Archive for the ‘research’ Category

Aluminium in Brain Tissue in Autism

https://www.sciencedirect.com/science/article/pii/S0946672X18302141?via%3Dihub

Aluminium in brain tissue in autism

Ivan Ivanovski, Ana Ivanovski, Dimitrije Nikolic, Petar Ivanovski

 

1. Introduction

The discovery of aluminum (Al) in quantities unexpectedly high in brain tissue in five patients with autism spectrum disorder [1] has immediately imposed to us the question: from where has this aluminum come? We live in what one leading researcher on the chemistry of aluminum has called “the Aluminum Age” [2] and concerns about the toxicity of ingested Al were expressed over hundred years ago [3] long before it became as widely used as it is today.

Al is the third most abundant element in the earth’s crust and occurs naturally in the environment, foodstuffs, and drinking water [4]. It is also used in: processed foods, materials and articles such as, Al-containing food packaging, Al foils, cooking utensils and baking trays. It has long been assumed that dietary Al is the main risk source of exposure to biologically available Al. Under physiologic conditions intestinal absorption of aluminum is impossible since biometals (Fe, Cu, Zn, Mn, Mo, Cr) and toxic metals (Pb, Hg, Ni, Cd,) are absorbed exclusively in their 2+ state. Aluminum as a trivalent under physiologic conditions cannot be absorbed. Trivalent Al can be absorbed through the intestinal mucosa only in the cases of mucosal damage (infection, inflammation, intoxication as was the case in 1988 in England [5]).

The Camelford water pollution incident [5] involved the accidental contamination of the drinking water supply to the town of Camelford, Cornwall, in July 1988, when twenty tonnes of aluminium sulphate was inadvertently added to the water supply, raising the concentration to 3000 times the admissible level. If present in the intestinal lumen while the mucosa is damaged, or is ingested in toxic quantities, Al3+ is absorbed probably by simple diffusion.

It has been suggested that acid digestion in the stomach would solubilise most of the ingested aluminum compounds. In acidic aqueous solutions with pH < 5 the aluminum ion exists mainly as Al3+, e.g. hydrated Al3+ [Al(H2O)6]3+. By passing from the stomach to the intestines the increase in pH results in the formation of complexes of aluminum with hydroxide and finally the formation of insoluble aluminum hydroxide at neutral pH. Therefore as the pH is neutralized in the duodenum the aluminum ion is gradually converted to aluminum hydroxide and the majority is then expected to precipitate in the intestine with subsequent fecal excretion, leaving only a minor fraction available for potential absorption. In conclusion, independently of the pH value Al in its compounds always retains its trivalent state. Divalent aluminum does exist. It has been detected in the gas phase after explosion of aluminized grenades in the upper atmosphere and in stellar absorption spectra [6]. Usually humans live very far from these events and spaces.

Aluminum can be potentially absorbed through the skin essentially if it is shaved or irritated by application of skin care creams, rejuvenation creams, sprays against unpleasant smells and sweats and after shave lotions that contain aluminum [7]. However, the use of these cosmetic products in newborns, infants, and children is not common. Al can be also absorbed across the lung or olfactory epithelia by persons working in workplaces where Al welding is carried out during electrolysis in Al production or in the processing industries (e.g., foundries, powder production). There are thus clearly different routes of Al exposure and what must be emphasized is that these are not necessarily equivalent with regard to the amount delivered per unit of time and more importantly with regard to the age at which the person is exposed to Al. The younger age carries greater probability for toxic effects.

Although it is commonly assumed that children obtain much more Al from diet than from vaccination [8], this notion contradicts basic toxicological principles. The route of exposure that bypasses the protective barriers of the gastrointestinal tract and/or the skin will likely require a lower dose to produce a toxic outcome [2]. In the case of Al only approximately 0.25% of dietary Al is absorbed into systemic circulation [9]. Much of the Al that enterally enters the human body is typically rapidly removed by the kidneys [10]. In contrast, Al hydroxide (the most common adjuvant form) injected intramuscularly may be absorbed at nearly 100% efficiency over time [11].
More importantly, wherever the anatomical place of vaccine application is, adjuvant Al enters into the circulation where it binds to transferrin. This adjuvant Al bound to transferrin, has a unique capacity to cross the blood-brain and blood-cerebrospinal fluid barriers, access the brain where it is deposited probably for the whole life [12] since adjuvant Al is poorly excreted [13].

Today we live in an era of aluminum. Aluminum is all around us. Therefore, one can rightly ask the question: were Mold et al. [1] aware in their research that there was no contamination with external aluminum during the acquisition of brain tissue and the procedure for determining the amount of aluminum in it? The same question can be posed to all other former researchers and to their research on the basis of which a ″Handbook on the Toxicology of Metals″ has been written [14].

In the paper of Mold et al. [1] the strangest and most intriguing fact is that the highest concentrations of aluminum were measured in the youngest person. The boy was only 15 years old (case A4). Generally accepted claim that dietary aluminum is the main source of exposure to aluminum, inevitably raises the question: how is it possible that in the course of only 15 years of life, this boy “absorbed” such amount of aluminum and deposited it in his brain? On the other hand the boy in that age probably did not use creams containing aluminum, antiperspirant sprays, nor shaved. He also could not have been present in1988 in Camelford, Cornwall (UK). At the age of 15 he could not be a worker in the aluminum industry where he would be exposed to aluminum dust and fumes. Even less it was likely that this boy lived near the place where aluminized grenades exploded! We also do not believe that the boy was a cosmonaut and he travelled in interstellar spaces where divalent aluminum is located. In the work of Mold et al. [1] the year of birth of persons shown in the work is not indicated. We can only assume that the 15-year-old boy was born around the year 2000.

Given all of the above under normal, usual, physiological conditions the most important, the most regular and most predictable even by the law legislated access of aluminum into the human body is through vaccines. According to the vaccination schedule which was established in 2000 in the USA, by the age of 18 months, approximately 4425 μg of aluminum is parenterally delivered into the human body through vaccines [15]. After 2005 with the introducing of new vaccines, the quantity of adjuvant Al has increased up to 4925 μg [15].

Aluminum neurotoxicity has been shown in experiments on mice [16]. Aluminum toxicity has been shown even in one clinical study in which 182 infants were treated with intravenous injections of nutritional formula that contained different quantities of aluminum [17] but received significantly less aluminum than the infants receiving aluminum via vaccines. Recently it was shown that another metal i.e. mercury is also neurotoxic for children even in much less quantities in comparison with aluminum [18]. Toxic effects of Al can be assigned to its physical and chemical properties. Owing to its 3+ charge Al attracts negatively charged ions and electrons but because it cannot transition to other oxidation states besides 3+, Al is not a direct component in any redox reactions but may participate indirectly in Fenton reactions. Moreover, the small ionic radius and the high charge of Al3+ are its important properties by which this metal can exert its toxic activity. The Al ion (0.054 nm) is roughly the same size as the ferric (Fe3+) ion (0.065 nm) and much smaller than magnesium (Mg; 0.072 nm) and calcium (Ca) ions (0.100 nm). Thus, in biological systems, Al can effectively replace these essential biometals in many enzymatic reactions [19,20].

2. Conclusion

Aluminum is undoubtedly neurotoxic. The main the most important “physiological” way to reach the human body is via vaccines in the form of a trivalent adjuvant. But on the other hand, vaccines have saved humanity from many deadly infectious diseases. So-called cost-benefit is in absolute overdose in favor of vaccination. One should never think about abolishing vaccination, but rather to work on finding ways to reduce the toxicity of adjuvant aluminum and if possible to completely eliminate it.

To achieve this goal, we suggest:

1

All aluminum containing vaccines must be postponed until the time when the child’s brain shows sufficient physiological maturation. That would be the day when the child loses its last primitive reflex, corresponding the age of 6–7 months, ideally, after 12 months. By this age most of so-called synaptic pruning is completed and consequently the child’s brain is probably less vulnerable to the deleterious effects of aluminum, in comparison with the brain vulnerability to the toxins given immediately after birth when the newborns on their first day of life are injected with 0.25 mg of Al3+ through the application of hepatitis B vaccine. The younger the time age of exposition to Al, carries the greater harm for Al toxicity and brain damage. This is in accordance with a recent review in which it has been calculated and shown, that the levels of aluminum suggested by the currently used limits place infants at risk of acute, repeated and possibly chronic exposures of toxic levels of aluminum in modern vaccine schedules [21]. Therefore, it has been suggested that vaccination in neonates and low birth-weight infants has to be re-assessed in the sense of aluminum dosage reduction in vaccines, according to the birth-weights. The main obstacle to this proposal is the unknown effect of this proposed reduction on the final antigenicity of the vaccine [21].

2

It is necessary to totally eliminate the metal(s) in all vaccines (especially aluminum and mercury), whether in children or in adults; it very much matters to be clear and totally intransigent, on this point. Complete elimination of vaccine aluminum neurotoxicity could be achieved by its replacement with some other element, or compound. Squalene could also be used to replace Al. In a recent review [22] it was reported that calcium phosphate could be as effective adjuvant as aluminum salts, with the following advantages: Calcium phosphate is present in the general monographic on human vaccines of the European Pharmacopoeia 8.0; calcium phosphate is classified as safe and biocompatible by the US FDA; calcium phosphate is a natural compound of the human body, thus suggesting its good tolerance for individuals; adsorption capability of calcium phosphate is equivalent to aluminum adjuvants depending on preparation mode, considered antigens, and particle size; calcium phosphate booster antigenicity is potentially better than with aluminum adjuvants [22].

Calcium phosphate was used in France until the mid-1980s mainly for the diphtheria-pertussis-tetanus vaccine group without any mention of adverse reactions by physicians. Until the early-1970s it was also successfully used in the pentavalent human vaccination (smallpox, yellow fever, measles, BCG, and tetanus) and also without any reported adverse reaction [23].

With all of this in mind it is very mysterious and curious that in the 1980s, vaccines manufacturers opted for replacing calcium phosphate, which was used as adjuvant for human vaccines with Al as preferred adjuvant. Since then most of the clinical experience has been gathered with the use of Al as vaccines adjuvant while calcium phosphate was only marginally investigated [24]. From the other side we do not insist but to our knowledge, we would like to suggest that zinc could be the element of choice to replace aluminum for the following reasons: 1. Both metals, Zn and Al are amphoteric; 2. Zinc is necessary for normal human life (zinc human body burden is between 200 and 300 mg); and finally; 3. so far, no zinc overload related disease has been described. In animal experiments zinc toxicity has been shown but normally and fortunately, humans do not live in “experimental” conditions, in which experimental animals are exposed to excessive, toxic quantities of various substances, including zinc. There are no literature data so far on the use of zinc as adjuvant. Therefore, vaccinologists and immunologists must start as soon as possible with the experiments with zinc compounds (hydroxide, sulphate or phosphate) as adjuvant. If it turns out after the experiment that zinc compound(s) have successfully replaced Al compounds as adjuvants, the amount of zinc that would be administered by vaccine in children up to 18 months of age would be about 5.000 μg ( = 5 mg), which is absolutely far beyond the domain of experimental Zn toxicity.

Naturally many scientists will not be in agreement with our arguments on the potential role of zinc in future vaccines. The fact is that we presently possess no critical perspective for zinc to be the substitution for Al, as well. Both of these statements should not at all be the arguments against our proposal for the experiments with zinc as adjuvant to find out whether zinc and its compounds could offer advantages over aluminum.

Conflict of interest statement

The authors declare no conflict of interest.

References

[1]
M. Mold, D. Umar, A. King, C. ExleyAluminium in brain tissue in autism
J. Trace Elem. Med. Biol., 46 (2018), pp. 76-82
[2]
C. ExleyAluminium and medicine
A.L.R. Merce, J. Felcman, M.A.L. Recio (Eds.), Molecular and Supramolecular Bioinorganic Chemistry: Applications in Medical Science, Nova Biomedical Books., NY, USA (2009), pp. 45-68
[3]
W.J. GiesSome objections to the use of alum baking-powder
JAMA, 57 (1911), pp. 816-821
[4]
EFSA (European Food Safety Authority)Safety of aluminum from dietary intake, scientific opinion of the panel on food additives, flavourings, processing aids and food contact materials
AFC). EFSA J. (2008), pp. 1-34
[5]
https://en.wikipedia.org/wiki/Camelford_water_pollution_incident; Accessed Feb 5, 2018.
[6]
https://en.wikipedia.org/wiki/Aluminium(II)_oxide; Accessed Feb, 5 2018.
[7]
A. Pineau, O. Guillard, F. Favreau, A. Marrauld, B. FauconneauIn vitro study of percutaneous absorption of aluminum from antiperspirants through human skin in the Franz™ diffusion cell
J. Inorg. Biochem., 110 (2012), pp. 21-22
[8]
P.A. Offit, R.K. JewAddressing parents’ concernes: do vaccines contain harmful preservatives, adjuvants, additives, or residuals?
Pediatrics, 112 (6 Pt 1) (2003)
1394-137
[9]
R.A. Yokel, C.L. Hicks, R.L. FlorenceAluminum bioavailability from basic sodium aluminum phosphate, an approved food additive emulsifying agent, incorporated in cheese
Food Chem.Toxicol., 46 (2008), pp. 2261-2266
[10]
L. TomljenovicAluminum and Alzheimerꞌs disease: after a centuryof controversy, is there a plausible link?
J. Alzheimers Dis., 23 (2011), pp. 567-598
[11]
R.A. Yokel, P.J. McNamaraAluminim toxicokinetics: un updated minireview
Pharmacol. Toxicol., 88 (2001), pp. 159-167
[12]
Z. Khan, C. Combadiere, F.J. Authier, et al.Slow CCL2-dependent translocation of biopersistent particles from muscle to brain
BMC Med., 11 (2013), p. 99
[13]
S.L. HemElimination of aluminium adjuvants
Vaccine, 20 (Suppl. 3) (2002), pp. S40-3
[14]
B. Sjögren, A. Iregren, J. Montelius, R.A. YokelAluminium
G.F. Nordberg, B.A. Fowler, M. Nordberg (Eds.), Handbook on the Toxicology of Metals (4th ed), Elsevier/Academic Press (2015)
Chapter 26.
[15]
N.Z. MillerAluminium in childhood vaccines is unsafe
J. Am. Phys. Surg., 21 (2016), pp. 109-117
[16]
G. Crépeaux, H. Eidi, M.-O. David, Y. Baba-Amer, E. Tzavara, B. Giros, F.-J. Authier, C. Exley, C.A. Shaw, J. Cadusseau, R.K. GherardiNon-linear dose-response of aluminium hydroxyde adjuvant particles : selective low dose neurotoxicity
Toxicology, 375 (2017), pp. 48-75
[17]
N.J. Bishop, R. Morley, J.P. Day, A. LucasAluminium neurotoxicity in preterm infants receiving intravenous feeding solutions
N. Engl. J. Med., 336 (1997), pp. 1557-1561
[18]
I. Prpić, A. Milardović, I. Vlašić-Cicvarić, Z. Špiric, J. Radić Nišević, P. Vukelić, J. Snoj Tratnik, D. Mazej, M. HorvatPrenatal exposure to low-level methylmercury alters the child’s fine motor skills at the age of 18 months
Environ. Res., 152 (2017), pp. 369-374
[19]
T.J. Shafer, W.R. MundyEffect of aluminum on neuronal signal transduction: mechanisms underlying disruption of phosphoinositide hydrolysis
Gen. Pharmacol., 26 (1995), pp. 889-895
[20]
W.R. Mundy, P.R. Kodavanti, V.F. Dulchinos, H.A. TilsonAluminum alerts calcium transport in plasma membrane and endoplasmic reticulum from rat brain
J. Biochem. Toxicol., 9 (1994), pp. 17-23
[21]
J. Lyons-Weiler, R. RicketsonReconsideration of the immunotherapeutic pediatric safe dose levels of aluminum
J. Trace Elem. Med. Biol., 48 (2018), pp. 67-73
[22]
J.D. Masson, M. Thibaudon, L. Bélec, G. CrépeauxCalcium phosphate: a substitute for aluminum adjuvants?
Expert Rev. Vaccines, 16 (3) (2017), pp. 289-299
[23]
C. Gateff, E.H. Relyveld, G. Le Gonidec, et al.Study of a new pentavalent vaccine combination
Ann. Microbiol. (Paris), 124 (1973), pp. 387-409
[24]
http://www.europarl.europa.eu/sides/getAllAnswers.do?reference=E-2017-001984&language=EN; Accessed Feb 5, 2018.

 

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For more:  https://madisonarealymesupportgroup.com/2017/09/21/aluminum-flawed-assumptions-fueling-autoimmune-disease-and-lyme/

 

https://madisonarealymesupportgroup.com/2017/11/28/biological-mechanisms-of-vaccine-injury/

https://madisonarealymesupportgroup.com/2018/08/21/aluminum-in-the-brain-in-multiple-sclerosis-regulatory-and-funding-agencies-silent-complicit/

https://madisonarealymesupportgroup.com/2018/10/16/altering-human-genetics-through-vaccination/

https://madisonarealymesupportgroup.com/2017/03/30/ty-bollinger-the-truth-about-vaccines-series/  I highlight a 9 part series on vaccines.  

https://madisonarealymesupportgroup.com/2018/09/08/acip-vote-yes-for-new-vaccine-despite-no-safety-studies-on-cumulative-effect-with-other-vaccines/

https://madisonarealymesupportgroup.com/2018/08/24/financial-kickbacks-for-vaccinations-abusive-illegal-fraudulent/

https://madisonarealymesupportgroup.com/2018/10/05/drug-companies-pay-fda-nih-to-fast-track-market-vaccines/

https://madisonarealymesupportgroup.com/2017/04/06/video-how-vaccines-are-made/

Autism and metals:  https://madisonarealymesupportgroup.com/2016/12/08/mercury-and-autism/

https://madisonarealymesupportgroup.com/2018/09/28/toxic-metal-pollution-linked-with-development-of-autism-spectrum-disorder/

https://madisonarealymesupportgroup.com/2017/09/19/autism-aluminum-adjuvant-link-corroborated/

https://madisonarealymesupportgroup.com/2018/06/15/canadian-data-more-autism-where-vaccine-coverage-is-highest/

https://madisonarealymesupportgroup.com/2018/06/01/immunoexcitotoxicity-as-the-central-mechanism-of-etiopathology-treatment-of-autism-spectrum-disorders-a-possible-role-of-fluoride-aluminum/

Vaccine fraud:  https://madisonarealymesupportgroup.com/2018/07/20/hhs-vaccine-fraud-proven/

https://madisonarealymesupportgroup.com/2018/03/21/congress-receives-vaccine-safety-project-details-since-the-cdc-fda-ignore-their-own-data-and-proclaim-vaccines-do-not-cause-autism/

https://madisonarealymesupportgroup.com/2018/10/08/vaccine-safety-efficacy-studies-that-are-the-bases-for-marketing-authorizations-are-a-complete-methodological-mess/

https://madisonarealymesupportgroup.com/2016/11/29/spider-attacks-cdc/

https://madisonarealymesupportgroup.com/2017/09/27/strange-case-of-poul-thorsen-vaccine-data-manipulator-extraordinaire/

Also, https://madisonarealymesupportgroup.com/2017/03/30/ty-bollinger-the-truth-about-vaccines-series/ , this link shows highlights of a 9 part series by Dr. Gentempo and it’s riddled with vaccine fraud everywhere.  There are links within the article on specific vaccines.

 

 

 

 

 

 

In vitro and in vivo Evaluation of Cephalosporins for the Treatment of Lyme Disease

https://www.ncbi.nlm.nih.gov/m/pubmed/30254421/

In vitro and in vivo evaluation of cephalosporins for the treatment of Lyme disease.

Pothineni VR, et al. Drug Des Devel Ther. 2018. doi: 10.2147/DDDT.S164966. eCollection 2018.

Abstract

Background: Lyme disease accounts for >90% of all vector-borne disease cases in the United States and affect ~300,000 persons annually in North America. Though traditional tetracycline antibiotic therapy is generally prescribed for Lyme disease, still 10%-20% of patients treated with current antibiotic therapy still show lingering symptoms.

Methods: In order to identify new drugs, we have evaluated four cephalosporins as a therapeutic alternative to commonly used antibiotics for the treatment of Lyme disease by using microdilution techniques like minimum inhibitory concentration (MIC) and the minimum bactericidal concentration (MBC). We have determined the MIC and MBC of four drugs for three Borrelia burgdorferi s.s strains namely CA8, JLB31 and NP40. The binding studies were performed using in silico analysis.

Results: The MIC order of the four drugs tested is cefoxitin (1.25 µM/mL) > cefamandole (2.5 µM/mL), > cefuroxime (5 µM/mL) > cefapirin (10 µM/mL). Among the drugs that are tested in this study using in vivo C3H/HeN mouse model, cefoxitin effectively kills B. burgdorferi. The in silico analysis revealed that all four cephalosporins studied binds effectively to B. burgdorferi proteins, SecA subunit penicillin-binding protein (PBP) and Outer surface protein E (OspE).

Conclusion: Based on the data obtained, cefoxitin has shown high efficacy killing B. burgdorferi at concentration of 1.25 µM/mL. In addition to it, cefoxitin cleared B. burgdorferi infection in C3H/HeN mice model at 20 mg/kg.

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For more on Dr. Lewis’ work:  https://madisonarealymesupportgroup.com/2018/08/06/meet-the-researcher-kim-lewis-ph-d/

https://madisonarealymesupportgroup.com/2016/10/31/news-story-on-researcher-kim-lewis-and-chronic-lyme/

https://madisonarealymesupportgroup.com/2018/08/24/identifying-vancomycin-as-an-effective-antibiotic-for-killing-bb/

 

“Super responders” Are Key to Personalized Lyme Disease Treatment

https://www.lymedisease.org/personalized-lyme-disease-treatment/

By Lorraine Johnson

LYMEPOLICYWONK: “Super responders” are key to personalized Lyme disease treatment

I’m excited to report that the first study using information from MyLymeData has just been published in the medical journal Healthcare.

Using patient-reported outcome data from 3,900 people enrolled in MyLymeData, we looked at how individual patients vary in their response to treatment. Finding out who responds well to which treatments—and then learning more about those people—is an important step towards developing personalized Lyme disease treatment.

Treatment studies of patients with late/chronic Lyme disease usually take an average of how people have responded to treatment. But guess what? The average Lyme patient isn’t average! Some people improve a lot with treatment, some improve a little bit, and some people don’t improve at all. A few may even get worse.

Super responders

However, if we can identify the “super responders”—the ones who did particularly well—and take a closer look at them, we may be able to learn things that can help other patients in a similar situation. This can help drive the development of personalized Lyme disease treatment.

For lots of diseases, such as tuberculosis, pulmonary disease, and cancer, scientists are now identifying high treatment responders, but our study is the first to use this approach in Lyme disease.

The reason it hasn’t been done before in Lyme disease is because identifying how different groups of patients respond to treatment requires large samples. The largest trial funded by the National Institute of Health for patients with chronic Lyme disease enrolled just 129 people—way too small a group to look at individual treatment variation.

So instead, they lumped all of the treatment responses together—the good, the bad and the ugly—and said how patients responded “on average.” On average, there wasn’t much improvement from treatment.

But treatment averages don’t tell the whole story. A famous mathematician, Des MacHale, explains it this way: The average person has one testicle and one breast. And we all know how ridiculous that is. You can’t average a male and a female like that and get any meaningful information.

It’s the same thing when you measure patient treatment response in Lyme disease. If one person gets better and the other gets worse after treatment, you can say that on average, treatment did nothing. However, for the patient who got better, it made a world of difference. Yet, when we use an average to calculate treatment response, the favorable response of one patient is cancelled out by the negative response of another.

A better approach looks at variations in how different patients respond. Most Lyme disease patients already know this. Some patients get better, others get worse, and some don’t change with treatment. Treatment response variation is lost when individual responses are averaged.

In our study, we included close to 4,000 patients, a large enough sample to look at variations in treatment response. Here’s what we found. Most patients (52%) responded positively to antibiotic treatment and some—roughly a third—responded very well to treatment. These patients said that they felt moderately to a very great deal better after taking antibiotics. Very few said that they felt worse after taking antibiotics (only 12%).

If I were a patient with chronic Lyme disease—which I was by the way–I would want to know that roughly a third of those in the sample were “high treatment responders”—meaning that they reported that after taking antibiotics their symptoms improved moderately to a very great deal. This is the type of information that patients want to know and that is why we conducted this study.

This is the first of many studies to be published using the data from MyLymeData.  So stay tuned! And if you are not enrolled in MyLymeData—I encourage you to stop what you are doing and sign up now. It is only by having patients pool their data that we will make progress in this disease.

Here is a short video I recorded explaining more about the study’s results.

Click here to read the full study.

Click here to enroll in MyLymeData.

Lorraine Johnson, JD, MBA, is the Chief Executive Officer of LymeDisease.org. You can contact her at lbjohnson@lymedisease.org. On Twitter, follow her @lymepolicywonk. If you have not signed up for our patient-centered big data project, MyLymeData, please register now.

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**Comment**

If you haven’t enrolled in this Bigdata research, please do.

The more people who do this, the more information we will have to look at.

Since the largest NIH study was done in 2008, EIGHT YEARS AGO, you’d think researchers & doctors would be a bit open-minded.  Can you imagine basing cancer or AIDS treatments on EIGHT YEAR OLD STUDIES?  https://www.niaid.nih.gov/diseases-conditions/chronic-lyme-disease.  Another, done in 2003 (15 years ago) only looked at 28 days of IV antibiotic compared to placebo in 55 patients, hardly a representative sample, and what’s 28 days of IV abx going to do with a persistent pathogen typically coupled with other pathogens making cases extremely complex?

No, The Cabal has run the research in a biased and skewed manner for over 40 years.  Time for a change.

Interestingly, an IDSA founder disagreed with their stance and used high powered antibiotics quite successfully:  https://madisonarealymesupportgroup.com/2017/07/09/idsa-founder-used-potent-iv-antibiotics-for-chronic-lyme/ 51 difficult cases are represented.

 

 

 

 

 

Study Finds Q Fever & Rickettsia (Typhus) in Australian Ticks and People

https://www.ncbi.nlm.nih.gov/m/pubmed/30270855/

Ixodes holocyclus Tick-Transmitted Human Pathogens in North-Eastern New South Wales, Australia.

Graves SR, et al. Trop Med Infect Dis. 2016.

Abstract

A group of 14 persons who live in an area of Australia endemic for the Australian paralysis tick, Ixodes holocyclus, and who were involved in regularly collecting and handling these ticks, was examined for antibodies to tick-transmitted bacterial pathogens.

Five (36%) had antibodies to Coxiella burnetii, the causative agent of Q fever and three (21%) had antibodies to spotted fever group (SFG) rickettsiae (Rickettsia spp). None had antibodies to Ehrlichia, Anaplasma, Orientia, or Borrelia (Lymedisease) suggesting that they had not been exposed to these bacteria.

A total of 149 I. holocyclus ticks were examined for the citrate synthase (gltA) gene of the SFG rickettsiae and the com1 gene of C. burnetii; 23 (15.4%) ticks were positive for Rickettsia spp. and 8 (5.6%) positive for Coxiella spp. Sequencing of fragments of the gltA gene and the 17 kDa antigen gene from a selection of the ticks showed 99% and 100% homology, respectively, to Rickettsia australis, the bacterium causing Queensland tick typhus.

Thus, it appears that persons bitten by I. holocyclus in NE NSW, Australia have an approximate one in six risk of being infected with R. australis. Risks of Q fever were also high in this region but this may have been due to exposure by aerosol from the environment rather than by tick bite. A subset of 74 I. holocyclus ticks were further examined for DNA from Borrelia spp., Anaplasma spp. and Ehrlichia spp. but none was positive. Some of these recognised human bacterial pathogens associated with ticks may not be present in this Australian tick species from northeastern New South Wales.

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**Comments**

Folks in Australia have been fighting the denial of authorities for decades regarding Lyme Disease:  https://madisonarealymesupportgroup.com/2018/08/21/our-battle-ongoing-lyme-disease-in-australia/

https://madisonarealymesupportgroup.com/2016/11/03/ld-not-in-australia-here-we-go-again/

https://madisonarealymesupportgroup.com/2018/10/03/aussie-widow-of-lyme-disease-victim-to-sue-nsw-health/  A SYDNEY woman launches a class action against NSW Health after autopsy results showed her husband was riddled with Lyme in his liver, heart, kidney, and lungs.  He was only 44 years old and was bitten by a tick while filming a TV show in Sydney.

Now how in the world did that happen?

While they still deny Lyme (borrelia) this recent study definitively shows a number of pathogens in Australian ticks and humans including Rickettsia (more commonly known as Tick & arthropod Typhus, Queensland typhus or Rickettsia australis), as well as Q Fever.

Tick Typhus is similar to Rocky Mountain spotted fever, but deemed not as severe.  Symptoms include:

  • Fever
  • Headache
  • Malaise
  • Bloodshot eyes
  • Red lump at tick bite site
  • Ulceration at tick bite site
  • Black scab at tick bite site
  • Enlarged local lymph nodes
  • Forearm red rash
  • Red body rash
  • Palm rash
  • Rash on soles of feet

Doxycycline is the front-line drug for typhus and broad-spectrum antibiotics aren’t helpful.

Fact sheet on typhus:  https://www.health.nsw.gov.au/Infectious/factsheets/Factsheets/typhus.PDF  The perps are typically lice, fleas, mites, and ticks.

https://madisonarealymesupportgroup.com/2018/08/19/monster-ticks-found-in-germany-threaten-europe-with-deadly-disease-crimean-congo-fever/  In this article, they found a tropical form of tick typhus in tropical ticks found in Germany. Typhus is making a comeback, particularly in the southern U.S. Migrating birds are transporting ticks as well as the diseases they carry worldwide 

Fact sheet on Q Fever: http://www.stopticks.org/ticks/qfever.asp

Caused by the bacteria Coxiella burnetii, it can cause pneumonia and hepatitis (liver inflammation) in its early stage, and infection of the heart valves (endocarditis) in its chronic stage.  Perps are the Brown Dog Tick (Rhipicephalus sanguine us), Rocky Mountain Wood Tick (Dermacentor andersoni), and the Lone Star Tick (Amblyomma americium).

https://coloradoticks.org/tick-borne-diseases/q-fever/  This article states it’s usually a mild disease with flu-like symptoms but sometimes it can resurface years later.  This more deadly, chronic form, of Q fever can damage heart, liver, brain and lungs. C. burnetii is highly infectious. Humans that are susceptible to this disease can be infected by a single organism. It is considered a significant threat for bio warfare and is classified as a Category B agent of bioterrorism.

The severity and combination of signs and symptoms vary greatly. About half the people infected with Q fever will get sick. Symptoms include:

  • High fever (up to 105°F)
  • Fatigue
  • Severe headache
  • General malaise
  • Myalgia
  • Chills or sweats
  • Non-productive cough
  • Nausea
  • Vomiting
  • Diarrhea
  • Abdominal pain
  • Chest pain

Doxycycline is also the front-line drug for this with quinolone antibiotics as an alternative.

Add the Ixodes holocyclus tick to this list as well.

And before you think it can only ever be in Australia, this article in the 2013 issue of the Australian Veterinary Journal shows the likelihood of a population of Ixodes holocyclus breeding outside their common range.  https://conference.ava.com.au/13097.

Well there goes the neighborhood.

Here’s a nifty chart:  https://www.lymedisease.org/lyme-basics/co-infections/other-co-infections/ (Please remember this is constantly changing)

Screen-Shot-2014-08-26-at-5.27.54-PM

If there’s one think I know for sure, it’s that nothing about ticks and the diseases they carry is sure.

They are finding tropical ticks in Germany (where they shouldn’t be)  https://madisonarealymesupportgroup.com/2018/08/19/monster-ticks-found-in-germany-threaten-europe-with-deadly-disease-crimean-congo-fever/ and they are finding Asian ticks in the U.S. (where they shouldn’t be)  https://madisonarealymesupportgroup.com/2018/10/03/1st-person-bitten-by-east-asian-longhorned-tick/.

When is the CDC going to get the memo and scrap the tick maps?

 

 

 

 

Removing the Mask of Average Treatment Effects in Chronic Lyme Disease Research Using Big Data & Subgroup Analysis

https://www.mdpi.com/2227-9032/6/4/124

Healthcare 2018, 6(4), 124; https://doi.org/10.3390/healthcare6040124

Removing the Mask of Average Treatment Effects in Chronic Lyme Disease Research Using Big Data and Subgroup Analysis

1MyLymeData, Chico, CA 95927, USA
2Analytic Designers LLC., Bethesda, MD 20817, USA
3Paul G. Allen School of Computer Science and Engineering, University of Washington, Seattle, WA 98195, USA
Author to whom correspondence should be addressed.
Received: 4 September 2018 / Revised: 9 October 2018 / Accepted: 9 October 2018 / Published: 12 October 2018
Full-Text   |   PDF [1495 KB, uploaded 12 October 2018]

Abstract

Lyme disease is caused by the bacteria borrelia burgdorferi and is spread primarily through the bite of a tick. There is considerable uncertainty in the medical community regarding the best approach to treating patients with Lyme disease who do not respond fully to short-term antibiotic therapy. These patients have persistent Lyme disease symptoms resulting from lack of treatment, under-treatment, or lack of response to their antibiotic treatment protocol. In the past, treatment trials have used small restrictive samples and relied on average treatment effects as their measure of success and produced conflicting results. To provide individualized care, clinicians need information that reflects their patient population. Today, we have the ability to analyze large data bases, including patient registries, that reflect the broader range of patients more typically seen in clinical practice. This allows us to examine treatment variation within the sample and identify groups of patients that are most responsive to treatment. Using patient-reported outcome data from the MyLymeData online patient registry, we show that sub-group analysis techniques can unmask valuable information that is hidden if averages alone are used. In our analysis, this approach revealed treatment effectiveness for up to a third of patients with Lyme disease. This study is important because it can help open the door to more individualized patient care using patient-centered outcomes and real-world evidence. View Full-Text

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**Comment**
Great work here.  We need to start the coinfection discussion; however, as Lyme is just one beast of many and the involvement of other pathogens muddies the water considerably and needs addressing.  Many, many patients WILL NOT improve on a Lyme only treatment.