I RECOVER Post Vaccine Protocol
I RECOVER Post Vaccine Protocol
I RECOVER Post Vaccine Protocol
- Section on anti-coagulation
- Reordering of preferred interventions
- Caution on Methylene Blue contraindications
Table of Contents
Summary of Suggested Therapies .......................................................................................... 3
Disclaimer ............................................................................................................................. 4
Contributors .......................................................................................................................... 4
Definition .............................................................................................................................. 4
Epidemiology......................................................................................................................... 4
Pathogenesis ......................................................................................................................... 5
Complications/ injuries caused by COVID injections ............................................................... 8
Treatment Approach ........................................................................................................... 10
Baseline Testing................................................................................................................... 11
Anticoagulation post-vaccination and the three clinical phenotypes of the vaccine injured ... 12
Antiplatelet drugs: ....................................................................................................................... 13
Direct oral anticoagulants (DOAC):................................................................................................ 14
Oral Fibrinolytic agents:................................................................................................................ 14
Provisional approach to anticoagulation in the post-vaccine phenotypes ....................................... 15
First-Line Therapies ............................................................................................................. 16
Adjunctive/Second-Line Therapies ....................................................................................... 24
Third Line Therapies ............................................................................................................ 26
Patients with elevated homocysteine levels ......................................................................... 27
Other Potential Treatments ................................................................................................. 28
Disease-Specific Therapeutic Adjuncts ................................................................................. 31
Small fiber neuropathy (SFN)/autonomic neuropathy ...................................................................31
Generalized neurologic symptoms/“brain fog”/fatigue/visual symptoms ......................................31
Depression ...................................................................................................................................32
Patients with elevated DIC and those with evidence of thrombosis ............................................... 33
Vaccine-induced myocarditis/pericarditis ..................................................................................... 33
Herpes virus reactivation syndrome .............................................................................................. 33
Tinnitus........................................................................................................................................ 34
Ageusia and anosmia (Loss of taste and smell) .............................................................................. 34
Bell’s palsy/facial paresthesia/visual issues ................................................................................... 35
Patients with new onset allergic diathesis/features of Mast Cell Activation Syndrome (MCAS)....... 35
Alopecia (hair loss) ....................................................................................................................... 35
References .......................................................................................................................... 37
Contributors
This protocol was a collaborative effort drawing on the expertise of a dozen world-renowned physicians.
Dr. Pierre Kory and Dr. Paul Marik are thankful for the contributions of: Dr. Keith Berkowitz; Dr. Flavio
Cadegiani; Dr. Suzanne Gazda; Dr. Meryl Nass; Dr. Tina Peers; Dr. Robin Rose; Dr. Yusuf (JP) Saleeby; Dr.
Eugene Shippen; Dr. Mobeen Syed; and Dr. Fred Wagshul.
We are also extremely grateful for the feedback of the many vaccine-injured people who shared their
experiences with us.
Definition
Although no official definition exists for ‘post-COVID-vaccine syndrome,’ a temporal correlation between
receiving a COVID-19 vaccine and the beginning or worsening of a patient’s clinical manifestations is
sufficient to diagnose as a COVID-19 vaccine-induced injury when the symptoms are unexplained by
other concurrent causes.
Since Phase 3 and Phase 4 clinical trials are still ongoing, the full safety and toxicity profile for COVID-19
vaccines cannot be fully determined. From a bioethical perspective, cases of any new-onset or worsened
signs, symptoms, or abnormalities following any dose of COVID-19 vaccine must be considered as an
injury caused by the vaccine, until proven otherwise.
Note that there are significant overlaps between the symptoms and features of long COVID/long-hauler
syndrome and post-vaccine syndrome. However, a number of clinical features appear to be
characteristic of post-vaccine syndrome; most notably, severe neurological symptoms appear to be
more common following vaccination. To complicate matters further, patients with long COVID are often
also vaccinated, making the issue of definition more difficult.
Epidemiology
The Centers for Disease Control (CDC), National Institutes for Health (NIH), Food and Drug
Administration (FDA), and World Health Organization (WHO) do not recognize post-COVID-19 vaccine
injuries as a specific medical condition, [1] even though there is a specific ICD-10 code. Curiously, the
code U12.9 is recognized in Europe but not in the United States. There have been no prospective studies
that have accurately classified and logged the incidence of this complication; therefore, the true
magnitude of post-vaccine syndrome is unknown.
However, as of December 2nd, 2022, 1 476 227 adverse events have been reported. This includes
32 621 deaths, 185 412 hospitalizations, 15 721 heart attacks, 35 718 cases of myocarditis and 60 758
cases of permanent disability according to OPEN VAERS, which tracks data recorded in the U.S. Vaccine
Adverse Event Reporting System (VAERS). Note that VAERS data is limited by underreporting, by a factor
of at least 30-fold. [2]
However, available data consistently and reproducibly demonstrates a rate of serious adverse events
(SAE) of about 8%. [2;3] Most importantly, the V-SAFE database administered by the CDC demonstrates
an 8% rate of SAE (https://www.cdc.gov/coronavirus/2019-ncov/vaccines/safety/vsafe.htm,
https://icandecide.org/v-safe-data/. Translated to the U.S. vaccinated population, this would mean
approximately 18 million vaccine injuries. A Pollfish survey released on July 4, 2022 reported that 8.64%
of adult respondents who had received a COVID-19 vaccine in the U.S. developed a vaccine injury. A
Rasmussen report published in December 2022 reported a 7% rate of SAE those jabbed. In a nationwide
cohort of U.S. veterans, an adverse reaction was reported in 8.5% of recipients of the Pfizer vaccine and
7.9% of those receiving the Moderna vaccine. [4]
As the mainstream medical community does not recognize this serious humanitarian disaster, these
patients have been shunned and denied access to the care they need and deserve. Furthermore, there is
limited clinical, molecular, and pathological data on these patients to inform an approach to treating the
condition. Consequently, our approach to the management of vaccine-injured patients is based on the
presumed pathogenetic mechanism, pharmacologic principles, as well as the clinical observations of
physicians and patients themselves.
Pathogenesis
The spike protein, notably the S1 segment, is likely the major pathogenetic factor leading to post-
vaccine syndrome (see Figure 1). [4-6] The S1 protein is profoundly toxic. Multiple intersecting and
overlapping pathophysiologic processes likely contribute to the vast spectrum of vaccine injuries: [1;7]
• The acute, immediate reaction (within minutes to hours) is likely the result of an acute type I
IgE-mediated hypersensitivity reaction. The type I response may be due to preformed antibodies
against mRNA, polyethylene glycol (PEG) [8;9], or other components of the nano-lipid particle. In
addition, PEG activates multiple ‘complement components,’ the activation of which may be
responsible for both anaphylaxis and cardiovascular collapse. [9-11] A prospective study on
64,900 medical employees, in which reactions to their first mRNA vaccination were carefully
monitored, found that 2.1% of subjects reported acute allergic reactions. [12]
• The acute myocarditis/sudden cardiac death syndrome that occurs post-vaccination (within
hours to 48 hours), noted particularly in young athletes, may be caused by a “stress
cardiomyopathy” due to excessive catecholamines produced by the adrenal medulla in response
to spike protein-induced metabolic aberrations. [13]
• The subacute and chronic myocarditis is likely the result of a spike protein-induced
inflammatory response mediated by pericytes and macrophages. [14;15]
• The subacute (days) and chronic (weeks to years) vaccine-related injuries likely result from the
overlapping effects of an S1-induced inflammatory response, the production of autoantibodies,
activation of the clotting cascade, and secondary viral reactivation.
• The inflammatory response is mediated by spike protein-induced mononuclear cell activation in
almost every organ in the body but most notably involving the brain, heart, and endocrine
organs.
The spike protein of SARS-CoV-2 has extensive sequence homology with multiple endogenous human
proteins and could prime the immune system toward development of both auto-inflammatory and
autoimmune disease. [11] As a consequence of molecular mimicry with the spike protein, a diverse
spectrum of autoantibodies has been reported. [36-46] These autoantibodies are the likely cause of
Guillain-Barré Syndrome (GBS), transverse myelitis, immune thrombocytopenia, and Small Fiber
Neuropathy (SFN)/Autonomic neuropathy. [47-54]
Many of these antibodies are directed against G-protein-coupled cell membrane receptors. [43;45] Anti-
neuronal antibodies likely contribute to the myriad of neurological findings. SFN/autonomic neuropathy
appears to be a characteristic disorder following vaccination and is strongly associated with a vast array
of autoantibodies. Further, autoantibodies may result in a number of specific syndromes, including anti-
phospholipid syndrome, systemic lupus erythematosus (SLE), rheumatoid arthritis, etc.
The spike protein is highly thrombogenic, directly activating the clotting cascade; in addition, the clotting
pathway is initiated via inflammatory mediators produced by mononuclear cells and platelets. [6]
Activation of the clotting cascade leads to both large clots (causing strokes and pulmonary emboli) as
well as micro clots (causing microinfarcts in many organs, but most notably the brain). Emerging data
suggest that the vaccines can induce an allergic diathesis (eczema, skin rashes, asthma, skin and eye
itching, food allergies, etc.) This appears to be due to a unique immune dysregulation with antibody
class switching (by B cells) and the production of IgE antibodies. There is an overlap with Mast Cell
Activation Syndrome (MCAS) and the distinction between the two disorders is not clear. [55;56]
However, by definition MCAS has no identifiable causes, is not caused by allergen-specific IgE, and has
no detectable clonal expansion of mast cells. [55]
And finally, due to altered immune function, the activation of dormant viruses and bacterial pathogens
may occur, resulting in reactivated Herpes Simplex, Herpes Zoster, Epstein Barr Virus (EBV), and
cytomegalovirus (CMV) infection, as well as reactivation of Lyme disease and mycoplasma. [57-60]
The common factor underlying the pathogenic mechanism in the vaccine-injured patient is “immune
dysregulation.” The development of immune dysfunction and the severity of dysfunction likely result
from several intersecting factors, including:
• Genetics: First-degree relatives of patients who have suffered a vaccine injury appear to be at a
very high risk of vaccine injury. Those patients with a methylenetetrahydrofolate reductase
(MTHFR) gene mutation [61] and those with Ehlers-Danlos type syndromes may be at an
increased risk of injury. MTHFR C677T polymorphism is the most common MTHFR single
nucleotide polymorphism (SNP) and the most common genetic cause of hyper-
The most common symptoms recorded in post-vaccine syndrome are presented in Figure 2. On average,
patients reported 23 distinct symptoms. (Results from PVS Survey Germany; Reproduced with
permission from React19.)
Figure 2. Post-Vaccine syndrome is a multi-symptomatic disease
• It is important to emphasize that there are no published reports detailing the management of
vaccine-injured patients. Our treatment approach is, therefore, based on the postulated
pathogenetic mechanism, pharmacologic principles, clinical observation, and feedback from
vaccine-injured patients.
• The core problem in post-vaccine syndrome is chronic “immune dysregulation.” The primary
treatment goal is to help the body to restore and normalize the immune system—in other
words, to let the body heal itself. We recommend the use of immune-modulating agents and
interventions to dampen and normalize the immune system rather than the use of
immunosuppressant drugs, which may make the condition worse. However, the concomitant
use of a controlled course of an immunosuppressant drug may be appropriate in patients with
specific autoimmune conditions.
• The treatment strategy involves two major approaches i) promote autophagy to help rid the cell
of the spike protein and ii) interventions that limit the toxicity/pathogenicity of the spike
protein.
• Treatment must be individualized according to each patient’s presenting symptoms and disease
syndromes. Not all patients respond equally to the same intervention; this suggests that the
treatment must be individualized according to each patient’s specific response. A peculiar
finding is that a particular intervention (e.g., Hyperbaric oxygen therapy) may be lifesaving for
one patient and totally ineffective for another.
• Patients should serve as their own controls and the response to treatment should dictate the
modification of the treatment plan. One (or at most two) new interventions should be added at
a time in order to evaluate what helps the patient and those interventions that are not helpful.
• Early treatment is essential; the response to treatment will likely be attenuated when treatment
is delayed.
• Patients should be started on the primary treatment protocol; this should, however, be
individualized according to the patient’s particular clinical features. The response to the primary
treatment protocol should dictate the addition or subtraction of additional therapeutic
interventions. Second-line therapies should be started in those who have responded poorly to
the core therapies and in patients with severe incapacitating disease.
• Patients with post-vaccine syndrome must not receive further COVID-19 vaccines of any type.
Likewise, patients with long COVID should avoid all COVID vaccinations.
• Patients with post-vaccine syndrome should do whatever they can to prevent themselves from
getting COVID-19. This may include a preventative protocol (see FLCCC protocols). In the event
they do contract the virus or suspect infection, early treatment is essential (see FLCCC
protocols). COVID-19 will likely exacerbate the symptoms of vaccine injury.
• Vaccine-injured patients are frequently desperate to try any medication or intervention they
believe may help them. Unfortunately, unscrupulous providers will take advantage of these very
vulnerable patients and sell them expensive and unproven remedies.
• Patients should avoid unscientific and poorly validated “Spike Protein Detox” programs.
• Hyperbaric oxygen therapy (HBOT) should be considered in cases of severe neurological injury
and in patients showing a rapid downhill course (see below).
• Once a patient has shown a clinical improvement the various interventions should be reduced or
stopped one at a time. A less intensive maintenance approach is then suggested.
The first is the “typical” post-vaccine, muti-symptomatic syndrome characterized typically by fatigue,
brain fog, and other multiple complex symptoms (see figure 2). This syndrome is characterized by
microvascular inflammation and microvascular thrombosis as part of the complex pathophysiology of
post-vaccine spike related disease (see Figure 1).
The second is that of sudden cardiac death within the first 2 weeks (usually first 7 days) following the
last dose of vaccination. The early sudden deaths are likely arrhythmogenic deaths related to
catecholamine-induced contraction band necrosis and spike-induced inflammatory myocarditis (often
focal myocarditis).
The third phenotype includes those otherwise healthy patients who “die suddenly” 4 to 6 months after
the last dose of the COVID vaccine. Patients with this phenotype typically lack the typical symptoms
characteristic of post-vaccine syndrome. While the pathology of this syndrome has not been studied (as
Dr. Steven R. Gundry, a cardiac surgeon, performed a biomarker-based cardiac risk assessment score
(the PULS Cardiac Test now available as the SMARTVascular Dx provided by SmartHealth Dx
https://www.smarthealthdx.com) in 566 patients 2 to 10 weeks following the 2nd mRNA COVID shot
and compared this score to the PULS score drawn 3 to 5 months prior to the jab. [69] The PULS score is a
marker of endothelial inflammation. In this study, the 5-year Acute Coronary Risk Score (ACS) increased
from a baseline of 11% to 25% after the jab. This study clearly demonstrates that the mRNA ‘jabs” lead
to progressive endothelial inflammation.
To complicate matters further, the clots (micro-clots and macro-clots) that develop in patients with
spike-related disease are distinctly different from “usual clots” and have a number of unique
characteristics. These clots are rich in fibrin with amyloid-like fibrils and are more resistant to
fibrinolysis. Immunohistochemical staining demonstrates a high concentration of spike protein within
the clots; this is important as spike protein via multiple mechanisms activates clotting as well as altering
the structure of fibrin resulting in amyloid-like fibrils.
Based on this information, it would seem intuitive that the use of anti-coagulants and the approach to
treatment would be different for these three phenotypes; however, the ideal approach has yet to be
determined. A provisional approach to anticoagulation is provided below. A review of the
pharmacological properties of the various anticoagulants available to the healthcare provider is
provided. The general approach to the management of the multi-symptom vaccine syndrome is then
reviewed.
The greatest risk with the use of anticoagulant drugs is clinically significant bleeding. A number of
factors increase the risk of bleeding; [70-72] these include age > 65 years (advanced age is a major risk
factor for bleeding), hypertension, renal impairment, diabetes, previous stroke, a previous bleed, and
male sex. Furthermore, the risk of bleeding increases exponentially as the number of anticoagulant/anti-
platelet drugs is increased. [71;73]
Antiplatelet drugs:
• Aspirin (ASA): ASA produces a clinically relevant antiplatelet effect by irreversibly acetylating
the active site of cyclooxygenase-1 (COX-1), which is required for the production of
thromboxane A2, a powerful promoter of platelet aggregation. These effects are achieved by
daily doses of 75 mg (and higher). The major adverse effect is bleeding. Bleeding most
commonly occurs in the gastrointestinal tract and is rarely fatal. Bleeding also occurs at other
sites, with intracranial bleeding being the rarest (approximately 4 per 10,000) but the most
serious (with a 50% case fatality rate).
• Clopidogrel (Plavix): Clopidogrel requires in vivo biotransformation to an active thiol metabolite.
The active metabolite irreversibly blocks the ADP receptors on the platelet surface, which
prevents activation of the GPIIb/IIIa receptor complex, thereby reducing platelet aggregation.
Similar to ASA, platelets blocked by clopidogrel are affected for the remainder of their lifespan
(~7 to 10 days). The usual dose is 75mg daily.
• “Typical” post-vaccine syndrome. The default treatment is low-dose aspirin (ASA) (81mg daily).
In patients at low risk of bleeding (see risk factors) nattokinase can be added. Pretorius et al
reported on the use of “triple therapy” in 24 patients with long COVID and the presence of fibrin
amyloid microclots on live blood analysis. [96] Patients were treated with one month of dual
antiplatelet therapy (Clopidogrel 75mg/Aspirin 75mg) once a day, as well as Apixaban 5 mg
twice a day. This was followed by ASA and nattokinase alone. These authors reported that “each
of the 24 treated cases reported that their main symptoms were resolved, and this was also
reflected in a decrease of both the fibrin amyloid microclots and platelet pathology scores.”
Triple therapy can be considered in patients at low risk of bleeding (see risk factors) who have
responded poorly to the combination of ASA and nattokinase alone; however, triple therapy
should only be instituted under the direct supervision and monitoring of a clinician with
expertise in the management of anti-coagulation.
• Early sudden death. Early post-vaccination sudden cardiac death is a condition of young
patients, especially men. This is the most problematic phenotype with no clear guidance on the
prevention of this fatal condition (except to stop vaccination in this high-risk group). Many of
the deaths occur during physical activity (sudden death in soccer players); consequently,
vigorous physical activity should be avoided for at least 3 weeks following vaccination.
Magnesium supplementation (see section on magnesium) may reduce the risk of arrhythmic
deaths. The role of anti-inflammatory agents (e.g., curcumin, resveratrol, Nigella sativa, Omega-
3 fatty acids) is unclear.
• Late cardiac deaths (4-6 months after “jab”). Ideally, these asymptomatic patients should be
risk stratified with the initiation of prophylactic measures in the moderate to high-risk groups.
Unfortunately, as this catastrophic disorder is not generally recognized and has therefore not
been studied, there is no data to allow for risk stratification. Serial cardiac risk biomarker
analysis may be helpful; [69] however, this test is expensive and not widely available. In the
absence of a risk stratified approach, the following interventions may reduce the risk of acute
myocardial infarction and sudden death: [97]
• ASA 81 mg daily
• Nattokinase 100-200 mg twice daily (in those with low risk of bleeding)
• Omega-3 fatty acids 2-4 g daily
• Resveratrol or flavonoid combination supplement
• “Green based diet”- Low carbohydrate, high fat diet (low in omega-6 vegetable oils)
Note that fasting is contraindicated in patients younger than 18 (impairs growth), malnourished
patients (BMI < 20 kg/m2), and during pregnancy and breastfeeding. Patients with diabetes,
gout, and serious underlying medical conditions should consult their primary care physician
before undertaking fasting, as changes in their medications may be required and these patients
require close monitoring.
Proton pump inhibitors (PPI) should be avoided as they prevent the acidification of lysosomes
and block autophagy. [105] Patients may develop rebound esophagitis if a PPI is suddenly
discontinued. H2-blockers (famotidine, ranitidine, etc.) may be an alternative. Aloe Vera
Stomach Formula (Aloe Vera contains over 200 biologically active components) and diluted
Apple Cider vinegar (tastes awful) have been suggested as an alternative to a PPI; however,
there is limited data to support these interventions. [106;107]
Chloroquine and hydroxychloroquine (HCQ) act by alkalinizing lysosomes and therefore interfere
with the autophagy process. [108;109] Based on this data, HCQ may limit the benefit of
intermittent fasting.
Paradoxically, while autophagy may prevent cancers, autophagy may promote the growth of
cells that have already undergone malignant transformation. Cancer cells, which have an
increased metabolic demand for energy and macromolecular building blocks to proliferate,
show elevated levels of autophagy to recycle nutrients. [110] High-dose HCQ (more than 800
mg/day) has been demonstrated to improve the outcome of patients with certain cancers by
inhibiting autophagy. [111-115] This data suggests caution in activating autophagy (fasting) in
patients with cancer. However, “fasting mimicking diets” as an adjunct to chemotherapy have
been reported to improve quality-of-life indicators. [116-118] Patients should discuss fasting and
fasting protocols with their treating oncologist.
A number of intermittent fasting plans can be adapted and modified to best suit the patient’s
lifestyle. [98] For timed fasting, begin slowly: start with a 12-hour eating window 5 days a week
and reduce weekly to an 8-hour eating window 7 days a week. This eating window can be
shortened to 4 hours or less over time. Timed fasting can be interspersed with 36- to 48-hour
It is important to stay well-hydrated during fasting periods; drink lots of water and/or an
electrolyte solution. In his book the “Complete Guide to Fasting,” Jason Fung, MD recommends
drinking coffee with added coconut oil (medium chain triglycerides)/heavy cream (no CHO or
protein) during fasting. [98] Remarkably, caffeine stimulates autophagy, [120-122] while
coconut oil has numerous health benefits. [123-125]
Several studies have suggested that intermittent fasting may not be as beneficial for pre-
menopausal women as it is for men. This is likely because calorie restriction in females is
associated with changes in the release of hypothalamic hormones, which may impact the
menstrual cycle.
Although there are no comparable human studies, experiments in rats have shown that 3–6
months of alternate-day fasting caused a reduction in ovary size and irregular reproductive
cycles in female rats. [126] Similarly, in a murine model, Kumar and Kaur demonstrated that
intermittent fasting negatively influences reproduction in young animals due to its adverse
effects on the complete hypothalamus-hypophysial-gonadal axis. [127] However, it should be
noted that, in this study, the female rats were very young (3 months old), which corresponds to
a human aged 9 years old. [128] Heilbronn et al reported that alternate-day fasting adversely
affected glucose tolerance in nonobese women but not in nonobese men. [129]
Changes in gonadotropins during fasting have only been assessed in one clinical trial to date. In
this trial by Li et al., young women with obesity and polycystic ovarian syndrome (PCOS)
followed an early 8-hour time-restricted eating regimen for 5 weeks. [130] At the conclusion of
the study, LH and FSH remained unchanged. It is possible that alternate-day fasting results in
greater disruption of the hypothalamus-hypophysial-gonadal axis than does 8-hour time-
restricted eating. In addition, the timing of time-restricted eating may be important. Jakubowicz
et al demonstrated that a large meal later in the day (at dinner) augmented estrogen levels in
women with PCOS as compared to eating earlier in the day. [131]
There are many anecdotal stories of women who have experienced changes to their menstrual
cycles after starting intermittent fasting (likely alternate-day or fasting > 24 hours). For this
reason, pre-menopausal women may need to follow a modified approach. To reduce any
adverse effects, women should take a mild approach to fasting: shorter fasts and fewer fasting
days. We would suggest beginning a program of time-restricted eating consisting of fasting for
12 hours for two to three days a week and increasing from there (see Figure 4). Furthermore,
the fasting window should begin at least 4 hours before going to sleep.
It is important to emphasize that patients should eat real food (as opposed to processed food)
and a low-carbohydrate, high-fat (LCHF) diet is preferred (e.g., Keto diet,). Fasting days should
be nonconsecutive and spaced evenly across the week (for example, Monday, Wednesday, and
Friday). With time, the fasting window can slowly be increased to 16 hours and the number of
fasting days per week increased. It has been suggested (with no published data) that the cycle of
intermittent fasting be linked to the menstrual cycle; namely, with a 16-hour fasting window
“I started 14:10 daily for a couple of weeks (14 hours fasting, eating for 10 hours); Then 16:8
daily for another two weeks (16 hours fasting; eating for 8 hours); Finally,18:6 for 3-4 days
out of a week with the rest of the week 16:8.
I try to stop any oral intake other than water three hours before bedtime — I found this is the
most critical factor in how I feel the next day. I have not noticed any side effects from
intermittent fasting other than a few pounds of unintentional weight loss. However, I have
experienced an improvement in my health.”
____________________________
• Moderating physical activity. Patients with long COVID and post-vaccine symptoms frequently
suffer from severe post-exertional fatigue and/or worsening of symptoms with exercise.
[133;134] Aerobic exercise is reported to be one of the worst therapeutic interventions for these
patients. Similar to patients with chronic fatigue syndrome, post-exertional fatigue may be
related to mitochondrial dysfunction and the inability to augment production of ATP.
[133;135;136] Magnetic resonance–augmented cardiopulmonary exercise testing suggests
failure to augment stroke volume as a potential mechanism of exercise intolerance in patients
with long COVID. [137] We recommend moderating activity to tolerable levels that do not
worsen symptoms, keeping the patient’s heart rate under 110 BPM. Furthermore, patients need
to identify the activity level beyond which their symptoms worsen, and then aim to stay below
that level of activity. Stretching and low-level resistance exercises are preferred over aerobic
exercises.
• Melatonin; 2-6 mg slow release/extended release before bedtime. Melatonin has anti-
inflammatory and antioxidant properties and is a powerful regulator of mitochondrial function.
[153-157] The dose should be started at 750 mcg (μg) to 1 mg at night and increased as
tolerated. Patients who are slow metabolizers may have very unpleasant and vivid dreams with
higher doses.
• Methylene blue; 10-30 mg daily. Methylene blue (MB) has several biological properties that
may be potentially beneficial in vaccine-injured patients. MB induces mitophagy (mitochondrial
autophagy) and has anti-inflammatory, antioxidant, neuroprotective, and antiviral properties.
[158;159] A study in 2013 found that methylene blue-induced neuroprotection is mediated, at
least in part, by macroautophagy through the activation of AMPK signaling. [160] MB easily
crosses the BBB and preferentially enters neuronal mitochondria. MB has high bioavailability in
the brain with brain tissue levels tenfold higher than serum levels. [161;162] Low-dose
methylene blue (LDMB) stimulates mitochondrial respiration by donating electrons to the
electron transport chain. MB can reroute electrons directly from complex I to complex III,
avoiding electron leakage and subsequent ROS production.
Low Dose Methylene Blue (LDMB) is a therapeutic option in patients with brain fog and other
neurological symptoms; this can be combined with transcranial photobiomodulation. Patients
and/or their healthcare providers must purchase high-quality, impurity-free, pharmaceutical-
grade methylene blue. Patients may purchase a 1% methylene blue solution (e.g.
https://www.bphchem.com/product/methylene-blue-1-usp-grade-50-ml-1-drop-contains-0-5-
mg-of-methylene-blue/), MB Buccal Trouches (https://troscriptions.com/products/), or MB in a
powder form requiring reconstitution into a 1% solution (e.g. from CZTL at
https://cztl.bz/?ref=Lwr85 ). Trouches will cause blue staining of the mouth and teeth; they can
be swallowed to avoid this effect.
Dosing of LDMB:
• Start with 5 mg (.5 ml or 10 drops) twice daily for the first week.
• Then gradually increase the dosage every 2-3 days (guided by symptoms - i.e.,
improvement in fatigue and/or cognitive improvement) until you reach a maximum of
30 mg (3 ml) per day (30 drops twice daily).
• Take the 7th day off every week to allow the body to “reset”.
The optimal dose is highly individualized and each patient needs to find the right dose for them.
LDMB will cause your urine to be blue or blue-green. Some patients may experience a Herx
reaction. A Herx reaction may cause fatigue, nausea, headache, or muscle pain. If you
experience a Herx reaction, stop the protocol for 48 hours and then resume again slowly.
CAUTIONS:
• Sunlight and Photobiomodulation (PBM). PBM is referred to in the literature as low-level light
therapy, red light therapy, and near-infrared light therapy. Our forefathers roamed the earth
and were exposed to sunlight daily, likely with profoundly important health benefits. [166] The
spectral radiance of solar radiation extends from 10 nm to about 3000 nm i.e., the spectrum
from ultraviolet (10-400 nm), visible (400-700 nm with red light 600-700 nm), near-infrared
radiation (750-1500 nm (NIR-A)) and mid-infrared radiation (1500- 3000 nm (NIR-B)).
Of all the wavelengths of sunlight, NIR-A radiation has the deepest penetration into tissues,
being up to 23cm. NIR-A in the range of 1000 to 1500 nm is optimal for heating tissues. Sunlight
has great therapeutic powers. Indeed, during the 1918 influenza pandemic, “open-air treatment
of influenzae” appeared to be the most effective treatment for seriously ill patients. [167] The
Surgeon-General of Massachusetts reported that “plenty of air and sunshine” was highly
effective for the treatment of influenza pneumonia. He reported that “very little medicine was
given after the value of plenty of air and sunshine had been demonstrated.” Further, he
comments “from being discouraged, the medical staff became enthusiastic, and the patients
were treated with the confidence that at last something had been found which would give good
results.”
A more recent large prospective study demonstrated that avoiding sun exposure is a risk factor
for all-cause mortality. [168] In this study, the mortality rate amongst avoiders of sun exposure
was approximately twofold higher compared with the highest sun exposure group. Apart from
UV radiation stimulating vitamin D synthesis, red and near-infrared (NIR) radiation have a
profound effect on human physiology, notably acting as a mitochondrial stimulant and
increasing ATP production. [169]
The most well-studied mechanism of action of PBM centers around enhancing the activity of
cytochrome c oxidase, which is unit four of the mitochondrial respiratory chain, responsible for
the final reduction of oxygen to water. In addition, one of the most reproducible effects of PBM
is an overall reduction in inflammation. PBM has been shown to reduce markers of M1
phenotype in activated macrophages. [169] Many reports have shown reductions in reactive
nitrogen species and prostaglandins in various animal models. In addition, PBM activates a wide
range of transcription factors leading to improved cell survival. It has also been suggested that
NIR light increases the production of melatonin in mitochondria. [170]
In an outstanding in vitro study, Aguida et al demonstrated that infrared light caused a marked
reduction in the TLR-4-dependent inflammatory response pathway in a human cell culture line.
[171] In this study, infrared light exposure resulted in a significant decline in NFkB and AP1
activity as well as a marked decrease in the expression of proinflammatory genes. The increased
body temperature induced by NIR-A and NIR-B activates the production of heat shock proteins
(which increase autophagy) as well as essential cell stress survival pathways.
Emerging data suggest that transcranial PBM has beneficial effects in a range of neuro-
psychiatric diseases including stroke, traumatic brain injury, Alzheimer's disease, Parkinson’s
disease, and depression. [172-175] PBM has been suggested to have a role in the prevention
and treatment of COVID-19. [176] A recent double-blind, sham-controlled study using an LED
The disadvantage of LED panels is they do not mimic that of solar radiation as they deliver 1-10
nm wide spiked emissions of red light at 660 nm and NIR-A at 830 nm. In contrast, ThermaLight®
bulbs (SaunaSpace® Saunas™) have a radiation spectrum closely resembling that of solar
radiation, but without UV radiation. About 39% of the emitted spectrum of the ThermaLight®
bulb is NIR-A (the solar spectrum has 41% IR-A) and about 41% of the radiation is in the IR-B
range; part of IR-A and IR-B (1000-3000 nm) contributes to the thermal effects of emitted
radiation, which promotes induced hyperthermia (sauna therapy) and is discussed below under
“Other Potential Therapies”.
• Magnesium; 100-400 mg daily. There are at least 11 different types of magnesium that can be
taken in supplement form with varying bioavailability. Generally, organic salts of Mg have a
higher solubility than inorganic salts and have greater bioavailability. [189] Magnesium citrate is
a widely used type of magnesium in salt form and is often recommended to treat constipation;
high doses may cause diarrhea and prolonged use should be avoided. Magnesium oxide and
magnesium citrate compounds, commonly prescribed by physicians, have poor bioavailability.
[190] Magnesium Malate, Taurate, Glycinate, and L-threonate have good bioavailability and will
readily increase RBC magnesium levels. Magnesium taurate and magnesium L-
threonate significantly increase magnesium levels in brain cells; hence they are used in the
treatment of depression and Alzheimer’s disease. [190;191] A starting dose of 100 to 200 mg
daily is suggested, increasing the dose as tolerated up to 300 mg (females) to 400 mg daily.
Endpoints of treatment include an RBC-Mag at the higher end of the normal range (between 4.2
and 6.8 mg/dL to be about 6.0 ng/dL). High intakes of magnesium from dietary supplements and
medications can cause diarrhea, nausea, and abdominal cramping.
• N-acetyl cysteine (NAC); 600-1500 mg/day [192-194] NAC is the precursor of reduced
glutathione. NAC penetrates cells where it is deacetylated to yield L-cysteine thereby promoting
GSH synthesis. [194] Based on a broad range of antioxidant, anti-inflammatory, and immune-
modulating mechanisms, the oral administration of NAC likely plays an adjuvant role in the
treatment of the vaccine injured. Several studies showed that NAC is well absorbed by the
intestine and that supplementation with NAC is effective for increasing GSH levels.
Oral glutathione is poorly absorbed and is generally not recommended. [195;196] However,
acetyl glutathione is more lipophilic than glutathione, sufficiently so to be taken up intact by
cells, and has been shown to rapidly raise intracellular GSH levels. A combination supplement
that contains acetyl glutathione, NAC, and Vitamin C may enhance the bioavailability of
glutathione. In addition, liposomal glutathione has been demonstrated to increase tissue levels,
antioxidant capacity, and immune function. [197]
• Nigella sativa; 200-500 mg encapsulated oil twice daily. Nigella sativa is a small shrub native to
Southern Europe, North Africa, and Southeast Asia. The seeds and oil of Nigella sativa have been
used as a medical agent for thousands of years. The most important active component is
thymohydroquinone. Nigella sativa has antibacterial, antifungal, antiviral (SARS-CoV-2), anti-
inflammatory, antioxidant, and immunomodulatory properties. [217;218] A dose of 200-500 mg
twice daily of the encapsulated oil is suggested. [217-220] It should be noted that
thymohydroquinone decreases the absorption of cyclosporine and phenytoin. Patients taking
these drugs should, therefore, avoid taking Nigella sativa. [221] Furthermore, two cases of
serotonin syndrome have been reported in patients taking Nigella sativa who underwent
general anesthesia (probable interaction with opiates). [222]
• Vitamin C; 1000 mg orally two to three times a day. Vitamin C has important anti-inflammatory,
antioxidant, and immune-enhancing properties, including increased synthesis of type I
interferons. [223-227] Avoid in patients with a history of kidney stones. Oral Vitamin C helps
promote the growth of protective bacterial populations in the microbiome.
• Vitamin D (4000-5000 units/day) and Vitamin K2 (100 mcg/day); The dose of Vitamin D should
be adjusted according to the baseline Vitamin D level. However, a dose of 4000-5000 units/day
of Vitamin D, together with Vitamin K2 100 mcg/day is a reasonable starting dose.
• Fluvoxamine; 50 mg twice daily: Start on a low dose of 12.5 mg/day and increase slowly as
tolerated. NOTE: Some individuals who are prescribed fluvoxamine experience acute anxiety,
• Intravenous Vitamin C; 25 g weekly, together with oral Vitamin C 1000 mg (1 gram) 2-3 times
per day. High-dose IV vitamin C is “caustic” to the veins and should be given slowly over 2-4
hours. Furthermore, to assess patient tolerability the initial dose should be between 7.5-15 g.
Total daily doses of 8-12 g have been well-tolerated, however, chronic high doses have been
associated with the development of kidney stones, so the duration of therapy should be limited.
[103-108] Wean IV Vitamin C as tolerated.
Third-Line Therapies
• Hyperbaric oxygen therapy (HBOT) [241-249]; HBOT has potent anti-inflammatory properties,
decreasing pro-inflammatory cytokines while increasing IL-10. Furthermore, HBOT polarizes
macrophages toward the M2 phenotype and improves mitochondrial function. Surprisingly, it is
the increased pressure, rather than the increase in the concentration of dissolved oxygen, that
appears to mediate these effects. HBOT is delivered at varying pressures, both with and without
oxygen. The addition of oxygen increases the clinical response. Maximal clinical response is
achieved via the use of high-pressure chambers (typically reaching 2.4 ATM) with 100% oxygen
for 60-90 minutes. If HBOT is delivered using lower pressure chambers (less than 1.5 ATM)
without supplemental oxygen, the clinical response, although present, is significantly less such
that a higher number of sessions will be needed to reach a clinical plateau.
• Hydroxychloroquine (HCQ); 200 mg twice daily for 1-2 weeks, then reduce as tolerated to 200
mg/day. HCQ is a potent immunomodulating agent and is considered the drug of choice for
systemic lupus erythematosus (SLE), where it has been demonstrated to reduce mortality from
this disease. Thus, in patients with positive autoantibodies or where autoimmunity is suspected
to be a prominent underlying mechanism, HCQ should be considered earlier. Further, it should
be noted that SLE and post-vaccine syndrome have many features in common. HCQ is safe in
pregnancy; indeed, this drug has been used to treat preeclampsia. [259-263] With long-term
usage, the dose should be reduced (100 or 150mg/day) in patients weighing less than 61 kg (135
lbs.). It should be noted that HCQ will limit the effectiveness of intermittent fasting.
• Low dose corticosteroid; 10-15 mg/day prednisone for 3 weeks. Taper to 10 mg/day and then 5
mg/day, as tolerated.
• Valproic acid [274;275]; Depakote, 250mg 2-3 times daily. Valproic acid has anti-inflammatory
effects and polarizes macrophages towards an M2 phenotype. [276] Histone deacetylase (HDAC)
inhibitors are being studied for neural regeneration. In addition, valproic acid has important
anticoagulant and anti-platelet effects [277] and is an inducer of heat shock proteins. [278]
Valproic acid may be helpful for neurological symptoms. Treatment should be limited to less
than 6 to 9 months due to the concern for the loss of brain volume particularly in those patients
with cognitive dysfunction. [279] In a cerebral ischemia/hypoxia model resveratrol markedly
enhanced the neuroprotective effects of valproic acid. [280] Furthermore, resveratrol has been
reported to reverse the toxicity of valproic acid, [281;282]. These data suggest that resveratrol
(in a dose of 500 mg – 1000 mg twice daily) should be recommended in patients prescribed
valproic acid.
• Induced hyperthermia and Cold Hydrotherapy. The role of sauna bathing and cold therapy
(cold showers, cold baths) in patients with long COVID and vaccine injury is unknown. [283;284]
Regular sauna bathing has been proven to reduce all-cause and cardiovascular mortality,
prolong lifespan, improve exercise performance, and improve the outcome of patients with
neuropsychiatric disease. [285-289] Induced hyperthermia increases the expression of heat
shock proteins, which activates autophagy. In addition, heat therapy increases the expression of
cell stress pathways, has antioxidant and anti-inflammatory effects, and improves mitochondrial
function. [283] Sauna bathing has very similar physiologic effects to that of aerobic exercise
(increase heart rate, stroke volume, and cardiac output). [290;291] As patients with long COVID
and the vaccine-injured are exercise intolerant (they cannot increase cardiac output) [137]
sauna bathing may be poorly tolerated. However, sauna bathing and induced hyperthermia
have been shown to improve endothelial and cardiac function in patients with chronic heart
failure. [292] Furthermore a recent meta-analysis reported that sauna bathing improved cardiac
function in patients with chronic heart failure. [293] Waon therapy (infrared dry sauna) has
shown promising results in patients with chronic fatigue syndrome. [294;295] Patients
interested in sauna bathing should determine their tolerance to short sessions (5-10 mins) and
increase the duration as tolerated (up to 20 minutes) three to four times a week. Similarly, the
• Pentoxifylline (PTX); PTX ER, 400 mg three times daily, should be considered in those patients
with severe microcirculatory disturbances. PTX is a non-selective phosphodiesterase drug that
has anti-inflammatory and antioxidant effects. [224] In addition, PTX improves red blood cell
deformability and reduces blood viscosity, so can mitigate the hyper-viscosity and RBCs hyper-
aggregation, which is linked with the development of coagulopathy in the vaccine injured.
• Maraviroc; 300 mg orally twice daily. If 6 to 8 weeks have elapsed and significant symptoms
persist despite the above therapies, this drug can be considered. Note Maraviroc can
be expensive and has a risk of significant side effects and drug interactions. Maraviroc is a C-C
chemokine receptor type 5 (CCR5) antagonist. While many long COVID and post-vaccine patients
have been treated with Maraviroc, the role of this drug requires further evaluation. [298]
• Sulforaphane (broccoli sprout powder) 500 mcg – 1g twice a day. While sulforaphane has many
potential benefits in patients with COVID, [299-301] long COVID and post-vaccine syndrome,
there is limited clinical data to support this intervention. Sulforaphane has immunomodulatory
effects by targeting monocytes/macrophages, suggesting a benefit in chronic inflammatory
conditions. [299-301] Sulforaphane is a beneficial supplement that may be useful for reducing
microglial-mediated neuroinflammation and oxidative stress. In addition, as has been well-
popularized, sulforaphane has an important role in cancer prophylaxis. The pharmacology and
optimal dosing of sulforaphane are complex. Sulforaphane itself is unstable. The supplement
should contain the two precursors, glucoraphanin and myrosinase, which react when the
supplement is consumed. Broccoli “extracts” are produced in a way that completely destroys
the activity of the myrosinase enzyme. As such, these extracts are incapable of producing
sulforaphane when consumed in a supplement or food. [302;303] We recommend a 100%
whole broccoli sprout powder, which maximally retains both glucoraphanin and
myrosinase whilst, at the same time, deactivating the inhibitors.
• Dandelion (Taraxacum officinale). The root, flower, and leaves of dandelion contain an array of
phytochemicals that have anti-inflammatory, antioxidant, hypolipidemic, antimicrobial, and
anticoagulant properties. [304;305] It is widely reported that dandelion is effective for
‘detoxifying’ spike protein. An in vitro study demonstrated that a dandelion leaf extract altered
the binding of SARS-CoV-2 spike protein to the ACE receptor. [306] It would appear that this
effect was due to alterations (binding) of the ACE-2 receptor rather than binding to the spike
protein. It, therefore, remains unclear whether dandelion extract actually binds to the spike
protein and would potentiate clearance of this protein. The European Scientific Cooperative on
Phytotherapy recommends a dose of 4-10 g TID (20-30mg/ml in hot water). [307] It should be
noted that Dandelion extract is considered contraindicated in those with liver and biliary
disease, bile duct obstruction, gallstones, cholangitis, and active peptic ulcer. [307] Furthermore
dandelion is rich in potassium and should be used cautiously in patients with kidney failure.
• C60 or C60 fullerenes [309;310]; C60, short for Carbon 60, is composed of 60 carbon atoms
forming something that looks like a hollow soccer ball and is considered as a “free radical
sponge.” C60 is considered the single most powerful antioxidant ever discovered. Robert Curl,
Harold Kroto, and Richard Smalley were awarded the Nobel Prize for chemistry in 1996 for its
discovery.
• Intravenous immunoglobulin (IVIG) treatment; The role of IVIG in the treatment of the vaccine
injured is unclear. The response to IVIG in the general population of vaccine-injured patients is
mixed, with very few showing long-term improvement. Many patients who report an initial
improvement will relapse in 2 to 3 weeks. Other patients report no benefit, while some appear
worsened. Due to the presence of non-neutralizing anti-SARS-CoV-2 antibodies and anti-ACE-2
antibodies, etc., the real possibility exists that IVIG will cause antibody-dependent immune
enhancement (ADE) with a severe exacerbation of symptoms.
IVIG is, however, recommended in specific autoimmune syndromes, which include Guillain Barré
Syndrome, transverse myelitis, and immune thrombocytopenia. These patients should
concomitantly be treated with the core immune-modulating therapies. IVIG proved to be
ineffective in an RCT that enrolled patients with small fiber neuropathy. [311]
The fact that many patients report an initial response to IVIG supports the notion that many
aspects of this disease are due to autoantibodies. IVIG will remove preformed antibodies, but
they do not prevent the B cells from ongoing antibody production; hence the response is likely
to be short-lived, and interventions that limit the production of autoantibodies are therefore
required (core immune-modulating therapies).
Depression
• Depression is a serious problem in long COVID and post-vaccine patients and, unfortunately, suicide
is not uncommon. [326-328] Patients with a history of depression and/or those taking SSRI
medications appear to be at particular risk of severe depression.
• Patients with depression are best managed by mental health providers with expertise in this area.
Long-term SSRI medications are generally not recommended due to the long-term effects of these
drugs on serotonin receptors, and intracellular messenger pathways as well genetic and epigenetic
effects. [329;330] Short-term fluvoxamine may have a role in these patients. It should be noted that
most SSRI/SNRI agents, but notably sertraline, paroxetine, venlafaxine, and duloxetine are
associated with self-inflicted harm, suicide, anger outbursts, physical violence, homicidal thoughts,
and homicide. [331-333] Patients who are treated with antidepressant agents, therefore, require
close monitoring for the development of these serious adverse reactions.
• There appears to be an interaction between vaccination, COVID-19, zinc levels, and depression.
[334-337] COVID-19 infection and COVID vaccines may lead to low zinc levels. Zinc deficiency is
associated with an increased risk of depression. Treatment with zinc has been shown to have
antidepressant effects and to act synergistically with SSRI medication. [338] 25 mg zinc daily
(elemental), together with the zinc ionophore quercetin is therefore suggested. [337]
• Non-invasive brain stimulation (NIBS) using transcranial direct current stimulation or transcranial
magnetic stimulation has been demonstrated to be highly effective in the treatment of depression.
[339-343] Indeed, The Fisher Wallace Stimulator® is FDA-approved for the treatment of depression,
anxiety, and insomnia. NIBS is painless, extremely safe, and easy to administer. NIBS is a recognized
therapy offered by many Physical Medicine and Rehabilitation Centers. Patients may also purchase
an FDA-approved device for home use (https://www.fisherwallace.com/).
• Methylene blue (dose as indicated above) has been proven to be beneficial in patients with
depression. [344;345] Do NOT TAKE FLUVOXAMINE, FLUOXETINE, BUPROPION, or any other SSRI-
NDRI with MB.
• Photobiomodulation and sauna bathing have been shown to be highly effective for the treatment of
depression. [288;346-348]
Vaccine-induced myocarditis/pericarditis
• ACE inhibitor/ARB, together with carvedilol as tolerated to prevent/limit progressive decline in
cardiac function.
• Colchicine in patients with pericarditis – 0.6 mg/day orally; increase to 0.6 mg twice daily if
required. Reduce dose if patients develop diarrhea. Monitor white blood cell count. Decrease
dose with renal impairment.
• Magnesium to reduce the risk of serious arrhythmias (see dosing above).
• Coenzyme Q (CoQ) 200-400mg/day. [362-365]
• Omega-3 fatty acids – EPA/DHA 2-4 g/day [366-368] Increase dose slowly as tolerated.
• Resveratrol/flavanoid combination for its anti-inflammatory and antioxidant properties.
• Referral to a cardiologist or ER in case of persistent chest pain or other signs and symptoms of
cardiac events are observed.
Tinnitus
• This a frequent and disabling complication reported in post-vaccine syndrome.
• Tinnitus refers to the sensation of sound in the absence of a corresponding external acoustic
stimulus and can, therefore, be classified as a phantom phenomenon. Tinnitus sensations are
usually of an unformed acoustic nature, such as buzzing, hissing, or ringing. Tinnitus can be
localized unilaterally or bilaterally, but it can also be described to emerge within the head. [379]
• Ideally, patients should be evaluated by an ENT specialist or audiologist to exclude underlying
disorders.
• Several treatment approaches exist to manage this disabling disease including [379-381]
o Cognitive behavioral therapy [382]
o Specialized therapy including tinnitus retraining therapy, hearing aids, sound therapy,
auditory perceptual training, and repetitive transcranial magnetic stimulation. [379]
o A number of pharmacologic agents have been used to treat tinnitus. Anticonvulsants
including carbamazepine have generally been disappointing. The following drugs have
shown some clinical benefit.
• Tricyclic antidepressant agents particularly nortriptyline and amitriptyline.
[383;384] In addition, the SSRI sertraline has shown some efficacy. [385]
• Clonazepam and or other benzodiazepines. These drugs may provide temporary
relief, however, due to issues of dependence, long-term use is not
recommended. [386]
• Melatonin slow release 2-6 mg at bedtime. [387]
• Oxytocin nasal spray. Oxytocin acts as a neurotransmitter affecting several neural circuits,
particularly in the hypothalamus and amygdala. [318] Oxytocin nasal spray has shown promising
results for the treatment of tinnitus (one puff to each puff nostril two times a day; a total dosage
of 16 IU per day). [388] Oxytocin must be avoided in pregnancy. Oxytocin nasal spray should be
compounded at 12 to 15 units/0.1ml (spray) and administered at onset aggressively to
upregulate receptors at 2 sprays each nostril BID (8-sprays per day) for the first week and then
maintenance at 2 sprays ea. nostril (4/d) once daily. [323] Oxytocin can also be delivered via SL
liquid or via lozenge.
• Non-invasive brain stimulation (NIBS) has proven to be effective in controlling treatment-
resistant tinnitus. [234;235]
Patients with new onset allergic diathesis/features of Mast Cell Activation Syndrome
(MCAS)
• The novel flavonoid luteolin is reported to be a potent mast cell inhibitor. [394-397] Luteolin 20-
100 mg/day is suggested.
• Turmeric (curcumin); 500 mg/day. Curcumin has been reported to block H1 and H2 receptors
and to limit mast cell degranulation. [398;399] Curcumin has low solubility in water and is poorly
absorbed by the body; [400] consequently, it is traditionally taken with full-fat milk and black
pepper, which enhance its absorption. Nano-curcumin preparations or formulations designed to
enhance absorption are encouraged. [401-404]
• H1 receptor blockers. Loratadine 10 mg/day, Cetirizine 5-10 mg/day, Fexofenadine 180 mg/day.
• H2 receptor blockers. Famotidine 20 mg twice daily as tolerated. [405]
• Montelukast 10 mg/day. Caution as may cause depression in some patients. The efficacy of
montelukast as a “mast cell stabilizer’ has been questioned. [55]
• Ketotifen. 1 mg in 5 ml. Start with 0.5 ml at night. Once they get used to it, as it has a strong
hypnotic effect, increase by 0.5ml increments up to 5ml. Some patients can increase up to 10 ml
daily (1 mg BID). Ketotifen has antihistamine effects and is a mast cell stabilizer. Ketotifen may
be particularly useful in patients with GI hypersensitivity. [406;407]
• Vitamin C; 1000 mg twice daily. Vitamin C is strongly recommended for allergic conditions and
MCAS. Vitamin C modulates immune cell function and is a potent histamine inhibitor.
• Low histamine diet.