Muscle Mass and Cancer
Cancer is a leading cause of death worldwide, with many patients experiencing malnutrition that affects 25% to 60% of individuals, depending on the cancer type and treatment. This malnutrition leads to loss of muscle mass, increased fat, and inflammation, resulting in poorer health outcomes and reduced quality of life. Muscle, which makes up over half of our body weight, is essential for metabolism, blood sugar regulation, and amino acid provision. Low muscle mass in cancer patients is linked to higher risks of complications from surgery and chemotherapy, making it a critical factor in patient care.
Cancer cachexia, a condition involving significant muscle mass and strength loss, affects up to 80% of advanced cancer patients and is challenging to treat with normal nutritional support. Low muscle mass exacerbates treatment challenges, leading to more severe chemotherapy side effects and difficulties in surgical recovery. The interplay between cancer, muscle loss, and inflammation further worsens patient outcomes. However, maintaining muscle mass through exercise, proper nutrition, and targeted supplements can improve prognosis, treatment tolerance, and overall quality of life. Collaborating with healthcare teams to develop individualized exercise and nutrition plans, alongside additional treatments for appetite and metabolism, can help counteract muscle loss in cancer patients.
Executive Summary
Cancer and Malnutrition: Cancer is a leading cause of death worldwide. Many cancer patients suffer from malnutrition, which can affect 25% to 60% of patients depending on the type of cancer and treatment. This malnutrition can lead to loss of muscle mass, increased fat, and inflammation in the body. These issues can result in poorer health outcomes and lower quality of life for cancer patients.
Importance of Muscle Mass: Muscle is a crucial part of our body, making up over half of our total body weight. It's not just for movement - muscle plays a vital role in metabolism, helps regulate blood sugar, and provides amino acids for various bodily functions. Low muscle mass in cancer patients is linked to poorer outcomes, including higher risks of complications from surgery and chemotherapy.
Cancer Cachexia: Many cancer patients experience a condition called cachexia, which involves significant loss of muscle mass and strength. This condition affects up to 80% of people with advanced cancer and is difficult to treat with normal nutritional support. Exercise may be particularly important for cancer patients to help maintain or regain muscle mass and strength.
Impact of Low Muscle Mass on Cancer Treatment: Having low muscle mass can make cancer treatment more challenging. Patients with low muscle mass often experience more severe side effects from chemotherapy drugs. This is because many of these drugs are distributed based on body composition, and having less muscle can lead to higher concentrations of the drugs in the body. Low muscle mass can also affect how well patients tolerate surgery and recover afterward.
Inflammation and Muscle Loss: Cancer and muscle loss are closely linked to inflammation in the body. When muscle mass decreases, it can lead to increased inflammation throughout the body. This inflammation, in turn, can contribute to further muscle loss and poorer cancer outcomes. Exercise has been shown to have anti-inflammatory effects, which may help break this cycle.
Muscle Mass and Blood Sugar Control: Muscle plays a key role in regulating blood sugar levels. When muscle mass decreases, it can lead to problems with blood sugar control and insulin resistance. These issues are associated with poorer outcomes in cancer patients. Maintaining muscle mass through exercise and proper nutrition may help improve blood sugar control and overall health in cancer patients.
Benefits of Maintaining Muscle Mass: Keeping or building muscle mass during cancer treatment can have several benefits. It may improve your prognosis, help you better tolerate treatment side effects, and enhance your overall quality of life. Even if you start exercising after your cancer diagnosis, it can still be beneficial. Exercise can help counteract some of the muscle loss caused by cancer and its treatments.
Strategies to Preserve Muscle Mass: There are several ways to help maintain muscle mass during cancer treatment. These include proper nutrition with adequate protein intake, specific supplements like creatine and certain amino acids, and regular exercise, especially resistance training. It's important to work with your healthcare team to develop a safe and effective plan tailored to your specific situation.
Exercise and Cancer Treatment: Exercise, particularly resistance training, can be very beneficial for cancer patients. It can help build muscle, improve strength and balance, reduce fatigue, and make daily tasks easier. Even during treatment, many patients can safely engage in some form of exercise. However, it's crucial to start slowly, listen to your body, and work with your healthcare team to develop an appropriate exercise plan.
Additional Treatments: Besides exercise and nutrition, there are other treatments that may help with muscle loss in cancer patients. These include medications to stimulate appetite, drugs to help with metabolism, and treatments to address inflammation. These approaches are often used in combination with exercise and nutrition strategies for the best results.
A Deeper Dive
According to the World Health Organization, cancer is one of the leading causes of mortality worldwide, accounting for one in every six deaths and causing more than 10 million fatalities in 2020 alone. Malnutrition is a prevalent feature among cancer patients, affecting 25% to 60% of them depending on the kind of cancer, diagnosis, and therapy. Malnutrition is caused by inadequate food and nutrient intake or absorption, and it may be linked to disease-related inflammation.
Cancer and its treatment negatively impact nutrient bioavailability and absorption, resulting in decreased lean mass, increased fat mass, and systemic inflammation (increased IL-6, IL-8, CRP, and TNF-α levels). Indeed, this vicious loop implies that around 79% of cancer patients have cachexia, or loss of lean muscle mass, as well as abnormalities in the architecture of the muscular sarcomere. Low muscle mass and malnutrition are both directly associated to poorer health-related outcomes, such as higher mortality, surgical complications, and increased likelihood of poorer treatment results and treatment toxicities, as well as a lower quality of life during and after cancer treatment and recovery.
Muscle mass and its general importance for overall health
Low skeletal muscle mass is frequently considered as an indicator for poor fitness and health condition, which can reduce resilience to the stresses associated with cancer and cancer treatment. Low skeletal muscle mass in cancer patients has been linked to poor clinical outcomes such as higher post-operative complication rates, higher chemotherapy toxicity, lower disease-free or progression-free survival, and higher overall mortality, though these associations are not direct.
Systemic inflammation, insulin-dependent glucose management, and changes in energy and protein metabolism, as well as pharmacokinetics, have all been hypothesized as pathophysiological processes explaining the link between reduced skeletal muscle mass and poor clinical outcomes in older cancer patients.
Understanding Muscle Mass
Skeletal (or striated) muscle is the biggest single component of the body, accounting for over half of total body weight in individuals. It also acts as the body's primary reservoir of protein and free amino acids. Aside from its locomotive duties, skeletal muscle is a vital metabolic organ. Metabolic activities are essential not only for movement but also for maintaining substrate homeostasis in the circulatory system and delivering amino acids for numerous physiological processes. Skeletal muscle mitochondria use oxidative phosphorylation to convert food energy into adenosine triphosphate (ATP).
For mechanical processes involving primarily movement, this chemical energy (ATP) is transformed into mechanical energy by the enzymatic (ATPase) activity of myosin and actin in the sarcomere. In this process, a significant percentage of the energy loss is ultimately lost as heat. Cold exposure and shivering thermogenesis highlight muscle's role as a "heater" for the body, as well as the resulting energy loss. Furthermore, skeletal muscle provides amine acids for protein synthesis in other tissues (essential during wound healing), immunological activities, and gluconeogenesis (alanine and glutamine) under catabolic circumstances. Skeletal muscle also oxidizes glucose and fatty acids and accumulates a significant quantity of glycogen postprandially.
Cancer and Cachexia (muscle wasting syndrome)
Cachexia of cancer is "a multifactorial condition characterized by an on-going loss of skeletal muscle mass (with or without loss of fat mass) that cannot be fully reversed by conventional nutritional support and leads to progressive functional impairment". Depending on the diagnosis, this syndrome affects up to 60-80% of people with advanced cancer, and there are currently few effective treatment options. Loss of muscular mass and strength is one of numerous variables linked to involuntary weight loss in cancer cachexia. Physical exercise may be especially important for cancer patients with advanced illness in the pre-cachectic or cachectic stages due to its possible impacts on muscle mass and strength.
Exercise has been shown in experimental trials to have anti-inflammatory benefits in cachectic mice, as well as to partially restore muscle mass and strength in tumour-bearing mice when paired with eicosapentiaenoic acid. Furthermore, a small number of clinical trials have shown that exercise can help minimize or postpone cachexia in people with chronic conditions other than cancer. Previous evaluations on the effects of physical exercise in patients with cachexia were narrative and not specific to cancer patients, or they largely explored the biological and pathophysiological effects of exercise on cachexia-related muscle wasting.
The Relationship Between Muscle Mass and Cancer
Impact of low muscle mass (sarcopenia) on prognosis, treatment tolerance, and recovery
Muscle mass begins to drop at the age of 40 years, with an average loss of 8% every decade until the age of 70. Above the age of 70, muscle mass loss accelerates to 25%-40% every decade.
Muscle mass loss is related to poor outcomes in chronic illnesses such as liver cirrhosis and cardiovascular disease, and is common in people with rheumatoid arthritis, diabetes, and HIV/AIDS. Low muscle mass in surgical patients has been linked to postoperative problems and can be used to assess patients' risk level prior to surgery. Low muscle mass has recently gained attention as a factor in cancer patients. In several tumor forms and treatment scenarios, individuals with reduced muscle mass appear to have worse survival compared with patients without low muscle mass.
Furthermore, individuals with poor muscle mass are more prone to have significant side effects from systemic anticancer medicines. Many chemotherapy medications are delivered to the fat-free compartment of the body. Low muscle mass is considered to result in substantially greater drug concentrations, as it is associated with a drop in the fat-free compartment, as well as the related toxicities. As a result, muscle mass may be a significant new predictive indicator for cancer patients' survival and therapy tolerance.
Muscle loss in cancer patients is most likely caused by both sarcopenia and cachexia-related mechanisms. Sarcopenia is a geriatric condition with several causes, including reduced muscle mass, poor muscular strength, or impaired physical performance. Sarcopenia in elderly persons is linked to death and physical impairment.
Mechanisms of Interaction
The mechanism of reduced muscle mass in cancer patients is not well understood. Physical inactivity and elevated levels of proinflammatory cytokines are etiological factors that contribute to cancer-related muscle wasting; however, the primary cause is most likely increased activity of the ubiquitin-proteasome system (UPS), which results in increased muscle protein degradation. This can occur in the absence of other cachexia-related factors such as weight loss, metabolic alterations, and muscle and adipose tissue loss. Furthermore, cancer therapy usually causes vomiting, improper food intake, and a lack of physical exercise, which can result in the loss of both fat and muscle mass. In addition, corticosteroids, which are commonly used in cancer patients, activate the UPS and produce insulin resistance, both of which contribute to muscle protein breakdown.
Systemic Inflammation
Skeletal muscle fibers can actively modify the immune system in both pro- and anti-inflammatory directions, controlling innate and adaptive immune responses. Low skeletal muscle mass relates directly to persistent low-grade local and systemic inflammation. Several clinical observational studies in older cancer patients found significant relationships between decreased skeletal muscle mass and greater inflammatory markers, such as a higher neutrophil-to-lymphocyte ratio and C-reactive protein levels. This dose-response relationship between low skeletal muscle mass and systemic inflammation persisted regardless of cancer stage, age, or gender. These inflammatory indicators have a substantial association with overall as well as cancer-specific mortality. Patients having a combination of low skeletal muscle mass and high inflammatory indicators had higher mortality rates than those with low skeletal muscle mass and low inflammatory markers.
One of the most common, well-documented, and supported theories is that reduced skeletal muscle mass leads to less myokine synthesis. Myokines are tiny chemicals produced by contracting skeletal muscle that have autocrine, paracrine, and endocrine effects on other tissues. Overall, myokine-adipokine imbalances can have a deleterious impact on the innate and adaptive immune systems.
Interleukin (IL)-15 and IL-6 have been widely investigated in relation to exercise and cancer immunology, and they influence the innate and adaptive immune systems. IL-15 regulates the number and function of natural killer cells and protects them from apoptosis. IL-15 knockout mice had practically no mature natural killer cells, and natural killer cells were killed when transplanted to the same knockout animals. Lower IL-15 release into the circulation as a result of poor skeletal muscle mass has been postulated to reduce natural killer cell quantity and survival, increasing the risk of infectious complications and shortening survival in cancer patients.
The major current concept for how exercise prevents and suppresses cancer growth is that it affects the host immune system by releasing exercise-induced substances (such as myokines and other mobilizing serum components) into the circulation. These beneficial benefits of exercise on immune function have been confirmed in cancer patients, as evidenced by an increase in natural killer cell cytotoxic activity, lymphocyte proliferation, and granulocyte count following prolonged aerobic and/or resistance exercise.
Insulin-Dependent Glucose Handling and Tumor Growth
Skeletal muscle plays a critical role in insulin-mediated glucose metabolism since it is the major target organ for insulin-dependent glucose uptake. In the event of atrophying skeletal muscle, lipid accumulation in muscle tissue might cause glucose intolerance via insulin resistance. On the other hand, glucose intolerance and insulin resistance have long been recognized as signs of malignancy. Insulin resistance has been linked to both overall and cancer-specific survival rates, as well as postoperative complications. Interestingly, anticancer medication therapy has been shown to raise the expression of the insulin-regulated glucose transporter, GLUT4, although the underlying mechanisms of these changes remain unclear. Because cancer tissue is known to absorb glucose, variations in insulin sensitivity in other organs must be investigated.
Because cancers frequently rely on glycolysis for cell survival and proliferation, elevated blood glucose levels may hasten cancer development and disease progression. Reduced blood glucose levels with calorie restriction or ketogenic diets have lately received attention in the literature, with conflicting outcomes and viewpoints. Such dietary treatments can hasten the loss of skeletal muscle mass, which would have serious effects.
Mitochondrial Function
A high skeletal mitochondrial function is often related to increased endurance and less fatigue during submaximal activity. As a result, poor skeletal mitochondrial activity can directly explain an increase in weariness in cancer patients. Cancer progression and anticancer treatments have both been shown to impair mitochondrial activity in skeletal muscle. Sarcopenia and cancer cachexia are both conditions characterized by mitochondrial dysfunction.
Cancer cachexia is characterized by altered mitochondrial dynamics, mitophagy, and decreased mitochondrial biogenesis, all of which reduce oxidative phosphorylation capability and increase reactive oxygen species (ROS) generation. These mechanisms most likely contribute to the development of muscle wasting in cancer patients. At the same time, numerous anticancer medicines have been shown to cause non-specific mitochondrial dysfunction in skeletal muscle cells. For example, doxorubicin is known to accumulate inside mitochondria, causing mitochondrial complex I malfunction and ROS production, ultimately lowering muscle growth and function through DNA damage, protein oxidation, and death. Other chemotherapeutics have similar effects and can alter mitochondrial DNA. The combination of cancer and current anticancer medicines causes mitochondrial damage, which eventually leads to a vicious spiral that degrades skeletal muscle bulk and function.
Low Protein Status and Poor Nutritional Status
Protein status changes play a significant role in the development of low skeletal muscle mass. Muscle protein synthesis rate is influenced by general health, nutritional availability, and physical activity levels. Low nutritional intake and muscular activation levels result in decreased protein anabolism and increased protein catabolism, both of which have a deleterious impact on skeletal muscle mass in animal models and human research investigations. Protein synthesis and function are inhibited when there is a lack of skeletal muscle bulk and activity.
Low protein status is commonly recognized as a sign of poor nutritional status, which is associated with poor clinical outcomes in cancer patients. Protein synthesis, on the other hand, takes place mostly in the liver, where ribosomes are found, although it also happens in skeletal muscle cells. Low skeletal muscle mass is associated with fewer ribosomes, resulting in decreased absolute protein synthesis rates, which may have harmful systemic consequences and impact clinical outcomes. Another notion is that muscle protein breakdown causes the efflux of stored amino acids into the circulation, making them available for the tumor to take up and stimulate cancer development. Furthermore, decreased protein levels impact the likelihood of chemotherapeutic toxicity.
Pharmacokinetics of Anticancer Drugs
Pharmacokinetics is crucial in cancer patients since the majority of them are treated with systemic medicines like chemotherapy. Patients with reduced skeletal muscle mass had a worse plasma clearance of several chemotherapeutics than those with normal skeletal muscle mass. Patients with poor skeletal muscle mass and limited clearance were also more likely to experience chemotherapeutic toxicity.
Other ways in which reduced skeletal muscle mass influences pharmacokinetics include inflammation and total protein status. The low-grade inflammatory condition associated with reduced skeletal muscle mass causes a reduction in liver cytochrome activity. As a result, the liver's metabolic capacity is reduced, increasing its exposure to chemotherapy and causing toxicity. Because of the reduced skeletal muscle mass, fewer skeletal muscle proteins may be accessible for potential chemical protein binding, increasing chemotherapeutic exposure and the risk of toxicity.
Benefits of Maintaining Muscle Mass in Cancer Patients
According to research, having adequate muscle mass may enhance your cancer prognosis while also allowing you to resist some of the negative effects of cancer therapy. Even if you don't start muscle-building activities until after you've been diagnosed, exercise may still be the best treatment for cancer cachexia.
A number of factors influence your body's capacity to preserve muscle mass while undergoing cancer therapy. Cancer can cause overall weakness, as well as treatment side effects such as nausea, vomiting, exhaustion, and discomfort, which can impair your ability to keep lean muscles. Muscle loss may be caused by the illness itself. Exercise may counteract some muscle loss and reduce the severity of therapy’s adverse effects.
Increased physical activity can minimize treatment-related toxicity by improving blood flow, controlling blood sugar levels, releasing endorphins, and so on. Physical exercise has been demonstrated to have systemic anti-inflammatory benefits in the body, whereas traditional cancer treatment promotes inflammation. Some diseases and cancer therapies eat away at the body's musculature, preventing it from gaining muscle mass—which cannot be restored merely by exercising more. Even in such situations, exercise may provide advantages.
Strategies to Preserve and Improve Muscle Mass During Cancer Treatment
Nutritional Interventions
Nutritional activity is crucial in the prevention and treatment of sarcopenia. A well-balanced diet rich in protein, vitamins, minerals, and antioxidants will help you maintain muscle mass, activity, strength, and function. Furthermore, sufficient hydration and frequent physical exercise are essential components of a successful treatment strategy. Consuming foods high in essential amino acids, such as lean meats, dairy, legumes, nuts, and seeds, can aid in maintaining muscular health. Antioxidant-rich foods, such as fruits and vegetables, can assist in lowering oxidative stress and inflammation, both of which have been linked to sarcopenia. Calcium, potassium, and vitamin D supplements can also assist in preventing bone loss while improving muscular strength and function.
Creatine and omega-3 fatty acid supplements may also be beneficial to muscular health. Nutritional therapies include sufficient protein consumption, improved dietary intake of key nutrients such as vitamins, minerals, and fatty acids, and supplementation with specific nutrients known to be involved in muscle health. Adequate protein consumption is essential for maintaining muscle mass, thus it should be a top focus for people suffering from sarcopenia.
A protein-rich diet stimulates muscle protein synthesis while inhibiting muscular atrophy. Muscle tissue formation and repair need the presence of proteins. Leucine is one of the amino acids required in these proteins to activate the mechanistic target of the rapamycin (mTOR) pathway, which is an important regulator of muscle protein synthesis. Antioxidants included in natural foods also combat oxidative stress, which is a major cause of muscle loss in sarcopenic individuals. Antioxidants such as vitamins C and E protect muscle fibers by scavenging free radicals. In addition, many natural diets contain bioactive chemicals such as plant polyphenols and omega-3 fatty acids, which have anti-inflammatory properties and can affect critical signaling pathways involved in muscle protein creation and breakdown.
Amino Acids: Citrulline, Leucine, and Beta-Hydroxy-Beta-Methylbutyrate
Amino acids help to avoid sarcopenia, which is the age-related decrease of muscle mass and strength. An adequate dietary intake of essential and branched-chain amino acids is required to maintain muscle mass, strength, and general physical function. These amino acids supply the body with the required building blocks to repair and create muscle, resulting in increased muscular strength and function. Furthermore, certain important amino acids, such as leucine, have a role in controlling muscle protein synthesis and may help avoid sarcopenia.
Citrulline, leucine, and beta-hydroxy-beta-methylbutyrate (HMB) are essential amino acids for preventing and treating sarcopenia, an age-related loss in muscle mass and strength. Citrulline promotes the generation of nitric oxide in the body, which improves blood flow and oxygenation to the muscles. Leucine is required for muscle protein synthesis and prevents muscular breakdown. HMB is a leucine metabolite that serves to inhibit muscle breakdown while increasing muscle synthesis. Together, these three amino acids can assist enhance muscle growth and strength, as well as stop or reverse sarcopenia.
Creatine
Creatine is an important supplement for those suffering from sarcopenia, a disease in which muscular mass and strength decline with age. It can help you gain muscular growth and strength, minimize tiredness during exercise, and recover faster. Creatine increases energy generation and improves muscular contraction efficiency, which can assist in halting the progression of sarcopenia. In addition, it can aid in muscle repair and regeneration, lowering the chance of injury. Creatine has been intensively investigated as a possible therapy for sarcopenia, or age-related muscle loss.
Creatine supplementation has been demonstrated in studies to improve muscular strength, size, and power in persons with sarcopenia. Furthermore, creatine can assist in building muscle mass, lowering the incidence of falls and fractures in older persons. Thus, creatine supplementation can be an effective and safe strategy to increase muscular strength and minimize the risk of impairment in persons with sarcopenia.
Physical Exercise
Increased physical exercise can help cancer patients by improving muscle mass, function, and metabolism while reducing treatment-related toxicity. Physical exercise produces systemic anti-inflammatory effects that limit protein degradation while increasing protein synthesis; moreover, training can enhance oxidative metabolism and maximize substrate use to prevent metabolic dysfunction. Furthermore, ketone bodies, chemical molecules produced from lipids, are oxidized during continuous exercise and used as fuel. Some ketone bodies may help to maintain redox balance in response to metabolic stress, decrease inflammation, and improve exercise performance.
Mechanical stimulation of protein synthesis pathways, along with other anabolic treatments, may offer a strategy to overcome anabolic resistance to nutrition and growth hormones. In fact, exercise combined with dietary therapy can enhance muscle mass and prevent tumor development in animal models.
Resistance training
Given the numerous areas where additional study is needed, exercise may be the most important therapy available currently for people with cancer cachexia, those who want to avoid developing it, or those suffering from comparable muscle-related adverse effects.
Evidence suggests that increasing resistance training increases lean muscle and consequently muscular strength. Evidence suggests that it can be done and is effective during and after a patient's therapy. Strength training during a patient's cancer therapy may help them endure the treatment better.
Strength training, cardiovascular activity, and stretching are all beneficial components of a well-rounded fitness regimen. However, based on the exact diseases or symptoms, each program must be adapted to each patient.
According to the American Society of Clinical Oncology (ASCO), strength exercise, also known as resistance training, can increase muscle mass while also improving balance, reducing tiredness, and making everyday tasks simpler. It states that a program may include hand weights, exercise machines, resistance bands, or the patient's body weight (via pushups or chin-ups).
Progressive strength training increases lean muscle development and general strength, benefiting everyday practical tasks such as walking, cleaning, cooking, and tolerance for leisure activities.
ASCO advises that cancer patients perform strength training.
Even if you're a regular exerciser, begin carefully.
Exercise in a safe area with little exposure to germs, such as at home or outside, and with fall protection.
Pay attention to your body and avoid doing too much.
Drink lots of water and eat a healthy diet.
Schedule frequent appointments with your doctor.
An inexperienced person should work out at a moderate intensity several times each week. A cancer patient should also exercise frequently to get the advantages of exercise and reduce negative effects such as muscle loss.
Pharmacological agents
The primary goal for these patients is to regain their lost appetite. Several drugs have been regarded as tools for promoting weight gain by increasing hunger and preventing muscle mass loss. Megestrol acetate, an active progesterone derivative, has been identified as one of the most often utilized appetite stimulants. Its method of action is unknown, although it is assumed to be related to its capacity to increase hunger by antagonizing the metabolic effects of catabolic cytokines, as well as its ability to increase lipogenesis, which also has a high safety profile. Cannabinoids have also been emphasized as an option to increase appetite in cancer patients, since they have the ability to activate the cannabinoid receptors (CB1 and CB2) in the CNS, hence raising food intake and restoring weight loss.
Finally, prokinetic medicines like metoclopramide or domperidone, which are used to treat early satiety associated with cancer cachexia, have been identified as valuable aids in the management of muscle loss associated with cancer. Both medicines have a similar mechanism of action in that they function as a dopamine-2 antagonist, resulting in gastric antral contraction, decreased postprandial fundus relaxation, and improved early satiety due to their stomach-emptying qualities.
In the realm of metabolic dysregulation, antidiabetics have been shown to improve muscle loss and body weight gain associated with cancer therapy. Rosiglitazone reduces glycemia and insulin resistance in adipose tissue, skeletal muscle, and liver, making it an effective antidiabetic. Thus, given the increased insulin sensitivity that may boost glucose absorption by skeletal muscle cells, rosiglitazone may aid in muscle loss recovery. In addition, past research has shown that rosiglitazone increases weight in cancer patients by lowering body wasting. Furthermore, metformin, a biguanide commonly used in diabetes treatment, demonstrated a potential ability to reduce lipolysis due to its ability to induce protein phosphatase 2A (PP2A), an enzyme with anti-lipolytic properties that could be useful in the treatment of cachexia in cancer patients.
Conclusion
Finally, the complex association between muscle mass and cancer emphasizes the vital need to preserve muscle health during cancer therapy and beyond. As this research shows, muscle mass has a major impact on cancer prognosis and treatment efficacy, in addition to physical strength and quality of life. Healthcare practitioners can reduce muscle loss and improve patient outcomes by including resistance training, proper nutrition, and early intervention methods in cancer treatment regimens. Moving forward, it is critical to have a better knowledge of the processes that relate muscle mass to cancer development and survival, paving the door for novel treatment approaches that meet cancer patients' holistic requirements.