Body dissatisfaction (BD) is a condition derived from negative thoughts and feelings about one's body and is a core symptom of the eating disorder anorexia nervosa (AN). Beingdissatisfied with one’s body is highly present in women and to some extent men. This might be a result of a skewed ideal in combination with social influences. In recent year, research on neurobiological risk factors as well as neuroscientific and cognitive mappings of AN and BD have gained traction, particularly when it comes to studies using neuroimaging- techniques and cognitive tests. Studies have identified brain regions (insular cortex, anterior cingulate cortex, parietal cortex, amygdala, dorsolateral and orbitofrontal areas of the prefrontal cortex) associated with the processing of body shape as well as dysfunctional processing of self-image and body satisfaction. Structural imaging studies of AN patients using CT and MRI have, in many cases, found reduced cerebral volume, increased spinal fluid (CSF) and enlarged ventricles. Usually, food and water restriction has been seen as the cause, and structural deficits in AN patients have shown to improve with weight gain after long-term recovery.

The aim of this review paper was to investigate variations in sex differentiation, andalso, examine what neurobiological underpinnings there are to gender identity andgender dysphoria. In addition, the most extreme form of gender dysphoria,transsexuality, will be described from a neurobiological perspective but also discussedin terms of the classification from DSM-5. One theory considered on how genderidentity originates is the fact that the sexual differentiation of the brain and thedifferentiation of sexual organs develop during different time periods. Alterationswere displayed in a demonstration of male-to-female (MTF) and female-to-male(FTM) transsexuals that showed reversed results in cell number in a part of thehypothalamus, acronymized INAH-3 and reversal volume results in another region,acronymized BSTc. Likewise, differences in grey matter in the right putamendepended upon their natal gender. It can be concluded that there is biologicalevidence for sex differentiation and indications that lead science into consideringbiological components for gender dysphoria. This conclusion suggests for futureresearch questions focused more on the possible genetic factors of gender identity,also, consider larger sample sizes and more replications. There is still incompleteknowledge of what exactly constitutes an individual’s gender identity.

In this essay, changes in the human hippocampal volume and function induced by stress, depression and physical exercise are examined. Hippocampus is crucially involved in the acquisition and retrieval of episodic and spatial memory, and hippocampal volume correlates with episodic and spatial memory performance. Hippocampus has substantial plasticity and changes with age, but also in response to experiential factors across life. Stress and, under at least some circumstances, also depression have negative effects on hippocampal volume and memory function. The negative effects are believed to accelerate age-related decline in volume and function, mediated by exaggerated cortisol levels and dysfunction in the HPA-axis. Physical exercise is examined from two perspectives; aerobic and strength exercise. Aerobic exercise increases hippocampal volume across various ages and decelerates age-related hippocampal degeneration, whereas support for strength exercise-induced effects are mixed and need to be studied further. The positive effects are believed to be mediated by increased BDNF levels and regional cerebral blood volume. Although hippocampal volume normally correlates with hippocampus-dependent memory, studies on exercise-induced changes in human hippocampus-dependent memory have reported inconsistent results. Animal studies have observed both the negative and positive effects on hippocampal volume to relate to changes in neurogenesis, cell proliferation, and dendritic complexity. The negative and positive effects on hippocampal volume have been observed to be non-permanent, suggesting that physical exercise may prevent, attenuate and possibly reverse hippocampal degeneration induced by stress and depression. Further, more studies on sex and age differences, exercise intervention designs and functional values of physical exercise would be of value.

Traumatic incidences happen all around the globe. Some of the people who experience trauma develop post-traumatic stress disorder (PTSD), while some do not. Even more interesting is that some also experience growth afterwards (post-traumatic growth; PTG). The purpose of this paper is to look at neural aspects of why some people develop PTSD and others PTG after a traumatic event. To fulfill the aim, both PTSD and PTG will be reviewed to create an image of the existing research in behavioral and neurological terms. In addition to looking at the constructs separately, a chapter will also look at studies where both PTSD and PTG are acknowledged collaterally in participants. When looking deeper into the theories of PTSD divisions occur, and more research is needed to establish the most prominent explanation of PTSD. PTG on the other hand has only been studied for a short period of time but yields important insights into trauma-related outcomes. These fields need to be submerged and new multidisciplinary definitions are needed for future research. The key to PTSD is suggested to emerge within the new field.

The connection between the heart and the brain was coined 150 years ago by Claude Bernard and has since then been an interesting topic of research. Scientists have for many years searched for biomarkers of stress and health to map the current status of the organism. Heart rate variability (HRV) has been presented as an emerging objective and promising marker to achieve just this. HRV refers to the beat-to-beat variations in heart rate (HR) and is thought to be a useful signal in understanding and providing valuable information of the autonomic nervous system (ANS). HRV has also been proposed as a marker of stress and health by sharing neural correlates and functions with several executive functions. This thesis identified several regions, including the ventromedial prefrontal cortex and the amygdala, in which significant associations across several studies were found between threat and safety perception, emotional regulation and HRV. This suggest that HRV may function as an index of the brain mechanism and structures that guide and govern adaptive functions and thus, provide researchers with valuable information regarding the stress and health of an organism. Two major theoretical frameworks, which articulate and explain the role of HRV as an indicator of individuals ability to adapt to environmental changes and cope under stress is presented. HRV can also be used in practice in several ways and a growing and promising field of application is HRV biofeedback.

Wellbeing and subjective wellbeing (SWB) has become some the most important goals of our time, both individually and societally. Thus, there is a need for reliable ways to measure SWB, as concerns regarding many current measures have been raised. Due to the interwoven nature of physiology and psychology, heart rate variability (HRV) has the potential to assess psychological processes in a physiological manner. HRV is an attractive measure since it is inexpensive, easy and non-invasive. Hence, the aim is to, from a cognitive neuroscientific standpoint, investigate whether HRV could serve as an objective measure to assess SWB. Most studies demonstrate associations between HRV and SWB, in particular between high frequency (HF)-HRV and positive affect (PA). However, the one study fully matching the theoretical framework only showed an inverse correlation between HRV and negative affect (NA). Plausibly implying that HRV does not serve as a reliable measure of SWB, but may be able to indicate inverse associations with NA, and possibly index certain aspect of SWB such as deactivated PA. The study of the relationship between HRV and SWB is still in its infancy and results are inconsistent. The lack of common standards regarding measurements, implementation details, and variable values, make results difficult to compare and generalize. Further standardizations and research are much needed before accurate conclusions can be drawn.

Distraction and cognitive reappraisal are two widely used types of emotional regulation strategies that are thought to be reliable when down-regulating our emotions to negative or unpleasant stimuli. Gross‘s process model of emotion generation (Gross, 1998) holds that they differ in the time they intervene in the emotiongenerative process and also how they impact emotional responses when they are used to regulate negative emotions. Distraction which involves attentional deployment is expected to operate earlier than reappraisal that entails meaning evaluation and reevaluation. Cognitive reappraisal encompasses various strategies that are used to regulate our emotions through reinterpretation. Self-focused and situation-focused reappraisal are two of them. The former is considered more efficient and thus would lead to a greater attenuation of the LPPthan the latter. To test this prediction, electrocortical responses to angry faces when using these strategies were measured using the late positive potential (LPP). Twenty four healthy participants were recruited for the study and were cued to down-regulate their emotions using these strategies while angry and neutral facial stimuli were seen on a computer screen. Contrary to prediction, distraction did not modulate the LPP earlier than reappraisal. However, supporting our hypothesis self-focused strategies largely modulated the LPP than situation-focused strategy. The pattern of result suggests that reappraisal might have an influence on the early neural processes of emotion generation and that the subcategories of cognitive reappraisal have a differential effect on emotional regulation.

Cognitive reappraisal is an emotion regulation strategy that has been shown effective in down-regulating negative emotions in both psychological and electrophysiological measures. Although there are many studies on cognitive reappraisal, only recently have there been studies differentiating between various ways of employing the strategy. This event-related potential (ERP) study sets out to compare the efficiency and temporal dynamics of three cognitive reappraisal techniques – situation-focused reappraisal, social distancing, and temporal distancing – by measuring their effects on emotional responses to aversive pictures, as indexed by the affective ERP component the late positive potential (LPP). EEG data was recorded from 17 participants. The results revealed no significant differences between emotion regulation strategies and baseline for the total ERP epoch (3,000 ms). When differentiating between early (400-800 ms), mid (800-1,500 ms), and late (1,500-3,000) periods of the epoch, significance was found in some conditions, but since no significant overall LPP activity was found, these numbers are difficult to interpret.

The present thesis deals with the concept of empathy for pain, its neurobiological underpinnings and modulations of the phenomenon. Empathy for pain is understood as the empathic response that occurs when recognising another in pain and entails at least the affective processes of actually felt pain in oneself. Cortical areas of importance for empathy for pain are the anterior insula and anterior cingulate cortex. Moreover, the phenomenon is correlated with high levels of empathy, as established by behavioural self-reports. Further, empathy for pain has been shown to be highly susceptible to modulatory factors giving rise to changes in the empathic response. Perceived fairness, perspective taking, intent and out-groups are all factors that can evoke change in the subsequent empathy for pain responses in humans. These modulatory factors provide insight into in- and out-group mechanisms. Cognitive strategies can regulate a diminished empathy for pain response, although further research is needed on how to cultivate and strengthen our ability to have empathy for another’s pain.

Peripheral neuropathy includes a wide range of diseases affecting millions around the world, and many of these diseases have unknown etiology. Peripheral neuropathy in diabetes represents a large proportion of peripheral neuropathies. Nerve damage can also be caused by trauma. Peripheral neuropathies are a significant clinical problem and efficient treatments are largely lacking. In the case of a transected nerve, different methods have been used to repair or reconstruct the nerve, including the use of nerve conduits, but functional recovery is usually poor. Autophagy, a cellular mechanism that recycles damaged proteins, is impaired in the brain in many neurodegenerative diseases affecting animals and humans. No research, however, has investigated the presence of autophagy in the human peripheral nervous system. In this study, I present the first structural evidence of autophagy in human peripheral nerves. I also show that the density of autophagy structures is higher in peripheral nerves of patients with chronic idiopathic axonal polyneuropathy (CIAP) and inflammatory neuropathy than in controls. The density of these structures increases with the severity of the neuropathy. In animal model, using Goto-Kakizaki (GK) rats with diabetes resembling human type 2 diabetes, activation of autophagy by local administration of rapamycin incorporated in collagen conduits that were used for reconnection of the transected sciatic nerve led to an increase in autophagy proteins LC3 and a decrease in p62 suggesting that the autophagic flux was activated. In addition, immunoreactivity of neurofilaments, which are parts of the cytoskeleton of axons, was increased indicating increased axonal regeneration. I also show that many proteins involved in axonal regeneration and cell survival were up-regulated by rapamycin in the injured sciatic nerve of GK rats four weeks after injury. Taken together, these findings provide new knowledge about the involvement of autophagy in neuropathy and after peripheral nerve injury and reconstruction using collagen conduits.