Can We Live Longer by Starving Cancer?

Audio Version:

Cancer is one of the most vicious and difficult-to-treat diseases we know of. Even using combinations of the newest surgical approaches, chemotherapy, and immunotherapy, doctors are often unable to effectively combat the progression of the disease. But what if I told you that by doing something as simple as changing our diets, we might be able to starve cancer and thus outlive it.

Now this might seem like a crazy idea, but let’s think about it. Cancer cells, just like any other cells, require energy to survive. For example, if we tried to culture them in a solution without any energy supply, they would quickly die. Or if one were to starve oneself to death, one’s cancer would quickly follow suit. Of course, starving oneself to fight one’s cancer is… counterproductive to say the least. We want to live longer and better, so starvation is out of the question. Even so, these examples illustrate an interesting angle of attack against cancer.

Cancer cells need energy to stay alive and replicate. Without energy, they stagnate and die.

That means, that if we could somehow selectively cut off the energy supply to the cancer, whilst maintaining nourishment for the rest of our body, cancer cells would slowly die, and the cancer would vanish, whilst we would continue to thrive. But is that even possibly? Since cancers reside within our bodies, they have access to anything our healthy cells have access to as well, and we can’t exactly build a fence around them to isolate them, either. If we want to find an answer to this question, we must look at how cells produce energy and how that metabolism might differ between healthy cells and cancerous cells, but don’t worry, I’ll dive just deep enough, so that everyone can understand it, and no deeper.

ATP is a molecule used by our cells as a sort of energy storage unit. It can be produced during the breakdown of energy sources, such as fat or sugar, and then later used to drive energy intensive processes, such as the contraction of our muscles (1). For healthy cells, most ATP is produced in various pathways, which together under the umbrella term of ‘cellular respiration’. The common factor between all these pathways is their requirement of oxygen, thus the ‘respiration’ part of the name. Whilst there is variation depending on the fuel used, our cells are capable of metabolising fats and sugars using this process (2).

Should oxygen not be available, cells are able to instead switch to something called anaerobic fermentation, where sugar can be broken down without the use of oxygen. This process is for example used in our muscles during high intensity work, when the blood does not supply enough oxygen (2).

Despite possessing the benefit of not requiring oxygen, fermentation is much less efficient than the pathways of cellular respiration. To give you a rough picture, metabolising one molecule of glucose (a simple sugar) through cellular respiration will yield about 15 times as much ATP in comparison to one molecule of glucose being fermented (with slight variations). This fuel inefficiency – and the resulting far higher amount of waste products for the same energy output – is the reason cells normally prefer relying on respiration instead of fermentation (2).

In contrast to the avoidance of fermentation by healthy cells unless strictly necessary, cancer cells exhibit significantly higher rates of fermentation, even when oxygen is widely available. This effect is named the Warburg Effect after Otto Warburg, who first discovered it in the 1920s (3).

Though the complete explanation for this unusual behaviour is still debated, it seems that mitochondria are of central importance. Mitochondria are a sort of subcellular compartment with quite a lot of different specialised functions, but for us it’s just important to know, that the last step of cellular respiration – called oxidative phosphorylation – occurs within these mitochondria (2). A cell must thus have functioning mitochondria to perform cellular respiration. The steps for fermentation in contrast do not occur within the mitochondria and thus don’t require them to be performed. This means, that cells, which don’t possess (functioning) mitochondria – which is normally the case with red blood cells, alone among all our cells (4) –, must rely on fermentation to synthesise ATP (remember: biologically available energy).

In contrast to red blood cells, cancer cells do possess mitochondria, though they are almost always abnormal and dysfunctional (5, 6). This reduces their capacity to produce ATP via oxidative phosphorylation and thus cellular respiration, irrespective of oxygen availability, and forces the cancer cells to compensate by increasing fermentation, explaining the unusual behaviour observed by Warburg (7).

But not all fuels can be broken down by fermentation. Thus, if we reduce the availability of fermentable fuels in our bodies, we can disallow this compensation by the cancer cells and restrict the energy they can produce, effectively starving them. The most common fermentable fuel in our bodies is glucose.

Completely eliminating glucose from our bloodstreams isn’t viable for various reasons. For one, red blood cells rely on fermentation of glucose to cover their energy needs (4). Furthermore, the liver works to maintain a minimum level of blood glucose. However, it is still possible to greatly reduce the availability of glucose within our bodies.

The simplest way to do so is by completely abstaining from consuming carbohydrates. Doing so causes the body to enter ketosis, a state where it switches from using glucose as the main fuel source to ketones – a type of fat derivative. During ketosis, blood sugar levels decrease and become perfectly stable. This is, because the normal blood sugar spikes caused by carbohydrate consumption are now absent (8). Effectively, this reduces the glucose, which cancer cells can draw upon to fuel fermentation, starving the cancer and achieving precisely what we set out to do (9, 10).

It is important to note that not all cancers have equally damaged mitochondria. Some might be more capable of utilising cellular respiration than others. Furthermore, glucose is not the only fermentable fuel, so some cancers might ferment glutamine – an amino acid – instead of glucose to produce sufficient amounts of ATP (11, 12). I want to emphasise this point, because it means that abstinence from carbohydrates isn’t a be-all end-all solution. It is merely one tool at our disposal to help you outlive cancer. It is best to combine this approach with different interventions that attack other aspects of cancer.

Diving into those at this point would go beyond the scope of this post. But, if you want to know more, we do have our free Mosaic Method Guide available on our homepage, wherein you can find the steps we can generally recommend to all cancer patients and our reasoning behind their recommendation.

And that already concludes it for this post.

I hope you learned something new, and I wish you a great day.

Cheers

1. Bonora, M., Patergnani S Fau - Rimessi, A., Rimessi A Fau - De Marchi, E., De Marchi E Fau - Suski, J.M., Suski Jm Fau - Bononi, A., Bononi A Fau - Giorgi, C., Giorgi C Fau - Marchi, S., Marchi S Fau - Missiroli, S., Missiroli S Fau - Poletti, F., Poletti F Fau - Wieckowski, M.R., et al. ATP synthesis and storage.

2. Alberts, B., Johnson, A., Lewis, J., Morgan, D., Raff, M., Roberts, K., and Walter, P. (2015). Cell Death. In Molecular Biology of the Cell, (Garland Science, Taylor & Francis Group, LLC), pp. 74-85.

3. Potter, M., Newport, E., and Morten, K.J. (2016). The Warburg effect: 80 years on. Biochem Soc Trans 44, 1499-1505. 10.1042/bst20160094.

4. Chatzinikolaou, P.N., Margaritelis, N.V., Paschalis, V., Theodorou, A.A., Vrabas, I.S., Kyparos, A., D’Alessandro, A., and Nikolaidis, M.G. (2024). Erythrocyte metabolism. Acta Physiologica 240.

5. Chen, Y., Cairns R Fau - Papandreou, I., Papandreou I Fau - Koong, A., Koong A Fau - Denko, N.C., and Denko, N.C. Oxygen consumption can regulate the growth of tumors, a new perspective on the Warburg effect.

6. Seyfried, T.N., and Shelton, L.M. (2010). Cancer as a metabolic disease. Nutrition & Metabolism 7, 7 - 7.

7. John, A.P. Dysfunctional mitochondria, not oxygen insufficiency, cause cancer cells to produce inordinate amounts of lactic acid: the impact of this on the treatment of cancer.

8. Nuttall, F.Q., Almokayyad, R.M., and Gannon, M.C. Comparison of a carbohydrate-free diet vs. fasting on plasma glucose, insulin and glucagon in type 2 diabetes.

9. Egashira, R.A.-O., Matsunaga, M.A.-O., Miyake, A., Hotta, S.A.-O., Nagai, N., Yamaguchi, C., Takeuchi, M., Moriguchi, M., Tonari, S., Nakano, M., et al. Long-Term Effects of a Ketogenic Diet for Cancer. LID - 10.3390/nu15102334 [doi] LID - 2334.

10. Weber, D.D., Aminzadeh-Gohari, S., Tulipan, J., Catalano, L., Feichtinger, R.G., and Kofler, B. Ketogenic diet in the treatment of cancer - Where do we stand?

11. Jiang, J., Srivastava, S., and Zhang, J. Starve Cancer Cells of Glutamine: Break the Spell or Make a Hungry Monster? LID - 10.3390/cancers11060804 [doi] LID - 804.

12. Alberghina, L., and Gaglio, D. (2014). Redox control of glutamine utilization in cancer. Cell Death & Disease 5, e1561-e1561. 10.1038/cddis.2014.513.t