The interface: marijuana and body weight.

“Acute marijuana use is classically associated with snacking behavior (colloquially referred to as “the munchies”). In support of these acute appetite-enhancing effects, several authorities report that marijuana may increase body mass index in patients suffering from human immunodeficiency virus and cancer…

Marijuana is a clinically controversial substance, but one potential medical benefit may be weight gain. According to available studies, appetite stimulation as well as weight gain may occur in patients with physical debilitation due to HIV/AIDS and/or cancer.

As for the effects of marijuana on body weight in the general population, use appears to be associated with a lower body mass index.

…marijuana may genuinely be a regulatory compound, increasing weight in those with low weight, but not in those who are normal or overweight.”

 http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4204468/

[Importance of the endocannabinoid system in the regulation of energy homeostasis].

“The endocannabinoid system is an endogenous signaling system that plays a role in the regulation of energy homeostasis and lipid and glucose metabolism-all of which can influence cardiometabolic risk. The endocannabinoid system appears to be a promising novel mechanistic pathway that modulates important aspects afcardiovascular and metabolic function. The endocannabinoid system is normally a silent physiologic system that becomes transiently activated, that is, only when needed. Evidence suggests that the endocannabinoid system is tonically overactive in human obesity and in animal models of genetic and diet-induced obesity. However, there is evidence in studies that the ECS is tonically overactivated in obesity, although it remains unclear whether overactivation of the ECS precedes or is consequent to expression of the obese phenotype. Rimonabant, a selective cannabinoid-1 receptor (CB1) blocker, has been shown to reduce smoking, body weight and improve and improves the profile of several metabolic risk factors in high-risk patients.”

http://www.ncbi.nlm.nih.gov/pubmed/23687711

http://www.thctotalhealthcare.com/category/obesity-2/

Mitochondria: A Possible Nexus for the Regulation of Energy Homeostasis by the Endocannabinoid System?

“The endocannabinoid system (ECS) regulates numerous cellular and physiological processes through the activation of receptors targeted by endogenously produced ligands called endocannabinoids. Importantly, this signalling system is known to play an important role in modulating energy balance and glucose homeostasis. For example, current evidence indicates that the ECS becomes overactive during obesity whereby its central and peripheral stimulation drives metabolic processes that mimic the metabolic syndrome. Herein, we examine the role of the ECS in modulating the function of mitochondria which play a pivotal role in maintaining cellular and systemic energy homeostasis, in large part due to their ability to tightly coordinate glucose and lipid utilisation. Because of this, mitochondrial dysfunction is often associated with peripheral insulin resistance and glucose intolerance, as well as the manifestation of excess lipid accumulation in the obese state. This review aims to highlight the different ways through which the ECS may impact upon mitochondrial abundance and/or oxidative capacity, and where possible, relate these findings to obesity-induced perturbations in metabolic function. Furthermore, we explore the potential implications of these findings in terms of the pathogenesis of metabolic disorders and how these may be used to strategically develop therapies targeting the ECS.”

http://www.ncbi.nlm.nih.gov/pubmed/24801388

http://www.thctotalhealthcare.com/category/obesity-2/

Obesity and cannabis use: results from 2 representative national surveys.

“We hypothesized that the prevalence of obesity would be higher in cannabis users than in nonusers… this analysis showed that even if cannabis consumption increases appetite, people using cannabis are less likely to be obese than people who do not use cannabis…

The authors conclude that the prevalence of obesity is lower in cannabis users than in nonusers.”

http://www.ncbi.nlm.nih.gov/pubmed/21868374
http://aje.oxfordjournals.org/content/174/8/929.long

Link between obesity and cancer – Science

 

“Link between obesity and cancer” http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3670342/

“Biological mechanisms linking obesity and cancer risk: new perspectives.” http://www.ncbi.nlm.nih.gov/pubmed/19824817

“Overweight/obesity and cancer genesis: more than a biological link.” http://www.ncbi.nlm.nih.gov/pubmed/18035514

“The Obesity-Cancer Link: Lessons Learned from a Fatless Mouse” http://cancerres.aacrjournals.org/content/67/6/2391.long

“Epidemiology and pathophysiology of obesity as cause of cancer.” http://www.ncbi.nlm.nih.gov/pubmed/17299670

“Obesity and cancer.” http://www.ncbi.nlm.nih.gov/pubmed/19924603

“Obesity and cancer: pathophysiological and biological mechanisms.” http://www.ncbi.nlm.nih.gov/pubmed/18465361

“Obesity and cancer risk: evidence, mechanisms, and recommendations” http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3476838/

 “The growing challenge of obesity and cancer: an inflammatory issue.” http://www.ncbi.nlm.nih.gov/pubmed/21793838

“Growth Signals, Inflammation, and Vascular Perturbations, Mechanistic Links Between Obesity, Metabolic Syndrome, and Cancer” http://atvb.ahajournals.org/content/32/8/1766.long

  “Obesity, metabolic dysregulation, and cancer: a growing concern and an inflammatory (and microenvironmental) issue” http://onlinelibrary.wiley.com/doi/10.1111/j.1749-6632.2012.06737.x/full

 “Obesity-induced gut microbial metabolite promotes liver cancer through senescence secretome.” http://www.ncbi.nlm.nih.gov/pubmed/23803760

“Overweight, obesity and cancer: epidemiological evidence and proposed mechanisms” http://www.nature.com/nrc/journal/v4/n8/full/nrc1408.html

“Overweight and obesity: a review of their relationship to metabolic syndrome, cardiovascular disease, and cancer in South America.” http://www.ncbi.nlm.nih.gov/pubmed/23452284

“Cytokines, obesity, and cancer: new insights on mechanisms linking obesity to cancer risk and progression.” http://www.ncbi.nlm.nih.gov/pubmed/23121183

“Obesity-driven inflammation and cancer risk: role of myeloid derived suppressor cells and alternately activated macrophages” http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3555202/

“Inflammation, autophagy, and obesity: common features in the pathogenesis of pancreatitis and pancreatic cancer.” http://www.ncbi.nlm.nih.gov/pubmed/23622129

“Obesity, energy balance, and cancer: new opportunities for prevention.” http://www.ncbi.nlm.nih.gov/pubmed/23034147

 “Obesity and colorectal cancer.” http://www.ncbi.nlm.nih.gov/pubmed/23481261

“Obesity and Risk of Colorectal Cancer: A Meta-analysis of 31 Studies with 70,000 Events” http://cebp.aacrjournals.org/content/16/12/2533.long

 “Obesity and Risk of Colorectal Cancer: A Systematic Review of Prospective Studies” http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3547959/

 “Central obesity and breast cancer risk: a systematic review.” http://www.ncbi.nlm.nih.gov/pubmed/12916817

“Role of Obesity in the Risk of Breast Cancer: Lessons from Anthropometry” http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3575614/

“The molecular contribution of TNF-α in the link between obesity and breast cancer.” http://www.ncbi.nlm.nih.gov/pubmed/21165572

“Subcellular Localization of Cyclic AMP-Responsive Element Binding Protein-Regulated Transcription Coactivator 2 Provides a Link between Obesity and Breast Cancer in Postmenopausal Women” http://cancerres.aacrjournals.org/content/69/13/5392.long

 “An IL-6 link between obesity and cancer.” http://www.ncbi.nlm.nih.gov/pubmed/23277002

 “Expression of microRNAs: potential molecular link between obesity, diabetes and cancer.” http://www.ncbi.nlm.nih.gov/pubmed/21767342

“Excess body weight and obesity–the link with gastrointestinal and hepatobiliary cancer.” http://www.ncbi.nlm.nih.gov/pubmed/21386810

“Obesity and gastrointestinal cancer.” http://www.ncbi.nlm.nih.gov/pubmed/20306531

 “The link between obesity and prostate cancer: the leptin pathway and therapeutic perspectives.” http://www.ncbi.nlm.nih.gov/pubmed/16344847

“The relationship between obesity and prostate cancer: from genetics to disease treatment and prevention” http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3523022/

 “Reducing the weight of cancer: mechanistic targets for breaking the obesity-carcinogenesis link.” http://www.ncbi.nlm.nih.gov/pubmed/18971125

“Overweight, obesity, and cancer risk.” http://www.ncbi.nlm.nih.gov/pubmed/12217794

“Obesity and cancer: the risks, science, and potential management strategies.” http://www.ncbi.nlm.nih.gov/pubmed/16053036

 “Overweight as an avoidable cause of cancer in Europe.” http://www.ncbi.nlm.nih.gov/pubmed/11169969

“Obesity management–an opportunity for cancer prevention.” http://www.ncbi.nlm.nih.gov/pubmed/19848061

 

Scales

Study Links Obesity, Cancer – News

“Study Links Obesity, Cancer” http://www.cbsnews.com/video/watch/?id=3438650n

“‘Direct link’ between cancer and obesity” http://www.independent.co.uk/life-style/health-and-families/health-news/direct-link-between-cancer-and-obesity-398386.html

 “Obesity link to cancer” http://news.bbc.co.uk/2/hi/health/1334311.stm 

“Study supports link between obesity and higher incidence of cancer, poorer prognosis” http://medicalxpress.com/news/2012-10-link-obesity-higher-incidence-cancer.html

“Obesity-Cancer Link Detailed” http://www.the-scientist.com/?articles.view/articleNo/36204/title/Obesity-Cancer-Link-Detailed/

  “Obesity Linked to Many Cancer Cases in U.S.” http://www.webmd.com/cancer/news/20091105/obesity-linked-to-many-cancer-cases-in-us

“Increased obesity means increased cancer cases” http://thechart.blogs.cnn.com/2010/08/05/increased-obesity-means-increased-cancer-cases/

 “Obesity responsible for 100,000 cancer cases annually” http://edition.cnn.com/2009/HEALTH/11/05/obesity.cancer.link/

“Obesity is now the leading cause of cancer” http://www.nydailynews.com/life-style/health/obesity-leading-cancer-article-1.403496

“Obesity as a Cause of Endometrial Cancer: Gynecologic Oncologists to Add Perspective on New Report” http://www.newswise.com/articles/obesity-as-a-cause-of-endometrial-cancer-gynecologic-oncologists-to-add-perspective-on-new-report

“Obesity Helps Spur Cancer’s Growth, Mouse Study Suggests” http://healthyliving.msn.com/diseases/cancer/obesity-helps-spur-cancers-growth-mouse-study-suggests

“Obesity makes cancer harder to treat – researchers” http://abclocal.go.com/kabc/story?id=9167668

“Childhood Obesity linked to Colorectal Cancer” http://www.hivehealthmedia.com/childhood-obesity-linked-colorectal-cancer/

“Childhood obesity linked to bladder, urinary cancer” http://india.nydailynews.com/business/007bed187246683db27f00329afb7e2a/childhood-obesity-linked-to-bladder-urinary-cancer

“Study links childhood obesity to cancer in adults”  http://www.jpost.com/Health-and-Science/Study-links-childhood-obesity-to-cancer-in-adults 

 “Weight Gain and Obesity Linked with Endometrial Cancer Risk” http://news.yale.edu/2011/03/16/weight-gain-and-obesity-linked-endometrial-cancer-risk 

 “Athlone scientist reveals link between obesity and oesophageal cancer” http://www.westmeathindependent.ie/news/roundup/articles/2013/07/03/4016553-athlone-scientist-reveals-link-between-obesity-and-oesophageal-cancer/

“Scientists uncover key mechanism that links obesity and diabetes with cancer” http://www.news-medical.net/news/20130201/Scientists-uncover-key-mechanism-that-links-obesity-and-diabetes-with-cancer.aspx

 “Obesity Gene Linked To Skin Cancer” http://www.medicalnewstoday.com/articles/257159.php

“Obesity linked to liver cancer, gallbladder cancer” http://www.foodconsumer.org/newsite/Non-food/Disease/obesity_liver_cancer_gallbladder_cancer_0917120712.html

“Obesity linked to womb cancer rise” http://www.nursingtimes.net/nursing-practice/clinical-zones/public-health/obesity-linked-to-womb-cancer-rise/5017506.article

“Obesity Linked to Ovarian Cancer” http://abcnews.go.com/Health/Healthday/story?id=6581157&page=1

“Obesity genes linked to uterine cancer” http://news.vanderbilt.edu/2012/01/obesity-uterine-cancer/

 “Obesity Linked to Ovarian Cancer” http://articles.washingtonpost.com/2009-01-05/news/36784799_1_ovarian-cancer-obese-women-normal-weight-women

“Obesity Linked to More Advanced and More Aggressive Thyroid Cancer” http://www.familypracticenews.com/news/more-top-news/single-view/obesity-linked-to-more-advanced-and-more-aggressive-thyroid-cancer/30971304ec4a03ee4ce8abd728da736c.html

“Obesity Linked to Higher Risk for Aggressive Thyroid Cancer” http://www.medscape.com/viewarticle/764234

 “Pancreatic cancer and obesity linked” http://latimesblogs.latimes.com/booster_shots/2009/06/pancreatic-cancer-and-obesity-linked.html

 “Obesity linked to rise in kidney cancer” http://www.cancerresearchuk.org/cancer-info/news/archive/pressrelease/2002-09-21-obesity-linked-to-rise-in-kidney-cancer

 “Obesity fuels record rise in kidney cancers” http://www.nhs.uk/news/2012/03march/Pages/Obesity-fuels-kidney-cancer-rise.aspx

 “Obesity Linked to Prostate Cancer, Study Finds” http://www.webmd.com/prostate-cancer/news/20130423/obesity-linked-to-prostate-cancer-study-finds

“Obesity Raises Risk of Aggressive Prostate Cancer” http://www.renalandurologynews.com/obesity-raises-risk-of-aggressive-prostate-cancer/article/202883/#

 “Obesity increases men’s risk of dying from prostate cancer” http://www.nbcnews.com/health/obesity-increases-mens-risk-dying-prostate-cancer-6C9566874 

“Researchers discover link between obesity gene and breast cancer” http://medicalxpress.com/news/2011-05-link-obesity-gene-breast-cancer.html

 

 “Breast Cancer Linked to Obesity Gene, New Research Suggests” http://www.sciencedaily.com/releases/2011/05/110523124402.htm 

 

“Research Piles Up on Links Between Cancer and Obesity” http://blogs.wsj.com/health/2009/06/23/research-piles-up-on-links-between-cancer-and-obesity/

Cannabis exposure associated with weight reduction and β-cell protection in an obese rat model.

“The aim of this study was to investigate the effect of an organic cannabis extract on β-cell secretory function in an in vivo diet-induced obese rat model and determine the associated molecular changes within pancreatic tissue…

These results suggest that the cannabis extract protects pancreatic islets against the negative effects of obesity.”

http://www.ncbi.nlm.nih.gov/pubmed/22421529

Therapeutic potential of cannabinoid medicines.

Drug Testing and Analysis

“Cannabis was extensively used as a medicine throughout the developed world in the nineteenth century but went into decline early in the twentieth century ahead of its emergence as the most widely used illicit recreational drug later that century. Recent advances in cannabinoid pharmacology alongside the discovery of the endocannabinoid system (ECS) have re-ignited interest in cannabis-based medicines.

The ECS has emerged as an important physiological system and plausible target for new medicines. Its receptors and endogenous ligands play a vital modulatory role in diverse functions including immune response, food intake, cognition, emotion, perception, behavioural reinforcement, motor co-ordination, body temperature, wake/sleep cycle, bone formation and resorption, and various aspects of hormonal control. In disease it may act as part of the physiological response or as a component of the underlying pathology.

In the forefront of clinical research are the cannabinoids delta-9-tetrahydrocannabinol and cannabidiol, and their contrasting pharmacology will be briefly outlined. The therapeutic potential and possible risks of drugs that inhibit the ECS will also be considered. This paper will then go on to review clinical research exploring the potential of cannabinoid medicines in the following indications: symptomatic relief in multiple sclerosis, chronic neuropathic pain, intractable nausea and vomiting, loss of appetite and weight in the context of cancer or AIDS, psychosis, epilepsy, addiction, and metabolic disorders.”

http://www.ncbi.nlm.nih.gov/pubmed/24006213

http://onlinelibrary.wiley.com/doi/10.1002/dta.1529/abstract

Pot smokers skinnier than non-tokers, study says – NBCNews

“We’re all familiar with the stereotype of the typical pot smoker — a lumpy, lazy couch potato with one hand wrapped around the remote and the other elbow-deep in a bag of nacho cheese Doritos.

But new research out of France gives a different spin to the stereotypical stoner.

“Cannabis is supposed to increase appetite,” says Dr. Yann Le Strat, a psychiatrist at Louis-Mourier Hospital in Colombes, France and co-author of a new study in the American Journal of Epidemiology. “So we hypothesized that cannabis users would be more likely to have higher weight than non-users and be more likely to be obese.”

Instead, Le Strat and his colleagues found just the opposite.

“We found that cannabis users are less likely to be obese than non-users,” he says. “We were so surprised, we thought we had [made] a mistake. Or that our results were due to the sample we studied. So we turned to another completely independent sample and found exactly the same association…”

“I know when we think about smoking pot, one of the jokes is that it gives you the munchies and dry mouth so you drink a bunch of water and eat a bunch of Cheetos,” she says.

“Maybe we need to adjust the stereotype.””

More: http://www.nbcnews.com/health/pot-smokers-skinnier-non-tokers-study-says-1C6437141

Peripherally restricted CB1 receptor blockers.

“Antagonists (inverse agonists) of the cannabinoid-1 (CB1) receptor showed promise as new therapies for controlling obesity and related metabolic function/liver disease.

These agents, representing diverse chemical series, shared the property of brain penetration due to the initial belief that therapeutic benefit was mainly based on brain receptor interaction. However, undesirable CNS-based side effects of the only marketed agent in this class, rimonabant, led to its removal, and termination of the development of other clinical candidates soon followed. Re-evaluation of this approach has focused on neutral or peripherally restricted (PR) antagonists.

Supporting these strategies, pharmacological evidence indicates most if not all of the properties of globally acting agents may be captured by molecules with little brain presence. Methodology that can be used to eliminate BBB penetration and the means (in vitro assays, tissue distribution and receptor occupancy determinations, behavioral paradigms) to identify potential agents with little brain presence is discussed.

Focus will be on the pharmacology supporting the contention that reported agents are truly peripherally restricted. Notable examples of these types of compounds are: TM38837 (structure not disclosed); AM6545 (8); JD5037 (15b); RTI-12 (19).”

http://www.ncbi.nlm.nih.gov/pubmed/23902803