Borrowing Concepts from Particle Physics to Better Frame the Mechanisms of Aging
An interesting idea is put forward in this open access paper, aimed at producing a greater and more useful unity of thought about the processes of aging. It is certainly the case that the field lacks a common conceptual foundation to build upon when it comes to working towards a better understanding of the mechanisms of aging. Hence the many theories of aging, focusing on quite different areas of molecular biology and evolutionary biology, and the persistent debate over whether aging is an evolved epigenetic program of late life dysfunction (the minority position), or an accumulation of damage that falls outside selection pressure for repair or prevention (the majority position).
We argue that some of the key principles of particle physics can be borrowed to study biological systems that age. Namely, these principles are: (a) Every interaction leads to a transformation of all interacting subjects. (b) Every process can be dissociated from the chronological time and considered as a sequence of discrete events. It is the order and the number of these events that predetermines the outcome, not time. (c) The threshold value is predetermined by a probability for a specific interaction to cause a specific transformation. An at-the-threshold event occurs not because of the accumulation of prior stimuli but because an increasing number of stimuli increased the probability of the observed event.
These principles can help understand the nature of aging or other biological processes. Cell functionality is determined by complex interactions of atoms within micro- and macromolecules with various cell structures and internal cell environments. During aging, discrete transformations in a cell eventually negatively affect cell system functionality. When atoms within molecules change their characteristics due to interactions and transformations, such as radioactivity, oxidation, reduction, etc., the macromolecule's whole functionality is altered. Alteration of functionality causes direct damage to a system by performing an alternative function or indirect damage defined by a loss of functionality.
In other words, systematic damage accumulation from the standpoint of a whole system leads to the decay of the system. Once damage in a system reaches a certain magnitude i.e. reaches a threshold, the system stops performing the originally designated function. When a cell can no longer maintain critical functionality, it finally transforms into a highly non-functional state. On an organism level, outcomes can look differently, e.g., senescence, cancer, coronary diseases, diabetes.
Therefore, biological aging may be defined as a sequence of highly discrete transformations caused by a combination of internal and external factors that lead to chronic damage accumulation and the consequent loss of functionality of a system. The transformations of damage repair mechanisms themselves may lead to their reduced functionality, representing critical thresholds since it would increase the rate of damage accumulation. However, some systems also exist where damage dilution, partitioning, clearance, decay and/or pre-emption support cell rejuvenation, thereby making the biological system appearing as non-aging (e.g. immortalized mammalian cell lines, germline, hydra).