Inflammation In Cancer Survivors Research Articles

MICROBIOME MODULATORS IN THE PREVENTION AND MITIGATION OF CANCER TREATMENT-INDUCED ACCELERATED AGING BIOLOGY

Abstract Advancements in oncology research have led to increased survivorship in patients with cancer. However, cancer treatments like chemotherapy cause debilitating side effects including multi-organ dysfunction and increased risk for chronic diseases, which mimic accelerated aging. Abnormalities in the gut microbiome composition (dysbiosis) increase inflammation, resulting in accelerated cognitive impairment with aging and a poor quality of life (QOL), which are all exacerbated by cancer treatments. We have screened, evaluated, and optimized our previously isolated human-origin live bacteria (probiotics) as well as pasteurized probiotics (postbiotics) for their anti-aging potential using Caenorhabditis (C.) elegans and mouse models. Probiotics improved the healthspan in C. elegans when given live and when fermented. Interestingly, PFM and LpD3.5 significantly protected from body weight loss, microbiome dysbiosis, and cognitive impairment in mice receiving 5-fluorouracil chemotherapy and protected from intestinal damage. We are planning a clinical trial where we will (1) cross-sectionally analyze the gut microbiome, leaky gut, and inflammation in cancer survivors with and without brain distress and (2) determine the safety, tolerance, and efficacy of PFM and LpD3.5 on microbiome diversity, inflammation, and cognitive health in cancer survivors with brain distress, using a 60-day open-label, randomized comparison study. These studies will improve our understanding of how cancer treatment-induced changes in the gut microbiome, inflammation, and gut permeability contribute to accelerated aging. Furthermore, they will establish the utilization of probiotics and postbiotics to improve QOL and mitigate cancer treatment-induced accelerated aging, which constitutes a debilitating public health concern among the increasing population of cancer survivors.

Cardiorespiratory fitness, visceral fat, and body fat, but not dietary inflammatory index, are related to C-reactive protein in cancer survivors.

The control of chronic inflammation has emerged as a target for improving the health of cancer survivors (CS). To examine differences in fitness and dietary characteristics of CS when grouped by low vs. moderate to high serum C-reactive protein (CRP). CS (N = 26, mean age = 68 ± 12 years) were evaluated for body mass index (BMI), body composition, cardiorespiratory fitness, dietary intake, dietary inflammatory index (DII), and serum CRP. Participants were assigned to one of two groups based on serum CRP concentrations: low CRP (≤1 mg/L) (LWC; n = 13) or moderate to high (CRP > 1 mg/L) (MHC; n = 13) and t-tests compared them. Data are presented as mean ± SD. LWC had higher VO2peak values (mL/kg/min) (p = 0.0003), and lower visceral fat area (cm2) (p = 0.02) and body fat mass (kg) (p = 0.04). Secondary analysis using Pearson's correlation coefficients, including all current study participant data, found significant negative relationships between CRP and total dietary fat intake (p = 0.02), saturated fat (p = 0.03), and polyunsaturated fat (p = 0.03). CS with moderate to high serum CRP concentrations had higher fat mass, visceral fat mass, and lower cardiorespiratory fitness. There was a significant negative relationship between dietary, fat, polyunsaturated and saturated fat, and CRP. However, these dietary fat related findings warrant further investigation. To summarize, improving cardiorespiratory fitness, maintaining lower body fat, may be helpful in altering chronic inflammation in CS.

Inflammation Modifies the Association of Obesity with Circulating 25-Hydroxyvitamin D Levels in Cancer Survivors.

ObjectiveObesity, inflammation, and circulating 25-hydroxyvitamin D (25-OHD) have distinct roles in cancer prognosis. We investigated their interplay by evaluating the associations of body mass index (BMI) with circulating 25-OHD levels in cancer survivors, and determining whether associations were modified by inflammation, defined by C-reactive protein (CRP) levels.MethodsData on cancer survivors were aggregated from the U.S. National Health and Nutrition Examination Survey (2001–2010). Multivariable linear regression models were used to evaluate the associations of BMI with circulating 25-OHD. We stratified the analyses by CRP levels: low <1.0mg/L, moderate 1.0–3.0mg/L and high >3.0–9.9mg/L.ResultsAmong 1,305 cancer survivors (mean age=60.8 years, mean BMI=28.0 kg/m2), circulating 25-OHD levels were 8.74 nmol/L lower (95%CI: 4.71 to 12.77) in cancer survivors with BMI ≥30kg/m2 compared to those with BMI <25kg/m2. This association was, however, limited to those with moderate CRP (−9.90 nmol/L, 95% CI: −16.45 to −3.36) and high CRP (−11.61 nmol/L, 95% CI: −18.71 to −5.05), but not among those with low CRP levels (−5.31 nmol/L, 95% CI: −12.66 to 2.04).ConclusionsA greater understanding of the interplay between 25-OHD and inflammation in cancer survivors with obesity should allow for targeted secondary prevention and help improve prognosis in these patients.