This study examined the relationship between cholesterol levels and impulsivity in a large sample of patients with mood symptoms. Three hundred and one patients with mood, anxiety, and personality disorders completed a battery of psychometric scales including the Barratt Impulsiveness Scale-Version 11 (BIS-11) and the Profile of Mood States (POMS). On the same day of psychometric assessment, blood samples were analyzed for total cholesterol (TC) and high-density lipoprotein cholesterol (HDL-C). Statistical analysis controlling for the confounding effects of age, gender, diagnosis, and current mood symptoms showed that lower TC levels were associated with increased attentional impulsivity. There was a weak linear correlation between TC and attentional impulsivity across the entire range of TC levels (110–295 mg/dL) but a highly significant difference between participants with TC levels lower than 165 mg/dL and the rest of the sample. The current study adds to the growing body of evidence pointing to the association between serum cholesterol and mental health. Considering that attentional impulsivity is a demonstrated risk factor for suicide, patients presenting with low cholesterol and mood symptoms may warrant increased clinical attention and surveillance.
Impulsivity has been defined as a predisposition toward rapid, unplanned reactions to internal or external stimuli with diminished regard to the negative consequences of these reactions to the impulsive individual or others (Moeller et al., 2001). Impulsivity is directly mentioned in the DSM-IV diagnostic criteria for several disorders and is implied in the criteria for others, including ADHD, personality disorders, mania, and substance abuse/dependence. Impulsivity not only has clinical implications, but also appears to be a relatively enduring trait that characterizes many people without diagnosable psychiatric disorders. Individual differences in the temperamental trait of impulsivity are continuously distributed as well as substantially heritable, and therefore are likely to result from additive or non-additive interaction of genetic variations with environmental influences (Lesch and Merschdorf, 2000 and Potenza and Taylor, 2009).
There has been considerable convergence in recent years on the neurobiological substrates of impulsivity. The neuroanatomical circuitry involved in impulsivity includes the prefrontal cortex, orbitofrontal cortex, and distinct sub-regions of the striatum (Dalley et al., 2008). Although the neurochemistry of impulsivity is likely to imply various neurotransmitters, including dopamine, noradrenaline, endocannabinoids, and glutamate (Pattij and Vanderschuren, 2008), the primary role of brain serotonin (5-HT) has clearly emerged from many experimental and clinical studies that have demonstrated an association between decreased 5-HT transmission and increased impulsivity (Carver and Miller, 2006 and Paaver et al., 2007).
Deficits in central serotonin transmission could also explain the link between low serum cholesterol and increased impulsivity (Buydens-Branchey et al., 2000, Pozzi et al., 2003 and Conklin and Stanford, 2008). Several studies have suggested that serum cholesterol may be a marker for central serotonergic activity (Steegmans et al., 1996, Terao et al., 2000 and Vevera et al., 2005). Experimentally decreasing the cholesterol content of cell membranes has been shown to reduce the binding affinity of a serotonin 5-HT1A receptor agonist, alter G-protein coupling of the receptor, and decrease activity of the serotonin transporter (Scanlon et al., 2001 and Pucadyil and Chattopadhyay, 2007). Kaplan et al. (1994) found that when monkeys (of the same weight and receiving the same caloric intake) were fed a low-cholesterol diet, they had lower levels of the serotonin metabolite, 5-hydroxyindoleacetic acid (5-HIAA), in their CSF than did monkeys on a high-cholesterol diet.
Compared to negative mood, aggression, suicide and self-harm, impulsivity has received less attention by studies focusing on the emotional and behavioral correlates of low-cholesterol levels (Troisi, 2009). What is more, the results of the few studies that have focused on impulsivity are discordant (Garland et al., 2007) and their generalizability is questionable because they were based on small samples and/or samples characterized by restricted demographic composition (mainly young men) and diagnostic range (primarily drug addiction and deliberate self-harm).
The present study was designed to overcome the methodological limitations of past research. We studied the relationship between cholesterol levels and impulsivity in a large sample of participants with a wide range of non-psychotic psychiatric disorders, not limiting our focus on those conditions characterized by extreme levels of impulsivity such as borderline personality disorder or substance abuse. Our sample included participants of both sexes and age spanning from adolescence to late adulthood. We took into account the confounding effect of present mood state on the assessment of impulsivity and distinguished between the different components of impulsivity when analyzing the data. Finally, we measured both total cholesterol (TC) and high-density lipoprotein cholesterol (HDL-C) to ascertain if a specific cholesterol fraction (pro-atherogenic or anti-atherogenic) was associated with impulsivity. Our hypothesis was that lower cholesterol levels were associated with greater impulsivity. The strong evidence linking impulsivity (Neufeld and O'Rourke, 2009) and cholesterol levels (Lester, 2002) to suicide risk attests to the clinical relevance of studying the relationship between cholesterol levels and impulsivity.
