THE MODEL OF LIFE: A FRESH PERSPECTIVE ON UNDERSTANDING DISEASE

The Model of Life

According to Schrödinger, life resists the entropy increase dictated by the second law of thermodynamics by absorbing energy to maintain or decrease its entropy, a concept he referred to as negative entropy. However, negative entropy is a broad concept and doesn’t concretely describe the entire life process. Assuming that an organism is entirely composed of cells, entropy measures the organism’s orderliness. An increase in entropy represents a transition from order to disorder within the organism, so the overall order of cells reflects the organism’s orderliness. When dysfunctional cells emerge, such as senescent or cancerous cells, the organism’s order is disrupted, decreasing its orderliness. Let’s assume these poorly performing cells, or those causing the loss of order, are collectively known as aging cells (including all types of dysfunctional and malignantly proliferating cells, with their main side effects being spatial occupation and disruption of order). The proportion of aging cells to the total cell count reflects the degree of disorder within the organism. This ratio is intuitive, making it a convenient measure of entropy increase.

We can create a model of life: the human body has approximately 50×1012 cells. When the proportion of dysfunctional aging cells (senescent cells) reaches a certain level, the person’s systemic functions will fail, leading to death. In this model, a local excess of dysfunctional cells beyond a threshold equates to the onset of a disease. The body’s natural functions, especially the immune system, work to slow down or reduce the accumulation of aging cells.

From birth, due to environmental or systemic influences, our body’s cells endure various damages. Once a certain threshold is reached, cells age and are cleared by the immune system. However, this clearance is incomplete. We use the immune system’s ability to clear cancer cells as a model for its capacity to clear aging cells. This capacity diminishes over time (according to the immunoediting hypothesis, cancer cells ultimately evade the immune system because its clearance ability decreases with time). This is an important variable as it not only reflects how aging affects the immune system but also how artificially altering the immune system can have long-term effects on the body’s ability to clear aging cells. Cells in the body have a lifespan; they don’t become senescent at a fixed point but accumulate damage over time, leading to senescence. This damage is likely to affect all cells, not just a subset. Therefore, as time progresses, the number of senescent cells increases at an accelerating rate.

In the animal kingdom, there’s a pattern: the heavier (or larger) an adult animal is, the longer its maximum lifespan tends to be. The size of an adult animal can explain 63% of its maximum lifespan. Assuming that an animal dies when a certain proportion of its cells become senescent, and given that all animals have the same rate of cellular damage, immune capacity, and rate of decline in immune function, then an animal’s lifespan would be solely related to its size.

Our model easily explains why larger animals live longer: larger animals have more total cells as adults, so they require more senescent cells to cause death. Since the number of senescent cells that accumulate without being cleared due to damage is related only to time, the larger the animal, the longer it takes to reach the critical proportion of senescent cells, and thus, the longer the animal’s lifespan.

Treatment or Prevention of Diseases

According to physical laws, when an animal becomes ill, it indicates that some of its cells are no longer functioning properly. The approach to treating diseases involves either repairing these dysfunctional cells or removing and replacing them with new ones. For example, in humans, when disease occurs, such as cells becoming inactive (losing function) or deteriorating (harming the body), these cells are considered senescent in our model. So, how do we treat these diseases? Physical laws suggest that we can only clear these damaged cells (since repairing a bad cell to a good one is almost impossible for humans), and then rely on the body’s own mechanisms, using remaining stem cells to regenerate normal cells to replace the ones that have been removed. Our model does not reflect the process of stem cell regeneration; we simply assume that this process will automatically occur after the bad cells are cleared. Since stem cells regenerate younger and healthier cells, if stem cell regeneration can occur naturally without other limitations, then according to our model, once the senescent cells are cleared, everything else happens naturally. Here, we assume this process occurs naturally.

Let’s assume a chronic disease occurs, such as diabetes, cancer, or Alzheimer’s disease, where the patient’s senescent cell accumulation grows exponentially. Without treatment, the patient is likely to die earlier than a healthy individual. If we apply an effective treatment, the result is reflected in the backward shift of the age cell accumulation curve.

According to our model, there are two types of treatments: 1) directly clearing senescent cells, and 2) enhancing immune capacity, which by being improved, increases the clearance of senescent cells. Either way, an effective treatment will result in the senescent cell accumulation curve shifting backward, thus moving the intersection with the death line further back, which equates to an extension of the patient’s lifespan. Many treatments can both directly clear senescent cells and boost immune capacity. For example, clearing senescent cells may present antigens to the immune system, bringing additional immune capacity to clear more senescent cells, thus pushing the senescent cell curve even further back, and extending lifespan even more.

In reality, ablation of tumors can increase patient survival; clearing senescent cells can extend animal lifespan. These real-world cases align with our model.

Unlike lethal cancers, the treatment of diabetes is more about prevention or reducing damage, since diabetes treatment does not seem to involve clearing senescent cells. Instead, it often involves lowering blood sugar to limit further damage from high blood sugar to the body’s systems, which may relate to the chronic nature of diabetes and the fact that there is no known cure for diabetes yet.

Toxic Excitatory Effect

Some treatment methods display a peculiar pattern where substances generally toxic to the human body, when administered in low doses, can benefit the elimination of diseases or cause an excitatory effect that is advantageous to the body.

For instance, it was commonly believed that free radicals (or ROS) inducing oxidative stress would damage normal cells, leading to cell loss or even cancer (akin to age cells in our model). However, it has been found that the body’s production of ROS is generally beneficial. Exercise, for example, generates ROS, but its benefits for diabetes and cancer are unquestionable. Increasing ROS can treat autoimmune diseases like arthritis. If the free radical harm theory held, people would need to take antioxidants daily to combat this damage. Yet, the observed toxic excitatory effects challenge this view.

Our model can easily explain this. We assess a treatment method by whether it increases or decreases the number of senescent cells. If the number grows, the treatment is deemed harmful; if it shrinks, the treatment is considered beneficial. Free radicals increase oxidative stress on normal cells, but since this damage accumulates gradually, there should be no dramatic fluctuations. Temporarily lowering free radical levels has a minimal impact. This perspective upholds the free radical damage theory. However, our model includes the function of immune clearance capacity. We know that ROS are crucial for the immune system, with neutrophils and macrophages clearing various senescent cells (like infected or cancerous cells) by elevating ROS levels to leverage their oxidative power. Clearly, while higher ROS levels may damage normal cells, they also enhance the immune system’s ability to clear senescent cells. When ROS levels are temporarily elevated after exercise, for example, it aids the immune system in clearing senescent cells, thus generally benefiting health.

Therefore, the toxic excitatory effect of free radicals relies on the short-term increase in ROS, which boosts the immune system’s capacity to clear more senescent cells than the number of new senescent cells caused by free radical damage to normal cells.

The Life Model and Chlorine Dioxide

In our pursuit of treating diseases, we have positioned extending survival as our ultimate goal. Within this framework, the preferred method of treatment for various diseases involves eliminating damaged cells and bolstering the immune system to enhance its clearing capability. For chronic diseases that lack effective treatments, our suboptimal strategy is to prevent further deterioration or minimize damage to other healthy cells.

ROS are known not only for their ability to clear damaged cells but also for their potential to boost immunity. Could chlorine dioxide have a similar effect? If we compare the human body to a complex machine, a disease is like a faulty component. Common sense dictates that a skilled mechanic would remove the damaged part and replace it. In this analogy, removing the bad part equates to clearing damaged cells, and the machine’s automatic replacement with new parts mirrors our body’s ability to regenerate healthy cells, provided the right conditions.

In our life model, we’ve developed a logical framework to explore the potential of chlorine dioxide’s oxidative properties in clearing damaged cells and to investigate if it could also promote tissue regeneration by simulating ROS.

Due to the rapid pace of redox reactions, effectively using oxidizing agents like chlorine dioxide to clear damaged cells requires ensuring they reach the affected areas directly. Free radicals have long been considered culprits in causing diseases, and chlorine dioxide could similarly harm healthy tissues or cells if misapplied. Until we fully understand whether such damage is reversible, we must exercise extreme caution when using chlorine dioxide to avoid contact with normal tissues or cells. This significantly raises the technical barrier for its medical application.

Fortunately, recent research has started to challenge the view that free radicals are entirely harmful. In particular, blindly following antioxidant regimens may not be beneficial to the human body and could even accelerate the progression of certain diseases. These findings provide a new perspective on the potential medical applications of chlorine dioxide. Numerous studies have found that supplementing ROS can aid in tissue regeneration, and my research also indicates that chlorine dioxide can promote this process.

In our life model, eliminating senescent cells is central to curing diseases. We previously assumed that once these cells were cleared, the body’s natural healing abilities would take over, stimulating the renewal of young cells and tissues. However, this assumption is not always solid because human regenerative capabilities are inherently limited, which is a significant bottleneck in our fight against diseases.

Against this backdrop, chlorine dioxide reveals its unique appeal. Besides its ability to clear senescent cells, it may also cause transient damage to healthy tissues. Yet, it is this damage that triggers a regenerative response in tissues, and this property of chlorine dioxide could be pivotal. It not only helps to fill the voids created by the removal of senescent cells but also promotes regeneration, aiding in the complete recovery of these damages. This dual effect offers us a fresh perspective to understand and harness the potential of chlorine dioxide in medical treatments, opening a new window for us.

In the MMS protocol, Jim Humble recommends methods of administration that include oral ingestion and topical application, with chlorine dioxide concentrations far below 3mg/mL (the saturation concentration at room temperature). Here, I must clarify that oral ingestion and low-concentration topical application are utterly ineffective in utilizing chlorine dioxide’s properties. Due to its rapid oxidative reaction, which completes within seconds upon contact with human cells, orally ingested chlorine dioxide almost certainly cannot reach areas beyond the mouth and esophagus. Moreover, oral administration of a highly concentrated solution of chlorine dioxide is hazardous, as it can cause severe corrosion of the esophagus and indiscriminately damage various types of cells.

Regarding low-concentration chlorine dioxide for topical use, such concentrations are almost ineffective in clearing diseased tissues and cells.

The Updated Disease Research Model

My life model falls under the category of systems biology and is part of complex science; it is a complex adaptive system. Current medical research exhibits a reductionist trend, emphasizing understanding life processes and pathological states by studying the most fundamental building blocks of organisms—molecules. This approach has its advantages, such as helping scientists uncover the molecular mechanisms of diseases and discovering new drug targets. However, reductionism has a fatal flaw:

(1) Neglecting Complexity: Biological systems are highly complex and dynamic, and changes in a single molecule may not suffice to explain changes in the entire system. Diseases are often the result of multiple factors interacting, and reductionism might overlook this system-level complexity.

(2) Overlooking Environmental Factors: The onset of diseases is related not only to individual molecular and genetic factors but is also influenced by a variety of factors such as environment, lifestyle, and psychological state. An excessive focus on the molecular level might neglect these important environmental and social factors.

(3) Limitations of Disease Models: Studying diseases at the molecular level often requires the establishment of simplified models, such as cell cultures or animal models. These models may not fully replicate the complexity of human diseases, thus limiting the applicability of research findings.

(4) Individual Differences in Treatment: Even with the same molecular targets, different individuals may respond differently to treatments. Reductionism may not adequately explain these differences between individuals.

While molecular research has significantly advanced medicine, the field is increasingly adopting a systems biology approach. This method integrates information across different levels—from molecules to cells, tissues, organs, and the entire organism—and factors in genetics, environment, and lifestyle for a more comprehensive understanding of disease. However, current systems biology theories often follow a reductionist path, attempting to exhaustively map relationships between variables at all levels. This seems unattainable. Aiming for a simple, elegant theory of life’s essence, like Schrödinger’s concept of negative entropy, is a more suitable goal for systems biology than constructing a complex model with all variables.

Upon analyzing the drug development process, it’s evident that aside from serendipitous discoveries, most new drugs originate from in-depth molecular studies, seemingly validating reductionism. Yet, when examining the effectiveness of current medical treatments, the number of curable diseases is disappointingly small compared to the vast array of human diseases. This suggests the need for new research approaches.

Similar to how mathematical modeling in complex sciences often omits certain details to highlight key variables, systems biology research should also discard variables that cancel each other out or are too complex to decipher. I propose a new method for systems biology research: stratifying complex systems and establishing clear boundaries between levels. We should focus on levels where human intervention can achieve specific goals. If a level’s variables are too numerous, the structure too complex, beyond our research and computational capabilities, or if comprehensive intervention is unfeasible, the research focus should shift to a higher level. For instance, if genomic research is too intricate, we might move to the proteomic level, and if that’s still unmanageable, we proceed to the cellular level. At the cellular level, we consider the average effects of genes and proteins instead of their specific variables.

I firmly believe that my exploration and development of the therapeutic potential of chlorine dioxide is rooted in this innovative research philosophy. Initially, in my study of chlorine dioxide, I focused on its effects at the cellular level, disregarding whether it damages the cell membrane or DNA. Additionally, I observed similarities between chlorine dioxide and certain substances in the body’s adaptive system. By simply mimicking ROS in experimental simulations, I found that chlorine dioxide exhibits a triple effect, including the elimination of abnormal cells, promotion of tissue regeneration, and modulation of immune responses. Considering the fundamental chemical properties of chlorine dioxide, I believe it is essential to deliver it directly to the affected areas as a core principle in disease treatment.

While I am convinced of the broad therapeutic effects of chlorine dioxide, I am also aware of the need to adhere to current medical regulations. I am committed to following the standard process for new drug development to advance it to clinical trials. I understand that many readers may be disillusioned with existing medical technologies. If you are confident in the therapeutic effects of chlorine dioxide but are unable to use it due to legal constraints, I suggest considering metformin as an alternative.

I suggest considering metformin for several reasons:

Firstly, numerous studies and clinical practices have shown that metformin has the potential to eliminate abnormal cells, promote tissue regeneration, and regulate immune responses. This may be achieved through its ability to generate ROS at the cellular level, similar to the mechanism of chlorine dioxide.

Secondly, the off-label use of metformin for non-diabetic treatment is legally permissible and does not pose any significant risks.

Thirdly, metformin is generally well-tolerated, with occasional diarrhea being the most common side effect.

Additionally, metformin has been found to have various beneficial effects, including weight loss, anti-aging properties, anti-cancer activity, and anti-inflammatory effects. These serendipitous discoveries parallel the potential benefits of chlorine dioxide. Unlike some existing drugs, such as targeted cancer therapies that can lead to drug resistance, metformin can be taken on a long-term basis.

Lastly, metformin is a cost-effective treatment option.