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mr peabody

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Research establishes antibiotic potential of CBD*

University of Queensland | Science News | 19 Jan 2021

Synthetic cannabidiol, better known as CBD, has been shown to kill the bacteria responsible for gonorrhoea, meningitis and legionnaires disease, which could lead to the first new class of antibiotics for treatment-resistant bacteria in 60 years.

The research collaboration between The University of Queensland and Botanix Pharmaceuticals Limited could lead to the first new class of antibiotics for resistant bacteria in 60 years.

The UQ Institute for Molecular Bioscience's Associate Professor Mark Blaskovich said CBD -- the main nonpsychoactive component of cannabis -- can penetrate and kill a wide range of bacteria including Neisseria gonorrhoeae, which causes gonorrhoea.

"This is the first time CBD has been shown to kill some types of Gram-negative bacteria. These bacteria have an extra outer membrane, an additional line of defence that makes it harder for antibiotics to penetrate," Dr Blaskovich said.

In Australia, gonorrhoea is the second most common sexually-transmitted infection and there is no longer a single reliable antibiotic to treat it because the bacteria is particularly good at developing resistance.

The study also showed that CBD was widely effective against a much larger number of Gram-positive bacteria than previously known, including antibiotic-resistant pathogens such as MRSA (methicillin-resistant Staphylococcus aureus) or 'golden staph'.

Dr Blaskovich said cannabidiol was particularly good at breaking down biofilms -- the slimy build-up of bacteria, such as dental plaque on the surface of teeth -- which help bacteria such as MRSA survive antibiotic treatments.

Dr Blaskovich's team at the Centre for Superbug Solutions mimicked a two-week patient treatment in laboratory models to see how fast the bacteria mutated to try to outwit CBD's killing power.

"Cannabidiol showed a low tendency to cause resistance in bacteria even when we sped up potential development by increasing concentrations of the antibiotic during 'treatment'."

"We think that cannabidiol kills bacteria by bursting their outer cell membranes, but we don't know yet exactly how it does that, and need to do further research.


The research team also discovered that chemical analogs -- created by slightly changing CBD's molecular structure -- were also active against the bacteria.

"This is particularly exciting because there have been no new molecular classes of antibiotics for Gram-negative infections discovered and approved since the 1960s, and we can now consider designing new analogs of CBD within improved properties."

Vince Ippolito, the President and Executive Chairman of Botanix, said the research showed vast potential for the development of effective treatments to fight the growing global threat of antibiotic resistance.

"Congratulations to Dr Blaskovich and his team for producing this significant body of research -- the published data clearly establishes the potential of synthetic cannabinoids as antimicrobials," Mr Ippolito said.

"Our Company is now primed to commercialise viable antimicrobial treatments which we hope will reach more patients in the near future. This is a major breakthrough that the world needs now."

Dr Blaskovich said collaborating with Botanix has sped up the research, with Botanix contributing formulation expertise that has led to the discovery that how cannabidiol is delivered makes a huge difference in its effectiveness at killing bacteria.

The collaboration has enabled Botanix to progress a topical CBD formulation into clinical trials for decolonisation of MRSA before surgery.

"Those Phase 2a clinical results are expected early this year and we hope that this will pave the way forward for treatments for gonorrhoea, meningitis and legionnaires disease.

"Now we have established that cannabidiol is effective against these Gram-negative bacteria, we are looking at its mode of action, improving its activity and finding other similar molecules to open up the way for a new class of antibiotics."


*From the article here :
 
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mr peabody

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University of Queensland

CBD shown to kill treatment resistant bacteria*

University of Queensland | Science Daily | 19 Jan 2021

CBD, has been shown for the first time to kill the bacteria responsible for gonorrhoea, meningitis and legionnaires disease.

The research collaboration between The University of Queensland and Botanix Pharmaceuticals Limited could lead to the first new class of antibiotics for resistant bacteria in 60 years.

The UQ Institute for Molecular Bioscience's Associate Professor Mark Blaskovich said CBD -- the main nonpsychoactive component of cannabis -- can penetrate and kill a wide range of bacteria including Neisseria gonorrhoeae, which causes gonorrhoea.

"This is the first time CBD has been shown to kill some types of Gram-negative bacteria. These bacteria have an extra outer membrane, an additional line of defence that makes it harder for antibiotics to penetrate," Dr Blaskovich said.

In Australia, gonorrhoea is the second most common sexually-transmitted infection and there is no longer a single reliable antibiotic to treat it because the bacteria is particularly good at developing resistance.

The study also showed that CBD was widely effective against a much larger number of Gram-positive bacteria than previously known, including antibiotic-resistant pathogens such as MRSA (methicillin-resistant Staphylococcus aureus) or 'golden staph'.

Dr Blaskovich said cannabidiol was particularly good at breaking down biofilms -- the slimy build-up of bacteria, such as dental plaque on the surface of teeth -- which help bacteria such as MRSA survive antibiotic treatments.

Dr Blaskovich's team at the Centre for Superbug Solutions mimicked a two-week patient treatment in laboratory models to see how fast the bacteria mutated to try to outwit CBD's killing power.

"Cannabidiol showed a low tendency to cause resistance in bacteria even when we sped up potential development by increasing concentrations of the antibiotic during 'treatment'."

"We think that cannabidiol kills bacteria by bursting their outer cell membranes, but we don't know yet exactly how it does that, and need to do further research. The research team also discovered that chemical analogs -- created by slightly changing CBD's molecular structure -- were also active against the bacteria."

"This is particularly exciting because there have been no new molecular classes of antibiotics for Gram-negative infections discovered and approved since the 1960s, and we can now consider designing new analogs of CBD within improved properties."


Vince Ippolito, the President and Executive Chairman of Botanix, said the research showed vast potential for the development of effective treatments to fight the growing global threat of antibiotic resistance.

"Congratulations to Dr Blaskovich and his team for producing this significant body of research -- the published data clearly establishes the potential of synthetic cannabinoids as antimicrobials," Mr Ippolito said.

"Our Company is now primed to commercialise viable antimicrobial treatments which we hope will reach more patients in the near future. This is a major breakthrough that the world needs now."

Dr Blaskovich said collaborating with Botanix has sped up the research, with Botanix contributing formulation expertise that has led to the discovery that how cannabidiol is delivered makes a huge difference in its effectiveness at killing bacteria.

The collaboration has enabled Botanix to progress a topical CBD formulation into clinical trials for decolonisation of MRSA before surgery.

"Those Phase 2a clinical results are expected early this year and we hope that this will pave the way forward for treatments for gonorrhoea, meningitis and legionnaires disease."

"Now we have established that cannabidiol is effective against these Gram-negative bacteria, we are looking at its mode of action, improving its activity and finding other similar molecules to open up the way for a new class of antibiotics."

*From the article here :
 

mr peabody

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Cannabis may slow or even prevent HIV's damaging effects on the brain*

by Randy Robinson | 24 Jan 2020

One of HIV’s lesser-known symptoms is neurodegeneration, a slow but progressive failure of the nervous system. But new data suggests cannabis may slow or, even prevent, HIV's damaging effects on the brain.

HIV and aging share one thing in common: They can both irreparably damage the nervous system. But cannabis may, potentially, halt both aging and HIV in their tracks when it comes to a deteriorating human brain.

A new study recently published in the Journal of Acquired Immunity Deficiency Syndrome found that HIV patients who consumed cannabis showed significantly less cognitive impairment compared to HIV patients who didn’t.

Here’s how the study went down. The researchers collected data from 679 people living with HIV and 273 people who didn’t have HIV. Participants’ ages ranged from 18- to 79-years-old. The researchers then assessed each participant to see how well their brain worked, their general state of health, and what kinds of drugs they were currently taking — FDA-approved or otherwise.

By the end of it, the researchers found that regular cannabis consumers living with HIV were at a 53 percent lower risk of developing cognitive impairments compared to people living with HIV who didn’t partake.

How could our favorite flower profoundly impact a disease that modern medicine still hasn’t found a (feasible) cure for? The researchers in the latest study concluded, “A possible mechanism of this result is the anti-inflammatory effect of cannabis, which may be particularly important for people living with HIV." They noted that “further investigations are needed to better understand how cannabis could work as a neuroprotective HIV medication."

HIV can cause neural degeneration, even though the virus solely targets human immune cells, not our nerves or brain cells. But HIV’s presence in the brain triggers inflammation due to toxins released by both the virus and the immune cells it destroys. Our neurons are incredibly fragile, and constant inflammation in the brain will cause those neurons to degenerate and eventually die. HIV-associated neurocognitive disorders, or HANDs, can permanently impair memory, motor coordination, natural reflexes, speech, and emotional regulation.

If a HAND progresses even further, it can develop into AIDS dementia complex (ADC), a condition that’s kind of like a cross between Parkinson’s and Alzheimer’s, both of which usually only affect aging populations. At the end stages of ADC, the individual essentially slides into a vegetative state, paralyzed and likely unable to communicate with others.

However, in industrialized countries such as the US, readily available anti-retroviral drugs can stop HIV from developing into AIDS — assuming the individual can afford the medications, that is. But seeing as cannabis is known to control several other HIV/AIDS symptoms, receiving additional neuroprotective benefits in one small, joint-sized package should qualify weed as an essential part of the standard HIV/AIDS pharmaceutical regimen.

*From the article here :
 
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mr peabody

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Injection prevents women from contracting HIV, study finds

Results so far suggest that the injectable drug cabotegravir was 89 percent more effective than pills at preventing HIV infection.

Al Jazeera | 9 Nov 2020

Researchers are stopping a study early after finding that a shot of an experimental medicine every two months worked better than daily pills to help prevent women from contracting HIV from an infected sexual partner.

The news is a boon for AIDS prevention efforts – especially in Africa, where the study took place and where women have few discreet ways of protecting themselves from infection.

Results so far suggest that the drug, cabotegravir, was 89 percent more effective at preventing HIV infection than Truvada pills, although both reduce that risk.

The results mirror those announced earlier this year from a similar study testing the shots versus the daily pills in gay men.

Cabotegravir is being developed by ViiV Healthcare, which is mostly owned by GlaxoSmithKline, with Pfizer Inc and Shionogi Limited. The study was sponsored by the United States National Institutes of Health (NIH), the Bill and Melinda Gates Foundation and ViiV. The drugs were provided by ViiV and Truvada’s maker, Gilead Sciences.

“This is a major, major advance,” said Dr Anthony Fauci, the top infectious disease doctor at the NIH. “I don’t think we can overemphasise the importance of this study.”

"The drug promises HIV prevention help to young women – those who need it the most,”
Fauci said.

Young women may be twice as likely as men to get HIV in some areas of the world, according to one study leader, Sinead Delany-Moretlwe of the University of the Witwatersrand in Johannesburg, South Africa.

“They need discreet options … without having to negotiate with their partners to use measures such as condoms," said Deborah Waterhouse of ViiV.

The study involved more than 3,200 participants in seven African countries who were randomly assigned to get either the shots every two months or daily Truvada pills. Independent monitors advised stopping the study after seeing that only 0.2 percent of women receiving the shots caught the AIDS virus versus 2 percent of women on the pills.

There were more side effects, mostly nausea, with the daily pills.

Cabotegravir’s makers are seeking approval from regulators to sell it for this purpose, and Truvada already is widely used.

“The urgent work now” is to make all prevention medicines affordable and more widely available," said Mitchell Warren, who heads AVAC, formerly known as the AIDS Vaccine Advocacy Coalition, a non-profit focused on prevention efforts that had no role in the study.

Condoms remain widely recommended because they help prevent a host of sexually spread diseases, not just HIV.

“People need choices for HIV prevention,” and this gives a new option," Warren said in a statement.

 
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mr peabody

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Medicinal plants: What you need to know about herbal antibiotics

by Mary Villareal | Matural News | 2 Aug 2021

Bacteria tend to develop resistance to industrial antibiotics sooner or later, but this isn’t the case with herbal antibiotics. Herbal antibiotics work in a way where bacteria resistance becomes unlikely, even futile.

Medicinal plants, including herbal antibiotics, have been used in the management of infectious diseases since ancient times. In modern times, the effectiveness of many of these remedies has been proven in scientific methodologies. While these mechanisms focused on plant-derived remedies are not fully understood, the fact remains that herbal medicine is effective in curing infectious diseases, and many plants are beneficial against illnesses.

Plants such as garlic and aloe vera are used as natural antibiotics for relief in burns, and respiratory tract infections. They are also known to enhance the immune system and even lower blood pressure. When the immune system is weak, unwanted microbes can infect and thrive in or outside our bodies, and the microbial activities of microorganisms can cause infections.

While not all bacteria are harmful, various strains of the same bacteria can cause symptoms like diarrhea and vomiting. Natural antibiotics such as herbs and spices have the desired properties that minimize the spread of harmful microbes in the body.

Natural antibiotics found in herbal medicine have fewer side effects. That said, while herbal medicinal or herbal products are considered for low risk for adverse effects compared to synthetic drugs, you should still take care when using them as taking too much may still lead to some adverse effects. To stay safe, be sure to consult with your healthcare professional before trying any new medicine, herbal or otherwise.

How plants work differently from pills

Unlike pills, plant chemistry is complex. They have dozens of distinct chemical compounds that make it impossible for bacteria to develop any kind of resistance to them. These compounds may defeat the bacteria, but they can also promote healing, provide pain relief and reduce inflammation to make recovery faster. When these plants and herbs are combined, chances are that improvements will be faster.

Fortunately, plants are easy to grow for medicinal purposes. While it does not take going to medical school to learn about them, it is still important to be aware of their interactions. Plants are safer than conventional alternatives, with fewer side effects. Adverse drug reactions are among the leading cause of death in the United States, and plants can help minimize such adverse effects. (Related: WHO warns world running out of synthetic antibiotics, but refuses to acknowledge power of natural herbal antibiotics.)

Powerful antibiotics in your kitchen

Prevent antibiotic overkill by using these plant alternatives instead:​
  1. Manuka Honey – one of nature’s best antimicrobial sources, it received even more attention because of its antibacterial properties as well. Clinical studies showed that Manuka honey can inhibit multiple drug-resistant pathogens and has a broad spectrum of antibacterial capabilities. Studies also showed that it can disperse and kill bacterial in biofilms or enclosed communities of cells; thus, it can be used to prevent bacteria in wounds and implanted devices.​
  2. Garlic – the chemical compounds in garlic have been proven to display antimicrobial activities that help kill pathogens responsible for common and rare infections. Garlic has been used for centuries to combat infectious diseases.​
  3. Oregano oil – one of the most powerful antibacterial essential oils, oregano contains antibacterial and antifungal compounds that make it effective against many strains of bacteria, including Escherichia coli (E. coli).​
Bonus: Probiotics can also reduce harmful and resistant bacteria while increasing good bacteria in your gut. Research showed that taking probiotics not only helps boost your immune system, it is also important to take them after antibiotics to replenish the good bacteria in your body.

Read more about alternative medicine in food at Medicine.news.

Sources include:

PrepSchoolDaily.BlogSpot.com

InTechOpen.com

Observer.com

 
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mr peabody

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Coronavirus vaccine technology is paving the way for a whole new approach to flu shots

by Lindsey Bever | Washington Post | 11 Apr 2021

Pfizer, partnering with BioNTech, and Moderna have created promising vaccines that scientists hope will lead to more medical breakthroughs using mRNA.

The technology used in two of the coronavirus vaccines authorized by the Food and Drug Administration may enable scientists to develop flu shots in record time, but also make inoculations that could be more effective and protect against numerous flu strains for years at a time.

The messenger-RNA technology — used in the Pfizer and Moderna coronavirus vaccines — would be a leap forward for flu shots, some of which still rely on a process developed in the 1950s involving chickens, petri dishes and dead viruses.

Researchers are hopeful that the success of those coronavirus vaccines will grease the wheels for mRNA flu shots and help expedite what is typically a lengthy process involving years of research, clinical trials and regulatory review and approval.

“It’s a very obvious progression given the success of the covid-19 vaccine to move right to flu,” said Andrew Pekosz, a professor of microbiology at the Johns Hopkins Bloomberg School of Public Health.

But researchers say the development and approval of an mRNA flu shot may take some time.

How long will the coronavirus vaccines protect you? Experts weigh in.

The idea that scientists can use messenger RNA for medical therapeutics is not new. Flu shots using mRNA technology have been in development for years.

In 2018, for example, Pfizer and BioNTech announced a partnership to start developing an mRNA vaccine that would prevent influenza. Moderna is working on a number of different mRNA vaccines, including one for the flu.

But using mRNA for vaccines shifted from experimental to critical last year. With a pressing need spurred by a global pandemic and billions of dollars in funding for vaccine development, scientists were able to repurpose their knowledge of mRNA to develop coronavirus vaccines.

“People who were slogging away for many years had money thrown at them to get it done. And they became laser-focused to bring something to market that would have ordinarily taken years,” said Paul Duprex, director of the Center for Vaccine Research at the University of Pittsburgh.

Why you shouldn’t get a covid antibody test after your vaccine

Currently, the most common influenza vaccine that is available in the United States is manufactured using an inactivated, or killed, virus and administered via a shot in the arm. But there is also a vaccine that uses a live, but weakened, virus and is given in the form of a nasal mist.

The flu viruses for these vaccines are grown in chicken eggs or in cells inside a petri dish. The viruses are then killed or weakened, and the resulting proteins — the important ingredient in the vaccine — are purified. When the shot is administered, the immune system starts making antibodies against those proteins.

“But the mRNA vaccine is very, very different,” Pekosz said, "mRNA vaccines can teach the immune system to fight a virus without ever coming into contact with it. They can also “generate a much stronger immune response than responses that are generated to the protein in a normal flu vaccine,” he added.

One limitation of the current flu vaccines is that they take about six months to develop, meaning scientists must choose which strains they think will be prevalent in the next flu season — even before the current one is over. So by the time the vaccines are ready for distribution, a different strain may have emerged as the better target.

An mRNA flu vaccine, on the other hand, can be developed in about a month or so, giving researchers plenty more time to determine which strains to protect against.

"All of this means you can much more accurately match an mRNA flu vaccine to the strains of virus that are circulating,” Pekosz said.

Messenger RNA vaccines still present challenges. The Pfizer and Moderna coronavirus vaccines, for example, must be kept at extremely cold temperatures, making transport and storage a challenge. It’s also not clear how long this vaccine-induced immunity will last. And although most side effects to the vaccine are not serious, some people have reported several days of things such as fatigue, body aches and nausea as their immune systems gear up to attack the coronavirus.

Still, researchers say mRNA vaccines are a success. "Because the mRNA vaccine platform that was used for the coronavirus vaccines is almost exactly the same platform needed for the flu, everything that has worked so beautifully for covid-19 could theoretically work in exactly the same way for influenza,” Pekosz said.

Researchers say mRNA flu shots are not likely going to be developed and approved in time for the upcoming flu season, and some researchers estimate that it could take several more years to get one on the market.

Even then, it will likely be a phased rollout with both traditional flu shots and mRNA flu shots available, Duprex said.

“It will be gradual,” he said. “You just don’t change technology overnight.”

 

mr peabody

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University of Queensland

CBD shown to kill treatment-resistant bacteria*

University of Queensland | Science Daily | 19 Jan 2021

CBD, has been shown for the first time to kill the bacteria responsible for gonorrhoea, meningitis and legionnaires disease.

The research collaboration between The University of Queensland and Botanix Pharmaceuticals Limited could lead to the first new class of antibiotics for resistant bacteria in 60 years.

The UQ Institute for Molecular Bioscience's Associate Professor Mark Blaskovich said CBD -- the main nonpsychoactive component of cannabis -- can penetrate and kill a wide range of bacteria including Neisseria gonorrhoeae, which causes gonorrhoea.

"This is the first time CBD has been shown to kill some types of Gram-negative bacteria. These bacteria have an extra outer membrane, an additional line of defence that makes it harder for antibiotics to penetrate," Dr Blaskovich said.

In Australia, gonorrhoea is the second most common sexually-transmitted infection and there is no longer a single reliable antibiotic to treat it because the bacteria is particularly good at developing resistance.

The study also showed that CBD was widely effective against a much larger number of Gram-positive bacteria than previously known, including antibiotic-resistant pathogens such as MRSA (methicillin-resistant Staphylococcus aureus) or 'golden staph'.

Dr Blaskovich said cannabidiol was particularly good at breaking down biofilms -- the slimy build-up of bacteria, such as dental plaque on the surface of teeth -- which help bacteria such as MRSA survive antibiotic treatments.

Dr Blaskovich's team at the Centre for Superbug Solutions mimicked a two-week patient treatment in laboratory models to see how fast the bacteria mutated to try to outwit CBD's killing power.

"Cannabidiol showed a low tendency to cause resistance in bacteria even when we sped up potential development by increasing concentrations of the antibiotic during 'treatment'."

"We think that cannabidiol kills bacteria by bursting their outer cell membranes, but we don't know yet exactly how it does that, and need to do further research. The research team also discovered that chemical analogs -- created by slightly changing CBD's molecular structure -- were also active against the bacteria."

"This is particularly exciting because there have been no new molecular classes of antibiotics for Gram-negative infections discovered and approved since the 1960s, and we can now consider designing new analogs of CBD within improved properties."


Vince Ippolito, the President and Executive Chairman of Botanix, said the research showed vast potential for the development of effective treatments to fight the growing global threat of antibiotic resistance.

"Congratulations to Dr Blaskovich and his team for producing this significant body of research -- the published data clearly establishes the potential of synthetic cannabinoids as antimicrobials," Mr Ippolito said.

"Our Company is now primed to commercialise viable antimicrobial treatments which we hope will reach more patients in the near future. This is a major breakthrough that the world needs now."

Dr Blaskovich said collaborating with Botanix has sped up the research, with Botanix contributing formulation expertise that has led to the discovery that how cannabidiol is delivered makes a huge difference in its effectiveness at killing bacteria.

The collaboration has enabled Botanix to progress a topical CBD formulation into clinical trials for decolonisation of MRSA before surgery.

"Those Phase 2a clinical results are expected early this year and we hope that this will pave the way forward for treatments for gonorrhoea, meningitis and legionnaires disease."

"Now we have established that cannabidiol is effective against these Gram-negative bacteria, we are looking at its mode of action, improving its activity and finding other similar molecules to open up the way for a new class of antibiotics."


*From the article here :
 
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mr peabody

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I was suffering from Human PapillomaVirus ( HPV) for over 2 years,i was hopeless until one of my friend directed me to a man called Dr Idedia, she said he cure Human PapillomaVirus (HPV) and also said he has helped her friend to cure HPV, and cure other people with different diseases, i never believed her but after a lot of talk, i decided to give the Dr Idedia a try, just few days later i contacted him and he told me what to do which i did and he prepared a herbal medicine and sent to me with prescriptions on how i will take it for a period of days. After i finished taking the medicine he told me to go for a test which i also did and when the result came out i was surprised to see that I'm Negative. Big thanks to him. You can also contact him on his email [email protected] +2349074505296.) if you need his help for heroes , fibroid, HERPES,HIV, CANCER, DIABETES, ANY TYPES OF INFECTION CURE,. and any type of infection. or if you have any problem contact him for help and you will be free with herbal medicine......
Very very interesting. Thank you so much for sharing!!

🙏
 

mr peabody

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Cannabis compound CBG a potent weapon in the fight against MRSA*

by Ian Sample | The Guardian | 19 Jan 2020

Mice cured of MRSA, raising hopes of treating antibiotic-resistant bacteria.

A compound made by cannabis plants has been found to wipe out drug-resistant bacteria, raising hopes of a new weapon in the fight against superbugs.

Scientists screened five cannabis compounds for their antibiotic properties and found that one, cannabigerol (CBG), was particularly potent at killing methicillin-resistant Staphylococcus aureus (MRSA), one of the most common hospital superbugs.

Tests in the lab showed that CBG, which is not psychoactive, killed common MRSA microbes and “persister” cells that are especially resistant to antibiotics and that often drive repeat infections. The compound also cleared up hard-to-shift “biofilms” of MRSA that can form on the skin and on medical implants.

Having seen how effective the substance was against bacteria in the lab, the researchers decided to test CBG’s ability to treat infections in animals. In a study that has not yet been published, they found that CBG cured mice of MRSA infections as effectively as vancomycin, a drug widely considered to be the last line of defence against drug-resistant microbes. The study is under review at the ACS Infectious Diseases journal.

Eric Brown, a microbiologist who led the work at McMaster University in Hamilton, Ontario, said “cannabinoids were clearly great drug-like compounds,” but noted it was early days in assessing the compounds for use in the clinic. “There is much work to do to explore the potential of the cannabinoids as antibiotics from the safety standpoint,” he said.

Antibiotic resistance has become a major threat to public health. England’s former chief medical officer Dame Sally Davies has said the loss of effective antibiotics would lead to “apocalyptic scenarios,” with patients dying from routine infections and many operations becoming too risky to perform.

In the study, the researchers describe how the rapid global spread of drug resistance, caused by microbes developing mutations that protect them against antibiotics, has driven an urgent need to explore new sources of drugs. Among antibiotics in use today, the newest date back to discoveries made more than 30 years ago.

Bacteria fall into two classes depending on the makeup of their cells. MRSA bugs are known as gram positive bacteria, and have a single, thick cell membrane. Gram negative bugs differ in having inner and outer cell membranes, and these infections can be harder to treat. In the World Health Organization’s priority list of drug-resistant bacteria, all three ranked as a “critical” priority are gram negative, namely Acinetobacter baumannii, Pseudomonas aeruginosa and Enterobacteriaceae.

Brown found that CBG and other cannabinoids did not work well against gram negative multi-drug resistant bugs. But the team went on to show that when CBG was used with small quantities of polymyxin B, an existing antibiotic that disrupts the outer membrane of gram negative bacteria, the cannabis compound wiped out the drug-resistant pathogens.

Cannabis plants are thought to make the compounds to fight off invading pathogens, but there are other ways to produce CBG. To study the compound, Brown’s team synthesised it in the lab using the chemicals olivetol and geraniol. “We are now pursuing the required paperwork to work with a wide variety of cannabinoids,” he said.

Mark Blaskovich, who studies antibiotic cannabis compounds at the University of Queensland, said cannabis seemed to be particularly rich in antibiotics, though other plants such as tea tree, garlic and the spices turmeric and curcurmin also contained antibacterials.

These are likely made as a defence mechanism to protect the plant from bacterial and fungal infections, but to date have not been very useful for human infections as they really only work outside the body,” he said. “That’s what makes this new report potentially exciting – evidence that cannabigerol is able to treat a systemic infection in mice.”

 

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Albert Hofmann

Anti-viral effects of Ibogaine

Dr. Vic Hernandez

Ibogaine in its administered forms has typically been applied to persons seeking a chemical dependence addiction treatment. The target population not only has had to contend with chemical dependence issues but issues concerning other infections, most notably HIV and/or HCV or co-infection. As antidotal and preliminary scientific information is noted concerning Ibogaine treatments, trends suggest potential applications to these pathogens. Medical science has not rigorously pursued investigation into the potential applications of Iboga alkaloids in in vitro work, animal and human studies.

I am a public health wonk. I have had the luxury of doing what interests me in what I call Public-Health. I get off on effecting and affecting the public's health. My work in HIV has concerned oxidative stress and HIV and its contribution to the understanding of pathogenesis and pathophysiology. I've been involved in developing guidelines for physicians treating HIV, trial design and methodology. I have worked on developing practitioner education forums to support understanding and treatment for isolated populations infected with HIV, notably active users. My unique relationship to communities affected by HIV, activism and passion for my work has brought me to unique understandings and relationships that I have brought to other public health work. I received a congressional citation for this work. Working with Lynn Mofenson at the NIH we moved to look at micro-nutrient intervention in HIV non-progressors to affect HIV progression and delay ARV intervention without compromising patient health by allowing HIV to run unabated. The fruits of this work have been born out in the African studies noted in US papers recently. Working with Lynn, Fauzi at Harvard and others, we established a treatment approach that was frowned upon when we started back in 1993 into accepted and respected reality.

Noted work included the resurrection of Alfa Lipoic Acid as a micronutrient effecting Liver toxicity. It would later be applied to HCV cases. In recent years, needing and wanting a break from HIV, I've worked in the realm of cancer, looking at the role of genetics in identifying trends in non-progressors utilizing non-conventional therapies or no therapeutic interventions. This work has allowed me to look at orthomolecular medicine (effect of micro-nutrients on the biochemistry of the body, pathogen infection, self cells run amuck and wellness and quality of life). Working with colleagues and mentors as Lynn Margulis at U Mass Amherst and Walter Willet at Harvard, I began to understand as Lynn puts it: the symbiosis of medicine, and as Walter puts it, as the effect of the basic building blocks of body systems and their abilities to stay healthy. Why mention this blather? You need to know where I am going with this information, so we can understand where we headed, now and in the future.

HIV. Where we are, and what it means

HIV research and treatment approaches have been checkered and somewhat baffling in approach and far too complex to delve into at this meeting or in this short of time. From a conventional medicine perspective, there are three steps required for HIV to enter cells: Attachment, Binding to a co-receptor, and Fusion of HIV into CD-4 cell. The currently available classes of drugs work to prevent the process of HIV reproducing itself and infecting new cells after HIV enters the CD-4 cell: They are Nucleoside Analogues, Non-nucleoside Analogues and Protease Inhibitors. These drugs have been administered in combination, at varied intervals, and in varying doses to tease out efficacy for the particular viral strain(s) expressed by the patient. Toxicities to body systems and healthy cells require strict and watchful management.

There is a new class of drugs called Entry Inhibitors which block HIV from entering CD-4 cells. They work by blocking the HIVs ability to enter and infect a cell. Essentially there are two steps to entry of HIV into the CD-4 cell. HIV attaches to the CD-4 cell and then fuses with it. After fusing with the cell, HIV can dump its genetic material into the CD-4 cell, the material it needs to reproduce itself in the CD-4 cell. There are two steps to attachment: attaching to the CD-4 receptor and then to a co-receptor, either CCR5 or CXCR4.

Basically, how Entry Inhibitors work is first by:

- Attachment
- Co-receptor binding
- Fusion

Currently available HIV drugs other than Fuzeon, prevent HIV from reproducing once HIV in the cell.

HIV Super-infection and HIV Drug Resistance. Let's start with HIV super-infection. Studies over the past two years suggest this is a real problem. Super-infection is when a person who has HIV gets infected with a second viral strain of HIV. Super-infection, based on study, occurs 5 to 13 months after estimated date of initial infection. The super-infection strain can be associated with ARV susceptibility and adherence. In some cases, a person can be infected with a drug resistant strain and then become infected with a super-infection wild-type or visa-versa. Initial co-infection cannot be ruled be ruled out. Molecular investigation determines evidence of super-infection coupled with progression and ARV response. The rate of the super-infection based on study hovers somewhere around 6.5% annually. Harm reduction counseling is recommended by the researchers.

There are some in the medical science community that are trying to link the super-infection to a patient zero that originated from New York. Nonsense! This was tried at the beginning of the HIV/AIDS pandemic by saying that HIV started in North America with a Canadian airline steward. It is impossible to narrow down such a claim. By the way, in that case, it was refuted by the testing of IDU blood samples from the early seventies that had been banked at Beth Israel. HIV was found in those cohorts, long before the Canadian air-steward stuff. At a recent conference, Paul Volberding MD from UCSF noted that the super-infection business hinged on one reliable case and that the bally-who was uncalled for. This should not minimize sound and reliable public health interventions such as safer sex practices.

Unfortunately, we are learning about HIV pathophysiology and pathogenesis as we go along instead of developing the understanding first. This may deal a blow to 18-MC, if applied to HIV or not.

As for HIV drug resistance, it was not until ICAAC in October of 2004 did the rates found seem alarmingly worrisome. Soon after, the media has grabbed a hold on this information. Studies are finding an escalation of HIV drug resistance during primary infection period (shortly after infection). And the resistances vary among drug classes. Drug resistant HIV acquired at time of infection can establish itself as the dominant virus population and become archived in the latent cellular reservoir. This may result in sub-optimal response to ARV interventions and promote the accumulation of mutations and jeopardize already limited treatment options. In further study, HIV drug resistance has been found in 1 of 7 treated in the US of a cohort of 317 in 40 US cities. The prominent resistance was found in the non-nukes class of drugs. Ethnic differences were noted. Latinos and Asian patients had a lower prevalence of reduced susceptibility (6 percent, with Caucasians at 27 percent, and Blacks at 23 percent. There were no gender differentiations or comparisons done. These were among male cohorts.

HCV and co-infection

HCV therapeutic interventions are limited in pharmaceutical application (interferon and pegalated interferon [riboviron and interferon]) are limited. There are surfacing reports indicating significant efficacy with TCM. In the co-infected individual, treatment options reduce due to the environment of the liver.

When Howard approached me with this paper, I read it and got excited. I like new ideas and approaches especially if the science is tight and is respectful of change. No one has the ace card and false hope, especially for patients, is highly unethical. Ask David Ho MD at Rockefeller's Aaron Diamond Center regarding the premature delivery of HIV cure based on invitro data. After reading the paper Howard shared, the questions flooded through my head and as we talked, he suggested I say a few words. Reluctantly, I accepted. I have been trying to avoid public gigs (especially those that risk pissing contests). The paper (above) by Silva et al from Brazil entitled: Anti-HIV-1 Activity of Iboga Alkaloid Congener 18-MC is a significant piece of work. It was an in vitro (in lab) study using human cells. The Iboga alkaloid 18-MC was introduced to human Peripheral Blood Mononuclear cells (PBMCs) and monocyte-derived macrophages. The result was the significant inhibition of isolates of HIV-1 in a dose dependent manner.

The approach of this anti HIV-1 inhibitory activity study went something like this: An in vitro study of donor PBMCs cells from healthy donors was executed with monocyte-derived human macrophages isolated from the PBMCs. This was not a formal clinical trial with subjects. Materials and methods seemed valid and reliable. Then HIV-1 primary isolates (3) were used. AZT, a nucleoside analogue was used as a control probably because the mechanism of action of 18-MC is as reverse transcriptase inhibitor and AZT is a nucleoside analogue used to affect reverse transcriptase. PBMCs were exposed to viral suspensions of HIV-1 P-24 antigen. Viral replication was assessed by measuring P-24 antigen. Dose ranges from 12.5 to 50 micromolers significantly effected HIV proliferation. Time durations varied from 3, 10, 14 and 21 days. A variety of doses, durations were done to observe safety, and effect. Compared to the control (AZT) which was rigorous as expected, 18-MC faired very well. It should be noted that the infection assays were performed with primary cells (acutely infected PBMCs and macrophages) to avoid the genotypic and phenotypic changes that might occur during viral changes that might occur during viral passages in tumor cell lines. They also used primary isolates, which are phenotypically closer to the viral population present in HIV-1 infected patients. Additionally, they looked at the naturally occurring COR and its anti HIV-1 effect and found significant results, but the data was not reported. They did report the indole alkaloid congener 18-MC molecule of the natural COR, presenting little to none of the adverse effects associated with the original molecule in this antiviral study reported. These study design considerations contributed to a tight study with valid and reliable outcomes.

Basically, 18-MC inhibits HIV-1 replication in human PBMCs and in monocyte-derived macrophages. This antiviral effect of the alkaloids may be due to their action on different steps of viral replication, such as inhibition of syncytium formation and reducing the activity of HIV-1 enzyme reverse transcriptase. So how this applies to the HIV treatment intervention picture is up for grabs. Certainly, further study needs to be done on the mechanisms by which 18-MC decreases HIV replication in vitro, in addition to inhibition of HIV reverse transcriptase. It is worth doing for a number of potential reasons:

1. 18-MC has a lower toxicity profile compared to the drugs in the study control class (nucleoside analogues). And I would venture to say in the other three classes that prevent the process of HIV from reproducing itself and perhaps infecting new cells after HIV enters the CD-4 cell.

2. 18-MC provides a potentially safe ARV therapeutic intervention in less virulent strains of HIV and minimizing toxicities.

3. Co-therapeutic intervention can be matched with micro-nutrient regimens which have been shown in study to delay ARV therapeutic intervention for up to 5 years, notably in women and infected infants.

4. 18-MC, based on its mechanism of action against HIV in comparable drug classes, could be applied to HIV infected pregnant women to affect mother to fetus transmission rates. The studies among these populations used AZT, the control for the 18-MC. I believe 18-MC has a less toxic profile than AZT even thought AZT showed significant interruption of mother to fetus HIV transmission.

5. Given the pharmacodynamics of Iboga alkaloids in the brain, the potential for crossing the blood brain barrier is significant.

6. As mentioned earlier in Dr. Onaivis presentation, the potential of Ibogaine to regulate inflammation (genetically) is significant for persons living with HIV/AIDS where inflammatory states are hallmark.

7. I believe it would be cost effective in poorer nations struggling with HIV infection.

There are issues here, too.

1. Since this 18-MC affects HIV-1 at reverse transcriptase, such as other classes of drugs, perhaps there is a chance for drug resistance as found in other drugs in that class or a shorter duration to it?

2. Perhaps it can be used in initial therapy in super-infections or drug-resistant strains until it succumbs to those viral expressions.

3. In combination with other drug classes such as nukes, non-nukes and protease, there is a strong potential for side effects. But given their toxicity to body systems and healthy cell lines that the nukes, non-nukes and protease inhibitors have, pairing them up with this group may not be wise. This is dependent on dose levels and state of the patient.

4. Perhaps it can be paired up with the new Entry Inhibitors to provide a well-rounded combination to thwart HIV. This I see as the most promising combination.

5. In the case of co-infection, particularly for those with HIV/HCV infection and dicey livers, this may prove to be questionable. I believe the verdict is not in, and further research is needed.

6. Regarding potential psychedelic effects, it should be noted that Sustiva reports similar side effects (like hypnogocic hallucinations) and has been controlled through a variety of provider and patient interventions.

What medical science needs to do

Simple, more study, but the politics of what gets studied and how it gets funded are sad realities. But history has shown us that vigilant activism can effect epistemology, study approach even study design and recruitment. For example, a medical treatment support group comprised of non-active injection drugs users (IDUs) based in the Bronx found the Hypericin study at Bellevue Medical Center in NYC to be of interest. But they found the route of administration (subcutaneous) a bit unwelcoming since it brought up potential triggers to use again. They met with the principal investigator (PI) Fred Valentine MD and persuaded him to add an arm that was orally administered. He agreed and they (the patients) help recruit for the study.

Since the study was done in Brazil and not in the US, the chances for further investigation are probably more promising. Based on this limited work, an Investigational New Drug (IND) designation can be developed, funding lined up, bring it up with Community Review Boards (CRBs), cultivate interested researchers are among the many avenues medical science must go with this. Working with the Institutional Review Boards (IRBs), who wheel a lot of political power to support pursuit of an Iboga-alkaloid as an anti-viral. This is most effective if you have a PI lined up with a clear focus, good science under his/her belt coupled with sufficient funding source(s).

What can patients and advocates do?

I believe there are many things that can be done here, to name a few:

1. Brainstorm with constituencies of patients in effected populations. Dr. Ken Alper and others have mentioned the comradery of the group having been treated with Ibogaine. These people serve as a constituency who can affect the fast tracking of treatments.

2. Develop proactive treatment support groups that can be involved in trial design, methodology, trial recruitment, trial implementation, and adherence. For example, I have started HIV/AIDS treatment support groups called AMEN (Attitude, Medications, Exercise, Nutrition). These groups encourage patients to be their own primary healthcare advocate. They are involved in all aspects of patient treatment intervention(s), advocacy, and often times drug development.

3. Treatment support group can not only promote such objects as patients being their own primary healthcare advocate but also informal researchers. For example, setting up simple databases that encourage the observation of trends of persons taking Ibogaine and the effect on say HCV or HIV. Blood work-up can be a point measure to observe trends.

4. Cultivate active and fruitful relationships between the treatment support group members and their healthcare providers, especially when it comes to understanding the population of active and non-active users, their medical conditions and predispositions, and above all the dynamic of behavior notably addiction.

Remember, some of the most profound discoveries and epistemology in medical science have come from non-medical and/or science trained patients and their advocates.

https://ibogainedossier.com/v_hernandez.html
 
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