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- #641
SweetSue's Class Notes
- Thread starter SweetSue
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- #642
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- #643
The importance of having a Gram stain done before they start you on antibiotics, which will mess up your gut and make everything else be compromised when you’re doing your best to heal. 
Knowing what I do now about the importance of gut health it chills me to recall all the times a doctor took the culture and said, “Start the antibiotics while we wait for the culture to come back.” *shudder*
Knowing what I do now about the importance of gut health it chills me to recall all the times a doctor took the culture and said, “Start the antibiotics while we wait for the culture to come back.” *shudder*
Brian420pm
Well-Known Member
@SweetSue , I started a thread in the "Cannabis Oil" forum about homogenizing CCO. I saw some posts here about nano emulsion and you mention you know of "someone" experimenting with it? Would love more chat about the subject, here or over there. I can't find a private message feature, or I would ask you if OK to put a link to my thread here?
Thank you!
Thank you!
overlord
Well-Known Member
For the PM feature, it is called "conversation" now.
Find your "inbox", then "start conversation"
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- #646
Thanks M’lord.
@Brian420pm, your link would be seen by more members and guests in the study hall I’d think. This thread is a dumping ground for research materials. Feel free to drop a link there.
- Thread starter
- #647
Project CBD has a new article on treating cancer, THC vs Breast Cancer highlighting a recent published study by Dr. Christina Sanchez. In the article I found this delicious tidbit shedding a bright light on dimers. 
As with hormone-sensitive breast cancer, THC’s antitumoral effect in HER2-positive breast cancer experiments was shown to be mediated by the CB2 cannabinoid receptor. Published in the Proceedings of the National Academy of Science, a subsequent report by Cristina Sanchez and other Spanish scientists noted that HER2 and CB2receptors are often found in the same exact place on cells.
CB2 actually conjoins with HER2 – forming what is called a dimer – and this dimerization is associated with poor treatment outcome for breast cancer. The PNAS report shed new light on THC’s anticancer mechanism of action: When THC binds to the CB2 receptor, it breaks up the CB2-HER2 dimer, triggering a chain reaction of signals that culminates in tumor regression.
Fascinating!
When THC binds to the CB2 receptor, it breaks up the CB2-HER2 dimer, triggering a chain reaction of signals that culminates in tumor regression.
I’ll see if I can access the published report. The puzzle pieces fall into place.
As with hormone-sensitive breast cancer, THC’s antitumoral effect in HER2-positive breast cancer experiments was shown to be mediated by the CB2 cannabinoid receptor. Published in the Proceedings of the National Academy of Science, a subsequent report by Cristina Sanchez and other Spanish scientists noted that HER2 and CB2receptors are often found in the same exact place on cells.
CB2 actually conjoins with HER2 – forming what is called a dimer – and this dimerization is associated with poor treatment outcome for breast cancer. The PNAS report shed new light on THC’s anticancer mechanism of action: When THC binds to the CB2 receptor, it breaks up the CB2-HER2 dimer, triggering a chain reaction of signals that culminates in tumor regression.
Fascinating!
When THC binds to the CB2 receptor, it breaks up the CB2-HER2 dimer, triggering a chain reaction of signals that culminates in tumor regression.
I’ll see if I can access the published report. The puzzle pieces fall into place.
- Thread starter
- #648
Link
Appraising the "Entourage Effect": Antitumor Action of a Pure Cannabinoid Versus a Botanical Drug Preparation in Preclinical Models of Breast Cancer
Sandra Blasco-Benito et al. Biochem Pharmacol. Nov 2018
Abstract
Breast cancer is the second leading cause of death among women. Although early diagnosis and development of new treatments have improved their prognosis, many patients present innate or acquired resistance to current therapies. New therapeutic approaches are therefore warranted for the management of this disease.
Extensive preclinical research has demonstrated that cannabinoids, the active ingredients of Cannabis sativa, trigger antitumor responses in different models of cancer.
Most of these studies have been conducted with pure compounds, mainly Δ9-tetrahydrocannabinol (THC). The cannabis plant, however, produces hundreds of other compounds with their own therapeutic potential and the capability to induce synergic responses when combined, the so-called "entourage effect".
Here, we compared the antitumor efficacy of pure THC with that of a botanical drug preparation (BDP). The BDP was more potent than pure THC in producing antitumor responses in cell culture and animal models of ER+/PR+, HER2+ and triple-negative breast cancer.
***This increased potency was not due to the presence of the 5 most abundant terpenes in the preparation.*** While pure THC acted by activating cannabinoid CB2receptors and generating reactive oxygen species, the BDP modulated different targets and mechanisms of action.
The combination of cannabinoids with estrogen receptor- or HER2-targeted therapies (tamoxifen and lapatinib, respectively) or with cisplatin, produced additive antiproliferative responses in cell cultures.
Combinations of these treatments in vivo showed no interactions, either positive or negative.
Together, our results suggest that standardized cannabis drug preparations, rather than pure cannabinoids, could be considered as part of the therapeutic armamentarium to manage breast cancer.
Appraising the "Entourage Effect": Antitumor Action of a Pure Cannabinoid Versus a Botanical Drug Preparation in Preclinical Models of Breast Cancer
Sandra Blasco-Benito et al. Biochem Pharmacol. Nov 2018
Abstract
Breast cancer is the second leading cause of death among women. Although early diagnosis and development of new treatments have improved their prognosis, many patients present innate or acquired resistance to current therapies. New therapeutic approaches are therefore warranted for the management of this disease.
Extensive preclinical research has demonstrated that cannabinoids, the active ingredients of Cannabis sativa, trigger antitumor responses in different models of cancer.
Most of these studies have been conducted with pure compounds, mainly Δ9-tetrahydrocannabinol (THC). The cannabis plant, however, produces hundreds of other compounds with their own therapeutic potential and the capability to induce synergic responses when combined, the so-called "entourage effect".
Here, we compared the antitumor efficacy of pure THC with that of a botanical drug preparation (BDP). The BDP was more potent than pure THC in producing antitumor responses in cell culture and animal models of ER+/PR+, HER2+ and triple-negative breast cancer.
***This increased potency was not due to the presence of the 5 most abundant terpenes in the preparation.*** While pure THC acted by activating cannabinoid CB2receptors and generating reactive oxygen species, the BDP modulated different targets and mechanisms of action.
The combination of cannabinoids with estrogen receptor- or HER2-targeted therapies (tamoxifen and lapatinib, respectively) or with cisplatin, produced additive antiproliferative responses in cell cultures.
Combinations of these treatments in vivo showed no interactions, either positive or negative.
Together, our results suggest that standardized cannabis drug preparations, rather than pure cannabinoids, could be considered as part of the therapeutic armamentarium to manage breast cancer.
- Thread starter
- #649
Eric Geisterfer has updated his list.
Updated 2/17/2019
People who beat cancer using cannabis oil ONLY
Updated 2/17/2019
People who beat cancer using cannabis oil ONLY
Derbybud
Well-Known Member
That's a big list of known people.
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- #651
Derbybud
Well-Known Member
I can read and watch those videos all night. Amazing.
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- #653
I know what you mean.
I can’t seem to stop. Lol! I’m researching prostate cancer for a member. The rabbit holes are difficult to pass by.
The role of cannabinoids in prostate cancer: Basic science perspective and potential clinical applications
Indian Journal of Urology: IJU: Journal of the Urological Society of India 28 (1), 9, 2012
Prostate cancer cells possess increased expression of both cannabinoid 1 and 2 receptors, and stimulation of these results in decrease in cell viability, increased apoptosis, and decreased androgen receptor expression and prostate-specific antigen excretion.
When they say "cannabinoids" are they speaking of THC? I thought that CBD doesn't bind to either CB1 or CB2 receptors (or I'm misremembering).
- Thread starter
- #655
Link
ncbi.nlm.nih.gov
The role of cannabinoids in prostate cancer: Basic science perspective and potential clinical applications
Juan A Ramos, Fernando J Bianco
Indian Journal of Urology: IJU: Journal of the Urological Society of India 28 (1), 9, 2012
Prostate cancer is a global public health problem, and it is the most common cancer in American men and the second cause for cancer-related death.
Experimental evidence shows that prostate tissue possesses cannabinoid receptors and their stimulation results in anti-androgenic effects. To review currently relevant findings related to effects of cannabinoid receptors in prostate cancer.
PubMed search utilizing the terms “cannabis,”“cannabinoids,”“prostate cancer,” and “cancer pain management,” giving preference to most recent publications was done. Articles identified were screened for their relevance to the field of prostate cancer and interest to both urologist and pain specialists.
Prostate cancer cells possess increased expression of both cannabinoid 1 and 2 receptors, and stimulation of these results in decrease in cell viability, increased apoptosis, and decreased androgen receptor expression and prostate-specific antigen excretion. It would be of interest to conduct clinical studies utilizing cannabinoids for patients with metastatic prostate cancer, taking advantage not only of its beneficial effects on prostate cancer but also of their analgesic properties for bone metastatic cancer pain.
Cannabinoid receptor as a novel target for the treatment of prostate cancer
Sami Sarfaraz, Farrukh Afaq, Vaqar M Adhami, Hasan Mukhtar
Cancer research 65 (5), 1635-1641, 2005
Cannabinoids, the active components of Cannabis sativa Linnaeus (marijuana) and their derivatives have received renewed interest in recent years due to their diverse pharmacologic activities such as cell growth inhibition, anti-inflammatory effects and tumor regression. Here we show that expression levels of both cannabinoid receptors, CB1 and CB2, are significantly higher in CA-human papillomavirus-10 (virally transformed cells derived from adenocarcinoma of human prostate tissue), and other human prostate cells LNCaP, DUI45, PC3, and CWR22Rν1 than in human prostate epithelial and PZ-HPV-7 (virally transformed cells derived from normal human prostate tissue) cells.
WIN-55,212-2 (mixed CB1/CB2agonist) treatment with androgen-responsive LNCaP cells resulted in a dose- (1-10 μmol/L) and time-dependent (24-48 hours) inhibition of cell growth, blocking of CB1 and CB2 receptors by their antagonists SR141716 (CB1) and SR144528 (CB2) significantly prevented this effect.
Extending this observation, we found that
ncbi.nlm.nih.gov
The role of cannabinoids in prostate cancer: Basic science perspective and potential clinical applications
Juan A Ramos, Fernando J Bianco
Indian Journal of Urology: IJU: Journal of the Urological Society of India 28 (1), 9, 2012
Prostate cancer is a global public health problem, and it is the most common cancer in American men and the second cause for cancer-related death.
Experimental evidence shows that prostate tissue possesses cannabinoid receptors and their stimulation results in anti-androgenic effects. To review currently relevant findings related to effects of cannabinoid receptors in prostate cancer.
PubMed search utilizing the terms “cannabis,”“cannabinoids,”“prostate cancer,” and “cancer pain management,” giving preference to most recent publications was done. Articles identified were screened for their relevance to the field of prostate cancer and interest to both urologist and pain specialists.
Prostate cancer cells possess increased expression of both cannabinoid 1 and 2 receptors, and stimulation of these results in decrease in cell viability, increased apoptosis, and decreased androgen receptor expression and prostate-specific antigen excretion. It would be of interest to conduct clinical studies utilizing cannabinoids for patients with metastatic prostate cancer, taking advantage not only of its beneficial effects on prostate cancer but also of their analgesic properties for bone metastatic cancer pain.
Cannabinoid receptor as a novel target for the treatment of prostate cancer
Sami Sarfaraz, Farrukh Afaq, Vaqar M Adhami, Hasan Mukhtar
Cancer research 65 (5), 1635-1641, 2005
Cannabinoids, the active components of Cannabis sativa Linnaeus (marijuana) and their derivatives have received renewed interest in recent years due to their diverse pharmacologic activities such as cell growth inhibition, anti-inflammatory effects and tumor regression. Here we show that expression levels of both cannabinoid receptors, CB1 and CB2, are significantly higher in CA-human papillomavirus-10 (virally transformed cells derived from adenocarcinoma of human prostate tissue), and other human prostate cells LNCaP, DUI45, PC3, and CWR22Rν1 than in human prostate epithelial and PZ-HPV-7 (virally transformed cells derived from normal human prostate tissue) cells.
WIN-55,212-2 (mixed CB1/CB2agonist) treatment with androgen-responsive LNCaP cells resulted in a dose- (1-10 μmol/L) and time-dependent (24-48 hours) inhibition of cell growth, blocking of CB1 and CB2 receptors by their antagonists SR141716 (CB1) and SR144528 (CB2) significantly prevented this effect.
Extending this observation, we found that
(a) WIN-55,212-2 treatment with LNCaP resulted in a dose- (1-10 μmol/L) and time-dependent (24-72 hours) induction of apoptosis
(b) decrease in protein and mRNA expression of androgen receptor
(c) decrease in intracellular protein and mRNA expression of prostate-specific antigen
(d) decrease in secreted prostate-specific antigen levels
(e) and decrease in protein expression of proliferation cell nuclear antigen and vascular endothelial growth factor
Our results suggest that WIN-55,212-2 or other non–habit-forming cannabinoid receptor agonists could be developed as novel therapeutic agents for the treatment of prostate cancer.
- Thread starter
- #656
IMO, that would have to be the case. CBD doesn’t directly activate any eCB receptors. It works through allosteric receptors.
I’m trying to figure out why I’m finding leads to using a CBD-rich medicine to treat prostate cancer.
I also want to dig out the list of mushrooms we had from K that will load the body up with anti-cancer metabolites. That info in in my notes back home. I know it’s here too, probably in Cajun’s thread.
I’m starting to see double,
a sure sign that I need to go back to being on vacation for a while. Lol!- Thread starter
- #657
They did the PSA test and didn’t bother to wait to see results before surgery. The test came back 4.1, down over less than two months from 10. The oncology standard is to wait when the PSA is 4.0
At 12:30 Dennis begins to lay out his casual regimen with what I’m assuming was CCO.
In 6 months, following two cycles of oil treatment (I’m figuring he did a gram a day?) he came up with clear labs. The prostate cancer was completely gone.
Tennessee Tim
Well-Known Member
Awesome , the power of herbs and positive thinking! The "corporate Doctors have to be dragged to the trough before admitting their approaches are not the only way,and indeed, are not as desirable in patient tolerance or outcomes, too frequently! If we can just get that core of controlling mentality corporate/government people to fully open up their resources to explore the cannabis human ecology, many peoples lives may be saved from pain ,suffering and early death!
- Thread starter
- #659
As per the speaker, individuals who want to avoid intermittent fasting:
* Brittle diabetics who can’t control their blood sugar
* Over 70
* Child or adolescent
* History of eating disorder of any kind (this can evoke that behavior)
* Pregnant
* Chronic heart issues
* Kidney disease
* Low body mass index
* Frail
* Recently hospitalized
It matters more when you eat than what you eat. Having said that, there are foods that’ll fuel you more efficiently than others.
Focus on real, whole foods, high in protein and complex carbohydrates.
- pasture-fed meat
- wild caught fish
- organic at every opportunity
- healthy fats (avocado, butter from grass-fed animals, nuts, coconut oil, fish oil omegas)
- complex carbs as much as possible. Instead of bread and pasta, substitute things like low glycemic berries, green, leafy vegetables, squash, quinoa, sweet potatoes.....
Limit sugar and alcohol. They can offset all the good you’re doing if you allow yourself to believe that
Stay well-hydrated. Plain coffee or tea in the fasting window. Green tea.... I can drink that plain.
She starts her patients on 12/12, increasing the fasting time by one hour a day until you’re up to a 16-hr fast.
I recall the study done that demonstrated women doing much better on a 14-15 hr fast. It also showed that the greatest gains in letting weight go were on a 6 AM to 2 PM schedule. I may put this to the test when I get back and get my Callanetics schedule back on track. Don’t want to release that much weight without also doing something to pull the skin in.
Living alone gives me a prime opportunity to try that seemingly crazy schedule.
MagicJim gets up at 5 AM. I could too.
TheRedDragon assures me black coffee is acceptable. Stevia is permitted too, to sweeten. I can’t stomach coffee black, but I do love me some sweet coffee. No creamer until the window opens. Remember you have green tea Susan.
Give it a solid 30 days before abandoning the concept. It may take 6-8 weeks to begin to see the full benefits of what you’re doing with IF.
If you have serious health concerns, speak to your medical support team before starting the fasting program.
This process is free, flexible, and simple to execute at home.
Drink a TON of water when you IF, this is a key piece that a lot of people miss. Magnesium is also a great supplement to get on which won’t break the fast. Mixing sea salt in water and drinking that while IF can also do a lot for your cells and opening them up so you get a deep flush with the water you drink. HUGE FAN of IF.
As per the speaker, individuals who want to avoid intermittent fasting:
* Brittle diabetics who can’t control their blood sugar
* Over 70
* Child or adolescent
* History of eating disorder of any kind (this can evoke that behavior)
* Pregnant
* Chronic heart issues
* Kidney disease
* Low body mass index
* Frail
* Recently hospitalized
It matters more when you eat than what you eat. Having said that, there are foods that’ll fuel you more efficiently than others.
Focus on real, whole foods, high in protein and complex carbohydrates.
- pasture-fed meat
- wild caught fish
- organic at every opportunity
- healthy fats (avocado, butter from grass-fed animals, nuts, coconut oil, fish oil omegas)
- complex carbs as much as possible. Instead of bread and pasta, substitute things like low glycemic berries, green, leafy vegetables, squash, quinoa, sweet potatoes.....
Limit sugar and alcohol. They can offset all the good you’re doing if you allow yourself to believe that
Stay well-hydrated. Plain coffee or tea in the fasting window. Green tea.... I can drink that plain.
She starts her patients on 12/12, increasing the fasting time by one hour a day until you’re up to a 16-hr fast.
I recall the study done that demonstrated women doing much better on a 14-15 hr fast. It also showed that the greatest gains in letting weight go were on a 6 AM to 2 PM schedule. I may put this to the test when I get back and get my Callanetics schedule back on track. Don’t want to release that much weight without also doing something to pull the skin in.
Living alone gives me a prime opportunity to try that seemingly crazy schedule.
MagicJim gets up at 5 AM. I could too.
TheRedDragon assures me black coffee is acceptable. Stevia is permitted too, to sweeten. I can’t stomach coffee black, but I do love me some sweet coffee. No creamer until the window opens. Remember you have green tea Susan.
Give it a solid 30 days before abandoning the concept. It may take 6-8 weeks to begin to see the full benefits of what you’re doing with IF.
If you have serious health concerns, speak to your medical support team before starting the fasting program.
This process is free, flexible, and simple to execute at home.
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