Healing Tree Naturopathic Medicine

10/14/2023

🌱In this study, researchers investigate the mechanisms underlying the anti-inflammatory effects of three minor phytocannabinoids including tetrahydrocannabivarin (THCV), cannabichromene (CBC), and cannabinol (CBN) using an in vitro system

Article: https://www.cannabisclinicians.org/2023/10/04/anti-inflammatory-effects-of-minor-cannabinoids-cbc-thcv-and-cbn-in-human-macrophages/

07/07/2022

Microdosing and Depression - Research study results

The use of psychedelic substances at sub-sensorium ‘microdoses’, has gained popular academic interest for reported positive effects on wellness and cognition. The present study describes microdosing practices, motivations and mental health ...

07/07/2022

Randomized Controlled Trial J Psychopharmacol 2022 Feb;36(2):151-158. doi: 10.1177/02698811211073759.

Efficacy and safety of psilocybin-assisted treatment for major depressive disorder: Prospective 12-month follow-up

Natalie Gukasyan 1, Alan K Davis 1 2, Frederick S Barrett 1, Mary P Cosimano 1, Nathan D Sepeda 1, Matthew W Johnson 1, Roland R Griffiths 1 3
Affiliations expand
PMID: 35166158 PMCID: PMC8864328 DOI: 10.1177/02698811211073759
Free PMC article
Abstract
Background: Preliminary data suggest that psilocybin-assisted treatment produces substantial and rapid antidepressant effects in patients with major depressive disorder (MDD), but little is known about long-term outcomes.

Aims: This study sought to examine the efficacy and safety of psilocybin through 12 months in participants with moderate to severe MDD who received psilocybin.

Methods: This randomized, waiting-list controlled study enrolled 27 patients aged 21-75 with moderate to severe unipolar depression (GRID-Hamilton Depression Rating Scale (GRID-HAMD) ⩾ 17). Participants were randomized to an immediate or delayed (8 weeks) treatment condition in which they received two doses of psilocybin with supportive psychotherapy. Twenty-four participants completed both psilocybin sessions and were followed through 12 months following their second dose.

Results: All 24 participants attended all follow-up visits through the 12-month timepoint. Large decreases from baseline in GRID-HAMD scores were observed at 1-, 3-, 6-, and 12-month follow-up (Cohen d = 2.3, 2.0, 2.6, and 2.4, respectively). Treatment response (⩾50% reduction in GRID-HAMD score from baseline) and remission were 75% and 58%, respectively, at 12 months. There were no serious adverse events judged to be related to psilocybin in the long-term follow-up period, and no participants reported psilocybin use outside of the context of the study. Participant ratings of personal meaning, spiritual experience, and mystical experience after sessions predicted increased well-being at 12 months, but did not predict improvement in depression.

Conclusions: These findings demonstrate that the substantial antidepressant effects of psilocybin-assisted therapy may be durable at least through 12 months following acute intervention in some patients.

06/17/2022

Tags: science, limbic system, cannabis history, cannabis research, endocannabinoid system Science Keynote, Ethan Russo, MD presents "Cannabis and Psychiatry ...

03/28/2022

Hashimoto’s Health Tip: Autoimmunity and Depression

Hey people!

This week, we’re covering some physiological causes of depression. Today, I’ll be covering how autoimmunity can lead to depression.

In the context of Hashimoto’s, hypothyroidism and depression, treatment is most often focused on thyroid hormone levels, antidepressant medication or a combination of the two. When this approach doesn’t help, then autoimmunity and inflammation should be investigated.

There is a relatively new model of depression which involves inflammation and immune cells (called cytokines). (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2995293/) Basically, the theory is that inflammation in the brain slows down communication between neurons. A common symptom of this slowed down communication is brain fog, but depression can also be a result.

If you experience both brain fog and depression and you have an autoimmune disease like Hashimoto’s, then you should suspect brain and/or neurological autoimmunity. One of the unfortunate realities of having autoimmune disease is that it can be found in multiple parts of your body.

Another unfortunate reality is that many doctors completely ignore this or are completely ignorant of it. But that doesn’t mean it’s not there. According to Dr. Datis Kharrazian, author of “Why Isn’t My Brain Working?”, the most common autoimmunity to co-exist with Hashimoto’s is brain autoimmunity, especially a part of the brain known as the cerebellum.

The cerebellum is found in the back of the brain and it helps with balance, maintains muscle tone in the neck and back and it orients you spatially in your surroundings. People with cerebellum autoimmunity may experience vertigo, difficulty with balance, chronic neck and back weakness, car sickness or nausea while driving or moving their heads quickly, etc.

In Hashimoto’s, this can be seen because it is triggered by gluten sensitivity. Gluten can lead directly to attacks on the cerebellum. In fact, there is a condition called “gluten-induced ataxia” that refers to a loss of balance caused by gluten. (https://www.ncbi.nlm.nih.gov/pubmed/18787912)

Continued in comments...

The reason why the cerebellum can be attacked is that gluten and cerebellar tissue both have proteins that are structurally similar. When a person who is sensitive to gluten eats gluten, the immune system attacks that gluten (because cerebellar proteins are so similar) and the immune system attacks the cerebellum too.

And something really important to understand is that the immune system in the brain is different than the immune system in the rest of the body. It has no “off” switch. Once activated, it won’t calm down.

This is why brain trauma is such a big deal, it can take years to recover from it.

So, what do we do about it?

1. Getting off of gluten 100% would be a good start. Even if you don’t have overt celiac disease, you may still have gluten sensitivity and this can lead to an attack your brain. Not good.
2. Test for additional autoimmunity. Cyrex labs, a leading lab for autoimmune testing has a few different panels that evaluate for neurological autoimmunity. I order these tests, if your’e interested, shoot me an email at marc@hashimotoshealing.com and I’ll send you more information.
3. Reduce inflammation. Working to keep inflammation at bay should be your #1 priority. Herbs like cur cumin and resveratrol are helpful in calming pathways that cause neurological autoimmunity.

Vitamin D and glutathione are also helpful in boosting TH-3 or the regulatory part of the immune system. This is like giving more power to the general to control his troops.

I’ll be covering other things this week that also must be addressed: these include stress (very inflammatory), blood sugar imbalance cues, poor circulation and more.

Have a great day! Unless you have other, dizzier plans.

03/13/2022

Find could lead to new treatments for obesity, depression

03/13/2022

Children with a complex motor disorder, characterized by a combination of movement and posture abnormalities (eg, spasticity and dystonia), were enrolled.

03/13/2022

Nicole Cain, ND, MA Tolle Causam As many as 1,080,168 children in the United States, ages 0-5, are taking a psychiatric drug.1 If we expand the age range to 0-17, that number jumps up drastically to 8,389,034. The primary types of medications prescribed for children include amphetamines, antidepress...

03/13/2022

CBDA, Cancer and Inflammation

Review Biomed Res Int 2018 Dec 4;2018:1691428. doi: 10.1155/2018/1691428. eCollection 2018.
Cannabis sativa L. and Nonpsychoactive Cannabinoids: Their Chemistry and Role against Oxidative Stress, Inflammation, and Cancer
Federica Pellati 1, Vittoria Borgonetti 2, Virginia Brighenti 1, Marco Biagi 2, Stefania Benvenuti 1, Lorenzo Corsi 1
Affiliations expand
PMID: 30627539 PMCID: PMC6304621 DOI: 10.1155/2018/1691428
Free PMC article
Abstract
In the last decades, a lot of attention has been paid to the compounds present in medicinal Cannabis sativa L., such as Δ9-tetrahydrocannabinol (Δ9-THC) and cannabidiol (CBD), and their effects on inflammation and cancer-related pain. The National Cancer Institute (NCI) currently recognizes medicinal C. sativa as an effective treatment for providing relief in a number of symptoms associated with cancer, including pain, loss of appetite, nausea and vomiting, and anxiety. Several studies have described CBD as a multitarget molecule, acting as an adaptogen, and as a modulator, in different ways, depending on the type and location of disequilibrium both in the brain and in the body, mainly interacting with specific receptor proteins CB1 and CB2. CBD is present in both medicinal and fibre-type C. sativa plants, but, unlike Δ9-THC, it is completely nonpsychoactive. Fibre-type C. sativa (h**p) differs from medicinal C. sativa, since it contains only few levels of Δ9-THC and high levels of CBD and related nonpsychoactive compounds. In recent years, a number of preclinical researches have been focused on the role of CBD as an anticancer molecule, suggesting CBD (and CBD-like molecules present in the h**p extract) as a possible candidate for future clinical trials. CBD has been found to possess antioxidant activity in many studies, thus suggesting a possible role in the prevention of both neurodegenerative and cardiovascular diseases. In animal models, CBD has been shown to inhibit the progression of several cancer types. Moreover, it has been found that coadministration of CBD and Δ9-THC, followed by radiation therapy, causes an increase of autophagy and apoptosis in cancer cells. In addition, CBD is able to inhibit cell proliferation and to increase apoptosis in different types of cancer models. These activities seem to involve also alternative pathways, such as the interactions with TRPV and GRP55 receptor complexes. Moreover, the finding that the acidic precursor of CBD (cannabidiolic acid, CBDA) is able to inhibit the migration of breast cancer cells and to downregulate the proto-oncogene c-fos and the cyclooxygenase-2 (COX-2) highlights the possibility that CBDA might act on a common pathway of inflammation and cancer mechanisms, which might be responsible for its anticancer activity. In the light of all these findings, in this review we explore the effects and the molecular mechanisms of CBD on inflammation and cancer processes, highlighting also the role of minor cannabinoids and noncannabinoids constituents of Δ9-THC deprived h**p.

In the last decades, a lot of attention has been paid to the compounds present in medicinal Cannabis sativa L., such as Δ[9] -tetrahydrocannabinol (Δ[9] -THC) and cannabidiol (CBD), and their effects on inflammation and cancer-related ...

03/03/2022

Cannabinoids and Bone remodeling

Cells 2021 Feb 17;10(2):414. doi: 10.3390/cells10020414.
Renal Proximal Tubule Cell Cannabinoid-1 Receptor Regulates Bone Remodeling and Mass via a Kidney-to-Bone Axis
Saja Baraghithy 1, Yael Soae 1, Dekel Assaf 1, Liad Hinden 1, Shiran Udi 1, Adi Drori 1, Yankel Gabet 2, Joseph Tam 1
Affiliations expand
PMID: 33671138 PMCID: PMC7922053 DOI: 10.3390/cells10020414
Free PMC article
Abstract
The renal proximal tubule cells (RPTCs), well-known for maintaining glucose and mineral homeostasis, play a critical role in the regulation of kidney function and bone remodeling. Deterioration in RPTC function may therefore lead to the development of diabetic kidney disease (DKD) and osteoporosis. Previously, we have shown that the cannabinoid-1 receptor (CB1R) modulates both kidney function as well as bone remodeling and mass via its direct role in RPTCs and bone cells, respectively. Here we employed genetic and pharmacological approaches that target CB1R, and found that its specific nullification in RPTCs preserves bone mass and remodeling both under normo- and hyper-glycemic conditions, and that its chronic blockade prevents the development of diabetes-induced bone loss. These protective effects of negatively targeting CB1R specifically in RPTCs were associated with its ability to modulate erythropoietin (EPO) synthesis, a hormone known to affect bone mass and remodeling. Our findings highlight a novel molecular mechanism by which CB1R in RPTCs remotely regulates skeletal homeostasis via a kidney-to-bone axis that involves EPO.