Pathology from persistent spike protein causes both "long-COVID" and anti-SARS-CoV-2 vaccine injuries.¹ It's difficult to understand how packaging this pathogenic protein in a vaccine was ever approved, unless we understand, that the entire approval flow for the lipid nanoparticle–encapsulated mRNA gene therapeutic anti-SARS-CoV-2 vaccines was shoddy.

Many of the claims, upon which approval was based, have since been called into question in independent experiments. Furthermore, approval was made without available long-term data, both for the specific drugs in question, but also for the technology at large.

That this was a horrendous failure on part of regulators, goes without saying, and that those involved in the obfuscation of the adverse effects of the vaccines remain at large, shows us the sordid state of our societies.² As of September 2022, 68% of the global population has received at least one dose of anti-SARS-CoV-2 vaccination, roughly 30% of which were administered the novel vaccines using lipid nanoparticle–encapsulated synthetic mRNA.

Two primary claims were made about these novel vaccines in support of their safety:

1. That the injection would stay at the injection site.
2. That they were inherently labile and would degrade within minutes.

Both these claims have been discredited since by virtue of spike-coding mRNA and the spike protein itself being found in organs and tissues far off from the injection site with an average persistence of 105 days in patients suffering from post-vaccination pathologies.¹ That is the average. The upper bound for persistence is unclear and probably depends on multiple physiological factors.

As teased above, spike protein itself is pathogenic. This is probably part of the reason why the COVID-19 vaccine has much higher occurrence of adverse effects compared to other vaccines, including having been involved in the killing of patients.^1–3

So, in this article, we'll look at exactly how spike protein harms patients, its significance to cancer and other chronic ailments, and then what therapeutic approaches we have available to support its clearance from the body to reinstate full patient health.

This article will mostly be interesting to healthcare practitioners and patients suffering acutely from long-COVID, post-vaccination injury, or latent infections with SARS-CoV-2.

How Spike Protein Harms Patients

This section will be a bit technical, but we'll go over the most important things from this section, when discussing the significance of spike-protein pathology for cancer and other chronic ailments.

Spike protein causes harm in multiple organ systems and in multiple ways.³ Spike protein lowers blood-brain barrier function, which can lead to central nervous system inflammation and following neuropsychiatric symptoms. It interacts with receptors used in immune signalling in a way, that promotes immune senescence under prolonged activation. It interacts with receptors used in controlling blood clotting, which can lead to thrombosis, haemolytic anaemia, myocarditis, and pericarditis. It interacts with an oestrogen receptor, which can cause menstrual abnormalities. It can lead to mitochondrial damage and thus metabolic dysregulation. It down-regulates the function of certain neural transmitter receptors, which makes motor and autonomous nervous signalling more difficult. And lastly, it's indicated to inhibit certain tumour suppressor genes, who's task it is to keep cell integrity under surveillance and terminate the cell, should cell integrity fall below a critical threshold.

Inhibition of tumour suppressor genes, engendering immune senescence, and metabolic dysregulation are probably the most significant to cancer development and treatment, but also for other ailments it becomes essential to support clearance of spike protein, as to free the body from long-term negative effects from SARS-CoV-2 infection and the catastrophically subpar mRNA-based anti-SARS-CoV-2 vaccines.

Its Significance in Cancer and Other Chronic Ailments

This section will be subdivided by mechanism of spike-protein pathology.

Changes to Blood-Clotting and Formation of Protein Aggregates

Changes in blood clotting can lead to thrombosis, which can block small blood vessels and capillaries. If such blood clots aren't efficiently removed, they lead to hypoxia (oxygen starvation). During low-grade hypoxia, mitochondrial function is boosted to improve aerobic metabolism despite dearth of oxygen, but if hypoxia continues to worsen mitochondrial function becomes largely suspended, and the cell either switches to fermentation for energy generation or dies.⁴

The waste product of our fermentation is acidic and in environments, where waste product clearance is compromised – such as in our thrombosis-compromised tissue –, this acidity builds up, leading to enhanced genomic instability of affected cells and the inactivation of incident immune cells, trying to clean up debris from dead cells.^5–9 This in turn gives us a highly cancer-promoting environment.

Such thrombotic plaques can of course also directly cause embolism in all organs, should they tear free from their site of creation and travel in the blood.¹⁰ Pulmonary embolism seems to be the most clinically relevant in patient mortality from spike protein, whether delivered by infection or vaccination, as spike protein alone suffices in the initiation of thrombosis.^10–11 Spike protein has also been found to indirectly (via fibrin) drive neuroinflammation, innate immune activation in the brain, and death of neurons independently of infection.¹²

Spike Protein–Induced Mitochondrial Damage

Spike protein also induces mitochondrial damage via a pathway independent from the above thrombotic-hypoxic pathway.¹ The mechanism by which spike protein does so has multiple prongs.

Spike protein directly damages mitochondria, lowering their metabolic rate and increasing the generation of reactive oxygen species – a highly reactive and toxic metabolic byproduct.¹ It also inhibits the pathway, by which such damaged mitochondria are normally destroyed and their materials recycled to form new mitochondria – a process known as mitophagy. Interestingly, this characteristic of spike protein of inhibiting mitophagy is at least partially counteracted by another protein encoded in the whole SARS-CoV-2 genome, which actually stimulates mitophagy.

Thus, whilst the problem of inducing mitochondrial damage isn't exclusive to the vaccines, the problem of sustained mitochondrial and thus metabolic dysfunction is especially bad in the mRNA vaccines and less prevalent in whole-virus infections.

Chronic mitochondrial dysfunction is heavily involved in the development and progression of cancer.^13–14 It's also implicated in insulin resistance and chronic inflammation.^15–17 Insulin resistance itself is a risk factor in type-2 diabetes, hypertension, cardiovascular disease, neuropathy, nephropathy, and retinopathy. The negative effects of chronic inflammation, we'll discuss in the next subsection, as spike protein also directly drives chronic-inflammatory immune senescence as well as other chronic-inflammatory complications.

Chronic-Inflammatory Immune senescence

Spike protein specifically interacts with the toll-like receptors 2 and 4 (TLR-2, -4). These receptors have important and versatile functions within the immune system.¹⁸ One of the downstream effects of TLR induction on dendritic cells (a type of immune response–directing cell) is the expression of interleukin 1, interleukin 6 (IL-6), and tumour necrosis factor alpha (TNF-a). Whilst this signalling profile is initially helpful for mounting an immune response, the chronic expression of IL-6 is immunosuppressive.

In fact, chronic IL-6 expression is used by mesotheliomata and many other cancers to induce immune senescence and thus enables them to evade immune destruction.^19–20 What's more, the precise expression profile of IL-6 and TNF-a is exhibited by senescent immune cells in the microenvironment of immune evasive lung cancers.²¹

This is disastrous for our mounting an effective anti-cancer immune response, but this also has implications in other chronic-inflammatory diseases. For example, it's logical that this immunosuppressive signalling enables persistent infection of the tonsil.²² Such persistent infection can lead to chronic tonsillar complications, so much so, that in one study 1 in 4 patients put through tonsillectomy have such persistent spike-protein to thank for their complications. It seems likely, that prolonged exposure to spike protein from vaccinations can indeed have the opposite effect of what we would expect from a vaccine. Catastrophically, this is precisely what we see in patients. Spike protein from SARS-CoV-2 vaccinations are actually suppressive to innate immune system function.²³

Such suppressed innate immune function isn't just bad for mounting an effective anticancer immune response, but for mounting any effective immune response, for the innate immune system is required to properly activate and co-stimulate the adaptive immune system, which in turn offers much more specialised immune cells to neutralise free viruses and destroy both infected and defective cells.²⁴ This would in turn be beneficial to cancer and pathogens, and thus detrimental to the patients.

Naturally, the question arises about what we can do against this.

Therapeutic Approaches to Counteract Persistent Spike Protein

There are multiple things we can do to stop the negative effects of persistent spike protein. The most obvious is that we can clear the spike protein from our body. Now, this itself can be done directly – by the administration of certain enzymes, which de-aggregate and digest spike protein – or indirectly – by improving autophagy. Clearance of spike protein may take time, so other actions could be made to counteract immunosuppressive signalling and reinstate proper anti-pathogenic and anticancer immune function.

So, how would we do that?

Direct Clearance through Pharmaceutical Intervention

The soy fermentation–derived enzyme nattokinase can be acquired as a "soft pharmaceutical" (i.e. one not requiring doctoral oversight). Nattokinase is thrombolytic (dissolves blood clots), fibrinolytic (dissolves the protein, by which blood clots and spike proteins are aggregated), and digests both free and membrane-bound spike protein.¹

It's unclear, whether nattokinase can efficiently cross the cellular membrane and unfold its spike-proteinolytic activity in the intracellular space. Computer simulations give it a high likelihood, but computer simulations of biological systems are flawed and inaccurate.

Nonetheless, nattokinase can effectively lower circulating spike protein, which would already counteract a lot of the negative effects of spike protein. Loss of free spike protein would normalise thrombotic signalling – which would in turn lower pro-inflammatory signalling –, reduce immunosuppressive signalling, lower the risk for embolisms and thrombotic hypoxia, improve blood-brain barrier function, and decrease oestrogen-disruptive signalling.

That's already a good start to solving our problem. The application of nattokinase isn't without risk, however. As nattokinase is a thrombo- and fibrinolytic, it hampers with the natural formation of blood clots, which can lead to nose bleeds, the formation of haematoma, longer bleeding from wounds, and inner bleeding in more extreme overdoses.

DO NOT EXCEED THE DOSE RECOMMENDED BY THE MANUFACTURER.

For effective therapy, we need to tap into the positive effects of nattokinase without exposing the patient to untenable adverse effects. The logic here is, that we don't want to thin the blood, but only counteract the blood-thickening signalling of spike protein. To ensure intracellular clearance of spike protein we luckily have other tools at our disposal.

Indirect Clearance through Boosting Autophagy

Beyond using nattokinase, we can also clear spike protein via autophagy. Autophagy is a natural cellular process, where cellular or foreign components are degraded. We can increase autophagy by various means, though it's probably recommendable to use all means at once, because – as mentioned above – spike protein hampers with autophagy.

Dietary Adaptations and Fasting

The primary and simplest way, in which we can boost autophagy is by adapting our dietary lifestyle. Autophagy is induced in some tissues during ketosis. Ketosis can be achieved either by eating a diet high in fat, low in carbohydrates, and moderate in protein or by fasting for extended periods.^25–26 How to do the former is extensively discussed in our Mosaic Method Guide.²⁷

The benefit of using fasting in addition to or above normal ketogenic nutrition – which in itself is healthy and does induce autophagy – is, that fasting seems to more robustly induce autophagy in a less tissue-dependent way.²⁸ Whilst ketosis alone does induce autophagy, it does lack the full pro-autophagic signal tone exhibited by fasting. Ketosis alone, for example, doesn't stimulate the pro-autophagic signal induced by amino acid or growth factor deprivation.^29–32 This supports fasting as a more intense stimulant of autophagy across all tissues.

Fasting for extended periods is superior to shorter fasting in inducing autophagy and induction is more significant at 48 hours over 24 hours of fasting.³³ One study in humans showed significant changes in the expression of two genes involved in autophagy with a time-restricted feeding pattern, where food intake was allowed for 6 continuous hours and disallowed for a following continuous 18 hours.³⁴ It's not entirely clear how robustly such a time-restricted feeding regimen induces autophagy compared to an intermittent fasting regimen with longer fasting times. Given the fact, that autophagic induction still rises from the 24- to 48-hour mark of continuous fasting, it's probably superior to employ the longer fasting regimen. Nonetheless, one study in mice found, that given the same daily caloric intake, mice were generally healthier, when feeding was restricted to two short windows, with complete food deprivation between feedings.³⁵ It thus seems to be wisest to combine the approaches of time-restricted eating with intermittent fasts one to four times every two weeks.

The most simple way of employing an extended fast to induce autophagy is probably to leave out a whole day of eating and skip breakfast on the following day. Given a latest food intake on day 0 at 2000 h, and a earliest food intake at 1200 h on day 2, this would give us a fasting window of 40 hours, thus solidly putting us into robust autophagic induction.

Autophagy-Stimulating Pharmaceuticals

We can also use pharmaceutical compounds to stimulate autophagy. One of the most powerful such autophagic stimulants is resveratrol, which is found in grape seeds and their extracts, but there are also other stimulants.³⁶ Many of the pharmaceuticals we use for cancer care are used because – amongst many other benefits – they stimulate autophagy. Such other autophagic stimulants are EGCG, curcumin, and astaxanthin, as well as extracts from Ganoderma lucidum and Cordyceps sinensis.^35,37–40 You can find dosage information on the former three in our Mosaic Method Guide and for the latter two in their respective posts.^27,41–42

For resveratrol, dosing shouldn't exceed 450 mg/d as this has been found to be safe via preclinical validation. In controlled environments, up to 5 g/d of trans-resveratrol have been used for 28 days, so staying below 450 mg/d should ensure safety.⁴³ Effect should be ensured at 300 mg/d, though results are varied.⁴⁴ For this reason a combinatory approach using all the herein recommended therapeutic interventions is probably most helpful in clearing spike protein efficiently.

Clearance of Chronic Inflammation and Latent Infections

As mentioned above mitochondria are involved in the perpetuation of inflammation and form a kind of vicious cycle, where prolonged inflammation will damage mitochondria and damaged mitochondria will prolong inflammation, eventually chronicising it.¹⁶ In such vicious cycles, it's obviously smartest to counteract all nodes of the cycle. So, in our given vicious cycle, we'd want to reconstitute mitochondrial health and function, as well as resolve chronic inflammation.

Reconstitution of Mitochondria

Energy metabolism in our cells can be divided into two principle modes: aerobic – which uses oxygen – and anaerobic – which does not.^45–46 Aerobic energy metabolism can only be performed within mitochondria. If we can enforce aerobic energy metabolism, we can thus force greater reliance on mitochondria and thus create a necessity for our cells' improving mitochondrial function.

There are principally two things we can do to promote aerobic energy metabolism. We can reduce the availability of fuels, which can be metabolised anaerobically (aka "fermentation"), and we can increase the availability of fuels, which can only be metabolised aerobically (aka "respiration"). Fuels, which can be fermented, are sugar and glutamate, and fuels, which can only be respired, are fats and ketones. To improve aerobic fuel availability and minimise anaerobic fuel availability, we thus want to change dietary patterns as to exclude or minimise carbohydrates and glutamate and maximise fat. This is commonly called a ketogenic diet and is already helpful in improving autophagy. In fact, there's emerging evidence, that patients undergoing androgen deprivation therapy (ADT) – a therapeutic invention, which slakes testosterone – as treatment for prostate cancer have improved energy, less fatigue, and improve metabolic function on ketogenic diets, despite ADT being damaging to mitochondrial health and function.^47–48

There is, however, more we can do for mitochondrial reconstitution.

Over their lifetimes, mitochondria take significant damage from metabolic byproducts produced during respiration. Like internal combustion engines, mitochondria can't go on forever. In internal combustion engines, we perform oil changes, gasket changes, and other repairs as the engine ages to stop it from breaking down from accruing damage. But even that will eventually not be enough, and the engine breaks down finally. Mitochondria are similar. They will constantly repair themselves and regenerate, they will fuse with one another, to improve function by balancing out the damaged components of the pre-fusion parts.^49–50 But eventually, even that won't be enough, and the damaged components need to be sequestered, destroyed, and their materials recycled for the cell to continue having functional mitochondria.⁵¹

This process of recycling damaged components is known as mitophagy. Mitophagy is the specific autophagy of mitochondria – hence the name. Mitophagy turnover is controlled by various signalling pathways, but limited by general autophagic flux.^29,52 Thus, increasing autophagic flux improves mitophagy. Autophagic flux can be – as discussed above – be induced via ketosis, fasting, and various pharmaceuticals.

It's not entirely clear how long mitochondrial reconstitution takes. It can thus be helpful to administer methylene blue in the short term to aid with mitochondrial respiratory capacity until they can be fully reconstituted. I've written at length about methylene blue, and about why it seems ill-advised to use it in the long run, but short-term therapeutic administration seems to be what it excels at.⁵³

Lastly, of course, proper nourishment with those essential nutrients mitochondria require is needed to endeavour proper reconstitution of mitochondrial function. Quite a lot of nutrients are used by the mitochondria and required for their function – namely these are iron, copper, zinc magnesium, selenium, calcium, most B-vitamins, as well as vitamins C, D₃, and E, as well as sulfur.^54–56 There are furthermore other so-called cofactors, which mitochondria require and which are produced by cells, but that can also be supplemented, such as coenzyme Q10 and L-carnitine.

Lastly, to help our mitochondria reconstitute and remain healthy over the long term, we must resolve chronic inflammation.

Resolving Chronic Inflammation

Chronic inflammation – as mentioned above, especially of the type engendered by spike protein – is highly immunosuppressive. So clearing this specific chronic inflammation has double benefit: we improve the longevity of our mitochondrial health and we improve the activity of our immune system in its destruction of infected or otherwise compromised cells, thus being able to clear the effects of long-COVID and vaccine injuries.^20,57

Principally, there are some nutrients we simply need in order for our body to even be able to clear inflammation and properly modulate the response of the immune system. Vitamins A and D₃, as well as omega-3 fatty acids are essential to this.^58–59 Without them, our body simply can't clear inflammation and properly modulate the immune system. A bonus to omega-3 is, that it can be used for anti-thrombotic signalling by the body.⁶⁰ An added benefit of vitamins A and D₃ is that they are involved in both positive and negative immune modulation, and thus allow for the immune system to adapt rapidly and precisely to changing requirements and stresses, thus acting more the scalpel than the brute's balled fist. It's obvious, why such a precise response would be beneficial in clearing latent infections, but there's more we can do.

As mentioned above, our chronic inflammation is specifically mediated by IL-6. Luckily for us, there exist fungal and plant extracts and compounds, which inhibit IL-6 signalling, which perhaps doesn't clear IL-6, but ameliorates it's effects, thus allowing our immune system to escape its suppressive signalling. Examples of such are extracts from Ganoderma lucidum, of which I have written at length priorly, and capsaicin from chilli fruits and seeds.^41,61

Thus modulating our immune response should allow us to eventually clear both the chronic inflammation – also by helping our reconstituted mitochondria – and the latent infections present. And as mentioned above, the very autophagy we induce to reconstitute mitochondria also directly sequesters and destroys cell-internal spike protein.

Closing Remarks

This has been a gargantuan article.

I apologise for the technical depth, but I hope I've been able to lay out the complex intricacies simply enough as to make them understandable. Nonetheless, I want to use these closing remarks to briefly summarise if not the effect of persistent spike protein, then at least the methods we can use to clear it, so that you have a condensed reference here.

We can clear spike protein by three principle methods:

1. Direct digestion through externally supplemented enzymes.
   • Administration of nattokinase from fermented soy. Caution to be taken due to fibrinolytic and thrombolytic properties.
2. Indirect digestion through induction of autophagy.
   • Mild induction through time-restricted eating (4–8 hours eating, 16–20 fasting).
   • Strong induction through intermittent fasting (8–12 hours eating, 36–40 hours fasting).
3. Immune destruction of compromised cells, for which we need:
   • Resolution of immunosuppressive chronic inflammation, for which we need:
     • Provision of vitamins A and D₃, as well as omega-3 fatty acids.
   • Reconstitution of mitochondrial health, for which we need:
     • Improving availability of aerobic fuels (fats, ketones).
     • Lowering availability of anaerobic fuels (carbohydrates, glutamate).
     • Induction of mitophagy.
     • Provision of B-vitamins, as well as vitamins C, D₃, and E, calcium iron, copper, selenium, zinc, manganese, magnesium, and sulfur.
     • Potential supplementation of coenzyme Q10, L-carnitine, taurine, and pyrroloquinoline quinone.
     • Potential short-term administration of methylene blue.

It's difficult to know, whether this list is complete, as it's inferred from disparate clinical data, mechanistic evidence, and cell-biological and immunological knowledge, but I trust that this should help a vast swath of patients suffering from spike-protein pathologies incurred as a result of the virus or the vaccines meant to protect against the virus.

As such I hope this helps. Should questions arise, don't hesitate to comment or reach out.

And should you want help with implementing all of this into your life alongside the rest of the Mosaic Method to help your body fight cancer and win, don't hesitate to reach out at marchward.com/outlive.

Swift healing and lasting health to you,
Merlin L. Marquard.

On the Impact of Persistent Spike Protein Pathology on Cancer and Its Allevation

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