## 1 Introduction  
The parapharyngeal fat pad is an accumulated fatty tissue located in the parapharyngeal space between the upper lateral region of the pharyngeal wall, the mascitor space and the parotid space [1, 2]. The distribution patterns of parapharyngeal fat tissue are associated with cervical mass lesions [3]. The increased amount of adipose tissue in this area is associated with obesity [4]. Parapharyngeal fat accumulation plays a role in the development of obstructive sleep apnea (OSA) as well by leading to upper airway narrowing [5]. OSA is defined by intermittent episodes of partial or total obstruction of the upper airways during sleep leading to hypoxia and sleep fragmentation [6]. OSA could contribute to a decrease in a patient's life quality and could increase the risk of developing heart and vascular, metabolic, or neurological diseases [7]. Several risk factors have been associated with OSA such as older age, male sex, smoking and craniofacial anatomical abnormalities [8; 9]. However, the leading factor contributing to the development of OSA currently is obesity by reducing lung capacity and by parapharyngeal fat tissue accumulation which could lead to the narrowing of the upper airways resulting in reduced air flow [10]. Obesity is considered a pandemic disease globally, and as the number of affected patients is growing every day, the prevalence of OSA patients is expected to increase drastically [11; 12].  
Carotid intima-media thickness (CIMT) is the thickness of the inner layers (tunica intima and media) of the carotid artery. The widening of the CIMT is a subclinical marker of atherosclerosis and has been associated with an increased risk of cardiovascular disease and stroke [13]. Inflammation could lead to increased CIMT as the repeated cycles of oxygen deprivation and arousal from sleep during OSA can contribute to the activation of inflammatory pathways and oxidative stress, which could lead to an increase in reactive oxygen species (ROS) and endothelial dysfunction [14]. This could result in the thickening of the CIMT and plaque development. Perivascular adipose tissue (PVAT) induces proinflammatory adipocytes which may lead to atherosclerosis as well [15].  
In a recent study, we examined the heritability of OSA-associated anatomical features in twins by measuring parameters on head and neck MRI scans [16]. In our study group, there was a strong heritability of the anteroposterior diameter of the tongue and the thickness of the submental fatty tissue of the neck, meanwhile, we found a strong environmental effect in the thickness of the parapharyngeal fatty tissue, the thickness of the pharyngeal wall, as well as the smallest diameter of the posterior upper airways [16]. Other parameters of the tongue, soft palate, uvula and parapharyngeal fat have proven to be similarly influenced by genetic and environmental factors [16].  
Our aim during this study was to further investigate the background of the measured traits by analyzing monozygotic twin pairs discordant for anatomic features associated with possible upper airway narrowing. We hypothesized that between these pairs the subjects with more accumulated fat tissue, a larger tongue, or thicker parapharyngeal wall would present higher values in markers for obesity (such as elevated cholesterol levels, higher body mass index (BMI), wider hip and waist circumference and higher body fat percentage) and would demonstrate thicker CIMT during carotid ultrasound (US) compared to their healthy twin control.