CBD-DrBob

CBD Reverses Anatomical Brain Damage caused by THC

It is well established that chronic marijuana use in the teen years causes functional and anatomical changes in the brain and that these changes are somewhat permanent but just how permanent was unknown.1-4

Chronic marijuana use causes thinning of the hippocampus in humans (and animals).  The hippocampus, together with its extensive interconnections with other neural systems, supports the flexible use of information in the brain.  It helps the brain develop lots of different abilities such as: memory, executive function, adaptive reasoning, attention, decision-making, character judgments, language use and main others.5  Chronic and acute marijuana use is known to impair all of these functions with chronic use causing persistence of impairment even after ceasing use of marijuana.1-4  It is thought that the anatomical changes and mental changes are interrelated with the anatomical thinning being representative of either the loss of neurons or the non-functioning of the neurons.1  (Note:  Non-functioning neurons are thought to get thinner if not used much like muscles).

Researchers from California have found that the anatomical changes in the brain persist throughout life and are still present up to 40 years after stopping using marijuana.6  They studied people in their 60’s (average age 66) who had used marijuana heavily during their teens (>20 times/month) but had essentially stopped using it by age 35 (<1-2 times/month).  These individuals still had thinning of the hippocampus in their brains caused by the use of marijuana in their teen years.

Recently, it has been shown that concurrent use of CBD with THC can minimize and possibly prevent the hippocampal thinning caused by THC exposure.2  However, even more recently, researchers found that individuals who were taking THC and  already had hippocampal thinning could have the thinning reversed with the addition of CBD, even if they kept ingesting THC.7

Even though the anatomical changes may be reversed the functional changes associated with THC use may or may not be reversed by CBD.  Pretreatment with CBD has been shown to reduce the hippocampal-dependent memory impairments seen with acute THC use.8  A different cognitive study found that CBD improved facial emotional recognition in THC users acutely. 9 However, a recent study found that the acutely-induced behavioral, subjective, or physiological effects of THC ingestion are not altered with CBD ingestion.10  These difference may be due to the fact that different parts of the brain are being connected by the hippocampus for different tasks.11

Therefore, there appears to be some potential for CBD to reduce some of the acute cognitive changes seen with CBD but whether the potential for CBD to reverse established changes due to chronic THC use is unknown.

Bottom Line:

CBD has the potential to prevent and reverse the anatomical changes in the brain caused by THC.   In addition, CBD has the potential to reverse some of the functional changes seen with acute THC use.  However, the potential for CBD to reverse some of the functional changes caused by chronic THC is unknown.

 

References:

  1. Ashtari M, Avants B, Cyckowski L, et al. Medial temporal structures and memory functions in adolescents with heavy cannabis use. J Psychiatr Res. 2011;45:1055–1066.
  2. Yucel M, Lorenzetti V, Suo C, et al. Hippocampal harms, protection and recovery following regular cannabis use. Transl Psychiatry. 2016;6:e710–e710.
  3. Solowij N, Battisti R. The chronic effects of cannabis on memory in humans: a review. Curr Drug Abuse Rev.2008;1:81–98.
  4. Broyd SJ, van Hell HH, Beale C, et al. Acute and chronic effects of cannabinoids on human cognition—a systematic review. Biol Psychiatry.2016;79:557–567.
  5. Rubin R, etal. The role of the hipposcampus in flexible cognition and social behavior.  Front Human Neuroscience 2014;8:742.
  6. Burggren A, etal, Subregional hippocampal thickness abnormalities in older adults with a history of heavy cannabis use. Cannabis & Cannabidiol Res 2018:3.1
  7. Beale C. etal. Prolonged cannabidiol treatment effects on hippocampal subfield volumes in current cannabis users.  Cannabis and Cannabinoid Research 2018;3:1.
  8. Englund A, etal.  Cannabidiol inhibits THC-elicited paranoid symptoms and hippocampal-dependent memory impairment.  J Psychopharmacol. 2013 Jan;27(1):19-27.
  9. Hindocha C, etal. Acute effects of delta-9-tetrahydrocannabinol, cannabidiol and the combination on facial emotion recognition: a randomized, double-blind, placebo-controlled study in cannabis users.  Eur Neuropsychopharmacol 2015;25(3);325-334
  10. Haney M, etal. Oral Cannabidiol does not alter the subjective, reinforcing, or cardiovascular effects of smoked cannabis.  Neuropsychopharmacology 2016;41(8):1974-82.
  11. Bhattacharyya S, etal. Opposite effects of delta-9-tetrahydrocannabinol and cannabidiol on human brain function and psychopathology.  Neuropsychopharmacology 2010;35:764-74.

 

 

 

How does CBD fight cancer?

I have been getting a lot of questions about this subject. At present, there are 9 ways that cannabinoids have been found to combat cancer.(1)

Cannbinoids:
1) Increase apoptosis of cancer (ca) cells (decreases the lifespan of ca cells).
2) Increase autophagy of ca cells (ca cells eating up themselves).
3) Inhibit metastasis (stops ca cells from breaking off a tumor and migrating to another area to start growing there).
4) Inhibit cancer cell proliferation (growing and dividing of ca cells)
5) Increase tumor immunity surveillance (improves the immune system’s ability to recognize ca cells as “foreign” and kill them).
6) Inhibit epithelial-to-mesenchymal transition (changing from a normal cell to a less developed cell).
7) Inhibit tumor cell invasion (ability of a tumor to grow into the normal tissue).
8) Cause cell cycle arrest (keeps the cancer cells from dividing and making more cancer cells).
9) Reduce drug resistance (keeps the cancer cells from becoming resistant to the effects of chemo and radiation therapy.

Notice that I did not say CBD or hemp oil but cannabinoids. However, CBD by itself has been shown to have all of the mechanisms of fighting cancer listed above. Other cannabinoids have been shown to induce some, if not all, of these mechanisms in cancer cells also. Little to no research has been done using CBD-enhanced hemp oil which contains a multiplicity of cannabinoids, terpenes, and flavonoids. It seems logical that, due to the entourage effect, all the components in CBD-enriched hemp oil would work together to produce a better clinical result that the individual cannabinoids when used alone.

More information on Cancer and Cannabinoid research will be coming soon in my disease list.
I hope the above information is helpful.

Note: At this time, hemp oil, CBD, or medical marijuana have not been approved by the FDA in the treatment of cancer nor for any of its complications nor for any side effects associated with cancer therapy.

References
1) Velasco G, etal. Anticancer mechanisms of cannabinoids. Curr Oncol 2016;23(S2):S23-S32.

Eczema (Atopic Dermatitis)

The Disease

Atopic Dermatitis (AD), commonly called “eczema, is a disease of the skin characterized by dry skin, severe itching, inflammation, abnormal skin barrier function, and secondary infection.  Often familial, most patients with severe AD have at least one abnormal gene for filaggrin, essential for maintaining skin hydration.  AD usually onsets in childhood and its severity usually decreases with age, however, it may persist into adulthood and be very debilitating.  Typically, the lesions will come and go, usually in the same areas of the skin.  The lesions are inflammatory, and scratching causes the inflammation to worsen and often leads to secondary infection.  Scratching is uncontrollable in most individuals but even those who can control the scratching while awake, scratch during the night.  The itch in AD is does not appear to be caused by one factor, however, recent research has shown that mast cells in the skin in AD patients release compounds that: 1) stimulate nerves in the skin causing the itch sensation and 2) trigger inflammatory reactions in the skin.  This scratching of the skin causes these mast cells to release more of these compounds causing the scratching and inflammation to increase leading to the development of the typical lesions seen in AD flare-ups.   Recent evidence suggests prevention of the itch (and subsequent scratching) may eliminate all the signs and symptoms of the disease.  This seems to be true even though the abnormalities in skin barrier function remain active.  Typical anti-itch medications, including antihistamines, may provide some temporary relief but do not eliminate the itch and scratching completely.  Creams and topical steroids have been shown to be helpful in treating and preventing AD, but relapses are common, and the side effects of chronic steroid use can great significant health problems. 

Research

The itching and subsequent scratching worsens the dermatitis in AD and causes the level of IgE (allergy antibodies) to increase, causing the skin to be more sensitive and react more violently to anything that person may be allergic to.1,2 Scratching causes mast cell activation which causes the release of inflammatory compounds and the opening of Transient Receptor Protein channels on the sensory nerves.  When sensory nerve TRP channels open, the nerve does 2 things:  1) it sends the “itch” message to the spinal cord, 2) it releases compounds that cause inflammation, and 3) it causes the nerve to make more TRP channels.3-6 The increase in TRP channels causes more itching and inflammation, further increasing the severity of the disease.   The reason that histamine doesn’t work well in AD patients is that activation of the TRP channels is what causes the majority of and the persistent itching in AD rather than histamine.7,8  Many of the TRP channels on the nerves are associated with and controlled by cannabinoid receptors.9,10  As severity of the disease increases, the TRP channels and their associated cannabinoid receptors increase together. 11   When cannabinoids bind to these receptors, they can modify the TRP channels making it harder for the nerve to be stimulated, which effectively controls the “itch” sensation.12,13 Studies have shown that CB1 receptor synthetic stimulators decrease the mast cell activation and CB2 receptor synthetic antagonists suppress the itch. 12,13 In addition to the effects of cannabinoid binding to CB1-2 receptors, CBD-like compounds that bind to G-protein coupled orphan receptors GRP55 and GRP119 inhibit itching in patients with chronic itching diseases.14   CBD has other anti-inflammatory effects which may help control the inflammation found in AD.15  

 

Bottom Line

Recent research has found that the itching in AD is caused by compounds that stimulate receptors in the “itch” nerves of the skin and that cannabinoids can suppress this itch.  This suggests that cannabinoids may have the potential to reduce the signs and symptoms of the atopic dermatitis. 

 

References:

  1. Mihara K. et al. Vital role of the itch-scratch response in development of spontaneous dermatitis in NC/Nga mice. Br J Dermatol 2004 Aug;151(2):335-45.
  2. Hashimoto Y, et al. Itch-associated scratching contributes to the development of dermatitis and hyperimmunoglobulinaemia E in NC/Nga mice.  Exp Dermatol. 2011 Oct;20(10):820-5.
  3. Wilson S, et al. TRPA1 is required for histamine-independent, Mas-related G protein-coupled receptor-mediated itch. Nat Neurosci 2011 May; 14(5): 595-602.
  4. Lui B, etal. TRPA1 controls inflammation and pruritogen responses in allergic contact dermatitis.  FASEB J. 2013 Sep; 27(9): 3549–3563.
  5. Feng J, etal. Sensory TRP channels contribute differentially to skin inflammation and persistent itch.  Nature Comm 2017;8:980.
  6. Sugimoto M, et al. Putative mechanism of the itch-scratch circle: repeated scratching decreases the cutaneous level of prostaglandin D2, a mediator that inhibits itching. Prostaglandins Leukot Essent Fatty Acids. 2007 Feb;76(2):93-101.
  7. Wilson S, et al. The Ion Channel TRPA1 Is Required for Chronic Itch. J Neurosci 2013 May; 33(22): 9283-9294
  8. Oh MH, et al. TRPA1-Dependent Pruruitus in IL-13-induced Chronic Atopic Dermatitis. J Immunol 2013 Dec 1; 191(11): 5371-5382.
  9. Ankopian AN, etal Role of ionotropic cannabinoid receptors in peripheral antinociception and antihyperalgesia. Trends Pharmacol Sci 2009; 30(2):79-84.
  10. Ru F, et al. Mechanisms of pruritogen-induced activation of itch nerves in isolated mouse skin.  J Physiol 2017; 595(11):3651-3666.
  11. Ueda Y, et al. Involvement of cannabinoid CB2 receptors in the IgE-mediated triphasic cutaneous reaction in mice. Life Sci. 2007 Jan 9;80(5):414-9.
  12. Nam G, et al. Selective Cannabinoid Receptor-1 Agonists Regulate Mast Cell Activation in an Oxazolone-Induced Atopic Dermatitis Model. Ann Dermatol 2016: 28(1): 22-29.
  13. Maekawa T, et al. The cannabinoid CB2 receptor inverse agonist JTE-907 suppresses spontaneous itch-associated responses of NC mice, a model of atopic dermatitis. Eur J Pharmacol. 2006 Aug 7;542(1-3):179-83. Petrosino S, et al. Anti-inflammatory Properties of Cannabidiol, a Nonpsychotropic Cannabinoid, in Experimental Allergic Contact Dermatitis. J Pharmacol Exp Ther. 2018 Jun;365(3):652-663.
  14. Ständer S, et al. Topical cannabinoid agonists. An effective new possibility for treating chronic pruritus. 2006 Sep;57(9):801-7.
  15. Biro T, et al. The endocannabinoid system of the skin in health and disease: novel perspectives and therapeutic opportunities. Trends Pharmacol Sci 2009 Aug; 30(8): 411-420.

Eczema (Atopic Dermatitis)

Eczema (Atopic Dermatitis) is characterized by dry skin, severe itching, and inflammation.   The itching is not caused by histamine (the chemical causing the symptoms in most allergies) but by another mechanism that doesn’t respond well to anti-histamines but does respond to CBD-enriched hemp oil. Along with its anti-inflammatory properties and moisturizing ability, CBD-enriched hemp oil should be a good candidate for treating atopic dermatitis.  At this time, the FDA has not approved hemp oil or CBD for use in atopic dermatitis.

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Pain: Nociceptive Pain

The Disease

Nociceptive pain is pain that originates because of stimulation of nerves located in the tissues in our body.  Let’s assume we cut some skin off our finger.  When this happens, receptors at the ends of the nerves in the skin of our finger are stimulated; this causes an “action potential” in the nerve which transfers the information along that nerve; that nerve will transfer the information to another nerve or nerves until it gets to the spinal cord; the spinal cord transfers this information up to our brain stem; the brain stem distributes this information to many different parts of the brain; each part “reports their analysis of this information” back to the brain stem;  the brain stem sends a “report” to the pain center in our brain, and our pain center analyzes this information and decides whether or not to let you know if your finger hurts.  I am sure many of you have cut your finger at some point and didn’t feel pain until you saw that you had cut your finger.  Until you saw the cut, your brain had decided that the information being sent to it from your nerves was false information.  When you saw the cut, your brain got more information from a different source, added this information the report, the pain center re-analyzed the situation and “changed its mind” and told you “your finger hurts”; and told you exactly where it hurt.  

As you can see from the above, lots of different kinds of nerves are involved in nociceptive pain, but it always starts by stimulation of receptors on the ends of the nerves.   Nociceptive pain can be caused by: mechanical forces (pinching, cutting, stretching, etc.), heat and cold, chemical irritation, and inflammation.  In all cases, the of these receptors are located on the ends of nerves and are stimulated via transient receptor potential (TRP) channels that sense and detect and damage occurring in the tissue.

Research Findings

As stated above, nociceptive pain occurs because of stimulation of transient receptor potential (TRP) channels on the ends nerves that lie in the tissues of our body.1  Only three of the six TRP sub-families, TRPV, TRPA, and TRPM, have been have been identified as being responsible for nociceptive pain.1 In each of these subfamilies only six specific channels (TRPV1,TRPV2,TRPV3, TRPV4, TRPA1 and TRPM8) are found to in nociceptive nerves.2,3  Activation of these nociceptive TRP channels by specific noxious and/or pain-producing stimuli serves as the principal mode of detection/transduction of pain under physiological and pathophysiological conditions.1  Some nerves will have only one specific TRP channel which allows them only to respond to the stimuli that activate that specific channel, i.e. certain nerves have only TRPM8 allowing them to respond only to pressure and shearing pain.1  However, most nerves have multiple TRPV channels allowing that nerve to respond to multiple types of pain.1  TRPV1 and TPRA1 are often found together on nerves and both activated in many noxious situations including inflammatory pain, visceral pain, migraines, etc.1    Nociceptive TRP channels are membrane proteins, and most are found in the neuronal/cell membrane.4 However, a significant number are present in intracellular organelle membranes of the nerves and these channels will migrate to the cell membrane when the cell undergoes significant and/or persistent injury or inflammation, increasing the intensity of the “felt pain” and leading to hyperalgesia (see neuropathic pain).1,5-9  Often inflammation in the tissue begins after the inciting stimulus.  This causes the release of various chemicals which cause vasodilation (the source of the redness and swelling associated with inflammation) and sensitization of the TRP channels leading to hyperalgesia (minor touching of the damaged area that normally doesn’t cause pain but now does).1,5-8,10  All of these changes result in constant activation and mobilization of the TRP’s which is responsible for the feeling of constant and increasing pain, even though the initial stimulus that caused the pain is no longer present.

CBD desensitizes TRPV1-4 and TRPA1 receptors such that they are unable to generate an action potential, causing the nerves to be unable to send “pain” messages to the spinal cord.11,12  In addition, CBD inhibits TRPM8 receptors which does the same thing.13 However, other cannabinoids including cannabinol (CBN), cannabichromene (CBC), cannabigerol (CBG), and THC also desensitize these receptors and inhibit the nerves from depolarizing and sending “pain” messages to the spinal cord.11  Often TRP channels are linked with other known cannabinoid receptors, i.e., CB2, 5-HT1A, etc.11  Cannabinoids binding to these receptors interact with their associated TRP channels causing desensitization and prohibition of generating nerve impulses.11

Numerous studies have been performed using chemically produced blockers of TRP’s and several have found them to be somewhat effective in the relief of specific types of nociceptive pain, however, because they all have been specific blockers of only one type of TRP (example: blocks only TRPV1 and not any others) and, in most painful situations, multiple TRP’s are being stimulated, they have not been universally useful in nociceptive pain.  However, because of its ability to block all the TRP’s associated with nociceptive pain, CBD-enhanced full spectrum hemp oil should be more effective in preventing nociceptive pain than chemically produced TRP blockers.  In addition, because it contains many other cannabinoids known to also block TRP’s, CBD-enriched hemp oil should be better at controlling nociceptive pain than CBD alone.

Bottom Line

Nociceptive pain is the most common type of pain and is caused by physical damage or potential damage to the body.  CBD-enriched hemp oil containing multiple other cannabinoids has great potential in being able to block sensory nerves from generating nerve impulses resulting in the elimination of nociceptive pain.  No studies of CBD-enriched hemp oil in nociceptive pain have been reported and, at this time, the FDA does not approve the use of CBD products for nociceptive pain.

 

References

  1. Mickle AD, etal. Nociceptive TRP channels: Sensory detectors and transducers in multiple pain pathologies. Pharmaceuticals 2016;9:72
  2. Marwaha L, etal. TRP channels: potential drug target for neuropathic pain.  2016 Dec;24(6):305-317.
  3. Sałat K, etal. Transient receptor potential channels – emerging novel drug targets for the treatment of pain.  Curr Med Chem. 2013;20(11):1409-36.
  4. Ferrandiz-Huertas C, etal. Trafficking of thermo-TRP channels. Membranes 2014;4:525–64.
  5. Mickle A.D, etal. Induction of thermal and mechanical hypersensitivity by parathyroid hormone-related peptide through upregulation of TRPV1 function and trafficking. Pain 2015;156:1620–36.
  6. Zhang X, etal. NGF rapidly increases membrane expression of TRPV1 heat-gated ion channels. EMBO J. 2005;24:4211–23.
  7. Schmidt M, etal. Nociceptive signals induce trafficking of TRPA1 to the plasma membrane. Neuron 2009;64:498–509.
  8. Meng J, etal. TNF alpha induces co-trafficking of TRPV1/TRPA1 in VAMP1-containing vesicles to the plasmalemma via Munc18-1/syntaxin1/SNAP-25 mediated fusion. Sci. Rep. 2016;6:21226.
  9. Bandell, M, etal. Noxious cold ion channel TRPA1 is activated by pungent compounds and bradykinin. Neuron 2004;41:849–57.
  10. Julius D. TRP channels and pain. Annu Rev Cell Dev Biol. 2013;29:355-84.
  11. Akopian AN, etal. Role of ionotropic cannabinoid receptors in peripheral antinociception and antihyperalgesia.  Trends Pharmacol Sci 2009;30(2):79-84.
  12. Iannotti FA, etal. Non-psychotropic plant cannabinoids, cannabidivarin (CBDV) and cannabidiol (CBD), activate and desensitize transient receptor potential vanilloid 1 (TRPV1) channels in vitro: potential for the treatment of neuronal hyperexcitability. ACS Chem Neurosci. 2014;5(11):1131-41.
  13. De Petrocellis L, etal. Plant-derived cannabinoids modulate the activity of transient receptor potential channels of ankyrin type-1 and melastatin type-8. J Pharmacol Exp Ther. 2008 Jun;325(3):1007-15.

 

 

 

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