Therapeutics for Supporting Immunity & Long Covid
2nd April ‘22 (Methylene blue)
10th April ‘22 (Various by John Paul)
24th April ‘22 (Lemon Balm)
27th April ‘22 (St John’s Wort)
28th April ‘22 (Cannabidiol)
1st May ‘22 (Persistent viral replication in the gut)
2nd May ‘22 (“Long COVID” Guardian article & media disinformation)
23rd May ‘22 (Berberine).
14th June ‘22 (Suggested stacks added to introduction)
15th June ‘22 (Artemisia)
16th June ‘22 (“Long COVID” Guardian article = “transfection injured”, again)
17th June ‘22 (FLCC program, Management of Post-Vaccine Syndrome)
30th June ‘22 (Substack title renamed)
16th July ‘22 (Echinacea)
24th August ‘22 (Gynostemma pentaphyllum)
25th September ‘22 (Doxycycline; a focus on quercetin)
Any extracts used in the following article are for non commercial research and educational purposes only and may be subject to copyright from their respective owners.
This is not an exhaustive list, has several contributors which unfortunately I can’t all credit and I will update the list accordingly as new therapies are presented. And please please add your own in the comments if you are shouting “why didn’t you mention Icelandic kelp extract??” or something like that, new studies are coming out all the time.
The “Long Covid’ condition is very complex, one size does not fit all but if we treat it as a combination of one or more pathologies comprising immune dysfunction, viral or spike protein persistence and oxidative stress then it explains why these therapies are effective for some and are gaining a following.
Combination therapies are also often more effective than a single therapeutic as effects can reinforce each other and multiple pathways can be targeted in a virtuous feedback cycle.
Additionally, as many of these therapeutics have strong antiviral efficacy and support the immune system in general (often including antitumor & autoimmunity moderating properties) a selection of them may be taken daily as prophylactics or at the first sign of infection.
Added 14th June ‘22:
A combination of two or more nootropic substances is called a “stack."
Combining several compounds into a stack can have synergistic effects, such as in the cases of the ingredients in green tea and coffee.
Combine Nootropics Into a "Stack?”, (2020),
For the full list and biochemistry research please read on and follow up the references, but here are a few basic stacks to get you started.
Although almost all are food or plant extracts with excellent safety profiles usual cautions apply as with any med.
Start by taking each in isolation at the lowest dose and take for a week, then start combining.
Don't expect instant miracles, these can take time to act systemically as your immune system and cellular health & metabolism recovers & gut biota stabilise. Antivirals start working within hours though.
Check with your doctor first if you are on any other meds for contraindications, have allergies to certain food groups etc and never just stop a med without consultation.
Check on webMD and other sites for cautions etc. These are good places to start:
Let's take turmeric: https://www.webmd.com/vitamins/ai/ingredientmono-662/turmeric
Check the botanical institute site for the same and dosage etc:
Cardiovascular & musculoskeletal:
Vitamin K2, MK-7, “fermented” or extracted from Natto for trans isomer. Even better with 5-10mg piperine. Take 200mg+ per day with meal or fatty food.
Take with D, magnesium, zinc, (ideally zinc with copper) as these are complementary for calcium management: out of your cardiovascular system and back in to teeth & bones eg via a daily multivitamin mineral sup. Zinc is also an essential complement to zinc ionophores like hydroxychloroquine & quercetin (hat-tip to the late Dr. Vladimir Zelenko's protocols).
Daily antiviral, immune & autoimmune health:
500mg - 2000mg milk thistle with 80% silymarin. Take at same time with:
Q10 30mg+ for cardiovascular & muscles.
Resveratrol 250-500mg +
Daily or weekly:
Hemp or CBD 1 gram = 1 teaspoon dried leaves as a tea or as oil do not exceed 60-70mg in total per day.
For joint pain/RA: Glucosamine sulphate 750mg+ and ideally with Chondroitin 75mg+ twice daily for at least 6 weeks.
Turmeric as above is also broad spectrum in efficacy. Take with 5-10mg piperine.
Further antiviral support when you get symptoms of an infection, early as possible ideally:
Quercetin 500-1000mg +
- Take quercetin with vitamin C and zinc, as above, for synergistic effects.
Artemisia is consumed on a daily basis in many African countries as an effective prophylactic against malaria & HIV.
Add to the above stack berberine or goldenseal 1000mg (750-2000 range). Ivermectin if you can get it but Berberine is just as good by many accounts.
Or/and at another part of the day Sweet Wormwood, Artemisia annua (NOT toxic Common Wormwood, A. absinthium) as 1 teaspoon dried leaves in porridge, as tea, or as infusion. It's bitter so add peppermint or fennel if needed.
Tincture, added to tea:
Take 0.7-2.0mL two to four times per day of a 1:4 tincture (in 50% alcohol).
To make an infusion, pour 1 cup boiling water over 1 teaspoon of dried leaf and infuse for 10-15 minutes. For therapeutic use it is recommended to drink 2 to 4 cups a day.
Echinacaea by tincture eg added to tea:
2.5ml, 3 times a day up to 10ml.
N-Acetyl Cysteine (NAC), 600mg once or twice a day.
I bookmarked the bones of this last May in case it might help someone?
Although useful for turning down the immune system (ie anti-inflammatory) general advice is try to avoid long term use of corticosteroids as these can lead to cardiovascular disease & osteoporosis.
Instead, CBD, D & Glucosamine are natural immune regulators and are considered preferential to corticosteroids long term.
I would also add for mitochondrial function Metformin, Resveratrol via 500mg supplements or/and red wine & black grapes (Malbec, Cabernet Sauvignon, Merlot), an antioxidant rich diet, NAC, Q10, K2 sources and Ivermectin (IVM) or Hydroxychloroquine (HCQ), 10ml high omega-3 fish oils, quercetin to clear any remnant RNA spike sources. HCQ helps neurological issues too, + glucosamine as an anti cancer agent and to reduce elevated inflammatory cytokine levels.
As an aside it's no coincidence that at least 6 of the above have been cited as having significant anti-cancer properties: Metformin, Resveratrol, CBD, IVM, HCQ & Glucosamine. Turmeric is a seventh.
@ShemNehm contributed the following:
"There are lots of papers, that look at anti-oxidants as a potential therapeutic for Covid, e.g:
Perusing the list above, you'll see the usual suspects: Vitamins C&D, NAC, Thymoquinone, Quercetin, Turmeric, etc. I was wondering. I wonder if Astaxanthin could be added to the list:
My aggregation of posts on therapeutics is here:
More therapeutics are listed without in-depth detail here:”
“Vaccine Injury: Long COVID and inflammatory vaccine reaction share the same cause Spike Protein. People are going to need to know about natural remedies. This thread will offer some papers with advice. First luteolin.
Long-COVID syndrome-associated brain fog and chemofog: Luteolin to the rescue
Zinc supplementation and immune factors in adults: a systematic review and meta-analysis of randomized clinical trials
Let's look at olive leaf extract as an anti-inflammatory that fits the damage profile.
Olive Leaf Extract Attenuates Inflammatory Activation and DNA Damage in Human Arterial Endothelial Cells”
* As ever this is not medical advice, you will need to check for suitability for you, do your own additional research for dosing, mode of action and for interactions plus consult a licensed medical practitioner who knows your full medical history. For example these may suppress other meds you are on or make a condition worse.
Some of the above in detail
In vitro antioxidant activity of olive leaf extract (Olea europaea L.) and its protective effect on oxidative damage in human erythrocytes (2018)
Olive leaves are an important source of antioxidants, such as phenolic compounds and flavonoids, which display effective antioxidant activity when various methodologies are used. OLE inhibits the action of reactive species that participate in cellular biochemical processes and protects human erythrocytes against oxidative damage. These results show that olive leaves are effective antioxidant in biological systems, suggesting that their intake may be related to prevention of oxidative stress in vivo, with consequent health benefits. Moreover, OLE have the potential to be used as natural antioxidants in preservation of food products, pharmaceuticals and cosmetics, in which chain reactions mediated by free radicals result in oxidative alterations.
The compounds responsible for the antioxidant effects of OLE are not yet fully understood. Thus, additional studies are required for identification and isolation of these compounds and their efficiency. In addition, further in vivo studies should be performed to confirm the results obtained so far.
Role of Mitochondria in the Mechanism(s) of Action of Metformin
Metformin is a drug from the biguanide family that is used for decades as the first-line therapeutic choice for the treatment of type 2 diabetes. Despite its worldwide democratization, owing to its clinical efficacy, high safety profile and cheap cost, the exact mechanism(s) of action of this anti-hyperglycemic molecule with pleiotropic properties still remains to be fully elucidated. The concept that metformin would exert some of its actions though modulation of the mitochondrial bioenergetics was initially forged in the 50s but undeniably revived at the beginning of the twenty-first century when it was shown to induce a weak but specific inhibition of the mitochondrial respiratory-chain complex 1. Furthermore, metformin has been reported to reduce generation of reactive oxygen species at the complex 1 and to prevent mitochondrial-mediated apoptosis, suggesting that it can protect against oxidative stress-induced cell death. Nevertheless, despite some recent progress and the demonstration of its key role in the inhibition of hepatic gluconeogenesis, the exact nature of the mitochondrial interaction between the drug and the complex 1 is still poorly characterized. Recent studies reported that metformin may also have anti-neoplastic properties by inhibiting cancer cell growth and proliferation, at least partly through its mitochondrial action. As such, many trials are currently conducted for exploring the repositioning of metformin as a potential drug for cancer therapy. In this mini-review, we discuss both historical and more recent findings on the central role played by the interaction between metformin and the mitochondria in its cellular mechanism of action.
Resveratrol induces mitochondrial biogenesis in endothelial cells (2009)
Pathways that regulate mitochondrial biogenesis are potential therapeutic targets for the amelioration of endothelial dysfunction and vascular disease. Resveratrol was shown to impact mitochondrial function in skeletal muscle and the liver, but its role in mitochondrial biogenesis in endothelial cells remains poorly defined. The present study determined whether resveratrol induces mitochondrial biogenesis in cultured human coronary arterial endothelial cells (CAECs). In CAECs resveratrol increased mitochondrial mass and mitochondrial DNA content, upregulated protein expression of electron transport chain constituents, and induced mitochondrial biogenesis factors (proliferator-activated receptor-coactivator-1alpha, nuclear respiratory factor-1, mitochondrial transcription factor A). Sirtuin 1 (SIRT1) was induced, and endothelial nitric oxide (NO) synthase (eNOS) was upregulated in a SIRT1-dependent manner. Knockdown of SIRT1 (small interfering RNA) or inhibition of NO synthesis prevented resveratrol-induced mitochondrial biogenesis. In aortas of type 2 diabetic (db/db) mice impaired mitochondrial biogenesis was normalized by chronic resveratrol treatment, showing the in vivo relevance of our findings. Resveratrol increases mitochondrial content in endothelial cells via activating SIRT1. We propose that SIRT1, via a pathway that involves the upregulation of eNOS, induces mitochondrial biogenesis. Resveratrol induced mitochondrial biogenesis in the aortas of type 2 diabetic mice, suggesting the potential for new treatment approaches targeting endothelial mitochondria in metabolic diseases.
Resveratrol: A Double-Edged Sword in Health Benefits (2018)
Resveratrol (3,5,4′-trihydroxy-trans-stilbene) belongs to polyphenols’ stilbenoids group, possessing two phenol rings linked to each other by an ethylene bridge. This natural polyphenol has been detected in more than 70 plant species, especially in grapes’ skin and seeds, and was found in discrete amounts in red wines and various human foods. It is a phytoalexin that acts against pathogens, including bacteria and fungi. As a natural food ingredient, numerous studies have demonstrated that resveratrol possesses a very high antioxidant potential. Resveratrol also exhibit antitumor activity, and is considered a potential candidate for prevention and treatment of several types of cancer. Indeed, resveratrol anticancer properties have been confirmed by many in vitro and in vivo studies, which shows that resveratrol is able to inhibit all carcinogenesis stages (e.g., initiation, promotion and progression). Even more, other bioactive effects, namely as anti-inflammatory, anticarcinogenic, cardioprotective, vasorelaxant, phytoestrogenic and neuroprotective have also been reported. Nonetheless, resveratrol application is still being a major challenge for pharmaceutical industry, due to its poor solubility and bioavailability, as well as adverse effects. In this sense, this review summarized current data on resveratrol pharmacological effects.
Keywords: resveratrol, physiological effects, pharmacological activity, antioxidant, anticancer, antimicrobial
Covid and/or spike protein exposure can lead to or exacerbate amyloidosis, accelerating dementia & Parkinsons:
Resveratrol for Alzheimer’s disease (2017)
The amyloid hypothesis suggests that the progressive accumulation and deposition of central nervous system amyloid with aging is the proximate cause of Alzheimer’s disease (AD). Thus, targeting molecular mechanisms of aging may represent a viable treatment approach. Caloric restriction prevents diseases of aging, including AD, in animal models, perhaps by activation of sirtuins. The sirtuins (such as mammalian SIRT1) are deacetylases that link energy balance (NAD+/NADH) to regulation of gene transcription. Resveratrol is a potent activator of SIRT1, and thus may mimic caloric restriction to prevent diseases of aging. We conducted a randomized, double blind, placebo-controlled, phase II trial of resveratrol for individuals with mild to moderate AD. Resveratrol (1) is detectable in cerebrospinal fluid (at low nanomolar levels), (2) is safe and well tolerated, (3) alters AD biomarker trajectories, (4) preserves blood–brain barrier integrity, and (5) modulates the CNS immune response. Further studies are needed to determine the safety and efficacy of resveratrol and the validity of this approach in the treatment and prevention of AD and other diseases of aging.
Keywords: Alzheimer’s disease, resveratrol, sirtuin, polyphenol, amyloid
Spike protein induced carcinogenesis via interactions with Snail protein and anti-cancer effects of the over-the-counter drug Glucosamine Sulphate
Modulation of inflammation and immunity by dietary conjugated linoleic acid (2016)
Depletion due to binding to spike protein has consequences
Serratiopeptidase, A Serine Protease Anti-Inflammatory, Fibrinolytic, and Mucolytic Drug, Can Be a Useful Adjuvant for Management in COVID-19 (2021)
Added 2nd April 22:
The pathway for MIS-C, Methylene Blue as protective supplement
And my favorite inhibitor
Unlike some of the other virus posts, this one will cover more than one paper. Second, and third, paper are good news.
Added 10th April
John Paul kindly let me share his findings.
Things Hidden series - How to heal yourself from post-Covid effects
And everything else.
Lots of useful referenced links.
We mustn't forget a balanced and especially a low carb diet, with sources of sulphur, cysteine & magnesium:
Things Hidden Since the Foundation of Cognition
Or how to fix a lifetime of physiological and cognitive damage
Melatonin, NAC & Astaxanthin:
Things Hidden Since the Splicing of SARS 2 S protein (part 1)
>Or how to avoid or minimize all potential damage from the super flu.
Vit C, D, Quercetin, Fisetin, B vits & niacin, NAC, R-ALA, Omega 3, Fucoidan, Fucoidan, Isatis, Smillax officinalis, Cryptolesis, Serrapetase (Lumbrokinase), Bromelain, Olive Leaf Extract/capsules, Elderberry, Ginger, Garlic extract:
Things Hidden Since the Splicing of SARS 2 S protein (part 2)
Bursting them proteins, son !
BHB and Niacin:
Things Hidden Since the Splicing of SARS 2 S protein (part 3)
Post-human warrior !
BPC-157. Body Protectice Compound 157:
The many wonders of a peptide
Aka, The Wolverine factor
Added 24th April:
Lemon Balm, which has many active ingredients such as quercetin and phenolics with antioxidant, antifungal, antibacterial and potent anticancer properties. May be infused in tea, which is how I take it at around 1 gram per cup:
Antitumoral effects of Melissa officinalis on breast cancer in vitro and in vivo (2012)
Background: There is a long standing interest in the identification of medicinal plants and derived natural products for developing cancer therapeutics. Here we investigated the antiproliferative properties of Melissa officinalis (MO) from Turkey on breast cancer.
Methods: MO extracts were studied for cytotoxicity against breast cancer cell lines (MCF-7, MDA-MB-468 and MDA-MB-231). In vitro apoptosis studies were performed by annexin V staining and flow cytometry analyses. Immunohistochemistry for Ki-67 and caspase 7 in the tumoral tissue sections of DMBA-induced mammary tumors in rats was also performed, along with TUNEL assays to detect apoptotic cells. In vivo anticancer activity testing was carried out with reference to inhibition of growth of DMBA induced mammary tumors in rats.
Results: MO showed cytotoxicity against three cancer cell lines, inducing increase in Annexin-positive cells. Expression of caspase-7 protein and TUNEL positive cells were much higher in rats treated by MO, compared with the untreated control group, while expression of Ki-67 was decreased. Furthermore, in vivo studies showed that mean tumor volume inhibition ratio in MO treated group was 40% compared with the untreated rats.
Conclusion: These results indicated that MO extrcts have antitumoral potential against breast cancer.
Melissa officinalis Extract Induces Apoptosis and Inhibits Migration in Human Colorectal Cancer Cells (2020)
Colorectal cancer (CRC) is one of the most frequently diagnosed cancers worldwide. Lifestyle-related factors, such as diet, are associated with the development of CRC. Cumulating evidence indicates noticeable chemopreventive effects of phytochemicals on CRC, suggesting that drinking herbal tea potentially reduces the risk of distal colon cancer via its antiproliferative and anti-angiogenic activities. We examine the antitumor effects of nine components frequently found in herbal tea and uncover the underlying molecular mechanism. Among them, the hot water extract of Melissa officinalis (MO) exhibited the highest anticancer activity on CRC cells. We revealed that MO reduced cell proliferation, induced cell cycle arrest at the G2/M phase, triggered caspase-dependent apoptotic cell death, and inhibited cell migration ability by modulating the epithelial–mesenchymal transition in HCT116 CRC cells. To examine the metabolite composition in the MO hot water extract, we applied mass spectrometry-based analysis and identified 67 compounds. Among them, the phenolic compounds, including lignans, phenylpropanoids, and polyketides, are widely found in natural products and possess various bioactivities such as anti-inflammatory, antioxidation, and anticancer effects. The results indicate that herbal tea consumption benefits CRC prevention and management.
Added 27th April. AKA St John’s wort.
Hypericum perforatum and Its Ingredients Hypericin and Pseudohypericin Demonstrate an Antiviral Activity against SARS-CoV-2 (2022)
For almost two years, the COVID-19 pandemic has constituted a major challenge to human health, particularly due to the lack of efficient antivirals to be used against the virus during routine treatment interventions. Multiple treatment options have been investigated for their potential inhibitory effect on SARS-CoV-2. Natural products, such as plant extracts, may be a promising option, as they have shown an antiviral activity against other viruses in the past. Here, a quantified extract of Hypericum perforatum was tested and found to possess a potent antiviral activity against SARS-CoV-2. The antiviral potency of the extract could be attributed to the naphtodianthrones hypericin and pseudohypericin, in contrast to other tested ingredients of the plant material, which did not show any antiviral activity. Hypericum perforatum and its main active ingredient hypericin were also effective against different SARS-CoV-2 variants (Alpha, Beta, Delta, and Omicron). Concerning its mechanism of action, evidence was obtained that Hypericum perforatum and hypericin may hold a direct virus-blocking effect against SARS-CoV-2 virus particles. Taken together, the presented data clearly emphasize the promising antiviral activity of Hypericum perforatum and its active ingredients against SARS-CoV-2 infections.
Keywords: COVID; SARS-CoV-2; coronavirus; plant extract; medicinal plants; antivirals; Hypericum perforatum; hypericin; pseudohypericin
Added 28th April:
Cannabidiol Inhibits SARS-CoV-2 Replication and Promotes the Host Innate Immune Response (preprint, 2021)
The rapid spread of COVID-19 underscores the need for new treatments. Here we report that cannabidiol (CBD), a compound produced by the cannabis plant, inhibits SARS-CoV-2 infection. CBD and its metabolite, 7-OH-CBD, but not congeneric cannabinoids, potently block SARS-CoV-2 replication in lung epithelial cells. CBD acts after cellular infection, inhibiting viral gene expression and reversing many effects of SARS-CoV-2 on host gene transcription. CBD induces interferon expression and up-regulates its antiviral signaling pathway. A cohort of human patients previously taking CBD had significantly lower SARSCoV-2 infection incidence of up to an order of magnitude relative to matched pairs or the general population. This study highlights CBD, and its active metabolite, 7-OH-CBD, as potential preventative agents and therapeutic treatments for SARS-CoV-2 at early stages of infection.
Cannabidiol from the cannabis plant has potential to prevent and inhibit SARS-CoV-2 infection
Quite an old paper but this kind of immunosuppression could be very useful to target autoimmunity & proinflammatory cytokines, but note that part of glucosamines’ autoimmune suppressing benefits are because it is a general immune suppressor, it may be contraindicated if you are already immunosuppressed.
Immunosuppressive Effects of Glucosamine (2002)
Glucosamine is a naturally occurring derivative of glucose and is an essential component of glycoproteins and proteoglycans, important constituents of many eukaryotic proteins. In cells, glucosamine is produced enzymatically by the amidation of glucose 6-phosphate and can then be further modified by acetylation to result in N-acetylglucosamine. Commercially, glucosamine is sold over-the-counter to relieve arthritis. Although there is evidence in favor of the beneficial effects of glucosamine, the mechanism is unknown. Our data demonstrate that glucosamine suppresses the activation of T-lymphoblasts and dendritic cells in vitro as well as allogeneic mixed leukocyte reactivity in a dose-dependent manner. There was no inherent cellular toxicity involved in the inhibition, and the activity was not reproducible with other amine sugars. More importantly, glucosamine administration prolonged allogeneic cardiac allograft survival in vivo. We conclude that, despite its documented effects on insulin sensitivity, glucosamine possesses immunosuppressive activity and could be beneficial as an immunosuppressive agent.
However, a recent report by Gouze et al. (27) demonstrated glucosamine-dependent inhibition of NF-κB activity in rat chondrocytes and IL-1β1bioactivity by up-regulation of the type II IL-1 decoy receptor.
Added 1st May:
"We have already observed the replication of SARS-CoV-2 virus in bacteria many times"🤔
What this means is that the virus is replicating in your gut bacteria or maybe acting as a latent pool of infection, affects your microbiota and possibly playing a part in long Covid. Watch those carbs!
SARS-CoV-2 and its bacteriophage abilities (and how to address it, and heal yourself)
Science finally catch up to me !
Added 22nd May ‘22:
Berberine has been researched widely as it has many different therapeutic properties, too many in fact to list here properly and a literature review in it's own right was warranted.
Several of the other therapeutics here regulate the same pathways so much of the research applies to ivermectin, quercetin, resveratrol etc too. Berberine must rate as a “supertherapeutic”.
Therapeutic properties of Berberine
A literature review (2022)
This Substack is a scientific literature review of much of the current research into the therapeutic benefits of berberine.
It explores the rational for finding effective antivirals against COVID-19 as a matter of some urgency.
Berberine as a compound is described along with common plant based sources of the drug.
Significant antiviral activity has been demonstrated against alphaviruses, cytomegalovirus, herpes simplex, COVID-19, SARS, RSV, hepatitis-C and influenza, including at higher viral loads in the later course of infection where it may be too late to use other treatments effectively.
Anticancer activity by interaction with several pathways has been evidenced. The most interesting of these is by upregulation of the key tumor suppressor p53. Efficacy against myeloma, non-Hodgkin lymphoma and as a potential antitumor agent for Primary effusion lymphoma (PEL) is also indicated.
A significant reduction of inflammatory cytokines in COVID-19 patients and other in vitro studies is discussed, along with a reduction of pulmonary fibrosis in COVID-19 patients.
Evidence for the efficacy of berberine in type 2 diabetes is presented, and related positive results when used to manage obesity.
Suppression of mast cell mediated allergic responses has been demonstrated in animal trials and in vitro.
Limited but significant evidence of reduction of hypertension was found from trials involving rats and randomised control trials of humans, along with favourable blood sugar markers, but more research is needed.
Berberine is beneficial for MS sufferers too by suppressing autoimmune responses according to a humanised mouse and other studies, and attenuation of the sphingosine kinase 1 (Sphk1) signalling pathway may also be beneficial for inhibiting tumorigenesis.
Berberine or a derivative can inhibit amyloidosis by disrupting at least 2 pathways: reducing neutrophil elastase levels and by disrupting cytochrome induced ROS generation. Amyloidosis and a possible correlation with cardiovascular incidents and excess deaths is explored.
A synergistic association with Ferulic acid and with the chemotherapeutic agent cisplatin is discussed, and finally bioavailability, warnings and dosing guidance is provided.
Added 15th June ‘22:
Therapeutic properties of Artemisia annua.
This is just for one mighty herb and I'm only reviewing a fraction of the research conducted to date.
This Substack is a scientific literature review of much of the research relevant to treating COVID-19 and transfection sequelae using the therapeutic herb Artemisia annua, including citations from other topic themed bibliography reviews.
Malarial treatments are discussed because the dosing techniques, toxicity and efficacy are relevant and well researched.
It explores the rational for finding effective antivirals against COVID-19 as a matter of some urgency, including a presentation of correlative anecdotal and official data on the harm being caused by currently adopted public health policy.
The botanical history of the herb Artemisia annua and its principle bioactive components and minerals are detailed.
A passage submitted by contributing author Charles Wright is featured: “THE WORLD HEALTH ORGANIZATION'S POSITION ON THE USE OF WHOLE LEAF AND CHEMICAL DERIVATIVES OF A. ANNUA”. This reports on how the stance of the WHO has changed in the last 20 or so years from supporting scientifically-proven traditional medicine to one of collaborating with social media platforms to suppress the discussion of the potential of whole leaf A. annua to treat SARS2.
A paper is reviewed that found strong anti-HIV activity with low toxicity when taken as a tea. As with malaria patients, this a very popular low cost and accessible treatment in Africa, with research studies findings of efficacy comparable to allopathic medications, although results varied according to sample sets used. No particular compound could be isolated that was responsible for this.
Research papers published into antiviral activity against COVID-19 are reviewed. One study concluded: “Results suggest that oral consumption of A. annua hot-water extracts (tea infusions), could provide a cost-effective therapy to help stave off the rapid global spread of these variants...” Another paper found via in vitro studies that later variants required greater artemisinin concentrations to achieve the same degree of viral inhibition.
Of particular note, greater efficacy than from hydroxychloroquine was indicated against mild to moderate COVID in one study. Another study concludes: “Artemisinin showed significant inhibition of 3CL protease activity but not Spike/ACE-2 binding.”
The water soluble artemisinin derivative artesunate shows particular promise as a compound which demonstrates anticancer, antimalarial and anti-amyloid properties, amongst others.
The next section further explores Artemisinin compounds and their anti-cancer properties. Research found multiple modes of action and synergistic effects for many of the therapeutic actions of A. annua.
Positive efficacy of artemisinin and its derivatives for the treatment of type 2 diabetes mellitus are reviewed. Once again, multiple modes of action are responsible.
A study by Kiss et al (2021) demonstrated that the artemisinin derivative artensuate attenuates levels of an amyloid precursor protein in an Alzheimer's disease (AD) mouse model.
A paper exploring therapeutic efficacy in the experimental model of multiple sclerosis using mice found that “The brain histology shows the absence of plaque formation in the artemisinin treated group.”
Another study found that dihydroartemisinin (DHA),an active form of artemisinin, alleviates pulmonary hypertension (PH) through the ELAVL2/miR-503/PI3K/AKT pathway (ie an autoimmune signalling pathway involving a microRNA), which might provide a basis for new therapeutic strategies.
The review concludes with dosing guidance from multiple sources, any contraindications, advice on growing, harvesting, drying and making tea infusions from A. annua and a further contribution by Charles on his recommendations for future research strategies.
Added 17th June ‘22:
Vaccine injury (COVID) and risk of severe outcome post vaccine; FLCCC program that has been devised to mitigate the risk of severe outcome, especially blood clots post COVID mRNA vaccine
Marik, Kory etc.
Dr. Paul Alexander
Management of Post-Vaccine Syndrome
Major public health authorities do not recognize post-COVID-vaccine injuries; and there is no specific ICD classification code for this disease. However, while no official definition exists, a temporal correlation between a patient receiving a COVID-19 vaccine and beginning or worsening of clinical manifestations is sufficient to diagnose as a COVID-19 vaccine-induced injury when the symptoms are unexplained by other concurrent causes.
Since there are no published reports detailing the management of vaccine-injured patients, our treatment approach is based on the postulated pathogenetic mechanism, clinical observation, and patient anecdotes. Treatment must be individualized according to each patient’s presenting symptoms and disease syndromes. It is likely that not all patients will respond equally to the same intervention; a particular intervention may be life saving for one patient and totally ineffective for another.
Early treatment is essential; it is likely that the response to treatment will be attenuated when treatment is delayed.
Program and with the input of your clinician (3 pages in order):
Added 16th July ‘22:
Therapeutic properties of Echinacea
A literature review
This Substack is a scientific literature review of research into the therapeutic benefits of three Echinacea species. A PubMed 10 year search for “Echinacea” returned 467 results. Some of the more cited research is presented here for review:
Echinacea purpurea was shown to broadly inhibit coronaviruses and SARS-CoV-2 in vitro. In 2021 Nicolussi et al used PCR testing to compare the rates of infection and viral loads in adults and children administered 2,400mg and 1,200mg respectively of Echinaforce extract tincture over 4 months vs the control with excellent results: viral loads in nasal secretions were significantly reduced by 98.5%.
For preventing and treating the common cold a controversial meta-analysis from 2014 by Karsch-Volk et al concluded there were either statistically insignificant or minor benefits.
In 2011, Hudson & Vimalanathan posted their meta analysis of reviews Echinacea—A Source of Potent Antivirals for Respiratory Virus Infections. They found that all strains of human and avian influenza viruses tested, including a Tamiflu resistant strain as well as herpes simplex, RSV and rhinoviruses (a common cold virus) were very sensitive to E purpurea preparations. Their results suggested intracellular inhibition and significant viricidal activity, including by inhibition of replication, although effects were sometimes weak at non-cytotoxic concentrations.
Fusco et al (2010) found that Echinacea-treated mice had lower systemic and pulmonary KC (human IL-8) and IL-10 levels and lower systemic IFN-γ levels following influenza infection. They suggested that E. purpurea alters the clinical course of influenza infection in mice through modulation of cytokines and not direct antiviral activity. Although aerial parts of the plant did not show antiviral activity, they found that root extracts did in fact demonstrate this.
Another finding was that “Echinaforce” inhibits mucin secretion, one of the most discomforting symptoms and the cause of coughs, sore throat or even bronchitis.
A further study by Vimananathan et al in 2017 indicated that virus-induced bacterial adhesion and cytokine storms associated with respiratory infections could be inhibited by E purpurea.
A 2009 murine study into the reduction of latent herpes simplex virus type-1 (HSV-1) reinfections demonstrated efficacy when taken as a prophylactic.
In 2007, a paper by Pillai et al further supports polysaccharides as being potent immunostimulants. Water soluble, but not fat-like extracts from all parts of the plant all produced substantial immunostimulatory activity.
Upregulation of NF-kB is a marker for infection. In 2008, Matthias et al identified 2 different alkyamides in Echinacea root extract, one of which stimulated the immune response, the other modulated it.
Prophylaxis appears important for reducing viral levels. Sharma, Schoop & Hudson (2009) used a standardised Echinacea preparation (Echinaforce) and concluded that symptoms may be reduced at any stage of infection: “under real life conditions of Echinacea consumption, the virus-induced stimulation of pro-inflammatory cytokines can be effectively reversed or alleviated.”
A study from 2007 by Zhai et al concluded that all three species promoted T-cell proliferation, anti-viral interferons and innate & adaptive immune responses, but E. angustifolia or E. pallida may have more anti-inflammatory potential.
A 2017 study by Chiou et al. (only abstract available) researched antioxidant, antidiabetic, and antihypertensive properties. They found that both chlorogenic acid and caffeic acid demonstrated high ACE-inhibitory activity. Their in vitro results suggested that E. purpurea extract and CAD have good potential for managing hyperglycemia and hypertension.
An interesting study by Tsai et al (2012) found that “cichoric acid has a strong growth-inhibitory effect against colon cancer cells, presumably resulting from the reduced telomerase activity and the induction of apoptosis.”
A human clinical trial by Yotsawimonwat et al (2010) showed an increase in overall skin hydration and a reduction in skin wrinkles by 10%-14% when using Echinacea as either a face cream or gel.
Contraindications, interactions with chemotherapeutic drugs, bioavailability and dosage recommendations are then considered.
Added 24th August ‘22:
Therapeutic properties of Gynostemma pentaphyllum (jiaogulan)
A literature review
This Substack is a scientific literature review of research into the therapeutic properties of Gynostemma pentaphyllum, also known as the immortality herb, five-leaf ginseng, poor man's ginseng, miracle grass, fairy herb, sweet tea vine, gospel herb, and southern ginseng. A PubMed 10 year search for “Gynostemma pentaphyllum” returned 298 results. Some of the more cited research is presented here for review:
From a paper published in 2021, Rehan and Shafiullah conducted an in silico molecular docking binding analysis of 60 saponins with the COVID-19 main protease 6LU7 Mpro.
Although they found that 34 saponins were more effective than hydroxychloroquine, chloroquine or nelfinavir, as this was software based analysis the results need confirming in vitro and in vivo, but it is extremely promising research.
Okoye et al (2012) investigated the antiviral effects of extracts of G. pentaphyllum against yellow fever virus infectivity of chicken egg embryos and mice, and the percentage inhibition of viral induced hemagglutination (ie red blood cells clumping together). Results were somewhat encouraging, especially as even today there are still no specific anti-viral drugs to treat yellow fever.
From the same year, 2012, the same author Okoye worked with Nworu to study “Inhibition of HIV-1 lentiviral particles infectivity by Gynostemma pentaphyllum extracts in a viral vector- based assay”. As with the previous study they performed solvent extraction from leaf powder using ethyl ether (EG), methanol (MG) or water (AG).
Again the results from this in vitro research pointed to potential antiviral drugs that could be developed using extracts from the herb.
Sornpet et al (2017) investigated the antiviral activity of five Asian medicinal plant crude extracts against H5N1 avian influenza virus.
In 2020, Shaito et al published a comprehensive review of the ethnopharmacological therapeutic potentials and medicinal properties against cardiovascular diseases (CVDS) of four widely used plants: Ginseng, Ginkgo biloba, Ganoderma lucidum, and Gynostemma pentaphyllum.
This review is unusual, so far, in that it considers available clinical trials data as well as safety, toxicity and side effects.
(2012), Li et al extracted 2 acidic polysaccharides and tested against cancer cells in vivo and in vitro. After using alcohol to remove lipid they used water at 90°C for 2 hours, x 3, to extract from dried stem and leaf material.
Cancer types: Human chronic myeloid leukemia K-562, breast adenocarcinoma MCF-7, colon adenocarcinoma HT-29, hepatocellular carcinoma HepG2 and mouse melanoma B16 cell lines.
For in vivo studies they used tumor bearing mice and melanoma injected male rats, feeding them or injecting the polysaccharides and various statistically significant results are presented.
In 2010, Peng, Zhou and Zhang investigated the antitumor activities of dammarane triterpene saponins from a different species, Bacopa monniera.
I reference this study due to the commonality of the dammaranes with G. pentaphyllum.
This herb is also known as water hyssop, waterhyssop, brahmi, thyme-leafed gratiola, herb of grace, and Indian pennywort. Their in vivo studies in mice demonstrated tumor inhibition of up to 90%.
Moving on to 2016 and Li et al performed an in vitro study into the anticancer activity of a nonpolar fraction from G. pentaphyllum.
They provided evidence for significant anticancer activities from previously unreported, non-dammarane compounds. This provides further evidence of broad spectrum anti-tumor efficacy and the potential for developing novel anticancer agents.
Also from 2016, Li et al published a comprehensive review of the literature associated with G. pentaphyllum (GpM) and anti-cancer activities and mechanisms of action.
The most recent paper in this review of anti-cancer properties is from 2021, by Liu et al. They investigated how gypenosides of G. pentaphyllum can induce apoptosis of renal cancer tells through decreasing the phosphorylation level of Akt and mTOR in the PI3K/Akt/mTOR signaling pathway.
In 2010, Choi et al reported neuroprotective effects of ethanol extracts from G. pentaphyllum in a rat model of Parkinson’s disease.
And in 2018, Dong et al published research into how gypenosides reverse depressive behaviour by inhibiting hippocampal neuroinflammation.
Then in 2022, Wang et al conducted an in silico analysis to screen for compounds that can inhibit neurologically damaging signalling pathways associated with Alzeimer’s disease (AD).
From 2020, Wang et al conducted an in vitro investigation in to how dammarane-Type saponins from G. pentaphyllum can prevent hypoxia-induced neural injury through activation of ERK, Akt, and CREB pathways.
Hong et al (2018) conducted a biomedical investigation integrated with an in silico assay into how G. pentaphyllum can attenuate the progression of nonalcoholic liver disease in mice.
In 2017, Wong et al demonstrated how G. pentaphyllum saponins attenuate inflammation in vitro and in vivo by inhibition of NF-κB and STAT3 signaling. This is also another tumorigenic pathway and one of the key pathways mediated by cellular exposure to spike protein due to COVID-19 infection or transfection.
Back in 2006, Megalli, Davies and Roufogalis conducted an in vivo investigation using rats into how extracts of G. pentaphyllum can improve the serum ratios of cholesterols, triglyceride, blood sugar and the insulin resistance profile.
In 2020, Yin et al reported on ten new dammarane-type saponins with hypolipidemia activity from G. pentaphyllum herbal tea.
Huang et al (2022) published a review focusing on the prebiotic and therapeutic aspects of saponins and polysaccharides of jiaogulan tea, and the indirect anticancer effects of a healthy gut biome.
Bioavailability, contraindications, interactions with chemotherapeutic drugs and dosage recommendations are then considered, to conclude the review.
Added 25th September ‘22:
Repurposing of the antibiotic Doxycycline as an antiviral and anti-cancer therapeutic
A literature review
This review begins with a brief introduction to doxycycline as a drug: its uses, side effects, history and chemical formula with the 5-ringed structure typical of the tetracyclines.
Doxycycline and its iron chelation mechanisms and effects are then described.
In 2021, Faure et al performed in vitro experiments to investigate the synergistic interactions between five tetracyclines and tobramycin with an iron chelator (CP762) against two reference strains and nine clinical isolates of Pseudomonas aeruginosa from cystic fibrosis patients.
They found that as it binds with high affinity to iron this inhibited its antibacterial effects by competing with the magnesium binding site on the bacterial ribosome. The addition of another iron chelator, CP762, synergistically restored the magnesium bridge binding.
In 1999 Alkawash et al appeared to find lactoferrin/doxycycline antibacterial synergy, and by a large margin of 32 to 64 fold against B. cepacia.
In 2015, Wu et al investigated its effects in vitro on the replication of vesicular stomatitis virus.
Of particular note here for also treating long covid/vaccine sequalae is that doxycycline acts as both an antiviral and an anticancer therapeutic agent by the induction of expression of the key tumor suppressor p53.
Induction of p53 expression by doxycycline is then discussed in more detail. Son et al (2009) conducted an in vitro investigation and concluded that the tumor suppressive effects on pancreatic cancer cells were due to the activation of proapoptotic genes, inhibiting IL-8 expression, and suppression of antiapoptotic genes.
In 2020, Mosquera-Sulbaran and Hernández-Fonseca published a review on the use of tetracycline as an anti COVID-19 therapeutic.
2 clinical trials using doxycycline and ivermectin are then discussed. No results were available from the first of these, but from the second the only participants to die of COVID-19 were 3 from the placebo group of 200. Duration and severity of symptoms in the treatment group were also significantly reduced.
Three papers investigating iron chelation, inhibition of tumors and metastasis are reviewed. Buss et al (2003) recognized the potential of using iron chelation in cancer therapy and their possible synergistic effects.
From 2013, Richardson et al review how the iron chelator DFO can inhibit key signalling pathways which induce epithelial mesenchymal transition (EMT) in pancreatic cancer and other tumors. EMT is described.
A paper by Morales and Xue (2021) reviews the targeting of iron metabolism in cancer therapy.
Ubiquitination is described, as is evidence for the HIF inhibitory effects of both lactoferrin and ivermectin. This is important for working synergistically with doxycycline to help avoid resistance from cancer cells.
To complete this review, four papers discuss the anticancer properties of doxycycline.
In 1998, Fife et al found that, in vitro, doxycycline can significantly inhibit the growth of prostate and breast cancer tumors by the inhibition of matrix metalloproteinases (MMPs) and induction of apoptosis.
From 2016, Zhang et al conducted an in vitro study using human breast cancer cell lines.
A paper by Zhu et al (2017) conducted an in vitro investigation into how doxycycline synergizes with the chemotherapeutic drug doxorubicin to inhibit the proliferation of castration-resistant prostate cancer cells, a condition that was previously untreatable.
And from 2019, Markowska et al conducted a review into the repositioning of doxycycline, salinomycin, monensin and ivermectin as cancer drugs.
To conclude this Substack, dosing and contraindications for doxycycline monohydrate are considered.
A Computational Study of Ivermectin and Doxycycline Combination Drug Against SARS-CoV-2 Infection;
What’s stopping doctors repurposing generic medicines? Answer - not a lot
A focus on quercetin
Dr Lynn Fynn cautions against taking this long term as it does interact with the gut biome. This may be a positive thing or a negative for some, so I have removed it from the daily prophylactic list.
But if you have completed a course of antibiotics, suffer from gut dysbiosis or leaky gut syndrome it may help restore the balance of your gut biome:
Quercetin improves gut dysbiosis in antibiotic-treated mice (2020)
The diversity and activity of the gut microbiota residing in humans and animals are significantly influenced by the diet. Quercetin, one of the representative polyphenols in human diets, possesses a wide range of biological properties. The aim of this study was to investigate the prebiotic effects of quercetin in antibiotic-treated mice. Gut dysbiosis was successfully induced in mice by treatment with an antibiotic cocktail. Gas chromatography and 16S rDNA high-throughput sequencing techniques were used to investigate short-chain fatty acid content and gut microbial diversity and composition. The results showed that quercetin supplementation significantly improved the diversity of the gut bacterial community in antibiotic-treated mice (P < 0.05). Meanwhile, intestinal barrier function was also recovered remarkably as indicated by a decrease in the content of serum d-lactic acid and the activity of serum diamine oxidase (P < 0.05). The length of intestinal villi and mucosal thickness were also significantly increased in response to quercetin treatment (P < 0.05). Furthermore, the production of butyrate in faeces was enhanced significantly in quercetin-treated mice (P < 0.05). In conclusion, quercetin is effective in recovering gut microbiota in mice after antibiotic treatment and may act as a prebiotic in combatting gut dysbiosis.
Quercetin modulates the gut microbiota as well as the metabolome in a rat model of osteoarthritis (2021)
Although the mechanism of osteoarthritis (OA) has been widely studied and the use of quercetin for OA therapy is well documented, the relevant characteristics of the microbiome and metabolism remain unclear. This study reports changes in the gut microbiota and metabolism during quercetin therapy for OA in a rat model and provides an integrative analysis of the biomechanism. In this study, the rats were categorized into 3 different groups: the OA model, quercetin treatment, and control groups. The OA rats was conducted using a monoiodoacetate (MIA) injection protocol. The rats in the quercetin group received daily intragastric administration of quercetin from day 1 to day 28. Stool samples were collected, and DNA was extracted. We used an integrated approach that combined the sequencing of whole 16S rRNA, short-chain fatty acid (SCFA) measurements and metabolomics analysis by mass spectrometry (MS) to characterize the functional impact of quercetin on the gut microbiota and metabolism in a rat model of OA. The use of quercetin partially abrogated intestinal flora disorder and reversed fecal metabolite abnormalities. Compared with the control rats, the OA rats showed differences at both the class level (Clostridia, Bacteroidia, and Bacilli) and the genus level (Lactobacillus and unidentified Ruminococcaceae). Acetic acid, propionic acid and 24 metabolites were significantly altered among the three groups. However, the changes were significantly abrogated in quercetin-treated OA rats. Consequently, this study provided important evidence regarding perturbations of the gut microbiome and the function of these changes in a potential new mechanism of quercetin treatment.
Keywords: Osteoarthritis; gut microbiota; metabolome; quercetin; regulation.
Quercetin metabolism by fecal microbiota from healthy elderly human subjects (2017)
Quercetin is a polyphenol found in food that has numerous health benefits. This study investigated the relationship between quercetin metabolism, gut microbiota composition, and dietary intake in elderly Japanese subjects. A food frequency questionnaire was used to assess dietary intake during the week prior to stool sample collection. Fecal suspensions from 56 subjects were anaerobically incubated with quercetin and fecal microbiota composition was analyzed by next-generation sequencing. Inter-individual variations in quercetin concentration and fecal microbiota composition at family level suggested differences in microbial quercetin metabolism. The abundance of Sutterellaceae (r = -0.292) and Oscillospiraceae (r = -0.334) was negatively correlated whereas that of Fusobacteriaceae (r = 0.361) and Enterobacteriaceae (r = 0.321) was positively correlated with quercetin concentration. Niacin (r = -0.313), vitamin B6 (r = -0.297), vitamin B12 (r = -0.266), vitamin D (r = -0.301), and ratio of animal protein to total protein (r = -0.27) were also negatively correlated with quercetin concentration. Bacterial abundance was positively or negatively related to intake of food components. This is the first report describing the relationship between fecal quercetin metabolism, human microbiota, and dietary intake in the elderly.
Long Covid & media disinformation.
Hat tip to Eugyppius. It was paywalled so I had to do my own investigations. And it was quite revealing, we see it so often with young people dropping dead. The V word is almost never allowed to be mentioned, it's always the elephant in the room, absence=confirmation.
This sort of sham article, whether accidental or deliberately pro narrative, serves to help no-one avoid or control their condition. A complicit medical profession, incompetent or just plain misinformed it's hard to tell?
The lack of a positive PCR, ever, rules out LC. No viral mRNA, no LC. The End.
You must call something what it is or you are wasting your efforts on the wrong treatments, misleading others and blaming government policy or Omicron when, as in this case, it's not that at all.
It was most likely complicated by an opportunistic infection at a time of induced immunosuppression.
What Rose and her GP appear to be wilfully blind to is that all these issues arose commensurate with the administering of the “Gulf War Syndrome” type jab combo.
These symptoms are identical to the now well known vaccine-associated adverse events.
Published May 1st:
I was a marathon runner with killer biceps – long Covid has stopped me in my tracks
Endurance athletes have been left using wheelchairs or barely able to walk. But the government acts like Covid is beaten
One of the mysteries of Covid is how it hits the fit. Before January, I was one of those people. I ran 30 miles a week. I could turn up to a 20-mile fell race on inadequate training and run it, thoughtlessly. I did yoga, weight training and cycling. I had a low resting heart rate and strong biceps. For a 52-year-old menopausal woman, I was in extremely good shape.
But then on 3 January I fell ill with a sore throat, then flu-like weakness, a cough that hasn’t left me since, and a constant and persistent headache that is resistant to every painkiller. In the months since, I have been not ill, but not well. I have days of feeling fine, and then I don’t. As a runner, I can say that long Covid feels like the wall at mile 18 in a marathon, when suddenly your energy has gone, and you feel like a different person and you don’t know why.
It’s appropriate to use a running analogy, because it seems that runners, triathletes, cyclists and other formerly fit people populate the long Covid forums in far greater numbers than you’d expect if, like me, you assumed that fitness and health were the perfect shield. My long Covid is suspected by my GP, since I never actually tested positive, but many on the forums had only mild infections and are still suffering. Some are now in wheelchairs, or confined to bed, or disabled, or dysfunctional, and they post on social media groups that can be wonderfully precise: Long Covid for Endurance Athletes is one group I found extremely helpful (a name that caused a Crohn’s-afflicted friend to say wistfully: “Is there a group for former TV writers with a poo bag?”).
I suppose I am lucky that I have long Covid now, when science believes in it and there are long Covid clinics. The NHS Covid recovery site must be helpful for many, and it discusses PEM (post-exertional malaise) which is the delayed-onset crash after exercise and is one of the most frustrating mysteries about any post-viral condition: you exercise and feel fine, and two days later you suddenly don’t. But the NHS site and most others seem meant for people who can’t walk upstairs, not ones who wonder whether they will be able to run in heart zone 3 again, or ever do more than three miles without fearing the consequences; the ones who are not disabled but not themselves.
I turned, of course, to Google. I learned that people with chronic fatigue syndrome (CFS), or myalgic encephalomyelitis (ME), have been floored by PEM for decades and only now are they being believed. I learned that perhaps Covid is lurking in my gut, or making my mast cells fire when they shouldn’t, and that I should be careful of my heart because doing too much can give me myocarditis. But my heart is fine, along with my X-rayed lungs and my blood, once a drop in my infection-fighting white blood cells had recovered. Whatever Covid is doing to me, it is doing it quietly and sneakily.
It is stealth that characterises long Covid’s baffling array of symptoms and sufferers’ equally baffling tendency to get better, then relapse, sometimes for no reason. A Lancet study found that long Covid sufferers reported on average more than 50 symptoms during their illness, across an average of 9.1 organ systems.
Yet Covid, according to our government, is no longer a concern. Never mind that everyone I talk to about long Covid knows someone with it, that more than a million Britons have it, and almost two-thirds of those say it has significantly limited their daily activities. One in 16 people now have Covid, according to Imperial College London’s April React study, 40% more than at Omicron’s “peak” in January, and the highest number ever.
Sometimes I feel as though I am gaslighting myself. I can walk around so I can’t be ill. I can work, so I can’t be ill. Sometimes I can run, so I can’t be ill. But then I remember: once there was a time when I didn’t always have a headache. I used to be able to laugh without coughing. I used to walk to the shops half a mile away without wondering how I would find the strength to walk home again.
I am so much better off than most, the ones who have debilitating brain fog, who cannot work or walk. But still I mourn the thoughtlessness of good health, the time when, to borrow a phrase from the writer Sinéad Gleeson, my body was an afterthought. I trusted it. Now I can’t rely on my body because I don’t know what’s happening to it, and neither does anyone else. “I’m so sorry,” said my lovely GP, phoning me from her home because she had Covid. “We’re in the dark.” As are employment lawyers, still struggling to understand whether workers missing with long Covid have a disability or an occupational health condition. What is certain is that long Covid is costing us hugely, and not just in money.
It's a sham article and it needs retracting. Here’s why, the backstory:
We know spike protein can persist for months in the lymph node germinal centres & monocytes, about ROS inactivated T cells & lymphopenia or even lymphoma, type 1 interferon reduction, TLR disruption, autoimmune disease, neurological cytotoxicity, endothelial damage, reverse transcription etc otherwise known as VAIDS:
Added 16th June ‘22:
“Long Covid” = “transfection injured”, again.
Such disinformation and gaslighting by the “experts” helps no-one to properly diagnose and treat their complex of symptoms.
Published June 11th:
Living with long Covid: ‘This is not a fake illness – on bad days all I can do is drag myself to the bathroom’
Sophie Raudnitz, 48, is a teacher and lives Northamptonshire, with her husband and their three children. Dr Raudnitz developed long Covid after contracting Covid over Christmas and has been unable to return to work since. She tells Katie Grant how, in addition to experiencing crippling fatigue and a host of other symptoms, she has also had to deal with long Covid-deniers who refuse to believe the illness even exists.
“I had Covid over Christmas really mildly – it was just a cold. But as the cold symptoms lifted the fatigue came down. I went back to work for two days when I’d had it for three weeks – I thought, ‘I can do this’. I was totally wiped out. I just knew I couldn’t go back.
The fatigue that comes with Long Covid is like no tiredness I’ve ever experienced before. It’s total. On the days that are really bad all I can do is lie in bed, look at the sky and drag myself to the bathroom.
When my fatigue is bad I get a raft of other symptoms, and my body is coming up with new ones all the time. They include breathing problems, gastrointenstinal issues and postural tachycardia syndrome (PoTS), which causes your heart to beat abnormally fast after sitting up or standing. For people with PoTS, rather than recovering from that after 20 seconds or so, their heartbeat continues to speed up and they can become lightheaded, experience breathing difficulties or faint. It is frightening.
I’ve got two dogs and I used to go out with them for an hour and a half. When I was really bad I couldn’t walk at all. Now I’ve just built it up to 25 minutes but I’m really exhausted from that.
The only things that have got me through with any kind of sanity are a yoga instructor I discovered on YouTube who had long Covid herself, and a colleague who also developed it.
Completely by chance, someone recommended I do a type of restorative yoga and I discovered the instructor, Suzy Bolt. She teaches live classes online targeted at people with long Covid and there is a whole community of fans on Facebook. It’s been a lifesaver for me. The group is so empathetic and kind.
With my colleague, it’s just so useful to have someone else going through exactly the same thing who gets it, because part of what is so destabilising about this illness is that recovery is so uneven. You might be fine one day and then crash the next and you don’t know why.
Where professional healthcare workers are concerned I think that body of knowledge is developing but it hasn’t really been disseminated in a very effective way to healthcare providers. I went to the GP quite early on, had blood tests and an ECG – everything came back normal, which is the usual story with long Covid. I fought very hard to be referred to a long Covid clinic.
When I finally got an appointment a couple of weeks ago, I’d really been hoping for a conversation about the various weird symptoms I get. But it became obvious really quickly that, with the best will in the world, this occupational therapist just didn’t have the detailed expertise to be able to go into this in any detail.
Having just had a conversation about how I get out of breath and my heart sky rockets when climbing the stairs, she said, ‘Pace yourself – if you usually run 5K, start with 3K.’ I was thinking, ‘I can’t even walk down the road, let alone run.’ I wanted to know, what is this illness I have? It’s really difficult living with an illness about which so little is known and for which there is so little help.
My family and friends have been fantastic and my work has also been really supportive. I attempted to have a return to work in late April but I had a relapse and couldn’t do it. I’m just in negotiations now about another return.
Long Covid returns are different from other illnesses – they have to be done so slowly and so carefully and the situation is really fragile. I am going back into it knowing I could relapse at any point.
Different people experience long Covid differently, which is partly why there has been so much scepticism around it I think, and why even in the medical community people are struggling to get to grips with it.
I’ve had some flack on Twitter from people who think long Covid is just a fake illness invented by skivers. I haven’t tried to battle trolls because I know they aren’t really open to logical argument. Their minds are made up and my energy has been so frayed I need to save it for things that are more important.
Often, people with long Covid don’t ‘look’ ill. Close friends and family can tell with me when the symptoms are biting hard but to people who don’t know me well, I probably look fine. I think this makes it far easier for people to dismiss this as a fake illness. It also makes it harder for people who don’t know much about the illness to understand it – it doesn’t look like you expect illness to look like.
Part of the growing body of medical knowledge about long Covid is that there are very real physical causes for our symptoms. Many medical practitioners are still approaching Long Covid as if it’s a mental issue but it’s a real, physical illness, and not in our heads.”
This isn’t to poke fun and humiliate but to get to the facts, which is a post transfection COVID-19 Omicron infection which should have been mild instead leading to a chronic condition with multiple symptoms including for cardiovascular and neurological damage.
And the “experts” should have right on top of that after 2+ years of research & clinical data in abundance.
Publishing only half the facts in a national newspaper, a very public forum, opens you up to public scrutiny and with good reason.
This site is strictly an information website about potential therapeutics. It does not provide medical advice, diagnosis or treatment. This content is not intended to be a substitute for professional medical advice, diagnosis, or treatment. Always seek the advice of your physician or other qualified health provider with any questions you may have regarding a medical condition. Never disregard professional medical advice or delay in seeking it because of something you have read on this website.