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Methylene Blue Trial

Updated: Feb 27, 2023

Help us and help others by helping yourself!

 

We are offering methylene blue treatment as part of a trial to determine the efficacy of this treatment, particularly against pathogens. It appears to be a "do no harm" treatment, as about 50 people in our program are currently using this approach - including myself.


To date, only one person has had an adverse reaction, and he is fine today. Importantly, this person is the only one taking methylene blue who got the jabs. Methylene blue is reported to deactivate the jab. We believe this "Herxheimer's Reaction" is not a coincidence. However, proving it destroyed the spike protein is not easily accomplished.


In the next blog, I will present the "offer" to be involved in our trial.


What follows is content on methylene blue from various sources.


Section 1: Thomas Levy, MD, JD: Resolving Colds to Advanced COVID with Methylene Blue

Section 2: Francisco Gonzalez-Lima, Ph.D.: Health Benefits of Methylene Blue

Section 3: Dr. Todd Maderis: Methylene Blue for Lyme Disease and Bartonella

Section 4: Thomas Levy, MD, JD: Myocarditis: Once Rare, Now Common

Section 5: Methylene Blue and Breast Cancer


To get to a section, do a "find" on "section."

 

Section 1

FOR IMMEDIATE RELEASE Orthomolecular Medicine News Service, Feb 4, 2023

Resolving Colds to Advanced COVID with Methylene Blue

Editorial by Thomas E. Levy, MD, JD Contributing Editor, OMNS

OMNS (Feb 4, 2023) Linus Pauling first coined the word "orthomolecular" in an article he wrote in the journal Science in 1968. Quite simply, ortho means correct or right, and molecular refers to the simplest building block of any substance. Dr. Pauling started the whole concept of orthomolecular medicine by pointing out that the only true way to prevent or treat any medical condition is to restore whatever important natural substances (nutrients, vitamins, minerals) that are depleted. And the corollary of this approach to healthcare is that no patient is sick because they have low levels of any synthesized agents (prescription drugs) that are not found in nature.


As a rule, a pharmaceutical agent impacts some metabolic pathway in such a manner that helps to alleviate a symptom without lessening the pathology causing that symptom to be present. With the rarest of exceptions, pharmaceutical agents reliably allow a disease to continue to evolve while one or more of the associated symptoms are chronically suppressed. However, when deficiencies of important natural substances are corrected, positive clinical results not known to (or acknowledged by) traditional medicine are consistently seen. Clinical improvement following the resolution of such deficiencies typically indicates that the underlying disease is no longer progressing and possibly even reversing. And depending on how chronic the condition was, an eventual return to physiological normalcy might also result.


Probably the most noteworthy of chronically depleted nutrients in a large majority of people around the world is vitamin C. The literature supporting its positive health impact when properly administered is massive and extending over 80 years now. [1] The benefits of vitamin C and many other important orthomolecular substances continue to be suppressed and even belittled in biased and sometimes frankly fraudulent medical articles. The patented drugs that are promoted relentlessly make knowing the benefits of an inexpensive natural remedy difficult for even sincere healthcare practitioners who want the best for their patients.


Such "education" on the "essential" role of pharmaceutical drugs begins in medical and osteopathic schools, and it never stops. Furthermore, without the endorsement of traditional medicine, many healthcare practitioners are reluctant to use such agents even when they are fully aware of the benefits. Also, as evidenced by the past three years of the COVID pandemic, it appears that a majority of pharmaceutical companies, along with too many hospitals and far too many physicians, place profits far ahead of patient welfare. The application of scientifically-based treatment protocols, many based on orthomolecular principles, continues to be ignored and even suppressed.


Methylene blue (MB), a powerful antioxidant with a clinical impact comparable to even vitamin C, is a major exception to the principles of orthomolecular medicine. It is not produced in the body, and it is not naturally present in any animal or plant.

Nevertheless, its documented beneficial health effects rival that of any other known substance, whether normally found in nature or coming out of a laboratory. Just like vitamin C, the true benefits of MB in so many different diseases remain unappreciated and unused by most clinicians, even though it has been safely utilized in many patients for a much longer time than even vitamin C.


The parallels between vitamin C and MB are also reflected in the fact that administering them in either their reduced or oxidized form is comparably beneficial to the patient. This is because the dose of vitamin C or MB is less designed to give a one-time boost to the electron stores of the body than it is to make sure newly-assimilated electrons get optimally distributed throughout the body.


A quality nutrition program is the best source of new (versus recycled) electrons in the body. And the qualities of super antioxidants like vitamin C and MB serve to make sure those electrons are optimally distributed and repeatedly exchanged in redox reactions throughout the body, which is the essence of optimal health.

For those who appreciate metaphors, good nutrition is the product (electron) manufacturing facility, and the premier antioxidants (vitamin C, MB) are the trucks that assure the optimal distribution and delivery of those products throughout the body (country). While it is logical and correct that delivering the antioxidant in its reduced form brings even more electrons into the body, the oxidized form is also highly effective without those extra electrons since it is the distribution and repeated give-and-take of electrons throughout the antioxidant matrix inside the cell that is of greatest therapeutic value. A clear example of this is seen in animal studies where dehydroascorbic acid (DHAA), which is the oxidized form of vitamin C, readily minimizes brain infarct size from induced ischemic stroke, facilitating rapid recovery. In fact, these studies also show that there is a precipitous decline in reduced vitamin C in the ischemic brain which is reversed by the infusion of DHAA. [2]


However, the presence of elevated blood levels of DHAA reported in patients with infectious disease does not mean DHAA is toxic per se. Rather, such elevated levels are just a reflection of increased oxidative stress in such a patient, not the cause of it. [3] Furthermore, any negative impact that DHAA has been reported to have in some in vitro studies does not reliably predict the positive effect that DHAA has in the intact plant, animal, or human, as such test tube studies are not receiving an ongoing new intake of electrons from quality nutrition or sun exposure. [4] Like the ascorbic acid and DHAA forms of vitamin C, the powerful clinical impact of MB appears equal whether administered in its oxidized (methylene blue) or reduced (leucomethylene blue) forms.


Methylene Blue (MB): A Brief History


Methylene blue (MB) is the first drug to be tested and used in humans. Chemically known as methylthioninium chloride, it was first synthesized in 1876, and it was used as an industrial dye. It was later found to be an excellent dye for staining microbes and human tissues as well. In 1891 it was found to be very effective as an anti-malarial agent by Paul Ehrlich. Of note, Ehrlich first coined the term "magic bullet" to refer to how effectively MB targeted and accessed the nervous system. [5] It has since been established to have a selective affinity for the nervous system, although it is highly effective in reaching all cells in the body.


As a powerful antioxidant with the ability to target the brain, MB was used as an antipsychotic drug for 50 years before phenothiazine became the first "official" antipsychotic drug. [6] It continues to be used as a dye for the staining of biological tissue specimens as well as a diagnostic tool in surgical procedures. [7] It has also been established to have numerous and very significant therapeutic purposes for a wide range of medical conditions. Some of the more significant conditions to be consistently and successfully treated by MB include the following:

  • Infections, from minimal to life-threatening, including those having progressed to septic shock. Also, acute respiratory distress syndrome (ARDS) and hypoxemia secondary to COVID or any of multiple different pathogens [8,9]; also used for disinfection of plasma to be used for transfusion [10-12]

  • Mitochondrial dysfunction [13-15]

  • Depression, dementia, psychosis, impaired memory, as well as multiple acute and chronic neurological conditions [16]

  • Methemoglobinemia, in which the oxygen-carrying capacity of the blood is critically depleted. [17] MB has FDA approval as a first-line therapy for this condition. [18,19]

Antioxidant Extraordinaire


An ideal antioxidant is one that is equally stable chemically in either its reduced or oxidized state, while having physical access to all the oxidized biomolecules in the body. Such a quality allows the continued giving and taking of electrons throughout the cellular and extracellular spaces, as that molecule does not resist being either reduced or oxidized. This redox (reduction-oxidation) property helps to conduct electron flow inside the cells. This helps to generate and sustain the microcurrents (a current is literally an electron flow) that have been identified inside cells, which work to maintain healthy transmembrane voltages. A sick cell always has a low transmembrane voltage, which directly reflects a redox balance skewed toward oxidation, with a limited influx of new antioxidant (nutrient) molecules available to deal with any new pro-oxidant (toxic) molecules. Normal transmembrane voltages are critical in maintaining healthy ion channels, transporters, pumps, and enzymes in the cell. [20] They are also critical for the optimal synthesis of ATP. [21]


A toxin always works to cause oxidation wherever it is found, or ends up. It is always pro-oxidant in its chemical impact, as it seeks to oxidize a biomolecule and then keep the electron it has "robbed." The electron it acquires makes the toxin much more stable chemically, and such a reduced toxin will not give up the electron again to another oxidized, or electron-depleted, biomolecule. This means that the electron-sated toxin will never re-donate its electron to an oxidized biomolecule, as would occur with an electron-sated, or reduced, antioxidant molecule.


In addition to increasing the numbers of oxidized biomolecules, this retention of electrons by toxins also impedes/decreases electron flow (microcurrents) since the newly acquired electrons are tightly held and never again released in the manner of an antioxidant that is continually giving and taking electrons. An antioxidant like vitamin C decreases the total number of oxidized biomolecules and supports optimal microcurrents, and a toxin does the opposite. [22]


It is the antioxidant properties of MB that results in the impressive clinical impact it has on so many conditions. In this regard, there is a striking parallel in what MB can do in the body with what vitamin C can do. Both vitamin C and MB are small molecules, and they effectively reach every cell in the body. However, MB requires no active or passive cell wall transporters as does vitamin C, and it has both lipid-soluble and water-soluble characteristics. Because of this, MB passes easily through lipid-rich cell walls, after which it disseminates throughout the water-based cell. [23,24] Also, while both MB and vitamin C access the brain, MB has been found to have a brain concentration up to tenfold higher than in the serum as quickly as one hour after intravenous administration. [25] Uptake is very rapid in the other organs as well. [26]


MB also has well-documented antitoxin properties like vitamin C, but the studies documenting them are much less prolific than those showing the similar effects of vitamin C on pro-oxidants and other poisons. MB helps protect the kidneys against the toxicity of the chemotherapeutic agent, cisplatin. [27] MB has also been shown to protect the brain against the toxicity of another chemotherapeutic agent, ifosfamide. [28,29] It also was shown to effectively treat the encephalopathy induced by ifosfamide after it had developed. And even though there is not an abundance of articles demonstrating the ability of MB to neutralize toxins and repair toxic damage, multiple researchers recommend it be routinely available as an emergency antidote for general use. [30,31]


Many toxins also inflict harm in some individuals by the formation of methemoglobin with a reduction of oxygen delivery to the tissues. Such toxin excesses or poisonings can be effectively treated with MB, as it is already the treatment of choice by many clinicians for methemoglobinemia. MB is always a good partner to be administered along with vitamin C for any toxin excess or overdose. [32,33] The addition of magnesium with MB and vitamin C to overdose patients offers additional protection against the development of fatal arrhythmias that can occur before the MB and vitamin C can resolve and block further toxic impact. [34]


Ideal Shock Therapy


Methylene blue is exceptionally beneficial for both infections in general and for hypotensive shock. This makes it a particularly optimal therapy for the very common cause of intensive care unit death around the planet: septic shock.

Refractory septic shock, a state of disseminated infection with vascular collapse and hypotension often unresponsive to all traditional measures, consistently responds positively to MB therapy, sometimes saving the patient from otherwise certain death.


As with vitamin C and many other non-traditional treatments, nearly all clinicians simply will not take the "leap" from clear-cut positive results in the literature to the application of those results in their patients. At best, they use these non-traditional therapies almost like a final gesture that they have done everything possible to save the patient, even though those therapies have little to no toxicity and should not be relegated to the last option in a treatment protocol. And, of course, this only applies to the clinicians who are even remotely aware of the existence of the data showing how effective and nontoxic these non-traditional therapies are. The many pearls in the medical literature remain completely unharvested by most clinicians. And many more clinicians are very diligent in doing everything possible to maintain the "mainstream status quo" to the point of ignoring and even suppressing anything that might threaten it.


An experienced and honest clinician will tell you that just one dramatic case report that is accurately reported has enormous value. When a patient is on the verge of death despite all that has been done, and one single intervention quickly stops the clinical deterioration and starts a clear recovery, the alert clinician does not need a large prospective, double-blind, and placebo-controlled clinical trial to take such a clinical response seriously. Such a trial would be unethical when the placebo group is not being given the benefit of some inexpensive, nontoxic, and highly effective agent. Especially in the setting of an advanced and rapidly progressing infection with unresponsive shock secondary to sepsis, seeing the patient normalizing only a short time after a treatment is administered compels serious attention.


A clear example of such a case report was reported on a 38-year-old male patient who presented with bilateral pneumonia that subsequently worsened and resulted in bacteria (Klebsiella pneumonia) being released into the bloodstream (septicemia). Lethargic with low blood oxygen when admitted to the hospital, he was given IV fluids with insulin and antibiotics. The oxygen levels continue to decline with increased difficulty breathing, and he was then intubated and supported on a ventilator. Hypotension requiring vasopressor infusion ensued. Broader antibiotic coverage was added. Metabolic acidosis with declining renal function followed, and a few hours later he had a cardiac arrest. Four hours after regaining a heart rhythm and only 25 hours after initial presentation, extracorporeal membrane oxygenation (ECMO) support was started. Nevertheless, critically low blood pressure unresponsive to multiple vasopressors continued.


At this point in time, a 172 mg IV bolus of MB was administered, and an infusion of MB at 0.51 mg/kg/hour was maintained for the next 10 hours. Blood pressure quickly improved and vasopressor support could be decreased. At the conclusion of the infusion, the clinical status stabilized for another 22 hours, but fever with a dropping blood pressure unresponsive to combinations of vasopressors at the highest doses returned. The MB infusion was restarted and blood pressure again responded promptly. This time the infusion was continued for 54 hours, and about seven days after this longer infusion was completed the patient was fully recovered and discharged from the hospital. [35] Another impressive case report on a clinically similar patient showed that MB had to be continually infused for a full 120 hours to prevent repeated clinical relapses, after which the patient stabilized and was eventually discharged. [36]


These case studies, in which the patients effectively serve as their own controls, showed clear improvement on MB when severely ill, clear deterioration back to a life-threatening point after MB discontinuation, and prompt improvement with complete clinical resolution when the MB was restarted and continued for a long enough period. No sincere and competent clinician giving his/her highest priority to patient welfare would ignore the importance of such a clinical response when treating similar patients in the future. And this is especially the case when it is realized that MB, dosed appropriately, has an impeccable safety profile, just like vitamin C. Also, like vitamin C, MB also enhances antibody production in the body. [37] This begs the question: Why not use MB first in such situations, rather than last, or never?


Multiple studies have demonstrated the benefits of MB in stabilizing and even resolving septic shock, which is the worst stage that any infection can reach before the inevitable progression to death. No reports of MB worsening the overall clinical status of septic patients could be found. The studies consistently show that MB always improves hypotension when appropriately administered. Furthermore, it has been shown that MB improves survival in shock of all causes (vasodilatory shock), including the shock of advanced sepsis. [38]


The refractory hypotension in septic shock is consistently seen in the setting of excessive nitric oxide production, which causes too great a decrease in vascular tone. [39] MB promptly counteracts this in restoring normal blood pressure. [40] Furthermore, over 120 years of MB use has clearly established the lack of significant toxicity. Toxic levels exist, as with nearly every other agent (including water), but the amounts needed are far beyond the recommended dosing in established treatment protocols. [41-43]

An open-minded clinician reviewing the literature for the first time to learn about the best treatment for septic shock would certainly utilize methylene blue as a first-line agent. Even low doses of MB and one-time boluses of MB consistently show clear benefit in septic shock.


However, the clinical response is much better and consistently achieved with a properly-dosed continuous infusion. [44,45] Septic shock still claims a lot of lives regardless of the therapy, and some clinical studies add MB seemingly as a last-ditch afterthought, after which MB is then reported to be ineffective for improving survival. And even now, some of the most recent clinical research continues to assert that "more studies are needed" on the impact of MB in septic shock, even though the very positive research on MB and septic shock now spans decades. [46-55] MB infusions in hypotensive neonates have also been shown to increase blood pressures rapidly and safely. [56-58]


The impact of MB on septic shock was addressed above in some detail since a patient cannot really be much sicker than having severe hypotension with massive infection and enormously increased oxidative stress throughout the body. However, it is important to realize that MB has also been shown to be very effective in treating different types of hypotensive shock that are unrelated to advanced degrees of infection. [59] Shock with unresponsive hypotension secondary to the ingestion of multiple drugs has responded rapidly to MB infusions, allowing the weaning of other vasopressor agents. [60,61] Shock secondary to anaphylaxis also responds well to MB. [62]


One patient with profound refractory hypotensive shock following a dihydropyridine calcium channel blocker overdose only responded positively to MB infusion and was eventually discharged. Prior to the MB infusion, no improvement in blood pressure was seen with saline infusion, several doses of calcium gluconate, glucagon, various vasopressor agents, and even high-dose insulin euglycemic therapy over a period of several hours. [63] Another type of hypotensive shock, cardiac vasoplegia, is also sometimes seen following cardiac surgery. This is effectively treated by methylene blue as well. [64-66]


All forms of hypotensive shock should be treated with MB, and it should be part of the treatment protocol at the outset. It should not just be held back as a last-ditch intervention to save the patient. [67]


Regarding ARDS secondary to COVID, a massive production of pro-inflammatory agents known as a cytokine storm typically precedes imminent death if not effectively terminated and neutralized. [68,69] MB has been uniquely shown to inhibit the production of all three of the major classes of pro-oxidants involved in the cytokine storm clinical picture (reactive oxygen species [ROS], reactive nitrogen species [RNS], and cytokines). [70-72] And as a potent antioxidant, MB is highly effective in neutralizing the wide array of pro-oxidants that have already been produced in the ARDS lungs.


MB also combines well with other antioxidants in providing clinical benefit. MB combined with vitamin C and N-acetyl cysteine was very effective in treating advanced COVID. [73]


Furthermore, patients who were severely ill with COVID but showing a steady clinical recovery still greatly benefit from MB. Very many "recovered" COVID patients have significant neurocognitive problems that are lessened or even blocked with adequate dosing of MB. With the known antioxidant properties of MB along with its predilection for targeting increased oxidative stress in the nervous system, it should be part of any COVID treatment, regardless of how well the infection is responding to other therapies. [74,75]


MB, Pathogens, and Photodynamic Therapy (PDT)


Logically, considering its documented impact on advanced septic shock, MB has also been shown to readily kill and/or neutralize a wide range of pathogens. While it can achieve this as a monotherapy, it is enhanced in effectiveness when accompanied by photodynamic therapy (PDT). A protocol using MB with PDT has even been shown to eliminate intracellular pathogens such as prions from the blood. [76] Another MB/PDT approach has shown rapid resolution of moderate to severe COVID in patients who did not require hospitalization. [77]MB has been shown to directly inhibit the initial binding of the COVID spike protein with the ACE2 receptor, a step necessary for the virus to enter the cell. [78-80]


MB and PDT have similar abilities to enhance mitochondrial function.

They both effectively bypass much of the Krebs cycle, producing normal amounts of ATP while generating less oxidative stress in the process of going through the entire cycle. [81] This can result in a complete clinical recovery from mitochondrial dysfunction syndromes.


ATP is produced in the mitochondria due to the shuttling of electrons through the four sequential complexes of the electron transport chain. The fourth complex transfers the electrons to the terminal electron acceptor, oxygen, ultimately resulting in ATP production. MB receives the electrons from the first complex and then directly passes those electrons on to cytochrome c in the fourth complex, bypassing the other complexes. [82] PDT with the photons from near-infrared light also energizes and enables the ability of cytochrome c to donate electrons to oxygen and result in the production of ATP. [83,84]


This bypassing of the earlier complexes of the electron transport chain lowers the production of reactive oxygen species (ROS) that would have been generated by those complexes, decreasing net oxidative stress in the cell. Yet, ATP production continues as though the entire electron transport chain was functioning normally. Less ROS production (mitochondrial oxidative stress) while achieving normal energy production goals is always a desirable, but rarely achieved therapeutic goal, and MB accomplishes this. [85,86] Because of these effects, MB has been promoted as an anti-aging drug. [87] In cultured fibroblasts, MB clearly extends the life span of these cells. [88]


When the mitochondria can be made more efficient in producing energy, every metabolic process in the body is positively impacted. Any of the mitochondrial dysfunction conditions can benefit from MB and PDT, but especially MB due to its antioxidant nature and its ability to be taken regularly in a supplemental fashion without the need to spend time receiving various applications of light therapy. Furthermore, the actions of MB or PDT can also serve to help restore to normal an electron transport chain that had accumulated too much oxidative damage to function with normal efficiency (mitochondrial dysfunction) by decreasing the pro-oxidants (ROS) normally generated in the process of making ATP. [89]


However, there is no need to enhance every MB treatment with PDT to get optimal benefit if the MB is properly-dosed. MB has been shown to inactivate a very large number of viruses and other pathogens in vitro, with and without PDT. [90-96] MB is especially well-suited to dealing with viral infections, as it works

  • directly against the virus, and

  • prevents virus entry into cells, and

  • inhibits viral replication after entry into the cell. [97]

As might be expected, the ability of MB to resolve viral infections indicates its likely positive impact in preventing viral infections as well. During the first wave of COVID-19 infections in France, it was reported that a cohort of 2,500 end-stage cancer patients being treated with a protocol that included 75 mg of MB three times daily had NO reported cases of influenza or COVID. [98]


There is significant research into methylene blue derivatives, which are also highly effective antiviral agents, including against viruses in the smallpox family. [99] Similarly, as MB is of clear-cut benefit in the treatment of depression, MB derivatives are being evaluated for the treatment of depression and neurological disorders. [100] Undoubtedly, the pharmaceutical industry recognizes the incredible abilities of MB, and much effort is going into finding related and effective agents that can be patented in order to generate astronomical profits.


MB and Cancer


On the PubMed website, the entry "cancer methylene blue" results in about 2,500 references. The articles that appear address primarily the role of MB in:

  • Localizing (staining) of cancerous tissues and/or identifying as many involved lymph nodes as possible [101-105]

  • The inhibition, inactivation, or killing of a wide array of different cancer cells in vitro, with and without the application of PDT [106-113]

  • The superiority of MB in treating tumors in mice over traditional chemotherapy [114]

  • In combination with PDT, the complete resolution of AIDS-related Kaposi's sarcoma skin lesions that had been unresponsive to chemotherapy with MB and toluidine blue [115]

  • The direct treatment of cancer in dogs [116]

  • The direct treatment of cancer in humans (only one article). While treating different types of cancer, the author asserted that MB reliably stopped pain secondary to cancer, improved general health, and added years of longevity. This was reported in 1907! [117]Another article asserted that MB was found to have anticancer effects over a century ago. [118] Of note, NO significant clinical applications of methylene blue on cancer patients were found other than the 1907 study cited above.

The efficacy of an inexpensive and safe agent like MB in many different and even advanced medical conditions make it an ideal general add-on or even stand-alone treatment most of the time. Furthermore, its potent anti-cancer effects in vitro make it especially puzzling why straightforward clinical studies on cancer patients with MB alone or in combination with other agents have not been reported. Even the positive effects of the much-ignored vitamin C on cancer patients have been published in many articles, yet the wonderful properties of MB have been known much longer now than vitamin C. The literature even suggests that MB could play a positive role in the treatment of cancer patients. [119]


MB: Safety and Dosing


The main side effect of MB is a blue discoloration of the urine. Rarely, some blue discoloration of the skin might be noticed when an extended administration of highly-dosed MB has occurred. Nevertheless, both effects are completely reversible in hours to a few days as the MB is eliminated out of the body. At very high doses of MB, some of the hemoglobin in the blood can be converted into methemoglobin, which is an abnormal state where MB is the treatment of choice when given at a lower dose. Even higher doses can result in greater toxic side effects, although higher doses can still be warranted for some critically ill patients who are not responding to other measures, as in terminal septic shock.


Also, in patients with depression who are on drugs known as serotonin reuptake inhibitors (SSRIs), the addition of MB is not advisable, as some of these patients can develop a potentially life-threatening development known as serotonin syndrome. [120,121] However, MB is an effective anti-depressant by itself at low doses. [122]

Because they are highly effective antioxidants, both MB and vitamin C have been cited to rarely precipitate red blood cell hemolysis in patients with glucose-6-phosphate dehydrogenase (G6PD) deficiency. Nevertheless, closely-monitored administration of these agents in such patients typically avoids such hemolytic problems.


In fact, when the G6PD-deficient patient presents with methemoglobinemia, a condition for which MB is typically the indicated treatment, properly-dosed vitamin C can resolve the condition without using MB. [123,124] Of note, G6PD deficiency resulting in hemolytic anemia from MB is very rare. In African children with malaria, MB therapy was shown to be very safe even when G6PD deficiency was present, as was the case with all 24 deficient children in one study. [125]Another study on 74 healthy but G6PD deficient adult men demonstrated no hemolysis when given MB along with chloroquine. [126]

Generally intravenous dosing is not necessary except for the critically ill patient, as in advanced hypotensive shock.


There is no standard, fixed regimen of MB recommended in such situations. Boluses of 2 mg/kg of MB can be given, often followed by infusions of various duration depending on the clinical status and response of the patient. Such infusions are often in the range of 0.5 mg MB/kg/hour over an extended period, but as much as 4 mg MB/kg can be infused over an hour. An effective infusion spanning 120 hours has been reported. Others report that infusions can range from 0.25 to 2 mg MB/kg/hour. [127,128]


For less critical patients, as well as for outpatients, oral MB dosing can range from 10 mg to 50 mg, and that dosage can be taken from one to three times daily, adjusted up or down in dose size and frequency depending on clinical response. Even higher doses can be comfortably used for limited times. 200 mg daily to stabilize COVID patients that are not yet critically ill is a very reasonable dose. A reasonable regular supplementation dose can range from 5 to 15 mg daily for general good health if there is no targeted symptom or medical condition.


As a practical point regarding regular supplementation, a dose of 5 to 15 mg of 1% MB solution (0.5 to 1.5 milliliters) can be added to a small amount of water. A teaspoon of ascorbic acid powder (not sodium ascorbate) can then be added. After sitting for 15 minutes or less, the solution will completely clear with just a slight residual blue tint. [129] This can then be quickly consumed with little staining of the tongue that readily occurs with the MB solution alone. Regardless, the staining resolves quickly. But without the added ascorbic acid, it is best to just put the MB straight into something like tomato juice and then drink that.


Methylene blue is not a nutrient. While having some important similarities with vitamin C, there are differences, including a narrower tolerance limit and higher risk safety profile. Less than 2 mg/kg MB is generally regarded as safe; over 7 mg/kg is more likely to induce side effects. MB administration is to be done with the guidance of a qualified health care provider.

Recap


Methylene blue (MB) is an antioxidant with high redox activity, able to rapidly "oscillate" between its oxidized and reduced forms, much like that seen in vitamin C. A small molecule with fat- and water-soluble characteristics, it reaches all areas and cells of the body, and it especially concentrates in the brain and central nervous system. Like vitamin C, MB is highly effective in maintaining a healthy distribution of electrons already in the body, along with the distribution of new electrons assimilated from the nutrients in a healthy dietary regimen.


MB has a unique ability among antioxidants and other biomolecules to relay electrons from the first complex in the energy-generating Krebs cycle in the mitochondria directly to the fourth complex. This allows the energized fourth complex to then produce ATP without the additional expenditure of energy in the steps of the electron transport chain that was bypassed. As such, MB allows dysfunctional mitochondria to produce healthy levels of ATP while producing less oxidative stress in the process, an optimal way both heal those mitochondria while promoting healing anywhere in the body. Photodynamic therapy (PDT) can also directly activate the energy production of the fourth complex in the electron transport chain.


Like vitamin C, MB is also a very powerful anti-pathogen It has been documented to salvage even late-stage COVID patients supported on ventilators with hypotension secondary to septic shock. For viruses in general, MB has the unique ability to attack the circulating virus, to block its binding of the virus to the cells of the body, and to stop the proliferation of the virus inside the infected cell. When administered as recommended, MB is exceptionally well-tolerated, with a safety profile that extends now over a period of more than 100 years of clinical use.

(OMNS Contributing Editor Dr. Thomas E. Levy [televymd@yahoo.com] is board certified in internal medicine and cardiology. He is also an attorney, admitted to the bar in Colorado and in the District of Columbia. The views presented in this article are the author's, and not necessarily those of all members of the Orthomolecular Medicine News Service Editorial Review Board. Readers should work in cooperation with their healthcare professional before and during application of this or any other approach to wellness.)

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10. Lozano M, Cid J, Muller T (2013) Plasma treated with methylene blue and light: clinical efficacy and safety profile. Transfusion Medicine Reviews 27:235-240. PMID: https://pubmed.ncbi.nlm.nih.gov/24075476/

11. Babigumira J, Lubinga S, Castro E, Custer B (2018) Cost-utility and budget impact of methylene blue-treated plasma compared to quarantine plasma. Blood Transfusion 16:154-162. PMID: https://pubmed.ncbi.nlm.nih.gov/27893348/

12. Gravemann U, Engelmann M, Kinast V et al. (2022) Hepatitis E virus is effectively inactivated by methylene blue plus light treatment. Transfusion 62:2200-2204. PMID: https://pubmed.ncbi.nlm.nih.gov/36125237/

13. Atamna H, Nguyen A, Schultz C et al. (2008) Methylene blue delays cellular senescence and enhances key mitochondrial biochemical pathways. FASEB Journal 22:703-712. PMID: https://pubmed.ncbi.nlm.nih.gov/17928358/

14. Kuliaviene I, Baniene R, Virketyte S et al. (2016) Methylene blue attenuates mitochondrial dysfunction of rat kidney during experimental acute pancreatitis. Journal of Digestive Diseases 17:186-192. PMID: https://pubmed.ncbi.nlm.nih.gov/26861116/

15. Duicu O, Privistirescu A, Wolf A et al. (2017) Methylene blue improves mitochondrial respiration and decreases oxidative stress in a substrate-dependent manner in diabetic rat hearts. Canadian Journal of Physiology and Pharmacology 95:1376-1382. PMID: https://pubmed.ncbi.nlm.nih.gov/28738167/

16. Rojas J, Bruchey A, Gonzalez-Lima F (2012) Neurometabolic mechanisms for memory enhancement and neuroprotection of methylene blue. Progress in Neurobiology 96:32-45. PMID: https://pubmed.ncbi.nlm.nih.gov/22067440/

17. Mak R, Liebelt E (2021) Methylene blue: an antidote for methemoglobinemia and beyond. Pediatric Emergency Care 37:474-477. PMID: https://pubmed.ncbi.nlm.nih.gov/34463662/

18. Clifton 2nd J, Leikin J (2003) Methylene blue. American Journal of Therapeutics 10:289-291. PMID: https://pubmed.ncbi.nlm.nih.gov/12845393/

19. Jiang Z, Duong T (2016) Methylene blue treatment in experimental ischemic stroke: a mini review. Brain Circulation 2:48-53. PMID: https://pubmed.ncbi.nlm.nih.gov/27042692/

20. Bezanilla F (2008) How membrane proteins sense voltage. Nature Reviews. Molecular Cell Biology 9:323-332. PMID: https://pubmed.ncbi.nlm.nih.gov/18354422/

21. Kaim G, Dimroth P (1999) ATP synthesis by F-type ATP synthase is obligatorily dependent on the transmembrane voltage. The EMBO Journal 18:4118-4127. PMID: https://pubmed.ncbi.nlm.nih.gov/10428951/

22. Levy T (2017) Hidden Epidemic: Silent oral infections cause most heart attacks and breast cancers. Henderson, NV: MedFox Publishing. See Chapter 4. To download free of book (English or Spanish): https://hep21.medfoxpub.com/

23. May J, Qu Z, Cobb C (2004) Reduction and uptake of methylene blue by human erythrocytes. American Journal of Physiology. Cell Physiology 286:C1390-C1398. PMID: https://pubmed.ncbi.nlm.nih.gov/14973146/

24. Bruchey A, Gonzalez-Lima F (2008) Behavioral, physiological and biochemical hermetic responses to the autoxidizable dye methylene blue. American Journal of Pharmacology and Toxicology 3:72-79. PMID: https://pubmed.ncbi.nlm.nih.gov/20463863/

25. Peter C, Hongwan D, Kupfer A, Lauterburg B (2000) Pharmacokinetics and organ distribution of intravenous and oral methylene blue. European Journal of Clinical Pharmacology 56:247-250. PMID: https://pubmed.ncbi.nlm.nih.gov/10952480/

26. DiSanto A, Wagner J (1972) Pharmacokinetics of highly ionized drugs. 3. Methylene blue-blood levels in the dog and tissue levels in the rat following intravenous administration. Journal of Pharmaceutical Sciences 61:1090-1094. PMID: https://pubmed.ncbi.nlm.nih.gov/5044808/

27. Usefzay O, Yari S, Amiri P, Hasanein P (2022) Evaluation of protective effects of methylene blue on cisplatin-induced nephrotoxicity. Biomedicine & Pharmacotherapy 150:113023. PMID: https://pubmed.ncbi.nlm.nih.gov/35483196/

28. Pelgrims J, De Vos F, Van den Brande J et al. (2000) Methylene blue in the treatment and prevention of ifosfamide-induced encephalopathy: report of 12 cases and a review of the literature. British Journal of Cancer 82:291-294. PMID: https://pubmed.ncbi.nlm.nih.gov/10646879/

29. Vakiti A, Pilla R, Moustafa M et al. (2018) Ifosfamide-induced metabolic encephalopathy in 2 patients with cutaneous T-cell lymphoma successfully treated with methylene blue. Journal of Investigative Medicine High Impact Case Reports 6:2324709618786769. PMID: https://pubmed.ncbi.nlm.nih.gov/30083561/

30. Baldo C, Silva L, Arcencio L et al. (2018) Why methylene blue has to be always present in the stocking of emergency antidotes. Current Drug Targets 19:1550-1559. PMID: https://pubmed.ncbi.nlm.nih.gov/29611486/

31. Kaiser S, Dart R (2022) The roles of antidotes in emergency situations. Emergency Medicine Clinics of North America 40:381-394. PMID: https://pubmed.ncbi.nlm.nih.gov/35461629/

32. Gebhardtova A, Vavrinec P, Vavrincova-Yaghi D et al. (2014) A case of severe chlorite poisoning successfully treated with early administration of methylene blue, renal replacement therapy, and red blood cell transfusion: case report. Medicine 93:e60. PMID: https://pubmed.ncbi.nlm.nih.gov/25144325/

33. Adhit K, Menon S, Acharya S, Siddhaarth K (2022) Toxin-induced methehemoglobinemia with kidney injury and hypoxic brain injury in a case of pesticide poisoning: a case report. Cureus 14:e32516. PMID: https://pubmed.ncbi.nlm.nih.gov/36654552/

34. Levy T (2019) Magnesium, Reversing Disease. Henderson, NV: MedFox Publishing. See Chapter 10. To download free copy of book (English or Spanish): https://mag.medfoxpub.com/

35. Jaiswal A, Kumar M, Silver E (2020) Extended continuous infusion of methylene blue for refractory septic shock. Indian Journal of Critical Care Medicine 24:206-207. PMID: https://pubmed.ncbi.nlm.nih.gov/32435102/

36. Dumbarton T, Minor S, Yeung C, Green R (2011) Prolonged methylene blue infusion in refractory septic shock: a case report. Canadian Journal of Anaesthesia 58:401-405. PMID: https://pubmed.ncbi.nlm.nih.gov/21246318/

37. Montegut L, Martinez-Basilio P, Moreira J, Schwartz L, Jolicoeur M (2020) Combining lipoic acid to methylene blue reduces the Warburg effect in CHO cells: from TCA cycle activation to enhancing monoclonal antibody production. PLoS One 15:e0231770. PMID: https://pubmed.ncbi.nlm.nih.gov/32298377/

38. Zhao C, Zhai Y, Hu Z et al. (2022) Efficacy and safety of methylene blue in patients with vasodilatory shock: a systematic review and meta-analysis. Frontiers in Medicine 9:950596. PMID: https://pubmed.ncbi.nlm.nih.gov/36237547/

39. Prauchner C (2017) Oxidative stress in sepsis: pathophysiological implications justifying antioxidant co-therapy. Burns 43:471-485. PMID: https://pubmed.ncbi.nlm.nih.gov/28034666/

40. Jang D, Nelson L, Hoffman R (2013) Methylene blue for distributive shock: a potential new use of an old antidote. Journal of Medical Toxicology 9:242-249. PMID: https://pubmed.ncbi.nlm.nih.gov/23580172/

41. Gebel F, Meng H, Michot F, Truniger B (1989) [Psychogenic water intoxication]. Article in German. Schweizerische Medizinische Wochenschrift 119:169-177. PMID: https://pubmed.ncbi.nlm.nih.gov/2648558/

42. Mercier-Guidez E, Loas G (2000) Polydipsia and water intoxication in 353 psychiatric inpatients: an epidemiological and psychopathological study. European Psychiatry 15:306-311. PMID: https://pubmed.ncbi.nlm.nih.gov/10954875/

43. Kirov M, Evgenov O, Evgenov N et al. (2001) Infusion of methylene blue in human septic shock: a pilot, randomized, controlled study. Critical Care Medicine 29:1860-1867. PMID: https://pubmed.ncbi.nlm.nih.gov/11588440/

44. Brown G, Frankl D, Phang T (1996) Continuous infusion of methylene blue for septic shock. Postgraduate Medical Journal 72:612-614. PMID: https://pubmed.ncbi.nlm.nih.gov/8977944/

45. Juffermans N, Vervloet M, Daemen-Gubbels C et al. (2010) A dose-finding study of methylene blue to inhibit nitric oxide actions in the hemodynamics of human septic shock. Nitric Oxide 22:275-280. PMID: https://pubmed.ncbi.nlm.nih.gov/20109575/

46. Schneider F, Lutun P, Hasselmann M et al. (1992) Methylene blue increases systemic vascular resistance in human septic shock. Preliminary observations. Intensive Care Medicine 18:309-311. PMID: https://pubmed.ncbi.nlm.nih.gov/1527264/

47. Keaney Jr J, Puyana J, Francis S et al. (1994) Methylene blue reverses endotoxin-induced hypotension. Circulation Research 74:1121-1125. PMID: https://pubmed.ncbi.nlm.nih.gov/8187278/

48. Daemen-Gubbels C, Groeneveld P, Groeneveld A et al. (1995) Methylene blue increases myocardial function in septic shock. Critical Care Medicine 23:1363-1370. PMID: https://pubmed.ncbi.nlm.nih.gov/7634806/

49. Preiser J, Lejeune P, Roman A et al. (1995) Methylene blue administration in septic shock: a clinical trial. Critical Care Medicine 23:259-264. PMID: https://pubmed.ncbi.nlm.nih.gov/7532559/

50. Andresen M, Dougnac A, Diaz O et al. (1998) Use of methylene blue in patients with refractory septic shock: impact on hemodynamics and gas exchange. Journal of Critical Care 13:164-168. PMID: https://pubmed.ncbi.nlm.nih.gov/9869542/

51. Memis D, Karamanlioglu B, Yuksel M et al. (2002) The influence of methylene blue infusion on cytokine levels during severe sepsis. Anaesthesia and Intensive Care 30:755-762. PMID: https://pubmed.ncbi.nlm.nih.gov/12500513/

52. Park B, Shim T, Lim C et al. (2005) The effects of methylene blue on hemodynamic parameters and cytokine levels in refractory septic shock. The Korean Journal of Internal Medicine 20:123-128. PMID: https://pubmed.ncbi.nlm.nih.gov/16134766/

53. Kwok E, Howes D (2006) Use of methylene blue in sepsis: a systematic review. Journal of Intensive Care Medicine 21:359-363. PMID: https://pubmed.ncbi.nlm.nih.gov/17095500/

54. Puntillo F, Giglio M, Pasqualucci A et al. (2020) Vasopressor-sparing action of methylene blue in severe sepsis and shock: a narrative review. Advances in Therapy 37:3692-3706. PMID: https://pubmed.ncbi.nlm.nih.gov/32705530/

55. Sari-Yavuz S, Heck-Swain K, Keller M et al. (2022) Methylene blue dosing strategies in critically ill adults with shock-a retrospective cohort study. Frontier in Medicine 9:1014276. PMID: https://pubmed.ncbi.nlm.nih.gov/36388905/

56. Driscoll W, Thurin S, Carrion V et al. (1996) Effect of methylene blue on refractory neonatal hypotension. The Journal of Pediatrics 129:904-908. PMID: https://pubmed.ncbi.nlm.nih.gov/8969734/

57. Goncalves-Ferri W. Albuquerque A, Evora P M, Evora P R (2022) Methylene blue not contraindicated in treating hemodynamic instability in pediatric and neonate patients. Current Pediatric Reviews 18:2-8. 34397332

58. Ismail R, Awad H, Allam R et al. (2022) Methylene blue versus vasopressin analog for refractory septic shock in the preterm neonate: a randomized controlled trial. Journal of Neonatal-Perinatal Medicine 15:265-273. PMID: https://pubmed.ncbi.nlm.nih.gov/34719443/

59. Manji F, Wierstra B, Posadas J (2017) Severe undifferentiated vasoplagic shock refractory to vasoactive agents treated with methylene blue. Case Reports in Critical Care 2017:8747326. PMID: https://pubmed.ncbi.nlm.nih.gov/29098094/

60. Fisher J, Taori G, Braitberg G, Graudins A (2014) Methylene blue used in the treatment of refractory shock resulting from drug poisoning. Clinical Toxicology 52:683-65. PMID: https://pubmed.ncbi.nlm.nih.gov/24364507/

61. Chalise S. Sahib T, Boyer G, Pathak V (2022) Methylene blue in refractory shock. Cureus 14:e31158. PMID: https://pubmed.ncbi.nlm.nih.gov/36505110/

62. Neto A, Duarte N, Vicente W et al. (2003) Methylene blue: an effective treatment for contrast medium-induced anaphylaxis. Medical Science Monitor 9:CS102-CS106. PMID: https://pubmed.ncbi.nlm.nih.gov/14586280/

63. Jang D, Nelson L, Hoffman R (2011) Methylene blue in the treatment of refractory shock from an amlodipine overdose. Annals of Emergency Medicine 58:565-567. PMID: https://pubmed.ncbi.nlm.nih.gov/21546119/

64. Omar S, Zedan A, Nugent K (2015) Cardiac vasoplegia syndrome: pathophysiology, risk factors and treatment. The American Journal of the Medical Sciences 349:80-88. PMID: https://pubmed.ncbi.nlm.nih.gov/25247756/

65. Arevalo V, Bullerwell M (2018) Methylene blue as an adjunct to treat vasoplegia in patients undergoing cardiac surgery requiring cardiopulmonary bypass: a literature review. AANA Journal 86:455-463. PMID: https://pubmed.ncbi.nlm.nih.gov/31584419/

66. Hohlfelder B, Douglas A, Wang L et al. (2022) Association of methylene blue dosing with hemodynamic response for the treatment of vasoplegia. Journal of Cardiothoracic and Vascular Anesthesia 36:3543-3550. PMID: https://pubmed.ncbi.nlm.nih.gov/35697643/

67. Evora P (2013) Methylene blue does not have to be considered only as rescue therapy for distributive shock. Journal of Medical Toxicology 9:426. PMID:

 

Chronic diseases have a root-cause explanation. According to Dr. Ewald, chronic diseases that inflict more than 60% of American adults are the true pandemic.


"If you are not testing, you are guessing." - Institute for Functional Medicine

"If you are not treating long-term, you are failing." - Thomas J. Lewis, Ph.D.

"There are no solutions, only trade-offs." - Thomas Sowell, Ph.D.

 

Section 2


Francisco Gonzalez-Lima, Ph.D., is a courtesy professor in the Department of Psychiatry and Behavioral Sciences. He also holds the George I. Sanchez Centennial Professorship at The University of Texas at Austin, where he is a professor in the departments of Psychology, Psychiatry, Pharmacology and Toxicology and the Institute for Neuroscience.

Gonzalez-Lima’s teaching experience includes undergraduate, medical, graduate and postdoctoral students, and he currently teaches the core graduate course in Functional Neuroanatomy. Gonzalez-Lima has been the research adviser of 22 Ph.D. students at UT Austin, and his trainees are world leaders in brain research on the relationship between brain energy metabolism, memory and neurobehavioral disorders.


Gonzalez-Lima graduated with honors from Tulane University in New Orleans with a Bachelor of Science in biology and Bachelor of Arts in psychology, and he earned his doctorate in anatomy and neurobiology from the University of Puerto Rico School of Medicine, which honored him with a Distinguished Alumnus Award. He completed postdoctoral training (behavioral neuroscience) at the Technical University of Darmstadt, Germany, as an Alexander von Humboldt research fellow.


Gonzalez-Lima has been a visiting neuroscientist in Germany, England, Canada and Spain and he has delivered more than 120 invited lectures about his brain research around the world. His research has been funded for more than 30 years with federal and private funds, and he has contributed to more than 350 scientific publications in peer-reviewed journals, conference proceedings, chapters and books.


Current research in the Gonzalez-Lima laboratory focuses on the beneficial neurocognitive and emotional effects of noninvasive human brain stimulation in healthy, aging and mentally ill populations. This research primarily uses transcranial infrared laser stimulation and multimodal imaging (EEG, fNIRS and fMRI) in collaboration with colleagues at UT Austin, The University of Texas at Arlington and University of Texas Southwestern Medical Center. Gonzalez-Lima supervises and trains students and residents to contribute to these ongoing brain research projects.

 

Section 3

Methylene Blue for Lyme Disease and Bartonella

PUBLISHED ON NOVEMBER 6, 2020 UPDATED ON FEBRUARY 6, 2022


Early in an infection, bacteria are in a growth phase where they divide rapidly to increase the number of bacteria to establish an infection. Bacteria then enter a stationary phase where bacterial growth slows down. The current antibiotic treatments for acute and chronic Lyme Disease and Bartonella primarily work in the bacterial growth phase. Still, these antibiotics are ineffective once the bacteria enter into the stationary phase. In recent years, researchers have conducted screening studies of drugs and natural compounds to identify effective treatments for Lyme Disease and Bartonella in a stationary phase. Surprisingly, a medication called methylene blue proved to be an effective treatment for stationary phase Lyme Disease and Bartonella.

What is Stationary Phase Lyme Disease and Bartonella

There are four phases of bacterial growth – lag, log (growth), stationary, and death. The lag phase is when the bacteria are preparing resources to grow. The log or exponential growth phase is when bacteria are rapidly dividing – one becomes two, two becomes four, four becomes eight, etc.). In the stationary phase, the rate of bacterial growth equals bacterial death, so there is no net change in the number of bacteria. The death phase is when the bacteria die off at a rate that exceeds bacterial growth.

“The conditions that sustain constant bacterial growth are seldom found in nature… The influence of harsh environmental factors, accumulation of toxic metabolic waste products during starvation, and antibiotics – all this threatens the survival of E. coli and other bacteria. For protection against harsh environmental influences, bacterial culture can enter a stationary phase where its internal systems of protection against stress become activated.” Survival guide: Escherichia coli in the stationary phase




Is it Post Treatment Lyme Disease Syndrome (PTLDS) or Chronic Lyme Disease (CLD)?

Lyme disease’s most controversial debate is whether or not the bacteria that causes Lyme disease (Borrelia burgdorferi) survives the commonly prescribed antibiotic regimens and continues to cause symptoms. The Infectious Disease Society of America (IDSA) refers to this phenomenon as Post Treatment Lyme Disease Syndrome (PTLDS). It suggests the infection with Lyme Disease has been adequately treated, and the symptoms remain due to another cause, such as an autoimmune response.

Several research studies have demonstrated the Lyme spirochete persists in humans following antibiotic therapy. The International Lyme and Associated Disease Society (ILADS) characterizes the persistence as Chronic Lyme Disease (CLD). Lyme Disease may persist and become chronic because the commonly used treatments are not effective at treating the stationary phase of the Lyme bacteria.

Stationary Phase of the Lyme Spirochete Causes More Severe Symptoms

In 2018 researchers from John Hopkins University published a study that looked at the severity of arthritis when the bacteria that causes Lyme Disease was in the growth phase, the stationary phase, and biofilm colonies. The research discovered the arthritis was more severe earlier in an infection in the stationary phase and biofilm groups than in the growth phase group. The researchers also concluded that currently used antibiotic regimens are less effective against the stationary and biofilm bacteria.



Methylene Blue for Lyme Disease

In 2014, researchers from Johns Hopkins University screened an FDA drug library for activity against Borrelia burgdorferi (the bacteria that causes Lyme disease). They identified 165 hits (drugs) with higher activity against Lyme disease than doxycycline and amoxicillin. The following year the same researchers narrowed the results down to the top 52 drugs that can be used in humans and effectively killed at last 65% of stationary phase bacteria.

The researchers discovered that various drugs used to treat other infections – including antibiotics, antivirals, antifungals, and antiparasitics – were effective at killing stationary phase Borrelia. One of the top hits was a medication called methylene blue. Methylene blue was originally an antimalarial medication currently used to treat a condition called methemoglobinemia and urinary tract infections. Methylene blue was almost as effective as daptomycin – a drug that has received attention for its ability to treat persistent Lyme disease.

Methylene Blue for Bartonella

An infection with the bacteria Bartonella may be more problematic than Lyme disease. Multiple vectors transmit Bartonella, diagnostic testing historically has not been accurate, and most physicians are not familiar with this infection, so rarely consider it as a diagnosis. If a Bartonella diagnosis is confirmed, a critical challenge is finding effective treatments. The commonly used antibiotics to treat Bartonella – rifampin, azithromycin, clarithromycin, ciprofloxacin, and doxycycline – work early in infection during the bacterial growth phase but are not effective during the stationary phase leading to poor treatment response. It is common for someone to feel better on these medications then have symptoms return as soon as the medications are discontinued due to bacterial resistance.

In 2019, some of the same researchers from Johns Hopkins University who performed the above Lyme disease study completed a drug screen to identify effective medications against the stationary phase Bartonella. Their research discovered 110 drug candidates from an FDA approved drug library that had better activity against Bartonella’s stationary phase than ciprofloxacin. The top 52 drug candidates from the primary screen were evaluated for their effectiveness by the number of bacteria remaining under microscopy. Similar to the previous drug screen findings for stationary phase Lyme disease, only 25% of stationary phase Bartonella bacteria remained following exposure to methylene blue.

The researchers confirmed their findings by performing minimal inhibitory

concentrations (MIC) study – the minimum amount of medication need to kill growing bacteria. Again, methylene blue performed very well. Interestingly, the drug daptomycin performed well against stationary phase Bartonella but was not effective against growing Bartonella. Rifampin – a commonly used antibiotic for Bartonella – worked well against growing Bartonella but was not effective at killing Bartonella’s stationary phase. Another challenge the researchers conducted was to test the effectiveness of the top 7 drugs from a stationary phase culture against Bartonella at various stages of growth to mimic the course of a natural infection. Here, the drugs were evaluated for their effectiveness against 1-day old growth phase 5-day old stationary phase. Again, methylene blue was a top performer proving its effectiveness against Bartonella in the infection’s growth and persistent stages.

Drug Combinations for Treating Bartonella

Researchers published the first study to evaluate drug combinations against Bartonella in the stationary phase and biofilms in 2020. Again, a team of researchers led by Ying Zhang, MD from Johns Hopkins University, expanded upon the single drug screen study from 2019. This research study evaluated the top-performing drugs from the 2019 trial and created 25 two-antibiotic combinations to test their efficacy against Bartonella in the stationary phase and biofilms.

Of the 25 combinations of antibiotics, four were able to completely eradicate stationary phase Bartonella in 24 hours – azithromycin/ciprofloxacin, azithromycin/methylene blue, rifampin/ciprofloxacin, and rifampin/methylene blue.

The next test was to determine how long it took for single and combination antibiotics to kill stationary phase Bartonella. Of the single and combination antibiotics, the methylene blue combinations with azithromycin and rifampin killed Bartonella’s stationary phase in the shortest time.

Biofilms are colonies of bacteria in a structure that improve the survival of the bacteria. In this same study, the researchers experimented to see how much bacteria in biofilms remained after exposure to single and combination antibiotics at two days, four days, and six days. None of the single or combination antibiotics were able to kill Bartonella after 2 and 4 days. However, the azithromycin/ciprofloxacin, azithromycin/methylene blue, rifampin/ciprofloxacin, and rifampin/methylene blue combinations eradicated Bartonella in biofilms after six days.



New Research, New Effective Treatment Options

Treatment options for chronic infections with Lyme disease and Bartonella have historically been inadequate. Recent research using drug screens to identify effective treatments for the stationary phase of infection has produced some promising options. The research has also confirmed the currently used antibiotics primarily work in the initial growth phase of an infection but not the stages that develop in chronic infection. Methylene blue is a promising treatment option for tens of thousands of people suffering from chronic Lyme disease and Bartonella.


 

Section 4

FOR IMMEDIATE RELEASE Orthomolecular Medicine News Service, Jan 5, 2023

Myocarditis: Once Rare, Now Common

Commentary by Thomas E. Levy, MD, JD

OMNS (Jan. 5, 2023) As an actively practicing clinical cardiologist for many years in three different communities, I knew about myocarditis. I just never saw it. Quite literally, I recall seeing ONE young woman who presented with a picture of acute congestive heart failure, and her echocardiogram study revealed a big and poorly contracting heart. Such a condition is diagnosed as an idiopathic congestive cardiomyopathy, which basically means the heart is enlarged and functioning very poorly, and you have no idea why. After treating her with traditional measures for congestive heart failure, she started getting better. To my great surprise, after six to nine months of follow-up, her echocardiogram had returned to normal.

Retrospectively, it was then clear that she had likely contracted a virus that focused on her heart. The virus-induced inflammation in her heart muscle cells then decreased the strength of her heart contractions to the point of clinical heart failure with heart enlargement. Presumably, her young immune system eventually "kicked in" and eliminated the viral culprit. Even as a clinician who also received many patients in consultation from other doctors, she represented the entirety of my cases of myocarditis. And at that, the diagnosis was only a retrospective conclusion.

COVID and Myocarditis

Today, the active clinical cardiologist is seeing myocarditis patients on a regular basis. The scientific literature indicates that myocarditis is occurring quite frequently in patients harboring the chronic presence of the COVID-related spike protein. This is being seen in many individuals with persistent chronic COVID, many of whom have been vaccinated, as well as in a substantial number of individuals who have been vaccinated and have never contracted COVID. [1-4] A study in mice showed that the injection of the mRNA vaccine (which produces the spike protein) reliably induced myopericarditis. [5] Regardless of the initial source of exposure to spike protein, it appears to be the reason for the pathology and symptoms seen in chronic COVID. [6]

While not yet clearly documented by any well-designed studies in the medical literature, a great deal of anecdotal information indicates that vaccine mRNA shedding can occur. And once transmitted, the mRNA directly leads to spike protein production. [7] Such mRNA shedding means that the spike protein is indirectly, if not directly as well, transmissible from one individual to another via inhalation or various forms of skin contact. In fact, Pfizer's own internal documents advise about the possibility of "environmental exposure" by "inhalation or skin contact" of the mRNA in the vaccine being transmitted from a vaccinated individual to another person. [8] Furthermore, while many try to dismiss such an "exposure" as too minimal to be of clinical consequence, such an assertion cannot be assumed to be true when dealing with an agent (spike protein) that appears capable of replication once it gains access to the body. The toxicity associated with spike protein would not be due to a one-time exposure, but one that could persist indefinitely because of this ability to replicate. A toxin that has such an ability is truly a clinical nightmare. It is never a good idea to overestimate the integrity of the pharmaceutical industry. [9]

The spike protein is the part of the COVID pathogen that facilitates its entry into various cells in the body. [10] This cellular entry occurs after the spike protein binds to ACE2 receptors present on the cell membranes found in a wide variety of tissues and organs. Spike protein binding to ACE2 receptors in the lungs, heart, and blood vessels has proven to be of particular importance in determining the severity of many COVID infections as well as the nature of the side effects seen following a spike protein vaccination. Deaths and severe complications have also resulted from vaccine-induced thrombosis occurring in the cerebrovascular circulation. [11,12] Autopsy evaluation of multiple vaccinated individuals who died shortly after receiving their vaccinations revealed acute myocarditis as the only logical cause of their deaths. [13]

Sufficient spike protein binding to ACE2 receptors on the endothelial cells lining the blood vessels has consistently resulted in increased blood clotting. Such clots are tiny in some people, which can then lead to various degrees of tissue and organ damage depending on how severely overall blood flow is impaired to those areas. [14,15] Other clots can rapidly increase in size and result in sudden death. [16] Spike protein can activate blood clotting by binding directly to the ACE2 receptors of platelets in the blood. [17,18] Also, circulating spike protein that has not yet been bound appears to stimulate hypercoagulation as well. [19] Of note, both Pfizer and Moderna appear quite proud to assert that their final formulations supply the "full-length" spike protein in the injections.

Myocarditis, which simply means inflammation of some or all of the muscle cells in the heart, can occur when the spike protein binds to the blood vessels in the heart, to the muscle cells themselves, or both. [20] Even when the myocardial blood vessels get more selectively targeted, inflammation of the heart muscle itself will still eventually ensue as the circulation of the heart gets progressively impaired by blood clotting and/or by an increased resistance to blood flow resulting from inflammation-induced vasoconstriction. Pre-pandemic myocarditis (cases not related to a spike protein presence) generally did not involve any predisposition to blood clotting in addition to the inflammation of the affected heart muscle cells.

Myocarditis presents no diagnostic challenge when it presents in its classical manner. Chest pain and rapid heart rate are often the earliest symptoms. If the myocardial inflammation is evolving rapidly, symptoms of congestive heart failure, including shortness of breath and swelling of the lower legs, can occur as well. Not uncommonly, an upper respiratory tract viral infection will be present or there will be a history of such an infection having recently resolved. Chest X-ray, electrocardiogram (ECG), and echocardiogram can all be used to help establish the diagnosis. An elevated troponin level on blood testing is extremely sensitive in picking up any ongoing heart muscle cell damage, and some elevation of this test will always be seen if any significant inflammation is present in those muscle cells.

Any continued elevation of troponin in the blood, however minimal, must be regarded with significant concern, even if there appears to be a complete clinical resolution of the myocarditis. Everyone should have this test done, even if they are feeling perfectly well, to both establish a baseline within the normal range or to detect any unsuspected low-grade myocardial inflammation.

The very high sensitivity of the troponin test has revealed that there are countless numbers of people post-COVID infection and/or post-vaccination that are continuing to have sustained subclinical degrees of myocardial inflammation. No matter how minimal the elevation of the test, any increase means that a gradual and continued loss of heart muscle function will occur over time. It also means that the heart is highly susceptible to an acute and potentially severe worsening of heart function when an additional exposure to more spike protein occurs, as is seen with the booster shots being vigorously promoted now. A heart with a minimal elevation of troponin is literally the perfect setting for a catastrophic clinical response when an additional spike protein-laden injection is given, much like what gasoline would do to smoldering coals. Not surprisingly, it has been shown that COVID patients with higher troponin levels were more likely to die than those with lower levels. [21]

Many abnormal troponin tests eventually resolve completely and many do not. The quality of nutrition, the strength of the immune system, and the quality of the nutrient/vitamin/mineral supplementation being taken are all critical factors in determining whether a minimal, subclinical degree of inflammation in the heart is capable of completely resolving with a return of the troponin level into the reference, or normal, range. With much of the world eating poorly and not supplementing at all, there is an ongoing presence of the spike protein in a very large number of people around the world. Clinical myocarditis is simply an advanced state of inflammation in the heart, with much higher levels of troponin being released into the blood. Cardiac injury was detected in 20% to 40% of patients hospitalized with COVID. [22,23] Any troponin elevation in hospitalized COVID patients was associated with an increased mortality. [24]

Troponin testing is currently the most important and widely accepted way to determine whether a suspected heart attack has occurred, with the troponin being released into the circulation as the heart muscle cells die. [25] Some degree of myocardial injury is felt to be present when any troponin level is detected beyond the 99th percentile upper reference limit, whether in the context of a suspected heart attack or the possible presence of any inflammation in the heart. [26,27] Even an increase in baseline troponin levels that remains below the established upper limits of normal has been shown to be significantly associated with increased mortality after noncardiac surgery. [28] Baseline troponin testing is a good idea for everyone, since normal ranges can vary from lab to lab, and because it appears myocardial injury can still be present when the troponin level rises significantly from a baseline point but remains short of the upper reference limit. [29]

The importance of the most minimal of troponin elevations has been established in several studies looking at the relationship of pre-operative troponin levels with long-term mortality following noncardiac surgery. Compared to patients with no troponin elevation, a significant increase in 30-day mortality was seen in patients having minor troponin elevations following noncardiac surgery. [30,31] Another similar study found over a doubling of the mortality rate when the two patient groups were evaluated at three years following the noncardiac surgery. [32]

In a recent Swiss study yet to be published at the time of this writing, troponin levels were measured on 777 hospital employees who received a booster injection after having received two shots previously. On the third day after the booster, troponin levels above the upper limits of normal were seen in 2.8% of those subjects. By the next day, half of the elevated troponin levels had come back into the normal range. [33] Longer-term follow-up data was not available. This study raises more questions than it answers. What would the troponin levels have been at one day post-injection? Did the troponin levels still elevated at day four post-injection resolve completely? If so, how long did that take to occur? Rather than be concerned that some myocardial damage was done by the vaccine, which is openly acknowledged in the study, it is dismissed as being of no importance since half of the elevated troponins resolved 24 hours later. And, as with all of the current papers downplaying the significance of any vaccine side effect, however significant, the authors always conclude that the vaccine is doing much more good than harm without any further qualification as to why such a conclusion is valid.

Having even the most minimal elevation of troponin not only raises the concern of some collective long-term heart damage, or the ease of having a "re-flaring" of inflammation with new spike protein exposures, as from a booster shot, it also raises the concern of electrical instability in some of the inflamed myocardial cells. There is always a possibility of electrical instability in any inflamed myocardial muscle cells, as it is their normal physiological nature to transmit electrical impulses from one cell to the next. Because of this, stressful events that release surges of adrenalin and catecholamines in the circulation, as is seen with peak physical exertion, can readily provoke such electrically unstable cells into starting, and sustaining, an abnormal heart rhythm. Literally hundreds of European soccer players have died or collapsed on the field of play in the last two years. Of note, they have not been seen to collapse while standing or sitting on the sidelines. Similarly, any pilot with even a minimal but otherwise symptom-free elevation of troponin can potentially sustain such a life-threatening arrhythmia when a significant stress-provoking emergency arises in the cockpit.

However, regardless of any benefits a COVID vaccine might have on the overall morbidity and mortality on those receiving it, it completely ignores that MANY effective treatments have emerged that either prevent most cases of COVID or readily cure them when properly applied after the infection has been contracted. [34-38]

With the availability of effective treatments, no vaccine side effect, especially one that has already resulted in many deaths, should be tolerated, unless the vaccine candidate is fully aware of all possible side effects and chooses not be bothered with measures proven to prevent and/or treat the infection.

To date, every vaccine that has ever existed has a significant side effect profile. This information, along with a full disclosure of effective non-pharmaceutical therapies for the condition the vaccine is supposed to prevent, should always be afforded to both physicians and their patients.

It is important to realize that most of the tissues and organs of the body do not have reliable laboratory markers indicating the presence and degree of ongoing spike protein damage. Tracking heart damage with troponin levels makes this organ relatively unique in this regard, and since ACE2 receptors are present in most organs and tissues, any continued elevation of troponin can also be considered a reliable indicator that spike protein damage is occurring in organs and tissues outside of the heart. Spike protein would be expected to bind ACE2 receptors wherever it finds them, and such binding would always be expected to cause cellular inflammation and damage. Blood testing for natriuretic peptides also reflects myocardial damage, but the primary focus should remain on troponin testing and doing whatever is necessary to return that test into the normal range. [39-45]

COVID, Arrhythmias, Heart Block, and Pilots

As would be logically expected, any agent that can cause inflammation in the heart would also be expected to sometimes involve the cells in the heart that generate and conduct each electrical spark that initiates every contraction of the heart. As myocarditis can be patchy and not affect all of the heart muscle cells uniformly, heart rhythm problems are not always part of the clinical presentation of myocarditis. However, various degrees of heart block have been reported because of the COVID-19 infection and/or because of the COVID-19 vaccination. [46-51]

A new condition known as multisystem inflammatory syndrome in children (MIS-C) has emerged since the onset of the COVID pandemic, appearing primarily in advanced COVID infections. [52,53] MIS-C, and MIS in adults, simply means the COVID infection has resulted in a widespread amount of inflammation in the body, often involving the heart and the lungs. Minimal to advanced heartbeat conduction problems have occurred secondary to MIS-C, ranging from the often-innocuous prolonged PR interval (see below) on the ECG to advanced and potentially life-threatening degrees of AV block. [54,55] When heart function is normal, the AV node allows a rapid conduction of the heartbeat throughout all of the heart muscle cells so that heart muscle contraction is synchronized and optimally efficient. AV block results in an abnormal slowing of the heart rate and sometimes fatal secondary arrhythmias, including complete stoppage of the heartbeat (asystole). It appears likely that the spike protein can damage the heart at any age, and that the spike protein can be present because of the infection itself and/or the vaccination targeted at the infection.

The PR interval is the amount of time that the heartbeat takes to traverse the atrial chambers in the heart before reaching the conduction-accelerating AV node. The normal PR interval ranges from 0.12 to 0.2 seconds. In younger individuals, especially well-trained athletes, a PR interval greater than 0.2 is usually completely normal. However, when PR interval measurements have always been 0.2 or less and then start to lengthen as an older adult, there should be significant concern that the aging conduction system might manifest more significant conduction abnormalities in the future.

In the setting of the pandemic, it is of particular concern when PR interval prolongation is seen for the first time following a bout of COVID and/or following a vaccination. This is a clear indicator of new inflammation in at least some of the heart cells, however minimal it may be. Regardless, it should not just be assumed to be of no importance. All disease has a spectrum of pathology, and the earliest stages of pathology should never be trivialized. [56] In a Harvard study that extended over a 30- to 40-year period, it was found that individuals with PR intervals greater than 0.2 seconds had twice the risk of atrial fibrillation, three times the risk of needing a pacemaker (meaning the presence of advanced degrees of heart block), and nearly a one and a half times increase in all-cause mortality. Furthermore, greater degrees of PR interval prolongation led to an even greater risk. [57]

However, ignoring the inherent pathology in a pandemic-induced prolonged PR interval is exactly what the Federal Aviation Administration (FAA) appears to have done. Facing a shortage of pilots due to both the vaccine requirement it initiated during the pandemic for the pilots to fly, along with many early retirements that resulted, the FAA decided to change the rules, disregarding long-standing parameters of normalcy based on medical science and not convenience. The FAA has now declared a PR interval of 0.3 seconds to be the "new normal" in the FAA Guide for Aviation Medical Examiners as of October, 2022. The October, 2021 standards asserted the PR interval was normal only at 0.2 seconds or less. When the pilot has "no symptoms" he or she can now obtain clearance to fly with a PR interval of 0.3 or less. And when that interval is greater than 0.3, a "current Holter and cardiac evaluation" are then required. Considering that the normal PR interval ranges between 0.12 and 0.20 seconds, an interval of 0.3 seconds represents a "permissible" increase in this interval by over 100% relative to the low normal interval of 0.12 seconds. This is not a nominal increase in PR interval, but a very large one.

Even now, a treadmill exercise stress test is not required to receive medical clearance to fly, even for commercial pilots. This is simply not a safe policy by the FAA and arguably a shocking one, as many pilots are in the age range when heart attacks occur without any early symptoms but with a normal ECG, the ECG being the only mandatory heart-related test. Roughly a third of all deaths around the world are due to cardiovascular disease. And in western countries sudden cardiac death occurs in about half of all coronary artery disease patients. [58,59] Much more vigorous cardiac evaluations should be performed in prospective pilots, and repeated at appropriate intervals. A normal ECG means a heart attack has not occurred, nothing more. A fatal heart attack from very advanced coronary artery disease could occur 10 minutes after the normal ECG was recorded. No pilot should ever fly when there is a persistent elevation of troponin levels and/or D-dimer levels (see below). It is irrelevant that the pilot might feel well, have a normal ECG, and have no clinical evidence of myocarditis.

COVID, Blood Clots, and D-dimer Levels

A D-dimer blood test is a measure of the degree to which blood clots already formed are breaking up (lysis) and releasing those breakdown products into the blood. It is not a measure of how prone the blood is to clotting in the first place (increased coagulability). However, it is a very sensitive test that will always be elevated when increased blood clotting is taking place, since those clots must still be broken down to keep the circulation from shutting down. Except when elevated in the setting of a very minimal number of chronic diseases, an elevated D-dimer test very reliably means there are blood clots breaking up because too many new blood clots are continuing to be formed. Only rarely is significant thrombosis seen in the absence of an elevated D-dimer level. [60]

In the setting of the pandemic with a history of active or chronic COVID infection, as well as a history of having had one or more vaccinations, an elevated D-dimer test is always a cause for GREAT concern. It is clear-cut evidence that there is an ongoing spike protein presence binding ACE2 receptors in the inner lining (endothelium) of blood vessels in the body, resulting in platelet activation and subsequent blood clotting. [61] Blood clots can range from microscopic to massive. Such clotting can also be part of a myocarditis presentation, although not necessarily so. Certainly, having both an elevated troponin level and an elevated D-dimer level is especially worrisome and warrants prompt treatment in order to normalize the pathology causing them.

Both the COVID vaccine and the COVID infection have been documented to cause increased blood clotting and thrombosis. [62,63] Viral infections in general have also been found to cause abnormal blood clotting. [64] In critically ill hospitalized COVID patients, elevated D-dimer levels were found about 60% of the time. [65] Not surprisingly, the longer that D-dimer levels remain elevated in COVID patients, the greater the morbidity and mortality. [66-68] Similarly, the higher the D-dimer level on hospital admission for COVID, the greater the chances of in-hospital mortality. [69]

When the underlying infection or other pathology can be resolved, D-dimer levels will generally resolve as well. If a thrombotic event occurs, resolves, and has no ongoing underlying pathology, D-dimer elevations will generally persist for only a few days before returning to normal. Chronic COVID infections often demonstrate persistent blood clotting problems. In one study, 25% of a recuperating group of COVID patients who were four months past the acute clinical phase of their infections demonstrated increased D-dimer levels. Also of note, the other common laboratory parameters of blood clotting had already returned to normal in over 90% of the patients, indicating the sensitivity that D-dimer testing has for detecting the blood clotting pathology. These other tests included prothrombin time, partial thromboplastin time, fibrinogen, and platelets. Even C-reactive protein and interleukin-6, tests that track inflammation, had typically also returned to normal. [70]

Platelet levels generally drop in the blood at the same time D-dimer levels are increasing, as they are consumed in the formation of the blood clots. [71] A post-COVID vaccination syndrome known as vaccine-induced prothrombotic immune thrombocytopenia (VIPIT) with these laboratory findings has been described. [72-75]

While the pandemic has given more attention to D-dimer testing than it ever had before, other conditions can cause a D-dimer elevation. [76] However, anyone today who is not acutely ill but found to have an elevation of their D-dimer levels is likely suffering from the consequences of persistent spike protein presence in their vasculature, whether due to lingering COVID infection and/or due to having received one or more COVID vaccinations. And even if such an individual never had COVID or received a vaccination, an extensive medical evaluation is warranted, since a D-dimer elevation is never normal. A persistently elevated D-dimer levels should never be dismissed as inconsequential just because the patient feels well.

Therapeutic Recommendations

Quite simply, the goal is to normalize both troponin and D-dimer levels in everyone under treatment. This can be more difficult to achieve in older patients with chronic medical conditions that are being clinically managed. But a concerted effort should still be made at the outset to normalize these tests.

Nearly all of the elevated troponin and D-dimer levels at this point in the pandemic will be secondary to persistent spike protein presence in the body following COVID infection, one or more COVID vaccinations, or both. The likely ease of spike protein transmission also means there will be some individuals who have elevated test levels without having knowledge of ever having been infected, and without a history of vaccination. In other words, these tests should be performed in everyone at this point in time, and any elevations should be aggressively treated. And if those tests are completely normal, they will still serve as excellent baseline data when dealing with future medical conditions or infections, COVID-related or otherwise.

There is no one set protocol for dealing with a persistent spike protein syndrome with elevated troponin and/or D-dimer levels. Some individuals will respond quickly and regain a normal health status after relatively minimal measures are taken. Others will require very aggressive and prolonged treatments, and still others will simply not normalize regardless of what is done. In younger patients, the inability to regain a normal health status should be extremely rare, especially when a quality regimen of nutrients, vitamins, and minerals is being introduced for the first time.

The following recommendations apply to an individual with elevated troponin and D-dimer levels, or with either one elevated and the other normal. Specific reference ranges, or normal ranges, for these tests should come from the laboratory running the tests, since significant variation in these ranges can be seen from one testing source versus another. These recommendations apply to both the clinically normal individual and someone who is suffering from chronic COVID or any of a variety of nonspecific symptoms. This protocol, and all variations thereof, should be administered with the guidance of a licensed healthcare professional.

  1. Intravenous vitamin C, dosed roughly between 50 and 150 grams (1 gram/kilogram body weight), infused over 60 to 120 minutes. Add 25 mg of hydrocortisone to each IV. If not available, take 50 mg of hydrocortisone orally about one hour before start of infusion. Also add 500 to 1,500 mg of magnesium chloride to each IV bag. For more information on vitamin C administration: [77] Alternatively, take 5 packets of liposome-encapsulated vitamin C orally three times daily. If available take 10 to 20 mg of hydrocortisone orally with each dose. Alternatively, 2 to 4 grams of sodium ascorbate in juice three times daily with 10 to 20 mg of hydrocortisone with each dose.

  2. Follow each vitamin C infusion with a separate infusion of methylene blue [a potent anti-pathogen proven to be of great benefit even in the most advanced stages of COVID] [79-84]: 50 mg of MB in 250 ml of 5% dextrose solution can be infused over 30 to 45 minutes. Alternatively, 50 mg of MB can be taken orally each day of vitamin C administration. 5 ml of 1% MB solution in juice (tomato a good option). Taking through a straw avoids temporary teeth and tongue staining. Prompt administration of 3% hydrogen peroxide removes skin stains.

  3. Hydrogen peroxide nebulizations as tolerated to eliminate low-grade colonizations of COVID and other pathogens in the aerodigestive and lower digestive tracts. [85]

Any, or all, of the following nutrient/vitamin/mineral supplements for general support of long-term health: [86]

  • Vitamin C

  • Magnesium chloride

  • Zinc and quercetin

  • Vitamin D

  • Vitamin K2

  • Olive leaf extract

  • Multivitamin, multimineral preparation that has no added calcium, iron, or copper

  • Nattokinase, lumbrokinase, and/or serrapeptase to minimize any future blood clotting problems

At the discretion of the healthcare professional, any of the following measures can be added:

  • Ozonated blood or ozonated saline infusions

  • Ultraviolet irradiation treatments of the blood

  • Intravenous infusions of hydrogen peroxide

  • Hyperbaric oxygen treatments

  • Chlorine dioxide treatments

  • Hydroxychloroquine or chloroquine

  • Ivermectin

Any modifications of these treatments, along with deciding how long they should be continued, must be determined on an individual basis with the help of the chosen healthcare professional working with the patient.

Recap

Myocarditis was once rare. Because of COVID vaccines and COVID itself, myocarditis has become genuinely common. The troponin test has shown that there are many individuals who continue to have low-grade myocardial inflammation after a return to clinical normalcy. This makes such individuals ticking time-bombs ready to develop a serious worsening of their underlying pathology when a booster shot is received or a recontraction of COVID or one of its variants occurs. The persistent inflammation in the heart means there is a persistence of the spike protein in that organ and very likely through much of the body. This sets the stage for a sudden and dramatic decline in health when more spike protein is administered or allowed to be replicated in the body.

Elevated D-dimer levels indicate an overactive state of blood clotting in the body, and when these levels remain elevated, the long-time prognosis is likely very poor in terms of morbidity and early mortality.

Heart rhythm problems and heart block can occur when troponin levels remain elevated. The FAA is currently changing its rules to allow more pilots to fly who have PR interval greater than 0.3 seconds, a development that should be of great concern to all who fly. PR intervals that lengthen in the older population can presage significant heart problems, including early death. Science should never be displaced by political expedience and the need to make ever greater amounts of money.

Any persistent elevations of troponin and D-dimer tests must be treated with the goal of normalizing them completely. Obviously, this is especially important in the pilot population. Measures to accomplish this along with recommended types of long-term supplementation are discussed.

(Cardiologist and attorney-at-law Thomas E. Levy is a Contributing Editor for the Orthomolecular Medicine News Service. Dr. Levy serves as a consultant to LivOn Labs. He may be contacted at televymd@yahoo.com)


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Section 5: Methylene blue photodynamic therapy induces selective and massive cell death in human breast cancer cells


Research article

Open Access

Published: 15 March 2017

Methylene blue photodynamic therapy induces selective and massive cell death in human breast cancer cells

Ancély F. dos Santos, Letícia F. Terra, Rosangela A. M. Wailemann, Talita C. Oliveira, Vinícius de Morais Gomes, Marcela Franco Mineiro, Flávia Carla Meotti, Alexandre Bruni-Cardoso, Maurício S. Baptista & Leticia Labriola

BMC Cancer volume 17, Article number: 194 (2017) Cite this article



Abstract

Background

Breast cancer is the main cause of mortality among women. The disease presents high recurrence mainly due to incomplete efficacy of primary treatment in killing all cancer cells. Photodynamic therapy (PDT), an approach that causes tissue destruction by visible light in the presence of a photosensitizer (Ps) and oxygen, appears as a promising alternative therapy that could be used adjunct to chemotherapy and surgery for curing cancer. However, the efficacy of PDT to treat breast tumours as well as the molecular mechanisms that lead to cell death remain unclear.


Methods

In this study, we assessed the cell-killing potential of PDT using methylene blue (MB-PDT) in three breast epithelial cell lines that represent non-malignant conditions and different molecular subtypes of breast tumours. Cells were incubated in the absence or presence of MB and irradiated or not at 640 nm with 4.5 J/cm2. We used a combination of imaging and biochemistry approaches to assess the involvement of classical autophagic and apoptotic pathways in mediating the cell-deletion induced by MB-PDT. The role of these pathways was investigated using specific inhibitors, activators and gene silencing.


Results

We observed that MB-PDT differentially induces massive cell death of tumour cells. Non-malignant cells were significantly more resistant to the therapy compared to malignant cells. Morphological and biochemical analysis of dying cells pointed to alternative mechanisms rather than classical apoptosis. MB-PDT-induced autophagy modulated cell viability depending on the cell model used. However, impairment of one of these pathways did not prevent the fatal destination of MB-PDT treated cells. Additionally, when using a physiological 3D culture model that recapitulates relevant features of normal and tumorous breast tissue morphology, we found that MB-PDT differential action in killing tumour cells was even higher than what was detected in 2D cultures.


Conclusions

Finally, our observations underscore the potential of MB-PDT as a highly efficient strategy which could use as a powerful adjunct therapy to surgery of breast tumours, and possibly other types of tumours, to safely increase the eradication rate of microscopic residual disease and thus minimizing the chance of both local and metastatic recurrence.


 

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