Verbal Fluency in Metabolic Syndrome

Abstract

Metabolic syndrome (MetS) or otherwise insulin resistance (IR) is described as a cluster of several commonly occurring disorders, including abdominal obesity; lipids disorders, such as hypertriglyceridemia; and low levels of high-density-lipoprotein cholesterol (HDL-C), hypertension (≥130/85 mmHg), and carbohydrates disorders, such as impaired fasting glucose or diabetes mellitus type 2. Type 2 diabetes (T2DM) constitutes insulin resistance, which is a strong risk factor for strokes. Patients with MetS are often prone to cognitive decline. Metabolic risk factors, hypertension, and diabetes, amongst them, have been hypothesized to play a great role in the pathogenesis of Alzheimer’s disease (AD) and the development of vascular dementia. For neuropsychological diagnostic and theoretical purposes verbal fluency is defined as a cognitive function that facilitates information retrieval from memory. It engages executive control and other cognitive processes, such as selective attention, selective inhibition, mental set shifting, internal response generation, and self-monitoring, as well as imagination and psychomotor skills. A total of 90 subjects, divided into 2 groups, patients with MetS (45) and healthy controls (45), were assessed. A significant difference in performance was found between the patients and controls, both in the phonetic (p < 0.01) and semantic fluency trials (p < 0.001). The MetS patients produced less words in the letter K and animal categories. The analysis of descriptive statistics shows that the group of patients with metabolic syndrome generated fewer words in both the phonetic and semantic categories. Our study shows that there is an association between metabolic factors and the verbal fluency performance of MetS patients. This is true, especially for phonetic verbal fluency, which is traditionally connected with the frontal cortex. Lower switching signifies possible executive dysfunctions amongst people with MetS. Subjects with this condition generated more diverse words and created less standard associations. This further implies the existence of dysexecutive syndrome and the need for diagnosing patients in this direction and involving this group of people in therapy. The proper correction of MetS components may improve cognitive function.

A latent clinical-anatomical dimension relating metabolic syndrome to brain structure and cognition

“…These associations were replicated by results from the group comparison highlighting worse performance in several cognitive domains in MetS (supplementary tables S5-6) being in line with previous reports. 10,[61][62][63] As a potential mechanism underlying these associations, altered cortical structure has been shown to mediate the relationship between MetS and cognitive performance in a pediatric study and elderly patients with vascular cognitive impairment. [64][65][66] The detected latent variable might represent a continuous disease spectrum spanning from minor cognitive deficits due to MetS-associated vascular risk factors to more severe vascular cognitive impairment and dementia.…”

Inflammatory Pathways in Overweight and Obese Persons as a Potential Mechanism for Cognitive Impairment and Earlier Onset Alzeihmer’s Dementia in the General Population: A Narrative Review

“…At the opposite end are motor and language/verbal skills, which are evaluated in a minority of studies [64]. The authors found patients with metabolic syndrome to perform worse in phonetic and semantic fluency tasks compared to normal subjects but found no correlation with waist circumference (although other components of the metabolic syndrome correlated with verbal performance) [65]. Phonemic verbal fluency (as well as delayed recall) was associated with abdominal obesity in another study on metabolic syndrome patients, while immediate recall and attention, mental flexibility, and visual-motor skills (evaluated by the Trial Making Test) were not [66].…”

NHANES 2011–2014 Reveals Decreased Cognitive Performance in U.S. Older Adults with Metabolic Syndrome Combinations

“…An example is the attenuation of proinflammatory phagocytosis in the early stages of plaque Aβ accumulation, which has deleterious effects that worsen tau protein pathology and increase synaptic loss [ 28 , 29 ]. On the other hand, numerous investigations have found contradictory results concerning these associations, even detecting no relationship [ 30 , 31 , 32 , 33 , 34 , 35 , 36 ]. Given that modifiable factors affect functional reserve, it is imperative to dissect their impact on CI.…”