Does Marijuana Help Parkinsons
With Parkinsons being the second most common neurological disorder among people in the U.S., its no surprise that a lot of research is being done into how to help patients. There has been research recently that specifically looks at marijuana and Parkinsons.
There are a few specific ways marijuana and Parkinsons may have a beneficial relationship with one another.
Other benefits of marijuana and Parkinsons together can include pain management and help with symptoms like sleep problems and nausea. Marijuana may help people with Parkinsons enjoy easier movement because it has muscle relaxing properties as well.
At the same time, with marijuana and Parkinsons there are risks. One of the biggest risks is that marijuana can potentially reduce dopamine levels in the brain, so researchers are looking at how they could accommodate this in the concept of marijuana and Parkinsons.
Possible downfalls to consider with marijuana and Parkinsons can include the mood and behavioral changes that can result from the use of marijuana, as well as loss of balance and the risk of lung cancer that comes with chronic marijuana use.
Medical Marijuana And Legislation By State
Thirty-five states and Washington, DC have passed legislation allowing the use of marijuana-based products.
In some states where medical marijuana is legalized, consumers must register to possess and use cannabis. Other states require consumers to acquire a document from a physician stating that the patient has an approved condition. Under federal law doctors cannot prescribe cannabis, but many states authorize them to issue certifications that allow patients to obtain medical marijuana.
PD is listed as a qualifying condition for medical marijuana in Connecticut, Florida, Illinois, Louisiana, Massachusetts, Michigan, Mississippi, Missouri, New Hampshire, New Mexico, New York, Ohio, Pennsylvania and West Virginia.
Medical marijuana is legal in Alaska, Arizona, Arkansas, California, Colorado, Connecticut, Delaware, Florida, Hawaii, Illinois, Louisiana, Maine, Maryland, Massachusetts, Michigan, Minnesota, Mississippi, Missouri, Montana, Nevada, New Hampshire, New Jersey, New Mexico, New York, North Dakota, Ohio, Oklahoma, Oregon, Pennsylvania, Rhode Island, South Dakota, Utah, Vermont, Washington, West Virginia and Washington, DC.
Strategies To Minimize Reverse Causality Bias
The impact of reverse causality bias in observational studies can be minimized by ensuring that information about exposures is collected before the onset of the disease excluding participants with previous disease at enrollment and excluding a relevant period of early follow-up to minimize distortion of results by cases of disease that were undetected at enrollment. Hence, the first 10 years of follow-up were excluded from all analyses to minimize the effects of reverse causality bias.,,
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Delaying Effect Of Smoking
The fact that proportional assumption hypothesis is verified demonstrates that the risk does not vary over the follow-up period, and this argues against a delaying effect of smoking on PD onset . Moreover, at odds with some previous reports,, our findings of an inverse relationship between smoking variables and risk of PD are not weakened when the analysis is restricted to old-age onset PD . Taken together, these results are not supportive of the hypothesis that smoking might delay, rather than prevent, PD onset, as previously suggested., However, despite this piece of evidence being important and informative per se, the distinction between delaying and preventing any disease onset is somewhat artificial, as these mechanisms might coincide from both a clinical and a biological point of view.
Parkinsons Foundation Centers Of Excellence And Medicinal Marijuana
The Parkinsons Foundation, in partnership with Northwestern University researchers, studied attitudes about cannabis at 40 Centers of Excellence. To the best of our knowledge, this is the first study to provide data on the practices, beliefs and attitudes of expert PD physicians concerning cannabis use.
The results were interesting: most experts said they knew what cannabis did, but disagreed on the details. While there is no general agreement on what the benefits might be for people with PD, the survey confirmed that cannabis is a popular subject within Parkinsons Foundation centers as 95 percent of neurologists reported patients have asked them to prescribe it.
Cannabis study results also included:
- Only 23 percent of physicians had any formal education on the subject of cannabis , thus 93 percent of physicians want cannabis taught in medical school.
- Physicians reported that 80 percent of their patients with PD have used cannabis.
- Only 10 percent of physicians have recommended the use of cannabis to patients with PD.
- In terms of memory: 75 percent of physicians felt that cannabis would have negative effects on short-term memory and 55 percent felt that cannabis could have negative effects on long-term memory
- Only 11 percent of physicians have recommended use of cannabis in the last year
This graph shows how physicians expect cannabis would improve, worsen, or show no effect to PD-related symptoms given their expertise and observations of patients with PD.
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Years Of Smoking Associated With Lower Parkinsons Risk Not Number Of Cigarettes Per Day
The American Academy of Neurology, an association of more than 22,000 neurologists and neuroscience professionals, is dedicated to promoting the highest quality patient-centered neurologic care. A neurologist is a doctor with specialized training in diagnosing, treating and managing disorders of the brain and nervous system such as Parkinsons disease, ALS , dementia, West Nile virus, and ataxia.For more information about the American Academy of Neurology, visit .
Tobacco Coffee And Parkinson’s Disease
This article has been corrected.
Parkinson’s disease belongs to that small group of conditions that occur less often among cigarette smokers than in non-smokers. The observation was first made in a case-control study over 30 years ago, but, as Hernán and colleagues have shown in their recent systematic review and meta-analysis, the finding has been replicated many times. The protective effect is largeaccording to the pooled data, current smokers have a 60% reduction in risk compared with those who have never smokedand consistent between studies in different settings. The fact that two very large prospective studies found a similar reduction in risk to that seen in retrospective studies rules out the possibility that the association can be accounted for by differential survival between smokers and non-smokers. Coffee drinking too, seems to protect against Parkinson’s disease. Here the pooled estimate is a 30% reduction in risk for coffee drinkers compared with non-drinkers.
One unachieved goal in the treatment of Parkinson’s disease is preventing it getting worse. If, as the epidemiological evidence implies, caffeine and nicotine are neuroprotective, some of the new pharmacological treatments currently being developed, such as adenosine A2A receptor blockers and nicotinic agonists, might not only improve symptoms but slow the relentless progression of the disease.
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Marijuana Should Be Studied For Pd Pain Relief
The researchers from this latest study say recent research has indicated that the endocannabinoid system plays an important role in PD. In detail, components of this system are highly expressed in the neural circuit of basal ganglia, which is part of a complex neuronal system, they say.
The neuronal system they mention organizes activities from certain cortical regions that are active in movement control.
When we started doing this review, says Prof. Loewy, the therapies out there were basically for motor symptoms, but Parkinsons also has non-motor symptoms that greatly impact the quality of a persons life.
To dig deeper, he and his team conducted a thorough literature review on studies of marijuana.
The most compelling finding was that chemical components of marijuana yield benefits in the wake of different PD symptoms.
For example, Prof. Loewy notes that marijuana has been found to relieve pain in other diseases, adding that it should be studied for pain relief in people with PD. Pain affects nearly 50 percent of people with the condition, the researchers note.
But why is marijuana specifically promising for PD? According to the team, the cannabinoid compounds in marijuana bind to dopamine receptors to reduce the effects of reduced dopamine in the brain.
Essentially, the compounds replace the normal compounds that are adversely affected by Parkinsons, Prof. Loewy says.
Nicotine And Hydroquinone Inhibit The
The early onset of familial PD is associated with the different missense mutations in the -synuclein gene, corresponding to A53T, A30P and E46K mutations in the -synuclein protein. Therefore, at the next stage, we evaluated the effect of hydroquinone, nicotine and nornicotine on fibrillation of the A53T mutant. represents the time-dependence changes in the ThT fluorescence intensity during the A53T fibril formation in the presence of different compounds at a concentration of 100 M. In agreement with earlier data, shows that the A53T mutant fibrillates faster than the wild type protein. A53T fibrillation was no affected by nornicotine, whereas hydroquinone and nicotine possessed an inhibitory effect. Similar to the wild type protein, nicotine was a better inhibitor of the A53T fibrillation.
Effect of different smoke compounds on the fibrillation kinetics of the A53T mutant. Mutant -synuclein incubated at 1mg/ml alone or in the presence of 100 M nicotine 100 M hydroquinone or 100 M nornicotine .
compares the effects of various nornicotine concentrations on the A53T fibrillation and shows that this compound did not effect the fibrillation even at 400 M concentration. On the other hand, show that hydroquinone inhibited the A53T fibrillation on a concentration-depended manner, whereas the fibrillation process was completely inhibited in the presence of the smallest nicotine concentration .
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Animal Experiments And Transgenic Mice
All procedures were performed according to guidelines and under supervision of the Institutional Animal Care and Use Committee of Cornell University. For all tests, we used both male and female 3-month-old mice. All transgenic animals were compared to corresponding wild-type littermates. Based on variability of prior collected data, necessary sample sizes were estimated using power analysis. No animals were excluded from the analysis assignment to treatment groups was done at random using animal ear-tag numbers and done separately for males and females. All mice were handled daily for two weeks prior to the behavioral tests to eliminate the influence of stress and anxiety on their behavior due to human handling.
Conditional SIRT6 mice
The SIRT6 conditional deletion allele has been described previously . To obtain brain-specific SIRT6 knockout animals , we crossed these mice, which have exons 2 and 3 of SIRT6 flanked by loxP sites , to a nestin-cre line of mice .
RNA sequencing and overrepresentation analysis
MPTP
In vivo MPTP and nicotine mouse experiments: MPTP was delivered by intraperitoneal injection at 10 mg/kg four times a day for four days a week . Mice were scarified for immunohistochemistry 1 month after the completion of MPTP administration. Mice were 3 months of age at the start of treatment.
Nicotine
Does Smoking Protect From Parkinsons Disease
In addition to the numerous studies that demonstrate that PD rates are lower in cigarette smokers than the general population, there are studies that show that the inverse relationship between smoking and PD is dose-dependent. That is, the more a person smokes, the less of a chance that he or she will develop PD. Another study investigated identical twin pairs in which one had PD and the other did not. The twin without PD tended to smoke more than the twin with PD. Since identical twins share the same DNA and often the same environment, many of the variables normally associated with a difference in risk of PD were removed except for smoking. The study is therefore cited as evidence that smoking is protective against PD.
Even if this theory is correct, and smoking does protect people from Parkinsons disease, all physicians and researchers agree, that this does not mean that increasing the rates of smoking among the general population is a desirable strategy to prevent PD. That is because epidemiologic studies have also consistently found that cigarette smoking is a risk factor for a variety of deadly diseases including lung cancer, emphysema, heart disease and stroke. Researchers have therefore tried to harness the possibly protective nature of cigarette smoke in other ways.
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Genetic Variants And Abundance Of Sirt6 Associate With Tnf And Parkinsons Disease In Humans
To investigate the connection between SIRT6 and PD in humans, we performed a meta-analysis of published GWAS studies. First, we analyzed data from the Religious Orders Study and Rush Memory and Aging Project ROS-MAP cohort, in which authors documented the medical history of participants, performed SNP genotyping, and measured genome-wide gene expression in the brain using RNA-sequencing. We analyzed thirteen SIRT6 SNPs reported in these studies and discovered that six SNPs, forming a linkage disequilibrium block in the N-terminus, have a significant impact on the expression of SIRT6 . We tested the association of these SNPs with the incidence of PD and found that SNPs that associate with elevated expression of SIRT6 strongly associate with increased risk of PD . We verified that the identified SNPs associate with the risk of PD in five additional PD GWAS studies , which confirmed our original discovery. It is worth noting that the SNPs with the greatest impact on SIRT6 expression associate with PD incidence most strongly , suggesting a functional link. Moreover, reanalysis of published genome-wide expression data from the substantia nigra of healthy controls and patients with sporadic PD revealed the latter tend to have elevated levels of SIRT6 transcripts .
Fig. 1
Nicotine Promotes An Increase In Survival Even When Treatment Begins In Aged Animals
We then decided to determine whether nicotine has a long-lasting effect even if treatment is suspended when flies age. We also studied whether starting the nicotine treatment in older animals is still effective at promoting fly survival. We determined that the half-life of animals that express Sph-1 is 60 days at this age, parkinsonian phenotypes are evident and there is an important decrease in the number of dopaminergic neurons . To determine if nicotine has a long-lasting effect even if treatment is suspended, we chronically treated Sph-1 expressing flies for 60 days and then suspended the treatment in this condition, a significant lifespan extension was observed compared with animals that were never nicotine fed . Interestingly, files that were not treated with nicotine for the first 60 days of their life and then received nicotine also had a significant extension of their lifespan . These results indicate that in the PD genotype nicotine has a beneficial effect on survival even when the drug is provided at older age, when the parkinsonian symptoms are already evident. Importantly, this effect appears to be very specific as suspension of the nicotine treatment slightly decreases flies survival.
Figure 7
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Tobacco And Nicotine Induce Suppress Sirt6 In Vitro And In Vivo
Since both tobacco and SIRT6 expression are linked to PD, we tested if tobacco smoke influences SIRT6 abundance in neurons in vitro. To do so, we prepared cigarette smoke extract and treated primary murine neurons. We found that like in human smokers, the levels of SIRT6 can be decreased by tobacco in vitro . To test if nicotine itself reduces SIRT6 levels, we treated primary neurons with various doses of nicotine and found a dose-dependent decrease of SIRT6 abundance . The decrease of sirtuin levels by nicotine seems specific to SIRT6, as we observed no changes in the levels of the functionally similar SIRT1 . The reduction of SIRT6 in response to nicotine occurred rapidly, within 90 min of application, without changes in SIRT6 mRNA levels , all of which suggested a degradation mechanism. In support of this hypothesis, nicotine is known to regulate the ubiquitin-proteasome pathway in neurons , and SIRT6 has been shown to be regulated in a proteasome-dependent manner . To test this, we treated primary neurons with nicotine and the proteasome inhibitor MG132. We found that neurons with inhibited proteasome function do not decrease SIRT6 abundance in response to nicotine exposure . These data suggest that nicotine can accelerate proteasome-mediated degradation of SIRT6.
Fig. 2
Sugar Makes You Aggressive
People who consume excess sugar are more likely to engage in aggressive behavior. Children with ADHD are also affected by sugar. For these children, too much sugar affects concentration and promotes hyperactivity. Thats why its a good idea for children to avoid eating sugar during school hours.
Bitter truth about sugar
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Sirt6 Regulates The Pro
Fig. 5
Characterization of brain-specific SIRT6 knockout and overexpressing mice. a Graphical representation of overrepresented pathways from RNA-sequencing analysis of BSKO, BSOX, and WT brains. All pathways shown were significantly altered after Bonferroni correction . The number of genes affected from each pathway and the pathway fold enrichment is shown. See also Additional file for complete data analysis. b Pile-up reads of SIRT6 from the RNA-seq analysis. BSKO mice lack reads for exons 2 and 3, while BSOX mice have increased reads at all exons. c Representative SDS-PAGE analysis of brain cortex lysates from BSKO, BSOX, and WT animals is shown. d Bar graph quantification of the ratio of phosphorylated AKT to total AKT from SDS-PAGE analysis, such as on c, showing a higher ratio in BSKO brains . e Bar graph quantification of full TNF, such as on C, show lower abundance of full length TNF in KO brains . f Bar graph quantification of cleaved TNF, such as on C, show lower abundance of cleaved TNF in KO brains and greater abundance in OX brains . g, h Relative survival of WT, KO, and OX primary neurons assessed by PI/Annexin-V staining with AKT inhibitor or TNF receptor inhibitor , and or 24 h of MG132 stress.
Sugar Contributes To Aging
We already know that sugar has a variety of health effects, but it also affects the skin. Thats in part due to glycation, the process whereby sugar molecules bind to collagen fibers. As a result, the collagen fibers lose their natural elasticity. Excess sugar also damages microcirculation, which slows cell turnover. That can promote the development of wrinkles, make you look older than your age.
Bitter truth about sugar
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