- Excerpt
Chronic inflammation can lead to obesity, early stage diabetes, cardiovascular problems and chronic pulmonary disease (COPD), which manifests itself in respiratory symptoms, shortness of breath and cough. Long COVID is a specific constellation of persistent signs of chronic inflammation, such as unremitting fatigue, post-exertional malaise, and a variety of cognitive and autonomic dysfunctions (heart rate, body temperature, breathing rate, digestion and sensation). What keeps all these degenerative chronic conditions going is oxidative stress, which leads to exhaustion of the body’s own anti-inflammatory hormone cortisol. OPCs not only directly mitigate inflammations but, by scavening free radicals, OPCs also diminish cortisol exhaustion and restore cortisol homeostasis.
Table of contents
- Inflammation … what does it really mean ?
- Oxidatieve stress is the “engine” of inflammation
- Cortisol, your body’s own anti-inflammatory agent
- Cortisol and Vitamine C are natural inflammatory inhibitors
- How cortisol breaks inflammation
- OPCs enhance the activity of cortisol
- Stabilizing cortisol homeostasis
- Long-haul Covid and Covid-19 Spike Protein Persistence
- OPCs ‘recharge’ vitamin C
- Cortisol en vitamin C need OPCs
Inflammation … what does it really mean ?
What we commonly refer to as “inflammation” is the immune system's perfectly natural and survival-oriented effort to repair and prevent damage. In other words, inflammation is a sign of the activity of the body’s innate natural healing impulse, known in the “old days” as the vis medicatrix naturae. The cause of an inflammation can always be found in some form of STRESS which the healing impulse tries to cope with and overcome. Stress can be pathogenic, for example in the case of bacteria or viruses (the Covid-19 virus and/or the Covid-19 ‘spike’ protein), but also chemical (oxidative) or physical (pressure/wear/overload). In the latter case, think of a tennis arm or wrist complaints as a result of using “the mouse” day in and day out. When the stress lasts too long and the process of recovery and healing must therefore go on and on, a downward spiral is set in motion in which the natural attempt to heal will eventually worsen the condition. Such a condition may result in “autoimmune diseases” such as metabolic syndrome, rheumatism and Covid-19 related chronic ‒ ‘long haul’ ‒ disorders.
Oxidatieve stress is the “engine” of inflammation
Free radicals and oxidative stress in general play the key role in keeping the healing impulse (the inflammation) going, because in the presence of oxidative stress, this impulse is kept going and does not “extinguish” on its own. The impulse turns into a self-reinforcing vicious circle. This happens, for example, when the vascular wall of the circulatory system is exposed too much, too often and for too long to ‘stressors’ such as free radicals and abnormal, oxidized, cholesterol. As a result, the vascular wall itself becomes so disturbed that it is perceived by the immune system as a ‘foreign’ and unwanted target that must be dealt with. Such vascular problems also arise when, under the influence of mRNA Covid-19 injections, the cells that line the inside of the vascular wall come under attack of the immune system because they secrete the foreign ‘spike’ protein
Cortisol, your body’s own anti-inflammatory agent
Fortunately, our body itself produces the substance that can “extinguish” inflammation. That can, in other words, turn off the healing impulse when it is no longer needed. This substance is called cortisol. Cortisol is an anti-inflammatory hormone that it is made in the cortex (outer layer) of the adrenal gland. Normally, there should be a healthy balance between cortisol and the inflammatory mediators, such that when the inflammation has performed its useful repair work, cortisol can extinguish and terminate the inflammation. By comparison, firefighters are needed when there’s a fire, but if there’s no fire, they will do more harm than good. When an inflammation (a “fire”) lasts too long or is too severe, pharmaceutical cortisol preparations (more “firefighters”) called corticosteroids such as Prednisone or Cortisone are commonly prescribed in regular medicine. But this approach overlooks the factor that fuels inflammations: oxidative stress. It is this stress that keeps the “fire” smoldering and eventually causes insensitivity to the body’s own endogenous and the additional pharmaceutical cortisol. The smoldering “fire” no longer responds to the “firefighters’” efforts to extinguish it. Increasing the dosage of corticosteroids then remains without result. The cortisol is there, but it is no longer capable of doing anything at the cellular level. We have entered the vicious circle called cortisol resistance or cortisol depletion.
Cortisol and Vitamine C are natural inflammatory inhibitors
In the Orthomolecular Medicine News Service of 11 December 2021, American physician Thomas E. Levy describes vitamin C and cortisol as the most important and most powerful synergistic natural anti-inflammatories. ( 1 ) They are, so wrote Levy, “literally designed by nature to interact together to optimize the antioxidant impact needed to resolve the disease- causing oxidation that always results from toxins, infections, and stress. As inflammation in a tissue is the direct result of the oxidation, metabolism, and depletion of vitamin C levels in that tissue, it is of primary concern to normalize cellular vitamin C levels as promptly and completely as possible. Quite literally, when intracellular vitamin C levels are normalized in an inflamed tissue, the inflammation is completely resolved, and the cells are once again in a non-diseased, normal state.” According to dr. Levy, “succumbing to an infection is a direct indication that more cortisol (and vitamin C) was needed by the body.” He refers to studies that have shown that cortisol increases the absorption of vitamin C by the cells of the body. ( 2 ) “This is very likely the primary function of cortisol in the body, as there is nothing more important for the resolution of tissue inflammation and the resulting tissue damage than normalizing elevated levels of intracellular oxidative stress as rapidly and completely as possible by normalizing intracellular levels of vitamin C.”
How cortisol breaks inflammation
Inflammatory reactions are ‘orchestrated’ by your DNA, which is located in the cell’s nucleus. The DNA comes to ‘expression’ when it has to defend the body against stress. Which means that you will experience this defense as an inflammatory reaction. Ideally, cortisol exerts its anti-inflammatory effect by “turning off” the pro-inflammatory genes in the DNA once the stress has been effectively handled. First, Cortisol penetrates into the nucleus of the cell by binding to a cortisol receptor. Arriving in the cell’s nucleus, where the DNA is located, the cortisol-receptor complex immediately silences the pro-inflammatory genes by binding specifically to the relevant DNA registers. But at the same time, the cortisol-receptor complex also recruits an enzyme (HDAC) that stabilizes the DNA itself, so that the pro-inflammatory DNA registers are “switched off.” In the tandem consisting of the cortisol-receptor complex and the gene-stabilizing enzyme, the latter, the HDAC, is the central but also the most sensitive of the two. Why sensitive? Because HDAC is extremely sensitive to oxidation. In pro-oxidative conditions, think of oxygen radicals, the HDAC is affected and no longer works. And so the effectiveness of the cortisol-receptor complex is also greatly hindered. If this situation is not handled by quenching the oxidative stress, we risk entering the phase of cortisol insensitivity. Taking pharmaceutical corticosteroids won’t help, because the HDAC in the cell’s nucleus will no longer function.
OPCs enhance the activity of cortisol
Knowing that several studies have shown that Masquelier’s OPCs can inhibit inflammation and quench oxidative stress led researchers Gesiele Verissimo, Antje Weseler and Aalt Bast of Maastricht University (Netherlands) to investigate whether these OPCs would be able to also break the vicious circle of cortisol depletion. To test their idea, the scientists used activated human white blood cells, macrophages, and first exposed them to oxidative stress to see if the inflammatory reactions described above would appear, which, indeed, they did. In these pro-oxidative circumstances, a reduced activity of HDAC was found in the cell nucleus, allowing pro-inflammatory gene expression. In addition to this, the researchers also saw that oxidative stress suppressed the production of active cortisol. The production of the active form of cortisol is regulated in the cells’ fluid part (the cytoplasm) by a specific enzyme. Like the HDAC enzyme that regulates the anti-inflammatory genes, the efficacy of this enzyme is also compromised by oxidative stress. All in all, oxidative stress inhibits cortisol production and disturbs the switching off of the anti-inflammatory genes. ( 3 )
Stabilizing cortisol homeostasis
When the Dutch researchers exposed macrophages incubated with OPCs prior to exposing them to the same amount and type of oxidative stress - at amounts that correlate with the amounts present in the human body after intake of the recommended dose - the adverse effects mentioned above did not occur. First of all, the OPCs maintained the cellular availability of the biologically active cortisol in the cytoplasm by maintaining the integrity of the enzyme that regulates cortisol production. Secondly, OPCs were able to keep the oxidation-sensitive HDAC enzyme in a healthy condition, thus inhibiting the pro- inflammatory gene expression. Both effects were attributed by the researchers to the effective anti-oxidative activity of OPCs. Differently put, it was shown in this study that OPCs were capable of maintaining an effective anti-inflammatory cortisol response in pro-oxidative conditions. It goes without saying that maintaining the integrity of all these interrelated anti- inflammatory processes, of cortisol homeostasis, is of great importance in maintaining whole body homeostasis, that is, maintaining the ability of the body to effectively and adequately deal with STRESS.
Long-haul Covid and Covid-19 Spike Protein Persistence
Back to the article by Dr. Levy and current health issues. Levy describes that both people who are disadvantaged by COVID mRNA injections and people who deal with ‘long-haul’ COVID are ideal candidates for a treatment consisting of a combination of medicinal corticosteroids and vitamin C. Corticosteroids wouldn’t even be necessary when taking very high doses of vitamin C. However, as most doctors and therapists know, prescribing very high doses of oral vitamin C is a problem for many patients. This is where the OPCs researched by the Maastricht scientists may come in handy, because these OPCs not only have a stabilizing effect on cortisol homeostasis, but they also have a vitamin C sparing effect. This is how OPCs not only help directly to ‘extinguish’ the inflammation, but they also do so indirectly because they support cortisol production and make more vitamin C available to the cells.
OPCs ‘recharge’ vitamine C
In 1976, Professor Jack Masquelier demonstrated this vitamin C sparing effect in a test he carried out with guinea pigs. They are just as dependent on vitamin C in the diet as we humans are. As a result, they respond to a vitamin C-deficient “scurvy” diet just like we do. In the test conducted by Masquelier and co-researchers, guinea pigs that received too little vitamin C in their diet lived significantly shorter lives than the piglets that ate enough vitamin> C. However, when OPCs were added to a diet given with very little vitamin C, the animals lived as long as those who received enough vitamin C. ( 4 ) The secret of this vitamin C sparing effect of OPCs lies in the capacity of OPCs to ‘recharge’ vitamin C. Whenever vitamin C neutralizes a free radical, it loses some or all of its oxidative power. To remain active as an anti-oxidant, vitamin C needs to be ‘recharged’ by another anti-oxidant. OPCs are the anti- oxidants of choice to recharge vitamin C. This is why the name “vitamin C co-factor” once< given to OPCs seems very appropriate.
Cortisol en vitamin C need OPCs
In other words, chronic inflammation and cortisol depletion are not only a problem caused by a lack of vitamin C and/or a disturbed cortisol homeostasis. These problems also have to do with the fact that vitamin C cannot ‘recharge’ itself after it has done its antioxidant work. OPCs gladly sacrifice themselves as donors of the ‘recharging’ electrons because they have a lot of them in stock and can make them available immediately. Add to that the fact that OPCs can normalize cortisol homeostasis by promoting the availability of active cortisol and dampening pro-inflammatory gene expression by exercizing their anti-oxidative effect, and it will be clear that OPCs play an indispensable role in the management of all kinds of chronic inflammation.
