Oxidative Stress

On Electricity, Electrons and Electron Flow.

The consistent common denominator of all diseases is the presence of Increased Oxidative Stress (IOS). And the lessening or resolution of that IOS is the key to the effective treatment of all disease. IOS is literally the single parameter that determines whether a cell or tissue is diseased. When no IOS is present, no disease is present. It’s that simple. – Dr Thomas Levy

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I’m reading Hidden Epidemic by Dr Thomas Levy at the moment (thanks Amelia!).

Chapter 4 is about Oxidative Stress, and I felt it warranted highlighting on its own.

It’s not every day you come across a meta explanation of disease.

I first wrote about IOS late last year, in connection to Vitamin C, after watching a Levy lecture. It was such a light bulb moment.

Vitamin C

"100 percent of chronic degenerative diseases, cancer, heart disease you name it have increased intracellular oxidative stress"

I was fortunate to interview Dr Levy early this year and got to ask him:

Interview with Dr Thomas Levy

Do you think of oxidative stress as a unifying theory of disease? Is that a fair description?

Absolutely. In my view, there is no other cause of disease. Some might question what about genetic defects? My response is that if you're deficient in a certain enzyme, your metabolism isn't running optimally, leading to inefficiencies and resultant oxidation. So, even if it's not due to the ingestion of a toxin, the root of diseased, malfunctioning cells and tissues is always elevated oxidative stress.

The real light bulb moment for me was understanding that what Levy was really talking about was an electrical phenomenon. Health is electrical. Disease is electrical.

Here again from our interview:

Would you like to add anything else about the particular role of electrons in this context?

Yes, there's a fascinating aspect of electrons that became apparent to me. It's about how diet brings in all new electrons, which, in essence, originate from the sun. The sun's energy irradiates plants, which through photosynthesis, produce nutrient substances rich in a natural array of electrons. This concept grabbed my attention during the COVID pandemic when I learned from a colleague in Colombia about the powerful antiviral properties of mango leaf and papaya leaf. It struck me that this could apply broadly across various plants.

Curious, I spent some time on PubMed and conducted a search for "leaf extract." I was presented with around 6,000 articles. Out of these, I managed to review the first 200 or so, which covered approximately 60 to 70 diverse plants. The findings were consistent: these leaf extracts exhibited anti-cancer activities and antioxidant properties, among other positive clinical effects. This research reinforced my understanding of the vital role plants—and by extension, their electrons—play in health and disease management.

It became clear to me that although certain plants can produce toxins, their primary function isn't to be poisonous. Even those that do produce toxins also generate substantial amounts of nutrient substances. This realization fits perfectly within a broader perspective. From my point of view — and this may not sit well with every physicist — the photonic energy from the sun is somewhat analogous to a diluted, airborne flow of electrons. The plants absorb this energy, converting it into electrons — although, it's worth noting, no one has actually seen an electron. These electrons, originating from sunlight photons, are then transferred to our bodies when we consume the plants or use them to make tea.

I find this concept incredibly intriguing. It has led me to believe that if one were stranded in the wild, there's an excellent chance that making tea from any leaf or stem found would be beneficial. Essentially, there's a high probability that these natural elements can sustain life, echoing the vital connection between the sun's energy and the nourishing properties of plants.

In fact, from Levy’s lecture he makes this quite precise point in relation to Vitamin C:

It is the "king" of antioxidants and plays a central role in redox reactions, donating electrons. Good health requires robust electron flow.

So, what we are talking about in not only electrons, but electron flow.

Health and disease are functions of electron flow.

I wonder how many doctors understand this?

I don’t think they do.

I think this is part of their, and our, constructed ignorance.

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Hidden Epidemic

Chapter 4: Increased Oxidative Stress: The Common Cause of All Diseases

Overview

All living systems require a continual exchange of electrons between biomolecules in order to function. This exchange is called reduction-oxidation (redox) and it occurs as one molecule takes one or more electrons from another molecule. The receipt of electron(s) by a biomolecule is called reduction and the loss of electron(s) by a biomolecule is called oxidation. A molecule cannot receive electrons unless another molecule loses them — one cannot happen without the other. In other words, redox requires one molecule to be oxidized so that another can be reduced.

Some chronic oxidation is a normal byproduct of all metabolic activity. But in healthy cells the oxidation is counterbalanced by antioxidants. Antioxidants ensure a healthy flow/supply of electrons as they reduce oxidized biomolecules by donating electrons. When antioxidant supplies become depleted, or when oxidation is occurring faster than the antioxidant system can neutralize, an abnormally high level of oxidized biomolecules results.

The state of disequilibrium caused by an excessive number of oxidized biomolecules, both inside and outside the cells, is called increased oxidative stress (IOS). The presence of IOS means that the high level of oxidized biomolecules present in a given group of cells is negatively impacting cellular function. Biomolecules include enzymes, proteins, sugars, lipids, and even nucleic acids. They can be part of the cellular structure, bound to other biomolecules, or roaming free in solution. When a biomolecule becomes oxidized, its biological function may be decreased to some degree or completely absent, depending on the biomolecule.

The presence of transition metal ions, like iron and copper, makes IOS even more pronounced since these agents are able to ramp up the production of the hydroxyl radical via the Fenton reaction. This radical is the most reactive redox molecule known to science. It is so reactive that the moment a hydroxyl molecule is formed it will immediately oxidize any adjacent biomolecule.

The consistent common denominator of all diseases is the presence of IOS. And the lessening or resolution of that IOS is the key to the effective treatment of all disease. IOS is literally the single parameter that determines whether a cell or tissue is diseased. When no IOS is present, no disease is present. It’s that simple.

The actual diagnosis and management of any chronic disease is considerably more complex. First, it is necessary to identify the specific causes of the IOS, and then the medical practitioner must find and employ effective means to mitigate those causes. Since the causes of IOS often come from multiple sources, failure to identify one chronic source—an undiagnosed oral infection, for example—means that treatment will be only partially effective or fail altogether.

The Consistent Cause of All IOS

What causes IOS? The answer is simple: toxins. Toxins are always pro-oxidant in their impact. They always, directly or indirectly, take electrons from biomolecules, either through a direct oxidation or by initiating one or more biochemical reactions that result in oxidation. Any free radical, pro-oxidant, or other molecule that produces an increase in oxidative stress is, by virtue of its activity, a toxin. In fact, the “toxicity” of a toxin is nothing more than the degree to which it can cause biomolecules to become oxidized and to remain so.

Antioxidant = Antitoxin

Because the toxicity of all toxins is due to the depletion of electrons in the affected biomolecules, it follows that antioxidants are the ultimate antitoxins because they donate electrons (reduction), sometimes directly to the electron-seeking toxins and sometimes just restoring a full complement of electrons to previously oxidized biomolecules, restoring their normal function. When an electron-seeking toxin receives its full complement of electrons, as from an antioxidant molecule, it loses its toxicity, since it cannot any longer take electrons from another molecule. This clear-cut and very potent antitoxin effect of all antioxidants remains little appreciated by mainstream medicine, as well as by much of integrative or complementary medicine. In fact, vitamin C, the prototypical antioxidant, has been documented to be a highly effective antitoxin against all toxins, or poisons, with which it has been tested. This includes in vitro and in vivo studies in plants, animals, and humans, as well as a wide variety of clinical studies.

Indeed, the modern poison control center need not exist at all, except to promptly administer high doses of vitamin C intravenously and orally, along with other selected antioxidant nutrients. The center could serve a role in evacuating the stomach of orally ingested toxins/poisons, along with the administration of an agent such as activated charcoal to bind and neutralize toxins still unabsorbed in the gastrointestinal tract. The administration of many antisera or species-specific antidotes, traditionally given after such events as a poisonous snakebite, often inflict their own additional toxicity and can harm as well as benefit the patient. Frederick Klenner, MD described treating a child with tetanus in conjunction with another physician and having to deal with the pronounced toxicity of the tetanus antitoxin doses that consistently appeared to work against the improvement seen after each intravenous vitamin C dose. Klenner also commented in this article that “massive doses of vitamin C” were “dramatically effective” in dealing with hundreds of poisonings and viral infections.

The effects of any pro-oxidant and any toxin at the molecular level are the same: they both cause, directly or indirectly, the oxidation of various biomolecules, and they result in IOS...

The effects of any pro-oxidant and any toxin at the molecular level are the same: they both cause, directly or indirectly, the oxidation of various biomolecules, and they result in IOS in the affected cells and tissues. As noted above, an antioxidant like vitamin C is a powerful antitoxin, since it will often directly neutralize the toxin, but also because it will always help to repair oxidized biomolecules. The best antisera or species-specific antidotes will never repair the damage already done by toxin, venom, or poison. They can only help to prevent the toxin from inflicting further oxidative damage, with the hope that the patient is not too far gone for the body to overcome the damage already done and to heal itself.

Antioxidant versus Reduced Toxin

The chemical nature of a toxin prevents redonation of the electrons taken in the oxidation of biomolecules. This is a basic difference between an antioxidant and a reduced toxin, both of which have a full complement of electrons. Because of this characteristic, an antioxidant such as vitamin C promotes electron exchange and flow, while the toxin molecules generally block electron exchange and flow. This is also why an antioxidant can repair an oxidized biomolecule, while a reduced toxin cannot. Although both the antioxidant and the reduced toxin have enough electrons to give them to an electron-deficient molecule, the chemical nature of the toxin only allows it to take and keep electrons. When a toxin acquires electrons, it becomes more chemically stable and holds onto the electrons relatively tightly, unlike the antioxidant molecule, which is not markedly more chemically stable in either its reduced or oxidized form.

Cellular Electricity

As noted directly above, the chemical stability of an antioxidant such as vitamin C is similar with or without a full complement of electrons. Because of this property, vitamin C gives and takes electrons, over and over. This contributes to a real electron flow inside cells that is manifest as microcurrents, while helping to facilitate the maintenance of healthy transmembrane electrical potentials (voltages). At rest, most cell membrane potentials range from -40 to -70 millivolts. Toxic, diseased cells have lower transmembrane voltages and lesser microcurrents. The importance of these microcurrents to the health of the cell is supported by many studies that show that the application of microcurrents to injured tissue can stimulate stem cell activity and promote healing. ¹⁰, ¹¹ Multiple membrane channels regulating the flow of calcium, sodium, and potassium ions are known as “voltage-gated” membrane channels and further contribute to cellular microcurrents. As calcium levels increase inside cells, oxidative stress is upregulated inside those cells, further impairing their ability to function normally and directly promoting all chronic diseases.

Different Toxin, Different Disease

Even though the final common pathological denominator of all chronic degenerative diseases is increased oxidative stress (IOS), multiple factors affect how the IOS clinically impacts the body. Factors that figure prominently in the variability of disease expression resulting from IOS include the following:

Degree of the IOS. IOS can vary widely in actual quantity, anywhere from minimal to massive.

Chronicity of the IOS. The circumstances can be acute and “one-time” or the conditions promoting ongoing IOS can be chronic and unremitting.

Location of the IOS. This includes extracellular, intracellular (cytoplasm), intracellular organelles (endoplasmic reticula, mitochondria), cellular nuclei, and cellular groupings (organ, tissue, or compartment).

Genetic predispositions in a given patient. If an enzyme is absent, deficient, or already oxidized, this represents an area in the body where the additional oxidative stress of a new toxin can have an even greater negative clinical impact.

Biochemical properties of the pro-oxidant molecules (toxins) that are promoting the IOS. Some of the more significant variables characterizing different toxins will be examined below.

Unique combination of the above five factors. Severe IOS resulting from the chronic exposure to a potent toxin in a particular organ might result in malignancy. On the other hand, mild intracellular and/or extracellular IOS in the muscles and joints could result in myalgias and arthralgias, but not necessarily an advanced disease.

...the degree to which a tissue, organ, or a specific microenvironment in the body is optimally functional (healthy) is directly related to the ratio of how many biomolecules are reduced to how many biomolecules are oxidized...

Generally, the biomolecules of the body exist in either a reduced (electron-saturated) or an oxidized (electron-depleted) state. Rarely, a biomolecule might act as if it were chemically inert and be intrinsically resistant to oxidation. However, technically it would still be in a reduced state since it would have a full contingent of electrons.

When reduced, the biomolecules are in their state of optimal physiological function. Oxidized biomolecules exhibit decreased to absent physiological function. Therefore, the degree to which a tissue, organ, or a specific microenvironment in the body is optimally functional (healthy) is directly related to the ratio of how many biomolecules are reduced to how many biomolecules are oxidized (reduction/oxidation). A higher redox ratio will reliably reflect better physiological function and health, while lower ratios will reflect differing degrees of disease. When a toxin results in the oxidation of extremely critical biomolecules, relatively severe disease and even death can result even though the overall redox ratio in the body is relatively good. Cyanide poisoning would be a good example of this, as this toxin rapidly inactivates critical biomolecules needed to incorporate oxygen into metabolic pathways, even though the total amount of toxin and the total number of oxidized biomolecules are relatively small compared to much less clinically potent toxins.

...the biochemical nature of the pro-oxidant agent, or toxin, plays a very large role in determining the clinical relevance of the IOS that is produced and what type of disease will result.

Item #5 noted above, the biochemical nature of the pro-oxidant agent, or toxin, plays a very large role in determining the clinical relevance of the IOS that is produced and what type of disease will result. Some of the most significant properties characterizing the nature of the toxin include the following:

Solubility properties. The toxin can be fat-soluble, water-soluble, or to some degree soluble in both fat and water (amphipathic).

Molecular size. The toxin can be a very small molecule with easy physical access to both intracellular and extracellular areas, or it can be a very large, complex molecule that only accesses a very limited number of areas.

Electrical state. Neutral or ionically charged. This characteristic not only affects where the toxin has physical access, it also impacts the degree of chemical reactivity of the toxin.

Unique molecular structure of the toxin. The physical configuration of a toxin, especially one with a higher molecular weight and extended branches that fold in a specific spacial manner, dictates the ability of the toxin to fit in a certain manner with target biomolecules, as in a lock-and-key relationship.

Direct impact of the oxidized biomolecule(s) on biochemical functions. One toxin might preferentially cause the oxidation of a relatively unimportant biomolecule, while another could cause the oxidation of one or more very critical biomolecules, such as those directly involved in energy production in the cell.

Tendency to produce oxidative chain reactions. When the toxin preferentially oxidizes and inactivates critical antioxidant enzymes, the resulting increased oxidative stress can be further magnified.

Chemical reactivity of the toxin. A chemical reaction can proceed very slowly or very rapidly, depending on the stability of the chemical configuration of the toxin. A toxin that requires a number of necessary chemical parameters to react with biomolecules in a given microenvironment will have a different clinical impact than one that reacts instantaneously, like the hydroxyl radical noted above.

Tendency to accumulate. Some toxins can build up physical stores inside cells and elsewhere. Even when the oxidative damage has already been inflicted, a sizeable accumulation of a toxin can physically impair or even prevent biomolecules from having needed interactions, serving to further block normal biological function.

Physical similarity to biomolecules. Some toxins can have enough physical similarities to particular biomolecules that they can act as inactive substitutes for those biomolecules, thereby decreasing the degree of normal function that would otherwise be present. Important receptors could be bound by certain toxins and rendered nonfunctional, as when a blank key fits a lock but will not open it.

Ease of access to excretion and elimination. Whether a toxin is intracellular, extracellular, bound to other molecules, existing freely in solution, or sequestered in various storage sites helps determine how readily that toxin can be mobilized, chelated, and/or excreted.

Levels of Intracellular Oxidative Stress

The basic metabolism of all cells results in metabolic byproducts that are pro-oxidant, and therefore toxic, in nature. As oxygen is processed and energy-rich molecules like ATP (adenosine triphosphate) are produced, waste products result as well. The degree of this oxidative stress can be of a physiologically normal degree, or it can be increased to various degrees. This depends on the type of cell and the level of its baseline metabolism, whether it is normal or already diseased, and on the amount of ongoing new toxin exposure. Of particular interest clinically is that all diseased cells demonstrate increased oxidative stress (IOS), especially intracellularly. Cancer cells, in particular, have the highest intracellular levels of IOS, and IOS has been shown to play a critical role in the malignant transformation of those cells. At least eight levels of intracellular oxidative stress can exist over the spectrum of normal, diseased, and cancerous cells:

Absent or non-detectable oxidative stress, as might be found in fully differentiated, non-replicating, and dormant cells

Minimal oxidative stress, as in cells with physiological levels of baseline metabolic activity

Minimal to moderate oxidative stress, intermittently upregulated. This level is present most of the time in normally functioning, non-diseased cells that are utilizing the physiological degrees of oxidative stress being produced in multiple intracellular signaling functions, upregulating or downregulating various metabolic reactions. ¹⁸

Moderate oxidative stress, chronically upregulated. While this level of oxidative stress can exist in a normal cell, this is usually the case only when this moderate degree is present transiently, as when a temporary burst of increased metabolic activity or energy is needed. When it is present most or all of the time, the cell can be characterized as being chronically diseased, with the stage being set for the cell to undergo malignant transformation if the intracellular oxidative stress is pushed any higher, in concert with the presence of other carcinogenic cofactors.

Moderate to elevated oxidative stress. When chronic, this is a level of oxidative stress inside the cells that is characteristic of established and replicating cancer cells.¹⁹ It is never found on a chronic basis inside normal cells, and it may also be present at times in chronically diseased but non-malignant cells that can easily be pushed into malignant transformation. When oxidative stress is high enough and prolonged enough, DNA damage can occur which then further promotes malignant transformation.

Elevated oxidative stress. This level of intracellular oxidative stress in seen in the most metabolically active of cancer cells, such as actively metastasizing cells, as well as in anaplastic, largely undifferentiated cancer cells. ²³ Since very high levels of intracellular oxidative stress are needed for a cell to die, this level of intracellular oxidative stress can also be briefly seen in an otherwise normal cell that is rapidly upregulating its oxidative stress in order to achieve programmed cell death, or apoptosis.

Greatly elevated oxidative stress. This is the level seen in cancer cells proceeding to apoptosis or even frank necrosis, as when the Fenton reaction in the cytoplasm has been upregulated by pro-oxidant agents, such as chemotherapy.

Maximal oxidative stress. This is the level of intracellular oxidative stress that is so elevated that the structural components of the cell are sufficiently oxidized to the degree that the physical integrity of the cell can no longer be maintained, and frank rupture occurs. This degree of oxidative stress can also exist in a previously normal or just chronically diseased cell acutely exposed to a very large toxin dose capable of inflicting enough intracellular oxidative stress to proceed directly to widespread cellular necrosis and rupture.

Conclusion

Increased oxidative stress, especially intracellularly, is the final common denominator in all chronic degenerative diseases, including heart disease and cancer. All pro-oxidant molecules are toxins, and all toxins inflict their damage by increasing the number of oxidized biomolecules. Pathogens are a major source of increased oxidative stress. All chronic infections strongly promote oxidative stress via associated endotoxins, exotoxins, and a wide variety of pro-oxidant metabolic byproducts are produced as tissue is damaged and also as pathogens eventually die and break down.

Although the cause of all disease is ultimately increased oxidative stress, the wide variety of diseases can be explained by various characteristics of the increased oxidative stress, as well as by the many different chemical characteristics of the offending pro-oxidants involved in producing the increased oxidative stress present in a given clinical syndrome or disease. Also, the degree to which intracellular oxidative stress is increased plays a major role in malignant transformation as well as in how invasive a given cancer might be.

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