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mr peabody

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DMT found to prevent recurrence of malignant lung and prostate cancers

Traditional medicinal use of DMT strongly suggests its medical potential. This suggestion is advanced by the discovery that DMT is an endogenous ligand of the sigma-1 receptor. This receptor can influence the energy utilization of cells, and its activation has therapeutic value in many pathological conditions such as ALS, Parkinson’s and cancer.

DMT may play a vital role in immunoregulation. For instance, DMT may help to coordinate the immune responses that fight cancer. This is based on the fact that the molecule's synthesis requires an enzyme called indolethylamine-N-methyltransferase (IMNT), which is produced by the IMNT gene, the expression of which has been found to prevent the recurrence of malignant lung and prostate cancers.

 
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mr peabody

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Is (R)-DOI a super-potent anti-cancer medicine?*

(R)-DOI (2,5-Dimethoxy-4-iodoamphetamine) is a psychedelic first synthesized by Alexander Shulgin. It is a potent inhibitor of Tumor Necrosis Factor-a inflammation, which exerts strong anti-cancer and anti-inflammatory effects through the modulation of innate and adaptive immune processes. (R)-DOI seems to be a superpower in regulating the 5HT2a receptor to inhibit TNF-α-mediated inflammation in the body. Activation of the 5-HT2A receptor represents a novel and extraordinarily potent therapeutic avenue for treating chronic inflammatory conditions, infections and cancer.

(R)-DOI is a psychedelic and mixed 5-HT2A/5-HT2C receptor agonist which acts via 5-HT2A receptors to inhibit the inflammatory effects of tumor necrosis factor (TNF)-α. Tumor necrosis factor-alpha (TNF)-α plays a key role in inflammation, and its production and signaling contribute to many inflammatory related diseases. Recently, we discovered that selective activation of serotonin 5-HT2A receptors with the agonist (R)-DOI produces a super-potent blockade of pro-inflammatory markers. Here we demonstrate that systemic administration of (R)-DOI can block the systemic effects of (TNF)-α in whole animal. Importantly, the mechanism underlying the systemic anti-inflammatory effects of (R)-DOI is activation of serotonin 5-HT2A receptors. Our results highlight a powerful new role for the serotonin 5-HT2A receptor in inflammatory processes, and indicate that agonism of serotonin receptors may represent an effective and novel approach to develop powerful small molecule therapeutics for inflammatory diseases.

*From the article here: http://pharmrev.aspetjournals.org/co...2/264.full.pdf
 
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mr peabody

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Treating breast cancer with P. harmala

The 'cancer patient in my life' who has Stage IV metastatic breast cancer has responded very well to a Syrian Rue tincture I prepared.

Her formerly aggressive, treatment-resistant tumors subsequently had become 'stable' despite the fact that her primary medication was no longer working. The patient and is firmly convinced that Syrian Rue has played a large part in that. For mood-enhancement alone, which is obviously very important in these situations too, rue is excellent IMO.

I made a tincture using 120g whole seeds, pressure-cooked in 800ml water for 2 hours. Filtered. The same seeds were then soaked in 200ml 95% ethanol for 48 hours, and this combined with the water-extract, to make about 1 litre. I think grinding seeds brings only problems, and mucilage...

Dosage: 5 ml/day first week. Then 10 ml following week. Then 15 ml until spent. This minimised adverse effects of harmalas in somebody with no prior experience.

I found that my patient observed positive changes soon after starting, because the metastatic tumors are in the spine (and affected mobility) and they reported increased mobility, after a lengthy period of decline and increasing pain, in that area.

https://www.dmt-nexus.me/forum/defau...=posts&t=75362
 
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Statins starve cancer cells to death

Johns Hopkins University | Medical Xpress | 12 Mar 2020

More than 35 million Americans take statin drugs daily to lower their blood cholesterol levels. Now, in experiments with human cells in the laboratory, researchers at Johns Hopkins Medicine have added to growing evidence that the ubiquitous drug may kill cancer cells and have uncovered clues to how they do it.

The findings, say the researchers, enhance previous evidence that statins could be valuable in combating some forms of cancer. In unrelated studies, other Johns Hopkins Medicine researchers have studied how statins may cut the risk for aggressive prostate cancer.

"There have been epidemiological indications that people who take statins long term have fewer and less aggressive cancers, and that statins can kill cancer cells in the laboratory, but our research was not initially designed to investigate possible biological causes of these observations," says Peter Devreotes, Ph.D., Issac Morris and Lucille Elizabeth Hay Professor of Cell Biology.

Results of the new research appeared Feb. 12 in the Proceedings of the National Academy of Sciences.

Devreotes and his team began the new study with an unbiased screen of about 2,500 drugs approved by the U.S. Food and Drug Administration (FDA) to see which ones had the best kill rate of cells genetically engineered to have a mutation in a cancer gene called PTEN. The gene codes for an enzyme that suppresses tumor growth. Among the thousands of drugs, statins and in particular pitavastatin, emerged as a top contender in cancer-killing ability. Most of the other drugs had no effect or killed normal and engineered cells at the same rate. Equal concentrations of pitavastatin caused cell death in nearly all of the engineered cells, but very in few normal cells.

Devreotes and his team then looked at the molecular pathways that statins were likely to affect. It's well known, for example, that statins block a liver enzyme that makes cholesterol, but the drug also blocks the creation of a small molecule called geranylgeranyl pyrophosphate, or GGPP, which is responsible for connecting cellular proteins to cellular membranes.

When the researchers added pitavastatin and GGPP to human cancer cells with PTEN mutations, the researchers found that GGPP prevented the statin's killing effects and the cancer cells survived, suggesting that GGPP may be a key ingredient to cancer cell survival.

Next, looking under a microscope at cells engineered to lack the enzyme that makes GGPP, Devreotes and his team saw that as the cells began to die, they stopped moving. Under normal circumstances, cancer cells are a bundle of moving energy, consuming massive amounts of nutrients to maintain their unchecked growth. They maintain this breakneck pace by creating straw-like protrusions from their surface to drink up nutrients from the surrounding environment.

"Suspecting that the non-moving cancer cells were literally 'starving to death,'" Devreotes says, "the scientists then measured the statin-treated cells' intake by adding a fluorescent tag to proteins in the cells' environment."

Normal human cells glowed brightly with the fluorescent tag, suggesting that these cells ingested protein from their surroundings regardless of whether the scientists added statins to the mix of nutrients and cells. However, human cancer cells with PTEN mutations took in almost no glowing proteins after the scientists added statins. The inability of the statin-treated cancer cells to make the protrusions needed take up proteins leads to their starvation.

Devreotes says his team plans further research on the effects of statins in people with cancer and compounds that block GGPP.

 
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mr peabody

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Consuming garlic in quantity significantly lowers colorectal cancer risk*

ScienceDaily | Asia Pacific Journal of Clinical Oncology | Feb 21, 2019

Consumption of garlic and onions (allium vegetables) has been linked with a substantially reduced risk of colorectal cancer in a study of men and women in China.

In the study, 833 patients with colorectal cancer were matched to 833 healthy controls by age, sex and residence area. Demographic and dietary information were collected
via face-to-face interviews using a validated food frequency questionnaire.

The odds of having colorectal cancer was 79 percent lower in adults who consumed high amounts of garlic and onions (allium) compared with those who consumed low amounts.

"It is worth noting that in our research, there seems to be a trend: the greater the amount of allium vegetables, the better the protection," said senior author Dr. Zhi Li, of the First Hospital of China Medical University. "In general, the present findings shed light on the primary prevention of colorectal cancer through lifestyle intervention."

*From the article here:


"I know of no faster way to restore optimum bowel health than to eat garlic in quantity! Buy already-peeled garlic in the big poly bag, and add lots of it to your favorite recipes!!" -pb





Natural compound in broccoli re-awakens function of a potent tumor suppressor*

ScienceDaily | May 16, 2019

Long associated with decreased risk of cancer, broccoli contains a molecule that inactivates a gene known to play a role in a variety of common human cancers. In a new paper published today in Science, researchers, led by Pier Paolo Pandolfi, MD, PhD, Director of the Cancer Center and Cancer Research Institute at Beth Israel Deaconess Medical Center, demonstrate that targeting the gene, known as WWP1, with the ingredient found in broccoli suppressed tumor growth in cancer-prone lab animals.

"We found a new important player that drives a pathway critical to the development of cancer, an enzyme that can be inhibited with a natural compound found in broccoli and other cruciferous vegetables," said Pandolfi. "This pathway emerges not only as a regulator for tumor growth control, but also as an Achilles' heel we can target with therapeutic options."

A well-known and potent tumor suppressive gene, PTEN is one of the most frequently mutated, deleted, down-regulated or silenced tumor suppressor genes in human cancers. Certain inherited PTEN mutations can cause syndromes characterized by cancer susceptibility and developmental defects. But because complete loss of the gene triggers an irreversible and potent failsafe mechanism that halts proliferation of cancer cells, both copies of the gene (humans have two copies of each gene; one from each parent) are rarely affected. Instead, tumor cells exhibit lower levels of PTEN, raising the question whether restoring PTEN activity to normal levels in the cancer setting can unleash the gene's tumor suppressive activity.

To find out, Pandolfi and colleagues identified the molecules and compounds regulating PTEN function and activation. Carrying out a series of experiments in cancer prone mice and human cells, the team revealed that a gene called WWP1 -- which is also known to play a role in the development of cancer -- produces an enzyme that inhibits PTEN's tumor suppressive activity. How to disable this PTEN kryptonite? By analyzing the enzyme's physical shape, the research team's chemists recognized that a small molecule -- formally named indole-3-carbinol (I3C), an ingredient in broccoli and its relatives -- could be the key to quelling the cancer causing effects of WWP1.

When Pandolfi and colleagues tested this idea by administering I3C to cancer prone lab animals, the scientists found that the naturally occurring ingredient in broccoli inactivated WWP1, releasing the brakes on the PTEN's tumor suppressive power.

First author Yu-Ru Lee, PhD, a member of the Pandolfi lab, notes "you'd have to substantial quantities of uncooked broccoli reularly to reap their potential anti-cancer benefit" - the reason Pandolfi's team is seeking other ways to leverage this new knowledge. The team plans to further study the function of WWP1 with the ultimate goal of developing more potent WWP1 inhibitors.

"Either genetic or pharmacological inactivation of WWP1 with either CRISPR technology or I3C could restore PTEN function and further unleash its tumor suppressive activity," said Pandolfi. "These findings pave the way toward a long-sought tumor suppressor reactivation approach to cancer treatment."

*From the article here:

 
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mr peabody

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Dr. Attila Szabo


Therapeutic potential of 5-MeO for cancer "very promising"

Research on the therapeutic potential of 5-MeO for cancer is still in the early stages, but the few studies that have been done are very promising. It has been shown to exert powerful anti-cancer and anti-inflammatory effects through the modulation of innate and adaptive immune processes. Its regulatory effect on the sigma-1 receptor, which plays a significant role in cancer, is especially interesting.

Classical psychedelics are psychoactive substances, which, besides their psychopharmacological activity, have also been shown to exert significant modulatory effects on immune responses by altering signaling pathways involved in inflammation, cellular proliferation, and cell survival via activating NF-kB and mitogen-activated protein kinases. Recently, several neurotransmitter receptors involved in the pharmacology of psychedelics, such as serotonin and sigma-1 receptors, have also been shown to play crucial roles in numerous immunological processes.

This emerging field also offers promising treatment modalities in the therapy of various diseases including autoimmune and chronic inflammatory conditions, infections, and cancer. However, the scarcity of available review literature renders the topic unclear and obscure, mostly posing psychedelics as drugs of abuse and not as physiologically relevant molecules or as possible agents of future pharmacotherapies.

In this paper, the immunomodulatory potential of classical serotonergic psychedelics, including N,N-dimethyltryptamine (DMT), 5-methoxy-N,N-dimethyltryptamine (5-MeO-DMT), lysergic acid diethylamide (LSD), 2,5-dimethoxy-4-iodoamphetamine, and 3,4-methylenedioxy-methamphetamine will be discussed from a perspective of molecular immunology and pharmacology.

Special attention is given to the functional interaction of serotonin and sigma-1 receptors and their cross-talk with toll-like and RIG-I-like pattern-recognition receptor-mediated signaling. Furthermore, novel approaches will be suggested feasible for the treatment of diseases with chronic inflammatory etiology and pathology, such as atherosclerosis, rheumatoid arthritis, multiple sclerosis, schizophrenia, depression, and Alzheimer’s disease.

Since both NF-kB and type I IFN signaling contribute to the transcriptional regulation of genes that are involved in cellular proliferation and survival, and many psychedelics exhibit in vitro anti-cancer potential through 5-HTRs, these compounds could be promising candidates in novel therapies of cancer.

Thus, as a target for future pharmacological investigations, DMT emerges as a potent and promising candidate in novel therapies of peripheral and CNS autoimmune diseases (such as Multiple Sclerosis or Amyotrophic Lateral Sclerosis) and cancer.

Here we demonstrate for the first time the immunomodulatory potential of NN-DMT and 5-MeO-DMT on human moDC functions via sigmar-1 that could be harnessed for the pharmacological treatment of autoimmune diseases and chronic inflammatory conditions of the CNS or peripheral tissues. Our findings also point out a new biological role for dimethyltryptamines, which may act as systemic endogenous regulators of inflammation and immune homeostasis through the sigma-1 receptor.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4500993/
 
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Even healthy tissues carry clusters of cells with mutations.


Study shows mutations are found even in healthy tissues throughout the body*

by Brittany Flaherty | June 6, 2019

"Just because you see a cancer-associated mutation, doesn't necessarily mean the patient has cancer..."

For years, the prevailing wisdom has been that our cells contain genes that are essentially carbon copies of each other. That notion is being dashed by studies painting a different picture — one in which even “normal” cells and tissues accumulate mutations over time.

New research out of the Broad Institute of MIT and Harvard has identified mutations in normal tissues throughout the body, including some known to drive cancer.

A large-scale analysis published Thursday in Science examined more than 6,700 samples of normal human tissue from 29 major tissue groups — from brain and bladder to breast and prostate tissue. The researchers used RNA sequencing data to look in these tissues for large mutational clones — groups of cells that have the same mutations. They found many more clones than they had expected, including some that contained mutations that drive cancer.

“This study opens up the big question of what is normal?” said Cristian Tomasetti, an associate professor of oncology at Johns Hopkins University who was not involved with the study. “This is now a picture of our normal tissues being quite messy and full of these mutational clones. We are really just at the beginning of knowing how to evaluate them.”

The team assessed normal tissue samples from nearly 500 different people and observed mutations in 95% of them.

“We didn’t know if we would find anything,” said senior author Gad Getz, professor of pathology at Harvard Medical School and director of the Cancer Genome Computational Analysis Group at the Broad Institute. “But we found macroscopic clones in essentially every tissue that we looked at in the body.”

Scott Kennedy and Rosana Risques, assistant professors of pathology at the University of Washington who weren’t involved with the research, said these findings are consistent with work from their lab and others that have uncovered cancer-associated mutations in normal skin and blood. But, they said, this new study is an important step toward understanding mutations found throughout the body. “Until we had the technology, we didn’t know all of these mutations existed in normal tissue,” said Risques. “Now that we have the methods, we really need to explore this.”

Getz and his colleagues leveraged an enormous RNA sequencing dataset gathered for a separate Broad Institute effort and developed a novel method to analyze the RNA data.

Keren Yizhak, the paper’s first author, conducted the study as a postdoctoral researcher at the Broad Institute."These findings could change the way we think about what constitutes normal tissue. Normal tissue is constantly developing and changing,” she said. “We are all like a puzzle made up of different cells.”

Scientists use the term “mosaicism” to describe this kind of cellular makeup, wherein an individual can have cells with different genetic material.

Some of the tissue types investigated in this study had more mutations than others. The researchers found that tissues of the lung, esophagus, and sun-exposed skin had the highest number of mutations. "This was somewhat expected, since these tissues are often subject to environmental factors like cigarette smoke, hot and cold beverages, and ultraviolet radiation that could incite mutations," said Getz. They also found an association between mutation number and age: tissue samples from older individuals had more mutations. Getz said future studies could reveal more about factors linked to a high number of mutations in normal tissue.

Genomic technologies now allow researchers to sequence the genetic makeup of tumors and identify the mutations found in tumor tissue. But Yizhak pointed out that analyzing a fully formed tumor provides little information about which mutations initially led to its formation. Understanding more about the mutations found in normal tissue and whether they develop into cancer could help researchers better understand how these diseases originate and progress.

Longitudinal studies that follow individuals for years could clarify how normal tissues change over time, as well as which mutations ultimately lead to cancer versus those that stop growing.

“We could detect mutations and then observe how they change in frequency during the course of the person’s lifetime and see whether they do develop into cancer,” said Selina Vattathil, a postdoctoral researcher at Princeton University who was not involved in the study. “But of course that’s really hard to do.” The technology for this type of work is available, Vattathil explained, but it is challenging to conduct studies of this kind and collect multiple samples from healthy individuals.

The emerging knowledge that normal tissues have more mutations than previously thought could throw a wrench into one ongoing area of research: the development of methods for the early detection of cancer.

Early detection is important and can improve treatment outcomes, but many tumors and blood cancers are elusive until after they have advanced to a more difficult-to-treat stage. To address this, scientists are developing techniques to identify disease-driving mutations sooner. The new findings about mosaicism present a challenge — figuring out which mutations are truly red flags that signal disease and which are harmless and normal.

Some early detection techniques, for example, involve collecting blood samples and sequencing cell-free DNA — genetic material that cells have shed into the bloodstream. Until recently, the detection of cancer-associated mutations suggested they were likely shed by cancerous or pre-cancerous cells. But the work by Getz’s team and others indicates that some of these mutations —even those known to drive cancer — may be shed by non-cancerous, normal cells.

“It really calls into question the specificity of seeing these mutations,” said Kennedy. “Just because you see a cancer-associated mutation, it doesn’t necessarily mean the patient has cancer. That’s something that diagnosticians and clinicians definitely have to take into account.”

Yizhak and Getz agree that scientists developing these techniques simply need to acknowledge the possibility that mutations they uncover may come from normal tissues.

“When we develop these tools of early detection, we want to make sure that we don’t have false positives in healthy people,” said Getz. “We just need to be careful.”

-----

*For years I've been saying 'everyone has cancer,' meaning we all "have" it, and the POTENTIAL for illness, when conditions which normally enable us to ward off the disease process fall below a certain threshold. Here now is the first documentary evidence that I was right. Cancer is quite simply the body spiraling out of control when it can no longer keep these mutations in check. -pb
 
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mr peabody

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Ayahuasca, neurodegenerative disorders, and cancer

by Daniel Gustafsson

Natural substances extracted from the ayahuasca plants have been found to possess unique restorative and strongly antioxidative properties on specific nerve cells in the brain and central nervous system – controlling neurotransmission, muscle/motor activity, memory and coordination. This gives probable cause to the theory that ayahuasca could be an effective treatment for neurodegenerative diseases such as ALS, Alzheimer’s, and Parkinson’s disease. Promising results as of date has also been obtained from studying the substance psilocybin, very closely related to the substances found in ayahuasca, naturally occurring in certain species of medicinal mushrooms consumed by the indigenous people where ayahuasca is also used.

According to Dr. Juan Ramos, head of the neurological disease department at the South Florida university, USA, initial studies show that these substances stimulate the development of new cells in the areas of the brain controlling the above mentioned functions. If this could prove to be an eventual cure through complete restoration of damaged or destroyed cells remains to be seen, but initial results indicate this could potentially be the case. There is also a growing interest in exploring the cell regenerative properties of these plants within the spinal chord injury support communities. Should people with this background eventually try and find the results of this treatment useful, medical science would be bound to take note. Cancer researchers have also shown interest in B. Caapi, as its different alkaloids has shown to be effective against the growth of cancer cells.

Ayahuasca could effectively be used in treatment of ALS and other motor neuron diseases based on the fact that studies suggest uniquely antioxidative effects that seem to protect brain/nerve cells, targeting motor neurons through a unique biochemical transport system, and that it and other molecularly similar substances, also naturally occurring, stimulate neurogenesis – the development of new brain/nerve cells, and the communicative capacity between these. In studies it has been found to reduce symptoms in Parkinson’s patients – all neurodegenerative diseases share common ground, thus making it likely that something that improves a given neurological condition could also be beneficial to other conditions nearly related. Also based on credible personal accounts from people having used ayahuasca for symptom relief from their multiple sclerosis (once again – the common ground of neurodegenerative diseases), documented in books about ayahuasca, and from descriptions of early stage minor improvement by those with various types of ALS now participating in the treatment project, already having used this medicine for a period of time. Studies also indicate ability to normalize metabolism in mitochondria, crucial to motor neuron survival, and to regulate and decrease levels of excitotoxicity in the central nervous system.

https://www.wakingtimes.com/2014/12/29/ayahuasca-natural-medicine-brain-disease-cancer-wellness/
 
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mr peabody

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Dr. Attila Szabo


Tryptamines: Endogenous regulators of inflammation and tumor immunity

Dr. Attila Szabo, University of Oslo, Norway

Tryptamines are members of a large family of monoamine alkaloids that are widespread in nature and abundant in all the three Kingdoms of life (plants, fungi, and animals). Their main feature is a common indole ring, a backbone that is structurally related to the amino acid tryptophan. This tryptamine backbone designates many biologically active compounds, such as psychedelics and neurotransmitters. To date, our knowledge about the immunomodulatory capacity of tryptamines is quite scarce. DMT is the only member of the family that has been investigated so far.

DMT is related to the neurotransmitter serotonin, the hormone melatonin, and other psychedelic tryptamines, such as bufotenin and psilocin. It is a naturally occurring indole alkaloid that is ubiquitous in plants, such as Diplopterys cabrerana and Psychotria viridis, which are used for the preparation of sacramental psychoactive brews including yage and ayahuasca. In addition to its ubiquitous presence in plant species, DMT has also been detected in animal tissues and is considered to be an endogenous trace amine. The milestones of DMT research were laid down by Szara and Axelrod who reported first the psychoactive effects and occurrence of this compound in the human brain. This led to the hypothesis that DMT is an endogenous psychedelic, and a neurotransmitter or neuromodulator. DMT was shown to act as an agonist at several serotonin receptors including 5-HT1A, 5-HT2A, and 5-HT2C as well as at sigmar-1.

The vast majority of the initial research into the reasons for the presence of psychoactive tryptamines in the human body has sought their involvement in mental illness. Until now, very little has been known about the function of DMT in cellular and general physiological processes, and the emphasis of research mostly aimed the understanding of its psychedelic properties. Recently, we and others demonstrated that DMT has the capability to modulate immune responses in in vitro human primary cell cultures. In these studies, DMT was shown to act as a non-competitive inhibitor of indoleamine 2,3-dioxygenase (IDO) and as a strong inducer of anti-tumor cytotoxic activity in the co-cultures of human PBMCs and a glioma cell line. Furthermore, DMT and its analog 5-MeO-DMT were found to exert potent anti-inflammatory activity through the sigmar-1 in human monocyte-derived dendritic cell (moDC) cultures.

The anti-cancer activity of ayahuasca has already been reviewed by Schenberg. However, it is important to keep in mind that ayahuasca is a complex decoction that, besides DMT, contains several other components according to the admixture plants used in the making process. Furthermore, ayahuasca can be administered in various ways (single-time, long-term, etc.), thus one should be particularly careful with the study design and interpretation of the data. Nevertheless, ayahuasca consumption in a highly controlled clinical setting emerges as a very promising model for investigating the possible immunomodulatory effects of DMT in humans. Importantly, it is possible that the observed anti-inflammatory and immunosuppressive effects may counteract with the anti-cancer activity, therefore further investigations are needed to elucidate the complex in vivo consequences of DMT administration.

The mentioned studies demonstrate and propose new biological roles for DMT, which may act as a systemic endogenous regulator of inflammation and immune homeostasis. According to these new results, DMT and 5-MeO-DMT possess the capability to inhibit the polarization of human moDC-primed CD4+T helper cells toward the inflammatory Th1 and Th17 effector subtypes in inflammatory ttings. This is of particular importance, since Th1 and Th17 cells and the cytokines they secrete are key players in the etiology and symptomatology of many chronic inflammatory and autoimmune diseases of the CNS and other tissues. Moreover, the mobilization of innate immune mechanisms is also well established in many psychiatric and neurological disorders. Thus, as a target for future pharmacological investigations, DMT emerges as a potent and promising candidate in novel therapies of peripheral and CNS autoimmune diseases such as Multiple Sclerosis, ALS, and cancer.

https://pdfs.semanticscholar.org/096...8ea779ba61.pdf
 
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How cannabis kills certain types of cancer cells*

by Kyle Jaeger | Jul 19 2019

Cannabis extracts can impair the survival of certain types of cancer cells and inhibit their spread. But the effects of those extracts vary significantly based on their specific chemical makeup.

Researchers found that treating cancer cells with isolated ingredients in cannabis, such as THC alone, does not appear to be especially effective—but full cannabis extracts showed more promise. However, with the plant containing hundreds of compounds that appear in different concentrations across strains and preparations, researchers had their work cut out for them in investigating how various cannabinoid combinations treated different types of cancer cells.

The team tested the antitumor effects of 12 whole cannabis extracts on 12 human cancer cell lines in order to “determine whether whole cannabis preparations with specific phytocannabinoid profiles could be advantageous as therapy for certain cancer sub-types.” The findings were published in the journal Oncotarget.

Each cell sample was treated with a cannabis extract in increasing doses (2-10 µg/ml) over the course of 24 hours. There were five preparations of cannabis that proved especially potent for a wide range of cancer types but, in general, the study shows there’s significant variability in effectiveness for different cancer types—even when the cancers originated in the same organ.

For example, two distinct forms of prostate cancer cells were found to be most sensitive to entirely different cannabis extracts.

The cannabis preparations also ranged widely in their effectiveness in preventing the proliferation of cancer cells. When applied to multiplying cells, there were three extracts that reduced the growths to 37-51 percent of their original size, compared to 68 percent for the control group. But there were other extracts that failed to reduce the spread in a statistically significant manner.

Some commonalities shared among the most potent cannabis extracts include a high concentration of THC and large amounts of phytocannabinoids in their decarboxylated form.

“Taken as a whole, we concluded that medical cannabis does not consist of a single therapeutic agent but rather a heterogeneous array of treatments,” the researchers wrote. “We propose that the fate of specific cancer cells following cannabis extract application is dependent upon the synergistic effects of its phytocannabinoid composition, concentration applied, along with the cell specific characteristics.”

The study concluded that “cannabis extracts were very potent in producing cell death and some of these extracts were of THC-rich type” and that, as previous studies have indicated, “using whole cannabis extracts is more effective in inducing cancer cell death than applying pure THC on the studied cells lines.”

“Furthermore, not all THC-rich extracts produce the same effects when applied at the same concentrations on a specific cancer cell line,”
the study authors wrote. “These findings indicate that compounds other than THC in these extracts might act together in a polypharmacology way and determine the extract efficacy as antitumor agents.”

Interestingly, the researchers also theorized that the the “presence or absence of cannabinoid receptors in the tested cell lines may explain the differential potency of the extracts towards reducing cell survival.”

The team has called for further research into the “specific properties and mechanisms of cancer cell insensitivity to cannabis extract effects.”

“We hope that this study will lay the groundwork for future preclinical studies and randomized controlled clinical trials in order to provide evidence for effective cannabis treatments for many cancer subtypes,”
they concluded.

*From the article here:

 
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Subjects who recovered from cancer were noted to have integrated a plant-based diet.


First study to show that DMT protects the body's immune system from cancer

New study led by Ede Frecska and Jordi Riba is the first to bring some clarity to the mystique surrounding this hotly-debated subject.

The team took 3 types of human cells – neurons derived from pluripotent stem cells (a cell that can develop into any other cell type), monocyte-derived macrophages and dendritic cells (these two are both key players in the body’s immune system, working to engulf and annihilate undesirable particles, such as harmful bacteria or cancer cells). The team then restricted the cells’ supply of oxygen (hypoxia). A few hours of severe hypoxia reliably kills the majority of neurons, and a significant proportion of the immune cells.

The scientists then tested whether DMT could protect the cells from this fate. And indeed, they found that DMT-treated cell cultures had a much higher survival rate! Moreover, the amount of DMT needed to protect the cells was relatively low.

Hypoxia usually causes dramatic alterations to unprotected cells. One of the most reliable markers of being oxygen-deprived –the hypoxic condition- is the presence of the so-called hypoxia-inducible factor (HIF)-1, which can be clearly visualised, but disappears when there is sufficient amount of oxygen. In the presence of DMT, there was significantly less HIF-1 detected in the cells, as well as the other oxygen-sensitive proteins. Therefore, DMT could be seen to actively reduce cellular stress in hypoxic environments.

So, the DMT-treated cells underwent – on a, literally, microcosmic level – a “near-death” experience, as opposed to a deadly one. The question is: How does DMT protect these cells?

Szabo et al. decided to investigate how important the action of the Sigma-1 receptors (Sig-1R) is in bringing about the protective effects of DMT. Located inside the immune and brain cells (and cells from other organs such as liver, kidney), these receptors have important functions in the synthesis of energy molecules, as well as facilitating stress signalling. On a molecular level, “stress,” does not correspond to the difficulties and hurdles of everyday life, but to all the nasty things that threaten a cell’s well-being, such as changes in oxygen level (used in this study), temperature, toxins and mechanical damage. DMT has been previously shown to bind to Sigma-1 receptors, and more DMT is detected in the central nervous system under stress.

Suspecting that the effects of DMT hinge on the action of these receptors, the team selectively silenced (i.e. switched off) the genes responsible for SIG-1R development. The results were drastic and immediately apparent: switching of the Sigma-1 receptors led to complete annihilation of the DMT-related effects on cell survival and HIF-1 markers! Therefore, the researchers concluded that Sig-1R receptors are absolutely instrumental in enabling the protective, anti-stress effects of DMT.

By finding out that these effects are mediated through the Sig-1 receptors, Szabo et al. have brought us one step closer to finding out mechanisms behind DMT’s neuroprotective effects. We can look more confidently to a future where the workings of DMT are better understood. Currently plausible hypotheses include the idea that DMT is fine tuning the regulation of oxygen metabolism, or relating to other molecules involved in cell survival.

Conclusion: “Our results suggest a novel and important role of DMT in human cellular physiology and point out to the relevance of DMT-mediated Sig-1R modulation in future therapies concerning hypoxia/ischemia-related pathologies.” If these results are applicable to other stressors and replicated in humans, the implications are huge. DMT could be administered to save neurones that would otherwise die from exposure to harmful events, such as to protect patients’ brains against damage caused by oxygen starvation – e.g. during heart attack or stroke. And the damage wrought by tragic neurodegenerative diseases, like Parkinson’s and Alzheimer’s – for which there are currently no cures – could potentially be redressed. On a biological level, DMT could be a life-saving agent, administered in order to give cells, and the bodies they belong to, a second chance at life.

http://beckleyfoundation.org/2016/09...-under-stress/
 
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There’s a troubling rise in colorectal cancer among young adults*

by Katarina Zimmer | The Scientist | Aug 26, 2019

Some experts blame our modern, sugary diet, while others think that gut microbiome changes and sedentary lifestyles may play a role. Altogether, the causes are far from clear.

achel Winegar, a mother of three from Colorado, has had trouble with her digestive system for as long as she can remember. So when she neared 30 and her problems intensified, colorectal cancer did not cross her mind. Her doctor figured it was perhaps a chronic condition like celiac disease, ulcerative colitis, or Crohn’s disease. She was suffering “rectal bleeding even while passing gas, full feeling, bloated, nauseous, low energy, feeling of sitting on something, pencil-thin stools,” she writes in an email to The Scientist.

After she finally went to a doctor, Winegar was scheduled for a colonoscopy. But instead of finding evidence for any of those conditions, her doctor discovered a mass the size of Winegar’s palm in her rectum, she recalls. It was stage 4 cancer. “My husband and our three kids and I have had our lives turned upside down because of the cancer diagnosis.”

Although still rare, affecting roughly 4 percent of adults over their lifetimes, according to the National Cancer Institute, colorectal cancer is becoming increasingly common in young adults, even as the incidence among older people is declining. The first reports of a rise among younger patients emerged a decade ago. “We thought this would level off with the newer data, but it continues to go up,” says Darren Brenner, a molecular cancer epidemiologist at the University of Calgary.

Brenner and his colleagues’ recent analysis of Canadian national cancer registry data found that the incidence of colorectal cancer diagnoses among women under 50 increased annually by nearly 4.5 percent from 2010 to 2015. Canadian men under 50 experienced an average per-year increase of nearly 3.5 percent from 2006 to 2015. “Among males and females, we are seeing the highest-ever recorded rates,” he says. Of the country’s population of 37 million, nearly 12,000 women and nearly 15,000 men of all ages were diagnosed with colorectal cancer in 2017, according to the Canadian Cancer Society.

A recent study in the journal Cancer described a similar trend among Americans, the figures being a little higher for rectal cancers than colon cancers. In 2004, 10 percent of diagnoses were in people under age 50, compared to 12 percent in 2015. The rise is not restricted to North America: In May, one analysis found significant increases in colorectal cancer among people under 50 in Denmark, New Zealand, and the UK over the last decade. Similarly, a study of 20 European countries found that over the past decade, the incidence of colorectal cancer had increased by nearly 8 percent per year among people in their 20s, by 5 percent for people in their 30s, and by 1.6 percent for those in their 40s.

Nowadays at the University of Texas MD Anderson Cancer Center, one in three new colorectal cancer diagnoses involves patients between 18 and 50 years old, according to Nancy You, a surgical oncologist there. What worries her in particular is that young adults are disproportionately affected by rectal cancer, which requires more complex treatment than cancer of the colon, she writes to The Scientist in an email. "In addition, they are disproportionately already at stages 3 or 4 at diagnosis—likely due to a lack of understanding of the disease in young people among patients and physicians," she says. The trends call for an urgent need to raise awareness of the issue and to understand its underlying causes. “It’s a really hard question to answer,” she says.

Factors contributing to colorectal cancers

Generally speaking, a small proportion of colorectal cancers—around 5 percent—are hereditary, including conditions such as Lynch syndrome, which is caused by mutations in genes responsible for repairing errors in DNA replication. Another 20 percent or so have a family history of colorectal cancer, although it’s not clear whether it’s predominantly genetic or environmental factors that cause the disease to aggregate in some families.

Most colorectal cancers occur in people who don’t have a family history or a known genetic predisposition, as is the case with Winegar. For these sporadic cases, different theories have emerged for the causes, including gut microbiome changes and a sedentary lifestyle. For instance, evidence published earlier this year linked prolonged time spent sitting watching TV with an increased risk of developing the disease in young Americans. General risk factors for colorectal cancer also include smoking and heavy alcohol consumption.

Given that the increase in cases in young adults has occurred within a relatively short timeframe, it’s most likely driven by environmental risk factors, rather than genetic changes in the population, according to Brenner. “The likely culprits are probably a combination of major lifestyle and exposure trends that have changed over the past forty years,” he says.

Some researchers blame diet-related changes in recent decades. “We know that people in those younger groups are eating less fiber and are eating more processed foods than previous generations have,” Brenner says. These are known risk factors for colorectal cancer, as well as processed meat and red meat. In addition, obesity rates are climbing in young populations, which several studies have linked to the rise in colorectal cancer among young adults.

“Colorectal cancer is one of the most sensitive cancers to diet,” notes endocrinologist Marcus Goncalves of Weill Cornell Medical College in New York, whose research focuses on the effects of diet on cancer.

Although the precise links between obesity and colorectal cancer are unclear, he sees several ways in which obesity could fuel tumor growth. By increasing fat reservoirs across the body and near the tumor, obesity could provide cancerous cells with fuel to grow. Obesity can also predispose a person to hormonal changes such as high amounts of insulin and estrogen, which can increase the rate of cell growth. The condition also leads to systemic inflammation of body tissues, releasing cytokines that further spur tumor growth. Dietary habits can also alter bacterial populations in the gut, which could affect tumor growth by changing the levels of metabolites and hormones, he adds.

Sugar intake may also be an important factor. “The tumor can just directly eat the sugar that you are eating. That’s unique to colorectal cancer,” Goncalves says. Recently, he and his colleagues conducted a study in mice that had a genetic predisposition for colorectal cancer, and fed them high-fructose corn syrup. In treated animals, those tumors became much larger and appeared to be more aggressive than in control animals that didn’t receive syrup. “But they did not become obese, so you can tease apart the independent effect of sugar,” he explains.

Colorectal cancers originate from benign polyps, or adenomas, which can become cancerous if not removed. Fructose in addition to glucose acts as a catalyst for glucose metabolism, which cells use to fuel the construction of macromolecules such as proteins, DNA, and lipids. In excess, these sugars could cause benign polyps to become cancerous. As cells grow and proliferate rapidly, this could increase the likelihood of new mutations to arise, such as in genes that regulate the cell cycle. “Our work would suggest that if you did have a benign polyp, and then you feed it a bit more sugar, that polyp could become cancerous faster,” Goncalves adds.

You, the MD Anderson oncologist, is wary of focusing too much on particular risk factors. “I definitely see patients who are vegetarians, they run marathons, they’re skinny, so it’s not exclusive,” she says. “The unfortunate reality [is that] many young people who ‘have done everything right’ are being diagnosed” as well, she adds.

Awareness needed for colorectal cancer in the young

Colorectal cancers in younger patients are often at advanced stages at the time of diagnosis. According to recent results of a social media survey of 1,195 colorectal cancer patients and survivors under 50, 71 percent said they were diagnosed at stage 3 or 4. “There’s a real disparity for them in being diagnosed in a timely manner,” says Ronit Yarden, the lead author of the research and the director of medical affairs at the Washington DC–based patient advocacy group Colorectal Cancer Alliance (CCA), which conducted the survey.

“What’s most devastating with colorectal cancer is that if caught early, it could be preventable, or at least the survival rate would increase significantly,” Yarden says. However, there are several major barriers to young adults in getting diagnosed early.

"Uninsured young people with symptoms of colorectal cancer typically don’t have access to a timely colonoscopy, which is considered the gold-standard diagnostic tool for colorectal cancers. But even for those with insurance, it can be difficult to get a colonoscopy because of the way US insurance companies classify the procedure: If a doctor finds no polyps in the colon that have to be removed, most companies will consider that a preventive procedure for people under 50 with symptoms," Yarden explains. But once a polyp is found and removed, even if it’s benign, payers typically consider that a diagnostic test, and as such it is often subject to various deductibles and premiums. “Some people who are maybe underinsured may not want to go and check themselves because they’re afraid the cost will be increased if they find something,” “she says. “That’s a loophole we have here in the US.”

"Within the medical community in the US, there have been ongoing debates about how to adapt screening guidelines to the rise in cases among young people,"
You says. Last year, the American Cancer Society (ACS) reduced its recommended screening age for colorectal cancer from 50 to 45, as most cancers that occur before 50 are during people’s 40s. "Some states have adopted that standard, but others are waiting for the American Preventive Services Task Force to adopt the ACS’s guidelines," Yarden says.

The fear around having a colonoscopy, an invasive procedure, may also deter people from going to the doctor. There are other, non-invasive screening methods available—such as fecal immunochemical tests—but a colonoscopy is considered the most efficient because polyps can be immediately removed during the visit, You says.

"Many young people may be simply unaware that symptoms such as rectal bleeding at a young age could be caused by colorectal cancer," Yarden adds. That was the case with Rachel Winegar. In fact, 41 percent of the CCA’s survey respondents reported that they waited at least six months after experiencing symptoms before talking to a doctor.

This may also be due to a lack of awareness among physicians. According to the survey, 67 percent of respondents saw at least two doctors before getting a correct diagnosis. “My doctors weren’t looking for colon cancer,” wrote one respondent. “My symptoms were pretty obvious in hindsight, but I don’t think they are used to seeing this diagnosis in young people.”

“Even though it’s only ten percent that are young-onset colorectal cancer, that is still significant,”
Yarden says. “Patients need to be aware of the symptoms and listen to their body and sometimes insist on getting a second opinion until getting checked thoroughly.”

Winegar, who says she’s experienced preliminary positive results after receiving a course of the anti-cancer drug Stivarga at a treatment center in Mexico, agrees. “People need to know what’s ‘normal’ and what’s cause for concern.”

*From the article here:

 
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Researchers unlock the profound anti-inflammatory properties of cannabis*

by Mark Taylor | Benzinga | Aug 23 2019

A new study deciphers for the first time the cannabis plant's biological blueprint for producing two molecules with anti-inflammatory properties, a discovery that could pave the way for expanded use of cannabis as medicine.

That study, which is published in the August 2019 issue of the journal Phytochemistry delineates for the first time the biosynthesis pathway outside of the actual cannabis sativa plant that allows reproduction of the molecules cannflavin A and cannflavin B.

Those cannflavins belong to the class of plant flavonoids, plant chemicals found in almost all fruits and vegetables, known as flavones, which occur in several plant lineages.

The study shows the medicinal versatility of the cannabis plant: Beyond the intoxicating ingredient THC and therapeutic oils that often contain cannabidiol (CBD), there exist many other specialized metabolites requiring further research.

The researchers at Guelph University in Ontario, Canada, unlocked the blueprint for producing the cannflavins, which were discovered in a 1985 study and were found to display “potent anti-inflammatory activity in various animal cell models.”

The new information in the Phytochemistry study opens a pathway to figure how to engineer plant metabolism to make medicine from the cannflavin A and B enzymes.

Tariq Ahktar, lead author and assistant professor of plant biochemistry at Guelph's Department of Molecular and Cellular Biology, told Weedmaps News that “for almost 30 years nobody touched these molecules or worked extensively on them. We thought it was a good time to look at these very promising molecules more closely.”

Ahktar said his laboratory utilizes plant chemistry and genomics to determine how plants produce certain molecules and compounds that have medicinal or industrial uses.

He said the cannaflavins A and B were discovered in the United Kingdom more than 30 years ago by researcher Marilyn Barrett. Her study also introduced the name cannflavin. Barrett's research showed that cannflavins A and B have nearly 30 times the power of aspirin to inhibit inflammation in cells.

Yet that discovery is just the beginning. Ahktar explained that the two cannflavins are present in cannabis in very low amounts.

“So if you want to gain the anti-inflammatory benefits, you would have to consume copious amounts of cannabis, which is both unlikely and impractical,” he said, "necessitating the need to reproduce the molecules outside of the cannabis plant."

He said cannflavins are “definitely encouraging news” for people suffering from acute and chronic pain, who have few effective alternatives to opioids, which work by blocking the brain's pain receptors. These cannflavins appear to take a different path by attacking cells that encourage inflammation, a primary cause of much pain.

Ahktar said that for decades American and Canadian researchers have been unable to research the medicinal properties of cannabis because of prohibitions against the cultivation and sale of the plant, still considered illegal by the U.S. federal government. Ahktar said his team has demonstrated a biochemical pathway for commercial producers to allow the production of cannflavins A and B from yeast, bacteria, plants, or other means.

“That way you don't have to grow huge fields of cannabis to obtain the benefits,” he said, noting that the Guelph researchers have patented the genes and licensed their research to Toronto-based Anahit International Corp., to biosynthesize those molecules.

The ability to “hack” other plants or microorganisms to produce their medicinal compounds offers great potential benefits to science and industry. Dr. Jeff Chen, Director of the University of California, Los Angeles (UCLA) Cannabis Research Initiative, spoke at the July 2019 Microscopes and Machines conference in Los Angeles about using biosynthesis as an alternative that is more scalable, consistent and continuous than plant farming to produce cannabinoids and other beneficial compounds.

Chen cautioned that science has a long way to go to find the most efficient method of producing the cannabinoids and other beneficial compounds. Patients, however, haven't been waiting.

Ahktar said he spoke with many patients who used cannabis successfully to treat a range of conditions and swore it improved their pain levels and reduced inflammation.

“Now that we have a mechanism for reproducing this, we can start producing it and performing side by side comparisons with existing pain relievers and test their relative efficacy,” he said.

The study comes amid an ongoing opioid crisis in the United States. According to the U.S. Centers for Disease Control and Prevention (CDC), U.S. healthcare providers prescribed more than 214 million prescriptions for opioid pain in 2016, with an estimated 11 million people misusing prescription opioids that year. More than two-thirds of the 63,632 drug overdose deaths in 2016 involved prescription or illicit opioids. From 1999 to 2017, almost 218,000 people died in the United States from overdoses related to prescription opioids.

Gregory Gerdeman, chief scientific officer for the St. Petersburg, Florida-based medicinal cannabis cultivator 3 Boys Farm and a neuroscientist who has studied the effects of cannabis on the brain for 22 years, said the takeaway from the study is that herbal cannabis takes a multifaceted approach to combating inflammation and that it may offer a greater therapeutic value than the THC or CBD alone.

“It also may point to potential drug development,” Gerdeman said. “I believe in herbal cannabis as a medicine. I think it already offers a very promising strategy for replacing opioids. We now know how the plant synthesizes cannflavins A and B and we're living in an age in which pharmaceutical companies are creating genetically modified cannabis that could allow drug factories to reproduce these molecules outside of the cannabis plant. This study shows how the science of cannabis as a medicine is being taken seriously today in the medical and pharmaceutical worlds. It was not that way in 1997 or even in 2007.”

He called cannabis the “queen of medicinal plants,” adding, “We have many secrets yet to learn from her.”

Gerdeman cautioned, however, that the Canadian study did not explore the precise role of cannflavins A and B in fighting inflammation or the molecules' potential therapeutic effects.

“The assertion from a 30-year-old study that these cannflavins offer anti-inflammatory effects 30 times the strength of aspirin requires much more research and study to validate. It would be premature to say that using isolated cannflavins as a drug would be desirable or without safety concerns.”

*From the article here:

 
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Drinking very hot tea nearly doubles risk of esophageal cancer

The Atlanta Journal-Constitution | Mar 25 2019

Like your tea served piping hot? Beware — you could be doubling your cancer risk, according to a new report.

Researchers from Tehran University of Medical Sciences in Iran recently conducted a study, published in the International Journal of Cancer, to determine the association between drinking hot tea and esophageal cancer.

To do so, they examined more than 50,000 people, aged 40-75, in Golestan, a province in northeastern Iran. They followed the participants for 10 years, tracking the temperature of the tea they drank as well as their overall health.

During the follow-up, 317 new cases of esophageal cancer were identified.

Furthermore, they found those who drank tea warmer than 60 degrees Celsius or 140 degrees Fahrenheit and consumed more than 700 ml of tea daily were 90 percent more likely to develop esophageal cancer, compared to those who drank less tea and at temperatures below 60 degrees Celsius.

“Many people enjoy drinking tea, coffee, or other hot beverages. However, according to our report, drinking very hot tea can increase the risk of esophageal cancer, and it is therefore advisable to wait until hot beverages cool down before drinking,” lead author Farhad Islam said in a statement.

Tea is rarely consumed at temperatures above 65 degrees Celsius in the United States or Europe. However, in places like Iran, Russia, Turkey and South America, it’s more common to serve tea at that temperature or hotter, Peter Goggi, president of the Tea Association of the USA, told CNN last year.

The scientists do not know why drinking hot tea is linked with esophageal cancer, but this isn’t the first study of its kind.

A 2018 study, published in Annals of Internal Medicine, found that consuming “hot” or “burning hot” tea is linked with a two- to five-fold rise in esophageal cancer, but only among individuals who also smoke or drink alcohol.

The analysts from that evaluation believe hot beverages may damage the tissue lining the esophagus, which could increase the risk of cancer from other factors, such as repeated irritation of the esophagus and the formation of inflammatory compounds.

https://billingsgazette.com/drinkin...cle_8f6681e4-0d2e-5c14-9fc9-75a8c05d7b98.html
 

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Study reveals how cannabis inhibits tumor growth*

by Kyle Jaeger | August 9, 2019

A recent scientific review shows that cannabis’s components can inhibit tumor growth and help with cancer management.

Researchers at Amity University in India detailed the scientific literature surrounding the effects of cannabinoids on different cancer types.

"Besides treating chemotherapy side effects, cannabis also shows potential in slowing the growth of cancer cells and even kill cancer cells in certain cases," the researchers wrote.

“THC and CBD exhibit effective analgesic, anxiolytic, and appetite-stimulating effect on patients suffering from cancer.”

But that’s not all. “Apart from exerting palliative effects, THC also shows promise in the treatment of cancer growth, and hence should be exploited accordingly,” an abstract of the study, published in the Journal of Cancer Research and Therapeutics, states.

The majority of the studies reviewed were based on in vitro experiments, meaning they did not involve human subjects but rather isolated cancer cells from humans, while some of the research used mice.

Cannabinoids appear to “exert potent anti-growth activity and activate various apoptotic mechanisms eventually leading to cell death” of cancer cells associated with glioma, an aggressive form of brain cancer.

At least once clinical trial showed that patients with recurrent glioblastoma multiforme who were treated with a “proprietary combination of THC and CBD” in addition to a traditional pharmaceutical had a higher one-year survival rate (83 percent) compared to a placebo group (53 percent).

Another study found blood cancer cells that were treated with two synthetic endocannabinoids activated receptors that “mediated apoptosis,” or the death of the cells.

In certain cell lines of prostate cancer, similar findings were observed. There was “significant cell growth inhibition followed by apoptosis in one particular cancer cell type in a study which was designed to evaluate the in vitro effects of endocannabinioids such as 2-arachidonoyl glycerol, anadamine, and its synthetic analog methazolamide.”

Less research has been conducted on the effects of cannabis on lung, breast, oral and liver cancers, but the study authors documented instances where mice with certain lung cancer types treated with THC experienced a “notable reduction of the subcutaneous tumor growth and lung metastasis of those cells, prompting its significance as a novel therapeutic molecule in lung cancer treatment.”

But while THC is a common study focus, other cannabinoids show particular potential in treating different cancer types, they found. For example, a synthetic CBD compound (940-CBD) was the most effective “in terms of antiproliferative effects and invasiveness” of a particular breast cancer cell line.

"When treated with THC, an oral cancer cell line that’s 'highly resistant to anticancer drugs,' showed increased 'cellular respiration inhibition,' whereas another conventional treatment option 'showed no such effect.' ”

While researchers have investigated a wide range of cancer treatments, “the utilization of THC and their derivatives is still unexplored pharmacologically owing to their ‘habit-forming’ nature,” the researchers concluded. “Specific targeting of cannabinoid receptors can be used to manage severe side effects during chemotherapy, palliative care and overall cancer management.”

“Furthermore, research evidences on cannabinoids have suggested tumor inhibiting and suppressing properties which warrant reconsidering legality of the substance,”
they said. “Studies on cannabinoid receptors, in case of cancers, have demonstrated the psychoactive constituents of cannabinoids to be potent against tumor growth.”

"Because the activation of CB1 and CBD2 cannabinoid receptors tends to limit human cancer cell growth, there may be a role of the endocannabinoid system as a novel target for treatment of cancers, and further explorations are required to exploit cannabinoids for an effective cancer management.”


The findings reflect another recent study that also explored the therapeutic potential of cannabis extracts in the treatment of different cancers. Like this new review, it demonstrated that while variation in cannabinoids that are used to treat distinct cancer cell lines is an important consideration, the growing data on marijuana’s ability to inhibit cell growth and kill cancer cells indicates that it should be a major area of research going forward.

*From the article here:

 
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Kambo and cancer

Kambo, the poison of the giant leaf frog 'Phyllomedusa bicolor,' is excreted through its skin. The secretion, long used by indigenous tribes in traditional rituals, is administered by applying it onto freshly inflicted burn wounds. Kambo is said to generate an altered state of reality, clear inner sight and a resurgence of long forgotten memories.

Years of research conducted at the University of Paris have shown Kambo to be very effective at killing certain types of cancer cells. Research at Queens University in Belfast recently won a prestigious award for their ground breaking work with cancer and Kambo.

Within Kambo exist the peptides Dermaseptin B2 and B3, which have the ability to cease and inhibit tumorous growths. Dermaseptin B2 has been shown to inhibit cancer cell (human prostatic adenocarcinoma) growth by more than 90%. This peptide penetrates cells and works by necrosis (active destruction), not apoptosis (normal or programmed cell death).

Kambo is one of the strongest, anti-inflammatory, antibiotic, antimicrobial and anesthetic substances on the planet. It is being studied for its effects on various types of cancer and for use in antibiotic resistant strains of bacteria.

http://www.kamboalchemy.com/medical-research-on-kambo/
 
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Ayahuasca – a natural medicine for brain disease and cancer

by Daniel Gustafsson

Natural substances extracted from the ayahuasca plants have been found to possess unique restorative and strongly antioxidative properties on specific nerve cells in the brain and central nervous system – controlling neurotransmission, muscle/motor activity, memory and coordination. This gives probable cause to the theory that ayahuasca could be an effective treatment for neurodegenerative diseases such as ALS, Alzheimer’s, and Parkinson’s disease. Promising results as of date has also been obtained from studying the substance psilocybin, very closely related to the substances found in ayahuasca, naturally occuring in certain species of medicinal mushrooms consumed by the indigenous people where ayahuasca is also used.

According to Dr. Juan Ramos, head of the neurological disease department at the South Florida university, USA, initial studies show that these substances stimulate the development of new cells in the areas of the brain controlling the above mentioned functions. If this could prove to be an eventual cure through complete restoration of damaged or destroyed cells remains to be seen, but initial results indicate this could potentially be the case. There is also a growing interest in exploring the cell regenerative properties of these plants within the spinal chord injury support communities. Should people with this background eventually try and find the results of this treatment useful, medical science would be bound to take note. Cancer researchers have also shown interest in B. Caapi, as its different alkaloids has shown to be effective against the growth of cancer cells.

Summary

Ayahuasca could effectively be used in treatment of ALS and other motor neuron diseases based on the fact that studies suggest uniquely antioxidative effects that seem to protect brain/nerve cells, targeting motor neurons through a unique biochemical transport system, and that it and other molecularly similar substances, also naturally occurring, stimulate neurogenesis – the development of new brain/nerve cells, and the communicative capacity between these. In studies it has been found to reduce symptoms in Parkinson’s patients – all neurodegenerative diseases share common ground, thus making it likely that something that improves a given neurological condition could also be beneficial to other conditions nearly related. Also based on credible personal accounts from people having used ayahuasca for symptom relief from their multiple sclerosis (once again – the common ground of neurodegenerative diseases), documented in books about ayahuasca, and from descriptions of early stage minor improvement by those with various types of ALS now participating in the treatment project, already having used this medicine for a period of time. Studies also indicate ability to normalize metabolism in mitochondria, crucial to motor neuron survival, and to regulate and decrease levels of excitotoxicity in the central nervous system.

https://www.wakingtimes.com/2014/12/29/ayahuasca-natural-medicine-brain-disease-cancer-wellness/
 
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Harmine found to suppress the proliferation of ovarian cancer cells

Jun Gao, Hong Zhu, Hong Wan, Xia Zou, Xiaoxin Ma, Guolan Gao

Harmine occurs in the psychedelic plants P. harmala and B. caapi (Ayuhuasca). P. harmala and B. caapi are both traditionally used for their psychoactive effects. Isolated from the plant Peganum harmala, harmine has already been shown to strongly inhibit the growth of cancer cells originating from breast, lung, bone and pancreas.

Ovarian cancer is the most lethal gynaecological cancer among Western women. In recent studies Harmine displayed obvious anticancer effects in several cancer cell types. In the present study, the effect of harmine on the cell proliferation and migration of ovarian cancer SKOV-3 cells and the underlying mechanism were investigated. Results indicate that Harmine significantly suppressed the proliferation of SKOV-3 cells in a dose-dependent manner. Interestingly, it also inhibited the epidermal growth factor (EGF)-induced proliferation of SKOV-3 cells. Moreover, the migration of SKOV-3 cells was markedly inhibited by Harmine treatment. Finally, Harmine significantly suppressed the expression of vascular endothelial growth factor (VEGF) and matrix metalloproteinase (MMP) family MMP-2, and MMP-9. In conclusion, our data revealed that Harmine inhibited the proliferation and migration of SKOV-3 cells, which might be mediated by ERK/CREB pathway. These findings elucidate that Harmine may act as a potential therapeutic drug for ovarian cancer treatment.

https://www.ncbi.nlm.nih.gov/pubmed/28901502
 
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The new non-invasive cervical pre-cancer test that's easily done at home*

Medical Xpress | Nov 4 2019

Researchers have developed a non-invasive test to detect cervical pre-cancer by analysing urine and vaginal samples collected by the women themselves.

In a presentation at the 2019 NCRI Cancer Conference today (Monday), Dr. Belinda Nedjai said that self-sampling test had proved popular with women taking part in the study and this meant that it was likely to improve participation in cervical cancer screening programmes.

"The initial use of self-sampling is likely to be for women who do not attend clinic after a screening invitation and countries without a cervical cancer screening programme. In the longer term, self-sampling could become the standard method for all screening tests. The study indicated that women much preferred doing a test at home than attending a doctor's surgery," said Dr. Nedjai, who is Senior Research Fellow and Director of the Molecular Epidemiology Lab at Queen Mary University of London, UK.

"To the best of our knowledge, this study is the largest to test a methylation classifier, called S5, in urine and self-collected cervical samples to detect pre-cancer lesions in women who have been referred for further investigation. We expect the self-sampling test to improve acceptance rates for cervical cancer screening, as well as reducing costs to health services and improving the performance of screening programmes."

The current gold-standard pap smear test is taken in the clinic and often follows a positive test for the human papilloma virus (HPV).

Dr. Nedjai said: "HPV testing is rapidly becoming the primary screening method for cervical cancer worldwide. It is a very sensitive method, very good at detecting true positives, but lacks specificity—in other words, a second test is needed to exclude HPV positive women that are not at increased risk of developing cancer. The choice of an appropriate strategy for high-risk HPV positive women is a key issue."

The S5 test developed by Dr. Nedjai and her colleagues at Queen Mary, measures DNA methylation—a chemical change to one of the four DNA base letters that make up the human genetic code. S5 looks at DNA methylation of four HPV types most strongly associated with cancer to produce a score that indicates the level of risk. If the score is above a selected cut-off it indicates an increased risk of a pre-cancer lesion, and the higher the score the higher the risk of cancer. They had discovered in earlier research that when S5 was used on cervical samples, it was 100% accurate at detecting invasive cervical cancer, and 93% accurate at detecting pre-cancer in women who had an HPV positive test.

Cervical cancer is preceded by the abnormal growth of precursor cells on the surface of the cervix—so called cervical intraepithelial neoplasia (CIN) or pre-cancer—that can develop into cervical cancer. It is divided into three stages (CIN1, CIN2 and CIN3), with the likelihood of the cells developing into cancer increasing at each stage.

"We decided to assess whether S5 could identify women who had CIN3 pre-cancer lesions using urine and vaginal samples," said Dr. Nedjai.

Women attending the colposcopy clinic at the Royal London Hospital as a consequence of an abnormal smear test or positive HPV result were asked to take part in a study led by Professor Jack Cuzick, Director of the Wolfson Institute of Preventive Medicine at Queen Mary. A total of 620 women provided vaginal samples, collected themselves using vaginal swabs, and 503 of these women also provided a urine sample. The researchers extracted and analysed the DNA in the lab and generated S5 scores.

"We found that S5 classifier with or without HPV testing worked well in both urine and vaginal samples," said Dr. Nedjai. "It distinguished between women who had no pre-cancerous lesions and those who had CIN3 or higher lesions. We evaluated two distinct ways that S5 could be used. We first tested S5 as a secondary test on HPV positive women to limit the number of patients sent to colposcopy. In urine, S5 was better at correctly identifying women who did have pre-cancer lesions than testing for the presence of HPV16 or 18; 96% of true CIN3 were identified with S5 compared to 73% with an HPV16 or 18 test. Secondly, we evaluated S5 as a standalone test, without first doing HPV testing. We adjusted the cut-offs to identify at least 85% of true positives. Urine performed as well as self-collected vaginal samples."

"We are currently working on new markers to try to improve the accuracy of the classifier even further, but these findings represent an advance in cervical cancer screening, especially for women who do not attend the clinic, such as older women, or women who find the smear test too painful or who do not have access to a screening programme in their country. We think it's promising."


In the future, Dr. Nedjai said the samples could be collected at home for both HPV and methylation analysis without the need to go to the clinic.

Dr. Manuel Rodriguez-Justo is a consultant pathologist at University College London (UK) and a member of the NCRI's sub-committee on early detection and prevention. He was not involved with the research. He commented: "This is exciting research that shows it's possible to detect cervical pre-cancer that is at high risk of developing into invasive cancer in urine and vaginal samples collected by women in the comfort and privacy of their own homes. This has the potential to revolutionise the way a positive HPV test is followed up, as well as making it easier for women in countries with no cervical cancer screening programme to be tested."

"The cervical screening programme in the UK has been very successful but there has been also a decline in its uptake, particularly in some areas in the UK and specific ethnic groups. If the results of this study are validated by other groups, the implementation of urine-based testing and self-sampled vaginal samples will, potentially, increase uptake and reduce costs for the screening programmes whilst achieving high sensitivity to detect pre-malignant lesions."


Cervical cancer is the fourth most frequently occurring cancer in women in the world. In 2018, there were an estimated 570,000 new cases of cervical cancer and 310,000 women died from the disease. Infection with HPV is almost the main cause of cervical cancer. More than 25 different types of HPV are transmitted through sexual contact and 12 of them carry a high risk of triggering the development of cancer cells by inactivating tumour suppressor proteins

*From the article here:

 
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CBD + chemotherapy triples cancer survival in mice

by David DiSalvo | Forbes

Mice with pancreatic cancer treated with a combination of cannabidiol (CBD) and chemotherapy survived nearly three times longer than those treated with chemotherapy alone, according to a new study that spotlights the potential for human treatment.

CBD, the non-psychoactive (non-intoxicating) compound in marijuana, has already been shown to improve side effects of chemotherapy like nausea and vomiting. The latest results provide more justification for testing in humans, building on prior animal research that uncovered possible anti-cancer properties of the compound.

"Cannabidiol is already approved for use in clinics in the UK, which means we can quickly go on to test this in human clinical trials," said lead researcher Marco Falasca from Queen Mary University of London.

While human trials involving CBD as a cancer treatment may move faster in the UK, similar efforts could face obstacles in the U.S., where CBD derived from marijuana is still considered an illegal substance under federal law. Progress is being made, however, with the US FDA approving the first drug comprised of CBD to treat severe forms of epilepsy.

Pancreatic cancer is among the deadliest forms of cancer in the world in terms of overall survival rates. According to the American Cancer Society, for all stages of pancreatic cancer combined, the one-year relative survival rate is 20%, and the five-year rate is just under 7%. It's the 12th most common cancer globally, with the highest incidence occuring in developed countries.

"The life expectancy for pancreatic cancer patients has barely changed in the last 40 years because there are very few, and mostly only palliative care, treatments available," Dr. Falasca added in a press statement. "Given the five-year survival rate for people with pancreatic cancer is less than seven percent, the discovery of new treatments and therapeutic strategies is urgently needed."

While this study hasn't yet been replicated in humans, the results underscore the importance of continued research involving marijuana compounds. As we've seen since the legalization movement started its push forward, studies have linked the compounds to multiple promising results, from easing migraine symptoms to improving stroke recovery to decreasing seizure severity, among others.

The more we learn about the potential of these compounds, the more it seems clear that decades of research being blocked by federal law deprived us of medical advances that are only now starting to surface.

https://www.forbes.com/sites/daviddi.../#502ba1c24630
 
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