Context: Declarative memory largely depends upon normal functioning temporal lobes (hippocampal complex) and prefrontal cortex. Animal studies suggest abnormal hippocampal function in hypothyroidism.Objective: The aim of the study was to assess declarative memory in overt and subclinical (SCH) hypothyroid patients before and after L-T 4 (LT4) replacement and in matched normal subjects. Design and Setting:A prospective, open-labeled interventional study was conducted at a teaching hospital.Participants and Intervention: Hypothyroid (n ϭ 21) and SCH (n ϭ 17) patients underwent neuropsychological tests at baseline and 3 and 6 months after LT4 replacement. Normal subjects were studied at the same time-points.Main Outcome: Tests of spatial, verbal, associative, and working memory; attention; and response inhibition and the Hospital Anxiety and Depression Scale were administered.Results: Baseline deficits in spatial, associative, and verbal memory, which rely upon the integrity of the hippocampal and frontal areas, were identified in patients with overt hypothyroidism. Spatial and verbal memory were impaired in SCH patients (P Ͻ 0.05). TSH levels correlated negatively (P Ͻ 0.05) with these deficits. After LT4 replacement, verbal memory normalized. Spatial memory normalized in the SCH group but remained impaired in the hypothyroid group. Associative memory deficits persisted in the overt hypothyroid group. Hospital Anxiety and Depression Scale scores did not correlate with cognitive function. Measures of attention and response inhibition did not differ from control subjects. Conclusion:Cognitive impairment occurs in SCH and more markedly in overt hypothyroidism. These impairments appear predominantly mnemonic in nature, suggesting that the etiology is not indicative of general cognitive slowing. We propose that these deficits may reflect an underlying disruption of normal hippocampal function and/or connectivity. (J Clin Endocrinol Metab 94: 3789 -3797, 2009) A lthough impairment of cognitive function in overt hypothyroidism has been recognized for more than a century, the nature and severity of this impairment and the degree of recovery after treatment remain unclear (1).Some studies have reported general cognitive slowing (2, 3), whereas others suggest a more specific mnemonic deficit (4, 5). Deficits in hippocampal-dependent memory tasks (6) that are reversible with thyroid hormone replace-

Cross-sectional data suggest that PUFAs modulated hormonal and lipid profiles and that supplementation with LC n-3 PUFAs improves androgenic profiles in PCOS. In bovine theca cells, arachidonic acid modulated androstenedione secretion, which suggests an indirect effect of n-3 PUFAs through the displacement of or increased competition with n-6 PUFAs. This trial was registered at clinicaltrials.gov as NCT01189669.

This study highlights the challenges facing clinicians in improving exercise levels in patients, and the need to identify the specific barriers to exercise in the individual to improve health outcomes.

HMW adiponectin is selectively reduced in women with PCOS, independent of BMI and IR. Gene expression analysis suggests that posttranscriptional/translational modification contributes to reduced HMW adiponectin in PCOS.

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