H/A: Monitoring of Food Intake (2009)
Joy T, Keogh HM, Hadigan C, Lee H, Dolan SE, Fitch K, Liebau J, Lo J, Johnsen S, Hubbard J, Anderson EJ, Grinspoon S. Dietary fat intake and relationship to serum lipid levels in HIV-infected patients with metabolic abnormalities in the HAART era. AIDS. 2007; 21: 1591-1600.PubMed ID: 17630554
- To evaluate dietary intake and its relationship to lipid parameters in HIV-infected patients with metabolic abnormalities
- To compare dietary intake in this population of HIV-infected patients with that of control individuals, using the 2005 US Department of Agriculture (USDA) Recommended Dietary Guidelines.
- HIV-infected patients aged 18 years to 60 years
- For patients receiving antiretroviral therapy, a stable regimen for a minimum of six weeks was required.
- HIV-infected patients with known wasting or evaluated for studies of AIDS wasting were not included in the analysis
- History of diabetes mellitus
- Receiving concurrent therapy with insulin, anti-diabetic agents, glucocorticoids, growth hormone, supra-physiologic testosterone replacement or anabolic steroids
- Current substance abusers
- Had a major opportunistic infection within the six weeks before the study
- Were pregnant or breastfeeding within the previous year
- HIV-negative control subjects were required to have no history of diabetes mellitus.
- HIV-infected patients and community-derived HIV-negative control subjects evaluated for metabolic studies between 1998 and 2005
- HIV-infected patients were recruited from newspaper advertisements, community and referral-based practices
- Patients could not be directly referred into the study by providers
- HIV-negative control subjects were recruited through hospital and local advertisements using many of the same community newspapers used to recruit HIV-infected individuals.
- P-values were derived from a mixed effects analysis of variance (ANOVA) model to determine differences between HIV-infected subjects and control subjects, adjusting for potential random effects of individual studies into which patients were recruited
- Further adjustments were done for age, race, sex, body mass index (BMI), insurance status, income quartile and use of lipid-lowering medications
- Among HIV-infected patients, the change in dietary consumption over time was assessed using a bivariate linear fit model with P-values derived from univariate regression analyses
- Effects of insurance status, lipodystrophy characterization or protease inhibitor use on dietary fat intake among HIV-infected patients were determined by ANOVA
- In HIV-infected patients, a least squares multiple regression model was used to evaluate the relationship between dietary intake and metabolic parameters, with adjustment for age, sex, BMI, race, protease inhibitor use, alcohol consumption, total fiber intake, impaired glucose tolerance/diabetes and use of lipid-lowering medications
- Study had 80% power to detect a difference of four grams per day in saturated fat between the HIV-positive and control groups.
Timing of Measurements
Dietary intake was evaluated in cases and controls evaluated for metabolic studies between 1998 and 2005. All participants were studied after an overnight fast of 12 hours.
- Height, weight, BMI
- Body composition measured using dual-energy x-ray absorptiometry
- Subcutaneous and visceral abdominal fat measured using cross-sectional abdominal computed tomography scans
- Resting energy expenditure and respiratory quotient measured through indirect calorimetry
- Standard 75-g oral glucose tolerance test
- Dietary intake was determined using four-day food records or 24-hour recalls
- Complete blood count, CD4 cell count, HIV viral load, and fasting concentrations of glucose, insulin, cholesterol, high-density lipoprotein (HDL) cholesterol and triglycerides were determined by standard laboratory methods.
- HIV infection
- Hip and waist circumference, waist/hip ratio
- Individuals were categorized as having lipodystrophy based on waist/hip ratio and evidence of fat redistribution.
- Zip code information compared with median income to provide an estimate of socioeconomic status
- Insurance status
- Income quartile
- Use of lipid-lowering medications
- Protease inhibitor use
- Alcohol consumption
- Total fiber intake
- Impaired glucose tolerance/diabetes.
356 HIV-infected patients (197 men, 159 women)
162 HIV-negative control subjects (73 men, 89 women).
Attrition (final N)
42 years±7 years for case subjects
41 years±10 years for control subjects.
Case subjects: 56.3% white, 28.4% African American, 9.9% Hispanic, 5.4% other
Control subjects: 61.1% white, 25.3% African American, 7.4% Hispanic, 6.2% other.
Other relevant data
- Mean CD4 count for HIV-infected patients: 444±254 cells/µl
- Mean viral load: 400 copies per ml (range, 50 copies per ml to 5,744 copies per ml)
- 66.8% were currently taking protease inhibitors
- 93.2% were currently taking nucleoside reverse transcriptase inhibitors
- 37.5% were currently taking non-nucleoside reverse transcriptase inhibitors
- 11.2% were not taking antiretroviral medications.
There were no statistically significant differences between groups in terms of age, sex, race, medication use and income quartile between the HIV-positive and HIV-negative groups.
|HIV-infected Group (N=356)||
Control Group (N=162)
|Subcutaneous adipose tissue (cm2)||225.5±149.2||320.1±190.2||0.07|
|Visceral adipose tissue (cm2)||125.4±69.0||131.0±86.4||0.24|
|Visceral:subcutaneous adipose tissue ratio||0.82±0.84||0.43±0.23||0.002|
|Total fat (kg)||20.4±10.0||26.1±13.5||0.13|
|Total lean (kg)||55.7±11.1||55.0±13.3||0.40|
|Total extremity fat (kg)||8.3±5.2||12.4±6.2||0.0008|
|Trunk:total extremity fat||1.5±0.6||1.0±0.4||<0.0001|
|Resting energy expenditure (REE) (kcal/day)||1,730±363||1,705±480||<0.0001|
REE/fat free mass (kcal/kg/day)
|Respiratory quotient (RQ)
|Total cholesterol (mg/dL)||196±52||178±37||0.003|
|HDL cholesterol (mg/dL)||41±13||48±14||<0.0001|
|Fasting glucose (mg/dL)||90±13||89±14||0.44|
|Glucose area under the curve (mg/dLx120 minutes)||16,980±3,855||15,224±3,468||0.02|
|Fasting insulin (µIU/ml)||13±12||12±10||0.03|
|% meeting criteria for metabolic syndrome||32.3||22.1||0.02|
Assessment of dietary intake in this group of HIV-infected patients demonstrated increased intake of total dietary fat (P<0.05), saturated fat (P=0.006) and cholesterol (P=0.006) as well as a greater percentage of calories from saturated fat (P=0.002) and from trans fat (P=0.02), despite similar energy intake as the control subjects.
A significantly higher percentage of HIV-infected patients consumed more than the 2005 USDA Recommended Dietary Guidelines for saturated fat (>10% per day, 76.0% HIV vs. 60.9% controls, P=0.003) and cholesterol (>300 mg per day, 49.7% HIV vs. 37.9% control subjects, P=0.04).
Saturated fat intake was strongly associated with triglyceride level [triglyceride level increased 8.7 mg per dL (parameter estimate) per gram of increased saturated fat intake, P=0.005] whereas total fat was inversely associated with triglyceride level [triglyceride level decreased 3.0 mg per dL (parameter estimate) per gram of increased total fat intake, P=0.02] among HIV-infected individuals.
There were no statistically significant differences in dietary carbohydrate, protein, monounsaturated fat and polyunsaturated fat intakes between the two groups. Fiber intake (P=0.03) and alcohol consumption (P=0.005) were significantly lower in HIV-infected patients compared to control subjects.
In terms of energy metabolism, HIV-infected participants demonstrated higher absolute REE values (P<0.0001), higher REE adjusted for fat-free mass (P<0.0001) and lower RQ (P=0.02) when compared with control subjects.
In conclusion, we investigated dietary intake in and relationship to lipid parameters in HIV-infected patients. The anthropometric and biochemical features of the HIV-infected patients in our study are consistent with the altered metabolic phenotype seen in a high proportion of HIV-infected individuals in the era of HAART. Our study demonstrates that this specific subset of HIV-infected individuals consumes a more "atherogenesis-promoting" diet compared with community-sampled controls, and a significantly greater percentage of HIV-infected subjects exceeded the 2005 USDA Recommended Dietary Guidelines for saturated fat and cholesterol. Importantly, saturated fat intake correlated directly and total fat correlated inversely with hypertriglyceridemia in these HIV-infected patients. Thus, based on these findings, the primary goal of dietary intervention in HIV-infected patients with metabolic abnormalities should be reduction in saturated fat, rather than an excessive reduction in total fat. Careful assessment of dietary intake and more aggressive dietary intervention may prove to be beneficial to the prevention of cardiovascular disease in this population of patients.
|Government:||NIH DKR01-49302, NIH DK-02844, NIH T32HD-052961, NIH M01-RR01066|
|University/Hospital:||University of Western Ontario Research Fellowship Fund|
Data collected over a seven-year period. Authors note the following limitations:
- Results cannot be generalized to larger group of HIV-patients without metabolic abnormalities nor to HIV-infected patients with wasting or undernutrition
- Patients were not followed longitudinally to determine relationship between changes in dietary intake and dyslipidemia.
Quality Criteria Checklist: Primary Research
|1.||Would implementing the studied intervention or procedure (if found successful) result in improved outcomes for the patients/clients/population group? (Not Applicable for some epidemiological studies)||N/A|
|2.||Did the authors study an outcome (dependent variable) or topic that the patients/clients/population group would care about?||Yes|
|3.||Is the focus of the intervention or procedure (independent variable) or topic of study a common issue of concern to dieteticspractice?||Yes|
|4.||Is the intervention or procedure feasible? (NA for some epidemiological studies)||N/A|
|1.||Was the research question clearly stated?||Yes|
|1.1.||Was (were) the specific intervention(s) or procedure(s) [independent variable(s)] identified?||Yes|
|1.2.||Was (were) the outcome(s) [dependent variable(s)] clearly indicated?||Yes|
|1.3.||Were the target population and setting specified?||Yes|
|2.||Was the selection of study subjects/patients free from bias?||Yes|
|2.1.||Were inclusion/exclusion criteria specified (e.g., risk, point in disease progression, diagnostic or prognosis criteria), and with sufficient detail and without omitting criteria critical to the study?||Yes|
|2.2.||Were criteria applied equally to all study groups?||Yes|
|2.3.||Were health, demographics, and other characteristics of subjects described?||Yes|
|2.4.||Were the subjects/patients a representative sample of the relevant population?||Yes|
|3.||Were study groups comparable?||Yes|
|3.1.||Was the method of assigning subjects/patients to groups described and unbiased? (Method of randomization identified if RCT)||Yes|
|3.2.||Were distribution of disease status, prognostic factors, and other factors (e.g., demographics) similar across study groups at baseline?||Yes|
|3.3.||Were concurrent controls or comparisons used? (Concurrent preferred over historical control or comparison groups.)||Yes|
|3.4.||If cohort study or cross-sectional study, were groups comparable on important confounding factors and/or were preexisting differences accounted for by using appropriate adjustments in statistical analysis?||N/A|
|3.5.||If case control study, were potential confounding factors comparable for cases and controls? (If case series or trial with subjects serving as own control, this criterion is not applicable.)||Yes|
|3.6.||If diagnostic test, was there an independent blind comparison with an appropriate reference standard (e.g., "gold standard")?||N/A|
|4.||Was method of handling withdrawals described?||Yes|
|4.1.||Were follow-up methods described and the same for all groups?||Yes|
|4.2.||Was the number, characteristics of withdrawals (i.e., dropouts, lost to follow up, attrition rate) and/or response rate (cross-sectional studies) described for each group? (Follow up goal for a strong study is 80%.)||Yes|
|4.3.||Were all enrolled subjects/patients (in the original sample) accounted for?||Yes|
|4.4.||Were reasons for withdrawals similar across groups?||N/A|
|4.5.||If diagnostic test, was decision to perform reference test not dependent on results of test under study?||N/A|
|5.||Was blinding used to prevent introduction of bias?||Yes|
|5.1.||In intervention study, were subjects, clinicians/practitioners, and investigators blinded to treatment group, as appropriate?||N/A|
|5.2.||Were data collectors blinded for outcomes assessment? (If outcome is measured using an objective test, such as a lab value, this criterion is assumed to be met.)||Yes|
|5.3.||In cohort study or cross-sectional study, were measurements of outcomes and risk factors blinded?||N/A|
|5.4.||In case control study, was case definition explicit and case ascertainment not influenced by exposure status?||Yes|
|5.5.||In diagnostic study, were test results blinded to patient history and other test results?||N/A|
|6.||Were intervention/therapeutic regimens/exposure factor or procedure and any comparison(s) described in detail? Were interveningfactors described?||Yes|
|6.1.||In RCT or other intervention trial, were protocols described for all regimens studied?||N/A|
|6.2.||In observational study, were interventions, study settings, and clinicians/provider described?||Yes|
|6.3.||Was the intensity and duration of the intervention or exposure factor sufficient to produce a meaningful effect?||N/A|
|6.4.||Was the amount of exposure and, if relevant, subject/patient compliance measured?||N/A|
|6.5.||Were co-interventions (e.g., ancillary treatments, other therapies) described?||N/A|
|6.6.||Were extra or unplanned treatments described?||N/A|
|6.7.||Was the information for 6.4, 6.5, and 6.6 assessed the same way for all groups?||N/A|
|6.8.||In diagnostic study, were details of test administration and replication sufficient?||N/A|
|7.||Were outcomes clearly defined and the measurements valid and reliable?||Yes|
|7.1.||Were primary and secondary endpoints described and relevant to the question?||Yes|
|7.2.||Were nutrition measures appropriate to question and outcomes of concern?||Yes|
|7.3.||Was the period of follow-up long enough for important outcome(s) to occur?||N/A|
|7.4.||Were the observations and measurements based on standard, valid, and reliable data collection instruments/tests/procedures?||Yes|
|7.5.||Was the measurement of effect at an appropriate level of precision?||Yes|
|7.6.||Were other factors accounted for (measured) that could affect outcomes?||Yes|
|7.7.||Were the measurements conducted consistently across groups?||Yes|
|8.||Was the statistical analysis appropriate for the study design and type of outcome indicators?||Yes|
|8.1.||Were statistical analyses adequately described and the results reported appropriately?||Yes|
|8.2.||Were correct statistical tests used and assumptions of test not violated?||Yes|
|8.3.||Were statistics reported with levels of significance and/or confidence intervals?||Yes|
|8.4.||Was "intent to treat" analysis of outcomes done (and as appropriate, was there an analysis of outcomes for those maximally exposed or a dose-response analysis)?||N/A|
|8.5.||Were adequate adjustments made for effects of confounding factors that might have affected the outcomes (e.g., multivariate analyses)?||Yes|
|8.6.||Was clinical significance as well as statistical significance reported?||Yes|
|8.7.||If negative findings, was a power calculation reported to address type 2 error?||Yes|
|9.||Are conclusions supported by results with biases and limitations taken into consideration?||Yes|
|9.1.||Is there a discussion of findings?||Yes|
|9.2.||Are biases and study limitations identified and discussed?||Yes|
|10.||Is bias due to study's funding or sponsorship unlikely?||Yes|
|10.1.||Were sources of funding and investigators' affiliations described?||Yes|
|10.2.||Was the study free from apparent conflict of interest?||Yes|