Are proinflammatory cytokines involved in an increased risk for depression by unhealthy diets?

Depression is a highly prevalent mental illness, which is associated with substantial functional impairment. Many factors, like especially genetic risk and stressful life events, are being discussed to be involved in the pathogenesis of the disease. There is also evidence that elevated levels of proinflammatory cytokines, which are frequently found in depressed individuals, could contribute to the development of the disease. Patients with metabolic syndrome also show a chronic low grade of inflammation. In addition, epidemiological studies suggest that an unhealthy dietary eating pattern, consisting of high amounts of refined grains and softdrinks, red and processed meat, fatty dairy products, and little amounts of vegetables, fruits and fish is associated with higher levels of major inflammatory cytokines, like Interleukin-6, and the acute phase C-reactive protein, even after controlling for body mass index. Furthermore, several recent studies suggest that an unhealthy diet quality is associated with an increased risk of depression. Therefore the connection between regular consumption of unhealthy foods, chronic inflammation, and increased risk for depression seems plausible.     

Is sickling trait associated with an increased risk for multiple myeloma?

In the US, multiple myeloma (MM) rates have been disproportionately higher in states with high proportions of African Americans. Understanding this disparity may assist in developing new control/prevention strategies for MM. Most of the known associated risk factors for MM are occupational and/or environmental. A possible chromosomal link between sickle cell disease and leukemia, a hematologic malignancy like MM, has been described. Interleukin-6 (IL-6) has been reported to be central to the pathogenesis of MM, inducing proliferation and inhibiting apoptosis in neoplastic plasma cells. IL-6 levels are also increased in healthy sickle cell disease patients. This role of IL-6 in the pathophysiology of MM and sickle cell disease makes it pertinent to ask whether persons with abnormal sickling erythrocytes are more at risk of developing MM than persons with no abnormal sickling erythrocytes. Abrogating the IL-6 signaling pathway will be of therapeutic interest for both MM and sickle cell disease.     

Does psychotherapy homework lead to improvements in depression in cognitive-behavioral therapy or does improvement lead to increased homework compliance?

The bidirectional causal relationships between psychotherapy homework (HW) compliance and changes in depression were assessed in 2 groups of depressed outpatients treated with cognitive-behavioral therapy using nonrecursive structural equation modeling techniques. The data were consistent with the hypothesis that HW compliance had a causal effect on changes in depression, and the magnitude of this effect was large. Patients who did the most HW improved much more than patients who did little or no HW. In contrast, depression severity did not appear to influence HW compliance. HW compliance did not appear to be a proxy for any other, unobserved (3rd) variable, such as motivation. Although the causal effect of HW on depression was large, the correlation between HW and depression was small. Some possible explanations, along with suggestions for future studies, are proposed.     

Can Mycobacterium tuberculosis infection lead to cancer? Call for a paradigm shift in understanding TB and cancer

Infections are known to cause tumours though more attributed to viruses. Strong epidemiological links suggest association between bacterial infections and cancers as exemplified by Helicobacter pylori and Salmonella spp. Infection with Mycobacterium tuberculosis (M. tb), the etiological agent of tuberculosis (TB), has been reported to predispose patients to lung cancers and possibly in other organs as well. While this etiopathogenesis warrant inclusion of M. tb in IARC’s (International Agency for Research on Cancer) classified carcinogenic agents, the lack of well-defined literature and direct experimental studies have barred the research community from accepting the role of M. tb as a carcinogen. The background research, case studies, and experimental data extensively reviewed in Roy et al., 2021; provoke the debate for elucidating carcinogenic properties of M. tb. Moreover, proper, timely and correct diagnosis of both diseases (which often mimic each other) will save millions of lives that are misdiagnosed. In addition, use of Anti Tubercular therapy (ATT) in misdiagnosed non-TB patients contributes to drug resistance in population thereby severely impacting TB disease control measures. Research in this arena can further aid in saving billions of dollars by preventing the superfluous use of cancer drugs. In order to achieve these goals, it is imperative to identify the underlying mechanism of M. tb infection acting as major risk factor for cancer.     

Is rheumatoid arthritis a consequence of natural selection for enhanced tuberculosis resistance?

Although the bubonic plague or "Black Death" is notorious for the toll it took on the population of Europe in the middle ages, another epidemic, the "White Death" of tuberculosis is responsible for millions of deaths worldwide over the past 300 years. With one in four deaths due to tuberculosis in Western Europe and the United States in the 19th century, this disease undoubtedly acted as a powerful genetic selective force. The epidemiology of modern day rheumatoid arthritis (RA) is strikingly similar to the epidemiology of tuberculosis 100-200 years ago, suggesting the possibility that genetic factors that enhanced survival in tuberculosis epidemics are now influencing susceptibility to RA. Recent advances in the analysis of genetic polymorphisms associated with disease have identified several genes linked to RA susceptibility that encode proteins involved in the immune response to Mycobacterium tuberculosis infection, including TNF-alpha, NRAMP1, PARP-1, HLA-DRB1, and PADI4. These results suggest that rheumatoid arthritis, and possibly other autoimmune diseases, are modern day manifestations of the genetic selective pressure exerted by tuberculosis epidemics of the recent past.     

How do women at increased risk of breast cancer make sense of their risk? An interpretative phenomenological analysis

Objectives

Offering breast cancer risk prediction for all women of screening age is being considered globally. For women who have received a clinically derived estimate, risk appraisals are often inaccurate. This study aimed to gain an in-depth understanding of women's lived experiences of receiving an increased breast cancer risk.

Design

One-to-one semi-structured telephone interviews.

Methods

Eight women informed that they were at a 10-year above-average (moderate) or high risk in a breast cancer risk study (BC-Predict) were interviewed about their views on breast cancer, personal breast cancer risk and risk prevention. Interviews lasted between 40 and 70 min. Data were analysed using Interpretative Phenomenological Analysis.

Results

Four themes were generated: (i) encounters with breast cancer and perceived personal significance, where the nature of women's lived experiences of others with breast cancer impacted their views on the significance of the disease, (ii) ‘It's random really’: difficulty in seeking causal attributions, where women encountered contradictions and confusion in attributing causes to breast cancer, (iii) believing versus identifying with a clinically-derived breast cancer risk, where personal risk appraisals and expectations influenced women's ability to internalize their clinically derived risk and pursue preventative action and (iv) perceived utility of breast cancer risk notification, where women reflected on the usefulness of knowing their risk.

Conclusions

Providing (numerical) risk estimates appear to have little impact on stable yet internally contradictory beliefs about breast cancer risk. Given this, discussions with healthcare professionals are needed to help women form more accurate appraisals and make informed decisions.     

Multinucleated spermatogonia in cryptorchid boys: A possible association with an increased risk of testicular malignancy later in life?

At birth, undescended testes contain germ cells, but after 1 year of life, a reduced number of germ cells is generally found. Microlithiasis and carcinoma-in-situ-testis occur in cryptorchid boys. Multinucleated germ cells, including at least 3 nuclei in the cell, exist in impaired spermatogenesis and in the senescent testis. AIM OF THE STUDY: We investigated whether multinucleated spermatogonia were present in undescended testes of cryptorchid boys, and if such a pattern is associated with special clinical features. RESULTS: Multinucleated spermatogonia occurred in 13/168 (8%) of 163 consecutive cryptorchid boys, who underwent surgery for cryptorchidism with simultaneous testicular biopsy showing seminiferous tubules. The patients with multinucleated spermatogonia more often exhibited a normal germ cell number (Fisher's exact test, p<0.0005), and were younger at surgery (Mann Whitney, p<0.005) than the rest of the patients. Before surgery, 3 patients underwent treatment with Erythropoietin because of renal failure. An intra-abdominal testis underwent clipping and division of the spermatic vessels, and a biopsy at final surgery 7 months later, exhibited multinucleated spermatogonia. In 1 case the undescended testicular position, a fixed retraction, was acquired after surgery for an inguinal hernia. Multinucleated spermatogonia were found in cases of carcinoma-in situ-testis in 2 cryptorchid boys. No case of multinucleated germ cells appeared in our normal material. CONCLUSION: Multinucleated spermatogonia are a further abnormality present in cryptorchidism. The cryptorchid boys with multinucleated spermatogonia in general exhibited rather many germ cells. This feature may be associated with an increased risk of testicular malignancy later in life, and we propose a careful follow up regime in these cases including ultrasound examination and a testicular biopsy in cases of symptoms or clinical findings.     

Magnesium deficiency in African-Americans: does it contribute to increased cardiovascular risk factors?

African-Americans are known to be disproportionately impacted by many chronic diseases such as diabetes, hypertension, cardiovascular, and renal disease. Lower levels of dietary and serum magnesium have been associated with an increased prevalence of hypertension, insulin resistance, and diabetes. Studies suggest a greater prevalence of occult magnesium deficiency among African-Americans compared to other populations. This increased prevalence of hypomagnesemia may contribute to increased insulin resistance leading to accelerated atherosclerosis and premature death. Trials that correct magnesium status/levels among African-Americans, whether through dietary intervention or direct magnesium replacement/supplementation need to be completed to characterize this relationship more completely.     

Symptoms of posttraumatic stress in parents of children with cancer: are they elevated relative to parents of healthy children?

Objective To examine posttraumatic stress symptoms (PTSS) inparents of children with cancer as a function of time sincediagnosis, treatment status, and relapse history, and as comparedto parents of healthy children. Method Participants includedparents of 199 children with cancer, comprising a cross-sectionalsample of diagnoses and treatment phases, ranging from currentlyon therapy to long-term survivors, and 108 parents of healthychildren obtained via acquaintance control methods. Parentscompleted a standardized self-report measure of PTSS. ResultsWithin the cancer group, parental report of PTSS differed asa function of treatment status and time since diagnosis. Parentsof children on active treatment endorsed similar levels of PTSSas control parents, whereas parents of children off treatmentreported significantly lower levels of PTSS than did controls.Similarly, parents of long-term survivors reported significantlylower levels of PTSS than did controls, while parents of recentlydiagnosed children did not differ from controls on PTSS. Incontrast, parents of children who had suffered a relapse reportedsignificantly higher levels of PTSS, and were much more likelyto be identified as a posttraumatic stress disorder (PTSD) case.Conclusions As a group, parents of children with cancer didnot demonstrate any evidence of increased PTSS relative to parentsof healthy children. Time since diagnosis, child treatment status,and relapse history are significant determinants of parent PTSS.Only parents of children who experienced a relapse appear tobe at increased risk of PTSD. The current results appear discrepantfrom the existing literature, and possible explanations forthese discrepancies are examined.