People who possess poor social skills have been hypothesized to experience negative events and consequently become vulnerable to psychosocial problems. This is characterized as the social skills deficit stress generation hypothesis. Two studies were conducted to examine this hypothesis. In study 1, 677 university students completed measures of social skills and negative life events that had occurred over the past three months. In study 2, 142 students participated in a 9 month, 3 wave longitudinal study that assessed social skills at times 1 and 3 and negative life events at times 2 and 3. Results of the investigations indicate generally negative associations between social skills and negative life events, but these associations were stronger concurrently than prospectively. Although social skills were predicted to be associated with negative life events that are social in nature, in most cases they were equally predictive of nonsocial negative life events. The associations between the social skills and life events were consistently small in magnitude.
The mediator's evolving hypotheses about what it is going to take to get agreement are the result of identifying the parties' desired outcomes, their interests, their underlying positive intentions and the principles (standards, criteria and rationales) that make sense to them.
The current study tests these questions in a longitudinal study of a sample followed from birth to early adulthood (with major study data collected at ages 15 and 20), who are at elevated risk for depression because of oversampling for maternal depression. The following specific hypotheses are tested: First, participants with at least one s 5-HTTLPR allele are predicted to show elevated rates of dependent stress across time points (including episodic stress at ages 15 and 20). Second, the presence of at least one 5-HTTLPR s allele is hypothesized to interact with depressive symptoms at age 15 to predict dependent (but not independent) stress at age 20. Based on studies suggesting that both stress generation (; ) and 5-HTTLPR (; ) may have stronger effects for women than men, gender effects were explored.
Second, 5-HTTLPR genetic vulnerability may interact with depressive symptoms to predict generation of stressful events. This idea differs from the above model (although the two are not necessarily mutually exclusive), in that instead of suggesting that 5-HTTLPR directly puts people at risk for generating stress, it proposes that the vulnerabilities introduced by the s allele presence will activate or amplify the stress-generating characteristics associated with depression, which may in turn put people at greater risk for increased depression. For example, proposed that the s variant increases psychological sensitivity to the social environment. Elevated sensitivity to negative social circumstances may instigate depression-related interpersonal processes (e.g., attachment disruptions, reassurance seeking) that may in turn generate stress (, ; ). Importantly, this hypothesis essentially expands and inverts existing 5-HTTLPR models, which have shown that the s alleles moderate the association between stressful life events and later depression, suggesting that the association between prior depression and stress generation is moderated by the s alleles. In fact, noted the failure to account for depression’s effects on stress occurrence as an important shortcoming of existing research on 5-HTTLPR.
There are two principal ways in which 5-HTTLPR could be associated with stress generation. First, the s allele may directly place individuals at greater risk for stressful life experiences, possibly due to passive (genetically associated parental traits affecting maladaptive parenting that results in social difficulties) or evocative (genetically associated youth traits that elicit negative reactions from others) gene-environment correlations (rGE). Although research has not directly focused on this hypothesis, studies that have examined stress x 5-HTTLPR interactions in predicting depression often report associations between stress and genotype, and generally these studies have not supported a main effect of genotype on stress (e.g., ; ; also see ), although existing studies have not distinguished between dependent versus fateful events.
Based on the literature it can be proposed that psychotherapists suffer from a high accumulation of occupational stressors. Psychotherapists may have a higher level of stress due to the poorly compensated high occupational demand as well as the financial concerns (Hypothesis1). The model of job satisfaction crisis postulates that an accumulation of stressors leads to an imbalance in social reciprocity. Therefore, it can be assumed that psychotherapists may show an imbalance in reciprocity at high expenditure aptness and low experienced reward (Hypothesis 2). Based on the model, an imbalance in social reciprocity affects the health of the psychotherapists. As shown in the literature, a psychotherapist may report a limited subjective state of health based on an imbalanced work load (Hypothesis 3).
In describing the conceptual basis of a stress intervention method, Emotional Brain Training (EBT), a program which integrates advances in neuroscience and stress physiology, we propose a new paradigm for health care. Many health care treatments focus on managing symptoms of stress-related disorders. In modern society stress is primarily psychological in nature and in its chronic form, the result of (non-homeostatic) neural circuits that amplify and prolong stress. The result is cognitive, emotional, behavioral and physiologic dysregulation resulting in wear and tear (allostatic load). The effectiveness of treating any one stress symptom is likely decreased because of the persistent allostatic state. Emerging understanding of neuroplasticity suggests that this circuitry is capable of change. EBT is based on the repeated use of techniques that mirror secure attachment and optimal self-regulatory processing to alter allostatic circuits through the process of reconsolidation, therefore decreasing allostatic load. This results in an improved state of well-being. We hypothesize that decreased dominance of allostatic neuronal circuits leads to improved health outcomes, offering a new paradigm for health care.
We hypothesize that the self-regulatory circuitry that responds to stress and reflects potentiation involves three phases: 1) quick sub-cortical processing phase (responses of the HPA and SMA axes), which is non-specific, evolutionarily based and primarily emotive (based in fear) (34); 2) cortical/cognitive processing of emotions into conscious feelings based on expectations and past experiences – the second phase concludes with the identification of needs; 3) generation of thoughts and actions to marshal a corrective response to meet those perceived needs. The process, if adaptive, returns the person to a state of well-being.
As illustrated in Figure 1, as arousal and stress increase, dominance shifts to more primitive areas of the brain. The limbic and reptilian brains have limited functions fo-cused primarily on survival. The stress-brain area dominance relationship impacts all domains of life, as the organization of the brain to facilitate survival draws upon all systems (40). Which brain area is dominant does not determine the precise symptom but rather the extent of deviation from homeostatic states associated with health and well-being. For example, an individual in brain state 4 may have one of various symptoms of emotional stress such as hostility, mania, depression or anxiety.
AB - Cardiovascular disease is frequent in chronic kidney disease and has been related to angiotensin II, endothelin-1 (ET-1), thromboxane A2, and reactive oxygen species (ROS). Because activation of thromboxane prostanoid receptors (TP-Rs) can generate ROS, which can generate ET-1, we tested the hypothesis that chronic kidney disease induces cyclooxygenase-2 whose products activate TP-Rs to enhance ET-1 and ROS generation and contractions. Mesenteric resistance arterioles were isolated from C57/BL6 or TP-R+/+ and TP-R-/- mice 3 months after SHAM-operation (SHAM) or surgical reduced renal mass (RRM, n=6/group). Microvascular contractions were studied on a wire myograph. Cellular (ethidium: dihydroethidium) and mitochondrial (mitoSOX) ROS were measured by fluorescence microscopy. Mice with RRM had increased excretion of markers of oxidative stress, thromboxane, and microalbumin; increased plasma ET-1; and increased microvascular expression of p22phox, cyclooxygenase-2, TP-Rs, preproendothelin and endothelin-A receptors, and increased arteriolar remodeling. They had increased contractions to U-46,619 (118±3 versus 87±6, P
Occupational stress. In the first hypothesis concerning occupational stress in psychotherapists it was postulated, that psychotherapists suffer from a high accumulation of occupational stressors.