Generalized anxiety disorder in primary care: mental health services use and treatment adequacy.

PURPOSE: Generalized Anxiety Disorder (GAD) is a common mental disorder in the primary care setting, marked by persistent anxiety and worries. The aims of this study were to: 1) examine mental health services utilisation in a large sample of primary care patients; 2) explore detection of GAD and minimal standards for pharmacological and psychological treatment adequacy based on recommendation from clinical practice guidelines; 3) examine correlates of treatment adequacy, i.e. predisposing, enabling and needs factors according to the Behavioural Model of Health Care Use. METHODS: A sample of 373 adults meeting DSM-IV criteria for Generalized Anxiety Disorder in the past 12 months took part in this study. Data were drawn from the "Dialogue" project, a large primary care study conducted in 67 primary care clinics in Quebec, Canada. Following a mental health screening in medical clinics (n = 14833), patients at risk of anxiety or depression completed the Composite International Diagnostic Interview-Simplified (CIDIS). Multilevel logistic regression models were developed to examine correlates of treatment adequacy for pharmacological and psychological treatments. RESULTS: Results indicate that 52.5 % of participants were recognized as having GAD by a healthcare professional in the past 12 months, and 36.2 % of the sample received a pharmacological (24.4 %) and/or psychological treatment (19.2 %) meeting indicators based on clinical practice guidelines recommendations. The detection of GAD by a health professional and the presence of comorbid depression were associated with overall treatment adequacy. CONCLUSIONS: This study suggests that further efforts towards GAD detection could lead to an increase in the delivery of evidence-based treatments. Key targets for improvement in treatment adequacy include regular follow up of patients with a GAD medication and access to psychotherapy from the primary care setting.

Organ-specific dietary fatty acid uptake in humans using positron emission tomography coupled to computed tomography.

A noninvasive method to determine postprandial fatty acid tissue partition may elucidate the link between excess dietary fat and type 2 diabetes. We hypothesized that the positron-emitting fatty acid analog 14(R,S)-[(18)F]fluoro-6-thia-heptadecanoic acid ((18)FTHA) administered orally during a meal would be incorporated into chylomicron triglycerides, allowing determination of interorgan dietary fatty acid uptake. We administered (18)FTHA orally at the beginning of a standard liquid meal ingested in nine healthy men. There was no significant (18)FTHA uptake in the portal vein and the liver during the 1st hour. Whole body PET/CT acquisition revealed early appearance of (18)FTHA in the distal thoracic duct, reaching a peak at time 240 min. (18)FTHA mean standard uptake value increased progressively in the liver, heart, quadriceps, and subcutaneous and visceral adipose tissues between time 60 and 240 min. Most circulating (18)F activity between time 0 and 360 min was recovered into chylomicron triglycerides. Using Triton WR-1339 treatment in rats that received (18)FTHA by gavage, we confirmed that >90% of this tracer reached the circulation as triglycerides. This novel noninvasive method to determine tissue dietary fatty acid distribution in humans should prove useful in the study of the mechanisms leading to lipotoxicity.

Mechanism of reduced myocardial glucose utilization during acute hypertriglyceridemia in rats.

PURPOSE: The purpose of the research is to study the effect of acute inhibition of intravascular lipolysis on myocardial substrate selection during hypertriglyceridemia using in vivo radiotracer analysis and positron emission tomography. PROCEDURES: We induced acute hypertriglyceridemia in vivo using an intravenous infusion of Intralipid 20% (IL) without and with acute inhibition of fatty acid delivery from circulating triglycerides with injection of Triton WR-1339 (TRI) during a euglycemic-hyperinsulinemic clamp in Wistar rats. We determined the effect of TRI on myocardial uptake of circulating triglycerides and free fatty acids using intravenous injection of [(3)H]-triolein and [(14)C]-bromopalmitate, respectively. Myocardial blood flow, oxidative metabolism, and metabolic rate of glucose (MMRG) were determined using micro-positron emission tomography (microPET) with [(13)N]-ammonia, [(11)C]-acetate, and 2-deoxy-2-[F-18]fluoro-D: -glucose (FDG). RESULTS: TRI reduced myocardial incorporation of [(3)H]-triolein but not [(14)C]-bromopalmitate showing that it selectively reduces myocardial fatty acid delivery from circulating triglycerides but not from free fatty acids. IL reduced myocardial blood flow and MMRG by 37% and 56%, respectively, but did not affect myocardial oxidative metabolism. TRI did not abolish the effect of IL on myocardial blood flow and MMRG. CONCLUSIONS: Hypertriglyceridemia acutely reduces myocardial blood flow and MMRG in rats, but this effect is not explained by increased myocardial fatty acid delivery through intravascular triglyceride lipolysis.

Increased postprandial nonesterified fatty acid appearance and oxidation in type 2 diabetes is not fully established in offspring of diabetic subjects.

BACKGROUND: It has been proposed that abnormal postprandial plasma nonesterified fatty acid (NEFA) metabolism may participate in the development of tissue lipotoxicity and type 2 diabetes (T2D). We previously found that non-diabetic offspring of two parents with T2D display increased plasma NEFA appearance and oxidation rates during intravenous administration of a fat emulsion. However, it is currently unknown whether plasma NEFA appearance and oxidation are abnormal during the postprandial state in these subjects at high-risk of developing T2D. METHODOLOGY: Palmitate appearance and oxidation rates and glycerol appearance rate were determined in eleven healthy offspring of two parents with T2D (positive family history, FH+), 13 healthy subjects without first-degree relatives with T2D (FH-) and 12 subjects with T2D at fasting, during normoglycemic hyperinsulinemic clamp and during continuous oral intake of a standard liquid meal to achieve steady postprandial NEFA and triacylglycerols (TG) without and with insulin infusion to maintain similar glycemia in all three groups. PRINCIPAL FINDINGS: Plasma palmitate appearance and oxidation were higher at fasting and during the clamp conditions in the T2D group (all P<0.05). In the postprandial state, palmitate appearance, oxidative and non oxidative rates were all elevated in T2D (all P<0.05) but not in FH+. Both T2D and FH+ displayed elevated postprandial TG vs. FH- (P<0.001). Acute correction of hyperglycemia during the postprandial state did not affect these group differences. Increased waist circumference and BMI were positively associated with elevated postprandial plasma palmitate appearance and oxidation. CONCLUSIONS/SIGNIFICANCE: Postprandial plasma NEFA intolerance observed in subjects with T2D is not fully established in non-diabetic offspring of both parents with T2D, despite the presence of increased postprandial plasma TG in the later. Elevated postprandial plasma NEFA appearance and oxidation in T2D is observed despite acute correction of the exaggerated glycemic excursion in this group.