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PubMed1994

Characterization of mice bearing subclones of colon 26 adenocarcinoma disqualifies interleukin-6 as the sole inducer of cachexia.

A subclone (clone 20) of chemically induced, murine colon adenocarcinoma with a potent ability to induce cachexia and another subclone (clone 5) without such an activity were transplanted to syngeneic mice (CDF1) and their tissue weights, blood components and cytokine levels in sera were compared. Mice transplanted with clone 20 showed a profound body-weight loss by 15 days after inoculation when the tumor accounted for less than 1% of the body weight, along with marked reduction of food and water intakes. Thereafter, they transiently gained in body weight with restoration of food and water intakes. Thus, the change in body weight was biphasic and not proportional to the tumor size. Body fat was lost preferentially, accompanied with a decrease in plasma triglyceride levels. The thymus contracted remarkably, and the peripheral lymphocyte count decreased extensively. Mice transplanted with clone 5, in contrast, did not show any of these changes characteristic of cachexia. Serum concentration of interleukin-6, which has been proposed as the principal inducer of cachexia in mice with colon 26, increased in mice with clone 5 to levels comparable to those in mice with clone 20. The changes in mice bearing clone 20 could not all be explained in terms of known biological activities of interleukin-6. Additional unknown factors, therefore, are presumed to contribute to cachexia in mice with clone 20. Identification of them should be helpful in the care of cachectic patients.

Adenocarcinoma↗
PubMed1995

Cytokine production in five tumor cell lines with activity to induce cancer cachexia syndrome in nude mice.

To identify the so-called toxohormone, which is a tumor-derived factor with activity to induce cancer cachexia syndrome in tumor-bearing animals, 5 human cancer cell lines with this activity were studied for cytokine production. Tumor cell products with activity to inhibit lipoprotein lipase (LPL) were shown to play an important role in the development of the cancer cachexia syndrome. All culture media conditioned by the 5 cell lines possessed LPL-inhibitory activity. However, the activity differed with the cell line. In order to characterize the activity, we examined whether the cultured cells produced cytokines with activity to inhibit LPL. A melanoma cell line, SEKI, and a neuroepithelioma cell line, NAGAI, were found to express a large amount of leukemia inhibitory factor (LIF) mRNA. Furthermore, both of these cell lines were demonstrated to produce a large amount of LIF protein, and plasma levels of LIF were extremely elevated in SEKI- and NAGAI-bearing nude mice, indicating that LIF produced by the tumor cells induced cancer cachexia syndrome in the animals. Thus, LIF fulfills the requirements for a toxohormone, except for suppressive activity on liver catalase. In contrast, the mechanisms responsible for cachexia in the MKN-1-, LX-1- and LS180-bearing mice remain unknown. These findings suggest that various types of bioactive substances produced by cancer cells could be toxohormones.

Animals↗
PubMed1988

Skeletal muscle and whole body protein turnover in cardiac cachexia: influence of branched-chain amino acid administration.

Muscle protein wasting commonly accompanies severe heart failure. The mechanism of this so-called cardiac cachexia has been investigated in eight patients with an average body weight decrement of 19%, whose results have been compared with those from 11 healthy control subjects. Exchanges of tyrosine and 3-methylhistidine across leg tissue were used as specific indicators of net protein balance and myofibrillar protein breakdown, respectively. Whole body protein turnover was measured using a stable isotope labelling technique with L-[1-13C]leucine as tracer. In patients with cardiac cachexia there were greater values, relative to those values in normal control subjects, of leg efflux of tyrosine (-8.1 +/- 0.6 nmol 100 ml leg tissue-1 min-1 vs. -4.2 +/- 0.3 nmol 100 ml-1 min-1 (P less than 0.01) and of 3-methylhistidine (-0.8 +/- 0.1 nmol 100 ml leg tissue-1 min-1 vs. -0.1 +/- 0.02 nmol 100 ml-1 min-1 (P less than 0.005), mean +/- SEM). The results suggest that in patients with cardiac cachexia the state of net negative protein balance across leg tissue is associated with an increased rate of myofibrillar protein breakdown. In cardiac cachexia, neither efflux of tyrosine (-8.4 +/- 0.7 nmol 100 ml leg tissue-1 min-1) nor of 3-methylhistidine (-1.0 +/- 0.2 nmol 100 ml leg tissue-1 min-1) were significantly altered by branched-chain amino acid (BCAA) infusion to plasma concentrations of 1300 +/- 14 mumol ml-1, i.e., four times normal plasma values (282 +/- 11 mumol ml-1).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed2005

Estimation of total body water from foot-to-foot bioelectrical impedance analysis in patients with cancer cachexia - agreement between three prediction methods and deuterium oxide dilution.

INTRODUCTION: Bioelectrical impedance analysis (BIA) is a useful bedside measure to estimate total body water (TBW). The aim of this study was to determine the agreement between three equations for the prediction of TBW using BIA against the criterion method, deuterium oxide dilution, in patients with cancer cachexia. METHODS: Eighteen measurements of TBW using foot-to-foot BIA in seven outpatients with cancer cachexia (five male and two female, age 56.4 +/- 6.7 years) at an Australian hospital. Three prediction formulae were used to estimate TBW - TBW(ca-radiotherapy) developed in patients with cancer undergoing radiotherapy, TBW(ca-underweight) and TBW(ca-normal weight) developed in underweight and normal weight patients with cachexia. TBW was measured using the deuterium oxide dilution technique as the gold standard. RESULTS: Mean measured TBW was 39.5 +/- 6.0 L. There was no significant difference in measured TBW and estimates from prediction equations TBW(ca-underweight) and TBW(ca-radiotherapy). There was a significant difference in measured TBW and TBW(ca-normal weight). All prediction equations overestimated TBW in comparison with measured TBW. The smallest bias was observed with TBW(ca-underweight) (0.38 L). The limits of agreement are wide (>7.4 L) for each of the prediction equations compared with measured TBW. CONCLUSIONS: At a group level, TBW(ca-underweight) is the best predictor of measured TBW in patients with cancer cachexia. For an individual however, the limits of agreement are wide for all prediction equations and are unsuitable for use. Practitioners need to be aware of the limitations of using TBW prediction equations for individuals.

Body Composition↗
PubMed1992

Diabetic neuropathic cachexia associated with malabsorption.

Diabetic neuropathic cachexia is characterized by neuropathic pain and severe weight loss of unknown aetiology. We describe four patients with diabetic neuropathic cachexia who were found to have malabsorption. Four diabetic patients presented with neuropathic pain, anorexia, depression and weight loss of 16 (range 10-21) kg. None complained of diarrhoea. There were three males and one female, median age 54 (46-67) years. A butterfat test showed a serum turbidity difference of 9 (6-10) light scattering units (normal greater than 60 units). The median serum xylose was low and there was delayed urinary xylose excretion. Urinary indicans, small bowel histology, liver function tests, and thyroid and renal function were normal. Ultrasound scans of liver, gall bladder and pancreas, and endoscopic retrograde cholangiopancreatogram were normal. The patients were treated with pancreatic supplements and a high calorie diet. Three have completely recovered and the other patient is improving. Thus these cases of diabetic neuropathic cachexia appeared to be associated with malabsorption which may be due to pancreatic dysfunction. It is suggested that the management of diabetic neuropathic cachexia should include the investigation and treatment of malabsorption.

Aged↗
PubMed1989

Studies of cachexia in parasitic infection.

Cachexia and septic shock, syndromes associated with chronic and acute infection, respectively, are mediated by endogenous factors. The search for humoral mediators of cachexia led to the isolation of the cytokine known as cachectin/TNF. A biologic role for cachectin/TNF in cachexia has been identified: it induces a catabolic state in adipose and skeletal muscle cells in vitro, and animals persistently exposed to it in vivo become cachectic. Cachectin/TNF was also discovered to be a primary, essential mediator of septic shock. The acute administration of the recombinant protein causes shock, tissue injury, and derangements of metabolic homeostasis that mimic endotoxemia and septic shock syndrome. Anti-cachectin antibodies protect against the lethal effects of septic shock and cachexia, suggesting that this mediator has a central role as a trigger to the inflammatory and deleterious host responses to infection. Future investigations will undoubtedly be directed towards the effects of inhibiting cachectin/TNF in the treatment of the complications of infectious disease.

Animals↗
PubMed1988

Tumor necrosis factor (cachectin) mediates induction of cachexia by cord factor from mycobacteria.

The mechanism by which cord factor (CF), a toxic glycolipid from mycobacteria, induces cachexia was studied in BALB/c mice. Body weight was markedly reduced 48 h after CF administration; the animals became severely wasted and exhibited hypertriglyceridemia, hypoglycemia, and high levels of tumor necrosis factor (TNF) in plasma. After CF administration, a transferable factor which caused cachexia and hypertriglyceridemia in recipient mice was detected in the blood. Dexamethasone partially inhibited the cachexia-inducing action of CF. Conditioned medium from adherent peritoneal cell cultures incubated with CF produced the same wasting symptoms when inoculated intravenously into mice. These studies also demonstrated that adherent peritoneal cells produced a humoral factor in response to CF which was related to CF-induced cachexia. Antiserum to recombinant TNF-alpha prevented the cachectin action in passive-transfer experiments. Our findings indicate that cachectin (TNF) plays a role as a central mediator of the wasting induced by CF.

Animals↗
PubMed1999

The endogenous balance of soluble tumor necrosis factor receptors and tumor necrosis factor modulates cachexia and mortality in mice acutely infected with Trypanosoma cruzi.

To better understand the role of tumor necrosis factor (TNF) during Trypanosoma cruzi infection in BALB/c mice, we have investigated the kinetics of circulating tumor necrosis factor (TNF), soluble TNF receptor 1 (sTNR1), and sTNFR2 levels, as well as the interactions between such factors, in relation to parasitemia, cachexia, and mortality of acutely infected animals. Our data show that the parasitemic phase of T. cruzi infection in mice is associated with high levels of circulating TNF and sTNFR2, resulting in the formation of cytokine-receptor complexes and some degree of neutralization of TNF bioactivity. Although sTNR2 levels always exceeded TNF levels, low sTNFR/TNF circulating ratios were associated with cachexia in all infected mice, whereas the lowest ratios were observed in dying animals harboring the highest parasitemia. We also studied the modulation of sTNFR/TNF ratios induced by anti-TNF antibodies administered to infected animals and their consequences on the outcome of the infection. The injection of anti-TNF monoclonal antibody (MAb) TN3 into infected mice resulted in a paradoxical overproduction of TNF (associated with a higher parasitemia), lowered the sTNFR/TNF circulating ratios, and considerably worsened cachexia and mortality of animals. Another anti-TNF MAb (1F3F3) decreased the in vivo availability of TNF as well as parasite levels and reduced cachexia. Altogether, such results highlight that, besides playing a beneficial role early in infection, TNF also triggers harmful effects in the parasitemic phase, which are limited by the in vivo simultaneous endogenous production of soluble receptors.

Acute Disease↗
PubMed2005

Thalidomide in the treatment of cancer cachexia: a randomised placebo controlled trial.

BACKGROUND: Proinflammatory cytokines, especially tumour necrosis factor alpha (TNF-alpha), play a prominent role in the pathogenesis of cancer cachexia. Thalidomide, which is an inhibitor of TNF-alpha synthesis, may represent a novel and rational approach to the treatment of cancer cachexia. AIMS: To assess the safety and efficacy of thalidomide in attenuating weight loss in patients with cachexia secondary to advanced pancreatic cancer. METHODS: Fifty patients with advanced pancreatic cancer who had lost at least 10% of their body weight were randomised to receive thalidomide 200 mg daily or placebo for 24 weeks in a single centre, double blind, randomised controlled trial. The primary outcome was change in weight and nutritional status. RESULTS: Thirty three patients (16 control, 17 thalidomide) were evaluated at four weeks, and 20 patients (eight control, 12 thalidomide) at eight weeks. At four weeks, patients who received thalidomide had gained on average 0.37 kg in weight and 1.0 cm(3) in arm muscle mass (AMA) compared with a loss of 2.21 kg (absolute difference -2.59 kg (95% confidence interval (CI) -4.3 to -0.8); p = 0.005) and 4.46 cm(3) (absolute difference -5.6 cm(3) (95% CI -8.9 to -2.2); p = 0.002) in the placebo group. At eight weeks, patients in the thalidomide group had lost 0.06 kg in weight and 0.5 cm(3) in AMA compared with a loss of 3.62 kg (absolute difference -3.57 kg (95% CI -6.8 to -0.3); p = 0.034) and 8.4 cm(3) (absolute difference -7.9 cm(3) (95% CI -14.0 to -1.8); p = 0.014) in the placebo group. Improvement in physical functioning correlated positively with weight gain (r = 0.56, p = 0.001). CONCLUSION: Thalidomide was well tolerated and effective at attenuating loss of weight and lean body mass in patients with cachexia due to advanced pancreatic cancer.

Aged↗
PubMed2006

IGF-1 is downregulated in experimental cancer cachexia.

Cancer cachexia is characterized by skeletal muscle wasting that is mainly supported by hypercatabolism. Muscle atrophy has been suggested to depend on impaired IGF-1 signal transduction pathway. The present study has been aimed at investigating the IGF-1 system in rats bearing the AH-130 hepatoma, a well-characterized model of cachexia. IGF-1 mRNA expression in the gastrocnemius of tumor hosts progressively decreases to approximately 50% of controls. By contrast, both IGF-1 receptor and insulin receptor mRNA levels increase in day 7 AH-130 hosts. IGF-1 and insulin circulating levels, as well as IGF-1 expression in the liver, are reduced. Muscle wasting in the AH-130 bearers is associated with hyperactivation of the ubiquitin-proteasome system. Consistently, the mRNA levels of ubiquitin and of the ubiquitin ligases atrogin-1 and MuRF1 are significantly increased in the gastrocnemius of day 7 AH-130 hosts. Exogenous IGF-1 administered to tumor bearers does not prevent cachexia. IGF-1 mRNA levels also have been evaluated in the gastrocnemius of AH-130 hosts treated with pentoxifylline, an inhibitor of TNF-alpha synthesis, alone or combined with formoterol, a beta(2)-adrenergic agonist. Both treatments partially correct muscle atrophy without modifying IGF-1 and atrogin-1 mRNA levels, whereas MuRF1 hyperexpression is reduced by the combination of pentoxifylline with formoterol. These results demonstrate for the first time that the IGF-1 system is downregulated in cancer cachexia, although the underlying mechanism remains unknown. Moreover, no simple relation linking IGF-1 and/or atrogin-1 mRNA levels and muscle atrophy could be observed in these experimental conditions. Further studies are thus needed to clarify both issues.

Adrenergic beta-Agonists↗
PubMed1992

Clinical management of anorexia and cachexia in patients with advanced cancer.

Cachexia occurs in the majority of cancer patients before death. It is the result of major metabolic changes produced by tumor-released substances as well as by cytokines and some endogenous peptides. The most significant clinical manifestation is profound anorexia. Aggressive parenteral nutrition has not been able to increase patient survival or produce any significant symptomatic improvement. Recent research, therefore, has focused on drugs that might result in symptomatic improvement, even if no significant nutritional changes are detected. Corticosteroids have been shown to increase appetite for a brief period of time, but they do not appear to improve caloric intake or nutritional status. In addition to appetite stimulation, corticosteroids also improve a number of other symptoms transiently. Progestational drugs have been found in a number of studies to increase appetite, caloric intake, and nutritional status. The most effective type and dose of progestational drugs have not been clearly established. Cyproheptadine, hydrazine sulfate, and cannabinoids have all been suggested to have beneficial effects on appetite; their effectiveness, however, needs to be confirmed in prospective, controlled trials. Some of these trials are currently under way. Current data suggest that megestrol acetate or other progestational agents could be useful--because of effects on not only appetite but also overall nutritional status--in patients who have profound anorexia as the main manifestation of cachexia, provided expected survival can be measured in weeks or months. In patients with shorter expected survival or those who have problems tolerating progestational drugs, a brief course of corticosteroids may provide short-term symptomatic effects. Future studies should focus on (1) improving understanding of both the pathophysiology of cancer cachexia and the interaction of some of the major syndromes of terminal cancer--e.g., pain, cachexia, and cognitive failure--and (2) characterizing the symptomatic effects of different drugs more completely.

Anorexia↗
PubMed1990

Tumor necrosis factor-alpha inhibits albumin gene expression in a murine model of cachexia.

The mechanisms responsible for decreased serum albumin levels in patients with cachexia-associated infection, inflammation, and cancer are unknown. Since tumor necrosis factor-alpha (TNF alpha) is elevated in cachexia-associated diseases, and chronic administration of TNF alpha induces cachexia in animal models, we assessed the regulation of albumin gene expression by TNF alpha in vivo. In this animal model of cachexia, Chinese hamster ovary cells transfected with the functional gene for human TNF alpha were inoculated into nude mice (TNF alpha mice). TNF alpha mice became cachectic and manifested decreased serum albumin levels, albumin synthesis, and albumin mRNA levels. However, even before the TNF alpha mice lost weight, their albumin mRNA steady-state levels were decreased approximately 90%, and in situ hybridization revealed a low level of albumin gene expression throughout the hepatic lobule. The mRNA levels of several other genes were unchanged. Hepatic nuclei from TNF alpha mice before the onset of weight loss were markedly less active in transcribing the albumin gene than hepatic nuclei from control mice. Therefore, TNF alpha selectively inhibits the genetic expression of albumin in this model before weight loss.

Animals↗
PubMed1993

Suramin interferes with interleukin-6 receptor binding in vitro and inhibits colon-26-mediated experimental cancer cachexia in vivo.

Neoplastic diseases are frequently associated with metabolic changes collectively known as cancer cachexia. The presence of cachexia complicates therapeutic intervention and is an important cause of death in cancer patients. At present there is no effective treatment for cachexia. Recently, the involvement of interleukin-6 (IL-6) in the wasting of colon-26 adenocarcinoma-bearing mice was demonstrated. The research presented here establishes an anticachectic role for the experimental drug suramin, since it partially blocks (up to 60%) the catabolic effects associated with the growth of this tumor in vivo. Suramin prevents the binding of IL-6 to its cell surface receptor subunits, as demonstrated by radioreceptor binding assay and affinity crosslinking experiments. Furthermore, the uptake of radioactive IL-6 by the liver is significantly reduced in suramin-treated mice. On the other hand, the drug is approximately 10-fold less potent in inhibiting the binding of tumor necrosis factor-alpha to indicator cell line in vitro and fails to block liver uptake of this cytokine in vivo. Collectively, these results suggest that suramin inhibits cancer-associated wasting, in part by interfering with the binding of IL-6 to its receptor. Whether suramin inhibits the action of other factors/cytokines that may also participate in colon-26-mediated cachexia is not yet known.

Adenocarcinoma↗
PubMedDate not supplied

Prevention of cancer cachexia by pyrrolidine dithiocarbamate (PDTC) in colon 26 tumor-bearing mice.

BACKGROUND: The precise mechanism of cancer cachexia is not fully elucidated. This study was aimed to assess the effect of pyrrolidine dithiocarbamate (PDTC, an inhibitor of NFkappaB) on interleukin (IL)-6 synthesis and cachexia in colon 26 tumor-bearing mice. METHODS: Murine colon 26 adenocarcinoma cells were inoculated subcutaneously in male BALB/c mice to induce cachexia. Saline and various doses of PDTC (10, 50, or 100 mg/kg/d) were given intraperitoneally daily from 7 days after tumor inoculation to killing. Body weight, food intake, and tumor volume were monitored daily. Serum and tumor tissue levels of IL-6, serum biochemical indicator, and activity of NFkappaB in tumor tissue were investigated in all mice. RESULTS: Significant tissue wasting was observed in all tumor-bearing mice. By day 16, carcass weights of untreated tumor-bearing mice were about 71.3% of healthy controls (p < .01), and the weights of gastrocnemius muscle and epididymal fat were lowered by 42.4% and 70.4% (p < .01), respectively. Furthermore, tumor-bearing caused a significant decrease of serum albumin, glucose, and triglyceride (p < .01) and increase of IL-6 (p < .01) in serum and tumor tissues. Administration of PDTC dose dependently inhibited the NFkappaB activation in tumor tissues, inhibited IL-6 synthesis of the tumor cells, and attenuated the wasting of carcass weight, gastrocnemius muscle, and epididymal fat. Tumor growth was inhibited by PDTC with 100 mg/kg (p < .05). No differences of food intake were found between groups (p > .05). CONCLUSIONS: These results suggest that PDTC, an inhibitor of NFkappaB, can attenuate the development of cachexia in colon 26 tumor-bearing mice through inhibition of IL-6 synthesis regulated by NFkappaB.

Adenocarcinoma↗
PubMed2003

Rethinking nutritional support for persons with cancer cachexia.

Cancer cachexia is a poorly understood syndrome of anorexia, weight loss, and muscle wasting that negatively impacts quality of life and survival in cancer patients. Research has clearly implicated pro-inflammatory cytokines in the biology of cancer cachexia. More recent research implicates products of arachidonic acid and suggests that cachexia may be a chronic inflammatory condition rather than a nutritional aberration. To date, nutritional support to slow weight loss has focused primarily on increasing calorie intake. Alternatively, many foods contain factors that can modulate the synthesis or activity of pro-inflammatory mediators, especially the synthesis of prostaglandin E2 from arachidonic acid. These factors and foods are sometimes called nutraceuticals, and research is needed to evaluate their efficacy in combating cancer cachexia.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMedDate not supplied

Cachexia in patients with advanced cancer.

Cancer cachexia generally is considered to be the end stage in the progression of nutritional deterioration and wasting of malignancy (Ottery, 1995). In patients with advanced cancer, this condition is very common and decreases quality of life, as well as survival (Fearon et al., 2001; Ottery; Smith & Souba, 2001; Whitman, 2000). However, if early diagnosis and intervention can control cachexia, the potential exists to greatly improve a patient's quality of life and prolong survival. Because metabolic alterations inhibit the effective use of conventional nutritional support, anti-inflammatory agents or fish oil are possible options. Orexigenic agents may be prescribed if patients wish to improve oral intake. Steroids and progestational agents may be used to attempt to improve mood and appetite. Nutrition affects symptoms that need to be managed effectively. Nurses should work aggressively to correct factors that contribute to decreased food intake (e.g., nausea, pain) and correct factors that worsen debility (e.g., anemia). Information must be presented so that informed choices can be made and realistic eating goals set. An interdisciplinary approach that involves the nurse, physician, dietician, and possibly social worker or case manager, as well as the patient and family, is necessary to identify nutritional alterations, assess specific needs, and plan individual interventions. Whitman (2000) stated that counseling is the most effective and least expensive intervention. It may be conducted by any member of the healthcare team and should be combined with other interventions. Palliation of cachexia in patients with advanced cancer is a challenge for nurses. Hopefully, early and judicious use of these interventions may decrease the significant morbidity and mortality that result from cancer cachexia.

Adenocarcinoma, Papillary↗
PubMed2005

Ratio of n6 to n-3 fatty acids in the diet affects tumor growth and cachexia in Walker 256 tumor-bearing rats.

In this study we investigate the impact of the dietary ratio of n-6 to n-3 fatty acids (FAs) from postweaning until adult age upon tumor growth, lipid peroxidation in tumor tissue, and metabolic indicators of cancer cachexia in Walker 256 tumor-bearing rats. Weanling male Wistar rats received a normal low-fat (40 g/kg diet) chow diet or high-fat diets (300 g/kg) that included fish oil (FO) or sunflower oil or blends of FO and sunflower oil to yield n-6 to n-3 FA ratios of approximately 6:1, 30:1, and 60:1 ad libitum. After 8 wk, half of each group was inoculated with 1 ml of 2 x 10(7) Walker 256 cells. At the 14th day after tumor inoculation, the animals were killed, and tumors and blood were removed. The different diets did not modify the blood parameters in the absence of tumor bearing, except the high-FO diet, which decreased serum cholesterol and triacylglycerol concentrations. Tumor weight in chow-fed rats was 19 g, and these rats displayed cancer cachexia, characterized by hypoglycemia, hyperlacticidemia, hypertriacylglycerolemia, loss of body weight, and food intake reduction. Tumor weight in FO-fed rats was 7.7 g, and these animals gained body weight (14.6 g) and maintained blood metabolic parameters similar to non-tumor-bearing animals. Tumor weight in rats fed the diet with an n-6 to n-3 FA ratio of 6:1 was similar to tumor-bearing, chow-fed rats, but they gained 2 g in the body weight and blood metabolic parameters were similar to those in non-tumor-bearing rats. However, a further increase in the n-6 FA content of the diet did not change the cachectic state associated with tumor bearing. In this experimental model, a dietary n-6 to n-3 FA ratio of 6:1 was able to increase food intake and body weight, restore the biochemical blood parameters of cachexia, and prevent the development of cancer cachexia.

Animals↗
PubMed2003

Fish oil supplementation in the treatment of cachexia in pancreatic cancer patients.

Patients with pancreatic cancer often experience a loss of weight and appetite, known as the anorexia-cachexia syndrome, which is associated with decreased quality of life and reduced survival. Research into the biological mechanisms of cachexia has demonstrated that an array of inflammatory mediators and tumor-derived factors cause appetite suppression, skeletal muscle proteolysis, and lipolysis,producing an overall hypercatabolic state that contributes to loss of fat and lean body mass. Omega-3 polyunsaturated fatty acids (n-3 PUFAs) have been shown to modulate levels of proinflammatory cytokines, hepatic acute phase proteins, eicosanoids, and tumor-derived factors in animal models of cancer and may reverse some aspects of the process of cachexia. Results of clinical trials of n-3 PUFAs in the form of fish oils have been mixed, but should encourage further investigation into dietary fish oil supplementation, including the most effective route of administration and the proper dosage to promote optimal weight maintenance and to limit side effects. Concerns about standardization and quality control should also be considered. With the current available evidence, a recommendation for the use of omega 3 polyunsaturated fatty acids in pancreatic cancer cachexia is premature.

Appetite↗