A one-year view on the association of metabolic syndrome and cognitive function in bipolar disorder – Preliminary data

Cognitive deficits are one of the major burdens of bipolar disorder (BD). Impairments can be found in a multitude of cognitive tasks, with reported impairment prevalence rates of 30–35 % (Cullen et al., 2016). Moreover, deficits seem to subsist even between acute episodes of BD, indicating that, as opposed to the general definition of BD, there is no full recovery during euthymia (Douglas et al., 2018). Deficits, even though observable globally, are especially pronounced in the domains of executive functions, verbal learning and memory, and attention with medium to large effect sizes (Cullen et al., 2016). In particular, reduced executive functioning and verbal learning and memory performances are related to poorer occupational outcome than the actual mood symptoms of BD, thus highlighting the importance of investigating neurocognition in BD (Xu et al., 2020).

Metabolic syndrome (MetS) is a highly prevalent condition in BD (MetS and BD: Bai et al., 2016; De Almeida et al., 2011; De Jong et al., 2018; Grover et al., 2020; Li et al., 2019; Vancampfort et al., 2015; Dalkner et al., 2021; Hubenak et al., 2015). The high prevalence is caused by a variety of risk factors frequently seen in BD, such as poor diet (Buhagiar et al., 2011), increased appetite (De Almeida et al., 2011), sedentary lifestyle (Stanton and Happell, 2014), and drug and alcohol abuse (De Almeida et al., 2011). Furthermore, psychotropic medication used in treating BD is known to change lipid and glucose metabolism, causing weight gain in patients with BD (Bai et al., 2016; De Almeida et al., 2011).

There is evidence for a two- to sevenfold risk of developing cognitive deficits among non-mentally ill individuals affected by MetS (Yaffe et al., 2009), with proven additional cognitive impairment in patients with BD, who are already affected by cognitive deficits by virtue of their diagnosis (Bora et al., 2019; Dalkner et al., 2021; Lackner et al., 2015). Although still controversial and in need of further investigation, there is some literature that suggests a progressive, neurodegenerative nature of cognitive decline in BD (Cao et al., 2016; Gildengers et al., 2009; Lim et al., 2013; Torrent et al., 2012) as well as MetS (Atti et al., 2019; Fan et al., 2017; Lin et al., 2014; Mora et al., 2017; Ng et al., 2016; Raffaitin et al., 2011; Siervo et al., 2014; Solfrizzi et al., 2011; Wu and Chen, 2021; Yaffe et al., 2009). Nevertheless, there is missing evidence if MetS is a predictor of cognitive decline in individuals with BD in the longitudinal course of illness.

Therefore, we investigated whether MetS has deteriorating effects on the one-year cognitive trajectory in BD. We expected patients with BD and additional MetS to reveal greater decline in global cognition, and the cognitive domains “verbal learning and memory”, “executive function”, and “processing speed and attention” over the course of one year when compared to patients without MetS.

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