Sutinen (2002b) studied lipodystrophy in 34 HIV-infected men on HAART and 35 HIV-negative controls. 25 of the HIV group had lipodystrophy, defined as subcutaneous fat loss +/- visceral fat increase or buffalo hump. Of the men on HAART, those with lipodystrophy had taken NRTIs for longer than the lipodystrophy-negative men (69 vs 45 months, p<0.05). The men with lipodystrophy had significantly higher levels of abdominal fat than the 2 other groups, and more intra-abdominal vs subcutaneous fat. Those with lipodystrophy also had a range of elevated metabolic parameters and greater liver fat content than the other 2 groups.

Grunfeld (2002) presented preliminary results from the Fat Redistribution and Metabolism (FRAM) study - a cross-sectional investigation of lipodystrophy in about 800 HIV-positive men (mean CD4 count 394, 14% had never taken antiretrovirals, 83% had taken NRTIs) with 370 age-matched controls. Of the HIV-positive group, both those with and without self-reported lipoatrophy had less subcutaneous fat than controls, although those with reported lipoatrophy had greater fat loss. Although a cross-sectional study, the authors reported greater fat loss from the arms and legs than from the trunk, while the upper trunk was least affected. Average visceral fat was slightly lower among HIV-infected subjects. Higher hip-to-waist ratios occurred among those with reported lipoatrophy, due to the relative preservation of trunk fat. The authors concluded that increased visceral abdominal fat is not related to HIV or antiretroviral therapy. Buffalo hump was detected in 12% of controls and 7% of HIV-positive men (non-significant) and was also deemed unrelated to HIV or HAART.

Gripshover (2003) and Saag (2003) presented further data from the FRAM study. Gripshover presented a comparison of 412 HIV+ men aged 33-45 to 153 age-matched controls form the CARDIA cohort. 56% of HIV+ vs 13.3% of the CARDIA control group reported fat loss at one or more peripheral sites and fat loss at one or more central sites (32.8% vs 15.1%) (both p<0.0001). Exam showed that more HIV+ men had reduced peripheral fat than controls (69% vs 39.2%, p<0.0001). Fewer HIV+ men had fat accumulation at central sites than controls (61% vs 81.6%, p<0.0001). Amongst individuals in whom self-report and exam proved concordant, 38.9% of HIV+ men had peripheral lipoatrophy, compared to 4.6% of controls (p<0.0001). Peripheral lipoatrophy was associated with central lipoatrophy in HIV+ men (OR 18.3), but not central fat accumulation (OR 0.70).

Saag presented a comparison of 158 HIV-positive men with lipoatrophy and 249 men without lipoatrophy to 153 male controls from the CARDIA cohort. Lipoatrophy was self-reported and confirmed by exam. DEXA scans were conducted in 60% of subjects and MRI data were available for 86% of subjects. Men with lipoatrophy had less limb and trunk fat than HIV-positive men without lipoatrophy, but both groups had lower limb fat than controls.

Zolopa reported on the prevalence of buffalo hump in the FRAM study in 412 HIV+ men and 151 age matched male controls from the CARDIA cohort. Subcutaneous and visceral fat in the lower and upper trunk were quantified by MRI. There was no significant difference in buffalo hump (8% vs 11.3%) between HIV+ and controls, and those with buffalo hump had higher trunk VAT and SAT. HIV+ men with buffalo hump had less lower trunk subcutaneous fat than controls with buffalo hump.

Laurenroth-Mai (2002) studied the prevalence of lipodystrophy in a cohort of 354 HIV-infected people (88% male). 10% had never taken antiretroviral therapy and 11% were not currently taking treatment although they reported previous exposure. Prevalence of lipodystrophy rose from 50% to 60% over the 12 month period (14% new cases, 4% resolution). After 12 months of treatment, 23% of patients had developed lipodystrophy, including 12% who experienced both fat loss and fat gain. Factors associated with any type of lipodystrophy were older age, more intense previous treatment, lower CD4 count, more advanced disease, duration of PI therapy (odds ratio 6.48), duration of NRTI therapy (OR 5.02), duration of d4T (OR 3.76) and duration of AZT (OR 3.74). Fat loss occurred more quickly than fat gain - after 62.3 vs 26.2 months on HAART, after 43.3 vs 19.6 months on PIs, and after 124 vs 107 months on NRTIs. Whether people had taken d4T or AZT did not impact on the frequency of lipodystrophy, but fat wasting was more likely in those who had taken AZT, while both fat wasting and fat gain was more likely in those who had taken d4T. The authors noted that this last finding may simply reflect longer time on therapy and greater PI exposure in the d4T group.

Kingsley (2001) updated Multicenter AIDS Cohort Study (MACS) data on the body fat changes in 868 HIV-positive and negative men. Overall, body fat changes occurred in 63% of positive men and 33% of negative men. 73% of positive men had received antiretroviral therapy. Of the HIV-infected men, 25-35% had thinning of the face, arms and legs compared to 2% of the HIV-negative group. However, fat accumulation was not more common among the HIV-infected group - 35% prevalence versus 26% in the HIV-negative group. The combination syndrome of a fat belly plus thinning of the arms and/or legs occurred in 20% of the men on HAART, among less than 3% of HIV-infected men and less than 1% of the negative men. Severe or moderate lipodystrophy occurred among 20% of the men on HAART and among 1-2% of antiretroviral-naive HIV-positive men. Prevalence of lipodystrophy stabilised after 2 years.

Martinez (2001) reported a prospective cohort study designed to investigate risk factors for lipoatrophy and/or fat accumulation in 494 consecutive, unrandomised individuals who started protease inhibitor therapy at the Hospital Clinic in Barcelona between 1996 and 1999. Body fat distribution was visually assessed by the clinician at baseline, and body fat changes were defined as changes reported by the patient and confirmed by the clinician on visual examination, and regional fat thickness was assessed by sonograph in a sub-group of patients in order to validate the clinical diagnosis. Median CD4 count at baseline was 204 cells/mm³ and median viral load was 4.9 log. Eighty four individuals were lost to follow up, died or stopped protease inhibitor therapy prior to development of lipodystrophy during the study. During a median 18 months of follow up, 17% (85) of patients developed lipodystrophy, and by Kaplan-Meier analysis it was estimated that 23% had some form of lipodystrophy after two years on therapy. Three patterns of fat redistribution were reported amongst the 85 patients who developed lipodystrophy: Central obesity alone (21%); Peripheral fat wasting (34%); Mixed syndrome of fat gain and fat loss (45%).Those who developed lipodystrophy had a greater increase in CD4 count, cholesterol and triglyceride levels than those who did not (+9 versus +6 cells per month increase after starting therapy in those who developed lipodystrophy, p=0.0067). Women were significantly more likely to develop lipodystrophy, and increasing age was also a risk factor (1.33 per 10 years older). Duration of exposure to d4T was associated with the risk of lipodystrophy accompanied by peripheral fat wasting, but even when patients who received d4T were excluded from the analysis, duration of exposure to HAART was still significantly associated with the likelihood of developing lipodystrophy with fat wasting, suggesting that the causes of peripheral fat wasting are multi-factorial and not solely linked to treatment with d4T.

Saves (2002) reported on the APROCO Study Group which enrolled people commencing PI-containing regimens over two periods in 1997 and 1998. 464 were examined at month 12 and 20 for lipodystrophy and metabolic disorders. 21% had fat loss in the arms, legs or face. 17% had isolated fat accumulation. 24% had mixed syndrome. About half had elevated triglycerides and glucose and 57% had elevated cholesterol. Age was associated with lipodystrophy and d4T associated with fat loss in particular.

Chene (2002) reported a cross-sectional analysis of ALBI-ANRS 070 of 151 individuals who took one of three NRTI regimens: AZT/3TC, or d4T/ddI alternating with AZT/3TC, or d4T/ddI. The initial study went for 24 weeks, at which time participants could add a PI or NNRTI. Follow-up to month 30 showed that 66 had remained on dual NRTI therapy. 31% had lipodystrophy/lipoatrophy. Multivariate analysis showed that commencing with d4T/ddI (odds ratio 6.7 vs AZT/3TC) and treatment with d4T/ddI throughout the 30 months (OR 26.4 vs AZT/3TC) were associated with lipodystrophy. Elevated lipids occurred in 25-40% of patients but there was no association with any particular regimen.

Tellol (2002) conducted a prospective, cross-sectional study of 89 HIV-infected children of whom 85 were taking antiretroviral therapy. 51 were taking protease inhibitors (PIs). 19 had lipodystrophy, including 18 who were taking PIs. 12 had increased trunk fat, 4 had fat wasting, and 3 had a combined syndrome. High cholesterol and high triglycerides occurred in 27 and 13 of 73 children without lipodystrophy and in 9 and 7 of the lipodystrophy group.

Thiebaut (2000) reviewed 581 HIV infected people from the Aquitaine Cohort for signs of lipodystrophy. 61% were taking protease inhibitor therapy. 37.9% were diagnosed with lipodystrophy, with 15.5% having peripheral fat wasting of the face or limbs. 12% had abdominal fat accumulation, 'buffalo hump', and/or enlarged breasts. 10% had mixed syndromes with elements of wasting and fat accumulation. 49% had lipid disorders and 20% had glucose disorders. Fat wasting was associated with older age, male sex, body mass index and duration of treatment. Mixed syndrome was associated with older age, AIDS stage, and waist-to-hip ratio. treatment with a PI. Fat accumulation was only associated with waist-to-hip ratio.

Jacquet (2000) conducted a cross-sectional study of 39 HIV-infected children aged between 3-18 years of whom 6 were non-symptomatic and 17 (40%) were severely immune suppressed. At the time of assessment, 33 children were taking triple therapy (29 taking 1 PI + 2 NRTIs), one was taking dual therapy, four were taking four or more drugs and two were not on treatment. One-third of the children had lipodystrophy: eight had excess fat around the abdomen and trunk, three had fat wasting in the limbs and face, and two children had both peripheral wasting and truncal fat accumulation. Children with body fat changes had higher fasting insulinaemia indicating insulin resistance. However, high cholesterol and high triglyceridaemia were not significantly different between the children with and without lipodystrophy (23 vs 15% and 15 vs 11% respectively).

Scarsella analysed 4025 patients from the US Chorus database and found a lipodystrophy incidence of 7% during mean follow-up of 26 months. LD was defined as either buffalo hump and/or peripheral fat wasting or increased abdominal girth. Predictors of LD were: age per 10 years (HR 1.6); AIDS diagnosis (HR 1.7); PI treatment (HR 6.0); NRTI/PI/NNRTI combination (HR 5.1) (all p>0.001); therapy with RTV/SQV/d4T/3TC (HR 5.7) (p=0.003); therapy with IDV/d4T/3TC (HR 3.6) (p=0.02); NRTI only treatment (HR 2.7) (p=0.04). No significant difference in risk of LD was observed between different PIs.

The Swiss HIV Cohort Study team conducted a cross-sectional analysis of side-effects among 1379 people taking antiretroviral therapy in August-September 1999 (Bernasconi 2000; Fellay 2001; Boubaker 2002). 47% had clinical side-effects and 27% had laboratory events probably or definitely associated with treatment. 1% had moderate or severe elevations in lactate levels. 42.4% had signs of fat redistribution: 28% had peripheral fat loss and 30% had fat accumulation. d4T and 3TC were associated with lipodystrophy. d4T and ddI were associated with elevated lactate. d4T and ritonavir were associated with elevated cholesterol and triglycerides. Lipodystrophy was not associated with use of protease inhibitors, although published data do not address fat loss and fat accumulation as possibly separate entities. Older age was associated with elevated lipids and blood glucose, and lipodystrophy.

Mauss (2002) reported on lipodystrophy among the LipART cohort of patients who all started HAART in mid-1996. After three years of treatment, 34% had lipodystrophy, most people exhibiting mixed fat loss and accumulation. Factors associated with lipodystrophy were d4T for more than 12 months (OR 2.1), CD4 nadir below 200 (OR 2.2) and high triglycerides (OR 2.3). Prolonged NNRTI treatment was associated with reduced risk of lipodystrophy.

Amaya (2002) conducted a cross-sectional study of 40 HIV-infected children who were receiving antiretroviral treatment. 18% had physical symptoms of lipodystrophy while two-thirds had high cholesterol. Adult dosing in children was associated with greater risk of physical signs of lipodystrophy.

Hillebrand (2000) reported risk factors for lipodystrophy for 207 patients enrolled in the SMART study were: longer HAART duration, older age, higher weight at HAART initiation. There was a non-significant trend towards higher baseline triglycerides and glucose among those with lipodystrophy. Previous NRTI exposure was not linked to occurrence of lipodystrophy. 15.5% developed lipodystrophy after a median follow-up time of 755 days.

Miller (1999) conducted a cross-sectional survey of clinics with high HIV caseloads in Australia. Data on 1,337 HIV-infected people were collected. 52% were asymptomatic. 82% were taking PIs, 13% taking ART without PIs and 5% were treatment naive. 58% reported body fat changes of peripheral fat loss and/or accumulated abdominal fat. Fat changes were associated with elevated LFTs, lipids, glucose, insulin and visceral fat.

Mallal (2000b) compared fat wasting in 227 Australian patients receiving various antiretroviral regimens including dual NRTI therapy or no therapy between December 1997 and May 1999. Body fat changes were assessed once by patient and physician report. Fat loss was assessed by whole body DEXA scan in 161 randomly selected patients. 56% of patients received dual NRTI therapy prior to commencing PI treatment, 16% remained treatment naive and 17% remained PI-naive. Association between drug exposure and fat loss was assessed by two parameters: cumulative drug exposure during the study period, and total duration of NRTI exposure prior to commencing PI treatment. The median time to appearance of fat wasting was 18.5 months in d4T recipients compared to 26 months in the AZT recipients. d4T increased the risk of fat loss 1.085-fold per month of exposure compared to AZT after adjustment for total duration of NRTI therapy, age, viral load and CD4 cell count. The rate of fat loss was significantly associated with adding a PI to NRTI therapy and to baseline regional fat percentage, with DEXA values of 10% or less associated with the lowest rate of change.

Lichtenstein (2003) conducted an assessment of 546 patients enrolled to the HOPS study. 337 had no evidence of lipoatrophy at baseline. 44 developed moderate to severe fat loss by the time of the follow-up visit two years later. White race, CD4 count below 100 cells/mm³, a viral load above 1,000 copies/mL and lower BMI were predictive by multivariate analysis. The strongest predictor of lipoatrophy was CD4 count at the second visit. In addition, an increase in CD4 count of less than 50 cells/mm³ in the two years of the study was also found to be a risk factor of fat loss. Nadir CD4 < 200 cells/mm³ (OR 2.91) at any time as early as 1994 was predictive of the emergence of lipoatrophy. No relationship was found between any anti-HIV drug and fat loss.

1077 HIV infected individuals from 8 US cities involved in the HIV Outpatient Study - HOPS. A total of 529 (49%) had one or more signs of fat maldistribution. 30% had abdominal fat accumulation, 26.5% had thinning of the arms and legs, 23% had thinning of the buttocks, 18.7% had sunken cheeks, 10.3% had buffalo hump and 9.8% had other facial changes. 143 (13.3%) of participants had only signs of peripheral fat loss, 142 (13.2 %) had only signs of fat accumulation, and 244 (22.7%). Severe fat loss occurred in 16% of participants, 10% had significant fat accumulation and 4.4% had both moderate/severe lipoatrophy and moderate/severe fat accumulation. Factors associated with moderate/severe fat loss were: older age, white race, duration and severity of infection, any PI therapy, use of d4T at any stage, use of indinavir, and more than a 2kg change in body mass index. Factors associated with moderate/severe fat gain were: increasing time on any anti-HIV regimen, lower peak viral load, higher body mass index throughout, and increasing time with undetectable viral load. The presence of non-drug risk factors for lipodystrophy and lipoatrophy acted synergistically with duration of d4T and indinavir treatment.

Muurahainen (2000) examined 210 people (160 men, 50 women) diagnosed with HIV-associated adipose redistribution syndrome (HARS) or lipodystrophy. CD4 counts ranged from 4-1456, and 51% had viral loads below 500. Fat accumulation (FA) was more common among people with a body mass index (BMI) over 28kg/m² compared with people under 21kg/m²: 94% vs 71% FA belly, 58% vs 24% FA breast, 60% vs 19% FA hump. In contrast, the underweight people were more likely than overweight people to experience fat depletion (FD): 71% vs 48% FD limbs, 67% vs 33% FD buttocks, 52% vs 15% FD face. Women had higher BMI and were more likely to experience fat accumulation, especially of the waist and breasts.

Rakotoambinina (2001) investigated a cohort of 196 HIV infected people on HAART including a PI. In January 1999, 14 had lipoatrophy (fat loss), 5 had obesity and 30 had obesity plus lipoatrophy after 20 months on treatment. People with fat disorders, versus those without fat disorders, had longer known HIV infection (103 vs 83 months) longer HAART (28.6 vs 22.3 months) and longer NRTI treatment prior to HAART (20.2 vs 8.6 months). People with fat loss alone were younger and had longer exposure to NRTIs prior to HAART (38.5 vs 20.2 months). High blood lipids were associated with PI therapy, independent of lipodystrophy.

Shevitz (1999) used dual x-ray energy absorptiometry (DXA) to assess 171 HIV infected people, of whom 101 were on PIs. After adjustment for total fat, people on PIs had 5% less of total body fat located in the arms and legs, and 5% more fat located in the trunk than people not on PIs.

Carr (2000) compared 14 people with NRTI-related wasting to 32 treatment-naive individuals, 28 non-wasted individuals on PIs/NRTIs, and 102 wasted individuals on PIs/NRTIs. The NRTI wasting syndrome developed after an average of 61 months on treatment, and was accompanied by fatigue, nausea, abdominal distension and elevated lactate and ALT levels. Average weight loss was 6 kg. Ten patients who stopped NRTI treatment for 3-4 months gained an average of 2.5 kg.

Mulligan (2001) compared five groups of people in a cross-sectional study of body fat to investigate which factors may affect body fat changes seen in HIV-infected people. The ratio of trunk fat to arm and leg fat was higher in those who had taken NRTIs compared to the HIV-negative controls and the HIV-positive people who had never taken treatment.

Garcia-Benayas (2002) reported the case of a woman who developed body fat wasting after 5 years of treatment with AZT monotherapy. 4 months after ceasing treatment (CD4 778, viral load 778 copies/ml), she developed abdominal fat and buffalo hump which subsequently improved significantly.

Fabre (2000) studied 102 people with lipodystrophy, of whom 15 had not taken PIs, and 13 controls. d4T and 3TC were associated with lipodystrophy. Visceral abdominal fat was greater among those with lipodystrophy, both PI and non-PI groups, and facial and limp wasting was very common. Body mass ratio, HOMA index, cholesterol and triglycerides were significantly higher in the PI group, as were impaired glucose tolerance and diabetes.

Pernerstorfer-Schoen (1999) reported on 20 HIV infected people and 17 people with AIDS treated for 6 months with a PI containing regimen. Both groups gained weight, increased their BMI and muscle significantly from baseline using BIA. AIDS patients only had a fat mass increased (average 24%) while resting energy expenditure fell significantly in both groups.

Saint-Marc (2000) observed body fat changes in 154 men, of whom 15 were therapy naﶥ, 39 were on long-term NRTI therapy and 100 were on a PI-containing regimen. 22% of participants had fat loss, 25% had both fat loss and intra-abdominal fat gain, 47% were normal and 6% were obese. Visceral fat was positively correlated with fasting insulin and total insulin. The use of d4T was correlated with fat wasting in both NRTI and PI recipients when compared with AZT. Saint-Marc (1999) also reported on 43 protease inhibitor-naive patients who took AZT and/or d4T for at least six months. Body fat mass as a percentage of total weight was lower among people taking d4T, as was the subcutaneous/visceral fat ratio. Fat wasting occurred in 63% of the d4T group and 19% of the AZT group. Five of 12 people who switched from d4T to AZT gained subcutaneous fat.

Moyle (1999b) investigated 5 individuals on PI-sparing regimens with body fat changes. Two were on dual NRTI therapy was were NNRTI/PI naive, while three were on an NNRTI plus NRTIs and were PI-experienced. In the PI-experienced group, none had reported body fat changes while on PI therapy. High lipids and insulin abnormalities were observed in 2 individuals, both PI-experienced. The mean total visceral fat to total adipose fat ratio was elevated (0.73).

Pedneault (2000) reviewed data from 4 amprenavir studies involving 490 people on amprenavir for signs of fat redistribution. PROAB3006 (n=245) found 4 cases of fat redistribution among people on amprenavir compared with 11 among people on indinavir. In PROAB3001 (n=113) one person on amprenavir developed fat redistribution versus no cases in the placebo group. CNAA2007 (n=99) found 6 people with fat redistribution although this group were PI-experienced. PROA2001 (n=9) found no cases of fat redistribution among people treated with 2 PIs.

Galli (2002) analysed 188 people being treated with dual nucleoside therapy (92 men, 96 women). 26% of women and 6.5% of men had some evidence of fat abnormalities. The following combinations were more likely to be associated with fat redistribution: AZT/3TC 7/77 (9.7%), AZT/ddC 1/10, AZT/ddI 2/24 (8.3%), d4T/3TC 19/70 (27.1%).

Galli reported on the Italian Cohort of Antiretroviral-Naﶥ Patients, which recruited 655 people from 34 treatment centres between September 1999 and March 2000. Study participants were followed-up every six months, with average follow-up lasting 86 weeks (range 52-107 weeks). 128 (19.6%) patients experienced some body fat changes. Abdominal fat accumulation was most frequently observed (72 people); loss of fat in the limbs (48 people) and cheeks (28) were the most commonly reported forms of lipoatrophy. RH of developing any morphologic alteration were: age per years 1.30, women 4.01, homosexual 4.95, HCV positive 2.43, addition of PI to initial dual NRTI therapy 3.66. RH of developing lipoatrophy: homosexual exposure category 12.93; heterosexual exposure 4.44; non-injecting drug use bloodborne 18.65; HCV-positive 4.74; each year on d4T 23.56. RH of fat accumulation: women 3.23; homosexual 6.86; non-injecting drug use bloodborne 8.86. Mixed fat accumulation and fat loss: Women 5.26; indinavir 4.78.

Qazi (2000) investigated breast enlargement in eleven men on HAART. The researchers used breast ultrasonography to assess the nature of breast swelling in the men who developed breast tissue changes whilst taking antiretroviral therapy. The breast changes were caused by glandular enlargement rather than fat deposition. However, levels of male and female hormones were normal in eleven patients.

Gharakhanian reported three patterns of body fat changes: atrophy (wasting) (20%), fat accumulation (16%) and a mixture of the two (41.7%). There was no significant difference between the three groups in the amount of time they had been taking PIs. There were marked differences in blood glucose levels and insulin sensitivity between the three groups.

Peyriere (1999) reported gynecomastia (breast growth and increased sensitivity) in men receiving HAART. Among 5 cases, the only common drug was d4T. Four out of 5 cases were not associated with any other body fat changes. Replacement of the PI did not result in improvement, but one patient who stopped d4T treatment did experience improvement.

Miller (2000) studied fat redistribution in 31 people treated with HAART during primary HIV infection. 15 people were on nelfinavir plus 2 NRTIs, and other combinations were indinavir plus 2 NRTIs (7), amprenavir plus 3 NRTIs (1), nevirapine plus 2NRTIs (2). Average time on therapy was 14.2 months. 14/31 self-reported fat redistribution, 7 with peripheral wasting and truncal obesity, 3 with peripheral wasting only and 4 with truncal obesity only. Doctor's assessment reported that 7 individuals had signs of lipodystrophy.

Polo (2000) analysed 150 individuals taking AZT/3TC/protease inhibitor (PI), or d4T/3TC/PI, or d4T/ddI/PI for signs of lipodystrophy (facial wasting, increased abdominal girth and elevated lipids). Incidence of lipodystrophy varied significantly between the groups: 1/46 (2%) of people on AZT/3TC/PI; 45/87 (52%) of people on d4T/3TC/PI and 15/17 (88%) of people on d4T/ddI/PI. PIs and demography were matched across the 3 groups. 10 people on d4T/ddI/PI switched to AZT/3TC while maintaining their PI, which led to improvements in lipid and fat measurements.

Staszewski (1999) reviewed the 006 study of efavirenz involving 1223 people followed for 24 weeks, 378 for 48 weeks and 132 for 72 weeks. Total incidence of lipodystrophy was 0.2% efavirenz /NRTIs, 2.3% efavirenz /indinavir and 2.9 indinavir /NRTIs.

Milano (1999) reported fatty or lipomatous growths in two people on HAART.

Dong (1999) studied 116 women on protease inhibitors, of whom 21(18%) reported body fat changes within 22 months of commencing treatment. These women reported increase in abdomen size (90%), increase in breast size (71%) and buffalo hump (19%). Cholesterol and triglycerides were elevated in these women. Dong reported on one woman who commenced aerobic exercise and noted only a small change in her body shape. Another woman started weight training which increased muscle size but did not affect fat distribution or wasting.

Ho (1999) reported on facial wasting among 24% of 29 people on indinavir for at least three months.

Hadigan reported on dietary intake and metabolic abnormalities in 62 men and 23 women with HIV who were taking antiretrovirals and had signs of body fat redistribution. Seventeen HIV-positive men without evidence of body fat changes and 35 HIV-negative men were also recruited as controls. The average ago of the people on the trial was 42, and the average time of HIV infection was a little over seven years. 41 percent had a viral load below 400 copies/ml. High consumption of fat, low dietary fibre intake and alcohol consumption were all associated with increased blood fat levels and insulin abnormalities. In particular, high polyunsaturated fat intake was a significant predictor of higher insulin levels. A low fibre intake also seemed to contribute to increased insulin levels, but did not impact on other lipids. High alcohol consumption was associated with the highest cholesterol levels. Of the 85 people enrolled on the trial, 53 percent had a dietary fibre intake lower than the daily 20 g recommended by the American Diabetes Association, and an increase of just five grams of dietary fibre a day was associated with a 14 percent decrease in insulin. However, fibre intake was not correlated with lipid abnormalities. The study also indicated that people with mixed lipodystrophy (a combination of lipoatrophy and adiposity) were more severely affected by insulin resistance.