With some types of cancer, it isn’t only about how much food a person takes in. Cancer isn’t a separate formation sitting quietly to itself. It stealthily builds connections with a large part of the body: the brain, muscles, fat tissue, and the immune system too. That way, it can change how the body uses food. A person tries hard to eat, and yet the mirror and the scale show a loss of muscle and fat mass. This condition is called cancer cachexia.
The definition
Weight loss is not the same as cachexia
The international consensus describes cachexia as a loss of more than 5% of body weight over 6 months. The criterion also applies to a loss of more than 2% if BMI is below 20 kg/m² or there is sarcopenia (loss of muscle mass) [1].
These are reference points for specialists, not a diagnosis to make on your own.
Let’s compare with a healthy person who has eaten less for a few weeks. Their body starts using its reserves, namely fat. Fatty acids are converted into ketone bodies to reduce the need for glucose. This spares protein and preserves muscle. In a healthy person, the body tries to protect muscle.
In cancer cachexia, things don’t work this way.
Mechanism
The main driver: inflammation
In theory, inflammation is a good mechanism: the body looks for the culprit, destroys it, and clears it out. The reality, though, is far more complicated.
A tumor isn’t just a pile of cancer cells. Around it there’s a whole “microenvironment”: immune cells, connective tissue, new blood vessels.
Particularly interesting is the ambiguous relationship between tumor cells and macrophages (a type of immune system cell). M1 macrophages act against the tumor: they fight it and want to destroy it. M2 macrophages act in favor of the tumor: they help build new vessels so the tumor can be fed and grow, and they break down the healthy tissue around it so it can make its way and metastasize.
This whole structure releases signaling molecules (cytokines): IL-1β, IL-6, and TNF-α.
IL-6 travels through the blood to the liver and tells the liver cells: “Stop, we’re halting the daily work. We’re going into war mode!” This war mode is the so-called acute-phase response. The liver starts producing more C-reactive protein (CRP) and reduces the synthesis of other proteins, including albumin.
What follows is something that’s often overlooked: albumin is a negative acute-phase protein. During active inflammation, its level drops regardless of food intake. That’s why it isn’t a good marker of nutritional status. It can also be low for other reasons (liver or kidney disease, protein loss, dilution), so it should never be interpreted on its own. But if inflammation continues, even a high intake of calories and amino acids doesn’t guarantee that albumin will rise [2,3].
ESPEN emphasizes that inflammation is a key element in assessing cachexia [4]. One of the tools used to measure it is the modified Glasgow Prognostic Score (mGPS). It evaluates systemic inflammation and has prognostic value [5]:
| Points | CRP | Albumin |
|---|---|---|
| 0 | ≤ 10 mg/L | irrelevant |
| 1 | > 10 mg/L | ≥ 35 g/L |
| 2 | > 10 mg/L | < 35 g/L |
What does this mean for eating?
Low albumin doesn’t automatically mean the patient needs “more food.” It’s a signal of inflammation. Food remains necessary because it provides energy and protein. But it can’t solve the problem on its own, so the goal is broader: to support the body and to treat the underlying disease.
The muscle
How inflammation reaches the muscle
Muscles constantly balance two processes: building proteins (anabolic) and breaking them down (catabolic). In a healthy person they’re relatively balanced. In cachexia, the balance shifts toward loss of muscle protein. This isn’t simply “the muscle breaks down because there aren’t enough calories.” It’s an active reprogramming of the cell.
The ubiquitin-proteasome system
Inflammatory signals, TNF-α among them, reprogram the muscle cell to produce enzymes that “tag” myofibrillar proteins (the ones that build the muscle). Tagged proteins go to the proteasome, the part of the cell that says: “Go ahead, break it down.” Let’s not blame it, it’s just doing its job. This is the normal quality-control system for proteins. The problem is that in cancer, inflammatory molecules activate it too often, and it starts breaking down everything in sight, including our own tissues.
Anabolic resistance
We’ve heard about insulin resistance, but this is something different. A patient takes, say, 25 g of protein and is expected to reach the so-called “leucine threshold,” after which mTORC1, the protein synthesis pathway, switches on. In cachexia, this response may be blunted. It isn’t enough to supply amino acids, the muscle also has to be able to use them [2].
This logic has led to ideas about larger protein doses per meal, leucine enrichment, or supplements like HMB. It sounds convincing at the molecular level, but the data in cancer patients isn’t sufficient for a routine recommendation. The practical takeaway is more modest: protein regularly throughout the day.
Energy
Fat: not just a “storage room”
Fat tissue is no longer understood as a passive storage depot, but as a metabolically active organ. In cachexia, inflammatory molecules activate the enzymes that break fat down into glycerol and free fatty acids. There’s also a pathological reprogramming of the tissue itself.
Interestingly, in some models of cachexia, white fat tissue takes on characteristics of brown fat. It’s known for the protein UCP1 in the inner membrane of mitochondria (the cell’s power plants). Normally, mitochondria make ATP, the main energy molecule. With UCP1, part of the energy is dissipated as heat. Fat stores shrink quickly, and no useful energy is produced. This mechanism is well described in animal models. In humans the data is more limited, and it’s probably only part of the picture [2].
Resting energy expenditure (REE)
REE (Resting Energy Expenditure)
The amount of energy the body needs at complete rest to maintain its basic functions.
In some patients it’s elevated. The causes are constant inflammation (an “alarm” that doesn’t switch off) and inefficient metabolic processes. One example is the Cori cycle: the tumor converts glucose into lactate (a waste product), and the liver spends more energy converting it back into glucose. It’s like withdrawing 20 euros from an ATM and having the bank charge you 60 for the transaction.
A caution, though: not every patient has an equally elevated REE. It depends on the type and stage of the tumor, inflammation, treatment, body composition, physical activity, infections and complications, and organ function.
So why doesn’t the body just use its fat stores?
In ordinary fasting, the body follows a clear plan: it breaks down fat and protects muscle. In cachexia, a tumor, inflammation, cytokines, and metabolic signals are added to the fasting. The plan goes wrong, and the body breaks down fat and muscle at the same time.
On the scale
BMI: much ado about nothing
An illustrative example:
Patient A
80 → 72 kg
- ~7 kg of fat
- ~1 kg of muscle mass
Patient B
80 → 72 kg
- ~3 kg of fat
- ~5 kg of muscle mass
The scale shows −8 kg for both. Clinically, these are two different situations. That’s why ESPEN recommends assessing muscle mass with appropriate methods, and where CT images are available, they can be used for this purpose [4].
Loss of muscle mass isn’t a cosmetic problem. It’s linked to lower physical function, smaller reserves, a higher risk of complications, and poorer tolerance of treatment. That’s why the approach is multimodal, not just a “diet”: nutrition + physical activity + symptom control + treatment of the underlying disease.
A metaphor
The house and the metabolic chaos
Imagine the body is a house, and food is bricks and firewood.
In a healthy person, the math is simple: you bring in more materials, the builders repair the walls (the muscles) and build up reserves. In cachexia:
Inflammation “puts them to sleep” (suppresses mTORC1, the pathway responsible for protein synthesis). No matter how many bricks you bring, there’s no one to lay them.
The house burns an enormous amount of firewood just to keep the fire going.
The demolition crew is working overtime. Machines keep knocking healthy bricks out of the walls and throwing them into the fire.
That’s why the formula “eat more → gain weight” doesn’t work here. Treatment is a strategy: reduce inflammation, “wake the builders” with movement and enough protein, and only then will the bricks start building the body up again.
Protocol
Okay, so what can we do?
The answer isn’t simply “eat more.” We work in several directions at once: enough energy and protein + preserving muscle + controlling symptoms + physical activity + treating the underlying disease.
1. Don’t start with a “diet,” start with food intake
The first goal isn’t for eating to become perfect, but for enough energy and protein to come in. When energy needs can’t be measured, the guideline is around 25–30 kcal/kg/day, and for protein ESPEN recommends more than 1 g/kg/day, up to about 1.5 g/kg/day where possible [3,4]. Specific needs are assessed individually. With kidney or liver failure, certain types of treatment, or complications, the targets may differ.
The principle is simple: when the body is losing weight and muscle mass, it’s not the time for arbitrary dietary restrictions.
2. Less quantity, more nutrition
The advice “just eat more” doesn’t help someone who finds it hard to finish even half of their usual portion. It’s better to make the same amount of food more nourishing:
- instead of a large portion of potatoes→potatoes + milk + olive oil + hard cheese
- instead of a large bowl of salad→a small salad + avocado + olive oil + egg
- instead of a large portion of meat→a moderate portion + rice or potatoes + a sauce made with olive oil or dairy
3. Protein: the building material
Good sources are eggs, fish, chicken and other meats, yogurt, cottage cheese, cheeses, legumes, tofu, and nuts. It doesn’t all have to be in one meal. It’s more practical to spread protein through the day:
That way, instead of trying to “catch up” in the evening, the body gets several opportunities across the day.
4. If you can’t eat enough
Food needs to become more concentrated:
adds energy to salads, soups, and purées.
small volume, high energy density.
into yogurt, desserts, snacks.
for sandwiches, salads, purées, if tolerated.
when there’s no reason to restrict it.
Here, “less fat is healthier” isn’t a good rule. For someone who struggles to meet their needs, fat is a convenient way to increase energy without a huge volume.
When that isn’t enough either, ESPEN recommends oral nutritional supplements (ready-made nutrition drinks) as an addition to eating. It’s best to choose the product and amount with a dietitian or your care team [4].
5. Several small meals instead of three big ones
With early fullness, you don’t need to wait until you’re hungry. You can try:
It isn’t a mandatory schedule. If a big portion is unbearable, split it into smaller ones.
6 · Symptoms
When symptoms get in the way of eating
Sometimes the problem isn’t a lack of desire to eat, but nausea, dry mouth, altered taste, pain when swallowing, or diarrhea. Then the strategy changes depending on the symptom.
Smaller, more frequent meals. Foods with a mild aroma are often better tolerated, and for some people cold or lukewarm foods are easier than hot ones. For example: yogurt + banana + a little tahini, chilled mashed potatoes with egg, or cold pasta with chicken and a mild sauce. With persistent or severe nausea, dietary measures don’t replace medication control.
Food can start to taste “unfamiliar.” Experiment with temperature, seasonings, marinating meat, sour or fresh flavors (if there’s no mucositis), and plastic cutlery if the metallic taste is pronounced. If a particular food puts you off, you don’t have to turn it into a test of character. There are other sources of protein.
Keep food soft, moist, and easy to swallow: cream soups, purées, eggs, yogurt, soft dairy desserts, well-cooked pasta, smoothies. Spicy, very sour, and crunchy foods are often best avoided temporarily.
The first priority is hydration. If it lasts more than a day or two, or there’s blood, a high fever, or signs of dehydration, contact your care team.
7 · Recipes
Not “superfoods,” but food that gets the job done
01
Creamy banana and tahini breakfast
- 200 g full-fat yogurt
- 1 banana
- 1–2 tbsp tahini
- 1 tbsp ground walnuts
- a little cinnamon
Stir together or blend.
02
Cheese and avocado omelet
- 2–3 eggs
- 30–40 g hard cheese
- ½ avocado
- 1 tsp olive oil
- a slice of soft bread
Cook the omelet in the olive oil, add the cheese at the end.
03
Mashed potatoes with salmon
- 250 g potatoes
- 100–120 g salmon
- 50–100 ml milk
- 1 tbsp olive oil
- a little yogurt or a mild sauce
Mash the potatoes with the milk and olive oil, serve the salmon on top.
04
Nourishing smoothie
- 1 banana
- 200 ml full-fat milk
- 150 g yogurt
- 1 tbsp peanut butter
- 1 tsp cocoa
Blend until smooth. Suitable on days when solid food is hard.
Nothing exotic, and that’s exactly the point. Not every meal has to be “anti-cancer.” Sometimes the most helpful food is simply the one the patient can manage to eat.
With lowered immunity (neutropenia), ask your team about food safety rules, for example about thoroughly cooking eggs and fish.
8–9 · Carbs and movement
What about carbs? And exercise?
8. What about carbohydrates?
“But doesn’t sugar feed cancer?” Tumor cells can use glucose. But it doesn’t follow that cutting out carbohydrates makes the tumor “starve” while healthy cells stay untouched. In a patient who is already losing weight, needlessly restricting whole food groups makes getting enough energy even harder. That’s why rice, potatoes, pasta, bread, and fruit aren’t “forbidden.” They’re part of the food.
9. What about exercise?
Muscle gets a signal from two directions: food gives it material, and movement tells it “I still need you.” In suitable patients, exercise, especially strength training, can be part of the strategy for maintaining muscle mass and function [3,4]. The goal isn’t burning calories, but preserving function.
You don’t need to start with the gym. Depending on your condition, it could be:
Even short sessions are a start.
But there’s one big “if”
With bone metastases, significant anemia, thrombocytopenia, severe neuropathy, recent surgery, cardiopulmonary problems, marked weakness, or other complications, exercise needs to be individualized with the medical team or a cancer rehabilitation specialist.
10 · A caution
What shouldn’t we do?
- Fasting to “starve the tumor.” There isn’t enough evidence that fasting around chemotherapy improves outcomes, and with a risk of malnutrition it can make the problem worse.
- Automatically cutting out carbohydrates. This can needlessly lower energy intake.
- Starting a ketogenic diet on your own. It’s restrictive, and there isn’t enough clinical evidence for it to be a universal strategy in cancer.
- Taking a pile of supplements “for muscle.” BCAAs, HMB, and other amino acid products sound logical at the molecular level, but the data on clinical benefit in cancer patients is insufficient. Discuss every supplement with your team, because some interact with treatment.
- Turning eating into yet another task. This may be the most important one. Eating during treatment is already hard. You don’t need to feel guilty that you didn’t finish the “perfect” anti-inflammatory bowl with seven kinds of seeds.
11 · Help
When to seek help
If weight loss continues, don’t wait for it to become obvious
Seek medical assessment if you have:
- unintentional weight loss
- persistently reduced appetite
- visible muscle loss or a marked drop in strength
- difficulty eating or swallowing
- ongoing nausea or vomiting, prolonged diarrhea
- mouth pain or sores
- being unable to take in enough food or fluids
The assessment shouldn’t be limited to the number on the scale. Weight, food intake, muscle mass, and physical function are tracked, and other clinical markers when needed.
Summary
In the end
Cancer cachexia shows that eating isn’t just calorie math. The body isn’t a calculator where calories in − calories out = weight. In illness, a whole biological system steps in between the two sides: inflammation, signaling molecules, muscle metabolism, fat tissue, energy exchange, and the treatment itself.
That’s why the approach is multilayered: food for energy and substrates, protein to maintain tissues, movement (when safe) as a signal to the muscle, symptom control so that eating is possible, and treatment of the underlying disease.
And perhaps most important: if you’re losing weight during cancer treatment, it doesn’t mean you’re not trying hard enough. Sometimes your body really has changed.
The task isn’t simply to give it more food, but to understand what happens to the food after you’ve eaten it.
This material is for educational purposes and doesn’t replace the judgment of your care team.
References
- Fearon K, et al. Definition and classification of cancer cachexia: an international consensus. Lancet Oncol. 2011;12(5):489–495.
- Baracos VE, et al. Cancer-associated cachexia. Nat Rev Dis Primers. 2018;4:17105.
- Arends J, et al. ESPEN guidelines on nutrition in cancer patients. Clin Nutr. 2017;36(1):11–48.
- Muscaritoli M, et al. ESPEN practical guideline: Clinical nutrition in cancer. Clin Nutr. 2021;40(5):2898–2913.
- McMillan DC. The systemic inflammation-based Glasgow Prognostic Score: a decade of experience in patients with cancer. Cancer Treat Rev. 2013;39(5):534–540.