In this study, cancer patients with pre-existing diabetes experience higher mortality than cancer patients without diabetes.

PMID:  Diabetologia. 2014 May ;57(5):927-34. Epub 2014 Mar 15. PMID: 24633676 Abstract Title:  Mortality after cancer among patients with diabetes mellitus: effect of diabetes duration and treatment. Abstract:  AIMS/HYPOTHESIS: The prognostic role of different diabetes treatment types has not been studied in detail. We compared mortality rates among cancer patients with and without diabetes, accounting for diabetes treatment and diabetes duration.METHODS: This register-based study included all cancer patients diagnosed in Denmark during 1995-2009. The patients were classified into four groups according to diabetes status at the time of cancer diagnosis: no diabetes, diabetes without medication, diabetes with only oral hypoglycaemic agent (OHA) or diabetes with insulin treatment. Poisson models were used to examine the association between pre-existing diabetes in cancer patients and mortality relative to the non-diabetic cancer population.RESULTS: Among 426,129 patients with incident cancer, we identified 42,205 patients with diabetes prior to cancer diagnosis. Overall, cancer patients with diabetes had higher mortality rates than non-diabetic cancer patients, highest among OHA- or insulin-treated patients. For all cancers combined and diabetes duration of 2 years at cancer diagnosis, insulin-treated patients experienced the highest mortality rate ratios starting from 3.7 (95% CI 2.7, 5.1) for men and 4.4 (3.1, 6.5) for women 1 year after cancer diagnosis, increasing to 5 (3.5, 7.0) for men and 6.5 (4.2, 9.3) for women 9 years after cancer diagnosis.CONCLUSIONS/INTERPRETATION: Our study provides strong evidence that cancer patients with pre-existing diabetes experience higher mortality than cancer patients without diabetes. The higher mortality seen among cancer patients treated with OHAs or insulin is in accordance with the existing evidence that more intensive diabetes treatment reflects a larger degree of comorbidity at the time of cancer diagnosis, and hence poorer survival.

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Preexisting diabetes mellitus may increase the risk of lung cancer, especially among female diabetic patients.

PMID:  Eur J Cancer. 2013 Jul ;49(10):2411-23. Epub 2013 Apr 3. PMID: 23562551 Abstract Title:  Diabetes mellitus as an independent risk factor for lung cancer: a meta-analysis of observational studies. Abstract:  BACKGROUND: Epidemiologic studies have demonstrated inconsistent associations between diabetes mellitus and the risk of lung cancer. To determine whether diabetes mellitus is associated with an increased risk of lung cancer, we performed a meta-analysis of observational studies.METHODS: PubMed, EMBASE and the Cochrane Library were searched for observational studies conducted prior to September 2012. We included prospective cohort studies that reported relative risks and case-control studies that showed odds ratios in the analysis. The pooled relative risk (RR) with 95% confidence intervals (CIs) was calculated with a random effects model. Sensitivity analysis was performed with studies which controlled for smoking status. Associations were assessed in several subgroups representing different participant and study characteristics.RESULTS: A total of 34 studies from 24 manuscripts (10 case-control studies and 24 cohort studies) were included in the analyses. Diabetes was significantly associated with the increased risk of lung cancer compared with non-diabetic controls when limiting the analysis to studies adjusting for smoking status (RR, 1.11; 95% CI, 1.02-1.20; I(2)=46.1%). By contrast, this association disappeared when the analysis was restricted to studies not adjusting for smoking status (RR, 0.99; 95% CI, 0.88-1.11; I(2)=96.7%). When stratifying by sex, an increased risk of lung cancer was prominent in diabetic women (RR, 1.14; 95% CI, 1.09-1.20; I(2)=0%), while there was no association in diabetic men (RR, 1.07; 95% CI, 0.89-1.28; I(2)=96.6%). Among diabetic women, significantly increased risks of lung cancer were found in the following subgroups: cohort studies (RR, 1.14; 95% CI, 1.08-1.20; I(2)=0%), studies controlling for major confounding variables such as age, smoking and alcohol (RR, 1.19; 95% CI, 1.00-1.43; I(2)=23.1%), studies with long-term follow-up (RR, 1.14; 95% CI, 1.08-1.20; I(2)=0%), and high-quality studies assessed by the Newcastle-Ottawa Scale (RR, 1.14; 95% CI, 1.08-1.20; I(2)=0%).INTERPRETATION: Preexisting diabetes mellitus may increase the risk of lung cancer, especially among female diabetic patients. Further large-scale prospective studies are needed to test specifically the effect of diabetes mellitus on lung cancer risk.

Protracted use of acetaminophen (1 week) may suppress fetal testosterone production, which could have adverse consequences.

PMID:  Sci Transl Med. 2015 May 20 ;7(288):288ra80. PMID: 25995226 Abstract Title:  Prolonged exposure to acetaminophen reduces testosterone production by the human fetal testis in a xenograft model. Abstract:  Most common male reproductive disorders are linked to lower testosterone exposure in fetal life, although the factors responsible for suppressing fetal testosterone remain largely unknown. Protracted use of acetaminophen during pregnancy is associated with increased risk of cryptorchidism in sons, but effects on fetal testosterone production have not been demonstrated. We used a validated xenograft model to expose human fetal testes to clinically relevant doses and regimens of acetaminophen. Exposure to a therapeutic dose of acetaminophen for 7 days significantly reduced plasma testosterone (45% reduction; P = 0.025) and seminal vesicle weight (a biomarker of androgen exposure; 18% reduction; P = 0.005) in castrate host mice bearing human fetal testis xenografts, whereas acetaminophen exposure for just 1 day did not alter either parameter. Plasma acetaminophen concentrations (at 1 hour after the final dose) in exposed host mice were substantially below those reported in humans after a therapeutic oral dose. Subsequent in utero exposure studies in rats indicated that the acetaminophen-induced reduction in testosterone likely results from reduced expression of key steroidogenic enzymes (Cyp11a1, Cyp17a1). Our results suggest that protracted use of acetaminophen (1 week) may suppress fetal testosterone production, which could have adverse consequences. Further studies are required to establish the dose-response and treatment-duration relationships to delineate the maximum dose and treatment period without this adverse effect.

Adenosine and P. distasonis have previously been shown to be anti-inflammatory in the colon and we postulate their reduction could promote tumorigenesis by de-repressing inflammation.

PMID:  Gut. 1973 Feb ;14(2):89-93. PMID: PMC4540493 Abstract Title:  Lymphocyte transformation in response to phytohaemagglutinin in primary biliary cirrhosis: the search for a plasma inhibitory factor. Abstract:  The aim of this study was to determine the importance of plasma inhibitory factors in producing the impaired phytohaemagglutinin (PHA)-induced lymphocyte transformation that is seen in some patients with primary biliary cirrhosis. Twenty-six normal subjects and 12 patients with primary biliary cirrhosis were studied. The lymphocytes from each subject were cultured in the presence of autologous plasma and also in the presence of homologous plasma from a normal subject or from a patient with primary biliary cirrhosis. The results confirm that a proportion of patients with primary biliary cirrhosis are anergic and that the impaired lymphocyte transformation to PHA in vitro can be partially accounted for by the presence of inhibitory factors in the plasma. However, these factors are unlikely to account completely for the impaired transformation, it being probable that there are also abnormalities of the T lymphocytes themselves.

THC may provide a protective effect against oxidative damage induced by diabetes.

PMID:  Cell Biochem Funct. 2014 Oct ;32(7):612-9. Epub 2014 Sep 3. PMID: 25187240 Abstract Title:  Oxidative stress and cannabinoid receptor expression in type-2 diabetic rat pancreas following treatment withΔ⁹-THC. Abstract:  The objectives of study were (a) to determine alteration of feeding, glucose level and oxidative stress and (b) to investigate expression and localization of cannabinoid receptors in type-2 diabetic rat pancreas treated withΔ(9)-tetrahydrocannabinol (Δ(9)-THC). Rats were randomly divided into four groups: control, Δ(9)-THC, diabetes and diabetes + Δ(9)-THC groups. Diabetic rats were treated with a single dose of nicotinamide (85 mg/kg) 15 min before injection of streptozotocin (65 mg/kg). Δ(9)-THC was administered intraperitoneally at 3 mg/kg/day for 7 days. Body weights and blood glucose level of rats in all groups were measured on days 0, 7, 14 and 21. On day 15 after the Δ(9)-THC injections, pancreatic tissues were removed. Blood glucose levels and body weights of diabetic rats treatedwith Δ(9)-THC did not show statistically significant changes when compared with the diabetic animals on days 7, 14 and 21. Treatment with Δ(9)-THC significantly increased pancreas glutathione levels, enzyme activities of superoxide dismutase and catalase in diabetes compared with non-treatment diabetes group. The cannabinoid 1 receptor was found in islets, whereas the cannabinoid 2 receptor was found in pancreatic ducts. Their localization in cells was both nuclear and cytoplasmic. We can suggest that Δ(9) -THC may be an important agent for the treatment of oxidative damages induced by diabetes. However, it must be supported with anti-hyperglycaemic agents. Furthermore, the present study for the first time emphasizes that Δ(9)-THC may improve pancreatic cells via cannabinoid receptors in diabetes. The aim of present study was to elucidate the effects of Δ(9)-THC, a natural cannabinoid receptor agonist, on the expression and localization of cannabinoid receptors, and oxidative stress statue in type-2 diabetic rat pancreas. Results demonstrate that the cannabinoid receptors are presented in both Langerhans islets and duct regions. The curative effects of Δ(9)-THC can be occurred via activation of cannabinoid receptors in diabetic rat pancreas. Moreover, it may provide a protective effect against oxidative damage induced by diabetes. Thus, it is suggested that Δ(9)-THC can be a candidate for therapeutic alternatives of diabetes symptoms.