Archive for the ‘research’ Category

A Scientist’s Rebuttal to the Danish Cohort Study on the MMR Vaccine

https://thevaccinereaction.org/2019/04/a-scientists-rebuttal-to-the-danish-cohort-study/

A Scientist’s Rebuttal to the Danish Cohort Study

by Brian S. Hooker, PhD, PE | Guest Writer
Published April 18, 2019
A Scientist’s Rebuttal to the Danish Cohort Study

 

The MMR vaccine study recently published by Hviid et al. (2019, Annals of Internal Medicine)1 entitled, “Measles, Mumps, Rubella Vaccination and Autism: A Nationwide Cohort Study,” leaves many more serious questions than definitive answers.

The authors claim that their work, “strongly supports that MMR vaccination does not increase the risk for autism, does not trigger autism in susceptible children, and is not associated with clustering of autism cases after vaccination.”

This is an extremely broad claim that unfortunately is not supported by the evidence they present. There are eight fundamental flaws in the research study that lead to questions about the accuracy of the conclusions.

1. Children were notably missing from the study sample

First and foremost is the underascertainment of autism cases within their data sample. The study authors used Denmark population registries of children born in Denmark of Danish-born mothers which should reflect the current reported autism incidence in Denmark at 1.65% (Schendel et al. 2018, JAMA).2However, the autism incidence within the sample of the Hviid et al. paper is 0.98%, meaning that approximately 4,400 autistic children are missing from this study. The authors do not discuss the discrepancy in the number of cases.

2. Many of the children in the sample were too young for an autism diagnosis

The most probable reason for the discrepancy in cases is that the sample in the Hviid et al. paper is too young to completely ascertain autism diagnoses. The average age of sample is 8.64 years with a standard deviation of 3.48 years. Age of autism diagnosis on average is reported as 7.22 years with a standard deviation of 2.86 years. Assuming that the age of diagnosis follows a standard bell curve, this would mean that 31.5% of the sample was too young to get an autism diagnosis. This could account for as many as 3,400 additional cases not included in the analysis, which would bias the outcomes to favor not finding a relationship between the MMR vaccine and autism.

3. Failure to eliminate those with autism related to genetic conditions from the sample

In addition, individuals who were diagnosed with genetic comorbidities (known to lead to autism) after age 1 were “censored,” meaning that they were followed until the time of diagnosis, but not removed from the study. Thus, they were counted among the sample with many of them most likely autistic due to a genetic condition.  These should have appropriately been eliminated from the sample.

4. Use of two different MMR vaccines

Also, two different MMR vaccines were used in this study. The GlaxoSmithKline Prolix® formulation was used from 2000 to 2007 and Merck’s MMR®II formulation was used from 2008 to 2013. Prolix® contains the Schwarz measles strain and MMR®II contains the Ender’s Edmonston measles strain. Thus, children using the Merck formulation were much too young to receive an autism diagnosis as the oldest they would be at the time of study is 6 years of age or younger. This is important for comparison to the experience in other countries, especially the U.S. where the Merck formulation was used exclusively for the entire study period.

5. Failure to control for the “dosage effect”

In addition, the age at which Danish children in the sample received their second dose of MMR vaccine was dropped from 12 years to 4 years in 2008. This means that children born after 2004 would get two MMR vaccines prior to the average age of an autism diagnosis, whereas children born prior to 2004 would have received only one MMR vaccine. If indeed there is a “dosage effect” of the MMR (i.e., where both doses were causally related to autism), this could not be elucidated in the sample and again, this would bias the results erroneously to not find a relationship.

6. Statistical method failed to capture those children with a delayed diagnosis of autism

The authors also used a non-transparent statistical method where “person-years” were considered following the MMR vaccine to an autism diagnosis where children who received a diagnosis soon after receiving their first MMR vaccine would be weighted more heavily than children with a delay in diagnosis. This makes no sense given that the age of autism diagnoses varies widely among populations based on access to services and severity of the autism case, among other factors.  This type of method is “borrowed” from infectious disease epidemiology where an exposure directly leads to a disease state rather quickly, for example, chicken pox. However, the method has no place in evaluating chronic sequelae to vaccination which may take a period of years to receive an accurate diagnosis.

7. Vaccinated male siblings of children with autism show more autism diagnoses

It is interesting to note the increased incidence of autism in boys with autistic siblings in the vaccinated group shown in Figure 2 of the article’s supplement.1The increase towards the end of the “survival curve” shows that more boys vaccinated with MMR (with autistic siblings) are diagnosed with autism than unvaccinated boys. The difference is not statistically significant but this may be an artifact of the very small subset of boys considered in this analysis.

The study authors also cite the CDC’s Destefano et al. 2004 study which actually shows a statistically significant relationship between MMR timing and autism incidence. This is discussed further in a reanalysis of CDC’s data in the Journal of American Physicians and Surgeons (Hooker, 2018).3

8. Conflict of interest of the study authors

It should be noted that three of the study authors are currently employed at the Statens Serum Institut which is a for-profit vaccine manufacturer in Denmark. In addition, this work was funded by a grant from the Novo Nordisk foundation. Novo Nordisk is a Danish multinational pharmaceutical manufacturer.

These are two serious conflicts of interest.

The lead author, Anders Hviid was the second author on the New England Journal of Medicine MMR autism paper from 2002 (Madsen et al. 2002).4 This research was completed despite the fact that the study authors had never received proper ethics approval to complete the study. A detailed analysis of this is featured by Children’s Health Defense.5

With these issues, this paper cannot be relied upon as evidence that the MMR vaccine does not cause autism.

References:

1 Hviid A, Vinsløv Hansen J, Frisch M, Melbye M. Measles, Mumps, Rubella Vaccination and Autism: A Nationwide Cohort Study. Annals of Internal Medicine Apr. 16, 2019.
2 Schendel DE, Thorsteinsson E. Cumulative Incidence of Autism Into Adulthood for Birth Cohorts in Denmark, 1980-2012. JAMA Nov. 6, 2018l; 320(17): 1811-1813.
3 Hooker BS. Reanalysis of CDC Data on Autism Incidence and Time of First MMR Vaccination. Journal of American Physicians and Surgeons Winter 2018; 23(4): 105-109.
4 Madsen KM, Hviid A, Vestergaard M, Schendel D, Wohlfahrt J, Thorsen P, Olsen J, Melbye M. A population-based study of measles, mumps, and rubella vaccination and autism. N Engl J MedNov. 7, 2002; 347(19): 1477-82.
5 The World Mercury Project. Poul Thorsen Fugitive Researcher. Children’s Health Defense August 2017.

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For more:  

https://madisonarealymesupportgroup.com/2019/03/15/medical-doctor-of-50-years-current-measles-hysteria-not-based-on-science-but-scientism-a-quasi-religious-faith-in-vaccines/

https://madisonarealymesupportgroup.com/2019/03/06/genetic-sequencing-science-breakthrough-just-proved-that-measles-outbreaks-are-caused-by-the-measles-vaccine/

https://madisonarealymesupportgroup.com/2018/10/27/measles-transmitted-by-the-vaccinated-gov-researchers-confirm/

https://madisonarealymesupportgroup.com/2019/04/03/sierra-avenue-school-exposed-to-measles-after-vaccinated-teacher-contracts-illness/

https://madisonarealymesupportgroup.com/2019/02/01/cnn-forced-to-correct-piece-on-measles/ https://madisonarealymesupportgroup.com/2019/03/15/us-warship-quarantined-at-sea-due-to-virus-outbreak/

https://madisonarealymesupportgroup.com/2018/12/17/for-health-officials-school-boards-asymptomatic-measles-infection-is-real/

https://madisonarealymesupportgroup.com/2019/03/13/vaccine-injury-is-free-as-long-as-we-deny-it/

https://madisonarealymesupportgroup.com/2019/03/21/measles-propaganda-can-have-dire-public-health-ramifications/

https://madisonarealymesupportgroup.com/2019/03/22/vaccines-best-video-yet/

The outcome of the Vaccine Culture War will determine what it means to be free. 101 Because if the State can tag, track down and force individuals against their will to be injected with biologicals of known and unknown toxicity today, then there will be no limit on which individual freedoms the State can take away in the name of the greater good tomorrow.

Category:

Activism, research, vaccines

New Strategy Fights Bacterial Antibiotic Resistance

https://www.bcm.edu/news/molecular-and-human-genetics/new-strategy-bacterial-antibiotic-resistance

New strategy fights bacterial antibiotic resistance

New strategy fights bacterial antibiotic resistance (970x444)

(713) 798-4710

Houston, TX –

A new strategy to combat antibiotic resistance has emerged from a study led by researchers at Baylor College of Medicine. Published in the journal Molecular Cell, the report reveals for the first time how bacteria evolve mutations that confer antibiotic resistance and that this process can be inhibited with FDA-approved drug edaravone.

“Antibiotic resistance is one of the most urgent threats to public health. Bacteria develop resistance thanks to the appearance of new mutations in their DNA that allow bacteria to overcome the deadly effects of the antibiotic,” said corresponding author Dr. Susan M. Rosenberg, Ben F. Love Chair in Cancer Research and professor of molecular and human genetics, of biochemistry and molecular biology and of molecular virology and microbiologyat Baylor.

Traditionally, antibiotic resistance has been countered with new antibiotics. In this study, however, the researchers looked to discover and then inhibit the molecular mechanisms that induce mutations conferring antibiotic resistance.

“We treated laboratory cultures of the bacterium Escherichia coli with low doses of the antibiotic ciprofloxacin, which are known to induce new mutations that confer antibiotic resistance,” said first author John P. Pribis, a student in the Integrative Molecular and Biomedical Sciences graduate program at Baylor and working in the Rosenberg lab. “In this system, we investigated in great detail the molecular pathways that were activated as the bacteria evolved antibiotic resistance.”

Pribis, Rosenberg and their colleagues discovered that ciprofloxacin induced DNA breaks, which were followed by bacteria releasing a burst of toxic compounds called reactive oxygen species. These compounds activated a general stress response that triggered error-prone DNA-repair, which resulted in mutations.

“We were surprised to find that the burst of reactive oxygen occurs only in 10 to 25 percent of the bacterial population, and that only these cells follow the next molecular steps that conclude in gene mutations,” Pribis said. “Some of these mutations may confer antibiotic resistance, but others will not and may be lethal for the bacteria. While these mutating ‘gambler’ cells sort of roll the dice on their genome generating mutations, the remaining bacteria do not mutate.”

“These findings suggest that bacteria that are exposed to low doses of antibiotic set in play a molecular strategy that confers a survival advantage to the bacterial population as a whole and is likely disadvantageous for some of the bacteria in an infection,” said Rosenberg, who also is leader of the Mechanisms in Cancer Evolution Program at the Dan L Duncan Comprehensive Cancer Center at Baylor.

“While a small segment of the population, the gamblers, takes the risk of generating mutations, the rest of the bacteria stay stable and do not follow that path. As a result, if those that mutated do not survive, there still is a portion of the original population that will.”

The researchers’ detailed study of the molecular pathways leading to antibiotic resistance provided new opportunities to slow down the process, therefore reducing the chance of bacteria developing resistance. Pribis, Rosenberg and their colleagues looked for drugs that could slow down the process.

“We realized that there are FDA-approved drugs that reduce the production of reactive oxygen species, one of the crucial steps leading to mutations,” Pribis said. “We found that the drug edaravone, which is used for treating amyotrophic lateral sclerosis and stroke, would fit in the molecular mechanisms we had described inhibiting the production of reactive oxygen species.”

“Indeed, when we tried it, it slowed down the development of mutations in bacterial cultures without losing its ability to kill bacteria. The drug prevented the rapidly evolving ‘gambler’ cell subpopulation from forming,” Rosenberg said.

The researchers plan to investigate next whether this drug is able to slow the course of an infection, with or without antibiotic treatment, in models of infections.

Other contributors to this work include Libertad García-Villada, Yin Zhai, Ohad Lewin-Epstein, Anthony Wang, Jingjing Liu, Jun Xia, Qian Mei, Devon M. Fitzgerald, Julia Bos, Robert Austin, Christophe Herman, David Bates, Lilach Hadany and P.J. Hastings. See a complete list of author affiliations.

This work was supported by NIH Grants R35-GM122598, R01-GM088653, R01-GM102679, R01-GM106373, T32-GM008231, Israeli Science Fund ISF 1568/13 and the Baylor College of Medicine (BCM) Integrated Microscopy Core funded by NIH (DK56338). Further support was provided by NIH: CA125123, the Dan L Duncan Comprehensive Cancer Center, postdoctoral fellowships RP160283 and 132206-PF-18-035-01-DMC (DMF) from the Cancer Prevention and Research Institute of Texas BCM Cancer Training Program and the American Cancer Society; the John S. Dunn Gulf Coast Consortium for Chemical Genomics and the BCM Cytometry and Cell Sorting Core (NIH: P30 AI036211, P30 CA125123, and S10 RR024574).

Dr. Rosenberg's lab team (970x444)Qian Mei, Jun Xia, Devon Fitzgerald, Susan Rosenberg, Yin Zhai, Libertad Garcia-Villada, Jinjing Liu and John Pribis.

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**Comment**

While I”ve heard Lyme docs state that borrelia has not become antibiotic resistant (even though as an organism it evades treatment by shapeshifting, and has efflux pumps to pump the drugsback out) some of the coinfections have.

LLMD’s (Lyme literate doctors) have always considered the possibility which is why they often pulse treatment and layer it with 2 or more drugs – not always of which are pharmaceutical antibiotics. 

For an example of what this looks like: https://madisonarealymesupportgroup.com/2016/02/13/lyme-disease-treatment/

https://www.treatlyme.net/guide/lyme-disease-antibiotic-guide (Dr. Ross does a great job explaining it all)

The real bone-heads in this drama are mainstream doctors using the mono therapy of doxycycline.

Professor Eva Sapi has shown that doxycycline throws the spirochete into the noncell wall form to emerge later: https://www.dovepress.com/evaluation-of-in-vitro-antibiotic-susceptibility-of-different-morpholo-peer-reviewed-article-IDR

My question has been and will always be, are we setting people up for Alzheimer’s & dementia later on in life?  This doctor seems to think so: https://madisonarealymesupportgroup.com/2017/06/10/the-coming-pandemic-of-lyme-dementia/

In essence, unresolved Lyme left in the brain can cause brain diseases:  https://madisonarealymesupportgroup.com/2019/03/09/researchers-identify-herpes-1-chlamydia-pneumoniae-several-types-of-spirochaete-as-major-causes-of-alzheimers/

https://madisonarealymesupportgroup.com/2017/01/18/a-bug-for-alzheimers/

https://madisonarealymesupportgroup.com/2016/06/09/alzheimers-byproduct-of-infection/

https://madisonarealymesupportgroup.com/2016/11/17/antibiotics-and-alzheimers/

https://madisonarealymesupportgroup.com/2016/06/03/borrelia-hiding-in-worms-causing-chronic-brain-diseases/

https://madisonarealymesupportgroup.com/2018/03/25/a-brief-history-of-neuroborreliosis-research-dementia-an-inside-look-at-two-researchers/https://madisonarealymesupportgroup.com/2016/11/17/alzheimers-lyme

https://madisonarealymesupportgroup.com/2018/10/03/chronology-of-research-on-lyme-disease-dementia-alzheimers-parkinsons-autism/

Category:

Activism, research, Treatment

First Study Showing Borrelia & Chlamydia Mixed Biofilms in Infected Human Skin Tissues

Borrelia_and_Chlamydia_can_form_mixed_biofilms_in_

Borrelia and Chlamydia Can Form Mixed Biofilms in Infected Human Skin Tissues

E. Sapi1*,K. Gupta1, K. Wawrzeniak1, G. Gaur1, J. Torres1, K. Filush1, A. Melillo1 and B. Zelger21
Received: 15 January 2019; accepted: 04 March 2019
Abstract
Our research group has recently shown that Borrelia burgdorferi, the Lyme disease bacterium, is capable of forming biofilms in Borrelia-infected human skin lesions called Borrelia lymphocytoma (BL). Biofilm structures often contain multiple organisms in a symbiotic relationship, with the goal of providing shelter from environmental stressors such as antimicrobial agents. Because multiple co-infections are common in Lyme disease, the main questions of this study were whether BL tissues contained other pathogenic species and/or whether there is any co-existence with Borrelia biofilms.
Recent reports suggested Chlamydia-like organisms in ticks and Borrelia-infectedhuman skin tissues; therefore, Chlamydia-specific polymerase chain reaction (PCR) analyses were performed in Borrelia-positive BL tissues. Analyses of the sequence of the positive PCR bands revealed that Chlamydia spp. DNAs are indeed present in these tissues, and their sequences have the best identity match to Chlamydophila pneumoniae and Chlamydia trachomatis. Fluorescent immunohistochemical and in situ hybridization methods demonstrated the presence of Chlamydia antigen and DNA in 84% of Borrelia biofilms. Confocal microscopy revealed that Chlamydia locates in the center of Borrelia biofilms, and together, they form a well-organized mixed patho-
genic structure.
In summary, our study is the first to show Borrelia–Chlamydia mixed biofilms in infected human skin tissues, which raises the questions of whether these human pathogens have developed a symbiotic relationship for their mutual survival.

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**Comment**

This study is important as once again, they show biofilm formation and the involvement of other pathogens. Mainstream medicine better wake up soon. The potential symbiotic relationship between these organisms shouldn’t be underestimated and they certainly should be factored into the problem with testing that only tests for one organism and treatments that only treat for one thing. Mainstream med isn’t even hitting the broad side of the barn on this one.

Chlamydia-like organisms are in ticks:  https://madisonarealymesupportgroup.com/2016/10/07/chlamydia-like-organisms-found-in-ticks/

Here, researchers identify chlamydia along with other pathogens in Alzheimer’s:  https://madisonarealymesupportgroup.com/2019/03/09/researchers-identify-herpes-1-chlamydia-pneumoniae-several-types-of-spirochaete-as-major-causes-of-alzheimers/

Chlamydia is best defined from the latin word: cloak. Yep. Another stealth pathogen.

Great read on the types of chlamydia:  https://articles.mercola.com/chlamydia/types.aspx The first two are mentioned in the abstract:

  • Chlamydia trachomatis can be passed from one person to another via unprotected sexual intercourse. Pain English: this is a STD.
  • Chlamydia pneumoniae (C. pneumoniae), a nonsexually transmitted disease that infects the lungs and causes bacterial pneumonia.
  • Chlamydia psittaci is another chlamydia strain that can lead to a rare condition called psittacosis, aka “parrot fever.”

 

 

Category:

Lyme, research, Testing, Ticks

Allergic Reaction Sparks Award-winning Science Fair Project For Missouri Teen

https://www.wpsdlocal6.com/2019/04/10/allergic-reaction-sparks-award-winning-science-fair-project-for-missouri-teen/  News Video Within Link

Allergic reaction sparks award-winning science fair project for Missouri teen

Jason Lindsey

JACKSON, MO — It all started with a tick bite for one southeast Missouri teenager. That bite caused a life-threating food allergy. It resulted in an award-winning science fair project.

Grant Roseman is a home-schooler in Jackson, Missouri. Grant will represent southeast Missouri in Arizona at the Intel International Science and Engineering Fair in May.

“For me, personally, I usually get hives that can last up to two weeks, and I’ve had anaphylactic shock before,” Grant says.

A  bite from a tick made him allergic to red meat.

“It made me really want to figure out how these ticks were getting on humans so much,” he says.

If you check out Grant’s science fair board, you can see he experimented with six different ticks. His goal was to show which one is attracted to carbon dioxide gas the most.

He used dry ice, frozen carbon dioxide gas, to represent the carbon dioxide gas produced by humans.

“I would set the ticks down, and release them with the dry ice on the other end, and see which ones got the farthest,” Grant says.

Here’s what he discovered.

“The Lone Star Tick — the one that causes an allergy — it’s the most aggressive,” Grant says.

Bottom line? The Lone Star Tick seeks out you and your family all because you produce carbon dioxide gas.

“So, the way it detects you is with two organs called the Haller’s organ. Those can detect carbon dioxide, heat, and movement,” he explains.

His research earned him first place at the SEMO Science Fair. Next stop, the Intel International Science and Engineering Fair.

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**Comment**

I’m telling you – it’s the tsunami of the infected who are going to move this mountain!

Well done Mr. Roseman! I’m rooting for you!

 

 

Category:

Activism, Alpha Gal Meat Allergy, research, Ticks

Ketamine – Reduces Depression-related Behaviors in Mice, Limits Bb in vivo, & Relieves Chronic Pain

https://neurosciencenews.com/ketamine-depression-reversal-11069/

Ketamine reverses neural changes underlying depression-related behaviors: Mouse study

Neuroscience NewsNEUROSCIENCE NEWS
FEATUREDNEUROSCIENCEOPEN NEUROSCIENCE ARTICLESPSYCHOLOGY5 MIN READ

Summary: The formation of prefrontal cortex dendritic spine formation sustains the remission of depressive related symptoms and behaviors following ketamine treatment by restoring lost spines.

Source: NIH/NIMH

Researchers have identified ketamine-induced brain-related changes that are responsible for maintaining the remission of behaviors related to depression in mice — findings that may help researchers develop interventions that promote lasting remission of depression in humans. The study, funded by the National Institute of Mental Health (NIMH), part of the National Institutes of Health, appears in the journal Science.

Major depression is one of the most common mental disorders in the United States, with approximately 17.3 million adults experienced a major depressive episode in 2017. However, many of the neural changes underlying the transitions between active depression, remission, and depression re-occurrence remain unknown. Ketamine, a fast-acting antidepressant which relieves depressive symptoms in hours instead of weeks or longer, provides an opportunity for researchers to investigate the short- and long-term biological changes underlying these transitions.

“Ketamine is a potentially transformative treatment for depression, but one of the major challenges associated with this drug is sustaining recovery after the initial treatment,” said study author Conor Liston, M.D., Ph.D., of Weill Cornell Medicine, New York City.

To understand mechanisms underlying the transition from active depression to remission in humans, the researchers examined behaviors related to depression in mice. Researchers took high-resolution images of dendritic spines in the prefrontal cortex of mice before and after they experienced a stressor. Dendritic spines are protrusions in the part of neurons that receive communication input from other neurons. The researchers found that mice displaying behaviors related to depression had increased elimination of, and decreased the formation of, dendritic spines in their prefrontal cortex compared with mice not exposed to a stressor. This finding replicates prior studies linking the emergence of behaviors related to depression in mice with dendritic spine loss.

In addition to the effects on dendritic spines, stress reduced the functional connectivity and simultaneous activity of neurons in the prefrontal cortex of mice. This reduction in connectivity and activity was associated with behaviors related to depression in response to stressors. Liston’s group then found that ketamine treatment rapidly restored functional connectivity and ensemble activity of neurons and eliminated behaviors related to depression. Twenty-four hours after receiving a single dose of ketamine, mice exposed to stress showed a reversal of behaviors related to depression and an increase in dendritic spine formation when compared to stressed mice that had not received ketamine. These new dendritic spines were functional, creating working connections with other neurons.

The researchers found that while behavioral changes and changes in neural activity in mice happened quickly (three hours after ketamine treatment), dendritic spine formation happened more slowly (12-24 after hours after ketamine treatment). While further research is needed, the authors suggest these findings might indicate that dendritic spine regrowth may be a consequence of ketamine-induced rescue of prefrontal cortex circuit activity.

This shows a brain

Although dendritic spines were not found to underly the fast-acting effects of ketamine on behaviors related to depression in mice, they were found to play an important role in maintaining the remission of those behaviors. Using a new technology developed by Haruo Kasai, Ph.D., and Haruhiko Bito, Ph.D., collaborators at the University of Tokyo, the researchers found that selectively deleting these newly formed dendritic spines led to the re-emergence of behaviors related to depression.

“Our results suggest that interventions aimed at enhancing synapse formation and prolonging their survival could be useful for maintaining the antidepressant effects of ketamine in the days and weeks after treatment,” said Dr. Liston.

“Ketamine is the first new anti-depressant medication with a novel mechanism of action since the 1980s. Its ability to rapidly decrease suicidal thoughts is already a fundamental breakthrough,” said Janine Simmons, M.D., Ph.D., chief of the NIMH Social and Affective Neuroscience Program. “Additional insights into ketamine’s longer-term effects on brain circuits could guide future advances in the management of mood disorders.”

ABOUT THIS NEUROSCIENCE RESEARCH ARTICLE

Source:
NIH/NIMH
Media Contacts:
Nick Miller – NIH/NIMH
Image Source:
The image is in the public domain.

Original Research: Open access.
Liston, C. et al. “Sustained rescue of prefrontal circuit dysfunction by antidepressant-induced spine formation”. Science. doi:10.1126/science.aat8078

Abstract

Sustained rescue of prefrontal circuit dysfunction by antidepressant-induced spine formation

The neurobiological mechanisms underlying the induction and remission of depressive episodes over time are not well understood. Through repeated longitudinal imaging of medial prefrontal microcircuits in the living brain, we found that prefrontal spinogenesis plays a critical role in sustaining specific antidepressant behavioral effects and maintaining long-term behavioral remission. Depression-related behavior was associated with targeted, branch-specific elimination of postsynaptic dendritic spines on prefrontal projection neurons. Antidepressant-dose ketamine reversed these effects by selectively rescuing eliminated spines and restoring coordinated activity in multicellular ensembles that predict motivated escape behavior. Prefrontal spinogenesis was required for the long-term maintenance of antidepressant effects on motivated escape behavior but not for their initial induction.

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**Comment**

Ketamine is used for starting and maintaining anesthesia and induces a trance-like state while providing pain relief, sedation, and memory loss. It can cause confusion and hallucinations as it wears off.  Discovered in 1962 it was used in the Vietnam War due to its safety and is on the WHO’s list of essential medicines.

It’s also used as a recreational drug in raves and as a club drug.  Due to this, it’s a schedule III substance in the U.S.

That said, it’s been shown to limit borrelia in vitro:  https://madisonarealymesupportgroup.com/2018/03/10/ketamine-limits-bb-in-vitro/

It’s also been shown to relieve her chronic pain, improve quality of life, reduce depression and suicidal ideation, and reduce opioid consumption:  https://madisonarealymesupportgroup.com/2017/09/14/iv-ketamine-in-ptls/

 

Category:

Activism, Psychological Aspects, research, Treatment