Plaque Formation is a Reaction, Not a Process
Updated: Jul 30
"Multiple Sclerosis, Diabetes, Parkinson's and Alzheimer's are not diseases. They are reactions to disease."
Over the past two decades, I have studied fat embolism and related mechanisms of tissue injury. Through this work, I have developed a hypothesis that challenges traditional views of plaque formation and the body's response to injury.
This proposed model suggests that plaque formation is not simply a metabolic consequence of elevated cholesterol, but rather a reactive biological response to cellular trauma. According to this hypothesis, chemical, physical, or environmental injury initiates what I describe as a "calcium ion crisis," a rapid release of intracellular calcium that may play a central role in the body's protective response.
In this model, cellular stress triggers the release of calcium ions from intracellular storage sites, including the sarcoplasmic and endoplasmic reticulum. The magnitude of calcium release is proposed to correspond to the degree of cellular injury. These calcium ions may then interact with circulating lipoproteins, including LDL, contributing to the transport of materials involved in tissue repair. Under this hypothesis, plaque formation represents an organized biological response intended to stabilize or protect injured tissue rather than simply the accumulation of excess cholesterol.
If supported through future research, this framework could offer a different perspective on conditions in which calcification or plaque deposition is commonly observed, including atherosclerosis, coronary artery disease, peripheral artery disease, kidney stones, gallstones, and other disorders involving abnormal mineral or lipid deposition. It also raises broader questions regarding the role of innate immune responses and tissue repair in chronic disease.
This concept further proposes that many pathological deposits traditionally viewed as the primary cause of disease may instead represent the body's attempt to contain or respond to underlying injury. While this hypothesis differs from prevailing scientific models, it highlights the importance of investigating the relationship between cellular injury, calcium signaling, inflammation, and tissue remodeling.
An additional area of interest is the role of calcium during the final stages of life. This hypothesis explores whether the calcium-dependent processes associated with rigor mortis may represent a continuation of the body's biological response following the cessation of normal cellular function.
This work remains a developing scientific hypothesis and requires further investigation through laboratory research, imaging studies, and clinical collaboration. Future research will be necessary to evaluate the proposed mechanisms, determine their biological significance, and assess whether they may lead to new diagnostic or therapeutic approaches.
Researchers, clinicians, and academic collaborators interested in exploring these concepts are encouraged to connect as this work continues to evolve.
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