MITCHONDRIA - CBD Cures - & My Letter to Charlie's Mom - Hempress

CHARLIE GARD

FOR LAST CHANCE TREATMENT

U.S.

7/21/2017

Connie,

I hope you are Charlie's Mother. Have you or are you able to treat your son with Cannabiniods? The CBD's from Cannabis directly affect and CURE brain disfunctions, PLEASE look this up. I will send you Cannabinoids – It would be a tragedy if Charlie goes without this treatment – Cannabinoids are natural components that center directly on the brain and the US is now starting to admit that this is extremely effective for many disfunctions... Please let me know you have received this message and please allow me to send this to you...

Hempress.

A FIGHT FOR THE LIFE OF THEIR CHILD

Charlie Gard : making world news in London as his parents are helpless in saving their son who is terminally set..  Courts are ruling out final treatments, but perhaps a possible last chance treatment can take place in U.S.? 

Cannabinoids - can it be a cure Mitichondrial? Does the U.S. have Cannabinoids in mind for their experimental therapy? Can his parents treat Charlie with Cannabinoids even if they wanted to?

After listening to the last CNN news casting this morning:   I wrote to Charlies Mother   gave her this link and pondered through articles to see if this poor child has ever been allowed CBD's to find the effects successful"  -

  
CONNIE YATES:  If you are reading this for your son -   Please read here what cannabinoids can do for your son's condition below, and this link: http://www.alternet.org/drugs/cbd-science-mitochondria-mysteries-homeostasis-renewal-endocannabinoid-system  

ARTICLES OF HISTORY:

STILL FIGHTING TO SAVE CHARLIE - July 20, 2017 - July 20, 2017

CHARLIE GARD - Should this go on without ability to try CBD'S? - July 21, 2017

THE WAIT



WHAT IS MITOCHONDRIAL AND HOW DO CANNABINOIDS EFFECT IT? - A scientific and real explanation.

Mitochondrial CB1 receptors. Embedded in cell membranes, cannabinoid CB1 receptors are the most prevalent G-coupled protein receptors to populate the human brain and central nervous system. An estimated fifteen percent of all CB1 receptors in neurons exist on the mitochondria. In certain kinds of muscle tissue, half of the CB1 receptors are localized on the mitochondria. In order to directly activate a mitochondrial CB1 receptor, THC must penetrate the outer cellular membrane and be chaperoned through the cell’s interior. Mitochondrial CB1 receptors are not structurally distinct from the prolific CB1 receptors that wrap around the cell’s outer surface, but their effects can be quite different. (Light switches may look the same from room to room, but they are connected to different circuitry throughout the house, and so turning the switch on or off in different places causes different outcomes.) Preclinical science suggests that activation of mitochondrial CB1 receptors usually decreases mitochondrial activity. This can protect the cell from oxidative stress and prevent apoptosis, but paradoxically it can also cause cell death in some conditions.

Membrane perturbation. The membrane of mitochondria are primarily made of lipids, such as fatty acids and cholesterol. As in the outer cellular membrane, the relative concentration of short and long chain fats, saturated and unsaturated fats, and cholesterol influences many aspects of the mitochondrial membrane. Lipophilic compounds like endocannabinoids and plant cannabinoids can also meld into the mitochondrial membrane, changing its fluidity and permeability. Mitochondria harness the energy of electrons by using proteins imbedded in the mitochondrial membrane; alteration of membrane fluidity can inhibit the mitochondria’s ability to produce energy and allow free radicals to more easily escape into the cell. Stephanie Seneff, a senior research scientist at MIT, reports that Monsanto’s Roundup herbicide interferes with ATP production by adversely affecting mitochondrial membrane permeability.

Non-cannabinoid receptors. Cannabidiol does not directly activate mitochondrial CB1 receptors. Instead, CBD binds to different receptors, including the sodium-calcium exchanger (NCX), on the mitochondria’s surface. Binding to NCX opens an ion channel, and ions, such as electrically charged calcium atoms, flow from high concentrations to low concentrations. Different levels of calcium ions have different effects.2 In conditions of low cellular stress, characterized by low intracellular calcium surrounding the mitochondria, CBD will increase stress by allowing calcium to flow out of the mitochondria. But in high stress conditions, characterized by copious intracellular calcium, CBD will do the exact opposite, allowing the flow of calcium from outside to inside the mitochondria (where calcium is stored) by opening NCX. The bidirectional calcium flow regulated by NCX is one of the mechanisms whereby CBD facilitates cellular homeostasis and neuroprotection.

CBD, calcium channels & homeostasis

Cannabinoids are well known among scientists for their trickster-like ability to exert opposite effects in different situations. In mitochondria, cannabinoid activity is even more complicated. At low-stress conditions, cannabinoids often increase mitochondrial activity and cellular respiration, triggering autophagic cellular repair. Cannabinoids will also buffer high stress conditions and protect cells by decreasing mitochondrial activity. But that’s not all. The dependence on stress is actually trimodular: In very high-stress conditions — such as those often present in cancer cells — endocannabinoids can create a positive feedback loop, increasing stress to the point where the cell undergoes apoptosis. Plant cannabinoids can also induce apoptosis under similar conditions. The death of cancer cells promotes homeostasis and the survival of the organism as a whole.3

The ebb and flow of calcium and stress, autophagy and cell death, the restoration of homeostasis on a cellular level are all regulated by CBD. A report by British researchers in the Journal of Neuroscience (2009) noted that “under pathological conditions involving mitochondrial dysfunction and calcium [Ca(2+)] dysregulation, CBD may prove beneficial in preventing apoptotic signaling via a restoration of calcium homeostasis.”

Examining CBD’s effect on mitochondria sheds light on how cannabidiol can protect against brain injury by regulating fluctuations in intracellular calcium. A November 2016 study in the European Journal of Pharmacologyfound that an “imbalance of sodium and calcium homeostasis trigger[s] pathophysiologic processes in cerebral ischemia, which accelerate neuronal brain death.” The good news for stroke victims, according to Iranian scientists at Shahid Beheshti University in Tehran, is that CBD can reduce the severity of ischemic damage by enhancing NCX receptor expression on the mitochondrial membrane.