Archive for the ‘research’ Category

The Effects of Light on the Human Body

http://  Approx. 30 Min

Why Sunlight Is the Most Powerful Drug 

March, 2026

Explore what a single photon of sunlight does to your body the moment it touches your skin — and why the physics your grandmother never knew explains everything she told you.

This video explores vitamin D photosynthesis, circadian entrainment, and nitric oxide release. Learn how one broken chemical bond controls over 200 of your genes, and find out why indoor living is quietly weakening your bones, disrupting your sleep, and raising your blood pressure.

Whether you are curious about what is really happening inside your body, fascinated by physics, or looking for explanations that actually make sense, this will change how you understand the sun, your health, and the biology you were built with. Watch now to discover what nobody tells you about sunlight.

CHAPTERS

  • 0:00 – Introduction
  • 0:42 – One Photon, One Bond
  • 2:21 The Vitamin D Factory
  • 5:23 – The Latitude Problem
  • 8:52 – Your Circadian Clock
  • 14:49 – Serotonin, Mood, and Sleep
  • 18:49 – Sunlight and Blood Pressure
  • 22:35 – The Real Risk: UV and DNA
  • 25:01 – Bones, Falls, and Immunity
  • 28:52 – Conclusion

https://gregreese.substack.com/p/the-effects-of-light-on-the-human?

The Effects of Light on the Human Body

Screen time leads to blindness and mind control
 
Greg Reese
May 22, 2025
 
Article Excerpts:

The blue light emitted by LED is a frequency band of 400 to 500 nanometers. Exposure to this has been shown to suppress melatonin production, a hormone critical for sleep. Blue light exposure will shift brain activity away from relaxed theta-dominant states, and towards heightened alert beta states. And so exposure in the evening will further complicate sleep patterns, which will negatively effect health in many ways.

The red light emitted is a frequency band of 620 to 700 nanometers. And it has been shown to promote bone and tissue repair and regeneration. It reduces inflammation and body fat, and it alleviates chronic and acute pain. The main reason that red light improves overall health, is because it enhances mitochondrial function throughout the entire body system. This leads to increased ATP production, reduced oxidative stress, and modulated cytokine activity.  (See link for article and video)

________________

https://sayerji.substack.com/p/the-ultimate-human-superpower-you

The Ultimate Human Superpower You Never Knew You Had: Melanin — The Hidden Solar Panel in Human Biology

Beyond Skin Deep: Melanin as a Biophotonic Engine
Sayer Ji
Jul 24, 2025
 
Article Excerpts:

For two centuries, this idea stuck: melanin as nature’s UV filter, nothing more.

Yet even as textbooks dutifully repeated melanin’s sunscreen status, scientists kept stumbling on puzzles that didn’t fit the simple story. For one, melanin pops up in places where sunlight scarcely shines. Consider the human brain: certain neurons in the deep brain (the substantia nigra and locus coeruleus) are loaded with neuromelanin, giving these regions a dark hue. Why would brain cells – tucked inside the skull – bother to produce a UV-blocking pigment? The inner ear is another enigma: the cochlea has melanocytes (pigment cells), and their dysfunction can cause hearing loss. Again, no sunshine reaches there. Even stranger, melanin is found in the heart valves of some animals and the lungs of certain seabirds. These “internal melanized sites” not obviously subject to light have puzzled researchers for years. Could melanin be doing something else there?

Laboratory observations added to the mystery. In one experiment, skin cells rich in melanin were found to contain far fewer mitochondria – the tiny organelles that generate ATP energy – than their non-pigmented counterparts, yet they grew and developed just as well. In these heavily melanotic cells, mitochondrial number dropped a whopping 83%, and respiration (the usual oxygen-burning energy process) was 30% lower, without impairing cell growth. It was as if the melanin was somehow compensating for the lost mitochondria.

Clinicians also noted paradoxes: melanin in the skin reduces UV DNA damage (protective), but an abundance of melanin can correlate with melanoma (cancer) risk; neuromelanin in the brain might be protective in some ways but is lost in Parkinson’s disease, possibly contributing to degeneration. Melanin, the pigment, was behaving less like a static shield and more like a dynamic player – one with a dual nature that scientists didn’t yet fully grasp.

Such anomalies prompted a few intrepid thinkers to ask uncomfortable questions. Was it possible that melanin had a metabolic function – that it could, under the right conditions, act as an energy source or catalyst for life’s processes?

One of the early proponents [of melanin being an unrecognized bioenergetic molecule] was Geoffrey Goodman, who published a speculative paper in 2008 titled “Melanin directly converts light for vertebrate metabolic use”.

Dr. Arturo Solís Herrera, a Mexican ophthalmologist and biochemist, stumbled onto melanin’s secret while studying diseases of the eye. In the 1990s, Solís-Herrera was investigating the causes of blindness like glaucoma and diabetic retinopathy…..anatomists knew the back of the eye is pigmented. But what struck Solís-Herrera was a question: Why would nature put a dense ring of melanin 2.5 centimeters deep inside the head, effectively behind the light-sensitive retina? It’s like finding solar panels buried in a cave – seemingly out of place.  (See link for article)

SUMMARY:

After a 12 year research journey Herrera’s team:

  • found melanin granules can dissociate water molecules, using light energy to split H₂O into hydrogen and oxygen – essentially the first step of photosynthesis.
  • demonstrated melanin’s water-splitting in vitro and measured the currents and reaction products and laid out their findings that melanin represents over 90% of cell energy requirements – and that a vast majority of our ATP energy might come from light and water via melanin while glucose is used to build biomass.

Over time more concrete evidence trickled in:

  • fungi that ‘eat’ radiation: melanin enabled fungus to harness radiation for metabolic energy – behaving like a broad-spectrum solar panel.
  • melanin rich mouse skin cells could function with 83% fewer mitochondria and 30% lower respiration rate, yet developed similar to non-pigmented cells implying that melanin was compensating and providing energy through another route.
  • it is hypothesized that the painted turtle can survive underwater without oxygen for months during winter hibernation due to the shell and skin containing melanin.
  • seeds: life’s solar-powered time capsules. Why would dormant seeds buried in soil away from light need a ‘sunscreen’ pigment? 
  • birds’ solar-powered eyes: darkly pigmented gel in a birds’ eye might directly convert light into metabolic energy to support the retina during 100 hours of flight without landing or eating.
  • photomodulation in humans (hairlessness advantage): red and near-infared light boost mitochondrial activity and ATP, reduce inflammation, and activate certain genes related to metabolism.
  • experiments by Dadachova’s group found that irradiating melanin with gamma, UV, visible, or infrared light all boosted the electron transfer rate – and to a similar extent regardless of the photon energy. This is telling: it suggests melanin absorbs across a broad spectrum (it is known to absorb UV through visible and into IR) and converts that absorbed energy into driving chemical reactions.
  • a 2014 discovery showed mammals can absorb dietary chlorophyll metabolites which then accumulate in mitochondria, allowing cells to harvest light to enhance ATP production.
  • Dr. Gerald Pollack’s research into the 4th phase of water—known as EZ water (Exclusion Zone water) opens the door to understanding how light, water, and pigment form a functional trinity at the heart of cellular energetics¹⁰.

This has far-reaching implications for health.

  • A 2012 paper states: “a failure in [the] light/melanin/water system” was posited as a cause of AMD and Alzheimer’s disease¹¹. 
  • some researchers think melatonin might synergize with melanin’s function to maintain mitochondrial health in the brain and retina. CF, metabolic syndromes, and developmental issues might involve melanin’s activity, opening new avenues for treatment: enhancing melanin’s function or compensating for its decline through light and other therapies.
  • 2012 research showed that mice receiving just 50 mg/kg of melanin showed 100% greater survival at 30 days compared to untreated mice. Perhaps equally important, the melanin showed no toxicity even at double this dose (100 mg/kg), suggesting a remarkable safety profile.
  • Another 2012 study showed 90% of mice fed a melanin-rich fungus one hour before exposing them to a massive 9 Gray dose of Cesium-137 radiation survived, but all control mice died within 13 days.  When the mice were fed white porcini mushrooms (which lack melanin but contain all the other bioactive mushroom compounds), they died almost as quickly as controls, but when the white mushrooms were supplemented with melanin, the mice gained the same radioprotection as those eating the melanized mushrooms, proving it was melanin that made the difference. (Chaga, Reishi and Turkey Tail mushrooms are all melanin dense, demonstrating anti-cancer and immune modulating properties)
  • In 2015, researchers in Mexico demonstrated a prototype melanin battery which could lead to novel solar energy storage systems.

For more:

Category:

Activism, research, Treatment

Bartonella and Babesia Detected in Patients With Chronic Illness

https://news.ncsu.edu/2024/07/bartonella-and-babesia-co-infection-detected-in-patients-with-chronic-illness/

Bartonella and Babesia Co-Infection Detected in Patients with Chronic Illness

July 16, 2024  
For Immediate Release
Tracey Peake
Edward Breitschwerdt

A small pilot study has found evidence of human co-infections from Bartonella and Babesia odocoilei, a protozoal tick-borne infection primarily found in deer, moose and other cervids. The co-infections were detected in six of seven patients suffering from chronic, non-specific illness, who were enrolled in a Bartonella study at North Carolina State University. The work presents some of the first definitive DNA evidence of this strain of Babesia infection in humans, and could impact treatments for patients with Bartonella, Borrelia or Babesia infections.

Bartonella are a group of vector-borne bacteria transmitted primarily via arthropods like fleas, lice and potentially ticks, but also by the animals that harbor them. There are at least 45 different known Bartonella species, of which 18 have been found to infect humans. Improved methods for detecting Bartonella infection in animals and humans have led to the diagnosis of bartonelloses in patients with a host of chronic illnesses, as well as in some patients with psychiatric symptoms.

In the U.S., the main Babesia species that infect humans are B. microti, B. duncani and B. divergens-like. Transmission occurs mainly by tick bite, but there are reports of transmission by transfusion of contaminated blood, organ transplantation and transplacental transmission. In addition to asymptomatic infection, babesiosis can be associated with non-specific symptoms such as fever, chills and night sweats, or with severe, life-threatening hemolytic anemia.

Babesia and Bartonella are often suspected as co-infections with Lyme disease, caused by the bacterium Borrelia burgdorferi.

“Doctors who work with Lyme patients often suspect co-infection with Babesia most often based on serology data and symptoms,” says Edward Breitschwerdt, Melanie S. Steele Distinguished Professor of Internal Medicine at NC State’s College of Veterinary Medicine and corresponding author of a paper describing the work. “So we decided to test for potential co-infections with this subset of our Bartonella study participants.”

The seven patients in the pilot study were already enrolled in a larger study aimed at detecting Bartonella in the blood of people with chronic illness and extensive animal contact. The participants’ ages ranged from two-and-a-half to 62 years old. Four were veterinary workers, one was a student and veterinary technician, one was a veterinarian’s daughter and one was a pre-school aged child. All submitted blood and tissue samples for testing.

Using digital droplet PCR testing, which identifies pathogens by their DNA sequences, the researchers discovered that all seven participants were infected with Babesia odocoilei, and that six of the seven were co-infected with at least one, and sometimes two or more, species of Bartonella.

“We were surprised by these findings for several reasons,” Breitschwerdt says. “First, this strain of Babesia – B. odocoilei – isn’t currently considered a cause of human infection. Second, these patients reside in locations around the U.S. and in Mexico, so the distribution may be geographically widespread. Finally, we were able to identify these seven infected individuals within a one-year time period, suggesting that this may be a more prevalent infection than currently appreciated.”

The findings could have implications for how patients with symptoms of vector-borne illnesses such as Lyme, babesiosis, or bartonellosis are tested and treated.

“The main symptom associated with babesiosis is acute, severe hemolytic anemia. None of these patients reported any such illness, a factor that could limit a doctor’s decision to test for Babesia infection,” Breitschwerdt says.

“This study primarily focused on patients with chronic illnesses and suspected bartonelloses. Most often, doctors don’t look for Babesia in these patients, but we now have good evidence that people can be infected by this organism, evidence that should be pursued in larger studies. Physicians who treat Lyme disease have often suspected co-infections with these pathogens, and it looks like their suspicions are correct, at least in a subset of patients.”

“We are committed to providing the best vector borne infectious disease testing results possible,” says Ricardo Maggi, research professor at NC State and first author of the study. “The cases presented in this manuscript reflect our team’s efforts to develop better approaches and diagnostic tools that can give answers to both patients and their doctors.”

The study appears in Parasites and Vectors and was supported by NC State’s Bartonella/Vector-Borne Diseases Research Fund and the Steven & Alexandra Cohen Foundation. NC State Ph.D. student Charlotte Moore, São Paulo State University Ph.D. student Ana Cláudia Calchi, and NC State research specialist Emily Kingston also contributed to the work.

For more:

Category:

Babesia, Bartonella, research

Magic Trick Reveal: How To Get Perfect Efficacy From a ‘Vaccine’ That Doesn’t Work. Two White Papers Call to Halt COVID Shots, But FDA Approves Non-mRNA COVID Shot

https://kirschsubstack.com/p/the-big-magic-trick-revealed?

The big magic trick revealed!

How can you get near perfect efficacy from a vaccine that doesn’t work? Thanks to Professor Jeffrey Morris, I now know the magic trick too! This one had me fooled me for years.

Steve Kirsch
May 16, 2025
The Secret Truth Behind Penn & Teller: Fool Us

I like Penn and Teller. But they don’t know jack about vaccines. Check out this video they did. They should apologize and re-do the video to tell the truth. YouTube will ban it though.

Executive Summary

If you have a policy of COVID testing where it is mandatory to test the unvaccinated 2x/week but the vaccinated can totally skip testing, this can massively skew all studies based on that data.

I just found out this was the case in the Czech Republic which is the only country where we have record level data.

That explains a lot, doesn’t it? A testing policy like that can make an ineffective vaccine close to perfect.

Bottom line: the only honest way to see if the vaccine worked is to compare the whole period all-cause mortality between those who got the shots and those who did not. Then you learn the truth.

Guess what? There isn’t a single study that does this.Zero. Zip. Nada.

So I calculated it for the Czech Republic. It shows that the vaccines should be stopped. But you already knew that, didn’t you?

And if you can’t get COVID, you can’t die from COVID!

BAM! The magic trick has been revealed. The next time you want to make a vaccine super effective, there is nothing like deploying a differential testing policy like this.

Therefore, in Czechia, you get a near perfect vaccine and can write papers about it and nobody is the wiser.  (See link for article)

_______________

**Comment**

These tactics need to be continually exposed for what they are: false and misleading – constituting scientific fraud.  Those in public health should be reviewing these things before they roll out a drug or medical product of any kind.

Hirsch then shows a table (to access, click top link) that shows when you actually compare whole period all-cause mortality between the injected and the non-injected you discover the shots are killing people.  But, reality is already showing this for those paying attention.

For more:

People have been shouting about these death shots for years.  There’s plenty of published science showing the myriad of problems.

Two White Papers Call For COVID Shot Halt

The IPAK-EDU White Paper 2025-ENDEUA states that when corrected efficacy curves and suppressed risks are taken into account, the mRNA covid shots fail the EUA standard.  The shots were based upon interim data from large-scale Phase III trials. The legal standard under §564 of the Federal Food, Drug, and Cosmetic Act requires that a product may be authorized for emergency use only if it is “reasonable to believe” that the product “may be effective” against a life-threatening condition, that the known and potential benefits outweigh the known and potential risks, and that no adequate alternatives are available. This report  demonstrates, through a rigorous retrospective analysis, that these criteria were never met.  

Go here to listen to Dr. Jeyanthi Kunadhasan, an Australian anesthesiologist and perioperative physician who was terminated from her hospital position after questioning the risk-benefit profile of COVID-19 vaccines in healthy individuals. Following her dismissal, she joined a group of international medical volunteers tasked with reviewing the 500,000+ pages of internal Pfizer documents released as part of a court-ordered FOIA request. This effort was coordinated by DailyClout and Dr. Naomi Wolf. As a result of that work, Dr. Kunadhasan has become one of the foremost experts on Pfizer’s pivotal mRNA vaccine trial, focusing specifically on discrepancies in reported deaths and adverse events.

What Dr. Kunadhasan uncovers raises grave questions about data integrity, regulatory failure, fraud, and the validity of the FDA’s EUA for the Pfizer-BioNTech COVID-19 shot.

And yet another White Paper is calling for an urgent halt on self-amplifying RNA ‘vaccine’ deployment until comprehensive safety studies are done to address contagiousness risks.  The paper discusses the significant theoretical risk including contagiousness through shedding, sexual transmission, and recombination with wild-type viruses.

FDA Commissioner Dr. Marty Makary and head of FDA’s Center for Biologics Evaluation and Research, Dr. Vinay Prasad, note that a number of other countries such as Australia and Germany only recommend the clot shots to certain populations while the U.S. has taken a ‘one size fits all’ approach because experts have argued Americans are too stupid to understand age-and risk-based recommendations.

But, even this approach ignores the elephant in the room: there are treatments for COVID which means a ‘vaccine’ isn’t even needed.  Then, there’s the fact they have negative efficacy.

What more is it going to take?

Evidently, a lot more……

The Food and Drug Administration issued an approval for Novavax’s Covid-19 ‘vaccine.’ This is the only non-mRNA vaccine.

The vaccine was approved for adults aged 65 and older and individuals aged 12 to 64 with at least one underlying health condition that increases their risk for severe COVID-19 outcomes. Reading the clinical trials prompts serious questions.

The trials included populations that had a single dose and populations that had two doses. The trials showed a reduction in symptomatic Covid 7 days after the second dose. But the FDA didn’t approve two doses. They only approved one. So is one dose even effective at all at preventing Covid? We don’t know, that wasn’t tested.  (Is this sounding familiar yet?)

There is also a noted risk of myocarditis and heart inflammation. There was also at least one vaccine recipient with “a serious event of Guillain Barré syndrome reported 9 days following the shot.  The FDA notes that Novavax has to follow up on any further cases if they observe it.

The FDA is also supposed to follow up on how the vaccine does when it is shipped to patients. They must submit a study called “Shipping Evaluation of SARS-CoV-2 rS (JN.1 Vaccine) Drug Product in Pre-Filled Syringe (PFS) Finished Good Presentation” by July of this year.

They approve vaccines not knowing how they will fare once they are shipped to doctor’s offices. They test it on us.

Don’t forget the low prevalence of Covid.

There is good news: there are at least 16 states with pending bills seeking to ban the clot shot mandates, establish a ‘vaccine’ bill of rights, or prohibit any immunization containing mRNA material.  Some bills would require manufacturers to label foods containing mRNA, according to data compiled by Bloomberg Government.

More than 2,500 ‘vaccine’-related bills have been introduced since 2021.

And top FDA official just disclosed she never got the clot shot due to her concerns about biodistribution.  She was concerned about excretion in breast milk since she was pregnant during the COVID ‘pandemic.’  When asked if information has emerged that validates her choice, said she thinks it does, but wanted to go on record that she was not speaking on behalf of the FDA.  

Researchers reported in a 2022 paper that messenger ribonucleic acid, which is in the Pfizer and Moderna COVID-19 shots, was detected in human breast milk. Another paper, in 2023, detailed similar findings.

Pfizer and Moderna did not return requests for comment.

And ‘Dilbert’ comic strip creator, Scott Adams, just admitted to having the same aggressive turbo cancer as former President Biden.

“The smartest, happiest people are the ones who didn’t get the vaccination, and they’re still alive.” ~ Scott Adams, Dilbert creator

It’s getting hot in the kitchen, folks.

Category:

Activism, research, vaccines

How Are MS & Chronic Lyme Related?

Although this article is about MS, I wanted to post this information from Dr. Makis on fibromyalgia since both have many similar symptoms:  https://makismd.substack.com/p/ivermectin-and-fibromyalgia-testimonials?

In short, fibromyalgia patients are experiencing great relief, and even cure with ivermectin.  Many are stating their pain is entirely or nearly gone.  A few MS patients claim ivermectin cured their MS.

https://www.lymedisease.org/multiple-sclerosis-chronic-lyme/

How are multiple sclerosis and chronic Lyme related?

By Bill Rawls, MD

April 21, 2025

Multiple sclerosis (MS) is a disease where the immune system attacks the protective covering (called myelin) around nerves in the brain and spinal cord.

Myelin acts like an insulator to keep nerves from touching each other and shorting out, much like the plastic coating on a copper wire.

This damage disrupts nerve signals, leading to symptoms such as fatigue, muscle weakness, numbness, vision problems, and coordination difficulties.

Undoubtedly, plenty of people who identify as having chronic Lyme disease struggle with these same symptoms. And demyelination of nerves has been documented for Lyme disease. Beyond that, many people with MS test positive for Borrelia, the Lyme bacteria. So what distinguishes MS from chronic Lyme?

The answer: arbitrary cut-offs.

So how do we differentiate?

There is no single test that is specific for MS. The diagnosis of MS is made using a combination of clinical evaluation, imaging, such as MRI, and laboratory tests of blood and spinal fluid.

If all of the findings are deemed significant enough by the clinician evaluating the patient, then the diagnosis of MS is made and the patient qualifies for treatment.

This means that a person could have all of the symptoms, and some or all of the findings, but not to the degree that would qualify for a diagnosis of MS.

That person might end up being diagnosed with some other neurological condition, fibromyalgia, or maybe wouldn’t get a diagnosis at all. Chronic Lyme disease is unlikely because it isn’t a diagnosis recognized by the conventional medical community.

No diagnosis, no treatment. But maybe that’s not such a bad thing.

Getting to the root cause

There are numerous drugs for treatment of MS. They work by blocking inflammation or blocking the immune system’s assault on myelin. The benefits are marginal at best and they carry significant side effects.

What the drugs don’t do is address why the body is attacking myelin in the first place. Without getting to the root causes of the problem, patients typically don’t get well. They live in a compromised state of relying on medications to mask the symptoms of their illness.

When you start looking for underlying causes, you’ll find that MS is listed as multifactorial. In other words, it’s not one specific cause, but rather multiple variable causes. This is also true of other chronic illnesses, including chronic Lyme disease.

A review paper published in the 2023 edition of the journal, NeuroSci, cataloged some of the known risk factors for MS that may be causative. These risk factors can be grouped into five categories.

  • Diets rich in processed foods and saturated fat, but low in vegetables and fruit
  • Chronic mental stress with inadequate sleep
  • Smoking or chronic exposure to other toxic substances
  • Sedentary lifestyle
  • Certain myelin-scavenging microbes, including (but not limited to) Chlamydia pneumoniae, Epstein-Barr Virus (EBV), Human Herpesvirus-6 (HHV-6), Mycoplasma pneumoniae and other mycoplasma species, and Borrelia burgdorferi

While the review didn’t go as far as defining how these factors might come together to cause MS, it doesn’t take much imagination to figure out a possible scenario.

A plausible explanation for MS

Myelin is contained within specialized cells called oligodendrocytes, which wrap around the shaft of a nerve to insulate it. Each of these microbes are known to invade oligodendrocytes to scavenge myelin as a resource for replication. While this provides one possible link to MS, that’s not the end of the story.

Evidence shows that the microbes can go dormant inside an oligodendrocyte after they invade it. Intracellular dormancy is a common survival mechanism used by many host-dependent microbes. It has been documented for borrelia and all the Lyme coinfections. Dormancy allows microbes to survive when conditions aren’t favorable for growth — in other words, when the cells they’ve invaded are healthy.

When cells are weakened by chronic stress factors — poor diet, chronic exposure to toxic substances, unrelenting mental stress and poor sleep, being sedentary — dormant microbes are able to reactivate, consume the cell, and then emerge to infect adjacent cells.

The immune system reacts by attacking the oligodendrocytes where microbes are emerging, in the process compounding the damage.

This is also a plausible explanation for chronic Lyme disease. The question remains: Why do some people progress to more advanced symptoms that are ultimately defined as MS?

The answer may be genetics. A variety of genetic mutations are common among people diagnosed with MS. You can’t do anything about genetic mutations, of course, but you can do something about the root causes of the problem.

A natural solution for MS and chronic Lyme

One obvious part of the solution is minimizing stress factors that weaken cells. Not surprisingly, there are many documented cases of people who went into stable remission from MS after modifying their health habits.

Improved health habits alone, however, don’t completely address the microbe factor. Fortunately, there is one thing that does — and it’s not antibiotics or other drugs.

Certain medicinal herbs demonstrate antimicrobial and immunomodulating properties that offer the potential for an ideal solution to support recovery from MS. They are already used widely for chronic Lyme disease and supported by sound evidence.

Among numerous studies, a study from Johns Hopkins University showed that certain herbs — cryptolepis, Japanese knotweed, and Chinese skullcap — were more effective for killing Borrelia than antibiotics.

Unlike an antibiotic, however, which is a single chemical agent specific for only certain microbes, an herb contains hundreds of chemical substances that act as a chemical defense system against a wide range of microbes, including bacteria, viruses, protozoa, and yeasts.

Never just one

This is important because it’s never just one microbe possibility. People identifying as having chronic Lyme disease typically test positive for co-infections. Chronic Lyme co-infections associated with demyelination include Chlamydia pneumoniae, Epstein-Barr Virus (EBV), Human Herpesvirus-6 (HHV-6), Mycoplasma pneumoniae and other mycoplasma species.

But these are just the ones that have been identified so far — there are probably many others.

Combining multiple herbs extends the range of coverage. This is possible because the potential for toxicity of the most commonly used herbs in Lyme protocols is inherently low.

Medicinal herbs and mushrooms that are commonly included in chronic Lyme protocols that could also be beneficial for MS recovery include:

  • Japanese knotweed (Polygonum cuspidatum)
  • Cat’s claw (Uncaria tomentosa)
  • Chinese skullcap (Scutellaria baicalensis).
  • Cryptolepis (Cryptolepis sanguinolenta)
  • Andrographis (Andrographis paniculata)
  • Reishi (Ganoderma lucidum)
  • Cordyceps (Cordyceps sinensis)
  • Berberine or berberine-containing herbs
  • Red sage (Salvia miltiorrhiza)
  • Rehmannia (Rehmannia glutinosa)

Very importantly, the complex chemistry of herbs and medicinal mushrooms also protects cells from a wide range of toxic threats, including free radicals, foreign toxic substances, and harmful radiation. This applies to all cells in the body, including cells that make up the nervous system.

Immunomodulators

The medicinal herbs and mushrooms listed are classified as immunomodulators, meaning they upregulate underactive parts of the immune system and downregulate overactive portions of the immune system. This is important for reducing inflammation and calming the autoimmune response.

A final advantage of antimicrobial herbs is specificity for pathogens. The antimicrobial properties of herbs and medicinal mushrooms are selective for pathogens, but do not disrupt normal flora in the gut and other areas of the body.

Low toxicity and low potential to disrupt the gut microbiome means that herbal therapy can be used for extended durations, months or even years, which is often what it takes for complete recovery.

What this all means is that therapy — with a targeted endpoint of wellness, not managed illness — can be started with or without having a formal diagnosis.

With over 30 years of medical experience, Dr. Bill Rawls specializes in the holistic treatment of chronic illnesses, particularly Lyme disease. His personal journey with Lyme disease inspired his mission to empower others with the knowledge and tools needed to regain their health naturally. Learn more about Dr. Rawls’ approach to treating chronic illness with herbal therapy at RawlsMD.com.

References

An X, Bao Q, Di S, et al. The interaction between the gut microbiota and herbal medicines. Biomed Pharmacother. 2019;118:109252.

Anderson C, Brissette CA. The Brilliance of Borrelia: Mechanisms of Host Immune Evasion by Lyme Disease-Causing Spirochetes. Pathogens. 2021;10(3):281.

Berer K, Mues M, Koutrolos M, et al. Commensal microbiota and myelin autoantigen cooperate to trigger autoimmune demyelination. Nature. 2011;479(7374):538-541.

Bjornevik K, Münz C, Cohen JI, Ascherio A. Epstein-Barr virus as a leading cause of multiple sclerosis: mechanisms and implications. Nat Rev Neurol. 2023;19(3):160-171.

Branton WG, Lu JQ, Surette MG, et al. Brain microbiota disruption within inflammatory demyelinating lesions in multiple sclerosis. Sci Rep. 2016;6:37344.

Eisenreich W, Rudel T, Heesemann J, Goebel W. Persistence of Intracellular Bacterial Pathogens-With a Focus on the Metabolic Perspective. Front Cell Infect Microbiol.

Feng J, Leone J, Schweig S, Zhang Y. Evaluation of Natural and Botanical Medicines for Activity Against Growing and Non-growing Forms of B. burgdorferi. Front Med (Lausanne). 2020;7:6.

Fritzsche M. Chronic Lyme borreliosis at the root of multiple sclerosis–is a cure with antibiotics attainable? Med Hypotheses. 2005;64(3):438-448.

Greening C, Grinter R, Chiri E. Uncovering the Metabolic Strategies of the Dormant Microbial Majority: towards Integrative Approaches. mSystems. 2019;4(3):e00107-19.

Ivanova MV, Kolkova NI, Morgunova EY, et al. Role of Chlamydia in multiple sclerosis. Bull Exp Biol Med. 2015;159(5):646-648.

Kriesel JD, et al. Spectrum of Microbial Sequences and a Bacterial Cell Wall Antigen in Primary Demyelination Brain Specimens Obtained from Living Patients. Sci Rep. 2019 Feb 4;9(1):1387.

Landry RL, Embers ME. The Probable Infectious Origin of Multiple Sclerosis. NeuroSci. 2023;4(3):211-234.

Libbey JE, Cusick MF, Fujinami RS. Role of pathogens in multiple sclerosis. Int Rev Immunol. 2014;33(4):266-283.

Livengood JA, Gilmore RD Jr. Invasion of human neuronal and glial cells by an infectious strain of Borrelia burgdorferi [published correction appears in Microbes Infect. 2015 Jun;17(6):e1]. Microbes Infect. 2006;8(14-15):2832-2840.

Pender M. The essential role of Epstein-Barr virus in the pathogenesis of multiple sclerosis. Neuroscientist. 2011;17(4):351-367.

Rittershaus ES, Baek SH, Sassetti CM. The normalcy of dormancy: common themes in microbial quiescence. Cell Host Microbe. 2013;13(6):643-651.

Thakur A, Mikkelsen H, Jungersen G. Intracellular Pathogens: Host Immunity and Microbial Persistence Strategies. J Immunol Res. 2019;2019:1356540.

Toledo A, Benach JL. Hijacking and Use of Host Lipids by Intracellular Pathogens. Microbiol Spectr. 2015;3(6):10.1128/microbiolspec.VMBF-0001-2014.

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**Comment**

A few points:

  • The Johns Hopkins study was in vitro, or the lab, which may not transfer over to the human body.
  • Antibiotics of daptomycin, doxycycline, and cefuroxime were used as controls at a final concentration of 5 μg/ml.  I’m not sure how this translates to oral dosages given patients, but according to Burrascano, dosages matter greatly.  It could be that these dosages were not high enough.
  • Doxy is a great front-line drug due to its action against many coinfections, but it is not the best and only drug to treat Lyme disease.
    • Eva Sapi found that while the use of doxy reduced spirochetal structures ~90%, round body forms increased about twofold.What this means is these round forms will simply lie and wait until conditions are better to reemerge. She found that tinidazole was the only antibiotic that reduced viable organisms by ~90%.  Recent research showed piperacillin effectively cured mice of Lyme at a dose 100 times smaller than doxycycline with virtually no impact on resident gut microbes.
So, for anyone paying attention, doxy has its limitations and all experienced Lyme literate doctors use multiple antibiotics in a combination therapy.

This, right here, is why mainstream medicine and research are worthless because this complex illness is treated as a one pathogen, one drug illness when typically more than one pathogen involved, and to complicate it further, the pathogens have multiple forms (pleomorphism) and strains that need to be addressed.

  • Daptomycin is an antibiotic that has been utilized recently in combination therapies. In a study through Johns Hopkins, when combined with doxycycline and ceftriaxone, daptomycin effectively cleared Lyme disease infection in vitro as well as in mice. However, daptomycin is relatively expensive and only available intravenously.  Notice it’s effectiveness is due to being used in a combo therapy.  I would say this is true of ALL antibiotics and why single antibiotics were not successful in the Johns Hopkins study Rawls refers to.
  • While cefuroxime has been found to have a minimum bactericidal concentration (MBC) similar to doxycycline; out of three borrelia species tested, two were susceptible while the third (borrelia hermsii) was less susceptible. The three antibiotics with similar MBCs in vitro, i.e., cefuroxime, doxycycline, and amoxicillin, demonstrated comparable activities in preventing borreliosis in B. burgdorferi-challenged hamsters (50% curative doses = 28.6, 36.5 and 45.0 mg/kg, respectively). So cefuroxime is far from perfect either when used alone.  Source

Using single antibiotics is really doing an injustice to what is known about successful treatment for Lyme since tindy is the most effective drug overall and combination drug protocols are by far the most effective.

Please remember too that Dr. Rawls manufactures and sells herbs and is financially compensated.

Don’t misunderstand – I’m not opposed to herbs.  I’ve used many myself and know of patients who have done well on them.  I just don’t want you to believe they are perfect or the only answer, either.  It takes everything AND the kitchen sink for this crap so keep an open mind.  And herbs are not harmless – there are interactions with other drugs as well as toxicity.

Nothing is ever simple.

For more:

Category:

Herbs, Lyme, research, Treatment

Why Doctor Treated Patient for Lyme – Even When His Test Was Negative

https://danielcameronmd.com/treated-lyme-negative-test/

Why I Treated Him for Lyme—Even When His Test Was Negative

Posted By: Dr. Daniel Cameron
May 13, 2025

Patients Deserve an Explanation

One of the most common—and most important—questions I hear from patients is:
“If my Lyme test is negative, why are you still treating me?”

It’s a fair question. And if you’re asking it, you deserve a clear and compassionate answer. The truth is, when it comes to Lyme disease, test results don’t always tell the full story.

Let’s break down why.

Lyme Disease Testing Isn’t Always Reliable

The standard test used to diagnose Lyme disease is called the two-tier system. It includes an ELISA screening test followed by a Western blot if the first result is positive. But this system is far from perfect—especially when the infection is in its early or late stages.

Here’s what you should know:

  • Early in the infection, your body may not have produced enough antibodies yet to trigger a positive result
  • Some patients never produce detectable antibodies at all
  • Co-infections like Babesia or Bartonella are not picked up by this test
  • Many rashes don’t appear in the textbook “bulls-eye” pattern—or don’t appear at all
So yes—you can absolutely have Lyme disease, even if your test is negative. And unfortunately, this is more common than many realize.

In Medicine, We Don’t Wait for Disease to Get Worse

In most areas of healthcare, we don’t wait for a serious event before we start treatment.

  • We don’t wait for a stroke to treat high blood pressure
  • We don’t wait for vision loss to manage diabetes
  • We don’t wait for full organ failure to address chronic kidney disease

We act early—because we know that early treatment improves outcomes. So why does Lyme disease often get treated differently?

When it comes to Lyme, many patients are told to “wait and see”—even when the symptoms are clear and distressing.

Waiting Is Not a Neutral Decision

Here’s what I tell my patients:
Waiting is not harmless. It’s a medical decision with consequences.

Delaying treatment can allow symptoms to worsen. It can allow the infection to persist or spread. In some cases, patients who were told to wait eventually end up with a label: Post-Treatment Lyme Disease Syndrome (PTLDS)—a condition where symptoms linger long after the initial infection was treated, or in some cases, never properly treated at all.

What if we had treated earlier? Could we have prevented months—or even years—of suffering?

In many cases, the answer is yes.

Clinical Judgment Is Not Guesswork

When I decide to treat someone for Lyme disease despite a negative test, it’s not a random decision. It’s based on:

• The full pattern of your symptoms

• Your medical history

• Your response to prior treatments

• Known or likely tick exposure

• And experience with thousands of Lyme patients

This is called clinical judgment. It’s a core part of good medical practice. I don’t ignore science—I apply it in context. Because Lyme doesn’t always follow the rules, and neither should we when those rules are failing real people.

You Know When Something Feels Wrong

I’ve met patients who’ve been told their symptoms are “just stress” or “hormonal” or “all in their head.” But they know their bodies. They’ve tracked their fatigue, their joint pain, their cognitive changes. They’ve seen something shift—and they’re right to speak up about it.

Many of those patients improve once treatment begins, even if their test results never confirmed the diagnosis. That’s not luck. That’s Lyme disease showing up in real life—even when it doesn’t show up in the lab.

It’s Time to Rethink How We Treat Lyme

We’re in a new era of medicine. Patients are more informed, more proactive, and more in tune with their own health than ever before. But too often, our Lyme diagnostic standards are stuck in the past—waiting for certainty while people lose months or years of their lives to untreated illness.

We need to bring clinical judgment back into focus. We need to listen more, wait less, and treat Lyme disease with the urgency it deserves.

Final Thoughts

If you’ve been told your test is negative, but you’re still struggling with symptoms—please know this:
You’re not imagining it. You’re not overreacting. And you’re not alone.

In my practice, I treat the whole patient—not just the lab result. Because when it comes to Lyme, early treatment can change everything.

Want to learn more? Follow my blog series for more insights on Lyme disease diagnosis and care—or reach out to my office if you’re looking for answers.
You deserve to be heard.

Related Articles:

Relying on a negative Lyme disease test can prove deadly

Don’t wait for a positive Lyme disease test

Can’t trust single dose of doxycycline to prevent Lyme disease

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**Comment**

A very needed article with crucial information for all to understand.

Testing for Lyme/MSIDS is abysmal.  Clinical judgement is required; however, doctors receive little training for tick-borne infections and whatever training they do receive is antiquated and biased.  The fact the needle hasn’t budged in 40 years is proof of this fact.

Dr. Cameron is an example of an independent doctor who could save your life.  He’s also a Lyme-literate doctor who has studied under ILADS and who has years of experience treating this.  Like many of his colleagues, he’s been attacked by the state medical board – which is common for these doctors because they do not partake in the globalist idea for ‘consensus-based’ medicine – which turns doctors into robots who blindly follow dictates from bureaucrats who are profiting from conflicts of interests including patents, drugs, and other metabolomics. 

Due to the horrific lack of education on all things Lyme/MSIDS, there is a parallel group to the tyrannical IDSA (Infectious Diseases Society of America) called ILADS (International Lyme and Associated Diseases Society) which holds their own medical conferences to educate doctors on what is happening in reality with Lyme/MSIDS and through independent, global research that the IDSA simply ignores or maligns. Their next conference, “The Complexity of Lyme: Diagnosing and Treating Tick-Borne and Related Diseases,” is June 7-8 in Philadelphia.

Our conference will include:

  • Introduction to diagnosing and treating vector-borne diseases
  • Case discussions with experts
  • Advanced topics in clinical treatments such as PANS/PANDAS, Mold toxicity, MCAS, supportive natural therapies and more.
  • Exhibitors showcasing medical services
  • CME credit available

The conference is open to healthcare professionals. Students enrolled in a medical degree program and PhD candidates conducting Lyme-related research are also eligible to attend and qualify for discounted rates. Email conference@ilads.org for more information.

Category:

Lyme, research, Testing, Treatment