Weight Loss In Cancer Patients Research Articles

A Mathematical Model of the Disruption of Glucose Homeostasis in Cancer Patients.

In this paper, we investigate the disruption of the glucose homeostasis at the whole-body level by the presence of cancer disease. Of particular interest are the potentially different responses of patients with or without hyperglycemia (including diabetes mellitus) to the cancer challenge, and how tumor growth, in turn, responds to hyperglycemia and its medical management. We propose a mathematical model that describes the competition between cancer cells and glucose-dependent healthy cells for a shared glucose resource. We also include the metabolic reprogramming of healthy cells by cancer-cell-initiated mechanism to reflect the interplay between the two cell populations. We parametrize this model and carry out numerical simulations of various scenarios, with growth of tumor mass and loss of healthy body mass as endpoints. We report sets of cancer characteristics that show plausible disease histories. We investigate parameters that change cancer cells' aggressiveness, and we exhibit differing responses in diabetic and non-diabetic, in the absence or presence of glycemic control. Our model predictions are in line with observations of weight loss in cancer patients and the increased growth (or earlier onset) of tumor in diabetic individuals. The model will also aid future studies on countermeasures such as the reduction of circulating glucose in cancer patients.

The Effect of Mediterranean Diet on Body Composition, Inflammatory Factors, and Nutritional Status in Patients with Cachexia Induced by Colorectal Cancer: A Randomized Clinical Trial.

Along with high calorie and high protein diet, a new comprehensive dietary approach is needed to control cachexia caused by cancer and its related outcomes. This study was done to evaluate the effect of a Mediterranean diet on body composition, nutritional status, and inflammatory markers among cancer cachexia patients. In this randomized clinical trial, 46 patients with colorectal cancer-induced cachexia were included. After randomization, 23 patients were allocated to the intervention group (Mediterranean diet) and 23 to the control group (nutritional counseling for weight gain and prevention of weight loss in cancer patients). The primary outcome including muscle health, nutritional status, and inflammatory markers along with secondary outcomes such as quality of life, and serum proteins were evaluated at the start and the eighth week of the study. Statistical analysis was performed according to the intention-to-treat concept. To compare changes in dependent variables between the 2 groups, analysis of covariance (ANCOVA) was performed. After adjustment for the baseline values, age, sex, and supplements use, in the Mediterranean diet group mean of weight (P < .001), lean body mass (P = .001), fat mass (P = .002), and muscle strength (P < .001) were significantly increased compared to the control group. Regarding inflammatory markers, the mean serum level of tumor necrosis factor-alpha (TNF-α) (P < .001), high sensitive-C-reactive protein (hs-CRP) (P = .01) and Interleukin 6 (IL-6) (P < .001) were significantly improved in the Mediterranean diet group. Moreover, in the Mediterranean diet group, the score for global health status (P = .02) and physical performance score (P < .001) were significantly increased. It appears that the implementation of the Mediterranean diet might be a strategy to improve nutritional status, quality of life, inflammatory markers, and body composition in patients with colorectal cancer cachexia. Iranian Registry of Clinical Trials (www.irct.ir); ID: IRCT20211027052884N1.

Understanding the molecular basis of anorexia and tissue wasting in cancer cachexia.

Cancer cachexia syndrome is a major cause of morbidity and mortality in cancer patients in the advanced stage. It is a devastating disorder characterized by nutritional impairment, weakness, and wasting, and it affects treatment success and quality of life. Two major symptoms of cancer cachexia are anorexia and weight loss. Weight loss in cachexia is not reversed through increased food intake, suggesting that anorexia and weight loss in cancer patients are regulated by independent molecular mechanisms. Although the wasting phenotype mostly occurs in skeletal muscle and adipose tissue, other organs, such as the brain, liver, pancreas, heart, and gut, are also involved in cachexia. Thus, cachexia is a multiorgan syndrome. Although the molecular basis of cancer cachexia-induced weight loss is known, the mechanism underlying anorexia is poorly understood. Here, we highlight our recent discovery of a new anorexia mechanism by which a tumor-derived humoral factor induces cancer anorexia by regulating feeding-related neuropeptide hormones in the brain. Furthermore, we elucidated the process through which anorexia precedes tissue wasting in cachexia. This review article aims to provide an overview of the key molecular mechanisms of anorexia and tissue wasting caused by cancer cachexia.

Weight Loss in Cancer Patients Correlates With p38β MAPK Activation in Skeletal Muscle.

Unintentional weight loss, a first clinical sign of muscle wasting, is a major threat to cancer survival without a defined etiology. We previously identified in mice that p38β MAPK mediates cancer-induced muscle wasting by stimulating protein catabolism. However, whether this mechanism is relevant to humans is unknown. In this study, we recruited men with cancer and weight loss (CWL) or weight stable (CWS), and non-cancer controls (NCC), who were consented to rectus abdominis (RA) biopsy and blood sampling (n = 20/group). In the RA of both CWS and CWL, levels of activated p38β MAPK and its effectors in the catabolic pathways were higher than in NCC, with progressively higher active p38β MAPK detected in CWL. Remarkably, levels of active p38β MAPK correlated with weight loss. Plasma analysis for factors that activate p38β MAPK revealed higher levels in some cytokines as well as Hsp70 and Hsp90 in CWS and/or CWL. Thus, p38β MAPK appears a biomarker of weight loss in cancer patients.

Magnoliae Cortex Alleviates Muscle Wasting by Modulating M2 Macrophages in a Cisplatin-Induced Sarcopenia Mouse Model.

Cachexia causes high mortality, low quality of life, and rapid weight loss in cancer patients. Sarcopenia, a condition characterized by the loss of muscle, is generally present in cachexia and is associated with inflammation. M2 macrophages, also known as an anti-inflammatory or alternatively activated macrophages, have been shown to play a role in muscle repair. Magnoliae Cortex (M.C) is a widely used medicinal herb in East Asia reported to have a broad range of anti-inflammatory activities; however, the effects of M.C on sarcopenia and on M2 macrophage polarization have to date not been studied. This study was designed to investigate whether the oral administration of M.C could decrease cisplatin-induced sarcopenia by modulating M2 macrophage polarization in mice. C57BL/6 mice were injected intraperitoneally with cisplatin (2.5 mg/kg) to mimic chemotherapy-induced sarcopenia. M.C extract (50, 100, and 200 mg/kg) was administered orally every 3 days (for a total of 12 times). M.C (100 and 200 mg/kg) significantly alleviated the cisplatin-induced loss of body mass, skeletal muscle weight, and grip strength. In addition, M.C increased the expression of M2 macrophage markers, such as MRC1, CD163, TGF-β, and Arg-1, and decreased the expression of M1-specific markers, including NOS2 and TNF-α, in skeletal muscle. Furthermore, the levels of like growth factor-1(IGF-1), as well as the number of M2a and M2c macrophages, significantly increased in skeletal muscle after M.C administration. M.C did not interfere with the anticancer effect of cisplatin in colon cancer. Our results demonstrated that M.C can alleviate cisplatin-induced sarcopenia by increasing the number of M2 macrophages. Therefore, our findings suggest that M.C could be used as an effective therapeutic agent to reverse or prevent cisplatin-induced sarcopenia.

N-3 fatty acid EPA supplementation in cancer patients receiving abdominal radiotherapy - A randomised controlled trial.

Malnutrition occurs frequently in patients with cancer during and after radiotherapy to the gastrointestinal (GI) and pelvic area and can lead to negative outcomes. N-3 fatty acids from fish, especially eicosapentaenoic acid (EPA) may possess anticachectic properties. The aim of this study was to investigate the effect of two nutritional interventions; dietary counselling and a daily oral nutritional supplement (ONS) containing 33.8g of protein and 2.2g EPA and 1.1g docosahexaenoic acid (DHA) or standard care, including dietary counselling and protein supplementation when needed. Outpatients commencing radiotherapy to the GI area were randomized to receive dietary counselling and daily supplementation over a 5-7-week period or standard care. Outcome parameters were measured at baseline (onset of radiotherapy), week 5, and 12 weeks after commencing radiotherapy, with one additional measurement of body weight at week 2. Quality of life (QoL) was measured using the EORTC QLQ-C30 questionnaire. Radiotherapy-related side effects were assessed using a questionnaire developed specifically for this study. Data from a historical control group collected in a previous observational study were included in this study to compare incidence of weight loss. In total, 30 patients were recruited to this study and 26 patients were enrolled and randomised. The rate of withdrawals was 7.7% at week 2, 15.4% at week 5, and 19.2% at week 12. In total, 22 patients completed the intervention. All the patients in the ONS-group and 85% in the control group experienced weight-loss. Using the intention to treat principle, there were no significant differences between groups in any of the outcomes. All patients experienced side effects. Five out of 11 patients consumed more than 75% of prescribed dose of the fish oil enriched oral nutritional supplement. Post hoc analysis showed that at week 2 the weight changed in high-compliant patients was+1.7% (1.0-2.6) compared with-0.7% (-2.8 to-0.1) in low compliant patients (p<0,01). The results indicated a dose-response relationship, as correlation analysis recovered a significant positive correlation between weight change and compliance to the fish oil enriched nutritional supplement at both week 2 and 5 (p<0.05 and p<0.01, respectively), but not at week 12, indicating a dose-response relationship during radiotherapy but not after. The proportion of patients experiencing weight loss throughout the study period was higher in this study (84.2%) than in the historical control group (73%) (p<0.05%). This study showed no effect from dietary counselling and intended protein/fish-oil supplementation on weight loss, quality of life, and nutritional intake, micronutrient status in plasma or radiotherapy-related side effects compared to the control group. However, the compliance to the fish oil enriched oral nutritional supplement was low. Post hoc analysis of dose-response relations indicate a positive correlation between the compliance and the ability to reduce weight loss in cancer patients during radiotherapy treatment. TRIAL REGISTRATION CLINICALTRIALS. NCT04687124.

Weight Loss in Cancer Patients Correlates with p38β MAPK Activation in Skeletal Muscle

Unintentional weight loss due to muscle wasting is a major threat to cancer survival without a defined etiology. We previously identified in mice that p38β MAPK mediates cancer-induced muscle wasting by stimulating catabolism. However, whether this mechanism is relevant to humans is unknown. In this study, we recruited men with cancer and weight loss (CWL) or weight stable (CWS), and non-cancer controls (NCC), who were consented to rectus abdominis (RA) biopsy and blood sampling (n = 20/group). In the RA of both CWS and CWL, levels of activated p38β MAPK and its effectors in the catabolic pathways were higher than in NCC, with progressively higher active p38β MAPK detected in CWL. Activated p38β MAPK correlated with weight loss. Plasma analysis for factors that activate p38β MAPK revealed higher levels in inflammatory cytokines, as well as Hsp70 and Hsp90 in CWS and/or CWL. Thus, p38β MAPK activation appears a key event associated with weight loss in cancer patients.

Association between Growth Differentiation Factor-15 (GDF-15) Serum Levels, Anorexia and Low Muscle Mass among Cancer Patients.

Simple SummaryIn our study, the novel inflammatory cytokine Growth Differentiation Factor-15 (GDF-15) has been found elevated in patients with gastrointestinal and lung cancer and associated with anorexia. Patients with gastrointestinal cancer were found more anorexic (based on the FAACT score) and showed higher GDF-15 serum levels than patients with lung cancer. We also evaluated the muscularity status of the patients by CT scan. No difference was found in GDF-15 levels between cancer patients with low muscle mass vs. those with moderate/high muscularity and between patients with body weight loss vs. those with stable weight. Based on our observations, we confirm the role of GDF-15 in the pathogenesis of anorexia in cancer, although the mechanisms of action of this cytokine in cancer should be further unveiled also regarding its potential involvement in changes in muscularity.The pathophysiology of cancer anorexia is complex and serum biomarkers, including growth and differentiation factor(s) (GDF), may be modulated. We explored the association(s) between GDF-15 serum levels and anorexia and, secondarily, with low muscle mass and body weight loss in cancer patients. We considered gastrointestinal and lung cancer patients (CP) and healthy BMI-matched controls. The FAACT-questionnaire was administered to diagnose anorexia and we calculated the L3-SMI by CT scan to assess low muscularity, setting their cutoff values at the lowest tertile. GDF-15 serum levels were assessed by ELISA. We enrolled 59 CP and 30 controls; among CP, 25 were affected by gastrointestinal and 34 by lung cancer. Anorexia was present in 36% of CP. Gastrointestinal CP resulted more anorexic compared to lung CP (p = 0.0067). Low muscle mass was present in 33.9% of CP and L3-SMI was lower in gastrointestinal compared to lung CP (p = 0.049). The GDF-15 levels were higher in CP vs. controls (p = 0.00016), as well as in anorexic vs. non-anorexic CP (p = 0.005) and vs. controls (p < 0.0001). Gastrointestinal CP showed higher GDF-15 levels vs. lung CP (p = 0.0004). No difference was found in GDF-15 between CP with low muscle mass and those with moderate/high muscularity and between patients with body weight loss and those with stable weight. Our data support the involvement of GDF-15 in the pathogenesis of cancer anorexia. The mechanisms of action of GDF-15 in cancer should be further clarified also regarding the changes in muscularity.

Altered Preoperative Nutritional Status in Colorectal Cancer: A Not So Infrequent Issue.

Introduction Malnutrition and weight loss in cancer patients is a common problem that affects the prognosis of the disease. In the case of CRC, malnutrition rates range between 30 and 60%. Objectives Description of the preoperative nutritional status of patients diagnosed with colorectal neoplasia who will undergo surgery. Materials and Methods A prospective observational study is performed. Results Of 234 patients studied, we observed that 139 (59%) had some degree of nutritional risk. Of all of them, 44.9% (N = 47) had 1-2 points according to MUST and 25% (N = 27) had more than 2 points. No differences were found when studying nutritional risk according to the location of the neoplasm. It was observed that 2.15% of the patients were underweight, 51% overweight, and 23% obese. 19.4% of patients lost less than 5 kg in the 3–6 months prior to diagnosis, 20.7% lost between 5 and 10 kg, and 2.1% lost more than 10 kg. In asymptomatic patients, the weight loss was lower than in symptomatic patients, loss <5 kg, 8.2% vs. 22.8%, and loss 5–10 kg, 16.2% vs. 29.3%, with a value of p = 0.016. 5% (N = 7) of the patients had hypoalbuminemia record. 16.5% (N = 23) had some degree of prealbumin deficiency and 20.9% (N = 29) of hypoproteinemia. Symptomatic patients had more frequent analytical alterations, 1-2 altered parameters in 48.8% (N = 20) of asymptomatic vs. 61.2% (N = 22) in the symptomatic, p = 0.049.

S1194 Bariatric Surgery Associated With Reduced Incidence of Rectal Cancer

INTRODUCTION: The impact of morbid obesity and weight loss surgery (WLS) on GI malignancy remains uncertain. We aimed to investigate if obesity and WLS could alter the risk of GI tumors (GITs). METHODS: The study aims to investigate the cross-sectional relationship between prior WLS and GITs. Data were obtained from 2016 National Inpatient Sample (NIS) database. Multivariate analyses were performed to study primary outcome, the incidence of GITs. RESULTS: Patients with GITs were less morbidly obese (MO) (6.1% vs. 10.7%), more cachectic (3.9% vs. 0.8%) and malnourished (18.1% vs. 4.7%) compared to patients without GITs. Given that multiple factors that can affect weight loss in cancer patients, we selected MO patients with BMI≥35Kg/m2. Out of 622,834 MO patients, 19,932 (3.1%) had undergone WLS. Patients who underwent WLS were older (55.3 vs. 53.8 years, P < 0.01), more females (74.4% vs. 64.5%, P < 0.01), and more White (72.0% vs. 66.9%, P < 0.01). The incidence of tumors among MO patients was 0.4% for colon, 0.1% for rectum, 0.1% for gastric, and < 0.1% for esophageal and small bowel tumors. Based on multivariate analysis; esophageal, gastric, small bowel, and colon tumors had no statistically significant association with a prior history of WLS. Only rectal cancer was associated with reduced incidence following WLS (adjusted OR = 0.31[0.15,0.61], P < 0.01]). CONCLUSION: In MO patients, WLS may be associated with a reduced incidence of rectal cancer. This study does not show any association with other types of GITs. Future prospective studies should clarify the multifactorial relationship between WLS and the development of GITs.

Cachexia in Cancer Patients: Systematic Literature Review

Introduction Cachexia in cancer patients, especially in advanced stage, is recently known as an emerging problem. Cachexia occurs in about half of all patients with neoplastic disease. The diagnosis of cachexia needs comprehensive evaluation of body weight and body composition for several months. Cachexia will give negative impacts such as increased mortality, chemotoxicity, and decreased quality of life. Here, we review the current evidence describing the definition, stages, mechanisms, diagnosis and treatment of cachexia in cancer patients. Methods We identified 75 studies and/or review articles evaluating cachexia and weight loss in cancer patients by searching PubMed and EMBASE databases. Results Cachexia is reported across all stages and types of cancers. The most recent definition of cachexia is reported in a 2011 paper by International Consensus. The mechanism of cachexia in cancer is complex and involved many factors which elaborate together to produce cachexia. The diagnostic evaluation and cut-off measurement of cachexia, especially in cancer varied across studies. The loss of weight that happens during chemotherapy will make a poor prognosis. Cachexia can worsen chemotherapy toxicity. Combination of dietary modification and exercise with supplementation of medication that control appetite and inflammation are important in the management of cachexia in cancer patients. Conclusion Patients with cancer are the population at risk for developing cachexia before and after chemotherapy. Cachexia diagnosis needs evaluation of body weight and body composition. Nonpharmacological treatments, such as dietary modification and physical exercise, are the best strategy to reduce cachexia in cancer patients.

RDN Interventions May Attenuate Weight Loss in Cancer Patients: A Quality Improvement Project

RDN Interventions May Attenuate Weight Loss in Cancer Patients: A Quality Improvement Project

Alterações no estado nutricional segundo IMC e perda de peso, em pacientes com câncer de cabeça e pescoço em uso de terapia nutricional enteral, em ambulatório de oncologia clínica em São Paulo

Introduction: Head and neck cancer (HNC) patients constitute a recognized risk group for malnutrition due to several factors, and may require enteral nutritional therapy (ENT). This study evaluated alterations in nutritional status and weight loss in patients with HNC using ENT followed at the Universidade Federal de São Paulo (UNIFESP) oncology outpatient clinic. Methods: This was a retrospective study conducted through database analysis, collected from January to December of 2018 at an UNIFESP oncology outpatient clinic. We selected all patients with HNC in use of ENT at some moment of the treatment during 2018. Weight and height were considered to calculate body mass index (BMI) and to classify nutritional status and the classification of weight loss for evaluation. Results: The sample consisted of 24 patients, 71% were elderly and 29% adults and 75% were men. At the first consultation in 2018, 6 (25%) patients were at normal weight and 15 (63%) had some degree of malnutrition (underweight). A total of 11 (46%) patients reported previous weight loss. After the analysis it was found that 54% of patients had weight loss in the period, however, only 1 patient had severe weight loss. Changes in BMI were observed in all patients, but in 88% of the cases there was no change in BMI classification. Conclusion: Although patients were on ENT, many had weight loss, which may be a result of decreased food intake, metabolic abnormalities caused by tumor activity, or a consequence of treatment-related symptoms. Most of the weight losses were not significant, and most patients had increased body weight, which may have been result of ENT use, which is responsible for delayed weight loss in cancer patients.

Enteral and parenteral nutrition in cancer patients, a comparison of complication rates: an updated systematic review and (cumulative) meta-analysis.

Weight loss in cancer patients is a worrisome constitutional change predicting disease progression and shortened survival time. A logical approach to counter some of the weight loss is to provide nutritional support, administered through enteral nutrition (EN) or parenteral nutrition (PN). The aim of this paper was to update the original systematic review and meta-analysis previously published by Chow et al., while also assessing publication quality and effect of randomized controlled trials (RCTs) on the meta-conclusion over time. A literature search was carried out; screening was conducted for RCTs published in January 2015 up until December 2018. The primary endpoints were the percentage of patients achieving no infection and no nutrition support complications. Secondary endpoints included proportion of patients achieving no major complications and no mortality. Review Manager (RevMan 5.3) by Cochrane IMS and Comprehensive Meta-Analysis (version 3) by Biostat were used for meta-analyses of endpoints and assessment of publication quality. An additional seven studies were identified since our prior publication, leading to 43 papers included in our review. The results echo those previously published; EN and PN are equivalent in all endpoints except for infection. Subgroup analyses of studies only containing adults indicate identical risks across all endpoints. Cumulative meta-analysis suggests that meta-conclusions have remained the same since the beginning of publication time for all endpoints except for the endpoint of infection, which changed from not favoring to favoring EN after studies published in 1997. There was low risk of bias, as determined by assessment tool and visual inspection of funnel plots. The results support the current European Society of Clinical Nutrition and Metabolism guidelines recommending enteral over parenteral nutrition, when oral nutrition is inadequate, in adult patients. Further studies comparing EN and PN for these critical endpoints appear unnecessary, given the lack of change in meta-conclusion and low publication bias over the past decades.

Endocrinopathies and cancer cachexia.

Cancer cachexia cannot be easily reversed by standard nutritional support and interventions directed at underlying metabolic derangements may be needed to prevent or reverse cachexia and maintain healthy body composition. The following review will highlight the contribution and potential therapeutic interventions for insulin resistance, alterations in ghrelin signaling, and hypogonadism in cancer patients. In addition to decreased caloric intake, chronic inflammation, and altered metabolism of glucose, proteins and lipids, endocrine abnormalities can propagate weight loss or changes in body composition in cancer patients. Cancer cachexia, loss of muscle mass with or without the loss of fat mass, is a multifactorial syndrome, which is associated with increased morbidity and mortality. Currently, limited therapeutic options for the treatment of weight loss in cancer patients exist, which lead to clinically meaningful improvements in weight gain and performance status. Treatment directed at underlying insulin resistance, low testosterone, and altered ghrelin sensitivity, in the future, may lead to potential therapeutic options for loss of lean body mass and cancer cachexia.

Combining optimal nutrition and exercise in a multimodal approach for patients with active cancer and risk for losing weight: Rationale and practical approach.

Weight loss and functional decline is a common and detrimental consequence of cancer. The interventions that are offered to patients with weight loss and functional decline often seem haphazard and varying from center to center. The lack of stringent management is probably based both on lack of knowledge of existing treatment guidelines and the current weak level of evidence of clinical effects of different nutritional and exercise interventions. Some studies evaluated multimodal interventions with various treatment combinations, including nutrition and exercise, that report clinically significant effects on cachexia outcomes. As of today, however, there is a paucity of large randomized controlled trials that incorporate both a fully structured exercise program and a well-described nutritional intervention. Studies investigating combinations of several interventions in patients with active cancer and risk for losing weight are too few and too heterogeneous to enable firm conclusions about effect, optimal dose, or timing of interventions. However, data presented in this review suggest an overall benefit, especially if interventions are started before weight loss and loss of function become too severe. Thus, the aim of this review was to examine the evidence for combined treatments targeting weight loss in cancer patients.

Measuring cachexia-diagnostic criteria.

Cancer cachexia is characterized by the loss of lean body mass with or without the loss of fat and is associated with increased susceptibility to treatment related toxicities, decreased quality of life, functional impairment, and increased cancer-related mortality. Uncontrolled symptoms which impair nutritional intake, metabolic derangements including elevated energy expenditure and increased catabolism, and chronic inflammation contribute to the development of cancer cachexia. Weight loss in cancer patients is not readily reversible by conventional nutritional support. The definition of cachexia and sarcopenia are evolving with time, as well as the assessment of weight loss in cancer patients. Clinicians should assess all cancer patients regardless of history of weight loss for risk for malnutrition at presentation and periodically throughout the trajectory of illness-pre-cachectic, cachexia, and refractory cachexia stage. For cancer patients with weight loss, assessments of BMI and percentage weight loss, symptoms which impact nutritional intake, quality of life, physical function, biological markers, energy expenditure, and body composition are ideally needed in order to measure cachexia and implement therapeutic interventions.

Nutrition support for treating cancer-associated weight loss: an update.

Patients with cancer present high risk for involuntary body weight loss and reduced food intake, which, contributing to progressive tissue wasting and affecting the nutritional status, are often under-estimated in the clinical practice. In this article, we aimed at focusing on cancer-associated weight loss and investigating recent evidences on the indications of nutritional interventions to treat this condition. During the last few years, increased emphasis has been addressed on the mechanisms underlying body weight loss in cancer that can be induced by either cancer metabolism and inflammation, either several side-effects of the anticancer treatments. This led to consider clinical parameters, such as BMI, body weight change and food intake, and their modification overtime, in predicting patient's overall survival. In this light, nutritional support has to be considered to maintain or restore nutritional status, improve tolerance to oncological therapies, and ameliorate physical performance and quality of life. Increased awareness on weight loss in cancer patients and on cancer cachexia is needed to carry out a nutritional assessment at an early stage of cancer journey and to establish its management and nutritional support to obtain advantages in terms of treatment tolerance and clinical outcomes.

A Novel Mobile Phone App (OncoFood) to Record and Optimize the Dietary Behavior of Oncologic Patients: Pilot Study.

BackgroundCatabolism and tumor-specific therapy lead to reduced nutrient intake and weight loss in cancer patients. Maintaining a specific individualized diet can be challenging for the patient as the nutritional counseling options are limited. Monitoring of nutrient intake and frequent feedback are, however, vital for successful nutritional therapy because they support the patient’s compliance and realization of dietary therapeutic goals.ObjectiveThis study aimed at investigating the feasibility and applicability of a novel mobile phone app to assess and evaluate dietary behaviors in oncologic patients.MethodsTo determine dietary habits and food preferences in oncologic patients, initially 1400 nutritional records were evaluated and analyzed. The results provided the basis for creating a nutritional mobile phone app. Key requirements for the app included simple handling, recording the daily intake, and a comparison of nutrient targets and current status. In total, 39 cancer patients were recruited for the study; 15 patients dropped out prior to the study. All patients received a nutritional anamnesis, nutritional analysis, and nutritional counseling. Individual energy and nutrient aims were defined. The intervention group (n=12) additionally used the app. Weight and body composition of each group were evaluated after 4 weeks.ResultsThe app group gained significantly more weight (P=.045; mean weight 1.03 kg vs –1.46 kg). Also, skeletal muscle mass showed a significant increase in the app group (P=.009; mean skeletal muscle mass 0.58 kg vs –0.61 kg) compared with the control group. There was no significant difference between groups relating to the daily protein intake (P=.06). Additionally, there was a decrease in macronutrient intake during the study period in the control group.ConclusionsOur study indicates that patients who track their daily dietary habits using a mobile phone app are more likely to reach their nutritional goals than the control patients. Further large-scale studies are needed to confirm these initial findings and test the applicability on a broader basis.

Insulin resistance and body composition in cancer patients

Cancer cachexia, weight loss with altered body composition, is a multifactorial syndrome propagated by symptoms that impair caloric intake, tumor byproducts, chronic inflammation, altered metabolism, and hormonal abnormalities. Cachexia is associated with reduced performance status, decreased tolerance to chemotherapy, and increased mortality in cancer patients. Insulin resistance as a consequence of tumor byproducts, chronic inflammation, and endocrine dysfunction has been associated with weight loss in cancer patients. Insulin resistance in cancer patients is characterized by increased hepatic glucose production and gluconeogenesis, and unlike type 2 diabetes, normal fasting glucose with high, normal or low levels of insulin. Cancer cachexia results in altered body composition with the loss of lean muscle mass with or without the loss of adipose tissue. Alteration in visceral adiposity, accumulation of intramuscular adipose tissue, and secretion of adipocytokines from adipose cells may play a role in promoting the metabolic derangements associated with cachexia including a proinflammatory environment and insulin resistance. Increased production of ghrelin, testosterone deficiency, and low vitamin D levels may also contribute to altered metabolism of glucose. Cancer cachexia cannot be easily reversed by standard nutritional interventions and identifying and treating cachexia at the earliest stage of development is advocated. Experts advocate for multimodal therapy to address symptoms that impact caloric intake, reduce chronic inflammation, and treat metabolic and endocrine derangements, which propagate the loss of weight. Treatment of insulin resistance may be a critical component of multimodal therapy for cancer cachexia and more research is needed.