TFR2 expression were both downregulated. There was a significant effect of ID for higher ARA-derived 15-HETE, but lower 5-HETE. Furthermore, there was a significant effect of ID for higher DHA-derived 17-HDHA, whereas 17-HDHA was lowered by n-3 FAD. When compared to the control group, 17-HDHA was significantly higher in the ID group but lower in the n-3 FAD group. 17-HDHA concentrations in the ID+n-3 FAD group did not differ from the control group (p = 0.99). HAMP expression correlated positively with 15-HETE and 17-HDHA and negatively with 5-HETE. Conclusion: As expected, both iron level-dependent genes BMP2 and TFR2 were downregulated by ID. However, the upregulation of HAMP expression by ID was unexpected and suggestive of inflammation. The presence of inflammation in an ID state was confirmed by the effect of ID for increased ARA-derived pro-inflammatory lipid mediators and DHA-derived inflammation-resolving 17-HDHA levels. N-3 FAD alone did not induce HAMP expression, but may compromise the inflammation-resolving capacity of rats with a concomitant ID. Masters

Background Recent studies are suggesting a U-shaped relationship between antenatal iron exposure and birth outcomes. Little is known about the iron status and associated birth outcomes of pregnant women in South Africa. Our aim was to assess iron status at early, mid- and late pregnancy, and to determine associations with gestational age and birth weight in women in Johannesburg, South Africa. Methods In this prospective study of 250 pregnant women, we measured haemoglobin, biomarkers of iron status and inflammation at, PLoS ONE, 14 (9), ISSN:1932-6203

Background Globally hypertension is stabilising, but in sub-Saharan Africa the incidence of hypertension remains on an increase. Although this might be attributed to poor healthcare and ineffective antihypertensive treatment, there is a limited understanding of population and individual-specific cardiovascular pathophysiology – necessary for effective prevention and treatment strategies in Africa. As there is a lack of longitudinal studies tracking the early pathophysiological development of hypertension in black populations, the African-PREDICT study was initiated. The purpose of this paper is to describe the detailed methodology and baseline cohort profile of the study. Methods and results From 2013 to 2017, the study included 1202 black ( N = 606) and white ( N = 596) men and women (aged 20–30 years) from South Africa – screened to be healthy and clinic normotensive. At baseline, and each 5-year follow-up examination, detailed measures of health behaviours, cardiovascular profile and organ damage are taken. Also, comprehensive biological sampling for the ‘omics’ and biomarkers is performed. Overall, the baseline black and white cohort presented with similar ages, clinic and 24-hour blood pressures, but black adults had lower socioeconomic status and higher central systolic blood pressure than white individuals. Conclusions The prospective African-PREDICT study in young black and white adults will contribute to a clear understanding of early cardiovascular disease development.