Monthly Archives: January 2013

Alzheimer’s Disease

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“Alzheimer’s disease (AD), also called Alzheimer disease, senile dementia of the Alzheimer type, primary degenerative dementia of the Alzheimer’s type, or simply Alzheimer’s, is the most common form of dementia. This incurable, degenerative, and terminal disease was first described by German psychiatrist and neuropathologist Alois Alzheimer in 1906 and was named after him. Most often, it is diagnosed in people over 65 years of age, although the less-prevalent early-onset Alzheimer’s can occur much earlier. In 2006, there were 26.6 million sufferers worldwide. Alzheimer’s is predicted to affect 1 in 85 people globally by 2050.

Although the course of Alzheimer’s disease is unique for every individual, there are many common symptoms. The earliest observable symptoms are often mistakenly thought to be ‘age-related’ concerns, or manifestations of stress. In the early stages, the most common symptom is inability to acquire new memories, observed as difficulty in recalling recently observed events. When AD is suspected, the diagnosis is usually confirmed with behavioral assessments and cognitive tests, often followed by a brain scan if available.

As the disease advances, symptoms include confusion, irritability and aggression, mood swings, language breakdown, long-term memory loss, and the general withdrawal of the sufferer as their senses decline. Gradually, bodily functions are lost, ultimately leading to death. Individual prognosis is difficult to assess, as the duration of the disease varies. AD develops for an indeterminate period of time before becoming fully apparent, and it can progress undiagnosed for years. The mean life expectancy following diagnosis is approximately seven years. Fewer than three percent of individuals live more than fourteen years after diagnosis.

The cause and progression of Alzheimer’s disease are not well understood. Research indicates that the disease is associated with plaques and tangles in the brain. Currently used treatments offer a small symptomatic benefit; no treatments to delay or halt the progression of the disease are, as of yet, available. As of 2008, more than 500 clinical trials have been conducted for identification of a possible treatment for AD, but it is unknown if any of the tested intervention strategies will show promising results. A number of non-invasive, life-style habits have been suggested for the prevention of Alzheimer’s disease, but there is a lack of adequate evidence for a link between these recommendations and reduced degeneration. Mental stimulation, exercise, and a balanced diet are suggested, as both a possible prevention and a sensible way of managing the disease.”

Video: http://www.medicalmarijuanainc.com/index.php/alzheimer-s-disease

The endocannabinoid system and Alzheimer’s disease.

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“The importance of the role of the endocannabinoid system (ECS) in neurodegenerative diseases has grown during the past few years. Mostly because of the high density and wide distribution of cannabinoid receptors of the CB(1) type in the central nervous system (CNS), much research focused on the function(s) that these receptors might play in pathophysiological conditions.

Our current understanding, however, points to much diverse roles for this system. In particular, other elements of the ECS, such as the fatty acid amide hydrolase (FAAH) or the CB(2) cannabinoid receptor are now considered as promising pharmacological targets for some diseases and new cannabinoids have been incorporated as therapeutic tools.

 Although still preliminary, recent reports suggest that the modulation of the ECS may constitute a novel approach for the treatment of Alzheimer’s disease (AD). Data obtained in vitro, as well as in animal models for this disease and in human samples seem to corroborate the notion that the activation of the ECS, through the use of agonists or by enhancing the endogenous cannabinoid tone, may induce beneficial effects on the evolution of this disease.”

http://www.ncbi.nlm.nih.gov/pubmed/17952652

Targeting the endocannabinoid system in Alzheimer’s disease.

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“The endocannabinoid system is rapidly emerging as a potential drug target for a variety of immune-mediated central nervous system diseases. There is a growing body of evidence suggesting that endocannabinoid interventions may have particular relevance to Alzheimer’s disease. Here we present a review of endocannabinoid physiology, the evidence that underscores its utility as a potential target for intervention in Alzheimer’s disease, and suggest future pathways of research.

Inflammation and oxidative stress are generally accepted as a critical risk factor for the development of AD, and interventions such as cannabinoids that attenuate these risks without arresting microglial activity and have innate neuroprotective benefits are attractive as potential preventative treatments for AD.

There is a potential for the development of CB1 interventions, whether agonists or antagonists, with applications for a variety of cognitive disorders including neurodegenerative disorders and schizophrenia. The recent discovery of a CB1 receptor Positron Emission Tomography tracer for clinical use may provide the opportunity to evaluate the impact of the regional distribution of CB1 receptors in brain on domain-specific cognitive performance (memory, executive function, praxis) in healthy individuals. Additionally, if AD is a disease of overproduction of eCBs, this may be visualized in case-control CB1receptor binding studies.

The emerging data suggest that the eCB system is a potential target for immune and/or cognitive intervention in AD. A wealth of available chemical compounds capable of intervening in the eCB system at a variety of levels and the success with which these compounds have been used in animal models suggest the potential for human drug development. What is missing is a clear direction for that development based on a concise conceptualization of eCB system function in both health and in neurodegenerative and inflammatory conditions such as AD. Focused experiments are now required to move the field forward.”

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2889705/

The role of the endocannabinoid system in Alzheimer’s disease: facts and hypotheses.

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“Unlike other neuroinflammatory disorders, like Parkinson’s disease, Huntington’s disease and multiple sclerosis, little is still known of the role of the endocannabinoid system in Alzheimer’s disease (AD). This is partly due to the poor availability of animal models that are really relevant to the human disease, and to the complexity of AD as compared to other neurological states. Nevertheless, the available data indicate that endocannabinoids are likely to play in this disorder a role similar to that suggested in other neurodegenerative diseases, that is, to represent an endogenous adaptive response aimed at counteracting both the neurochemical and inflammatory consequences of beta-amyloid-induced tau protein hyperactivity, possibly the most important underlying cause of AD.

Furthermore, plant and synthetic cannabinoids, and particularly the non-psychotropic cannabidiol, might also exert other, non-cannabinoid receptor-mediated protective effects, including, but not limited to, anti-oxidant actions. There is evidence, from in vivo studies on beta-amyloid-induced neurotoxicity, also for a possible causative role of endocannabinoids in the impairment in memory retention, which is typical of AD.

 This might open the way to the use of cannabinoid receptor antagonists as therapeutic drugs for the treatment of cognitive deficits in the more advanced phases of this disorder. The scant, but nevertheless important literature on the regulation and role of the endocannabinoid system in AD, and on the potential treatment of this disorder with cannabinoids and endocannabinoid-based drugs, are discussed in this mini-review.”

http://www.ncbi.nlm.nih.gov/pubmed/18781980

Marijuana nutrients found to help prevent Alzheimer’s disease

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“A study conducted by scientists at Scripps Research Institute in California has found that, contrary to marijuana’s reputation, the ingredients of the drug can actually fight off the memory-impairing effects of Alzheimer’s disease.The researchers found that the active ingredient in marijuana — delta-9-tetrahydrocannabinol, or THC — is responsible for the positive effect, as it can prevent the breakdown of the neurotransmitter acetylcholine even better than commercially marketed prescription drugs.

The study also showed that THC could completely prevent the enzyme acetylcholinesterase (AchE) from forming amyloid plaques, whereas twice as much donepezil and tacrine — the two drugs approved for Alzheimer’s treatment — only reduced such clumping by 22 and 7 percent, respectively, the researchers reported in the journal Molecular Pharmaceutics. This led the scientists to conclude that a more effective Alzheimer’s drug could be developed in the future.”

Read more: http://www.naturalnews.com/020667_Marijuana_Alzheimers_drugs.htm

Alzheimer’s, Mom and Cannabis

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“It is Skunk PharmResearch’s policy to let patients tell their own story, but in the case of mom, as her daughter and 24/7 caregiver, I will speak for her.  She is in the late seventh and final stage of Alzheimer’s and would want her story told.

Mom was diagnosed as late stage six when she came to me from Seattle four years ago.  She was given six more months to live. She began displaying symptoms before 1998, but she wasn’t diagnosed until 2001, following her first husband’s death.  It took that long to resolve other health issues and get her to a neurologist.

Just the thought of Alzheimer’s frightened her so, that we eventually had to trick her, to get her to a doctor for testing.   Once tested and diagnosed, they put her on Aricept, which brought back cognitive skills, with slow decline for the next seven years while my step brother cared for her in her own home.  Along with other western meds, this was her medical course.

When Mom’s Alzheimer’s progressed to the point that she became combative and personal hygiene became an issue, my brother planned to put her in a nursing home, but I quit my job to look after her.  I moved her to Portland with me and took over her care, to focus on the quality of her remaining life.

For five months prior to her arrival, I immersed myself into learning as much about Alzheimer’s as possible, researching and joining The Alzheimer’s Association, as well as the Online Alzheimer’s Support Group, spending as much time as possible conversing with patients and caregivers alike, to prepare myself for the task.

When Mom arrived, besides being on five over the counter drugs, she was on three inhalers and a pill for asthma, blood pressure meds, allergy meds, anti psychotics that made her angry, anti seizure meds that made her delusional, plus three others I have no idea what they were used to combat.

We got her an OMMP card immediately upon her arrival.  She had smoked cannabis recreationally with me for over thirty years, but never medically until she came toOregon. Cannabis was my only means of mitigating her despicable behavior (psychotic).

Her physical health was also poor, so I changed her diet, eliminated dairy, wheat and gluten. I prepared and feed her home cooked meals, using whole organic ingredients, supplemented with quality vitamins and minerals.

I’ve continued to work with her doctor to straighten out her mishmash of meds.  He started with large doses of anti psychotics to combat the behavioral issues (with potential seizure/death side effect), and we systematically took her off as many of the other drugs as possible.  Meanwhile, I started trying the different forms of cannabis concentrates.

The first extractions were cannabis essential oils using hot grape seed oil, but she didn’t like the flavor and refused to ingest it.

Given that unused meds are 100% ineffective, I next tried honey elixir, thinking she might go for the sweetness of the honey, but no luck.

No luck with fudge either, even though she loves chocolate.

I quickly determined that the only way to get substantial doses into mom would be via concentrates, so after experimenting with bubble hash combined with coconut oil as a menstruum, I focused on hash oil in an effort to improve consistency and homogeneity for consistency in dosing.

More specifically I began to experiment on my version of the Holy Anointing Oil from Exodus, using coconut oil instead of olive oil, and brewed from essential oils, as opposed to using the biblical perfumer’s extraction practices.

More on that medication at:  http://skunkpharmresearch.com/holy-anointing-oil-and-holy-shit/

It worked beautifully!  The flavor of the cannabis was concealed by the remaining essential oils in the ingredients.  She loved it, and to my delight, she became happier and less combative.

Mom transformed from aggressive and angry to the cheerful woman I knew from childhood.  Instead of slapping my cheeks, she caressed them tenderly and moved my hair from my face as she told me she loved me.  From her isolation came the interaction and humor required to joke with us.   From frantic shuffling and hiding of objects she began offering them for my use.  Rather then kicking, biting and hitting, she became happily compliant, even cooperative.  She literally became a social butterfly!

Mom also suffered extensively from muscle spasms, particularly in her legs, typically relieved by dancing the night away together. But one night I thinned some HAO oral with coconut oil, to reduce the cinnamon oil below topical TLV as an irritant and to improve penetration.  After slathering her leg with the modified HAO, the cramps went away, allowing her to go back to sleep.  She woke 20 minutes later complaining of the other leg.  Again, HAO topical and back to sleep! HAOT was born.

It took nearly two years working with her doctor to get her medical care stabilized and a permanent “Primary Care Practitioner” (PCP) established.  We were able to get her off of most of the original drug regiment, and determined that her psychotic episodes were directly related to urinary tract infections, for which she is susceptible.

With cultures and medications, we were able to get the UTIs in check which eliminated the need for the anti psychotic, Seroquil.  We determined that it was medicating the behavioral issues related to UTI’s, rather then psychotic behavior associated with dementia.  Since Seroquil has black box warnings (death) for the elderly, I was more than pleased to eliminate it.

She had begun having seizures after starting seroquil. a potential side effect even with anti seizure meds.  The pharmaceutical consultation revealed anti seizure meds also cause seizures if doses are missed, late or low dose was taken.  Once on anti seizure meds, one must stay on them.  He warns that it permanently lowers the resistance to seizures, although other pharmacists suggested a slow taper is possible.

The delusional side effects of Dilantin, her original medication, are ill advised for a demented patient.   It took me nearly two and a half years to talk the doctors into letting me try a slow wean off the Dilantin, hoping the fact she had not taken Seroquil for over six months and that her cancer doses of cannabis might stop potential seizures.  Although her cognitive capabilities were notably and significantly improved, she still seized, even with using a slow taper and cannabis.

We next went to Depekote, which gave her diarrhea.  We weaned her slowly, as it is also an antidepressant.  That took nearly three weeks.  The diarrhea kept her in constant battles with UTIs, which tend to promote seizures in demented patients, a vicious downward spiral.  We began feeding her Metamucil cookies.  It seemed like that was all she ate.

We then put her on Lamotragine.  When she seized, the dose was increased…..which gave her diarrhea.  Back to that vicious cycle.  More cookies and holy root balm to rescue her poor little raw butt! I used MU’s recipe with my twist (thanks MU!).

Next we tried Gabapentin, hoping that she would acclimate to the initial drowsiness.  Again she seized on the dose, so we increased the night dose to compensate.  The results were diarrhea….more cookies.

Keppra is well accepted for seizures, but it too gives Mom diarrhea.  Opium tincture is the last choice drug for its control.  Dosing is easier and we have more time and room for nutritious/delicious food.  It was time for closer supervision; she was placed on in home hospice care.  Weekly she gets visits from health care, social and spiritual sectors.

I don’t know what we will try next; perhaps, if Mom had never gone on anti seizure meds (off label for muscle spasms), she would only be on cannabis today.  She has never had seizures until now, nor have there been any record of seizures in our family…ever!  She was given Dilantin for muscle spasms, when western medicine quit prescribing Quinine, deeming it damaging to the body, and seizures are not?  But, perhaps the seizures are caused by Alzheimer’s itself, an unusual but occasional occurrence.

The good and interesting news is, with all of what has been happening to mom, I began a mega dose (two plus grams/day) to try and alter her mood.  We dose her every two hours (or our life is hell).  During that period of time, I increased her dose to between .3 and .5 grams.  That is six or seven doses a day or on the light side, 62 grams per month….more then a cancer cure…in one month.

The results were quite unexpected.  The cognitive changes were unmistakably positive.  She began to interact appropriately, become more animated and loving, and appropriately reactive, choosing short phrases.  In short, her cognitive thinking had improved!  She even played jokes on us. When Dino came to visit; she hugged him and kissed him and said “it’s been so long since I seen you.”  Then demanded another round of hugs and kisses!

Even her doctor, whom does not normally sign for medical cannabis cards, noticed the dramatic improvement, saying, “I wish all my Alzheimer’s patients were on cannabis.  Look at her quality of life!”  She signs Mom’s renewals no questions asked.

Where everyone I know (even those with huge tolerances) would be stupid, asleep or puking on two plus grams of cannabis oil in ten hours; mom has gained cognitive capacity!  Who’d of thought?

I read that CBD’s are the anti seizure cannabinoid, so I grew some plants with balanced THC/CBD to see if they can save Mom from seizures and I can add mitigation of seizures, to the list of ailments for which she no longer takes western medication.  To date, those include asthma, arthritic pain, agitation and anxiety of Alzheimer’s, sleeplessness, blood pressure, and muscle spasms.

Mom lost another ten pounds from diarrhea trying the different western meds, but I have Hippie Chicken hanging and will be extracting her soon.  Hopefully, mom will eat then.  (It has become obvious that high CBD strains induce appetite.  She eats well after anti seizure cannabis medication. Hopefully others can watch that tendency to see if this is an isolated response.)

After getting Mom on the high CBD medications, we took our time weaning her off anti seizure meds, ten days on each reduction, with four total reductions.  She did fine during the reduction, but the balanced CBD cannabis did not give her the needed behavioral change of psychotic effects of THC, so we backed her off to .1 mg per dose in balanced CBD/THC oil and the rest of her cannabis dose in high THC strains.

Once off western anti seizure meds, she faired well for nearly three weeks before she seized, at which time we adjusted the dosing to try and compensate for the lowered level of CBD in her system.  Just prior to bed we gave her a full gram of balanced CBD/THC oil, then again as she slept in the morning such that it would wear off by the time she woke.    Six days later she seized again, so we put her on immediate doses of Lorazapam, then back on Keppra, with liquid Opium to combat the diarrhea.

Next I’d like to try Betane Hydrochloride to aid in digestion for the diarrhea.  Although Mom’s life is limited in length, it would be nice if she did not have to take the opiates.  Updates will follow.

For now, she is on anti seizure meds, opiates for diarrhea, cannabis for asthma, blood pressure, muscle spasms, arthritic pain and sleeplessness, anxiety, aggression of Alzheimer’s.  She weighs 86 pounds at 5’4” now.  She eats and drinks but not enough to sustain.  (Even hippie chicken didn’t work as well as i had hoped.)  But, fourteen years after initial symptoms, she is mostly happy and loving….as long as she gets her cannabis dose!”

http://skunkpharmresearch.com/alzheimers-mom-and-cannabis/

 

Medical Marijuana as Effective Treatment for Alzheimer’s Disease

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“Regular low dose cannabis smoking might keep Alzheimer’s away, according to marijuana research by professor Gary Wenk and associate professor Yannic Marchalant of the Ohio State Department of Psychology. Wenk’s studies show that a low dosage in the morning of a certain cannabinoid, a component in marijuana, reversed memory loss in older rats’ brains. In his study, an experimental group of old rats received a dosage, and a control group of rats did not. The old rats that received the drugs performed better on memory tests, and the drug slowed and prevented brain cell death.”

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“Alzheimer’s is a disease unique to humans…, but rat brains are similar enough to human brains to serve as partial models for humans, Wenk said.

… marijuana is the first substance that has worked on older brains in experiments.”

 

Read more: http://alzheimers-review.blogspot.com/2009/11/medical-marijuana-as-effective.html

 

Alzheimer’s: Marijuana as Effective Medicine

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“Cannabis is getting much positive publicity and seems to be regaining its popularity of one hundred years ago when it was the most widely used drug for about 100 different diseases. There is a big toodoo nowadays about Alzheimers which has turned into almost an epidemic for old folks with some even in their 50’s. So far nobody seems to have put a handle on it and I won’t either.The latest information seems to be that there are senile plaques in the cerebral cortex and subcortical grey matter but whether these plaques are a cause or effect seems to be up for grabs.

I don’t know either. My Merck manual says that four million Americans have it, mostly those over 60 years old. It is a very expensive disease for nursing homes and nursing care probably at least 100 billion dollars per year.

As a Medical Marijuana doctor, I jumped into this fracas when I heard that a lady spouse of an Alzheimers patient went to a Medical Marijuana Advisory Committee meeting of The Oregon Medical Marijuana Program (OMMP) and demanded that her husband be given a permit. She was successful and the medical statistics from OMMP indicate that somewhat less than 50 people have Marijuana permits for this disease. It is called Alzheimers Rage.

The above really didn’t surprise me because there are several Central Nervous System (CNS) diseases for which Cannabis/Marijuana (C/MJ) works very well. These include ALS, Epilepsy, Multiple Sclerosis, Parkinsonism, PTSD and Traumatic Brain Injuries (TBIs). I don’t know if anyone has figured out why C/MJ works for these conditions but why ask if those suffering say that C/MJ works.

Tod Mikiyuria, the foremost scholar in this area, says that C/MJ works as a modulator which is a term of general meaning which possibly just means that it works.

The standard drugs are almost worthless, many seem to be Cholinergics related to Acetyl Choline, the standard Neuro transmitter nerve cell to cell and nerve cell to muscle. At any rate C/MJ seems to work better than any of the heavily advertised drugs.

Cannabis/Marijuana is simultaneously getting much positive publicity and seems to be regaining its popularity of one hundred years ago when it was the most widely used drug for about 100 different diseases.

Those of us advocates for Medical Marijuana who have suffered scorn and derision for DEVIL WEED causing REEFER MADNESS can finally say

WE TOLD YOU SO!!!” –
 
Dr. Phil Leveque 
 

Marijuana and Alzheimer’s – How Marijuana Outperforms Drugs for Alzheimer’s Disease

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“Marijuana and Alzheimer’s – Alzheimer’s Help without Nasty Drug-Induced Side Effects.”

marijuanaplants 235x147 Marijuana and Alzheimers How Marijuana Outperforms Drugs for Alzheimer’s Disease

“The war on drugs has most people believing there is no legitimate argument for marijuana, causing it to be highly looked down upon and illegal under federal law throughout the United States. But there is an exceptionally large body of research pointing to the positive impact marijuana can have on various health ailments, with recent research revealing a link between marijuana and Alzheimer’s – showing that THC, the psychoactive component of marijuana, may be beneficial for Alzheimer’s patients.

As published in the journal Molecular Pharmacology, a Skaggs Institute for Chemical Biology study shows that Δ9-tetrahydrocannabinol (THC) both “competitively inhibits the enzyme acetylcholinesterase (AChE) as well as prevents AChE-induced amyloid β-peptide (Aβ) aggregation.” In other words, cannabinoid molecules found in cannabis could halt the progression of Alzheimer’s disease.”

Read more by  : http://naturalsociety.com/marijuana-and-alzheimers-outperforms-harmful-drugs/

“A Molecular Link Between the Active Component of Marijuana and Alzheimer’s Disease Pathology” – Free full text: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2562334/

Cannabidiol affects the expression of genes involved in zinc homeostasis in BV-2 microglial cells.

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“Cannabidiol (CBD) has been shown to exhibit anti-inflammatory, antioxidant and neuroprotective properties. Unlike Δ(9)-tetrahydrocannabinol (THC), CBD is devoid of psychotropic effects and has very low affinity for both cannabinoid receptors, CB(1) and CB(2). We have previously reported that CBD and THC have different effects on anti-inflammatory pathways in lipopolysaccharide-stimulated BV-2 microglial cells, in a CB(1)/CB(2) independent manner. Moreover, CBD treatment of BV-2 cells, was found to induce a robust change in the expression of genes related to oxidative stress, glutathione deprivation and inflammation. Many of these genes were shown to be controlled by Nrf2 and ATF4 transcription factors. Using the Illumina MouseRef-8 BeadChip platform, DAVID Bioinformatics and Ingenuity Pathway Analysis, we identified functional sets of genes and networks affected by CBD. A subset of genes was found to be regulated by the metal responsive element (MRE)-binding transcription factor-1 (MTF-1) and is shown to be related to zinc homeostasis. We found that CBD upregulates the expression of the mRNAs for metallothionein 2 (Mt2), N-myc-downstream regulated gene 1 and matrix metalloproteinase 23 as well as of the zinc transporters ZnT1/Slc30a1 and Zip4/Slc39a4 but downregulates the expression of the mRNA for the zinc transporter Zip10/Slc39a10 as well as for the zinc finger protein 472. Among these genes, ZnT1, Mt2 and the zinc transporters ZIPs are known to function together to control the intracellular zinc concentration. These results show that CBD, but much less so THC, affects the expression of genes involved in zinc homeostasis and suggest that the regulation of zinc levels could have an important role through which CBD may exert its antioxidant and anti-inflammatory effects.”

http://www.ncbi.nlm.nih.gov/pubmed/22178458