Ageing as a Multi-System Chronic Disease Caused by Accumulation of Protein Damages

Ageing is a complex, multi-system chronic condition that stems from the progressive accumulation of protein damage. This protein damage, driven by both endogenous and exogenous factors, compromises the structural and functional integrity of proteins, leading to cellular and systemic dysfunction. This article introduces a unifying theory that positions protein damage as the central mechanism of ageing, weaving together various established theories. It highlights the role of protein damage in enzymatic dysfunction, DNA damage, telomere alterations, and organ deterioration, presenting ageing as a chronic disease rooted in molecular dysfunction.

The enigma of ageing has captivated scientists for centuries, yielding diverse theories that seek to explain its mechanisms. From the wear-and-tear theory to genetic and free radical theories, these frameworks often focus on isolated aspects of ageing rather than a holistic understanding.

This article posits that the central driver of ageing is the gradual accumulation of protein damage. This perspective integrates existing theories into a cohesive model, focusing on how protein damage disrupts cellular and systemic processes over time. By linking molecular damage to broader biological dysfunctions, this theory offers a comprehensive explanation of ageing as a chronic, multi-system disease.

Proteins are vital for maintaining cellular structure and function. Their precise three-dimensional conformation enables biological activity. However, protein damage—induced by oxidative stress, environmental toxins, and metabolic byproducts—compromises this conformation, leading to dysfunction. This framework explores protein damage as the linchpin of ageing, with implications for enzymatic activity, DNA integrity, telomere maintenance, and organ function.

Enzymes are particularly vulnerable to damage due to their critical roles in cellular processes. Enzymes involved in DNA synthesis and expression, such as DNA polymerases and histone methyltransferases, are essential for genomic stability. Damage to these enzymes results in errors in DNA replication and transcription, and DNA damage that exacerbates protein dysfunction in a self-reinforcing cycle.

Telomeres, protective caps at the ends of chromosomes, are maintained by telomerase and associated proteins. Damage to telomerase enzymes impairs telomere maintenance, accelerating cellular ageing.

This theory reinterprets telomere shortening as a downstream effect of protein damage rather than a primary cause, shifting the focus from genetic determinism to molecular degradation.

Protein damage extends beyond cellular processes to impact organ systems. Structural and functional proteins in the heart, nervous system, muscles, kidneys, and other organs suffer cumulative damage, disrupting cellular homeostasis. Over time, this leads to progressive organ failure, along with clinical manifestations of ageing, such as cognitive decline, reduced muscular strength, and chronic illnesses.

Protein damage arises from the interplay of internal metabolic processes and external environmental influences.

Metabolic byproducts such as reactive oxygen species (ROS), free radicals, and advanced glycation end products (AGEs) contribute to protein damages leading to ageing process. Dysregulated cellular signaling molecules, including hormones, cytokines, and antibodies also play a role. Failures in cellular repair mechanisms, leave damaged proteins uncorrected.

Environmental pollutants, radiation, and chemical exposure, dietary additives, preservatives, and drugs that interact adversely with proteins, and infectious agents that damage cellular components belong to the exogenous components of peotein damaging.

The progressive accumulation of protein damage parallels the molecular pathology of chronic diseases such as diabetes, cardiovascular disease, and neurodegenerative disorders. By redefining ageing as a chronic disease, this perspective underscores its gradual onset from early life, and shared molecular pathways with other chronic conditions, particularly protein dysfunction.

This paradigm shift has profound implications, treating ageing not as an inevitable decline but as a modifiable condition.

Understanding ageing as a chronic disease caused by protein damage opens the door to innovative strategies for prevention and treatment. Reduce oxidative stress by neutralizing reactive oxygen species, and enhancing cellular repair systems via pharmacological or genetic interventions , are importantant in managing ageing process.

From a homeopathic standpoint, addressing the root causes of protein damage could mirror the approach used to manage other chronic diseases, emphasizing personalized care. Since antibodies generated in the body against alien proteins play a role in causing protein damages and ageing process, antimiasmatic homeopathic treatment is very much important.

Lifestyle Modifications, such as reducing intake of harmful additives and oxidants, minimizing exposure to toxins and pollutants, and enhancing metabolic efficiency and reducing oxidative stress, are important.

This article presents a unified theory of ageing, framing it as a chronic disease driven by the accumulation of protein damage. This perspective synthesizes existing theories, linking molecular dysfunction to systemic ageing processes. Recognizing ageing as a chronic condition provides a new lens for understanding its prevention and treatment, with the potential to improve healthspan and quality of life.

Ageing is a chronic disease caused by the accumulation of protein damages that starts from infancy. By redefining ageing in this way, we pave the way for innovative approaches to delay its onset, manage its progression, and transform how we view the human lifespan.