Is the Second Law of Thermodynamics Able to Classify Drugs?

Laurent Schwartz, Assistance Publique des Hôpitaux de Paris

Luc Benichou

Jules Schwartz, Assistance Publique des Hôpitaux de Paris

Maxime Pontié, Université d’Angers, Faculté des Sciences, Groupe Analyses et Procédés, Angers

Marc Henry, Institut Le Bel, Université de Strasbourg/CNRS, Strasbourg

This paper is one of a series of publications trying to merge medicine back into physics. Accordingly, the combination of theory and subsequent experiments was the cause of major progress in physics. We aim at describ-ing diseases and thus treatment as physical features. But in medicine, meas-urements of physical data such as calculation of entropy are missing. Entropy production and dissipation has never been measured in human cells. We are, at a stage, where we can only raise hypothesis based of indirect markers of the fluctuation of entropy.

We have based our reasoning on data based on the metabolic flux centered by the mitochondria, the place within a cell, providing the maximum production of entropy as heat. We also have used clinical data. For example, if the patient is more active (like after treatment with thyroid hormones) one can assume that the entropy flux has increased. Similarly, if the temperature decreases (like after antibiotic treatment for infection) one may deduce that there is a decrease in entropy released in the outer space. In this paper, we have tried to merge biological and medical data, focusing on their impact on entropy. The second law of thermodynamics tells us that entropy can only increase in a closed system. When discussing the second law of thermodynamics, one should always define its reference. Here we consider the human body as the reference point. The entropy can be excreted from the patient and thus locally decreases. But, the entropy of the universe is always going up, as the contribution from our body, compared to the Sun-Earth system, is almost negligible.

In the vast majority of diseases, there is a shift toward increased synthesis of biomass. In cancer, there is increase in cellular proliferation. In neurodegenerative diseases, there are protein deposits like the amyloid plaques in Alzheimer’s disease or the bodies of Lewy in Parkinson’s disease. In inflammation, there is secretion of proteins such as lymphokines and cytokines and proliferation of inflammatory cells. The Nobel Prize, Otto Warburg (1883–1970) in the 1920s, first described this shift toward anabolism in cancer cells. The Warburg’s effect is a modified cellular metabolism based on aerobic fermentation, which tends to favor anaerobic glycolysis rather than oxidative phosphorylation, even in the presence of oxygen. In epithelial cells, the Warburg’s effect results in cancer. The Warburg’s effect is a bottleneck. The cells cannot burn the glucose because the pyruvate cannot be degraded in the Krebs’ cycle. Evidence of the central role of the Warburg’s effect comes when the researcher injects into cancer cells, with a micropipette, normal mitochondria. The growth will stop. These cells have become benign. The injection of the nuclei of cancer cells into normal cells does not increase growth. These cells can still burn glucose because the mitochondria are normal and do not form tumors [1 and references therein]. The inhibition of the oxidative phosphorylation results in the activation of the anabolic pathway, such as the Pentose Phosphate Pathway (PPP), that is necessary for DNA and RNA synthesis [1 and references therein]. The Warburg’s effect results in the release of lactic acid in the extracellular space, the concomitant activation of the Pentose Phosphate Pathway, and anabolism.The Warburg’s effect results in the synthesis of new proliferating cells. More recently, metabolic shifts have been described in Alzheimer and Parkinson’s diseases. Similar shifts toward anaerobic glycolysis have been described in most common disease. To name a few, among others, as published in: autism, schizophrenia, Alzheimer, Parkinson’s disease, Huntington’s disease, stroke, infection, fibrosis, cirrhosis, emphysema, arthritis, scleroderma, lupus. To the difference to the Warburg effect, these shifts toward glycolysis and increased lactate secretion may be transient and reversible in the presence of oxygen.


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