Category Archives: Anorexia

Biomedical benefits of cannabinoids?

Posted on by
Reply

“Cannabinoids appear to be of therapeutic value as antiemetics, antispasmodics, analgesics and appetite stimulants and may have potential uses in epilepsy, glaucoma and asthma.

This paper reviews the clinical trials which have been carried out with cannabinoids including Δ⁹-tetrahydrocannabinol (THC) and synthetic cannabinoids such as nabilone and levonantradol, and discusses the advantages and adverse effects of cannabinoids in clinical use.

The place of cannabinoids in modern medicine remains to be properly evaluated, but present evidence suggests that they could be valuable, particularly as adjuvants, for symptom control in a range of conditions for which standard drugs are not fully satisfactory.”

Very low doses of delta 8-THC increase food consumption and alter neurotransmitter levels following weight loss.

Posted on by
Reply

“We have investigated the effect of 0.001 mg/kg delta(8)-tetrahydrocannabinol (THC) on food consumption, cognitive function, and neurotransmitters in mice…

Cognitive function showed a tendency to improve in the THC-treated mice…

Delta(8)-THC increased food intake significantly more than did delta(9)-THC, while performance and activity were similar.

Thus, delta(8)-THC (0.001 mg/kg) caused increased food consumption and tendency to improve cognitive function, without cannabimimetic side effects.

Hence, a low dose of THC might be a potential therapeutic agent in the treatment of weight disorders.”

http://www.ncbi.nlm.nih.gov/pubmed/15099912

[Cannabinoids in medicine].

Posted on by
Reply

“Cannabinoids have been known for many centuries because of their various effects in healthcare. They are primarily effective in reducing nausea, vomiting, pain, anorexia, spasticity and depression. Some other effects are known, all seem to be mediated by cannabinoid receptors in the central nervous system. In the past years, medical use has been proven in several studies. Today, the therapeutical use of cannabinoids in medicine is increasing, and access was made easier. Especially in pain-management and palliative care, they seem to be a valuable therapeutic option.”

http://www.ncbi.nlm.nih.gov/pubmed/19165445

Negative Regulation of Leptin-induced ROS Formation by CB1 Receptor Activation in Hypothalamic Neurons.

Posted on by
Reply

“The adipocyte-derived, anorectic hormone, leptin, was recently shown to owe part of its regulatory effects on appetite-regulating hypothalamic neuropeptides to the elevation of ROS levels in arcuate nucleus (ARC) neurons.

Leptin is also known to exert a negative regulation on hypothalamic endocannabinoid levels and hence on cannabinoid CB1 receptor activity.

Here we investigated the possibility of a negative regulation by CB1 receptor of leptin-mediated ROS formation in the ARC…

We conclude that CB1 activation reverses leptin-induced ROS formation, and hence possibly some of the ROS-mediated effects of the hormone, by preventing PPAR-γ inhibition by leptin, with subsequent increase of catalase activity.

This mechanism might underlie in part CB1 orexigenic actions under physiopathological conditions accompanied by elevated hypothalamic endocannabinoid levels.”

Modulation of sweet taste sensitivities by endogenous leptin and endocannabinoids in mice.

Posted on by
Reply

“Leptin is an anorexigenic mediator that reduces food intake by acting on hypothalamic receptor, Ob-Rb. In contrast, endocannabinoids are orexigenic mediators that act via cannabinoid CB1 receptors in hypothalamus, limbic forebrain, and brainstem.

In the peripheral taste system, leptin administration selectively inhibits behavioral, taste nerve and taste cell responses to sweet compounds. Opposing the action of leptin, endocannabinoids enhance sweet taste responses.

Taken together, our results suggest that circulating leptin, but not local endocannabinoids, may be a dominant modulator for sweet taste in lean mice; however, endocannabinoids may become more effective modulators of sweet taste under conditions of deficient leptin signaling, possibly due to increased production of endocannabinoids in taste tissue.”

http://www.ncbi.nlm.nih.gov/pubmed/25728242

The role of cannabinoids in regulation of nausea and vomiting, and visceral pain.

Posted on by
Reply

“Marijuana derived from the plant Cannabis sativa has been used for the treatment of many gastrointestinal (GI) disorders, including anorexia, emesis, abdominal pain, diarrhea, and others.

Several cannabinoid receptors, which include the cannabinoid receptor 1 (CB1), CB2, and possibly GPR55, have been identified throughout the GI tract.

These receptors may play a role in the regulation of food intake, nausea and emesis, gastric secretion and gastroprotection, GI motility, ion transport, visceral sensation, intestinal inflammation, and cell proliferation in the gut.

…the regulation of nausea and vomiting by cannabinoids and the endocannabinoid system has shed new knowledge in this field.

Novel drug targets such as FAAH and monoacylglycerol lipase (MAGL) inhibitors appear to be promising in animal models, but more studies are necessary to prove their efficiency.

The promise of emerging drugs that are more selective and peripherally acting suggest that, in the near future, cannabinoids will play a major role in managing an array of GI diseases.”

http://www.ncbi.nlm.nih.gov/pubmed/25715910

Hypothalamic POMC neurons promote cannabinoid-induced feeding.

Posted on by
Reply

“Hypothalamic pro-opiomelanocortin (POMC) neurons promote satiety. Cannabinoid receptor 1 (CB1R) is critical for the central regulation of food intake.

Here we test whether CB1R-controlled feeding in sated mice is paralleled by decreased activity of POMC neurons.

We show that chemical promotion of CB1R activity increases feeding, and notably, CB1R activation also promotes neuronal activity of POMC cells…

Together, these results uncover a previously unsuspected role of POMC neurons in the promotion of feeding by cannabinoids.”

http://www.ncbi.nlm.nih.gov/pubmed/25707796

“Yale Study Finds “Marijuana Munchies” Linked to Brain Neurons”   http://wnpr.org/post/yale-study-finds-marijuana-munchies-linked-brain-neurons

“Mulling the marijuana munchies: How the brain flips the hunger switch” http://news.yale.edu/2015/02/18/mulling-marijuana-munchies-how-brain-flips-hunger-switch

“Effects Of Marijuana: Smoking Weed Gives You ‘The Munchies’ Because Of The Hunger Switch In Your Brain”  http://www.medicaldaily.com/effects-marijuana-smoking-weed-gives-you-munchies-because-hunger-switch-your-brain-322534

“Researchers discover truth about the munchies”                              http://www.west-info.eu/researchers-discover-truth-about-the-munchies/

The interface: marijuana and body weight.

Posted on by
Reply

“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/

The Neuroscience Of Munchies: Why The Scent Of A Burger Gives Us A High – npr

Posted on by
Reply

We Didn't Make This Up: The scientists who performed the study on how cannabis triggers the munchies through the sense of smell commissioned an artist to put this illustration together.

“From cinnamon buns in the morning to a burger after a long run, food never smells as good as when you’re superhungry.

Now scientists have uncovered a clue as to why that might be — and it lies in the munchies and marijuana.

Receptors in the brains of mice that light up when the animals are high are also activated when the critters are fasting, French scientists reported Sunday in the journal Nature Neuroscience.

In other words, skipping a meal triggered the same hunger-inducing brain receptors that marijuana does. And it works, at least in mice, by boosting the sense of smell, neuroscientist Giovanni Marsicano and his team at the Universite de Bordeaux report.

That’s because the receptors that get activated are located in the smelling center of the brain. And sense of smell is known to be a key factor driving appetite.

In case you’re wondering, the mice didn’t toke up. The researchers injected the rodents withTHC, the active ingredient in marijuana.”

http://www.npr.org/blogs/thesalt/2014/02/10/274660785/munchies-neuroscience-why-the-scent-of-a-burger-gives-us-a-high?live=1&utm_content=socialflow&utm_campaign=nprfacebook&utm_source=npr&utm_medium=facebook

“The endocannabinoid system controls food intake via olfactory processes.” http://www.ncbi.nlm.nih.gov/pubmed/24509429

The endocannabinoid system controls food intake via olfactory processes.

Posted on by
Reply

“Hunger arouses sensory perception, eventually leading to an increase in food intake, but the underlying mechanisms remain poorly understood. We found that cannabinoid type-1 (CB1) receptors promote food intake in fasted mice by increasing odor detection.

CB1 receptors were abundantly expressed on axon terminals of centrifugal cortical glutamatergic neurons that project to inhibitory granule cells of the main olfactory bulb (MOB).

Local pharmacological and genetic manipulations revealed that endocannabinoids and exogenous cannabinoids increased odor detection and food intake in fasted mice by decreasing excitatory drive from olfactory cortex areas to the MOB.

Consistently, cannabinoid agonists dampened in vivo optogenetically stimulated excitatory transmission in the same circuit.

Our data indicate that cortical feedback projections to the MOB crucially regulate food intake via CB1 receptor signaling, linking the feeling of hunger to stronger odor processing.Thus, CB1 receptor-dependent control of cortical feedback projections in olfactory circuits couples internal states to perception and behavior.”

http://www.ncbi.nlm.nih.gov/pubmed/24509429