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J U N E 2 0 0 7                                 T H E S O U T H E R N A F R I C A N J O U R N A L O F H I V M E D I C I N E2 2

1. NUTRITION, WEIGHT LOSS AND 
HIV IN AFRICA

1.1 INTRODUCTION
The HIV epidemic affects large numbers of people living in the
southern African region.2 Despite more than 2 decades of
research, a cure remains elusive.3 The implementation of
proven preventive interventions has had limited success; and
the uptake of antiretroviral (ARV) drugs has lagged far behind
the estimated numbers in need.4 Furthermore, the production
of food in Africa may well be adversely influenced both by the
epidemic itself and by global warming.5 Nutrition, specifically
the use of food, special diets, micronutrients and so-called
immune boosters and supplements, has been suggested as an
affordable and practical means of ’delaying the onset of
advanced HIV infection’.6 Is this true? And if it is, how secure is
access to food and good nutrition in Africa? Floods, drought,
famine, poverty, war and political instability define much of
the everyday life of millions on this continent. Secure and
reliable access to food is extremely important in these
circumstances. In some instances, sex will be exchanged for
food and employment far from home may result in risky sexual
behaviour. The science of nutrition is more than the science of
food itself.5 It is about people, their access to food of a suitable
quality and quantity, and in addition it is about the production
of food and its utilisation. It is also about maintaining access
to food over decades so as to ensure that the children and
adults of Africa – including those who are HIV-infected – grow
and realise their full potential. 

Discussion about food and diet in the HIV era also requires that
due attention be given to the interactions and toxicities of the
ARV group of drugs. These have revolutionised the manage-
ment of HIV infection. Sooner or later all who are infected will

need to take these agents. Some ARVs are best given on an
empty stomach, some with food and others with a fatty meal.
Many give rise to metabolic alterations, such as insulin
resistance and glucose intolerance, fat abnormalities
(lipodystrophy, hyperlipidaemia), lactic acidosis, liver enzyme
abnormalities, anaemia and osteopenia.7 Certain herbs and
foods interfere with the bioavailability of the ARVs. Various
micronutrients have been shown to benefit the HIV-infected.
Home-grown diets, herbal concoctions and vitamin
supplements have been advanced by some as alternatives to
the ARVs and as cures of the disease, but without providing
evidence of their benefit.8 Where denial and stigma and
commercial interests have dictated the political and social
response to this epidemic, it has been a simple matter to add
nutritional nonsense and personal economic gain to the
general confusion that has defined public discussion.9

The science of nutrition and HIV infection intersect at several
strategic levels. Evidenced-based research confirms the
following four concepts:

■ Weight loss predicts death.10

■ Energy and nutrient needs are increased in the HIV-
infected.11

■ Adequate food – and not just vitamins and so-called
immune boosters – constitutes an appropriate supplement
for those in need.12

■ Nutritional security: Food alone is not enough. Children
and adults who are malnourished, whether they are
infected, exposed or affected, need comprehensive medical
and nutritional care and social support.13

These concepts will be discussed in detail in later chapters.

1.2 EPIDEMIOLOGY AND BASIC SCIENCE 
The human immunodeficiency virus (HIV) crossed into the
human race from its primate host in the early decades of the
20th century.14 Since that time it has spread throughout the
globe and has caused more than 20 million deaths
worldwide.15 Sub-Saharan Africa has borne the greatest
burden of the infection. Without access to ARV drugs average

G U I D E L I N E S

Nutrition and HIV/AIDS
Nutritional Guidelines for HIV-infected Adults and Children

in Southern Africa: Meeting the Needs

D C Spencer, C Harman, T Naicker, S Gohre, for the Nutrition Focus Group of the SA HIV Clinicians Society

Reviewers: N Rollins, D Labadarios, M Visser

‘Despite progress in boosting democracy, ending wars and improved economic growth, Africa is the only region in the world
becoming less able to feed itself’.1

Members of the Nutritional Focus Group: D C Spenser (Chair), 
C Harman, C Egbers, A Caradas, E Hefer, T J Dlamini, B Ndzungu, 
C Julsing, Z Makasi, T Naicker, S Gohre, F Venter, M Yssel, 
T Robinson.



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survival is about 10.3 - 10.8 years.16 The HIV virus is spread
from human to human via direct contact with sexual fluids
and blood (blood products) and to infants and children during
pregnancy and lactation.17 Since the mid-1990s, drugs called
antiretrovirals (ARVs) have been used to control viral
replication, and to prevent neonatal transmission and
accidental exposure to the virus. These interfere with the
growth cycle of the virus. Some prevent the virus from
entering the human cell (viral entry inhibitors), while others
inhibit viral enzymes that assist in the reproduction of the
virus: the nucleoside and nucleotide reverse transcriptase
inhibitors (NRTIs and NtRTIs) and the non-nucleoside reverse
transcriptase inhibitors (NNRTIs). The protease inhibitors (PIs)
block the assembly of newly formed viral proteins. A further
class of ARVs, the integrase inhibitors, impair the integration
of viral DNA into the human genome. Interactions with food
and other drugs, including herbs and the so-called immune
boosters, are well documented. These interactions may impair
viral control by a variety of mechanisms. 

The virus targets the cells of the immune system, particularly
the CD4 lymphocyte (the 'helper-T cells’).18 Despite the
increased production of these cells, they are ultimately
sacrificed to the virus. Eventually this progressive immune
deficiency leads to life-threatening infections and cancers: the
acquired immunodeficiency syndrome (AIDS). Once within a
cell, HIV-1 reproduces rapidly. From a single infected cell
thousands of new viral particles are released into the
bloodstream. In the laboratory this is measured as the viral
load. Nevertheless, most of the virus remains undetectable
within the cells of the body.19 Together with the medical
history and examination, the measurement of the CD4 cell
count and the viral load (VL) provide a platform from which to
assess the patient. Because of the effect of the infection on
nutritional status, this assessment should include the
nutritional evaluation of the patient. What does growth failure
and loss of weight mean in HIV-infected children and adults? 

1.3 WEIGHT LOSS IN HIV-INFECTED CHILDREN AND
ADULTS 

Weight loss is a strong predictor of death in HIV-infected
adults and children.20

During the 1980s and early 1990s, ‘Slim Disease’ was a term
used throughout central Africa to characterise a patient with
end-stage HIV infection or AIDS.21 Indeed, weight loss is used
in both the World Health Organization (WHO) and the Centers
for Disease Control (CDC) adult staging systems: unintentional
weight loss of < 10%  = WHO stage II and > 10% = stage III
and CDC stage C, i.e. is AIDS defining.22 In children older than

a year, weight loss resulting in a fall of 2 or more percentile
lines is AIDS defining if accompanied by chronic diarrhoea or
fever. Also AIDS defining is a child in the 25th percentile of
weight-for-height (on consecutive measurements separated
by more than 30 days).23 Severe wasting in adults is defined by
the CDC as a body mass index (BMI) < 18.5 (kg/m)2 or
unintentional weight loss of > 5% of usual body weight within
6 months.24 Growth faltering and stunting are common in
children with HIV infection and occur early in life.25-27 In
children, wasting is particularly associated with the loss of
lean body mass and failure to gain height.27

In adults both lean mass and fat are lost, though the loss of
lean mass predominates.24 In contrast, starvation leads
primarily to fat loss.24 Both the loss of lean mass and poor
linear growth in HIV-infected children are closely associated
with poor survival and protecting lean body mass prolongs
survival.24, 27

Weight loss in the HIV-infected is the sum of a number of
causes. Energy requirements are increased even in the
asymptomatic state.28, 29 These needs soar under periods of
stress and during malnutrition.29 Cytokines such as tumour
necrosis factor-� (TNF-�) and interleukin-1 (IL-1) released
during episodes of infection and even during the
‘asymptomatic’ phase of HIV infection, promote increased
metabolism, glucose recycling, muscle catabolism and
negative nitrogen balance.29, 30 They may also reduce appetite
even when there is no overt opportunistic disease. This results
in the characteristic wasting associated with AIDS.31 Levels of
interferon-� (INF-�) are persistently elevated in full-blown
AIDS.29, 31 Apart from these underlying metabolic factors, the
inability to eat or to swallow food and the increased loss of
dietary nutrients from vomiting and diarrhoea will lead to
wasting and malnutrition. Wasting also accompanies the
opportunistic infections and cancers of advanced HIV-
infection.

1.4 WEIGHT LOSS: ITS CAUSES AND INCREASED
ENERGY REQUIREMENTS (Table 1.1) 

1.4.1 Increased and often unmet energy requirements
during all stages of HIV infection

Energy requirements are likely to increase by 10% just to
maintain body weight and normal physical activity in
asymptomatic HIV-infected adults and to maintain normal
growth in asymptomatic, infected children. During sympto-
matic stages and particularly during AIDS (opportunistic
diseases) these energy requirements increase by 20 - 30%.
Energy needs may even increase to levels of 50 - 100% above

Weight = heaviness measured in kilograms 

Lean body mass = the total of all body components except
storage lipid (fat) and bone

Fat-free mass = the same as lean body mass 

WEIGHT LOSS PREDICTS DEATH
• Low weight reflects advancing disease

• Weight loss often indicates opportunistic infections or
progressive disease

• Weight loss should be a warning to the doctor/nurse to
initiate investigations and treatment



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normal in children who are severely malnourished and who
are experiencing weight loss.28, 29 When enriched with various
fats (peanut butter) or oils (olive, canola), food will provide
greater ‘energy content’. This ‘enriched’ food is needed to
supplement the daily, baseline dietary requirements if the
malnutrition and weight loss are to be corrected.

1.4.2. Decreased energy intake and the increased loss
of nutrients

Anorexia, nausea, gingivitis, oral sores and dysphagia will
impair food intake and promote weight loss. At times the ARVs
and the anti-TB drugs are poorly tolerated – nausea, anorexia,
and vomiting. Fortunately this situation is generally short-
lived and usually restricted to the first weeks after the start of
therapy. Depression and anxiety suppress appetite and result
in weight loss. Religious and cultural practices that require
regular fasting, purging and dietary restrictions may be
harmful in the context of advanced HIV infection.  Food access
and food security can be significantly affected when material
resources are lost - income, the inability to work. Chronic
diarrhoea and malabsorption may cause wasting: direct viral
invasion of gastrointestinal cells (HIV-enteropathy) can be
demonstrated in some patients.32 Both localised gastro-
intestinal and overwhelming generalised infections are

frequent in Africa. Pulmonary and extra-pulmonary TB,
salmonella, Escherichia coli, cryptosporidia and isosporiasis
may present with fever, anorexia, nausea, vomiting and
diarrhoea. Undiagnosed and untreated, these infections will
lead to wasting and ultimately death.

The prevention and treatment of weight loss is a priority for
patients who are HIV-infected. What can be done for patients
who are at risk? 

1.5 WEIGHT LOSS. ASSESSMENT AND TREATMENT 

1.5.1 Assessing weight loss 
All infected children and adults must be regularly followed up.
This includes taking a medical and nutritional history. The
patient must be thoroughly examined.  It goes without saying
that in southern Africa, every effort MUST BE MADE to identify
the infected so as to offer them protection from advancing
HIV disease and facilitate the control of the epidemic.  The
following measurements are essential: weight, height/length
in children, the mid-upper arm circumference (MUAC) and the
CD4 and viral load. MUAC is a useful means of assessing lean
body mass. Additional investigations are discussed in a
subsequent section. 

1.5.2  Managing weight loss
Attention must be given to the causes of weight loss and the
diagnosis and control of anorexia. Poverty, food insecurity and
related socio-economic issues ought to be recognised and
managed in as practical a way as possible. The timeous
provision of ARV therapy is a very appropriate means of
preventing weight loss and the secondary opportunistic
infections associated with it.33

Provide food. Provide nutritional counselling. Provide support
– but aim to make the patient and their family independent of
food parcels and short-term solutions. A team approach
(nurse, doctor, dietician and trained nutritional advisor) works
best. Diagnose and treat intercurrent disease. Check the CD4
and viral load and any other relevant tests as suggested by the
clinical examination. Consider starting ARV therapy where
appropriate. ‘The best way to achieve protein repletion in
clinically severe HIV/AIDS is to establish effective ARV
therapy.’34 Once an adult has achieved his/her normal body
weight, discourage further weight gain in those on ARVs.
Obesity is to be avoided. Fat redistribution, hyperglycaemia
and insulin resistance, the metabolic syndrome, hyper-
lipidaemia and cardiovascular disease are recognised
complications.35-37 Wasting and severe malnutrition may
require enteral and parenteral feeding. This is usually
undertaken in a hospital or clinic. Nutritional supplements
such as fortified porridges and food itself ought to be
accessed on behalf of the patient. The use of specific
micronutrients generally follows recommendations for the
population at large.  Safety, tolerability and cost are the
important drivers in this regard.24 The role of individual
supplements will be discussed later. Exercise – including
resistance training – has been found to improve the patient’s
quality of life, to build up lean body mass, and in those on

MANAGING WEIGHT LOSS EFFECTIVELY
• Record weight at each visit, usually 3 - 4 visits annually. 

• Identify the reason for the weight loss

• Control the HIV infection where indicated: ARVs may be needed

• Treat malnutrition: Food, supplements, micronutrients where

needed

• Diagnose and treat opportunistic disease

• Symptomatic control of: Nausea, anorexia, vomiting, diarrhoea

• Examine the oral cavity: Treat thrush, gingivitis and oral ulcers

• Stop smoking, alcohol abuse and recreational drug use

• Exercise and strength training may have a role in some

• Exclude hypogonadism (rare) and consider use of appetite

‘stimulants’ such as megesterol acetate, anabolic steroids and

dronabinol for nausea where appropriate (benefit controversial)

• Involve social support mechanisms: Social worker, income

grants, NGOs including faith-based groups that provide

nutritional support, exclude depression and anxiety, consider

incorporating a family member or ‘concerned other’.

HIV- Energy
positive phase

Adults and adolescents Asymptomatic 10%  

Symptomatic (mild) 20 - 30%  

Children Asymptomatic 10%

Symptomatic (mild) 20 - 30% 

Symptomatic 

(moderate to severe) 50 - 100%   *

*In the presence of severe malnutrition.

TABLE 1.1. INCREASED ENERGY NEEDS OF HIV-INFECTED
ADULTS, ADOLESCENTS AND CHILDREN28, 29

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ARVs, to improve serum lipid profiles.38, 39 The simplest monitor
of nutritional recovery in adults is the measure of sequential
weight gain.  But weight alone will not discriminate between
the return of lean muscle and/or fat, or for that matter
indicate the return of good health. Other measurements in
addition to that of weight will be needed.

REFERENCES
1. Christian Science Monitor. Hunger is spreading in Africa. August 01, 2005.

http://www.csmonitor.com/2005/0801/p01s02-woaf.html
2. Merson MH. The HIV-AIDS Pandemic at 25 – The Global Response. N Engl J Med

2006; 354: 2414-2417.
3. Hammer SM, Saag M, Schechter M, et al. Treatment for adult HIV infection:

2006 recommendations of the International AIDS Society-USA panel. JAMA
2006; 296: 827-843.

4. Hassan F, Bosch D. Monitoring the Provision of ARVs in South Africa: A Critical
Assessment. Aids Law Project, University of the Witwatersrand. ALP Briefing for
TAC, NEC on 17 and 18 January 2006, Cape Town. 

5. de Waal A, Whiteside A. New variant famine: AIDS and food crisis in southern
Africa. Lancet 2003; 362: 1234-1237. 

6. Smetherham J-A. Mrs v d Maas and the AIDS diet. Cape Times. 2004; 27
February.

7. Montessori V, Press N, Harris M, Akagi L, Montaner JSG. Adverse effects of
antiretroviral therapy for HIV infection. CMAJ 2004; 170: 229-238.

8. http://www4.dr-rath-foundation.org/THE_FOUNDATION/press_release
20050615.htm 

9. Health Ministry backs AIDS muti. City Press report on News24.com, 13 February
2006. http://www.news24.com/News24/South_Africa/Aids_Focus/ 0,,2-7-
659_1880449,00.html

10. Wheeler DA, Gilbert CL, Launer CA, et al. Weight loss as a predictor of survival
and disease progression in HIV infection. J Acquir Immune Defic Syndr 1998; 18:
80-85.

11. Mangili A, Murman DH, Zampini AM, Wanke CA. Nutrition and HIV infection:
Review of weight loss and wasting in the era of highly active antiretroviral
therapy from the Nutrition for Healthy Living Cohort. Clin Infect Dis 2006; 42:
836-842.

12. Young H, Borrel A, Holland D, Salama P. Public nutrition in complex
emergencies. Lancet 2004; 365: 1899-1909.

13. Finch L. Fighting for food aid – the struggle to assist groups affected by
HIV/AIDS. Lancet 2004; 364: 1650-1651.

14. Stebbing J, Gazzard B, Douek DC. Where does HIV live? N Engl J Med 2004; 350:
1872-1880.

15. Sepkowitz K. AIDS – the first 20 years. N Engl J Med 2001; 344: 1764-1772.
16. The UNAIDS Reference Group on Estimates, Modelling and Projections.

Improved methods and assumptions for the estimation of the HIV/AIDS
epidemic and its impact: recommendation of the UNAIDS Reference Group on
Estimates, Modelling and Projections. AIDS 2002; 16: W1-W14.

17. Schreibman T, Friedland G. Human immunodeficiency virus infection
prevention: Strategies for clinicians. Clin Infect Dis 2003; 36: 1171-1176.

18. Rosenberg ES, Walker BD. HIV Type 1-specific helper t cells: a critical host
defence. AIDS Research Human Retrovir 1998; 14 (Suppl 2): S143-S147.

19. Kilby JM. Human immunodeficiency virus pathogenesis: insights from studies
of lymphoid cells and tissues. Clin Infect Dis 2001; 33: 873-884.

20. Tang AM, Forrester J, Spiegelman D, Knox TA, Tchetgen E, Garbach SL. Weight
loss and survival in HIV-positive patients in the era of highly active
antiretroviral therapy. J Acquir Immune Defic Syndr 2002; 31: 230-236.

21. Serwadda D, Mugerwa R, Sewankambo N. Slim disease: a new disease in
Uganda and its associations with HTLV-III infection. Lancet 1985; 2: 849-852.

22. The WHO International Collaborating Group for the Study of the WHO Staging
System. Proposed ‘World Health Organisation Staging System for HIV Infection
and Disease’: preliminary testing by an international collaborative cross-
sectional study. AIDS 1993; 2: 711-718. 

23. Bailey RC, et al. Growth of children according to maternal and child HIV,
immunological and disease characteristics: a prospective cohort study in
Kinshasa, Democratic Republic of the Congo. Int J Epidemiol 1999; 28: 532-540.

24. Grinspoon S, Mulligan K. Weight loss and wasting in patients infected with
human immunodeficiency virus. Clin Infect Dis 2003; 36 (Suppl 2): S69-78).

25. Bobat R, Coovadia H, Moodley D, Coutsoudis A, Gouws E. Growth in early
childhood in a cohort of children born to HIV-1 infected women from Durban,
South Africa. Ann Trop Paediatr 2001; 21; 203-210.

26. Miller TL et al. Growth and body composition in children infected with the
human immunodeficiency syndrome virus-1. Am J Clin Nutr 1993; 57: 588-592.

27. Arpadi SM. Growth failure in HIV-infected children. WHO Consultation on
Nutrition and HIV/AIDS in Africa: Evidence, lessons and recommendations for
action. Durban, 10-13 April 2005. Geneva: World Health Organization, 2005.

28. Food and Nutrition Technical Assistance (FANTA) Project. HIV/AIDS: A Guide for
Nutritional Care and Support. 2nd ed. Washington, DC: Academy for
Educational Development, 2004: 86.

29. Hsu J W-C, Pencharz PB, Macallan D, Tomkins A. Macronutrients and HIV/AIDS:
A review of current evidence. WHO Consultation on Nutrition and HIV/AIDS in
Africa: Evidence, lessons and recommendations for action. Durban, 10-13 April
2005. Geneva: World Health Organization, 2005: 1, 2.

30. Roubenhoff R, Grinspoon S, Skolnik PR, et al. Role of cytokines and testosterone
in regulating lean body mass and resting energy expenditure in HIV-infected
men. Am J Physiol Endocrinol Metab 2002; 283: E138-145.

31. Hazenberg MD, Otto SA, van Benthem BHB, et al. Persistent immune activation
in HIV-1 infection is associated with progression to AIDS. AIDS 2003; 17: 1881-
1888.

32. Kotler DP. HIV infection and the gastrointestinal tract. AIDS 2005; 19: 107-117.
33. Gazzard B. Antiretroviral therapy for HIV: medical miracles do happen

(Editorial). Lancet 2005; 366: 346-347.
34. Shevitz AH, Knox TA. Nutrition in the era of highly active antiretroviral therapy.

Clin Infect Dis 2001; 32: 1769-1775.
35. Grunfeld C, Feingold KR. Metabolic disturbances and wasting in the acquired

immunodeficiency syndrome. N Engl J Med 1992; 327: 329-337.
36. Dube MP. Disorders of glucose metabolism in patients infected with human

immunodeficience: effects on parameters related to fatigue, dyspnea, weight
and body composition in HIV-infected adults. AIDS 2001; 15: 693-701.

39. Roubenoff R, McDermott A, Weiss L, et al. Short-term progressive resistance
training and lean body mass in adults infected with human immunodeficiency
virus. AIDS 1999; 13: 231-239.

2. NUTRITION, HIV AND CLINICAL
MEASUREMENT

2.1 NUTRITION: TAKING A DIETARY HISTORY
‘A simple nutritional assessment is available to all and requires
only an interview, a scale and a tape measure.’1 This
assessment begins with history taking: ‘What do you eat on a
typical day?’ ‘When last did you have a meal?’ ‘Tell me
everything you’ve had to eat or drink in the last 24 hours.’ The
nutritional history needs to give the interviewer a clear sense
of the client’s diet, its contents, amounts of food taken, regular
and reliable access to good food, and in the context of the HIV
epidemic, the stage of the infection and use by the client of
prescribed medication, herbs and traditional or so-called
complementary treatments.

It may be helpful to use actual plates, cups and spoons to
estimate the size of food portions. A diary card may be helpful:
‘Record everything you eat and drink for the next week. Add in
the amounts that you consume …’2 If the patient is an infant,

enquire as to what feeds are being given. Formula? Breast?
Exclusive or mixed breastfeeds? How is the food prepared?
What understanding does the client have of hygiene and
food? ARV drugs may cause physical changes: ask about
weight loss and breast enlargement and the loss of fat on the
face, arms and legs. What is the stage of HIV infection? Have
opportunistic diseases such as TB been experienced? Co-
morbid conditions such as diabetes, liver and cardiovascular
disease will require dietary advice and the outlining of
potential ARV drug and food interactions.3, 4 ‘Do you or the
family ever go without food?’ Enquire about the patient’s
access to an income and food. In busy public clinics trained
caregivers from the community can assist with history taking,
and the weighing and measuring of patients. The goal of the
dietary analysis is to prevent weight loss and optimise
nutrition: the counselling that takes place will foster the
patient-doctor/nurse relationship and improve communi-
cation.5,6 However, providing specific advice is difficult. Diets
vary between and within populations. Familiarity with local
foods, food preparation and the culture and traditions of a



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community will root any advice offered within the context of
the patient’s life. Dietary advice needs to be culture sensitive
and feasible. See also Appendices 1 and 2 for action to be
taken in response to nutritional risk.

2.2 NUTRITION: MEASUREMENT

Medical science is built upon practices that have measurable
and reproducible outcomes. The measurement of human
nutrition is based upon anthropometric, biochemical, clinical
and dietary parameters – the so-called ‘ABCD’ of nutritional
assessment.7, 8 Included in the anthropometric measurement
are body weight, length or height, the body mass index
(BMI) and the mid-upper arm circumference (MUAC). If
performed reliably, these form a baseline from which to judge
growth failure or abnormality. Often the measurements can be
carried out by a trained non-medical clinic or community
member. Results must be tabulated in the clinic file at each
visit, preferably before the patient is seen by the nurse or
doctor. A reduction in lean body mass in children is detectable
before a deceleration in linear growth (length/height) and is
important to document and act upon.9 Waist circumference is

a measure of cardiovascular risk, type 2 diabetes, hypertension
and increased cholesterol risk in non-HIV infected adults. This
may also be a helpful measurement in patients on ARVs at risk
for the metabolic complications of therapy.10

Paediatric growth charts record both height and weight:
height-for-age, weight-for-age, and weight-for-height. All
three measurements must be plotted at each visit.8 In young
children, body length will replace height. MUAC and
subscapular and triceps skin-fold thickness reflect lean body
mass and fat stores in adults and children older than 1 year.
About 50% of body fat is subcutaneous.11,12 MUAC is generally
the preferred measurement. MUAC is an essential component
of malnutrition assessment and is routinely used in World
Health Organization (WHO) and UNICEF-sponsored relief
programmes.6 Intercurrent illness will alter these measure-
ments: repeated measurement reveals the emergence of
trends and the early onset of new disease.

In adults the body mass index, BMI = weight (kg)/height (m)2

(Table 2.1), is a sensitive measure of both under and over
nutrition. (The BMI can be read directly from a nomogram –
usually present in most practices, or worked out from the
above equation.)

DIET HISTORY

A diet history is a detailed dietary record that may include a 24-

hour recall, a food frequency questionnaire and other information

such as weight, history, previous dietary changes, the use of

supplements and known food intolerance. 

NUTRITIONAL QUESTIONNAIRE

Question 1. Baseline assessment. What is your usual weight and
height (adult)? Is the child being regularly weighed and having

his/her height/length measured at the clinic? May I see the child's

clinic card, please? 

Question 2. Weight loss: Have you recently lost weight? Do your
clothes still fit? Have you noticed weight gain and body changes on

the antiretrovirals (ARVs)? 

Question 3. Appetite: Has your appetite changed? 
Question 4. Digestion: Do you have any of the following:

• Difficulty with swallowing?

• Discomfort or pain in the mouth?

• Nausea and vomiting?

• Diarrhoea?

Question 5. Food access and food security: In the past week have
you missed any meals?  Do you or your children ever go hungry?

Are you able to eat meat or fish regularly? How often? 

Question 6. Non-prescription medication. Do you take any
immune boosters, vitamin supplements or traditional medicines?

How much alcohol and/or recreational drugs do you take each day

or each week? 

Question 7. Prescription medication. Do you know which of your
ARVs need to be taken with or without food/a meal? What

medicines other than ARVs are you taking?

Question 8. Stage of HIV infection: Have you been admitted to
hospital or been diagnosed with tuberculosis in the last 3 to 5

years? Do you know your most recent CD4 level? 

MUAC IN ADULTS AND CHILDREN
By convention the tape is placed around the left upper arm midway

between the tip of the acromion process (shoulder) and the

olecranon (elbow). Values in adult men of < 23 cm and women of

< 22 cm represent malnutrition. Paediatric measurements vary

with age and will be detailed in the (later) paediatric chapter. 

WEIGHING THE PATIENT
Subjects are weighed in light underclothing without shoes. Heavy

items of jewellery, wallet, keys, etc. should be removed and the

patient advised that a large meal just prior to the measurement and

a full bladder at the time of measurement will increase the reading.

Where available a beam or lever balance is more reliable. Bathroom

scales are generally unreliable. The scale must be regularly serviced

and checked, preferably monthly. Babies are weighed naked and

without their nappies. 

Classification BMI (kg/m2)

Severe undernutrition < 16

Underweight < 18.5

Normal 18.5 - 24.9

Overweight 25.0 - 29.9

Obesity, class I 30.0 - 34.9

Obesity, class II 35.0 - 39.9

Extreme obesity, class III > 40
Source: National Heart, Lung and Blood Institute, National Institutes of Health, USA.
Clinical Guidelines on the Identification, Evaluation, and Treatment of Overweight
and Obesity in Adults. NIH Publication  No. 98-4083. 

TABLE 2.1. THE BODY MASS INDEX (BMI) – A MEASURE OF
THE RISK OF UNDERNUTRITION AND OBESITY



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2.3 NUTRITION: THE LABORATORY 

Laboratory tests in HIV patients are restricted to those with
clinical value. The CD4 cell count and viral load are essential
and provide a direct measure of the patient's immune system
and the virus. Often included in the routine workup are tests
that indicate whether vital organs are functioning normally:
blood, the full blood count (FBC); liver – the alanine
aminotransaminase (ALT) level; and kidneys – urea or
creatinine and urine dipstix. From time to time sophisticated
diagnostic tests are indicated (blood cultures, malaria smears,
sputum analysis for TB and urine microscopy), but tests that
directly measure the micronutrient status of the patient are
seldom required. In general, the clinical evaluation and
anthropometric measurements discussed above will guide the
clinician in deciding what additional investigations are
necessary. 

2.3.1 Anaemia

Anaemia is an independent predictor of mortality in HIV
patients. It is therefore important to document and to follow
and act upon.13 The common nutritional deficiencies
associated with anaemia are iron, folate and vitamin B12.
However the most common cause of anaemia in HIV-infected
patients is 'the anaemia of chronic disorders', an anaemia seen
in many chronic inflammatory or infective conditions and not
related to any nutritional deficiency.14 The haemoglobin, red
cell mass and haematocrit are decreased. The laboratory will
provide a comment on the peripheral blood smear and record
the mean corpuscular volume (MCV), a measure of the size of
the red cell. The MCV is usually normal in the anaemia of
chronic disorders (normocytic anaemia), while in iron
deficiency the red cells are small and the MCV is less than
normal (microcytic anaemia). In folate and B12 deficiencies, the
MCV will usually be elevated (macrocytic anaemia). Other
causes of anaemia are occasionally present: red cell
haemolysis, drug-induced toxicity (the ARVs: zidovudine,
combivir), bone marrow infiltrate (e.g. tumour or infection
such as TB) or infection with HIV itself. Not every HIV-infected
person requires iron supplementation. Indeed most have an
excess of storage iron (ferritin), and added iron may be
harmful.15,16 Nevertheless during pregnancy and lactation
supplementation with iron, folate and multivitamins is given
to both HIV-infected and non-infected women. In other
circumstances, iron supplementation should only be provided
if iron deficiency has been confirmed on laboratory testing.  In
many parts of Africa malaria and hookworm infestation are
common. These must be excluded in any investigation of
anaemia in patients from rural or endemic areas.17

2.3.2 Serum micronutrients in the HIV-infected patient

The persistent presence of the virus in the human host ensures
that the immune system is chronically stimulated. Hence the
frequently elevated total proteins in HIV-positive patients –
resulting from the chronic overproduction of gamma
globulins, including antibodies. Intercurrent illnesses cause
additional inflammatory stress. An ‘acute-phase response’
follows. For the clinician, elevated erythrocyte sedimentation

rate (ESR) and C-reactive protein (CRP) level help to define
such periods.18,19 Local and systemic cytokine levels rise and
fall. Micronutrient concentrations mirror these changes. Some
increase, others decrease.20, 21 Some micronutrients such as
vitamins A, C and E, and zinc may behave as antioxidants. Low
serum levels may therefore indicate utilisation rather than an
underlying deficiency.22, 23 Blood levels are an incomplete
measurement of the body's micronutrient status.  Without the
clinical context of the patient and knowledge of the
micronutrient status of the community, the meaning of an
individual result is of limited value.24 Studies from the Cape
and KwaZulu-Natal confirm generally low levels of
micronutrients among HIV-infected South African children
and adults.25-27 Furthermore, micronutrient supplementation
with vitamin A reduces morbidity, growth failure and death,
while zinc supplementation reduces the duration of diarrhoea
and associated fluid losses in young HIV-positive children.27,28

Selenium and zinc also behave as acute-phase reactants: their
levels fluctuate during infection. The value of observational
and cross-sectional micronutrient studies and studies that
ignore the acute-phase phenomenon remain difficult to
interpret.29-31 Any measurement of individual micronutrients
must place the result within its clinical context. Where these
issues are ignored, clinical studies fail to provide convincing
data.29 The routine measurement of micronutrients is
expensive, difficult to interpret and generally not warranted in
the southern African situation. But it goes without saying that
well-planned clinical studies in this area are urgently needed
to supplement the sparse data currently available. 

2.3.3 Liver function tests: albumin and serum ALT 

A low serum albumin level may indicate poor nutrition, and
indeed low serum albumin predicts both death and length of
stay in hospitalised HIV-positive patients.5 But malnutrition is
just one of several causes of low albumin: liver disease with
decreased protein synthesis, renal disease with protein loss
(albuminuria), enteric infections with chronic diarrhoea and
malabsorption are also associated with low albumin levels. In
addition, as an acute-phase reactant, a low albumin level may
simply behave as a marker of an active inflammatory state.

Liver-related disease has become a significant cause of death
of patients on long-term ARV therapy.32 Prolonged survival on
ARVs has increased exposure to the following:

■ Persistent liver damage resulting from uncontrolled
hepatitis B or C virus infection.33

■ Non-alcoholic steatohepatitis (NASH) may result from HIV
infection itself and from exposure to the metabolic side-
effects of the ARVs.34, 35

■ Direct drug toxicity. All drugs are potential hepatotoxins
but certain ARVs are more frequently associated with liver
toxicity, e.g. nevirapine in women with CD4 counts
> 250 cells/µl and men with CD4 counts > 400/µl, the
combination of stavudine and didanosine, and the
protease inhibitor ritonavir.32, 35, 36

Elevated transaminases, e.g. ALT, may accompany liver damage
and must be checked two or three times a year while on the



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ARVs. Elevated transaminases ought to direct the physician to
excluding alcohol (GGT>>AST >>ALT) and the activity of the
hepatitis viruses (HBV and HCV) as possible causes.37, 38

Elevated alkaline phosphatise and gamma-gluteryl transferase
(GGT) may suggest an infiltrative process including the
presence of hepatic granulomas, e.g. TB or cotrimoxazole-
induced hepatitis.39

2.3.4 Miscellaneous tests

Amylase levels are checked in symptomatic patients with
suspected pancreatitis: abdominal pain, nausea, vomiting
while taking didanosine or the combination of didanosine and
stavudine, and rarely, lamivudine in children. Concomitant use
of alcohol, pentamidine, hydroxyurea and steroids including
anabolic steroids, will increase the risk.40 Serum amylase is not
tested routinely. 

Fasting plasma cholesterol and triglycerides, glucose (or urine
dipstix) are suggested at baseline assessment and annually in
patients with known risk factors for cardiovascular disease,
diabetes, etc. Patients on ARVs associated with lipodystrophy
are at an increased risk of cardiovascular disease and insulin
resistance. These will also need annual or bi-annual fasting
lipids and sugars.4

2.4  NUTRITION: THE CLINICAL ASSESSMENT

See also Appendices 1 and 2.

The assessment of the nutritional status of HIV-infected
patients begins with the initial interview. A clinical
examination follows. This is combined with measurements
that are repeated during subsequent follow-up visits: weight,
height/length to enable a BMI measurement to be made,
MUAC, and in patients on lipid-altering ARVs, waist

NUTRITIONAL ASSESSMENT OF THE HIV-INFECTED PATIENT7

Laboratory tests (baseline assessment 
History Examination and as indicated clinically thereafter) 

Weight loss Weight Full blood count and haemoglobin (anaemia)
Dietary history Height or length Serum iron studies only if significantly 

Access to food and food security Body mass index (BMI) (normal anaemic, Hb < 8 - 10 g/dl

Stage of HIV infection value: 18.5 - 24.9 kg/m
2) otherwise clinically indicated

Use of medication including the Mid-upper arm circumference (MUAC) Viral hepatitis serologies (HBV, HCV)

antiretrovirals (normal values: adult males > 23 cm; and additional liver tests as clinically indicated 

Pregnancy, lactation and the adult females > 22 cm; Plasma fasting cholesterol and triglyceride
‘child under 5’ pregnant females > 23 cm) Plasma fasting blood glucose
Micronutrient and vitamin use Waist circumference, 'at risk values' The albumin level, and specific micronutrient 
Family and/or community support (adult males ≥ 102 cm, levels are not routinely assessed

adult females ≥ 88 cm) Serum amylase not routinely assessed
Clinical examination of the patient: 
signs of wasting, evidence of stunting 
in children, signs of advanced HIV 
infection, signs of specific nutritional 
deficiency syndromes, signs of 
treatment-related fat redistribution 

What to do? 

History: Examination Laboratory tests
Identify food insecurity Weight loss is significant and is Anaemia, low serum albumin levels indicate

Assist families/patients with associated with mortality in the an increased risk of death in the HIV infected.

accessing government support HIV infected. Check measurements All abnormal investigations must be explained
and welfare grants to exclude significant weight loss and and acted upon

Identify lack of nutritional 
malnutrition (weight, BMI)

Anaemia: check the MCV and find the likely
knowledge Lower than normal MUAC levels: cause and correct this

Refer to counsellor to assist with loss of lean body mass Serum iron, % saturation, transferrin
practical support of the mother/ Correct underlying malnutrition and and ferritin levels may be helpful if iron
child/patient ensure virus is brought under control deficiency is suspected

Identify a responsible Assess food access, intake and utilisation Elevated ALT: check the AST, alkaline
home or community member who Examine patient to exclude active phosphatase, GGT and HBV, HCV antibody
can assist opportunistic disease and uncontrolled tests. Decide whether this is a medication-

Identify opportunities to HIV infection related toxicity or an opportunistic process. If

prevent HIV transmission Increased abdominal circumference: necessary follow up with a hepatic ultrasound

Assist the pregnant patient with check which ARVs are being used and
to exclude a space-occupying lesion, fatty liver

making informed choices including confirm metabolic abnormalities with
or NASH, enlarged abdominal lymph nodes

exclusive breastfeeding appropriate investigations

Where weight loss is confirmed, Give dietary advice and refer where
examine and investigate to exclude available to dietician
opportunistic disease, e.g. tuberculosis, Weight reduction and exercise
advanced HIV programme may be indicated



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circumference can be considered. Baseline and follow-up
blood and urine tests complete the assessment and permit
clinical staging of the patient.  At this time the patient will
want to know whether ARV drugs are needed and what if any,
is the role of diet, micronutrient supplements and vitamins.
These topics will be addressed in the next chapter. 

REFERENCES
1. Shevitz AH, Knox TA. Nutrition in the era of highly active antiretroviral therapy.

Clin Infect Dis 2001; 32: 1769-1775.
2. Truswell AS. Measuring nutrition. BMJ 1985; 291: 1258-1262.
3. Nerad J, Romeyn M, Silverman E, et al. General nutrition management in

patients infected with human immunodeficiency virus. Clin Infect Dis 2003; 36
(Suppl 2): S52-62.

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

5. Souba WW. Nutritional support. N Engl J Med 1997; 336: 41-48.
6. Young H, Borrel A, Holland D, Salama P. Public nutrition in complex

emergencies. Lancet 2004; 364: 1899-1909.
7. Knox TA, Zafonte-Sanders M, Fields-Gardner C, Moen K, Johansen D, Paton N.

Assessment of nutritional status, body composition and human
immunodeficiency virus-associated morphologic changes. Clin Infect Dis 2003;
36 (Suppl 2): S63-68.

8. Jones JM. The methodology of nutritional screening and assessment tools.
J Hum Nutr Dietet 2002; 15: 59-71.

9. Arpadi SM. Growth failure in HIV-infected children. WHO Consultation on
Nutrition and HIV/AIDS in Africa: Evidence, lessons and recommendations for
action. Durban, 10-13 April 2005. Geneva: World Health Organization, 2005: 4.

10. Hadigan C, Meigs JB, Corcoran C, et al. Metabolic abnormalities and
cardiovascular disease risk factors in adults with human immunodeficiency
virus infection and lipodystrophy. Clin Infect Dis 2001; 32: 130-139.

11. American Dietetic Association. HIV/AIDS Medical Nutrition Therapy Protocol:
Medical Nutrition Therapy Across a Continuum of Care. Chicago, III.: American
Dietetic Association, 1998.

12. Heller LS. Nutrition support for children with HIV/AIDS. J Am Diet Assoc 1997;
97: 473-474.

13. Weinberg GA, Boelaert JR, Weinberg ED. Iron and HIV infection. In: Friis H, ed.
Micronutrients and HIV Infection. Boca Raton: CRC Press, 2001: 135-157.

14. Weiss G, Goodnough LT. Anemia of chronic disease. N Engl J Med 2005; 352:
1011-1023.

15. Boelaert JR, Weinberg GA, Weinberg ED. Altered iron metabolism in HIV
infection: mechanisms, possible consequences and proposals for management.
Infect Agents Dis 1996; 5: 36-46.

16. Gangaidzo IT, Moyo VM, Mvundura E, et al. Association of pulmonary
tuberculosis with increased dietary iron. J Infect Dis 2001; 184: 936-939.

17. Spivak JL. The blood in systemic disorders. Lancet 2000; 355: 1707-1712.
18. Feldman JG, Goldwasser P, Holman S, DeHovitz J, Minkoff H. C-reactive protein

is an independent predictor of mortality in women with HIV-1 infection.
J Acquir Immune Defic Syndr 2003; 32: 210-214.

19. Munford RS. Statins and the acute-phase response (Editorial). N Engl J Med
2001; 344: 2016-2018.

20. Tomkins A. Assessing micronutrient status in the presence of inflammation.
J Nutr 2003; 133; 1649S-1655S.

21. Grunfeld C, Feingold KR. Metabolic disturbances and wasting in the acquired
immunodeficieincy syndrome. N Engl J Med 1992; 327: 329-336.

22. Halliwell B, Gutteridge JM. The antioxidants of human extracellular fluids. Arch
Biochem Biophys 1990; 280: 1-8.

23. Nike E. Antioxidants in relation to lipid peroxidation. Chemistry and Physics of
Lipids 1987; 44: 227-253.

24. Brown KH et al. Potential magnitude of the misclassification of a population's
trace element status due to infection: example from a survey of young Peruvian
children. Am J Clin Nutr 1993; 58: 549-554.

25. Eley BS, Sive AA, Abelse L, Kossew G, Cooper M, Hussey GD. Growth and
micronutrient disturbances in stable, HIV-infected children in Cape Town. Ann
Trop Paediatr 2002; 22: 19-23.

26. Visser ME, Maartens G, Kossew G, Hussey GD. Plasma vitamin A levels in HIV
infected adults in Cape Town, South Africa. Br J Nutr 2003; 89: 475-482.

27. Bobat R, Coovadia H, Stephen CV, et al. Safety and efficacy of zinc
supplementation for children with HIV-1 infection in South Africa: a
randomised double-blind placebo-controlled trial. Lancet 2005; 366: 1862-
1867.

28. Coutsoudis A, Bobat R, Coovadia H, Huhn L, Tsai W, Stein Z. The effects of
vitamin A supplementation on the morbidity of children born to HIV infected
women. Am J Public Health 1995; 85: 1076-1081.

29. Truswell AS. Levels and kinds of evidence for public-health nutrition. Lancet
2001; 357: 1061-1062.

30. Nichol C et al. Changes in the concentrations of plasma selenium and
selenoproteins after minor elective surgery: further evidence for a negative
acute phase response? Clin Chem 1998; 44: 1764-1766.

31. Lawlor DA, Smith GD, Bruckdorfer KR, Kundu D, Ebrahim S. Those confounded
vitamins: what can we learn from the differences between observational versus
randomised trial evidence? Lancet 2004; 363: 1724-1727.

32. Morcroft A, Soriano V, Rockstroh J, et al. Is there evidence for an increase in the
death rate from liver-related disease in patients with HIV? AIDS 2005; 19: 2117-
2125.

33. Bonacini M, Louie S, Bzowej N, Wohl AR. Survival in patients with HIV infection
and viral hepatitis B or C: a cohort study. AIDS 2004; 18: 2039-2045.

34. Pol S, Lebray P, Vallet-Pichard A. HIV infection and hepatic enzyme
abnormalities: Intricacies of the pathogenic mechanisms. Clin Infect Dis 2004;
38 (Suppl 2): S65-72.

35. Duval X, Journot V, Leport C, et al. Incidence and risk factors for adverse drug
reactions in a prospective cohort of HIV-infected adults initiating protease
inhibitor-containing therapy. The Antiprotease Cohort, APROCO. Clin Infect Dis
2004; 39: 248-255.

36. Van Leth F, Andrews S, Grinszteyn B, et al., for the 2NN Study Group. The effect
of baseline CD4 cell count and HIV-1 viral load on the efficacy and safety of
nevirapine or efavirenz-based first-line HAART. AIDS 2005; 19: 463-471.

37. Pratt DS, Kaplan MM. Evaluation of abnormal liver-enzyme results in
asymptomatic patients. N Engl J Med 2000; 342: 1266-1271.

38. Kew M. Serum aminotransferase concentrations as evidence of hepatocellular
damage. Lancet 2000; 355: 591-592.

39. Kreisberg R. Clinical problem solving. N Engl J Med 1995; 332: 945-949.
40. Dube M. Disorders of glucose metabolism in patients infected with HIV. Clin

Infect Dis 2000; 31: 1467-1475.

The following chapters of this Guideline will appear in
subsequent issues of the Journal.



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ENTRY AND EXIT CRITERIA: ADULTS > 14 YEARS 
NUTRITION RISK SCORE
If the total score exceeds 6 points, the patient can be seen as nutritionally at risk and requires food and to be provided with long-term

nutritional support and access to government or NGO assistance or welfare grants. Where practical, the patient should be referred to a

dietician for appropriate nutritional intervention.

DATE AND SCORE

1. Weight loss in 3 months
• None 0

• 3 kg (< 1clothes size) 1

• 3 - 6 kg (1 - 2 clothes size) 2

• > 6 kg (> 2 clothes size) 3

2. BMI
• ≥ 18.5 0

• 17.0 - 18.4 1

• 16.0 - 16.9 2

• ≤ 16 3

3. Appetite
• Good (most of plate) 0

• Poor (half of plate eaten) 1

• Unable to eat  (no food in 2 days) 2

4. Ability to eat
• No problems 0

• Mild vomiting/diarrhoea 1

• Difficult swallowing/chewing 2

• Severe vomiting/diarrhoea 2

• Need help feeding 3

5. Stage of infection (WHO stage classification) 
• Stage I 0

• Stage II 1

• Stage III 2

• Stage IV 3

6. Other problems
• None 0

• TB 2

• Pregnant/lactation 2

• Social problems 2

TOTAL SCORE

Source: Harman C. Nutritional Assessment Chart. Nutrition Unit, Department of Paediatrics, Chris Hani Baragwanath Hospital, Soweto, 2007.

APPENDIX 1



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ENTRY AND EXIT CRITERIA: CHILDREN < 14 YEARS 
NUTRITION RISK SCORE
If the total score exceeds 6 points, the child is nutritionally at risk and needs to be given food and provided with long-term nutritional

support and access to government or NGO assistance or grants.  Where practical, the patient should be referred to a dietician for an

appropriate nutritional intervention.  Where acute malnutrition is diagnosed, this child MUST BE ADMITTED to hospital and provided with

appropriate formula feeding as per WHO guidelines. RTHC = Road to Health Chart.

DATE AND SCORE

Is this child malnourished?
1. Present weight:

0 - 3 years (RTHC)
• Following a curve on the RTHC 0

• Inadequate weight gain, growth faltering 2

• ≤ 3rd percentile RTHC 4

• ≤ 60% of expected weight on the RTHC 6

2 - 14 years BMI
• ≥ 50th percentile 0

• < 50th percentile 2

• ≤ 25th percentile 4

• < 3rd percentile 6

3. Appetite
• Good (5 meals a day) 0

• Poor (less than 3 meals daily) 2

• Unable to eat (no food in 2 days) 4

4. Ability to eat
• No problems 0

• Mild vomiting/diarrhoea 1

• Difficult swallowing/chewing 2

• Severe vomiting/diarrhoea 4

5. Stage of infection
• Stage I 0

• Stage II 1

• Stage III 2

• Stage IV 3

6. Other problems
• None 0

• TB 2

• Pregnant/lactation 2

• Social problems 2

TOTAL SCORE

Source: Harman C. Nutritional Assessment Chart. Nutrition Unit, Department of Paediatrics, Chris Hani Baragwanath Hospital, Soweto, 2007.

APPENDIX 2