Menopause Analytical Hormonal Correlate Outcome Study (MAHCOS) and the Association to Brain Electrophysiology (P300) in a Clinical Setting

Abstract

Various studies have demonstrated that increased leptin levels and obesity are inversely related to cognitive decline in menopausal women. It is hypothesized that adiposity is inversely correlated with cognitive decline, as women with increased weight are less vulnerable to diminishing cognition. However, it is increasingly observed that menopausal women, even with increased adiposity, experience significant cognitive decline. Positron emission tomography (PET) has been used to analyze cognitive function and processing in menopausal women. Evoked potentials (P300) and neurophysiologic tests have validated brain metabolism in cognitively impaired patients. Post-hoc analyses of 796 female patients entering PATH Medical Clinic, between January 4, 2009 and February 24, 2013, were performed as part of the “Menopause Analytical Hormonal Correlate Outcome Study” (MAHCOS). Patient age range was 39–76 years (46.7±0.2). P300 latency and amplitude correlated with a number of hormones: follicle stimulating hormone (FSH), luteinizing hormone (LH), estradiol, estrone, estriol, DHEA, pregnenolone, progesterone, free and total testosterone, thyroid stimulating hormone (TSH), Vitamins D 1.25 and D 25OH, leptin, and insulin-like growth factor-binding protein 3 (IGF-BP3). Corrected statistics did not reveal significant associations with P300 latency or amplitude for these hormones except for leptin plasma levels. However, factor analysis showed that FSH and LH clustered together with Vitamin D1.25 and Vitamin D25OH, P300 latency (not amplitude), and log leptin were found to be associated in the same cluster. Utilizing regression analysis, once age adjusted, leptin was the only significant predictor for latency or speed (p = 0.03) with an effect size of 0.23. Higher plasma leptin levels were associated with abnormal P300 speed (OR = 0.98). Our findings show a significant relationship of higher plasma leptin levels, potentially due to leptin resistance, and prolonged P300 latency. This suggests leptin resistance may delay electrophysiological processing of memory and attention, which appears to be the first of such an association.

Neurocognitive performances of visuospatial attention and the correlations with metabolic and inflammatory biomarkers in adults with obesity

“…prolonged P3 latency) seen in individuals with obesity or obesity‐linked disorders, such as type 2 diabetes (Harvey, ; Braverman et al . ). Given that individuals with excessive body fat or higher body mass index (BMI) show higher concentrations of leptin because of greater leptin resistance (Considine, ; Haleem, ), the impaired neurocognitive performances in adults with obesity could thus be associated with higher leptin concentrations (Harvey, ; Gunstad et al .…”

Predictors and Protectors of Pathological Menopause

“…The premorbid background for the development of the pathological course of menopause is a burdened somatic and obstetric-gynecological anamnesis. An earlier onset of menopause (46.7±0.2 years) in women in the region was identified, in contrast to global data (50±2 years) [17,18]. The question of premature and early onset of menopause in almost every tenth woman in the region remains relevant.…”

Differences in neurocognitive performance and metabolic and inflammatory indices in male adults with obesity as a function of regular exercise

“…Indeed, animal studies suggest that obesity‐induced chronic low‐grade inflammation constitutes a pathway causing impaired cognition much earlier, independent of obesity‐induced co‐morbidities (Bilbo & Tsang, ; Pistell et al., ). Also, chronically high insulin levels and leptin/insulin insensitivity in the central nervous system play a role in neurocognitive impairments (Braverman et al., ; Vanhanen et al., ). Therefore, reducing blood levels of energy metabolic (e.g.…”