Archive for the ‘Alzheimer’s’ Category

Lost Link – ALS & Lyme  by Huib Kraaijeveld, October 2017

The lost link between ALS and Lyme disease

Knowledge about emergent diseases normally increases over time. Lyme Disease seems to be an exception to this rule. Claims that governments and scientists made around 1990, seem to have been forgotten. This article explores the lost link between ALS and Lyme. ALS is also known as Motor Neurone Disorder (MND) or as Lou Gehrig’s Disease, after the famous Yankee baseball player who died from it in the 1940’s. It is still claimed there is no known cause nor cure for it. 


A few weeks ago I visited a friend to admire her new house. She wasn’t as happy as I’d expected. She told me that a good friend of hers (46) was just diagnosed with ALS. ALS is considered a progressive and lethal disease, without a known cure for it.

Two months earlier, her friend had sudden deterioration of her memory, impairment of cognitive function and lost the use of the muscles in one arm. I’m not medically trained myself, but found this to be a peculiar combination of symptoms for ‘ALS’.

Some clinical tests for other illnesses were checked off, no blood work was done and she was basically sent home to write her will and say goodbye to her young child and husband. Memory loss and the sudden inability to think straight were not included in the diagnosis process.

My friend asked me for some sources about a potential link between Lyme and ALS. I’d like to share these sources with you as well in this current article, as a timely example how knowledge can somehow be ‘forgotten’.

Media coverage

There is a specific reason to write this article now. This week, on October 18, a highly disputed broadcast by Zembla International called ‘deceit or Borrelia‘ seems to be repeated on Dutch TV.

It attacked a specialized German lab, using the edited stories of Danish Lyme patients, who could not get help in their own country.

The patients did not give their consent for the broadcast, and when they realized where the broadcast was heading, they found that they were unable to withdraw their cooperation. This led to a ‘counter’ documentary of their own making, which you can see below.

Tabitha, the first lady who you can see in this documentary, was also told that she would live another six months at most and should say goodbye to her young daughter. Her diagnosis was also ALS.

She found that Lyme was likely the cause of her deterioration in health, got treated for it and stopped the progression of the ‘ALS’. She’s still alive now, although hardly after the damage the original documentary had done to her care plan.

Differential diagnosis

A differential diagnosis is what specialists call ‘detective work’. Clinicians look for symptomatic and laboratory clues, have hunches, order testing and perform exams, and then rule diagnoses in or out, especially when one or more illnesses have similar symptoms or even lab findings.

Part of that detective work is simply doing diagnostics by way of treatment. If a patient does not respond to a treatment for a specific disease, too bad, but then you can exclude it. But if they do, great news! Wouldn’t you think, in case of a lethal condition?

Allan Sheppard’ story, which was featured by the BBC, tells another tale. After the UK medical system NHS kept him in Intensive Care for two years with alleged ‘ALS’ and refusing his daughter to get a Lyme test from another specialized German lab, he is now improving while being treated for Lyme. Despite the UK government trying to stop her.

The story of Eivind Markhus is even more sinister. After he was told he would die from ALS, he had an American lab test his blood and found Lyme to be the real cause of his problems. He also improved after initial treatment and the progression of his ALS symptoms stopped.

Yet instead of spending 150,000 dollar on Lyme treatments, he spent that amount on legal cases, because his Norwegian government forbade him to get treated. He lost both the lawsuit and his life.

Recently, a male Dutch ALS patient (34, with three little children), who had been previously tested – with the standard unreliable serological test – for Lyme in a so-called (ALS) ’Expert Center’, had to learn from a chronic Lyme patient and a Lyme Literate US doctor how to improve the diagnostics.

By buying antibiotics online in New Zealand and taking them for a few days, his body started to produce antibodies for Lyme. So suddenly the test was positive in another (Lyme) ‘Expert Center’, where they apparently don’t know how to do this.

He is now crowdfunding to undergo an experimental treatment, which his insurance refuses to cover as it is not considered ‘evidence based’.

The story of Dr. Martz, who is featured in the award-winning documentary ‘Under Our Skin’ is the icing on the cake. He was told he would die of ALS as well, but found out by coincidence that he actually had Lyme and a co-infection, was treated for both of them and recovered so much he could give lectures in 2011.

Ice buckets

A relationship between ALS / MND and Lyme makes sense, looking at the findings of the 1990 research that was published in the article ‘Immunological Reactivity against in Borrelia burgdorferi in Patients with Motor Neuron Disease’ by Halperin et al.

This study showed that in almost 50% of the 19 people diagnosed with ALS, Lyme was the cause. Once treated, several of these patients improved. In that same year, 1990, the CDC published its first definition about Lyme and described the complex, systemic, multi-symptom and sometimes devastating chronic disease experienced by many Lyme patients – then and still today.

Did anyone ever do a follow-up on this promising research? No. It was simply hidden away and Halperin chose to become a co-author of the 2006 IDSA Lyme Guidelines instead, which maintain that ‘Lyme is a mild disease that is hard to get, easy to treat and hardly ever becomes a chronic condition’. Any possible connection with ALS or any other of the serious and previously acknowledged debilitating or even deadly conditions was no longer mentioned. Any long-term health issues are reasoned away, using semantics rather than ‘evidence based’ science.

These 2006 IDSA Lyme Guidelines have become worldwide policy, even though they were removed from the National Guidelines Clearinghouse and named as a case of bad ‘evidence based’ guidelines by the Institute of Medicine in 2011. To this day, both the CDC and WHO wholeheartedly support them, regardless of the hundreds of scientific publications that dispute them.

Today, 27 years after the Halperin study, people with ALS are routinely not (properly) tested nor treated for Lyme. Instead, friends and families are encouraged to empty ice buckets over each other’s heads to collect money for new research for a new cure for ALS.

The patient stories mentioned above will simply be discarded as ‘anecdotical’ by both mainstream scientists, doctors and policymakers. So will the fact that Lou Gehrig actually owned a house in Old Lyme, Connecticut.

Yet, if these stories are not shared anyway, the knowledge in them will be lost and so is hope for other people like Eivind, Allan, Tabitha, my friend’s friend and their children.

Choices of media channels such as the BBC or Zembla are decisive which knowledge is made available to the public. I asked the editors of Zembla to reconsider broadcasting it again, but have not yet received a reply.

An intellectual ice bucket

Most of these diagnoses are simply words on a form, which either best fit the symptoms or simply fit the codes of the insurances. Almost all of them are based on clinical diagnoses only and can mean a life-sentence to the patients.

Yet they need to prove with 100% certainty that Lyme is the actual cause? How can they do so, with blood tests that produce over 500 times more false negatives than the current HIV tests? Even the ‘experts’ now state that they should no longer be used

The intellectual ice-bucket is that one disease (causative agent) can show up as many different ‘disease images’, fooling doctors, patients, immune systems and statistics alike. Although it happened before in history, with Syphilis, many people seem to find this idea hard to grasp.

In this current article I only used ALS, which is considered a lethal and incurable disease to all afflicted, as an example to open up your imagination. Yet I could have also used any of the other 364 known potential misdiagnoses of Lyme as well.

Odds are about 100% that you personally know people who suffer from several of these illnesses, as the list includes MS, Parkinson, Alzheimer, ME, Fibromyalgia, ADHD and so on.

This is why I wrote my book for people like my friend, as it’s much easier for her to see the scope and possibilities than for the people like her friend, who are disabled and so frightened that will tend to believe their medical ‘death sentence’.

Is Lyme always the cause? Most likely not, as with anything in life, but without a 100% reliable test we will never know for sure in how many cases it is. Can it be? Of course it can, in the current climate of ‘lost knowledge’. Here are just a few more examples.

In 1988, the Canadian Department of Health reported several cases of congenital Lyme infection. In 2017: silence.

In 2012, the WHO stated in an instruction about blood donation (p.84) that Lyme Borrelia infection can “occur after the bite of a tick, mosquito or horsefly and can survive blood storage temperatures“.

Did you know? Does your doctor? Not if they don’t stumble upon it in their private lives, as retired MD Dr. Al Miller did. He recently discovered his daughter-in-law (43) was wrongly diagnosed with – again – ALS and that her health improved, after she was (properly) tested and treated for Lyme. Dr. Miller has become very vocal about it.


Using normal human, scientific or professional logic does not really help to understand the current bias against Lyme as a potential cause for many different illnesses. It simply does not fit the current model.

So change will not come from ‘above’. Throughout history, it never has, because ‘above’ has no interests in changing a status quo. Both the CDC and the WHO are political organizations.

The main insight you may need to fully understand why a severe and widespread disease – or rather pandemic – is so systematically ignored, downplayed or simply denied to exist in the first place, is to appreciate what it means that Lyme is called a ‘political disease’.

This quote might give you a hint: “a patient cured is a customer lost”. That is why a paradigm shift entails more than just ‘finding a cure for ALS’ (or those 364 other diseases) and emptying a next bucket of ice cubes; no matter how well-intended the gesture is.


Neurodegenerative and Fatiguing Illnesses, Infections and Mitochondrial Dysfunction: Use of Natural Supplements to Improve Mitochondrial Function. Garth L. Nicolson, Robert Settineri and Rita R. Ellithorpe. Functional Foods in Health and Disease 2014; 4(1):23-65 (page 23 of 65)

Lyme disease-induced polyradiculopathy mimicking amyotrophic lateral sclerosis. Burakgazi AZ1. Int J Neurosci. 2014 Nov;124(11):859-62. doi: 10.3109/00207454.2013.879582. Epub 2014 Feb 7.

Chronic or Late Lyme Neuroborreliosis: Analysis of Evidence Compared to Chronic or Late NeurosyphilisJudith Miklossy. The Open Neurology Journal. 2012; 6: 146–157.

Dr. Richard Horowitz has a section in his second book ‘How Can I Get Better?‘ (page 282) where he says “Yet, if Lyme disease, co infections and environmental toxins are the sole causes of ALS, I would expect to see even more of these patients coming in with the disease.

Huib Kraaijeveld

Author of ‘Shifting the Lyme Paradigm‘, chairman of the On Lyme Foundation and founding member of the Ad Hoc Committee for Health Equity in ICD



Bravo Huib!

Dr. Miller:

Silent Epidemic of Early-Onset Alzheimer’s

The “Silent Epidemic” of Early-Onset Alzheimer’s

young woman with hands on shoulders


An estimated 200,000 to 275,000 people in the United States alone are believed to have early-onset Alzheimer’s disease…

A study published in the journal Surgical Neurology International in 2015 highlighted a growing trend in the onset of dementia among people under 65 years of age. The study, authored by Colin Pritchard and Emily Rosenorn-Lanng of Bournemouth University in England, found that dementia and other neurological diseases among people in 21 Western countries between the ages of 55 and 74 had dramatically increased during 1989-2010. By 2010, the average age of people developing dementia was 10 years less than in 1989.1 2 3

Dementia is increasingly being diagnosed in people in their 30s, 40s, and 50s. This phenomenon, known as “early-onset” (or “younger-onset”) dementia, has been referred to as a growing “silent epidemic” affecting younger people3 4—so much so that the media has begun to notice and report on individual cases.

People magazine recently highlighted the story of 32-year old ski instructor and photographer Becky Barletta who was diagnosed with early-onset dementia shortly after her marriage in 2015. There was the case of 29-year old mother-of-two Zoe Bottrill and the case of father-of-three Ken Dodson, also 29. The media is also reporting cases of childhood dementia, such as that of nine-year old Isobel Jeffery, two-year old Kade Gibbons, and one-year old Marian McGlocklin.5 6 7 8 9 10

An estimated 200,000 to 275,000 people in the United States alone are believed to have early-onset Alzheimer’s disease. (Alzheimer’s is the most common form of dementia.) This represents up to five percent of the estimated 5.5 million Americans with Alzheimer’s. Most people with early-onset dementia are diagnosed to have Alzheimer’s.11 12 13 14 15

The Alzheimer’s Association is projecting that by the year 2050 there will be 13.5 million Americans with Alzheimer’s.16 If the percentage of people in the U.S. with early-onset Alzheimer’s compared to the total number of people with Alzheimer’s remains constant, we may expect to have almost half a million Americans with early-onset Alzheimer’s in the next four decades. If growth trends in early-onset Alzheimer’s continue, however, we could have more than a million young to middle-aged Americans with this disease within two generations.

According to the Alzheimer’s Society, “The earlier the symptoms start, the more likely the disease is to be genetic.” This genetic form of the disease, known as “familial Alzheimer’s disease,” is caused by “rare mutations” in three genes—mutations found in 7-12 percent of people with early-onset Alzheimer’s.17 

So what accounts for the remaining roughly 90 percent of people with early-onset Alzheimer’s? The study by Pritchard and Rosenorn-Lanng suggests “environmental factors.”1 Although the study did not specify which environmental factors, some of these could include greater exposure to petrochemicals and toxic herbicides and insecticides.18 

Exposure to mercury could also be a contributing factor. In 2010, the Journal of Alzheimer’s Disease published a study showing that long-term exposure to mercury may produce Alzheimer’s-like symptoms in people.19 Neuropharmacologist Richard Deth, PhD, one of the study’s authors, concluded, “Mercury is clearly contributing to neurological problems, whose rate is increasing in parallel with rising levels of mercury. It seems that the two are tied together.”

There have also been journal studies showing exposure to aluminum could be another factor in the onset of Alzheimer’s symptoms.20 21 22 An author of one of those studies, bioinorganic chemist Chris Exley, PhD, has observed that high levels of aluminum have been found in the brains of people with early-onset Alzheimer’s. “I don’t believe [aluminum] is the only factor, but I think it is an important one which should be considered very seriously,” says Dr. Exley.22

Mercury and aluminum are found in some foods, medications, personal care products, and other consumer goods like compact fluorescent light bulbs (CFLs) and cookware. Both mercury (in the form of thimerosal) and aluminum are also used in vaccines—the former as a preservative and the latter as an adjuvant.23 24 25 26 27 28 29 30 31



There has been invaluable research in Lyme Land revealing that infections such as tick borne illness(es) including nematodes can be players in Alzheimer’s/dementia, antibiotics can often help these patients as well as anthelmintics, and due to the persistence of borrelia, we should prepare ourselves for an upcoming dementia pandemic.

There also has been great information coming out about the dangers of mercury and aluminum in vaccines:

Info on the Lyme Vaccine: (This link has many more listed at the end of the article)


Autism-Aluminum Adjuvant Link Corroborated

New Canadian study: Autism-Aluminum adjuvant link corroborated

BY J.B. HANDLEY September 18, 2017

In the December 2017 issue of the Journal of Inorganic Biochemistry and released online today, Dr. Christopher Shaw and colleagues at the University of British Columbia have established convincing biological evidence linking aluminum adjuvant used in vaccines to autism.

“This is the paper I have been waiting for. This paper reports measurements of cytokines in the brains of animals injected with aluminum adjuvant as neonates. The same cytokines are elevated as in human autism. IL-6 and CCL2/MCP-1 are elevated for example. Male animals are more strongly affected. It’s a perfect match to human autism.”

VANCOUVER, British Columbia — Just two weeks ago, I wrote about a study from France that raised major concerns about aluminum adjuvant used in vaccines. The French study authors wrote: “Concerns about its [aluminum adjuvant’s] safety emerged following recognition of its unexpectedly long-lasting biopersistence within immune cells in some individuals, and reports of chronic fatigue syndrome, cognitive dysfunction, myalgia, dysautonomia and autoimmune/inflammatory features temporally linked to multiple Al [aluminum]-containing vaccine administrations.”

In a nutshell, the French study found that when smaller doses of aluminum adjuvant were consistently injected over a short period of time — like during childhood vaccinations —the aluminum was more likely to end up in the brain, and the French scientists issued a stern warning about the use of aluminum adjuvant in vaccines:

In the context of massive development of vaccine-based strategies worldwide, the present study may suggest that aluminium adjuvant toxicokinetics and safety require reevaluation.

Canadian researchers establish direct link

In the December 2017 issue of the Journal of Inorganic Biochemistry and released online today, Dr. Christopher Shaw and colleagues have established convincing biological evidence linking aluminum adjuvant to autism. The study’s title alone should cause concern for parents everywhere:

Subcutaneous injections of aluminum at vaccine adjuvant levels activate innate immune genes in mouse brain that are homologous with biomarkers of autism

As the study authors state:

“It thus appears that Al [aluminum adjuvant] triggered innate immune system activation and altered cholinergic activity in male mice, observations which are consistent with those in autism. Female mice were less susceptible to Al exposure as only the expression levels of NF-κB inhibitor and TNFA were altered. Regional patterns of gene expression alterations also exhibited gender differences, as frontal cortex was the most affected area in males and cerebellum in females. Thus, Al adjuvant promotes brain inflammation and males appear to be more susceptible to Al′s toxic effects.”

It’s critical to note that the researchers found gender differences in how the mice responded, with male mice showing higher susceptibility, which is consistent with what we are seeing in autism: roughly 80% of the cases are boys.

The Canadian researchers included a diagram in their study that showed how aluminum adjuvant can contribute to an inflammatory cascade in the brain that leads to autism.

What does this mean in plain English?

Six months ago, I wrote an article about how close it appeared international scientists were to establishing a clear biological basis for how aluminum adjuvant can create autism. My article has been read more than 250,000 times, and I have heard from scientists from all over the world (most unwilling to let me quote them in public, which is its own great tragedy), including a scientist who has created a great website called Vaccine Papers. I asked “VP” about the importance of this study, and words were not minced:

This is the paper I have been waiting for.

This paper reports measurements of cytokines in the brains of animals injected with aluminum adjuvant as neonates. The same cytokines are elevated as in human autism. IL-6 and CCL2/MCP-1 are elevated for example. Male animals are more strongly affected. It’s a perfect match to human autism.

The paper includes a number of strong statements about vaccine causality.

This paper is hugely important because it shows IL-6 elevation in the brain, which of course provides a firm link to the immune activation literature. It is strong evidence supporting the al adjuvant IL-6 autism hypothesis.

Vaccines are given to babies during key phases of brain development

A Clear Hypothesis

If you would like to understand this complex issue in greater detail, I hope you will consider reading my widely read article from six months ago:

For the sake of brevity, here are the four key scientific discoveries I discussed in this lengthy article, most of which has happened in the last thirty-six months, appearing to show a clear link between aluminum adjuvant from vaccines and autism.

Discovery #1: “Maternal Immune Activation” can cause autism

Studies that support Discovery #1:

  1. Pregnancy, Immunity, Schizophrenia, and Autism.

2. Neuroglial activation and neuroinflammation in the brain of patients with autism

3. Microglial Activation in Young Adults With Autism Spectrum Disorder

4. Maternal Immune Activation Alters Fetal Brain Development through Interleukin-6

5. Activation of the Maternal Immune System During Pregnancy Alters Behavioral Development of Rhesus Monkey Offspring

6. Brain IL-6 elevation causes neuronal circuitry imbalances and mediates autism-like behaviors

Some helpful quotes from the above research to help contextualize Discovery #1:

“As we learn more about the connections between the brain and the immune system, we find that these seemingly independent networks of cells are, in fact, continually talking to each other. As an adult, the activation of your immune system causes many striking changes in your behavior — increased sleep, loss of appetite, less social interaction — and, of course, headaches. Conversely, stress in your life (as perceived by your brain) can influence immune function — the brain regulates immune organs, such as the spleen, via the autonomic nervous system.

Recent evidence shows that this brain-immune conversation actually starts during the development of the embryo, where the state of the mother’s immune system can alter the growth of cells in the fetal brain. As we shall see, such alterations can lead to an increased risk of schizophrenia or autism in the offspring.” — Dr. Paul Patterson, CalTech

Dr. Paul Patterson, CalTech

“There is also very striking evidence of immune dysregulation in the brain itself. Just last year, a group led by Carlos Pardo at Johns Hopkins found what they’re calling a “neural inflammation” in postmortem examination of brains of patients with autism who died between the ages of eight and 44 years. But these people weren’t infected — they died of such things as drowning or heart attacks. The study found that the microglial cells, which act as the brain’s own immune system, were activated. The study also found amazing increases of certain cytokines in the brain, and of others in the cerebro- spinal fluid. This is is a landmark paper, in my opinion. It presents the first evidence that there’s an ongoing, permanent immune-system activation in the brains of autistic people. It’s a subclinical state, because there’s no overt infection. But it’s there.” — Dr. Paul Patterson, CalTech

“In conclusion, the present PET measurements revealed marked activation of microglia in multiple brain regions of young adults with ASD. The results strongly support the contention that immune abnormalities contribute to the etiology of ASD.” — Dr. Carlos Pardo, Johns Hopkins

“Cytokines are produced by the white blood cells, and their levels in the blood increase when we get an infection…We think that maternal immune activation alters brain circuits…there’s that permanent, subclinical, altered immune state in the autistic brain — those increased cytokine levels…are they [cytokines] actually interacting with the brain in an ongoing fashion, with consequences visible in the patients’ behavior? I favor [the cytokine] hypothesis.” — Dr. Paul Patterson, CalTech

“Here we show that the cytokine interleukin-6 (IL-6) is critical for mediating the behavioral and transcriptional changes in the offspring. A single maternal injection of IL-6 on day 12.5 of mouse pregnancy causes prepulse inhibition (PPI) and latent inhibition (LI) deficits in the adult offspring.” — Dr. Paul Patterson, CalTech

“In this rhesus monkey model, MIA yields offspring with abnormal repetitive behaviors, communication, and social interactions. These results extended the findings in rodent MIA models to more human-like behaviors resembling those in both autism and schizophrenia.” — UC Davis MIND Institute

“In summary, our study supports a critical role of IL-6 elevation in modulating autism-like behaviors through impairments on synapse formation, dendritic spine development, as well as on neuronal circuit balance. These findings suggest that manipulation of IL-6 may be a promising avenue for therapeutic interventions.” —Dr. Xiaohong Li, Shanghai Jiao Tong University School of Medicine

Discovery #2: Aluminum Adjuvant causes immune activation and is far more neurotoxic than previously thought

Studies that support Discovery #2:

  1. Aluminum Adjuvant Linked to Gulf War Illness Induces Motor Neuron Death in Mice
  2. Aluminum hydroxide injections lead to motor deficits and motor neuron degeneration
  3. Mechanisms of aluminum adjuvant toxicity and autoimmunity in pediatric populations
  4. Slow CCL2-dependent translocation of biopersistent particles from muscle to brain

5. Biopersistence and brain translocation of aluminum adjuvants of vaccines

6. Non-linear dose-response of aluminium hydroxide adjuvant particles: Selective low dose neurotoxicity

Some helpful quotes from the above research to help contextualize Discovery #2:

“In addition, the continued use of aluminum adjuvants in various vaccines (i.e., Hepatitis A and B, DPT, and so on) for the general public may have even more widespread health implications. Until vaccine safety can be comprehensively demonstrated by controlled long-term studies that examine the impact on the nervous system in detail, many of those already vaccinated as well as those currently receiving injections may be at risk in the future. Whether the risk of protection from a dreaded disease outweighs the risk of toxicity is a question that demands urgent attention.” — Dr. Christoper Shaw, University of British Columbia

“Overall, the results reported here mirror previous work that has clearly demonstrated that aluminum, in both oral and injected forms, can be neurotoxic. Potential toxic mechanisms of action for aluminum may include enhancement of inflammation (i.e., microgliosis)…” — Dr. Christoper Shaw, University of British Columbia

“…it is somewhat surprising to find that in spite of over 80 years of use, the safety of Al adjuvants continues to rest on assumptions rather than scientific evidence.For example, nothing is known about the toxicology and pharmacokinetics of Al adjuvants in infants and children…Yet, in spite of these observations children continue regularly to be exposed to much higher levels of Al adjuvants than adults, via routine childhood vaccination programmes.” — Dr. Lucija Tomljenovic, University of British Columbia

“However, continuously escalating doses of this poorly biodegradable adjuvant in the population may become insidiously unsafe, especially in the case of overimmunization or immature/altered blood brain barrier…” —Dr. Josette Cadusseau, Université Paris

“Thus alum and other poorly biodegradable materials taken up at the periphery by phagocytes circulate in the lymphatic and blood circulation and can enter the brain using a Trojan horse mechanism similar to that used by infectious particles. Previous experiments have shown that alum administration can cause CNS dysfunction and damage, casting doubts on the exact level of alum safety.” — Dr. Josette Cadusseau, Université Paris

“We conclude that Alhydrogel [aluminum adjuvant] injected at low dose in mouse muscle may selectively induce long-term Al cerebral accumulation and neurotoxic effects. To explain this unexpected result, an avenue that could be explored in the future relates to the adjuvant size since the injected suspensions corresponding to the lowest dose, but not to the highest doses, exclusively contained small agglomerates in the bacteria-size range known to favour capture and, presumably, transportation by monocyte-lineage cells. In any event, the view that Alhydrogel neurotoxicity obeys ‘the dose makes the poison’ rule of classical chemical toxicity appears overly simplistic.” —Dr. Romain K. Gherardi, Université Paris Est Créteil (UPEC)

“In the context of massive development of vaccine-based strategies worldwide, the present study may suggest that aluminium adjuvant toxicokinetics and safety require reevaluation.” — Dr. Romain K. Gherardi, Université Paris Est Créteil (UPEC)

Discovery #3: Aluminum can increase IL-6 in the brain

Studies that support Discovery #3:

  1. Neuroprotective Effect of Nanodiamond in Alzheimer’s Disease Rat Model: a Pivotal Role for Modulating NF-κB and STAT3 Signaling

2. Brain IL-6 elevation causes neuronal circuitry imbalances and mediates autism-like behaviors

Some helpful quotes from the above research to help contextualize Discovery #3:

“The results also showed that aluminum administration increased the hippocampus pro-inflammatory cytokines TNF-α by 3.8-fold, IL-6 by 4-fold, and iNOS by 3.8-fold compared to the normal control group.” —Dr. Mosaad A. Abdel-Wahhab, Cairo University

Most vaccines contain aluminum, and aluminum is a proven neurotoxin, in amounts received from vaccines. Vaccines in combination can result in toxic aluminum overload. Even the aluminum in a single vaccine can be harmful because the aluminum is in a form that is more dangerous than ingested aluminum. Specifically, vaccine aluminum is in nanoparticulate form, which is harder for the body to eliminate, and because it is transported around the body differently than ingested aluminum.

It is natural and normal to ingest small doses of aluminum from food and water. Its not good for you, but the body has adequate defenses. Absorption of ingested Al is low, about 0.3%, so about 99.7% is eliminated in feces. Ingested aluminum is in ionic form (individual charged atoms), which is readily removed by the kidneys. Also, ionic aluminum is blocked from entering the brain by the blood brain barrier. The low absorption, rapid elimination by the kidneys and barrier to brain entry adequately protects the brain from aluminum.

However, nanoparticulate aluminum from vaccines cannot be removed by the kidneys. The particles are far too large to be filtered out by the kidneys. The Al nanoparticles do dissolve slowly (converting to ionic aluminum). But long before they can dissolve completely, the Al nanoparticles are “eaten” by immune system cells called macrophages. In other words, the particles wind up inside the macrophages. Once loaded with the Al nanoparticles, the macrophages spread aluminum as they travel through the body. This is dangerous, because the Al-loaded macrophages carry Al nanoparticles to tissues (e.g. the brain) that are damaged by very small amounts of aluminum. — Vaccine Papers

“Here we show that mice with elevated IL-6 in the brain dis- play many autistic features, including impaired cognitive abilities, deficits in learning, abnormal anxiety traits and habituations, as well as decreased social interactions. IL-6 elevation caused alterations in excitatory and inhibitory synaptic formations and disrupted the balance of excitatory/inhibitory synaptic transmissions. IL-6 elevation also resulted in an abnormal change in the shape, length and distributing pattern of dendritic spines. These findings suggest that IL-6 elevation in the brain could mediate autistic-like behaviors, possibly through the imbalances of neural circuitry and impairments of synaptic plasticity.” —Dr. Xiaohong Li, Shanghai Jiao Tong University School of Medicine

Discovery #4: Hepatitis B vaccine induces IL-6 in postnatal rats

Studies that support Discovery #4:

[Author’s note: This fourth discovery was really the subject of my extensive article, because it discussed a new paper that seemed to tie everything together. The Canadian paper above ties everything together even more tightly.]

  1. Neonatal vaccination with bacillus Calmette–Guérin and hepatitis B vaccines modulates hippocampal synaptic plasticity in rats

Some helpful quotes from the above research to help contextualize Discovery #4:

“An important new study by Li et al. reports the effects of bacillus calmette-guerin (BCG) vaccine (for tuberculosis) and hepatitis B vaccine on brain development in infant rats. The study relates the observed brain changes to the type of immune activation (Th1 or Th2, explained below) stimulated by the vaccines. The BCG and hep B vaccines had opposite effects on the brain (BCG being beneficial, and hep B being detrimental), and a combination of both vaccines resulted in cancellation of the effects.

This is the first study to test the effects of immune activation by vaccination on brain development. All other studies of immune activation have used essentially pathological conditions that mimic infection and induce a strong fever. A criticism I have heard often from vaccine advocates is that the immune activation experiments are not relevant to vaccines because vaccines cause a milder immune activation than injections of poly-IC or lipopolysaccharide (two types of immune system activators).

This new study demonstrates that vaccines can affect brain development via immune activation. Hence, the immune activation experiments are relevant to vaccines…The hep B vaccine increased IL-6 in the hippocampus (the only brain region analyzed for cytokines).” — Vaccine Papers

Four discoveries, a clear path to autism

Here’s a simple graphic that I think spells out the process of triggering autism very clearly, as demonstrated by the published science I have shared with you above through the four discoveries.

The new Canadian study, just published, makes these findings even more clear, and more robust, and provides even greater detail into HOW aluminum adjuvant leads to autism.

Image created by Vaccine

Now what?

When I published my article back in February, I heard from scientists from all over the world. I heard from pediatricians. I heard from board members at Autism Speaks. Many agreed with me: this was disturbing and important work, and it may well describe where all this autism is coming from. What’s happened since that time? Nothing.

There’s no mechanism for reviewing or putting all this published science together. The scientists doing this great work are perpetually nervous that they will lose their funding source or get “Wakefielded.” There’s no group responsible for putting all these published scientists in a room and figuring out what we do about this giant mess, and what all this information means. Every minute, a new child is diagnosed with autism, and every minute, it strikes me that autism may be completely AVOIDABLE. If you’re reading this, all I can ask is that you share the information widely, and that if you happen to be in a position of influence, please help save our kids.

In my opinion, we are much, much closer to understanding how autism has been triggered in so many children, and I hope this article is another step on the path to the truth. And, for so many of you out there doing everything you can to help you son or daughter with autism live the best possible life, perhaps a clearer understanding of how their autism was triggered will improve their chances for recovery.


For those of you interested in hearing from Dr. Shaw directly, here’s a video excerpt (just under 2 minutes) from the movie The Greater Good where Dr. Shaw discusses an earlier study he and his colleagues conducted looking at aluminum adjuvant (Aluminum hydroxide injections lead to motor deficits and motor neuron degeneration):

J.B. Handley is the father of a child with Autism. He and his wife co-founded Generation Rescue, a national autism charity. He spent his career in the private equity industry and received his undergraduate degree with honors from Stanford University. He is also the author of “The Only Vaccine Guide a New Parent Will Ever Need” , An Angry Father’s Guide to Vaccine-Autism Science”, and “7 reasons CDC employees should be “crying in the hallways” Mr. Handley has started a podcast called “How to End the Autism Epidemic” — you might enjoy his first six interviews:



I’m posting this because it should be important to everyone; however, whenever you talk about the immune system and cytokines, Lyme/MSIDS patients should sit up and take notice.  Due to a pathogen storm, we have a cytokine storm, confusing our immune systems and giving us boatloads of pain among other horrific symptoms.  This is also a sound warning about receiving any vaccinations while infected as they are designed to introduce many foreign substances into the body so the body mounts a response.  Our immune systems are already confused by a pathogen invasion.  In fact, the question truly begs to be asked, are vaccines ever safe for infected patients?  Also, it is important to point out that it is believed that children can get infected congenitally, which means they come out of the shoot compromised.  What does vaccination do to them?

So much is unknown and unproven.  Our children are too important not to search out the answers as inconvenient as they may be.

Every Lyme/MSIDS patient I know has regressed after a vaccination.  Food for thought.

For more on vaccines:  Dark Ages of Immunization Medicine Are NOW

Info on the Lyme Vaccine:  (This link has many more listed at the end of the article)


MS Cure?

Photo Credit: UK Business Weekly  by Erin Elizabeth, Health Nut News, Aug. 31, 2017

Multiple sclerosis is a terrible and debilitating disease where the body’s immune system is directed against the central nervous system. When that happens, according to the National MS Society:1

  • Within the CNS, the immune system attacks myelin — the fatty substance that surrounds and insulates the nerve fibers — as well as the nerve fibers themselves.
  • The damaged myelin forms scar tissue (sclerosis), which gives the disease its name.
  • When any part of the myelin sheath or nerve fiber is damaged or destroyed, nerve impulses traveling to and from the brain and spinal cord are distorted or interrupted, producing a wide variety of symptoms.

Currently, there is no cure. Medication can often help make symptoms like double vision, blindness, as well as psychological or muscle issues more bearable but ultimately it robs people of their lives and shortens life expectancies. But that may all be changing.

Dr. Su Metcalfe believes that the attack on the nerve cells can be stopped thanks to a new medical development her company LIFNano has created. 2

She said in an interview:

“Some people get progressive MS, so go straight to the severe form of the disease, but the majority have a relapsing or remitting version.

It can start from the age of 30, and there’s no cure, so all you can do is suppress the immune response, but the drugs that do that have side effects, and you can’t repair the brain. The cost of those drugs is very high, and in the UK there are a lot of people who don’t get treated at all.” 3

Using the stem cell particle LIF, which is a part of the immune cell and is able to control and confine the attack on our bodies, she found a “small binary switch” which is able to regulate itself INSIDE the immune cell to NOT attack our body. However, it can attack when it needs to.

She went on to say,

“That LIF, in addition to regulating and protecting us against attack, also plays a major role in keeping the brain and spinal cord healthy. In fact it plays a major role in tissue repair generally, turning on stem cells that are naturally occurring in the body, making it a natural regenerative medicine, but also plays a big part in repairing the brain when it’s been damaged.” 4

Much more research needs to be done but this breakthrough seems quite promising and the team has set their sights on having found the cure by 2020.

Dr. Metcalfe also believes she and her team might be able to tackle dementia as well because LIF is a “major health factor for the brain.5 Therefore, if they can get into the brain and protect it, it serves that they could prevent dementia.


This is indeed great news for Lyme/MSIDS patients due to the fact many with MS, dementia, and Alzheimer’s are initially misdiagnosed with those labels but are actually infected and vice versa.  All in all, many autoimmune diseases will potentially benefit from this treatment.

Iowan, Jack Gordon, is a case discovery of 2 diseases NEVER found together before on 11.22.2015: Lewy Body Dementia, causing violent hallucinations, and Lyme Disease/MSIDS. Using his medical files, he was bitten by a tick 35 yrs. ago, but the doctors never acknowledged it by diagnosing or treating him.

You may recognize Lewy Body Dementia as what Robin Williams’ autopsy revealed:


Drexel Prof: Lyme Persists by Lauren Ingeno July 18, 2017

Original Title: I.pacificus(F)_55sRGBBlacklegged ticks are known vectors for the bacteria Borrelia burgdorferi, which is the pathogen responsible for Lyme disease. Summer is tick season. (CDC / James Gathany)

Pennsylvania is the Lyme disease epicenter, with over 7,000 cases diagnosed in 2015.

The disease is caused by the spirochete bacteria Borrelia burgdorferi, which is carried by ticks and then transmitted to humans. When treated early, antibiotics can cure most patients. But making a diagnosis is often challenging, and chronic symptoms — such as memory problems, digestive issues and joint conditions — can linger for years, even after treatment.

Chronic Lyme is a controversial issue, dividing frustrated patients and some in the medical community who do not view their disease as a persistent infection. The Infectious Diseases Society of America, for instance, does not recommend longer courses of antibiotics even when symptoms continue.

Garth Ehrlich, PhD, a professor of microbiology and immunology at Drexel University College of Medicine, studies how chronic bacterial pathogens prevail after antibiotic therapy, and he was recently quoted in an Associated Press story about a Lehigh Valley woman who contracted the disease.

Below, he weighs in about chronic Lyme disease and why it is so hard to eliminate.

 What is the connection between your research and Lyme disease?
Lyme disease, in its persistent form, is most likely due to the bacteria forming a biofilm. I study bacterial biofilms, which are multicellular forms of bacteria, providing for increased resistance to antibiotics. If Lyme disease patients are not treated early enough or long enough, then it is possible the bacteria will form biofilms, and their acute disease will become chronic.

How is Lyme disease currently treated, and does that treatment work?
In many cases, Lyme can be treated by antibiotics, but it does not necessarily mean the disease won’t become chronic. There are many factors that contribute to the course of the disease, including the overall health and immune status of the patient, as well as the particular strain of the Lyme disease bacteria that they contract.

Why is there disagreement among the medical and scientific communities about chronic Lyme disease?
A few physicians involved in characterizing the disease in the early stages of its recognition staked their reputations on the fact that it only had an acute phase. But the bacteria that causes Lyme is a spirochete, and spirochetes are primarily associated with chronic infections, like gum disease and syphilis.

How is Lyme disease diagnosed? What are the challenges?
There is a huge problem with diagnosing it, and there are many reasons why it is difficult. There are two stages for the standard testing: an ELISA (enzyme-linked immunosorbent assay) is used to detect antibodies against B. burgdorferi proteins and a Western blot (used to separate and identify specific antibody proteins), which is more specific and used for confirmation of the ELISA.

Scientists are working to develop DNA-based tests, but they are not widely available yet, and they won’t be perfect. The problem with both types of testing is that there is enormous variability among the bacterial strains that cause the disease. Thus, an assay based on one strain might very well miss variant strains. And different individuals mount more or less of an immune response to the infection. If the infection becomes focal, then you might not be able to detect it with a DNA blood test.

What do we need to do to better combat Lyme disease?
The most important thing is to develop better diagnostics. And the next most important thing is better therapeutics. My lab is trying to develop drugs against biofilm bacteria.

For media inquiries, contact Lauren Ingeno at or 215.895.2614.



Fantastic article revealing Oz behind the curtain:  biofilms.

I appreciate the careful wording about treating early – that it can cure most patients; however, the caveat is that treatment has to be early enough AND long enough.  I would add, and smart enough.

That said, there is an elephant in the room.  Since Eva Sapi discovered in vitro that doxycycline throws the spirochete into the cyst form, is it hiding out to reemerge later?  Many think so, and believe Lyme can be contributing to dementia and Alzheimer’s which means treatment should also include not only something that addresses biofilms, but something that addresses the non-cell wall form (even in acute cases).  For more:

The other elephant standing by the first is the prevalence of coinfections.  Research is absent on the compounding factors of coinfections.  For more:


Wisconsin – 117% Increase in Human Version of Mad Cow Disease

In a recent article by Dr. Mercola,,  statistics reveal there is a a 117% increase in Wisconsin and an 85% increase in the U.S. of the human version of mad cow disease, Creutzfeldt-Jakob, which is a contagious neurological disease caused by eating beef contaminated with brain, spinal cord or other central nervous system tissue from infected cattle.

Now the Canadian Government is warning that chronic wasting disease (CWD), a similar disease found in the deer family may jump to humans as well.  Both mad cow disease and chronic wasting disease cause transmissible spongiform encephalopathies (TSE).

The deer family is also known to pick up hitchhiking ticks and carry them long distances.

This warning is due to a study which found CWD was transmitted to three out of five macaque monkeys infected with white tail deer meat.  There is also a systematic literature review showing CWD could also be transmitted to squirrel monkeys.

There is a potential for transmission to humans exposed to deer through diet, health products containing antler velvet, slaughter, velvet harvest, field dressing, preparing trophies and hunting lures.

The state of Wisconsin offers free CWD testing to hunters.

The Milwaukee Journal Sentinel states,

“Wisconsin Department of Natural Resources (DNR)] figures show that tens of thousands of hunters are killing deer in areas where CWD is prevalent and are not submitting them for testing. In 2016, in a CWD-prone area that the DNR describes as the southern farmland zone, 442 deer tested positive for disease out of 3,760 samples. More than 65,000 deer were killed in that zone and were not tested, according to DNR figures.”

Animals infected with CWD shed prions in saliva and urine and remain contagious for life and contaminate land and water.

Similar to Chronic Lyme Disease, CWD does not evoke a detectable immune response or inflammatory reaction. It is different; however, in that it is smaller than most viruses.  It also persists in the environment which is why animals raised in captivity are more likely to infect each other.  Avoid meat from those who force natural herbivores to eat animal parts (routine in concentrated feeding operations).

Researchers have also found an infectious protein (TDP-43) in Alzheimer’s patients is quite similar to prions in mad cow disease and CWD and was found in 200 of 340 autopsied brains of Alzheimer’s patients.  Patients with TDP-43 are 10 times more likely to have been cognitively impaired at death.

A 2005 study published in the journal Medical Hypotheses, stated:

“In the opinion of experts, ample justification exists for considering a similar pathogenesis for Alzheimer’s, Creutzfeldt-Jakob and the other spongiform encephalopathies such as Mad Cow disease. In fact, Creutzfeldt-Jakob and Alzheimer’s often coexist and at this point are thought to differ merely by time-dependent physical changes. A recent study links up to 13 percent of all ‘Alzheimer’s’ victims as really having Creutzfeldt-Jakob disease.”

**Please have your meat tested.  It’s free and it may save your life.**

A Bug for Alzheimer’s?

Please read the article above, written by Melinda Wenner Moyer, edited by Pam Weintraub.

A brief summary:

Robert Moir, a neurologist at Massachusetts General Hospital in Boston, believes that beta-amyloid, a key player in Alzheimer’s, might be a good guy who is actually protecting the brain from pathogens.

This idea is coming from numerous corners of the world and has been labeled ‘pathogen hypothesis.’ Others pointing this out are pathologist Alan MacDonald, neuropathologist Judith Miklossy, and microbiologist Tom Grier.

Moir has published mouse studies showing that their brains create amyloid plaques within hours of contracting infections and they actually kill pathogens.

This observation flies in the face of accepted dogma about beta-amyloid and it is rarely discussed in AD groups.

A meta-analysis of 25 published studies has shown that infected folks are 10 times more likely to develop AD, leading international researchers to co-sign an editorial begging others to consider pathogens in relation to AD.

But, the cabal isn’t having it. Moir’s 2016 paper was rejected six times without even a review before finally getting the nod.

The author reminds the reader that infections in the brain are nothing new and a short list of them includes: Syphillis, Herpes simplex encephalitis, tick borne disease, HIV, Toxoplasma gondii, Chlamydia pneumoniae, HSV-1, and Zika.

The journalist also points out that pathogen causation is not proven and that Alzheimer’s patients might be prone to infection but that some studies suggest the infections came first. She also says that the majority of folks suggesting the ‘pathogen hypothesis’ do not feel the infections work alone but rather can cause a domino effect that over time can accumulate causing AD.

And lastly, if beta-amyloid causes AD then removing these plaques should get rid of symptoms, but when 145 beta-amyloid-reducing drugs were tested, not one slowed progression of the disease.

Once again, proving a science cabal exists, Moir recounts how at a Korean conference, attendees were asked to raised hands if they thought infections played a part in AD and a majority of hands went up.

“Ten years ago, it would have been four guys in a corner, all huddled together, not talking to anyone else, Moir says.

Isn’t that sad?