Mike, what kind of breast cancer (invasive ductal, I presume)? How many of her lymph nodes were positive? How big was the primary tumor? Reason I ask is that in women with Stage I or IIA tumors that are estrogen-and progesterone-receptor-positive and HER2-negative (ER+/PR+/HER2-) with three or fewer positive lymph nodes, there is a genomic assay test on a sample of the tumor, called OncotypeDX, that will tell doctors whether chemo is necessary or would even work at all. Medicare covers that test 100%.That type of breast cancer mentioned above, which I had as Stage IA, is treated in postmenopausal women with anti-estrogen drugs called aromatase inhibitors(aka AIs: anastrazole, letrozole, or exemestane)which have as a side effect joint pain. CBD oil is effective for this joint pain it is not, I repeat, NOT a substitute for chemo, radiation or these anti-estrogen drugs.So don’t assume your mom’s cancer will require chemo; but if it does, CBD helps with those side effects as well. If she lives in a state where medical marijuana is legal, there are doctors who sub-specialize in certifying applications for a medical marijuana card, and in the interim before the card is issued can advise as to the appropriate dose of CBD oil (legal and over-the-counter in all 50 states). Some (though not most) medical oncologists will certify their own patients’ medical marijuana card applications so she need not seek out another doctor; and will advise the appropriate dose for her symptoms. Once she gets her card, the “budtenders” in the licensed dispensaries can advise her as to the right CBD product (with or without THC), strength, and dosage. If she lives in a state where recreational weed is legal, the “budtenders” in the marijuana shops can steer her to the right strength of CBD oil and the right dosage.
Karl W. Hillig, a graduate student in the laboratory of long-time Cannabis researcher Paul G. Mahlberg at Indiana University, conducted a systematic investigation of genetic, morphological, and chemotaxonomic variation among 157 Cannabis accessions of known geographic origin, including fiber, drug, and feral populations. In 2004, Hillig and Mahlberg published a chemotaxonomic analysis of cannabinoid variation in their Cannabis germplasm collection. They used gas chromatography to determine cannabinoid content and to infer allele frequencies of the gene that controls CBD and THC production within the studied populations, and concluded that the patterns of cannabinoid variation support recognition of C. sativa and C. indica as separate species, but not C. ruderalis. The authors assigned fiber/seed landraces and feral populations from Europe, Central Asia, and Turkey to C. sativa. Narrow-leaflet and wide-leaflet drug accessions, southern and eastern Asian hemp accessions, and feral Himalayan populations were assigned to C. indica. In 2005, Hillig published a genetic analysis of the same set of accessions (this paper was the first in the series, but was delayed in publication), and proposed a three-species classification, recognizing C. sativa, C. indica, and (tentatively) C. ruderalis. In his doctoral dissertation published the same year, Hillig stated that principal components analysis of phenotypic (morphological) traits failed to differentiate the putative species, but that canonical variates analysis resulted in a high degree of discrimination of the putative species and infraspecific taxa. Another paper in the series on chemotaxonomic variation in the terpenoid content of the essential oil of Cannabis revealed that several wide-leaflet drug strains in the collection had relatively high levels of certain sesquiterpene alcohols, including guaiol and isomers of eudesmol, that set them apart from the other putative taxa. Hillig concluded that the patterns of genetic, morphological, and chemotaxonomic variation support recognition of C. sativa and C. indica as separate species. He also concluded there is little support to treat C. ruderalis as a separate species from C. sativa at this time, but more research on wild and weedy populations is needed because they were underrepresented in their collection.
No, as long as the plant is used correctly then no it’s not a bad thing. I’m sure there’s probably more good capability about that plant that people know or don’t know. No matter how it’s administered, as long as used properly it’s a good thing. It probably has more healing capabilities than people know about and since big Pharma or whoever it is out there discovered this, that’s probably why they made it illegal for all we know. Yes, I know there’s no money in cure which would hurt big Pharma but oh well! If they want to keep us away from the cure and keep us all sick, I say go for it anyway and go for the cure.
exhaustion and pain that kept her on the couch much of the day. The 58-year-old Seattle speech coach didn’t want to take opioid pain-killers, but Tylenol wasn’t helping enough. Roth was intrigued when women in her online chat group enthused about a cannabis-derived oil called cannabidiol (CBD) that they said relieved pain without making them high. So Roth, who hadn’t smoked weed since college but lived in a state where cannabis was legal, walked into a dispensary and bought a CBD tincture. “Within a few hours of placing the drops in my mouth, the malaise and achiness that had plagued me for weeks lifted and became much more manageable,” she says. She took the drops several times a day and in a few weeks was back to her regular life.
Liquid CBD Oil/Tinctures/Extracts: Drops or tinctures should have a “suggested serving size” and the total milligrams of CBD listed on their packaging. From there, you can determine the amount of CBD you would like to ingest. Simply place the correct quantity of drops under your tongue using the dropper and hold the CBD oil in place for a minimum of 60 seconds. The 60 second hold allows for absorption via the blood vessels underneath your tongue – efficiently bypassing first-pass metabolism. Once 60 seconds has passed, swallow the CBD oil.
In December 2013, Uruguay became the first country to legalize growing, sale and use of cannabis. After a long delay in implementing the retail component of the law, in 2017 sixteen pharmacies were authorized to sell cannabis commercially. On June 19, 2018, the Canadian Senate passed a bill and the Prime Minister announced the effective legalization date as October 17, 2018. Canada is the second nation to legalize the drug.
Former President Barack Obama defined industrial hemp as a distinct crop from marijuana in the 2014 U.S. Farm Bill, authorizing higher education institutions and state agricultural departments to give the green light to "regulate and conduct research and pilot programs." But with its classification as a Schedule 1 drug still in effect, the path toward cultivating industrial hemp hasn't been an easy one.
In 1972, the Dutch government divided drugs into more- and less-dangerous categories, with cannabis being in the lesser category. Accordingly, possession of 30 grams or less was made a misdemeanor. Cannabis has been available for recreational use in coffee shops since 1976. Cannabis products are only sold openly in certain local "coffeeshops" and possession of up to 5 grams for personal use is decriminalised, however: the police may still confiscate it, which often happens in car checks near the border. Other types of sales and transportation are not permitted, although the general approach toward cannabis was lenient even before official decriminalisation.
Synthetic cannabis is illegal in New Zealand. It is designed to imitate the effects of cannabis and is usually dried plant material sprayed with chemicals known as synthetic cannabinoids. It is also available in liquid form. Little is known about the chemicals used in synthetic cannabis and the effects can be unpredictable, especially when mixed with other substances.
μ-Opioid receptor agonists (opioids) (e.g., morphine, heroin, hydrocodone, oxycodone, opium, kratom) α2δ subunit-containing voltage-dependent calcium channels blockers (gabapentinoids) (e.g., gabapentin, pregabalin, phenibut) AMPA receptor antagonists (e.g., perampanel) CB1 receptor agonists (cannabinoids) (e.g., THC, cannabis) Dopamine receptor agonists (e.g., levodopa) Dopamine releasing agents (e.g., amphetamine, methamphetamine, MDMA, mephedrone) Dopamine reuptake inhibitors (e.g., cocaine, methylphenidate) GABAA receptor positive allosteric modulators (e.g., barbiturates, benzodiazepines, carbamates, ethanol (alcohol) (alcoholic drink), inhalants, nonbenzodiazepines, quinazolinones) GHB (sodium oxybate) and analogues Glucocorticoids (corticosteroids) (e.g., dexamethasone, prednisone) nACh receptor agonists (e.g., nicotine, tobacco, arecoline, areca nut) Nitric oxide prodrugs (e.g., alkyl nitrites (poppers)) NMDA receptor antagonists (e.g., DXM, ketamine, methoxetamine, nitrous oxide, phencyclidine, inhalants) Orexin receptor antagonists (e.g., suvorexant)