Recent scientific breakthrough:
Regulation of the body at the deepest level is now possible! Namely epigenetic, in other words, reversible heritable changes in gene function without altering the DNA in the cell nucleus. CBD and THC oil are not the long-term solution! THE ENDOCANNABINOÏDE SYSTEM (ECS)?= Endocannabinoids + cannabinoid receptors + enzymes. The endocannabinoid system is the "master regulator" in the body. "Endo" means "inside" and "cannabinoid" refers to any molecule that activates these receptors. All of our bodily systems are in a constant state of balance. Endocannabinoids help maintain this state when needed. The ECS plays a modulating role in the following systems:
- Central and peripheral nervous system
- Hormone System
- Immune System
- Metabolism
The six main features:
- Reducing cellular, oxidative, nitrosative, mitochondrial, chemical, mechanical, immunological, physiological, psychological and other forms of stress;
- Reducing chronic, inflammatory and acute pain;
- Ontstekingsremmend;
- Regulates the release and processing of traumatic experiences;
- Preventing and fighting cancer and neurodegenerative diseases;
- Social: promoting connection and reducing social anxiety and stress.
Pain and inflammation The endocannabinoid system (ECS) is central to fighting pain and inflammation. Most, if not all pain and inflammation inhibitors such as opioids, paracetamol, NSAIDs and aspirin, work through activating the ECS and the endorphin system. The ECS interacts with the endorphin system at a deeper level. So the endocannabinoid system consists of endocannabinoids, cannabinoid receptors and specific enzymes. A further explanation.
- Endocannabinoids
These are molecules produced by the body itself that activate endo cannabinoid receptors and bind to them. The two main endocannabinoids in the body are anandamide and 2-AG.
- Cannabinoid receptors
Receptors are a kind of antennae on cells on which molecules can hook up. Cannabinoid receptors play a fundamental role in the functioning of the ECS. They help pass messages of endocannabinoids between cells, as well as from outside the cell to the inside. The two main receptor types of the endocannabinoid system are called CB1 and CB2. These receptors are found on many cell types throughout the body. Various cannabinoids bind to, block or modulate the activity of these receptors. These include endocannabinoids, phytocannabinoids (found in plants) and synthetic cannabinoids (made in a lab such as medications). According to researchers, TRPV1 (transient receptor potential vanilloid one) is also part of the network. Namely, it serves as a receptor for CBD, THC and anandamide. CB1 regulates the release of dopamine via endorphin receptors (MOR) during rewards CB2 regulates the release of endorphins during inflammation and inflammatory pain
- Enzymes are substances that catalyze chemical reactions. The ECS contains enzymes that both build up and break down endocannabinoids. Fatty acid enzyme amidohydrolase (FAAH) is one of primary enzymes in the system. This breaks down anandamide
Anandamide Anandamide is a substance released in response to all kinds of stress. E.g. pain, stress from endurance sports, hyperglutamate, cellular stress, injury and stress hormones. Anandamide activates reward via endorphins and dopamine. The reward effect of anandamide is more intense than dopamine. The nine main functions of Anandamide are:
- Antidepressant: along with BDNF, it is a strong feel-good substance;
- Activates anti-cancer genes;
- The strongest pain inhibitor (stronger than endorphins and enkephalins) via inhibiting the synaptic activity of glutamate and other pain mediators;
- Along with 2-AG the strongest glutamate inhibitor (very strong neurotransmitter that acts strongly on other nerve cells);
- Anandamide reduces anxiety and social stress;
- Has an anti-inflammatory effect;
- Restores Th1/Th2 balance (immune system); It reduces Th2 dominance = anti-allergic effect. It additionally acts as an antihistamine just like kaempferol, -an FAAH inhibitor- which inhibits the release of histamine from mast cells and has a beneficial effect in the treatment of lgE mediated conditions such as asthma, hay fever and other allergic respiratory diseases;
- Stimuleert de aanmaak van melanine. Melanine is tot 34 keer sterker dan EDTA om zware metalen te ontgiften. Cannabis (THC) vermindert (!) melanine met 75%;
- (not actually a function but an obvious relationship) Estrogen connection: estrogen stimulates the release of anandamide.A deficiency or malfunctioning endocannabinoid molecule anandamide in relation to disease:
Anandamide Pathology
- Anandamide is decreased in ADD/ADHD, autism high sensitivity, depression, PTSD and most disorders and complaints with chronic hyperglutamate;
- Anandamide dysfunctions cause anxiety, dejection, social stress and stress hypersensitivity;
- Trauma causes impaired functioning of anandamide via epigenetic dysfunctions of the FAAH gene and the anandamide gene, making one hypersensitive to stimuli and stress. In a study of people with PTSD, FAAH inhibitors have a beneficial effect in reducing fear conditioning and anxiety;
- SNPs (single-nucleotide polymorphism: variation in DNA) are a major cause of anandamide dysfunctions;
- Dysfunctions of anandamide can lead to short- and long-term memory problems.
- Connection to insulin; Overstimulation causes hyperinsulinemia (too much insulin production), insulin resistance, a chronic feeling of hunger, and inhibits GLUT4, an insulin-regulated glucose transporter that removes glucose from the bloodstream to the cell;
- Neural anti-inflammatory and neuroprotective function;
- Cardioprotective: prevents heart attacks, arrhythmias and lowers blood pressure;
- Prevents amyloid-P induced neurotoxicity.: e.g. Alzheimer's disease, Parkinson's disease;
- It is a tumor suppressor receptor;
- Stimulates processing of traumatic experiences;
- Anxiety-inhibiting, facilitates social interaction: being social is no longer a stressor but a rewarding factor;
- Reduces gastrointestinal complaints such as abnormal defecation pattern (diarrhea, constipation) unexplained abdominal discomfort, cramps, gas accumulation, etc., which occur in irritable bowel syndrome(PDS) or IBS, among others;
- Regulates the sensitivity and release of leptin. Leptin is a hormone that activates satiety when eating and is produced in white fat cells. CB1 suppresses the action of leptin in the hypothalamus. This is triggered by such things as a linoleic acid-rich diet, cannabis or antidepressants, causing one to experience a false sense of hunger and continue to eat.
- BDNF depletion: BDNF is the epigenetic protector of CB1;
- Glutathione depletion: glutathione regulates intracellular absorption of vitamin D!
- Linoleic acid-rich diet enhanced by combination with sugars, flavor enhancers and high-glycemic index agents such as beer, alcohol, corn, starches and exorphins (protein structures from gluten, cow's milk, soy and spinach), junk food and processed foods;
- Frequent use of alcohol;
- Hyper Cortisol: greatly reduced CB1 expression in the hippocampus;
- Acute, toxic and traumatic stress: PTSD, abuse, traumatic experiences, parental stress such as rejection and violence within the family, "social defeat" stress;
- Use of drugs: cannabis (THC), XTC, amphetamines;
- Use of pain medications: opioids, paracetamol, NSAIDs, aspirin (the latter enhances the effects of CB1 and CB2 receptors);
- Use of psychopharmaceuticals: antidepressants, benzodiazepines, antipsychotics.
- A weak partial CB2 agonist (agonist and antagonist), it increases the activity and density of CB2;
- A NAM (negative allosteric modulator) of CB1, the latter means that CBD blocks the binding of anandamide to CB1 receptors. CBD is not a CB1 antagonist, it has no effect on CB1 density. CBD eliminates the action of anandamide. For this reason, CBD is to be avoided;
- A FABP inhibitor, it inhibits the transport of anandamide to FAHH. It increases anandamide, but that effect is negated by NAM on CB1. CBD has no effect on CB1 expression and density.
How do I ensure that my Endocannabinoid System can function optimally?
- Take as little medication below as possible (in consultation with the doctor, of course):
- Paracetamol: causes anandamide resistance (downregulation of the CB1 receptors), glutathione depletion, endorphin resistance, Th2 dominance (asthma and allergic reactions), leaky cell membranes, mitochondrial damage and strong increase in nitric oxide (NO), increasing nitrosative stress. Furthermore, it has been linked to autism.
- Paroxetine: cause anandamide resistance via downregulation of CB1 receptors. These drugs cause BDNF depletion.
- Fluoxitini: cause anandamide resistance via downregulation of CB1 receptors. These agents cause BDNF depletion.
- Limit Linoleic acid intake and ensure proper omega-6 / omega-3 balance by using appropriate fatty acids
- Safflower oil and grape seed oil: 80%
- Sunflower oil: 70%, a 15 g serving of mayonnaise contains 10 g of linoleic acid
- Hemp oil: 50-70%
- Walnut oil: 57%
- Corn oil: 55%
- Soybean oil: 50%
- Rice oil: 40%
- Peanut oil: 25%
- Rapeseed oil: 20%
- Avocado oil: 13% (50% oleic acid)
- Olive oil: 8% (75% oleic acid)
- Coconut oil: 2%
- DHA and EPA (omega-3) play an important role in the regulation of the expression and density of CB1 and CB2 receptors. DHA stimulates the production and expression of BDNF and thus is a central substance in the regulation of the ECS;
- DHA (not EPA) reduces overexpression of CB1 receptors in a linoleic acid-rich diet;
- DHA (not EPA) increases leptin sensitivity in the hypothalamus;
- DHA and EPA provide flexibility to the cell membrane, improving cell metabolism and signaling of neurotransmitters and hormones.
- At normal weight, 20 to 25% of body weight consists of white adipose tissue. Overweight people have too much white adipose tissue.
- Linoleic acid stimulates the production of white adipose tissue.
- Alpha-linolenic acid (ALA) is an omega-3 fatty acid. It is considered the "mother omega-3" because ALA is converted into EPA and DHA;
- ALA increases the expression of CB2 receptors in humans when one supplements 2.5 grams of ALA from flaxseed oil for 10 weeks. The effect begins from the third week;
- Linoleic acid is the competitor of alpha linolenic acid, gamma linolenic acid, EPA and DHA. The DHA and EPA deficiency occurs because of the typical Western diet rich in linoleic acid;
- The highest concentration of ALA is found in flaxseed oil (75%), perilla oil (60%) and chia seeds (55%).
- Oleic acid or olein is the main unsaturated fatty acid; it belongs to the omega-9 fatty acids. Unlike omega-3 and omega-6, it is not an essential fatty acid;
- Oleic acid is the precursor of oleoylethanolamide, which increases upon FAAH inhibition. Oleoylethanolamide activates the PPAR-alpha receptors that inhibit nitric oxide (NO), thus contributing to lowering nitrosative stress. Presumably one of the reasons why a Mediterranean diet is healthy. Oleic acid inhibits neuropeptide Venghrelin, reducing appetite when CB1 is overstimulated by a high-fat diet;
- Oleic acid increases the expression of the "anti-obesity" CB2 receptors in fat cells, thus helping to reduce the inflammatory effects of fat cells due to stress, obesity and excessive CB1 stimulation. Oleic acid stimulates the sense of satiety;
- Olive oil contains the most oleic acid at 75%, followed by macadamia nut (60%),hazelnut (52%), pecan (43%), rice oil and sesame oil (42%), almond (35%) and cashew (28%).
- Avocado oil: 50% oleic acid, 13% linoleic acid
- Olive oil: 75% oleic acid, 8% linoleic acid
- Coconut oil: 6% oleic acid, 2% linoleic acid, also suitable for frying
- Ossewit: frying
- Drastically reduce linoleic acid;
- Bring ratio of omega 6:omega 3 to the ratio of 1:1;
- Measurement in blood of Vitamin D and Glutathione. In case of measured deficiency supplementation;
- Employ 2 specifically developed supplements to enhance CD1 and CD2 receptors.