Cancer cachexia: a nutritional or a systemic inflammatory syndrome?

McGovern, Josh; Dolan, Ross D.; Skipworth, Richard J.E.; Laird, Barry; McMillan, Donald C.

doi:10.1038/s41416-022-01826-2

Cited by 74 publications

(60 citation statements)

References 50 publications

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“…A typical feature of cancer cachexia is increase in systemic inflammatory response, which leads to tumor growth and organ failure through a cascade of inflammatory factors. 261 The treatment of cachexia‐related inflammatory factors has been a focus of research. 262 As a powerful HT‐1A receptor agonist in an animal study, espindolol can bind to HT‐1A receptors in the brain and increase muscle content and body weight.…”

Section: Treatment Of Cancer Cachexiamentioning

confidence: 99%

Targeting cancer cachexia: Molecular mechanisms and clinical study

Wang

Lin

et al. 2022

MedComm

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Cancer cachexia is a complex systemic catabolism syndrome characterized by muscle wasting. It affects multiple distant organs and their crosstalk with cancer constitute cancer cachexia environment. During the occurrence and progression of cancer cachexia, interactions of aberrant organs with cancer cells or other organs in a cancer cachexia environment initiate a cascade of stress reactions and destroy multiple organs including the liver, heart, pancreas, intestine, brain, bone, and spleen in metabolism, neural, and immune homeostasis. The role of involved organs turned from inhibiting tumor growth into promoting cancer cachexia in cancer progression. In this review, we depicted the complicated relationship of cancer cachexia with the metabolism, neural, and immune homeostasis imbalance in multiple organs in a cancer cachexia environment and summarized the treatment progress in recent years. And we discussed the molecular mechanism and clinical study of cancer cachexia from the perspective of multiple organs metabolic, neurological, and immunological abnormalities. Updated understanding of cancer cachexia might facilitate the exploration of biomarkers and novel therapeutic targets of cancer cachexia.

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Section: Treatment Of Cancer Cachexiamentioning

confidence: 99%

Targeting cancer cachexia: Molecular mechanisms and clinical study

Wang

Lin

et al. 2022

MedComm

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“…Inflammatory cytokines induce signaling in the central nervous system (CNS) and peripheral tissues to alter metabolism, increasing catabolic and decreasing anabolic signaling. The involvement of inflammation in cachexia has been extensively reviewed ( 1 , 13 – 15 ), and is associated with cancer-related weight loss in humans ( 16 ). Additional non-inflammatory mediators including activin A, myostatin, GDF15, and lipocalin-2, have also been implicated in catabolic signaling in cachexia ( 17 ).…”

Section: Cancer Cachexia Pathophysiologymentioning

confidence: 99%

“…In healthy individuals, intentional weight loss from reduced food intake and increased exercise favors loss of fat and preservation of muscle. In contrast, weight loss in a disease state such as cancer leads to significant loss of both fat and lean tissue, particularly skeletal muscle, due to the presence of non-inflammatory ( 17 ) and inflammatory ( 15 ) mediators. Inflammatory cytokines act to upregulate catabolic signaling ( 37 , 38 ) and impair regeneration ( 39 ) in skeletal muscle, particularly through the transcription factor NF-kappaB.…”

Section: Cancer Cachexia Pathophysiologymentioning

confidence: 99%

Cancer cachexia: Pathophysiology and association with cancer-related pain

Law

2022

Front. Pain Res.

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Cachexia is a syndrome of unintentional body weight loss and muscle wasting occurring in 30% of all cancer patients. Patients with cancers most commonly leading to brain metastases have a risk for cachexia development between 20 and 80%. Cachexia causes severe weakness and fatigue and negatively impacts quality and length of life. The negative energy balance in cachectic patients is most often caused by a combination of increased energy expenditure and decreased energy intake. Basal metabolic rate may be elevated due to tumor secreted factors and a systemic inflammatory response leading to inefficiency in energy production pathways and increased energy demand by the tumor and host tissues. A growing body of research explores physiological and molecular mechanisms of metabolic dysregulation in cachexia. However, decreased energy intake and physical functioning also remain important contributors to cachexia pathogenesis. Pain associated with metastatic malignancy is significantly associated with inflammation, thus making inflammation a common link between cancer pain and cachexia. Pain may also influence appetite and food intake and exacerbate fatigue and functional decline, potentially contributing to cachexia severity. Cancer pain and cachexia often occur simultaneously; however, causal relationships remain to be established. Appropriate assessment and treatment of pain in advanced cancer patients may positively impact nutrition status and physical functioning, slowing the progression of cachexia and improving quality and length of life for patients.

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“…Based on recent data from the literature, McGovern et al suggest that cancer-cachexia should be seen in perspective as an inflammatory systemic response syndrome that opens new horizons for cancer-cachexia treatment [ 15 ].…”

Section: Introductionmentioning

confidence: 99%

Nutritional Interventions to Improve Cachexia Outcomes in Cancer—A Systematic Review

et al. 2022

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Background and Objectives: The prevalence of cachexia has increased across all of the cancer types and accounts for up to 20% of cancer-related deaths. This paper is a systematic review of nutritional interventions aiming to improve cachexia outcomes in cancer, focusing on weight gain. Materials and Methods: A search in Medline and Elsevier databases for articles up until the 23 January 2022, was conducted. Results: Out of 5732 screened records, 26 publications were included in the final analysis. Four randomized clinical trials showed a significant body weight (BW) increase in patients treated with eicosapentaenoic acid (EPA), β-hydroxy-beta-methyl butyrate (β-HMB), arginine, and glutamine or marine phospholipids (MPL). An upward BW trend was observed in patients treated with L-carnitine, an Ethanwell/Ethanzyme (EE) regimen enriched with ω-3 fatty acids, micronutrients, probiotics, fish oil, a leucine-rich supplement, or total parental nutrition (TPN) with a high dose of a branched-chain amino acid (BCAA). Conclusions: Although clinical trials relating to large numbers of nutritional supplements present promising data, many trials provided negative results. Further studies investigating the underlying mechanisms of action of these nutritional supplements in cancer cachexia are needed. Early screening for cancer cachexia risk and nutritional intervention in cancer patients before aggravating weight loss may stabilize their weight, preventing cachexia syndrome. According to the GRADE methodology, no positive recommendation for these nutritional supplements may be expressed.

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Cancer cachexia: a nutritional or a systemic inflammatory syndrome?

Cited by 74 publications

References 50 publications

Targeting cancer cachexia: Molecular mechanisms and clinical study

Targeting cancer cachexia: Molecular mechanisms and clinical study

Cancer cachexia: Pathophysiology and association with cancer-related pain

Nutritional Interventions to Improve Cachexia Outcomes in Cancer—A Systematic Review

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