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Wellness Check: Mental Health | 2 Minute Medicine

Internet Based Cognitive Behavioural Therapy Reduces Cardiac Anxiety And Frequency Of Chest Pains In Individuals With Non-Cardiac Chest Pains

  1. Internet-delivered cognitive behavioral (iCBT) therapy reduced cardiac anxiety in people with non-cardiac chest pains but was not superior to psychoeducation.
  2. iCBT reduced the frequency of chest pains in people with non-cardiac chest pains.

Evidence Rating Level: 1 (Excellent)

Chest pain is one of the most concerning presenting symptoms in the clinical setting. The differential diagnosis of chest pain includes highly concerning life-threatening diseases from pulmonary embolism to myocardial infarction. Fifty percent of chest pain presentations to the emergency department, however, are typically non-cardiac chest pains (NCCP). The association of chest pains with heart disease makes symptoms very distressing to patients. This is termed cardiac anxiety (CAx). CAx negatively impacts quality of life and leads to an increase in chest pain frequency. Cognitive behavioral therapy (CBT) is the treatment of choice for CAx. The effectiveness of internet-delivered CBT (iCBT) on CAx has not been fully investigated.

This nonrandomized control trial investigated the effectiveness of nurse-led iCBT on the treatment of CAx compared to psychoeducation in Sweden. There were 109 individuals with NCCP that were randomized to the two treatment arms; 54 in the iCBT group, and 55 in the psychoeducation group. Swedish-speaking participants over the age of 18, with an NCCP complaint in the last 6 months, diagnosed CAx (score >24 on cardiac anxiety questionnaire (CAQ)), and who had access to a computer were included. Participants who did not meet these criteria were excluded. Participants received 5 weeks of either iCBT or psychoeducation depending on their treatment group. CAx was assessed after the study, then at 3-, 6-, and 12-months post-intervention. The primary outcome measured was CAx using the CAQ. Secondary outcomes included fear of bodily sensations, depressive symptoms, and chest pain frequency.

Concerning the primary outcome, while iCBT did show success at reducing CAx, it was not superior to psychoeducation alone. Concerning secondary outcomes, iCBT did not show superiority to psychoeducation at reducing fear of bodily sensations or depressive symptoms. iCBT was, however, statistically significant in reducing chest pain frequency. A limitation of this study is that researchers did not consider further healthcare utilization a participant might have taken in working up their chest pain. For example, if an individual with NCCP utilized further medical investigation to reassure them their chest pain was not cardiac related, their anxiety would be less than an individual who only adhered to the treatment arms utilized in the study. Nevertheless, iCBT’s ability to reduce CAx in general and reduce chest pain frequency is a valuable finding. Increased frequency of chest pains leads to further utilization of healthcare by patients impacting their daily activities and quality of life overall. This study shows iCBT is a viable, and convenient option for the treatment of CAx.


Specific Inflammatory Cytokines May Impact Depression Severity, Suicidal Ideation, And Behaviour

  1. Interleukin-1β levels are significantly associated with depression severity, but not suicidal ideation and behaviour
  2. Tumor necrosis factor-α is significantly associated with suicidal ideation and behaviour

Evidence Rating Level: 2 (Good)

Depression affects around 8% of the total adult American population. The pathophysiology underlying this common mental health disorder remains under investigation. Previous research has shown inflammation to be associated with depression. However, further research remains to be conducted to clarify the specific inflammatory markers associated with depression.

This cohort study conducted in China measured the plasma cytokines of 82 participants. Participants over the age of 18 and confirmed DSM-V diagnosis of depression by a psychiatrist were included. Individuals comorbid with another mental health disorder like schizophrenia and bipolar disorder, who had an infection or antibiotics use in the past 3 months, or who have an autoimmune disorder or are on immunosuppressive therapy were excluded. Specifically, 14 plasma cytokines were measured at baseline by drawing venous blood samples in the morning after a period of fasting the night before. Participant’s depression severity was also gathered at baseline using the Patient Health Questionnaire-9 (PHQ-9). Depression severity was followed up at 1, 2, and 3 months. Participant’s suicidal ideation and behaviour was also assessed at the 3-month mark using the Hamilton Depression Rating Scale (HDRS). The participant’s age, BMI, education, social support, and depression treatment were also taken into consideration during data analysis and interpretation. The primary outcome measured depression severity.

The results showed that interleukin-1β (IL-1β) levels were significantly associated with depression severity at all monthly follow-ups, even when adjusted for by considering external factors (age, BMI, education, antidepressant drug, and baseline PHQ-9). Tumor necrosis factor-α was significantly associated with suicidal ideation and behaviour, while IL-1β was not. A limitation of this study is the lack of a healthy control group. Certainly, gathering data on inflammatory markers from healthy individuals would allow researchers to accurately compare differences and make further comments on the pathophysiological association between specific cytokines and depression. Nevertheless, the study offers deeper insight into the physiology underlying depression and provides education on specific inflammatory markers that could potentially be targeted in future therapy.


Levels Of MMP-2 and TNF-α May Be Associated With The Inflammatory Processes Underlying Schizophrenia

  1. Inflammatory markers MMP-2 and TNF-α were higher in treatment-resistant (TRS), and chronically medicated schizophrenia (CMS) groups, respectively compared to a healthy control group.
  2. MMP-2 and TNF-α showed no correlation to cognitive function in individuals with schizophrenia.

Evidence Rating Level: 2 (Average)

The role of inflammation in the pathogenesis of many psychiatric illnesses is an ongoing area of research. Schizophrenia is classified as a severe mental illness that affects approximately 0.5% of the American population. Understanding the physiological mechanisms underlying schizophrenia can help researchers create targeted therapies for this life-altering illness. The specific inflammatory markers underlying the pathophysiology of schizophrenia remain to be further explored.

This was a cross-sectional study with a case-control design that compared the levels of tumor necrosis factor-α (TNF-α), and matrix metalloproteinase-2 (MMP-2) of male patients with schizophrenia to that of a healthy control group. Thirty-one individuals with treatment-resistant schizophrenia (TRS), 49 individuals with chronically medicated schizophrenia (CMS), and 53 healthy individuals were enrolled in the study. Han Chinese males between the ages of 18-60, with a confirmed diagnosis of schizophrenia by DSM-IV criteria, and who have not been on anti-inflammatory medication or antibiotic therapy for the past 4 weeks were included in the study. Individuals with any major medical issue, an endocrinological disorder, degenerative brain disease, or substance abuse disorder were excluded. TRS criteria required a poor response to 6 months of therapy with two antipsychotics, and a Positive and Negative Syndrome Scale (PANSS) score over 3 on each subscale. CMS was defined as those who experienced effective treatment on one antipsychotic for 6 months with PANSS<3 on each subscale. Serum MMP-2 and TNF-α were measured from blood drawn in the morning. A clinical assessment was performed by two psychiatrists immediately after which consisted of PANSS to assess for symptom severity and Repeatable Battery for the Assessment of Neuropsychological Status (RBANS) to assess cognitive function. The primary outcome measured levels of MMP-2 and TNF-α.

The results showed that compared to the control group levels of MMP-2 were higher in the TRS group and levels of TNF-α were higher in the CMS group. The levels of both of these markers were not significantly different between the TRS and CMS groups. Interestingly, the levels of MMP-2 and TNF-α had no association with cognitive function. A limitation of this study is that people with schizophrenia tend to be on different medications. The researchers made their best efforts to control differences in medication by converting dosages of these medications to a chlorpromazine-equivalent. However, this cannot control for the different mechanisms of action of these drugs and therefore, cannot control for the way these differentially affect levels of MMP-2 and TNF-α. Nevertheless, this is likely the first study of its kind to provide insight into the associations between these specific inflammatory markers and schizophrenia potentially opening new paths for investigation and future treatment.

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