Tuesday, December 2, 2014

Marijuana fights Alzheimer’s disease, new study indicates

http://blog.sfgate.com/smellthetruth/2014/11/29/marijuana-fights-alzheimers-disease-study-indicates/


Another study is adding evidence to the case for the treatment and prevention of Alzheimer’s disease with the compounds in cannabis.
Research published in the Journal of Alzheimer’s Disease this September “strongly suggest that THC [the main active ingredient in marijuana] could be a potential therapeutic treatment option for Alzheimer’s disease through multiple functions and pathways.”
More than five million Americans have Alzheimer’s today. One in three seniors will die with Alzheimer’s or another dementia, and Alzheimer’s is the sixth leading cause of death in the nation, costing America about $203 billion in 2013.
Chuanhai Cao and other researchers at the University of South Florida and Thomas Jefferson University wanted to investigate the “potential therapeutic qualities of Δ9-tetrahydrocannabinol (THC) with respect to slowing or halting the hallmark characteristics of Alzheimer’s disease.”
So they treated Alzheimer’s research cells (N2a-variant amyloid-β protein precursor (AβPP) cells) with THC and examined them for amyloid-β at the 6, 24, and 48-hour time markers. Amyloid-β is a type of protein that is linked to Alzheimer’s symptoms. The researchers found THC “to be effective at lowering Aβ levels … in a dose-dependent manner.”
The main active ingredient in pot “directly interacts” with amyloid-β, “thereby inhibiting aggression”. THC was also effective at lowering other key Alzheimer’s Disease markers. Furthermore “no toxicity” was observed from the THC. The researchers also found THC “enhances” the function of the cell’s energy factories — the mitochondria.
“THC is known to be a potent antioxidant with neuroprotective properties, but this is the first report that the compound directly affects Alzheimer’s pathology by decreasing amyloid beta levels, inhibiting its aggregation, and enhancing mitochondrial function,” stated study lead author Chuanhai Cao, PhD and a neuroscientist at the Byrd Alzheimer’s Institute and the USF College of Pharmacy.
“Decreased levels of amyloid beta means less aggregation, which may protect against the progression of Alzheimer’s disease. Since THC is a natural and relatively safe amyloid inhibitor, THC or its analogs may help us develop an effective treatment in the future.”
Other research in the same journal that month indicates THC boosts the body’s natural anti-Alzheimer’s fighting mechanism — the endocannabinoid system.
Alzheimer’s Disease is thought to result from a lifetime of brain inflammation. Cannabis is one of the most safe anti-inflammatories in medicine. Some neuroscientists believe a bout of pot smoking in early adulthood may prevent Alzheimer’s onset later in life. Cannabis slows brain aging, Time reported in 2012.
Smoking, vaping, or eating the pot molecules THC and CBD directly effects nerve cell function, reducing chronic brain inflammation, oxidative stress, and cellular dysfunction — all the while promoting stability of the human body’s internal environment (homeostasis) and healthy brain cells (neurotrophic support), studies show.
“What we found was that not only did the single puff a day reverse the memory impairment but also restarted neurogenesis,” Ohio State University, Gary Wenk told the Seattle Post Intelligencer this year.
Other studies have shown THC inhibits other key pathological markers of Alzheimer’s Disease.
The U.S. government has patented marijuana molecule CBD as a neuroprotectant, evan as it maintains that cannabis is a schedule 1 drug with no medical use and high potential for abuse. The federal drug war is blocking deeper research into cannabis’ impacts on brain disease, Wenk states.

Wednesday, November 19, 2014

Cannabis ‘Dramatically Reduces’ Growth of Brain Cancer Cells: New Study

http://naturalsociety.com/cannabis-dramatically-reduces-growth-brain-cancer-cells-new-study/ 

http://mct.aacrjournals.org/content/early/2014/11/12/1535-7163.MCT-14-0402.abstract

The Combination of Cannabidiol and Δ9-Tetrahydrocannabinol Enhances the Anticancer Effects of Radiation in an Orthotopic Murine Glioma Model

  1. Wai M. Liu*
+ Author Affiliations
  1. Department of Oncology, Division of Clinical Sciences, St George's, University of London, London, United Kingdom.
  1. *Corresponding Author:
    Wai Liu, Department of Oncology, Division of Clinical Sciences, St George's, University of London, Second Floor, Jenner Wing, London, SW17 0RE, United Kingdom. Phone: 44-20-8725-5037; Fax: 44-20-8725-0158; E-mail: w.liu@sgul.ac.uk

Abstract

High-grade glioma is one of the most aggressive cancers in adult humans and long-term survival rates are very low as standard treatments for glioma remain largely unsuccessful. Cannabinoids have been shown to specifically inhibit glioma growth as well as neutralize oncogenic processes such as angiogenesis. In an attempt to improve treatment outcome, we have investigated the effect of Δ9-tetrahydrocannabinol (THC) and cannabidiol (CBD) both alone and in combination with radiotherapy in a number of glioma cell lines (T98G, U87MG, and GL261). Cannabinoids were used in two forms, pure (P) and as a botanical drug substance (BDS). Results demonstrated a duration- and dose-dependent reduction in cell viability with each cannabinoid and suggested that THC-BDS was more efficacious than THC-P, whereas, conversely, CBD-P was more efficacious than CBD-BDS. Median effect analysis revealed all combinations to be hyperadditive [T98G 48-hour combination index (CI) at FU50, 0.77–1.09]. Similarly, pretreating cells with THC-P and CBD-P together for 4 hours before irradiation increased their radiosensitivity when compared with pretreating with either of the cannabinoids individually. The increase in radiosensitivity was associated with an increase in markers of autophagy and apoptosis. These in vitro results were recapitulated in an orthotopic murine model for glioma, which showed dramatic reductions in tumor volumes when both cannabinoids were used with irradiation (day 21: 5.5 ± 2.2 mm3 vs. 48.7 ± 24.9 mm3 in the control group; P < 0.01). Taken together, our data highlight the possibility that these cannabinoids can prime glioma cells to respond better to ionizing radiation, and suggest a potential clinical benefit for glioma patients by using these two treatment modalities. Mol Cancer Ther; 1–13. ©2014 AACR.
  • Received May 12, 2014.
  • Revision received September 8, 2014.
  • Accepted September 23, 2014.

Tuesday, September 16, 2014

Clinical endocannabinoid deficiency (CECD) revisited: Can this concept explain the therapeutic benefits of cannabis in migraine, fibromyalgia, irritable bowel syndrome and other treatment-resistant conditions?

http://www.ncbi.nlm.nih.gov/pubmed/24977967

Neuro Endocrinol Lett. 2014 Jun 30;35(3):198-201. [Epub ahead of print]

Abstract

OBJECTIVES:

Ethan B. Russo's paper of December 1, 2003 explored the concept of a clinical endocannabinoid deficiency (CECD) underlying the pathophysiology of migraine, fibromyalgia, irritable bowel syndrome and other functional conditions alleviated by clinical cannabis.

METHODS:

Available literature was reviewed, including searches via the National Library of medicine database and other sources.

RESULTS:

A review of the literature indicates that significant progress has been made since Dr. Ethan B. Russo's landmark paper, just ten years ago (February 2, 2004). Investigation at that time suggested that cannabinoids can block spinal, peripheral and gastrointestional mechanisms that promote pain in headache, fibromyalgia, irritable bowel syndrome and muscle spasm.

CONCLUSION:

Subsequent research has confirmed that underlying endocannabinoid deficiencies indeed play a role in migraine, fibromyalgia, irritable bowel syndrome and a growing list of other medical conditions. Clinical experience is bearing this out. Further research and especially, clinical trials will further demonstrate the usefulness of medical cannabis. As legal barriers fall and scientific bias fades this will become more apparent.
PMID:
24977967
[PubMed - as supplied by publisher]

Thursday, September 11, 2014

CANNABINOIDS INCREASE LUNG CANCER CELL LYSIS (cell breakdown) BY LYMPHOKINE-ACTIVATED KILLER CELLS VIA UPREGULATION OF ICAM-1

http://www.ncbi.nlm.nih.gov/pubmed/25069049

Biochem Pharmacol. 2014 Jul 25. pii: S0006-2952(14)00420-1. doi: 10.1016/j.bcp.2014.07.014. [Epub ahead of print]

Abstract

Cannabinoids have been shown to promote the expression of the intercellular adhesion molecule 1 (ICAM-1) on lung cancer cells as part of their anti-invasive and antimetastatic action. Using lung cancer cell lines (A549, H460) and metastatic cells derived from a lung cancer patient, the present study addressed the impact of cannabinoid-induced ICAM-1 on cancer cell adhesion to lymphokine-activated killer (LAK) cells and LAK cell-mediated cytotoxicity. Cannabidiol (CBD), a non-psychoactive cannabinoid, enhanced the susceptibility of cancer cells to adhere to and subsequently lysed by LAK cells, with both effects being reversed by a neutralizing ICAM-1 antibody. Increased cancer cell lysis by CBD was likewise abrogated when CBD-induced ICAM-1 expression was blocked by specific siRNA or by antagonists to cannabinoid receptors (CB1, CB2) and to transient receptor potential vanilloid 1. In addition, enhanced killing of CBD-treated cancer cells was reversed by preincubation of LAK cells with an antibody to lymphocyte function associated antigen-1 (LFA-1) suggesting intercellular ICAM-1/LFA-1 crosslink as crucial event within this process. ICAM-1-dependent pro-killing effects were further confirmed for the phytocannabinoid Δ9-tetrahydrocannabinol (THC) and R(+)-methanandamide, a stable endocannabinoid analogue. Finally, each cannabinoid elicited no significant increase of LAK cell-mediated lysis of non-tumor bronchial epithelial cells, BEAS-2B, associated with a far less pronounced (CBD, THC) or absent (R(+)-methanandamide) ICAM-1 induction as compared to cancer cells. Altogether, our data demonstrate cannabinoid-induced upregulation of ICAM-1 on lung cancer cells to be responsible for increased cancer cell susceptibility to LAK cell-mediated cytolysis. These findings provide proof for a novel antitumorigenic mechanism of cannabinoids.
Copyright © 2014. Published by Elsevier Inc.


Lysis

From Wikipedia, the free encyclopedia
This article is about the biological definition of the word Lysis. For other uses, see Lysis (disambiguation).
Lysis (/ˈlsɪs/; Greek λύσις lýsis, "a loosing" from λύειν lýein, "to unbind") refers to the breaking down of a cell, often by viral, enzymic, or osmotic mechanisms that compromise its integrity. A fluid containing the contents of lysed cells is called a "lysate".

Monday, July 14, 2014

New research reveals how cannabis compound could slow tumour growth

http://www.uea.ac.uk/mac/comm/media/press/2014/July/cancer-cannabis

Mon, 14 Jul 2014

Scientists at the University of East Anglia have shown how the main psychoactive ingredient in cannabis could reduce tumour growth in cancer patients.

Research published today reveals the existence of previously unknown signaling platforms which are responsible for the drug’s success in shrinking tumours.

It is hoped that the findings could help develop a synthetic equivalent with anti-cancer properties.

The research was co-led with the Universidad Complutense de Madridin, Spain. The team used samples of human cancer cells to induce tumours in mice. They then targeted the tumours with doses of the cannabis compound THC (Tetrahydrocannabinol). They found that two cell receptors in particular were responsible for the drug’s anti-tumour effects.

Dr Peter McCormick, from UEA’s school of Pharmacy, said: “THC, the major active component of marijuana, has anti-cancer properties. This compound is known to act through a specific family of cell receptors called cannabinoid receptors. However, it was unclear which of these receptors were responsible for the anti-tumour effects of THC.

“We show that these effects are mediated via the joint interaction of CB2 and GPR55 - two members of the cannabinoid receptor family. Our findings help explain some of the well-known but still poorly understood effects of THC at low and high doses on tumour growth.

There has been a great deal of interest in understanding the molecular mechanisms behind how marijuana, and specifically THC, influence cancer pathology.

“There has also been a drive in the pharmaceutical industry to create synthetic equivalents that might have anti-cancer properties.

“By identifying the receptors involved we have provided an important step towards the future development of therapeutics that can take advantage of the interactions we have discovered to reduce tumour growth.”

Dr McCormick added that cancer sufferers should not be tempted to self-medicate.

“Our research uses an isolated chemical compound and using the correct concentration is vital. Cancer patients should not use cannabis to self-medicate, but I hope that our research will lead to a safe synthetic equivalent being available in the future.”

‘Targeting CB2 –GPR55 receptor heteromers modulates cancer cell signalling’ is published in the Journal of Biological Chemistry.

Monday, April 28, 2014

Cannabis extract treatment for terminal acute lymphoblastic leukemia with a Philadelphia chromosome mutation.

Authors
  • 1Brampton, Ont., Canada.
  • 2Ajax, Ont., Canada.

Abstract

Acute lymphoblastic leukemia (ALL) is a cancer of the white blood cells and is typically well treated with combination chemotherapy, with a remission state after 5 years of 94% in children and 30-40% in adults. To establish how aggressive the disease is, further chromosome testing is required to determine whether the cancer is myeloblastic and involves neutrophils, eosinophils or basophils, or lymphoblastic involving B or T lymphocytes. This case study is on a 14-year-old patient diagnosed with a very aggressive form of ALL (positive for the Philadelphia chromosome mutation). A standard bone marrow transplant, aggressive chemotherapy and radiation therapy were revoked, with treatment being deemed a failure after 34 months. Without any other solutions provided by conventional approaches aside from palliation, the family administered cannabinoid extracts orally to the patient. Cannabinoid resin extract is used as an effective treatment for ALL with a positive Philadelphia chromosome mutation and indications of dose-dependent disease control. The clinical observation in this study revealed a rapid dose-dependent correlation.

KEYWORDS:

Acute lymphoblastic leukemia, Cannabinoids, Hemp oil, Philadelphia chromosome

http://www.ncbi.nlm.nih.gov/pubmed/24474921






Tuesday, April 22, 2014

The Side Effects of Chemotherapy on the Body


Cancer cells divide more quickly than healthy cells, and chemotherapy drugs effectively target those cells. Unfortunately, fast-growing cells that are healthy can be damaged too. There are many different chemotherapy drugs with the potential for many different side effects. These effects vary from person to person and from treatment to treatment.

The Side Effects of Chemotherapy on the Body Cancer cells divide more quickly than healthy cells, and chemotherapy drugs effectively target those cells. Unfortunately, fast-growing cells that are healthy can be damaged too. There are many different chemotherapy drugs with the potential for many different side effects. These effects vary from person to person and from treatment to treatment.

Factors that play a role in side effects include other ongoing treatments, previous health issues, age, and lifestyle. Some patients experience few side effects while others feel quite ill. Although most side effects clear up shortly after treatment ends, some may continue well after chemotherapy has ended, and some may never go away. Chemotherapy drugs are most likely to affect cells in the digestive tract, hair follicles, bone marrow, mouth, and reproductive system. However, cells in any part of the body may be damaged. 

See more at: http://www.healthline.com/health/cancer/effects-on-body#sthash.FCZnXkCW.dpuf

Friday, January 31, 2014

Cannabis oil helping leukemia

Cannabis extract treatment for terminal acute lymphoblastic leukemia with a Philadelphia chromosome mutation.

 

Case Rep Oncol. 2013 Nov 28;6(3):585-92. doi: 10.1159/000356446. eCollection 2013.

Abstract

Acute lymphoblastic leukemia (ALL) is a cancer of the white blood cells and is typically well treated with combination chemotherapy, with a remission state after 5 years of 94% in children and 30-40% in adults. To establish how aggressive the disease is, further chromosome testing is required to determine whether the cancer is myeloblastic and involves neutrophils, eosinophils or basophils, or lymphoblastic involving B or T lymphocytes. This case study is on a 14-year-old patient diagnosed with a very aggressive form of ALL (positive for the Philadelphia chromosome mutation). A standard bone marrow transplant, aggressive chemotherapy and radiation therapy were revoked, with treatment being deemed a failure after 34 months. Without any other solutions provided by conventional approaches aside from palliation, the family administered cannabinoid extracts orally to the patient. Cannabinoid resin extract is used as an effective treatment for ALL with a positive Philadelphia chromosome mutation and indications of dose-dependent disease control. The clinical observation in this study revealed a rapid dose-dependent correlation.

KEYWORDS:

Acute lymphoblastic leukemia, Cannabinoids, Hemp oil, Philadelphia chromosome