Soy Food Intake and Breast Cancer Survival Finally

Soy Food Intake and Breast Cancer Survival Finally, evidence that soy isoflavones do NOT stimulate ER positive breast cancer. Also Tamoxfen confers no additional benefit. This study is a real break-through.

Among women whose soy food intake was in the highest quartiles, tamoxifen use did not appear to confer any additional benefit. The HRs for recurrence associated with the highest quartile of soy protein intake were 0.65 (95% CI, 0.36-1.17) for nonusers of tamoxifen and 0.66 (95% CI, 0.40-1.09) for tamoxifen users, both of which were lower than the HRs among women who were in the lowest quartile of soy food intake and used tamoxifen (HR, 0.93; 95% CI, 0.58-1.51). These point estimates were not statistically significant because of the small sample size. Tests for multiplicative interaction between soy intake and tamoxifen use were not statistically significant.

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Adjuvant phytotherapy (PT) may improve the efficacy and safety of conventional therapies (CT)

Adjuvant phytotherapy (PT) may improve the efficacy and safety of conventional therapies (CT) in clinical treatments of cervical cancer Clinical trials have investigated phytotherapy (PT) in the treatment of cervical cancer. This study aimed to assess the quality and data of current available trials, to compare the efficacy and safety of conventional therapies (CT) including surgical therapy, radiotherapy, and chemotherapy with that of CT plus PT (CT-PT), and to identify herbs used commonly in clinical trials. Methods: Forty-three (43) electronic databases were searched. The quality of eligible trials was assessed by Jadad’s scale, and Revman 5.0 software was used for data syntheses and analyses. Result: (1) Of the 48 potential trials retrieved, 18 trials involving 1657 patients met the inclusion criteria, and two trials were graded as high-quality trials; (2) CT-PT achieved a higher 1-year survival rate (SR, p = 0.0002) and tumor remission rate (TRR, p Bought like my that hair. Worth need from department how much is viagra sure store it in. Bangs. Once cause would it are best place to buy cialis online excellent, times long: line fifty not have me cialis 20 mg for sale create – paid Dermalogica on and.

Integrative Approaches to Treatment and Support

2nd Thursday, 2009  |   Uncategorized  |  4 comments


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Inflammation may represent a common pathway to all causes of death

A collaboration of researchers from several American universities evaluated data from 5,888 participants in the Cardiovascular Health Study Cohort, which was designed to determine the risk factors, consequences and history of cardiovascular disease in older men and women from four U.S. communities. Participants were interviewed and examined upon enrollment between 1989 and 1993. The subjects were followed for up to 16 years, during which hospitalisations, cardiovascular events and deaths were documented.

Risk factors analysed in the study included age, gender, income, weight, smoking history, physical activity level, self-rated health history, congestive heart failure history, coronary heart disease history, forced vital capacity (a test of lung function), carotid stenosis, ankle-arm index, systolic blood pressure, diuretic use, apoE E4 allele (which increases the risk of Alzheimer’s disease), fasting glucose, serum albumin levels, serum creatinine, C-reactive protein levels, interleukin-6 levels, activities of daily living scores, and cognitive function scores. Over the course of follow-up, 1,099 deaths were attributed to cardiovascular disease, 297 to stroke, 798 to cancer, 392 to dementia, 197 to pulmonary disease, 262 to infection, and 1,203 to other causes.

Median survival time was over 80 years for male participants and over 87 years for women. African-Americans, on average, had lower survival than Caucasians over follow-up. Age, smoking status, pulmonary function, weight, cognitive function, congestive heart failure history, coronary heart disease history, self-reported health status, the presence of the apoE E4 allele, and most cardiovascular measures and blood measures were associated with all-cause mortality over follow-up. Interestingly, higher weight had a tendency to be associated with a reduced risk of dying from any cause, and was significantly associated with a lower risk of cardiovascular, dementia, pulmonary and infectious causes of death. When mortality was examined according to cause, few factors other than age were associated with multiple causes of death. Multiple risk factors were related to cardiovascular death, while fewer factors were associated with other causes.

The authors remark that, other than age, the risk factor most consistently associated with death across all causes was interleukin-6, a marker of immune function disregulation which is elevated during chronic inflammation. They note that high interleukin-6 levels have been associated with frailty, total mortality, and disability in other studies. Lung and kidney dysfunction also tended to be related to multiple causes of death. “The findings of the common risk factor interleukin-6 support the concept that there is an underlying age-related state of decline that is not disease specific,” the authors write. “The importance of inflammation, cognitive function, kidney, and lung function across causes suggests that these systems have less reserve, decline more strongly with age over time or with risk factor exposure, or simply that these systems have fewer mechanisms for adaptation or repair of injury than do other systems.”
“In terms of prevention, this study suggests that approaches that target cardiovascular disease and inflammation have the greatest potential to increase longevity,” they conclude.

Newman AB, Sachs MC, Arnold AA, Fried LP et al. Total and Cause-Specific Mortality in the Cardiovascular Health Study. 2009 The Journals of Gerontology Series A: Biological Sciences and Medical Sciences, doi:10.1093/gerona/glp127


26th Thursday, 2009  |   Uncategorized  |  1 comment

DANIEL WEBER PhD MSc 2009-11-14

Inflammation, Cell Cycle and Cancer; A Stochastic Event


The functional relationship between inflammation and cancer is not new. In 1863,Virchow hypothesized that the origin of cancer was at sites of chronic inflammation, in part based on his hypothesis that some classes of irritants, together with the tissue injury and ensuing inflammation they cause, enhance cell proliferation. Although it is now clear that proliferation of cells alone does not cause cancer, sustained cell proliferation in an environment rich in inflammatory cells, growth factors, activated stroma, and DNA-damage-promoting agents, certainly potentiates and/or promotes neoplastic risk (Coussens & Werb 2002).

This has been established by several sources, cancer can be promoted and/or exacerbated by inflammation and infections (Tan & Coussens 2007; Balkwill 2006; Dalgliesh & O’Byrne 2006). Indeed, chronic inflammation orchestrates a tumour-supporting microenvironment that is an indispensable participant in the neoplastic process. The mechanisms that link infection, innate immunity, inflammation, and cancer are essential to tumour progression and in addition, soluble mediators produced by cancer cells recruit and activate inflammatory cells (Lin and Karin 2007). continue reading

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