The presence of frailty with NCI was associated with a greater risk of falls, disability or death in PLWH than NCI alone. Interventions that target prevention or reversal of both frailty and NCI (such as increased physical activity) may significantly limit poor health outcomes among PLWH.
Purpose
To analyze clinically relevant interactions between the apolipoprotein E (
APOE
) ε2, ε3 and ε4 alleles and nutritional factors on glycemic control and lipid levels in a cohort of type 2 diabetes (T2D) patients from western Mexico.
Patients and Methods
In this cross-sectional study of the cohort of T2D patients, a total of 224 individuals were selected for interaction studies. Clinical and anthropometric data were obtained from pre-designed medical records. Dietary intake was assessed by validated three-day food consumption records. Biochemical measurements were determined by automated methods.
APOE
genotyping was performed by a real-time allelic discrimination assay. Gene–diet interactions were tested by corrected multiple linear regression analyses, which were adjusted by potential confounding factors such as age, sex, energy intake, BMI and anti-hyperglycemic therapy (Metformin, Glibenclamide or Insulin), and years with T2D.
Results
Seventy-six percent of patients with T2D were on Metformin therapy. The frequencies of the
APOE
alleles were ε2 (5.8%), ε3 (74.1%) and ε4 (20.1%). After statistical settings, significant
APOE
alleles-by-diet interactions in relation to the metabolic profile were found. Interestingly, higher blood levels of total cholesterol (p int. = 0.016), non-HDL-c (p int. = 0.024), and LDL-c (p int. = 0.030) were found only in carriers of the
APOE
ε2 allele with a low consumption of MUFA. In contrast, carriers of the
APOE
ε4 allele with a high ω-6:ω-3 PUFA ratio in the diet had higher %HbA1c blood concentrations (p int. = 0.035).
Conclusion
This study suggests a differential metabolic impact of
APOE
alleles on lipid/glycemic phenotypes depending on the dietary intake, with important potential implications in the personalized medicine and nutritional management of patients with type 2 diabetes mellitus.
Background
Neurocognitive impairment (NCI) and frailty are more prevalent among persons with HIV (PWH) compared to those without HIV. Frailty and NCI often overlap with one another. Whether frailty precedes declines in neurocognitive function among PWH or vice versa has not been well-established.
Setting
AIDS Clinical Trials Group (ACTG) A5322 is an observational cohort study of older PWH. Participants undergo annual assessments for NCI and frailty.
Methods
ACTG A5322 participants who developed NCI as indexed by tests of impaired executive functioning and processing speed during the first 3 years were compared to persons who maintained normal cognitive function; those who demonstrated resolution of NCI were compared to those who had persistent NCI. Participants were similarly compared by frailty trajectory. We fit multinomial logistic regression models to assess associations between baseline covariates (including NCI) and frailty, and associations between baseline covariates (including frailty) and NCI.
Results
929 participants were included with a median age of 51 years (IQR 46-56). At study entry, 16% had NCI and 6% were frail. Over 3 years, 6% of participants developed NCI; 5% developed frailty. NCI was associated with development of frailty (odds ratio [OR]=2.06; 95% confidence interval [CI]=0.94, 4.48; p=0.07). Further adjustment for confounding strengthened this association (OR=2.79; 95% CI=1.21, 6.43; p=0.02). Baseline frailty however was not associated with NCI development.
Conclusions
NCI was associated with increased risk of frailty, but frailty was not associated with development of NCI. These findings suggest that the presence of NCI in PWH should prompt monitoring for the development of frailty and interventions to prevent frailty in this population.
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