Abstract
Malnutrition has been reported in alcohol use disorder patients as having a possible influence on cognitive function. The aim of this study was to analyse the prevalence of ascorbic acid (AA) deficiency in inpatients admitted for alcohol detoxification and the associated factors, including cognitive impairment in the early period of abstinence. A retrospective chart review was conducted. The AA level was categorised into three groups: deficiency (AAD) (<2 mg/L), insufficiency (AAI) (2–5 mg/L) and normal level. The cognitive impairment was screened using the Montreal Cognitive Assessment (MoCA). Ninety-six patients were included (74 men; mean age 49.1 years (±11.5)). Twenty-seven AAD (28.1%) and twenty-two AAI (22.9%) were observed. In multivariate analysis, risk factors for AAD versus normal AA level were men (OR 17.8, 95%CI (1.63–194)), compensated cirrhosis (OR 9.35, 95%CI (1.60–54.6)) and street homelessness (OR 5.76, 95%CI (1.24–26.8) versus personal housing). The MoCA score was available for 53 patients (mean MoCA score: 25.7 (±3.3)). In multivariate analysis, the natural logarithm of AA (β = 1.18, p = 0.037) and sedative use disorder (β = −2.77, p = 0.046) were associated with the MoCA score. AAD and AAI are frequent in inpatients admitted for alcohol detoxification. A low level of AA was associated with cognitive impairment in the early period of abstinence.
Highlights
Malnutrition contributes to acute alcohol-related cognitive impairment in patients with alcohol use disorder (AUD) through several mechanisms, not limited to thiamine deficiency or thiamine dysmetabolism [1,2,3]
Nutritional support aims at taking care of the highly prevalent malnutrition observed in this specific population [6] due to altered intakes and variable alterations of nutrient metabolism in AUD patients [7]
ascorbic acid deficiency (AAD) increases the risk of cardiovascular diseases, infectious diseases or cancer
Summary
Malnutrition contributes to acute alcohol-related cognitive impairment in patients with alcohol use disorder (AUD) through several mechanisms, not limited to thiamine deficiency or thiamine dysmetabolism [1,2,3]. Uncertainties remain about the real prevalence due to heterogeneity in these studies’ design, including small sample size [8,10] or specific settings such as intensive care units [11]. This high prevalence of AA deficiency in patients with AUD may play an important role in the vulnerability of those patients to several pathophysiological processes, as the antioxidant roles of Vitamin C were shown to be protective in cardiovascular diseases, infectious diseases or cancer [14,15]
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