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MCT infused Cannabis oil is best for cancer


Cannabis oil, is cannabis oil, right? It offers great benefits for anyone suffering from cancer, but what you may not know is that we need to ensure that patients are accessing the best type of oil. This article describes the differences when Cannabis oil has been infused using MCT oil, as opposed to alcohol, as well as other facts around cannabis oil and cancer.

MCT Oil (medium chain triglyceride) is derived from coconuts. We all know that coconuts are really good for us. The humble coconut has gathered much fame for its health benefits over the last decade as an oil, a milk and a drink amongst others.

So it is no surprise that MCT oil made from coconuts has some magical qualities.

When you consume (eat or drink it), the MCT’s are easily digested and head straight for your liver.

MCT molecules are smaller than those in most of the fats you eat (long-chain triglycerides [LCT]) which makes them easier to digest. So the great news is that with MCT oil, you can absorb this in your bloodstream quicker than with an oil that has been infused using alcohol.

Should you have problems accessing this product, feel free to email us here

The many benefits of MCT oil

MCT oil has many health benefits. One of it’s stand out features are that it is really good for your brain and can help your body make ketones which is an energy source for your brain that doesn’t have any carbohydrates. If you have a cognitive disorder, then adding some MCT oil to your diet will help you recover cognitive abilities and can also restore memory.

Research indicates that MCT oil also helps with pain, inflammation, sleep, relaxation, arthritis and more.

The science behind MCT oil is relatively simple, but also incredibly effective. MCTs go directly from the digestive system to the bloodstream, without being digested first. This also makes MCT oil ideal for people with digestive disorders.

In our experience, this quick delivery directly into the blood stream means that the cannabis infused MCT oil effects are quicker than other fat based infusions.

Whilst butter and coconut oil do contain a certain amount of MCT’s, it is best to choose an oil that is pure in MCT fatty acids and so in this concentrated form is a higher “energy oil” than butter, or coconut oil.

We also use a full spectrum MCT oil derived from organic coconuts that is solvent free and cold pressed.

It’s also great for making stronger blends, due to the fact it is easily diluted.

The problem with alcohol infused cannabis oils

The problem we found with the dark sticky alcohol extraction was always the solvents.

What is the problem with solvents?

Residual solvents can be harmful to the body. Here is the complete list of solvents and limits that we are aware of.

All of which can be avoided with an MCT infusion:



Limit (parts per million)

Acetic acid

Cannabis oil



Cannabis oil



Cannabis oil



Cannabis oil



Cannabis oil



Butane (sum of n- and iso-)

Cannabis oil


Butyl acetate

Cannabis oil


Tert-Butylmethyl ether

Cannabis oil


Carbon dioxide

Cannabis oil

No limit

Dimethyl sulfoxide

Cannabis oil



Cannabis oil


Ethyl acetate

Cannabis oil


Ethyl ether

Cannabis oil


Ethyl formate

Cannabis oil


Formic acid

Cannabis oil



Cannabis oil


Isobutyl acetate

Cannabis oil


Isopropyl acetate

Cannabis oil


Methyl acetate

Cannabis oil



Cannabis oil


Methylethyl ketone

Cannabis oil



Cannabis oil



Cannabis oil

No limit


Cannabis oil



Cannabis oil



Cannabis oil



Cannabis oil



Cannabis oil


Propyl acetate

Cannabis oil



Cannabis oil



Cannabis oil

No limit


Have in mind that the MCT infused oil is much thinner, which does not make it weaker, The strength is the same as the alcohol extractions.

Note, it also has a pleasant taste.

We source oils that are doubly infused, which makes for a higher quality product.

M-Oil ranges

We recommend a product called M oil.

This comes in 12 strengths and types. For the purpose of this article we will only include the oils relevant to cancer.

It is important to ensure that patients with hormone receptive cancer receive no more than 5% THC per dosage. 

M oil no. 4  – Mainly used for depression, arthritis, Autism, joint pain, sleep issues and general health

Very low THC 4%, CBD, CBDV, CBG, CBC, CBN, THCV, Zatador, Vitadox and MCT oil

M oil no. 6 – used for many reasons to include reproductive organ cancers, Autism, pain and much more

low THC, THCV, CBDV, CBG, CBC, CBN, Zatador, MCT oil, Vitadox

M oil no. 8 – Used for Autism and many immune issues as well as many other immune related Illnesses.

Low THC, THCV, Higher CBDV, Higher CBD, CBG, CBC, CBN. Zatador and MCT oil and Vitadox.

M oil no. 10 –  This product is used for most forms of cancer, epilepsy, parkinsons, Cancers not affecting the reproductive organs and life threatening ailments.
Higher THC, THCV, Higher CBDV, Higher CBD, CBG, CBC, CBN. Zatador and Coconut oil.

M OIL no. 12 – Mainly used for Brain Tumors Skin cancers and cancers exteral:
High THC, THCV, Higher CBDV, Higher CBD, CBG, CBC, CBN. Zatador and Vitadox.

Brain cancers:  High THC, CBDV, CBG, CBC, CBN

M oil  no. 9 – All cancer except the above: medium THC, CBD

Please see here for example, for a full range of M-oils

You may consider rectal application for certain types of cancer requiring high THC.

One way to allow the absorption of cannabis oil is through the medicinal patch in the rectum.
The reason that rectal administration is best for cannabis oils, is the rectal mucosa has a blood and lymph supply that is capable of effective systemic absorption.

The rectum is relatively underused in some societies as a route for safe administration of medicines, arguably due to the intimacy of the site compared with more socially accepted and visible routes, such as oral, topical, or intravenous.

In addition to being a viable option for patients who can’t ingest cannabis, the advantages to applying it rectally:

  • It starts to work quicker, at around 10–15 minutes, compared to orally where it might not be felt for 30–40 minutes, as it has to travel through the intestine and liver
  • It lasts for a longer period of time (4 to 8 hours)
  • It’s 50-70 percent more efficient, whilst digesting cannabis oil by mouth is only around 20 percent efficient and therefore has a “superior bio-availability”

Reduces side effects

As well as being a more effective route of delivery, rectal administration also reduces some side effects that the oral administration may induce such as gastric irritationnausea and vomiting (Tortora and Derrickson, 2008). Euphoric effect.

You will feel less of the THC effect than by mouth, which will have a greater impact on your day and improve your quality of life.

The rectum

The rectum constitutes the final 20cm or so of the terminal gastrointestinal tract; approximately 2-3cms of this is the anal canal. Absorption from within the anal canal is via its highly vascular mucous membrane that is divided into folds or pillars, known as anal columns (Tortora and Derrickson, 2008).

Once carefully inserted into the rectum and inserted far enough inside the medication (see this article for instructions) should not cause pain. The anal canal is divided into areas above and below the Pectinate line; the area below (distal) is sensitive to pain, touch and temperature, whereas the area above (proximal) is only sensitive to stretch.

The metabolism of THC

The speed as to which this can then be delivered is a marked advantage, for it is in the liver that the mystical THC to 11-Hydroxy-THC metabolism takes place.


11-OH-THC does not naturally exist in the cannabis plant, but is formed within the human body after THC has entered the body. The amount of 11-OH-THC formed in your body can vary wildly depending on whether you take cannabis as an edible (high levels), or smoke it (low levels) and for the very best results taken rectally.

Metabolism of THC to 11-OH-THC
Metabolism of THC to 11-OH-TH

After THC is ingested, your liver goes to work on it, converting it into other molecules in order to eliminate it from your body. These other molecules are called metabolites. Usually metabolites are less active than the parent molecule, but sometimes you get one that is even more potent!

The drug-metabolizing enzymes are present in your GI tract and these enzymes get to work quickly creating 11-OH-THC.

The second factor is that all blood flow from your GI tract goes to the liver first before entering the general circulation (a phenomenon called first pass metabolism). This is one more chance for 11-OH-THC to be created in high quantities.

However, after taking cannabis rectally, the average levels of 11-OH-THC vary from 25% of THC to more than 300% of THC levels, depending on which study you look at. These are just averages of a group of people – there is even further variation at the level of individuals. So some people will have well over 3 times more 11-OH-THC in their body than THC after absorbing cannabis rectally.

11-OH-THC also penetrates the blood brain barrier making it very effective for brain cancer.

The endocannabinoid system

Let us make something very clear for those patients who may see a taboo with cannabis. We’re all born with a form of cannabis in our bodies. It’s called the “endocannabinoid system”… Like it or not, each and every one of us is fundamentally wired to respond to cannabis.

 Ground breaking research in the 1990s discovered that we all contain 2 different vital Cannabinoid receptors (CB) that are essential to our mental and physical health. 

The simple view of the endocannabinoid system is that there are two receptors, CB1 and CB2. Some may mention rumors of a third.

The endocannabinoid system
The endocannabinoid system

A brief History of the Endocannabinoid System

In the dark ages of the mid-1980’s, many thought that THC worked by perturbing cell membranes. This was proved wrong in 1988, when we saw that cannabinoids could bind to specific receptor sites in the brains of rats.

In 1990, the human CB1 receptor was identified as the primary receptor that mediated the effects of THC.

Anandamide (AEA) was the first endocannabinoid discovered to activate the CB1 receptor, produced on demand by a set of enzymes.

This ground-breaking research was followed by the discoveries of a second cannabinoid receptor, mostly expressed in immune cells, and a second endocannabinoid,2-arachidonylglycerol (2-AG).

Undoubtedly, this decade of the mid-80’s to mid-90’s will remain one of the most important in the history of cannabinoid research.

However, for some reason, much of the research from the following decade is largely ignored by many.

For example, the list of endocannabinoids and endocannabinoid receptors has expanded. We now know that many effects of endocannabinoids are not mediated through either the CB1 or CB2 receptor.

Below, I will give an overview of the different receptors that are either part of the endocannabinoid system, or are part of a different signaling system, yet are still modulated by endocannabinoids.

Cannabinoid CB1 Receptor

The CB1 receptor is hands down the most famous of the endocannabinoid system. This receptor, like the next 4 that I describe, are part of a class of receptors called G protein-coupled receptors (GPCRs). These receptors sit within the cell membrane and upon activation, start a signaling cascade within the cell that leads to specific effects. The two most common endocannabinoids to activate CB1 are anandamide and 2-AG.

The highest levels of CB1 expression are in the central nervous system (CNS). In fact, there are more CB1 receptors in the brain than any other type of GPCR. However, despite descriptions as the “brain receptor” it is also found throughout the body in many different tissues: cardiovascular, reproductive, immune, gastrointestinal, and peripheral nerves to name a few important ones.

In 1999, the first mouse with a genetically-deleted CB1 receptor (i.e. a “CB1 knockout”) was reported. An excellent book chapter has reviewed the many functions of the CB1 receptor discovered through this approach.

Given the wide distribution of the CB1 receptor, it is not surprising that it seems to be involved in, well, just about everything. I can only give a high level summary, as any one of these points could be an entire article in itself:

  • Allergic and autoimmune inflammatory diseases
  • Osteoporosis (loss of bone mass)
  • Neurodegenerative diseases
  • Ischemic injury from stroke or heart attack
  • Chronic pain
  • Hepatic (liver) injury and disease
  • Alcohol and nicotine addiction
  • Weight gain
  • Stress responses

The CB2 receptor is located primarily in the periphery instead of the CNS. It is mainly expressed in immune cells, giving it an important role in inflammation. However, we now know that CB2 is expressed in a variety of cells, including those in the CNS, liver, and bone. CB1 is no longer considered to be the only cannabinoid receptor that affects memory and cognition.

The amino acid sequence of the CB2 receptor is relatively similar to the CB1 receptor. So not surprisingly, the CB2 receptor is activated by similar cannabinoids as the CB1 receptor, including anandamide and 2-AG.

Using mice with the genetically-deleted receptor, many functions of CB2 have been elucidated. Mice lacking CB2 had had more severe conditions in a variety of disease models:
Allergic and autoimmune inflammatory diseases
Osteoporosis (loss of bone mass)
Neurodegenerative diseases
Ischemic injury from stroke or heart attack
Chronic pain
Hepatic (liver) injury and disease
Alcohol and nicotine addiction
Weight gain

“Atypical” Cannabinoid Receptors

In most articles on the endocannabinoid system, the story stops there. However, let’s get to the exciting new research from the last two decades that is rarely talked about.
We have known for some time that the CB1and CB2 receptors do not mediate all the actions of cannabinoids. How could we know this? Mice with genetically-deleted CB1 and CB2 receptors were crossbred to create mice that had neither receptor. If no other receptors were activated by cannabinoids, then there should be no effect of THC or anandamide in these mice.
However, starting with the first report in 1999, we have observed many different effects of cannabinoids in these double knockout mice. For example, cannabinoids were still able to affect blood pressure, pain, inflammation, and gastric motility in the absence of CB1 and CB2 receptors.

At this point, the hunt was on to find new cannabinoid receptors! Since then, we have discovered that endocannabinoids bind to many receptors that were not considered part of the endocannabinoid system.


This receptor was discovered in 1997, but for several years it was an “orphan receptor”, meaning that they did not know what its ligand was. In 2006, a surprising discovery was made – this receptor could be activated by endocannabinoids!
GPR18 can be activated by anandamide, but it’s main endocannabinoid ligand appears to be N-arachidonyl glycine (NAGly), which is a metabolite of anandamide.
The GPR18 receptor is expressed highly in the spinal cord, small intestine, immune cells, spleen, bone marrow, thymus, lungs, testis and cerebellum.

GPR18 activation can lower blood pressure. It also has significant functions in immune cells. It acts as a powerful chemoattractant – meaning it induces migration of immune cells.

This receptor has a similar story to GPR18. It was an orphan receptor for many years until its ligands were discovered. GPR55 is activated by the endocannabinoids 2-AG and anandamide, but its main ligand appears to be another putative endocannabinoid called lysophosphatidylinositol (LPI).
This receptor is expressed at high levels in the central nervous system, as well as adrenal glands, gastrointestinal tract, lung, liver, uterus, bladder and kidneys. It’s wide tissue distribution gives it roles in a variety of body systems.

GPR55 activation causes hypotension (lowers blood pressure), is anti-inflammatory, and is in some cases anti-nociceptive (pain blocking). GPR55 regulates energy intake and expenditure, which could impact diseases such as obesity and diabetes. It is also expressed in bone cells with a possible role in osteoporosis. GPR55 is neuroprotective and decreased neurodegeneration in models of multiple sclerosis.


GPR119 expression is restricted to a limited number of tissues. It is primarily found in the pancreas and gastrointestinal tract – hinting that it’s role is the regulation of energy and metabolism.
GPR119 is activated primarily by the endocannabinoid OEA, with minimal activation by other endocannabinoids such as anandamide and 2-AG.
Activation reduces food intake, improves handling of blood sugar, and decreases body weight. These effects appear to be mediated through regulation of hormones such as insulin and GLP-1.

Vanilloid Receptors

Transient receptor potential vanilloid 1 (TRPV1) is an ion channel expressed both on sensory neurons and in the brain. In sensory nerves, TRPV1 acts a sensor for things that could potentially cause tissue damage. It is activated in response to heat and proinflammatory substances, sending a pain signal to the brain. The most famous activator of TRPV1 is capsaicin, the ingredient found in chili peppers that causes a burning pain. Dysregulation of TRPV1 is also involved in chronic pain.
Interestingly, anandamide is an activator of the TRPV1 channel. Sensory neurons often co-express both the CB1 receptor and the TRPV1 receptor, making the role of anandamide in generating pain signals unclear.

TRPV1 plays a very different role in the brain, where its activation by anandamide seems to reduce pain.

Serotonin Receptors

There are many different serotonin (5-HT) receptor subtypes that mediate the different effects of serotonin. The 5-HT3 subtype is unique among the 5-HT receptors since it is a ligand-gated ion channel instead of a GPCR.

The 5-HT3 receptor is most well-known for mediated nausea and vomiting, particularly after chemotherapy. Several anti-nausea drugs work by inhibiting this ion channel. It also has a role in neuropathic pain.
Anandamide can directly bind to the 5-HT3 receptor and inhibit its activation. However, it doesn’t work by blocking the main serotonin binding site on the receptor. Instead, it binds to a different site and acts as a negative allosteric modulator. In other words, it changes the conformation of the receptor to minimize activation by 5-HT.

This inhibition of 5-HT3 is at least partly responsible for the analgesic effects of cannabinoids that are not mediated through the traditional CB1 or CB2 receptors.

Glycine Receptors
Glycine receptors (GlyRs) are ligand-gated ion channels which inhibit nerve activation. GlyRs are expressed in spinal interneurons, where they regulate pain transmission to the brain.
Anandamide is capable of directly binding to GlyRs and increasing channel activation. Anandamide does not bind the main agonist site, nor can it activate GlyRs by itself. Like with 5-HT3 receptors, anandamide acts as an allosteric modulator. It binds a different site on the GlyR and enhances activation by glycine.

This is another mechanism, independent of the CB1 and CB2 receptors, that endocannabinoids may reduce pain by acting at the spinal level.

Peroxisome Proliferator-Activated Receptors

Peroxisome proliferator-activated receptors (PPARs) are fundamentally different than the receptors described above. Rather than sit within the cell membrane, PPARs reside within the cell and can directly bind to DNA sequences and change transcription of targeted genes. There are three isoforms of PPAR: α, β, and γ.
Anandamide and 2-AG are potentially able to activate PPARα, but activation is much stronger by the endocannabinoids OEA and PEA. Anandamide and 2-AG may also be able to activate PPARγ.

PPARs regulate cellular functions in almost every tissue. Some of the effects of endocannabinoids which may be at least partially attributed to either PPARα or PPARγ activation include neuroprotection against ischemia and neurodegeneration, reduced nicotine addiction, analgesia, anti-tumor effects, vasorelaxation, weight reduction, and reduced inflammation.

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We do hope that the above has been useful.

We do the research. You decide.

We do the research you decide,
Love and Light
The Healing Oracle Team
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