Department of Nutrition and Dietetics
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Item Iron deficiency in rural Ghanaian children.(2001-05) Agyei-Frimpong, M.T.; Asare, G.; Owiredu, W.K.B.A.; Yeboah, F.A.OBJECTIVES: To compare the prevalence of iron deficiency among Ghanaian children in different residential settings and to see whether 200mg ferrous fumerate B.P. could correct iron deficiency anaemia in observed cases of iron deficiency. DESIGN: Prospective case-finding study using an iron-deficiency society questionnaire, laboratory data and general practice records. Crude prevalence was calculated using the hospital's mid-year estimates. SETTING: Nkoranza in the Brong Ahafo Region of Ghana, Komfo Anokye Teaching Hospital, Kumasi, Ghana SUBJECTS: Rural-dwelling children entering as out-patients, urban-dwelling children entering as controls and newly diagnosed iron-deficient children entering as in-patients. MAIN OUTCOME MEASURES: Crude prevalence rates (per quinquennia) for three groups of children. Corrected deficiencies expressed as percentage after management. Age, haemoglobin, iron status, residential status, symptoms at entry and after therapy. RESULTS: Following a 30-day administration of ferrous fumarate, the mean serum iron for the rural children increased significantly by 3.3 micromol/l representing an improved iron status of 20.0%(P<0.0001). Iron deficiency anaemia defined by serum Hb<12.0 g/dl and Fe<12.5 mmol/l decreased by 10% in the rural subjects. Comparatively, iron deficiency among the newly diagnosed anaemia group, fell by 17.6% whilst their ambulant urban counterparts employed as the control group had an iron deficiency anaemia of 0.0%. CONCLUSION: The study clearly indicates that the-prevalence of iron deficiency anaemia among children in rural Ghana is about ten times that of the urban-dwelling children and that iron-deficiency anaemia accounts for a greater percentage of all anaemic cases among children in our hospitals. It was also shown that taking appropriate iron supplements like 200 mg of ferrous fumerate for thirty days can substantially improve the iron status of iron-deficient children.Item Dietary iron overload in the African and hepatocellular carcinoma.(Wiley Blackwell, Blackwell publishing, MA, 2007) Kew, C.M.; Asare, A.G.Dietary iron overload occurs commonly in parts of sub-Saharan Africa. It results from the consumption of large volumes of traditional beer that is home-brewed in iron pots or drums and consequently has a high iron content. The liver becomes iron overloaded and may develop portal fibrosis or, less often, cirrhosis. A genetic predisposition to the condition has been suggested, but no putative gene has yet been identified. Although originally believed not to cause hepatocellular carcinoma, recent case-control studies have shown African Blacks with dietary iron overload to be at increased risk for the tumour and a causal association has been confirmed in an animal model. The mechanisms of iron-induced malignant transformation are yet to be fully characterised, but the close association between cirrhosis and hepatocellular carcinoma in patients with hereditary haemochromatosis and the lesser association in those with dietary iron overload, suggests that chronic necroinflammatory hepatic disease contributes to the malignant transformation. Increased hepatic iron may, however, also be directly carcinogenic. Probable mechanisms include the generation of reactive oxygen intermediates and the resultant chronic oxidative stress that damages hepatocytes and proteins, causes lipid peroxidation, and induces strand breaks, DNA unwinding, and mutations in tumour-suppressor genes and critical DNA repair genes.Item Interactions between aflatoxin B1 and dietary iron overload in hepatic mutagenesis.(Elsevier, Ireland, 2007) Asare, A.G.; Michelle, B.; Vivash, N.; Kew, C.M.BACKGROUND/AIM: Dietary aflatoxin B(1) (AFB(1)) exposure and iron overload are important causes of hepatocellular carcinoma in sub-Saharan Africa. The aim of this study was to investigate if the two risk factors have an interactive effect. METHODS: Four groups of Wistar albino rats were studied for 12 months. Group 1 (control) was fed the normal chow diet; group 2 (Fe) was supplemented with 0.75% ferrocene iron; group 3 (Fe+AFB(1)) was fed 0.75% ferrocene throughout and gavaged 25 microg AFB(1) for 10 days; group 4 (AFB(1)) was gavaged 25 microg AFB(1) for 10 days. Iron profile, lipid peroxidation (LPO), 8-hydroxydeoxyguanosine (8OHdG), oxidative lipid/DNA damage immunohistochemistry, superoxide/nitrite free radicals, cytokines IL6, IL-10, transaminases (ALT/AST) and Ames mutagenesis tests were performed. RESULTS: LPO and ALT showed a significant (p<0.05)/additive effect and 8OHdG a significant (p<0.05)/multiplicative effect in the Fe+AFB(1) group. IL-6 produced a negative synergy as against an additive antagonistic effect with IL-10. Massive deposits of 4-hydroxynonenal (4-HNE) and 8OHdG were observed in liver sections of the Fe+AFB(1) group, suggestive of multiplicative synergy. Significant levels of mutagenesis (p<0.001) were observed in the Fe+AFB(1) group. This multiplicative synergy was five-fold. CONCLUSION: Dietary iron overload and AFB(1) have a multiplicative effect on mutagenesis.Item African diet: A toxic/protective dilemma(Transworld Research Network, Kerala, India, 2009) Mossanda, K.S.; Asare, G. A.Food shortages and high prevalence of poverty-related chronic diseases including HIV/AIDS, malaria and tuberculosis have culminated in health crisis in African continent. The diet of the majority of African populations consists largely of maize and cassava flour. Apart from being deficient in essential amino-acids, important vitamins and micronutrients, maize and cassava flour are prone to fungal infestation and thus to contamination by mycotoxins which increases the risk of cancer development mostly in HIV/AIDS individuals. In addition, digestive cancers and especially squamous cell carcinoma of the oesophagus (SCCE) are become the most common cancers in Southern African black men (incidence: 14.5%). Among other factors including hepatitis B and C, excessive intake of dietary iron as a result of drinking homebrewed in iron pots constitutes one of the most important factors leading into hepatocellular carcinoma (HCC). Alcohol consumption has been also implicated in the aetiology of both SCCE associated with cigarette smoking, low intake of dietary antioxidants, consumption of compounds such as polycyclic hydrocarbons, nitrosamines, heterocyclic amines found in African diet and HCC associated with increased hepatic iron stores inducing successively fibrosis and cirrhosis which finally progress into liver cancer. Despite our progress in antioxidant, environmental, genetic and carcinogenic studies, the mechanism of induction of those two types of cancer is still not fully understood. Our histological findings and the immuno-histochemistry evidence of DNA damage by the presence in situ (biopsies) of 8-hydroxy-deoxyguanosine (8-OHdG) and that of lipid peroxidation by the presence in situ of 4-hydroxy-nonenal (4-HNE) increasing with the disease progression, have provided a consistent correlation between low intake of dietary antioxidant and the occurrence of carcinoma. In contrast to those toxicological aspects of African diet leading to the occurrence of digestive and liver cancers in African populations, an expanding body of evidence from epidemiological and laboratory studies demonstrated that edible plant as whole, or their ingredients have substantial protective effects on human carcinogenesis. We have recently demonstrated the anti-oxidative and anti-mutagenic properties of some African indigenous edible plants: Bambara groundnut (Vignea subterranean) and beverage: Rooi bos tea (Aspalathus linearis). Their chemo-preventive and antiinflammatory activities have been tested in cell culture using human breast epithelial (MCF-10A) cells and in animal model using mouse skin. Methanolic extracts of some other African plants (Sutherlandia fructescens and Harpagophytum procumbens) used as beverages showed inhibition of 12-O-tetradecanoyl-phorbol-13 acetate (TPA)- induced cyclo-oxygenase (COX-2) expression in mouse skin, which appears to be mediated through blocking of catalytic activity of extracellular signal-regulated protein kinase (ERK) and through inhibition of activator protein-1 (AP-1) and cylic AMP response element binding (CREB) protein activation, suggesting their chemopreventive and chemo-protective activities. Due to the fact that inhibition of COX-2 is now regarded as an effective and promising strategy for prevention of anti-inflammatory process precluding the initiation and tumor stage, more research on African food plants and beverages should be conducted using this strategy in order to understand the molecular mechanism underlying those specific activities. In the light of these data, the extensive use of African foodstuffs and beverage bearing preventive and protective factors should be recommend in the diet of African populations for reducing the incidence of digestive and liver cancers in those areas.Item Effects of exogenous antioxidants on dietary iron overload.(The Society for Free Radical Research, Japan, 2009) Asare, G. A.; Kew, M.C.; Mossanda, K.S.; Paterson, A.C.; Siziba, K.; Kahler-Venter, C.P.In dietary iron overload, excess hepatic iron promotes liver damage. The aim was to attenuate free radical-induced liver damage using vitamins. Four groups of 60 Wistar rats were studied: group 1 (control) was fed normal diet, group 2 (Fe) 2.5% pentacarbonyl iron (CI) followed by 0.5% Ferrocene, group 3 (Fe + V gp) CI, Ferrocene, plus vitamins A and E (42x and 10x RDA, respectively), group 4 (Fe - V gp) CI, Ferrocene diet, minus vitamins A and E. At 20 months, glutathione peroxidase (GPx), superoxide dismutase (SOD), Oxygen Radical Absorbance Capacity (ORAC), Ames mutagenicity test, AST, ALT and 4-hydroxynonenal (4-HNE) immunohistochemistry were measured. 8OHdG levels of the Fe + V and Fe - V groups were 346 +/- 117 and 455 +/- 151, ng/g w.wt, respectively. Fe + V and Fe - V differences were significant (p<0.005). A positive correlation between DNA damage and mutagenesis existed (p<0.005) within the iron-fed gps. AST levels for Fe + V and Fe - V groups were 134.6 +/- 48.6 IU and 202.2 +/- 50.5 IU, respectively. Similarly, ALT levels were 234.6 +/- 48.3 IU and 329.0 +/- 48.6 IU, respectively. However, Fe - V and Fe + V groups transaminases were statistically insignificant. 4-HNE was detected in Fe + V and Fe - V gp livers. Vitamins A and E could not prevent hepatic damage.