Lipidemia Status and Associated Factors among HIV Positive Persons on HAART


As global treatment efforts mature and more people receive life-long treatment for this chronic disease, progressively more patients who are already receiving HAART are switching to new programs for care, either to evaluate alternative programs, or to receive care closer to home. Thus, this group of patients is forming an increasing portion of the clinic population whose outcomes and needs may differ significantly from HAART-naïve patients who have been the focus of the majority of studies citing clinical treatment success in resource-limited settings

Infection with HIV is associated with subtle changes in lipid metabolism. Slight reductions in high density lipoprotein cholesterol occur early in the course of the infection. This is followed by an increase in the number of small, dense type B low density lipoprotein particles. Later on, as patients begin to develop symptomatic HIV disease, plasma triglyceride levels and Low Density Lipoproteins may rise. The initiation of antiretroviral therapy also affects lipid metabolism, and protease inhibitors appear to further worsen the patient’s atherogenic profile. However, Highly Active Antiretroviral Therapy (HAART) leads to lipid changes with increases in both total cholesterol and triglycerides (Riddler et al., 2003).

HAART is indicated in all HIV-positive adults and adolescents with the following: WHO clinical stage 1 or 2 and a CD4 count ≤ 350 cells/mm; WHO clinical stage 3 or 4 regardless of CD4 count; HIV and TB co-infection regardless of the CD4 count; patients with HIV/HBV co-infection with evidence of active liver disease and cirrhosis or other evidence of chronic liver disease (NASCOP, 2011).

Evidence indicates that lifestyle changes such as diet and physical activity have a major influence on health. While many chronic diseases develop slowly, changes in lifestyle and dietary behaviours transpire with a steady speed. It is possible that people who are already ill may be more likely to be physically inactive and change their diet as a result of prevalence of the diseases (Chiuve, 2006).

Although HIV infection can now be treated effectively with combination of antiretroviral medications, significant toxicities such as hyperlipidemia, as well as the potential for significant drug-nutrient interactions present new challenges for the management of persons infected with HIV. However, the issue is complex, because HAART has improved life expectancy, changed the nutrition profile, and presented new challenges for persons living with HIV infection (Faintuch, 2006).

Hyperlipidemia is a condition with abnormally elevated levels of any or all lipids and or lipoproteins in the blood. High-density lipoproteins (HDL) form a class of lipoproteins, varying somewhat in their size (8-11 nm in diameter) and contents, which carry cholesterol from the body tissues to the liver. Because HDL can remove cholesterol from atheroma within arteries and transport it back to the liver for excretion or re-utilization, they are seen as “good” lipoproteins. HDL is the smallest of the lipoprotein particles. Low-density lipoproteins (LDL), on the other hand are very-low density lipoprotein (VLDL), and lipoprotein (a) are the 3 major apolipoprotein-B–containing lipoproteins found in blood. Diagnosis of lipidemia is typically based on medical history, physical examination, and blood tests (done after overnight fasting) in order to determine the specific levels of low density lipoprotein cholesterol, high density cholesterol, and triglycerides.

Despite the tremendous benefits of highly active antiretroviral therapy (HAART) use on HIV disease progression and survival, micro and macronutrient malnutrition remain strong independent predictors of mortality among HIV-positive individuals in both high and low resource settings (Hogg et al., 2001). A growing body of evidence suggests that socio-economic determinants may also adversely impact survival among people living with HIV/AIDS (McMahon et al., 2011).

The consequences of HIV infection for societies, health and economies are devastating everywhere, but most especially so in poor, vulnerable and disadvantaged populations such as those already infected with HIV Virus. Research evaluating the role of nutrition in HIV infection focused initially on loss of weight or Lean Body Mass (LBM) and wasting (Forrester et al., 2002). The lean body mass and wasting was found to be associated with increased risk of opportunistic infections and death. Even in the era of Highly Active Antiretroviral Therapy (HAART), unintentional weight loss is associated with increased risk of mortality (Tang et al., 2002).

Unfortunately, HAART regimens are associated with the development of chronic metabolic complications, including peripheral lipoatrophy, centripetal fat accumulation and lipidemia (Carpentier et al., 2005). HIV replication alone in human T-cells, without any influence of antiviral drugs or other factors, can stimulate the production of novel cellular enzymes and proteins that enhance fatty acid synthesis, increase the quantity of low density lipoproteins, secrete triglycerides, alter the lipid transport and metabolism, and oxidize lipids (Rasheed et al., 2008).

Debate continues about lipidermia whether deranged status is a direct result of the drugs alone or whether it is primarily from the course of HIV disease or from combination of HIV disease progression plus anti- HIV drug effects. Other factors which have been identified as affecting the development of metabolic complications include age of patient and economic status (Boyle et al., 2002).

Overview of HIV, HAART therapy and Lipidemia

Sub-Saharan Africa remains the region heavily affected by HIV. The most dramatic increases in antiretroviral therapy coverage according to UNAIDS 2011 report on the world AIDS day have occurred in sub-Saharan Africa, with a 20% increase between 2009 and 2010 alone. HIV prevalence among adults aged 15 to 64 years decreased nationally from 7.2%, as measured in KAIS (2012) to 5.6% in 2012. This corresponds to approximately 1,192,000 persons living with HIV infection with 4.4% being men (KAIS, 2012). Fifty-eight percent of HIV-infected persons aged 15-64 years were eligible for Highly Active Antiretroviral Therapy (HAART) treatment for HIV infection based on a CD4+ T-cell count of 350 cells/μl or less or reported history of current tuberculosis treatment. Of those, 63% were currently on HAART (KAIS, 2012).

The past decade has witnessed a revolution in the treatment and long term prognosis for patients with HIV infections. The advent of highly active-antiretroviral therapy (HAART) has made HIV infection a chronic and manageable disease for many patients (Koutkia, 2004). HAART is the therapy composed of multiple antiretroviral drugs. The HAART include one nucleoside analog (DNA chain terminator), one protease inhibitor and either a second nucleoside analog (“nuke”) or a non-nucleoside reverse transcription inhibitor (NNRTI).

HAART is indicated in all HIV positive adults and adolescence patients with WHO clinical stage 1or 2 and a CD4 counts ≤ 350 cells/mmᶾ, WHO stage 3 or 4 regardless of CD4 count, HIV and TB co infection regardless of CD4 counts and HIV/HBV co infection with evidence of active liver disease, cirrhosis or the evidence of liver disease. HIV-infected patients on treatment with Highly Active Antiretroviral Therapy (HAART) have been linked to the development of lipidermia, a clinical condition characterized by elevated levels of plasma lipids (Carr, 2000.) HAART regimens, especially those including protease inhibitors (PIs), cause lipidemia mostly associated in HIV patients taking long-term HAART.

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However, Pre-HAART lipidemia was confirmed in a study, characterized by an initial decrease in serum levels of total cholesterol, High-Density Lipoproteins (HDL), and Low-Density Lipoproteins (LDL), followed by elevations in triglyceride levels during the advanced stages of HIV disease (Penzak and Chuck, 2000). This study desired to establish the lipidermia status among HIV positive adult male receiving HAART at the Comprehensive Care Centre. 

Demographic and socio economic characteristics of the HIV positive persons

There is now a wealth of compelling evidence from a wide range of settings across the world and at various scales to suggest that location and place shape our health, our exposure to environmental features that impact on our health and our access to those goods and services that either promote health or treat episodes of diseases that we encounter (Gatrell and Rigby, 2004). People and the factors that cause diseases are dispersed, often unevenly, across communities and regions, and the processes that bring the people and the disease-causing agents into contact are geographically variable too (Cromley and McLafferty, 2002).

The heterogeneity in the HIV patterns has been thought to be a product of local, social and economic determinants. Among the factors are relative gender distribution in the communities, culture, socioeconomic status and religion. Chronic conditions like lipidemia are frequently incorrectly considered to have limited impact on the burden of disease in Sub-Saharan Africa, because of the known high relevance of the infectious diseases like HIV.

For the patients receiving HAART, there are emerging challenges associated with metabolic disorders such as lipidemia and fat redistribution, which are increasingly common and are receiving tremendous attention in the world of research.

Nutritional status of HIV positive patients on HAART treatment

Individuals living with HIV/AIDS have special nutritional needs irrespective of whether they are on ART or not. Proper nutrition helps to strengthen the immune system, manage opportunistic infections, optimize response to medical treatment, and may contribute to the slowing down of the progression of the disease (Castleman et al., 2004).

Evidence from studies indicates that poor nutrient status in HIV-infected individuals worsens their immune status, rendering them vulnerable to infections and further deterioration in nutrient status (Anabwani et al., 2005). Malnutrition compromises an individual’s immunity thus increasing susceptibility to infections (including HIV). Infection leads to increased nutrient requirements which if not sufficiently met results in wasting. HIV-associated wasting has been recognized as a predictor of progression to AIDS and is a major contributor to the development of malnutrition in HIV-infected individuals early in the epidemic (Koethe and Heimburger, 2010). Furthermore the increased incidence of opportunistic infections such as diarrhoea causes poor absorption and use of fat-soluble vitamins A and E. This can further compromise nutrition and immune status (Piwoz and Preble, 2000). Nutritional care and support helps people living with HIV to manage HIV-related complications, promotes good responses to medical treatment, and improves the person’s quality of life by maintaining strength, comfort, level of functioning, and human dignity (FANTA, 2004).

Many of the nutritional problems that occurred among HIV infected persons in the era prior to HAART still persist even today. Weight loss remains a prevalent feature of persons with HIV infection, used as one of the indicators for staging the progression of the disease, and the incidence of wasting appears to be unaffected by HAART therapy. Decreased lean body mass, in particular, continues to be associated with decreased quality of life among the HIV patients receiving HAART (Wilson et al., 2000). Gastrointestinal problems are frequent in persons infected with HIV and also among those receiving HAART. Diarrhoea is very common, and malabsorption continues to be found in HIV infected persons with or without chronic diarrhoea (Knox et al., 2000). For example, in developing countries more than 90% of HIV-positive individuals get diarrhoea compared with less than half in developed countries (Call et al., 2000).

According to the 2005-2010 Kenya National HIV/AIDS strategic plan, the Government of Kenya identified good nutrition as a key component of the national response to the HIV/AIDS epidemic, this in keeping with the global recognition that nutrition is essential for the promotion of health and quality of life for HIV infected patients (Ministry of Health, Government of Kenya, 2007). However, effective interventions to achieve this are still deficient due to resource constraints. The study wished to appraise the nutritional status in relation to HIV of the adult HIV positive male patients receiving care and treatment. 

Dietary intake and food consumption pattern of the HIV positive adult persons on HAART

The Highly Active Antiretroviral Therapy interrupts the replication of HIV and results not only in clinical and immune functions improvement but rapid and significant weight gain, provided that the diet contains adequate energy, protein and micronutrients to enable nutritional recovery (Brown et al., 2008). However, reduced body mass index is still predictive of mortality even with antiretroviral treatment, and highlights the value of appropriate nutritional monitoring and support in addition to antiretroviral medications (Van der Sande et al., 2004). Furthermore, reduced food intake can reduce the efficacy of HAART treatment regimens, as some drugs may not be properly absorbed or can cause significant side effects if not taken with adequate food.

Piwoz and Preble (2000) also noted that HIV infection affects the production of some hormones that are involved in metabolism of macronutrients including fat. Body fat loss is due to poor dietary intake, in conditions where there is inadequate energy intake; body fat is used as fuel source (Hsu et al., 2005). The dietary changes witnessed in many regions including South Rift Valley of the nutrition transition involve large increases in the consumption of fat (especially saturated fat) and sugar, marked increases in animal products, and a decline in unrefined cereal and, thus, in fiber intakes (Popkin, 2001a). Body fat oxidation increases in HIV-positive patients (Hsu et al., 2005)

However, it is important to appreciate that the association of individual nutrient intakes with disease outcomes can be difficult to detect; that is because nutrients are not consumed in isolation and act synergistically in the body (Kant, 2004; Newby et al., 2004). The study therefore enquired about the dietary patterns and its influence on the serum lipid status and body fat percentage through the measurement skin fold.

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Lipidemia status in HIV positive patients receiving HAART

Highly Active Antiretroviral Therapy (HAART) associated lipidemia is characterized by elevated serum concentrations of total cholesterols, triglycerides, low density lipoproteins (LDL-C) , very low density lipoprotein ( VDLD) and apolipoprotein B and low levels of high density lipoproteins profile (Dronda, 2004). These lipid changes occur within three months of initiating HAART and plateau after six to nine months (Sherer, 2003).

In a large cross-sectional study by Friis-Møller et al., (2003), the prevalence of lipidemia as per the classes of lipoproteins was suggested to be 10 to 27 percent for hypercholesterolemia (>6.2 mmol/L), hypertriglyceridemia (>2.3 mmol/L), and low HDL-cholesterol (<0.9 mmol/L) depending on the HAART regimen . However, the prevalence of low density lipoprotein has not been highlighted in the study by Friis- Moller et al., (2003).

Protease inhibitors may inhibit several proteins involved in lipid metabolism and adipocyte regulation, including LDL receptor–related protein and cytoplasmic retinoic acid–binding protein-1, which share a high degree of homology with PIs’ catalytic site (Brinkman et al., 1999). However, emerging in vitro data suggest a more complicated mechanism, since different protease inhibitors (PIs) have differential effects on these systems (Mooser and Carr, 2001). Exposure to PIs is clearly associated with this entire range of metabolic abnormalities. Fat redistribution and lipidemia are correlated in patients on HAART. Most studies have not found an association between CD4 lymphocyte count or HIV viral load and lipid abnormalities.

The nutritional status of HIV-infected patients such as weight loss and protein depletion, contributes to reduction in the high density lipoprotein-cholesterol or elevation of low density lipoprotein-cholesterol levels (Grunfeld et al., 1992). Several path physiologic models have been proposed to explain the development of lipidemia in HIV-infected patients, involving several studies which postulated the interactions between the virus, antiretroviral therapies, and host factors (Brinkman et al., 1999; Safrin & Grunfeld, 1999; Lenhard et al., 2001; Mooser and Carr, 2001).

The pathogenesis of hyperlipidemia is incompletely understood and appears to be associated with a number of factors. It is not possible to derive a precise incidence rate for lipidemia from these studies (Behren et al., 2005; Carr et al., 1998; Vergis et al., 2001) since they use different observation period and cut off points for hyperlipidemia and included patients with lipid disorders at baseline. The study by Almeida observed significant increase in total cholesterol, triglycerides and glucose in 110 patients after the treatment with the HAART. The glucose levels were increased due to the HAART in this study.

Nevertheless, the mechanisms that promote lipid alterations in HIV infected patients are still not completely understood, and may be potentiated by genetic and environmental factors as well as by medications (Grinspoon & Carr, 2005). Kramer et al., (2009) reported dyslipidemia in the HIV patient who makes use of HAART characterized by increased VLDL (the greatest triglyceride transporter) and LDL-cholesterol levels and reduction of the HDL-cholesterol level.


Since HIV has become a chronic disease as a result of the efficacious use of HAART, discussion has turned to questions about how to address the metabolic changes associated with the potent use of HAART. Highly active anti retroviral associated lipidemia is characterized by elevated serum concentrations of triglycerides, low density lipoprotein (LDL-c), very low-density lipoprotein (VLDL), and apolipoprotein B (apoB), and low levels of high density lipoprotein (HDL-c), constituting an atherogenic lipid profile.

Nutritional care and support helps people living with HIV to manage HIV-related complications, promotes good responses to medical treatment, and improves the person’s quality of life by maintaining strength, comfort, level of functioning, and human dignity (FANTA, 2004). Having proper nutrition in HIV/AIDS includes consuming diversified or variety of foods that will provide the body with the necessary energy, protein, fats, vitamins and minerals (MOH, 2006). According to the Kenyan National Guidelines on Nutrition and HIV/AIDS (2006), dietary intake, along with regular exercise, controlling weight, avoiding alcohol intake, smoking and other narcotic drugs make up nutrition related healthy life styles. Dietary diversity, the consumption of an adequate variety of food groups, is an aspect of dietary quality and can be considered an indicator of general nutritional adequacy (Nontobeko et al., 2008). Poor dietary diversity, a component of food insecurity, has been associated with mortality among HAART-naïve individuals in Uganda (Rawat et al., 2012). As the HIV infection becomes a more chronic disease and the management becomes increasingly sophisticated, the ability to ensure HIV-infected persons have access to high quality, nutritious food choices that promote optimal dietary patterns, rather than just sufficient quantities of food, is significant (Faintuch et al., 2006; Fields-Gardner et al., 2004).

Kramer, et al., (2009) reported dyslipidemia in the HIV patient who makes use of HAART characterized by increased VLDL (the greatest triglyceride transporter) and LDL-cholesterol levels and reduction of the HDL-cholesterol level. The author also suggests that the facts which would lead the HIV patient to present lipidemia are not totally elucidated yet. It is not clear whether it directly occurs due to the use of HAART or if it is a product of many factors such as: HAART treatment, genetic predisposition, diet and physical exercise or other factors such as the host response to the infection by the HIV. However, it remains uncertain whether these complications are related to each other, and whether they are exclusively associated with protease inhibitor administration (Penzak et al., 2002). Nevertheless, the mechanisms that promote lipid alterations in HIV/AIDS patients are still not completely understood, and may be potentiated by genetic and environmental factors, as well as by medications (Grinspoon and Carr, 2005).


Anabwani G, Navario P. (92005). Nutrition and HIV/AIDS in sub-Saharan Africa: an overview. Nutrition 21(1):96-99.CrossRef, PubMed, Web of Science.

Behrens, G. M. N. (2005). Metabolisches Syndrom und Hyperlipidämie bei HIV-positiven Patienten. Herz Kardiovaskuläre Erkrankungen, 30(6), 458-466. doi:10.1007/s00059-005-2722-5.

Boyle B.A. (2002) Guide to Management of Protease Inhibitor. Toxicities and side effects. 1: pg1

Brinkman K., Smeitink J.A., Romijn J.A., Reiss P (1999). Mitochondrial toxicity induced by nucleoside-analogue reverse-transcriptase inhibitors is a key factor in the pathogenesis of antiretroviraltherapy-related lipodystrophy. Lancet;354:1112-5.

Brown J.E., J Isaacs, N Wooldridge, B Krinke, and M Murtaugh. 2008. Nutrition Through the Life Cycle. 3rd ed. Belmont, CA: Wadsworth Publishing.

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Call S.A., Heudebert G., Saag M., Wilcox C.M. (2000). The changing etiology of chronic diarrhea in HIV-infected patients with CD4 cell counts less than 200 cells/mm3. Am J Gastroenterol;95:3142-6.

Carpentier, A., Patterson, B. W., Uffelman, K. D., Salit, I., & Lewis, G. F. (2005b). Mechanism of highly active anti-retroviral therapy-induced hyperlipidemia in HIV-infected. In J.E. Forrester, D. Spiegelman, E.

Carr, A. (2000). HIV Protease Inhibitor-Related Lipodystrophy Syndrome. Clinical Infectious Diseases, 30(Supplement 2), S135–S142. doi:10.1086/313854

Castleman, T., Eleonore, S. F. and Cogill, B. (2004). Food and Nutrition Implications of Antiretroviral Therapy in Resource Limited Settings. Technical note. FANTA

Chiuve S.E., McCullough ML, Sacks FM, Rimm E.B., (2006) Healthy lifestyle factors in the primary prevention of coronary heart disease among men: benefits among users and nonusers of lipid-lowering and antihypertensive medications.

Cromley, E.K. and S.L. McLafferty, 2002. GIS and Public Health. 1st Edn., The Guilford Press, New York.

Dronda F. (2004). Cardiovascular risk in patients with chronic HIV-1infection: a controversy with therapeutic, clinical and prognostic implications. Enferm Infecc Microbiol Clin.

Faintuch J., Soeters P.B., Osmo H.G. (2006). Nutritional and metabolic abnormalities in pre-AIDS HIV infection.

Fields-Gardner C., Fergusson P. (2004). ADA reports: position of the American Dietetic Association and Dietitians of Canada: nutrition intervention in the care of persons with human immunodeficiency virus infection. J Am Diet Assoc.

Food and Nutrition Technical Assistance (FANTA). (2004) HIV/AIDS: A Guide for Nutritional Care and Support. Academy for Educational Development, 2nd edition, Washington DC.

Forrester J.E., Spiegelman D., Tchetgen E., Knox T.A., Gorbach S.L., ( 2002). Weight loss and body-composition changes in men and women infected with HIV. Am J Clin Nutr.

Friis-Møller, N., Weber, R., Reiss, P., Thiébaut, R., Kirk, O., d’ Arminio Monforte, A.,… Pradier, C. (2003). Cardiovascular disease risk factors in HIV patients–association with antiretroviral therapy. N Engl J Med.

Gatrell A.C. and Rigby, J.E. (2004) .Spatial perspectives in public health. In, Goodchild, M.F. and Janelle, D.G.(eds.) Spatially Integrated Social Science: Examples in Best Practice. Oxford University Press, NewYork.

Grinspoon S., Carr A. (2005). Cardiovascular risk and body fat abnormalities in HIV infected adults. N Engl J Med.; 352:48–62.

Grunfeld, C., Pang, M., Doerrler, W., Shigenaga, J. K., Jensen, P., & Feingold, K. R. (1992). Lipids, lipoproteins, triglyceride clearance, and cytokines in human immunodeficiency virus infection and the acquired immunodeficiency syndrome. Journal of clinical endocrinology and metabolism, 74(5), 1045–1052.

Hogg R.S., Yip B., Chan K.J., Wood E., Craib K.J., (2001) .Rates of disease progression by baseline CD4 cell count and viral load after initiating triple-drug therapy. JAMA 286.

Hsu, W.C., Pencharz, P.B., Macallan, D., Tomkins, A. (2005). Macronutrients and HIV/AIDS: review of current evidence; Consultation on Nutrition & HIV/AIDS in Africa. Durban South Africa.

Kant A.K. (2004). Dietary patterns and health outcomes. J Am Diet Assoc.; 104:615–635.

Knox T.A., Spiegelman D., Skinner S.C., Gorbach S. (2000). Diarrhea and abnormalities of gastrointestinal function in a cohort of men and women with HIV infection. Am J Gastroenterol ;95:3482–9

Koethe J.R., Heimburger D.C. ( 2010). Nutritional aspects of HIV-associated wasting in sub-Saharan Africa.Am J Clin Nutr.

Koutkia, P.,Grinspoon, S.(2004). HIV associated lipodystrophy: pathogenesis, prognosis, treatment, and controversies. Annual Rev Med.

Kramer A.S., Lazzarotto A.R., Sprinz E., Manfroi W.C. (2009). Metabolic abnormalities, antiretroviral therapy and cardiovascular disease in elderly patients with HIV. Arq Bras Cardiol.

Lenhard J.M., Croom D.K., Weiel J.E., Winegar D.A. (2000). HIV protease inhibitors stimulate hepatic triglyceride synthesis. Arterioscler Thromb Vasc Biol; 20:2625–9.

McMahon J., Wanke C., Terrin N., Skinner S., Knox T. (2011) Poverty, hunger, education, and residential status impact survival in HIV. AIDS Behav 15: 1503–1511. doi: 10.1007/s10461-010-9759-z.

Ministry of Health Kenya (MOH). (2007). Kenyan National Guidelines on Nutrition and HIV/AIDS. Ministry of Health, Government of Kenya.

Mooser V., Carr A. (2001). Antiretroviral therapy-associated hyperlipidaemia in HIV disease. Curr Opin Lipidol;12:313-19.

National AIDS and STI Control Programme (2012) Kenya AIDS Indicator Survey (KAIS) 2012: Preliminary Report, Nairobi, Kenya. Nairobi: Ministry of Health, Kenya. Available at

National AIDS and STI Control Programme. National Guidelines for Antiretroviral Therapy in Kenya, 4th Edition, Nairobi, Kenya 2011. Available at:

Newby P.K., Muller D., Tucker K.L. (2004). Associations of empirically derived eating patterns with plasma lipid biomarkers: a comparison of factor and cluster analysis methods. Am J Clin Nutr;80:759–767

Nontobeko,. M., Broeck, J. V., Meera, C., Luabeya, A., Ayesha, J., and Bennish, M. L. (2008). HIV Infection Is Associated with Decreased Dietary Diversity in South African Children. J Nutr. 2008 Sept; 138(9): 1705–1711.

Penzak, S. R., & Chuck, S. K. (2002). Management of protease inhibitor-associated hyperlipidemia. Am. J. Cardiovasc. Drugs 2:91-106.

Piwoz E. G. and Preble E. A (2000) HIV/AIDS and Nutrition. A review of the Literature and Recommendations for Nutritional Care and Support in Sub-Saharan Africa.

Popkin, B. M (2001a) .The nutrition transition and obesity in the developing world. J. Nutr.

Rasheed S., Yan J.S., Lau A., Chan A.S. (2008). HIV replication enhances production of free fatty acids, low density lipoproteins and many key proteins involved in lipid metabolism: a proteomics study. PLoS ONE. Article ID e3003.

Rawat R, McCoy S.I., Kadiyala S. (2012) Poor diet quality is associated with low CD4 count and anemia and predicts mortality among antiretroviral therapy naive HIV-positive adults in Uganda.JAcquir Immune Defic Syndr 62: 246–53.

Riddler S.A., Smit E, Cole SR, Li R, Chmiel JS, Dobs A, Palella F, Visscher B, Evans R & Kingsley LA (2003) . Impact of HIV infection and HAART on serum lipids in men. Journal of the American Medical Association.

Safrin, S., & Grunfeld C. (1999). Fat Distribution and metabolic changes in patients with HIV infection;AIDS 13:2493-505.

Sherer R. (2003). HIV, HAART, and hyperlipidemia: balancing the effects. J Acquir Immune Defic Syndr. ;34 Suppl 2:S123–9.

Tang A.M., Forrester J.E., Spiegelman D., Knox T.A., Tchetgen E., Gorbach S.L. (2002). Weight loss and survival in HIV-positive patients in the era of highly active antiretroviral therapy. J Acquir Immune Defic Syndr .

Van der Sande M.A., Schim van der Loeff MF, Aveika A.A., Sabally S., Togun T., Sarge-Njie R., (2004). Body mass index at time of HIV diagnosis: a strong and independent predictor of survival. J Acquir Immune Defic Syndr;37:1288-94.

Vergis, E.N., Paterson, D.L., Wagener, M.M., Swindells, S., & Singh, N. (2001). Dyslipidaemia in HIV-infected patients: association with adherence to potent antiretroviral therapy. Int J STD AIDS.;12(7):463-8.

Wilson I.B., Roubenoff R., Knox TA., Spiegelman D., Gorbach S.L., (2000). Relation of lean body mass to health-related quality of life in persons with HIV. J Acquir Immune Defic Syndr;24: 137–46


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