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The Endocannabinoid System and Alzheimer's Disease

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posted on Mar, 27 2017 @ 06:22 PM
The Endocannabinoid System and Alzheimer's Disease

This is a spinout thread from the diabetes one. I apologize in advance for specifically focusing on Alzheimer's as I know all neurodegenerative diseases are equally debilitating in their own ways. I have a personal interest in Alzheimer's because my aunt died from this at the age of 58. Alzheimer's is simply saddening to witness, the progression timeline of the disease will blast off randomly, and before you know it, that once normal and heathly individual is in a nursing home and resembles nothing of who and how you know them as. Obviously, I am sure most realize there is a connection with diabetes and Alzheimer's as well. My aunt did not have any medical conditions, other than suffering from PTSD (intruders came into the home and kidnapped her and my uncle and cousin), which I am convinced this traumatic experience is what induced the neurodegenerative process that lead to Alzheimer's. There is research published about the link between PTSD and Alzheimer's, but regardless, I do not wishfully intend this thread to focus on my personal attachment, but rather the importance of what regulates all neurodegenerative diseases. So again, I apologize for this being Alzheimer's specific, but this just correlates with the previous thread and also my own personal interests.

The endocannabinoid system acts as the body's homeostatic regulatory system. In the brain, the endocannabinoid system regulates numerous important and crucial signaling, cognitive and motor function processes. The ECS in the brain orchestrates complex regulatory functions, some of them are: memory, emotions/mood, pain, appetite, mitochondria activity, neurogenesis, and provides neuro-protective qualities such as antioxidant protection and is a key neuro-protectant during traumatic brain injury. More than likely it is the regulator of dream generation.

Below are some studies I have bookmarked that seemed significant to me at the time. I want to share them with you all.

Active endocannabinoids are secreted on extracellular membrane vesicles

Our findings, by providing evidence for the activation of CB1 in GABAergic neurons by microglia-derived MVs, suggest that microglia may crucially regulate positioning and circuit formation of CB1-expressing interneurons through secretion of AEA-storing EVs during brain development.

Here, we show that endocannabinoids are secreted through extracellular membrane vesicles produced by microglial cells.

We demonstrate that microglial extracellular vesicles carry on their surface N-arachidonoylethanolamine (AEA), which is able to stimulate type-1 cannabinoid receptors (CB1), and inhibit presynaptic transmission, in target GABAergic neurons. This is the first demonstration of a functional role of extracellular vesicular transport of endocannabinoids.

Retrograde signaling is the principal mode by which eCBs modulate synaptic function. N-arachidonoylethanolamine (AEA) and 2-arachidonoylglycerol (2-AG), the most active eCBs as yet discovered, are synthesized in the postsynaptic compartment of neurons and act retrogradely to inhibit GABA or glutamate release from presynaptic terminals; this process is mediated by activation of type-1 cannabinoid (CB1) receptor 3, 5.

However, there is also evidence suggesting that eCBs indirectly signal at the synapse via glial cells by triggering gliotransmission 6 and that glial cells directly produce eCBs 7.

Indeed, microglia release eCBs 8, 9, 10 and produce in vitro 20-fold higher amounts than neurons or astrocytes, likely representing the main source of these substances in the inflamed brain 11. Microglia also respond to eCBs through functional type-1 (CB1) and type-2 (CB2) cannabinoid receptors, which likely regulate microglia behavior and phenotype 11.

Additionally, we now show that microglial MVs directly suppress the GABAergic tone through CB1 activation on interneurons, thereby contributing to alteration of excitation/inhibition balance.

Amyloid proteotoxicity initiates an inflammatory response blocked by cannabinoids

Cannabinoids such as tetrahydrocannabinol stimulate the removal of intraneuronal Aβ, block the inflammatory response, and are protective

THC is protective, removes intraneuronal Aβ and completely eliminates the elevated eicosanoid production in induced MC65 cells

Prostaglandins tend to be neuroprotective and leukotrienes potentiate toxicity, whereas the activation of cannabinoid receptors prevents Aβ accumulation and toxicity

Both intracellular Aβ accumulation and nerve cell death are potentiated by 5-LOX metabolites and proinflammatory cytokines.

Endocannabinoids can be produced in response to stress,44,45 and in rodent AD models cannabinoids reduce Aβ accumulation and improve memory.46,47

THC also reduces inducible huntingtin overexpression in PC12 cells,48 and both THC and endocannabinoids reduce inflammation.49,50 Several synthetic, plant derived and endogenous cannabinoids are able to prevent the accumulation of intraneuronal Aβ, reduce the production of eicosanoids, and block nerve cell death.

Cell death can only be completely prevented by 5-LOX inhibitors, cannabinoids and caspase inhibitors.

However, once the cell death process is underway, death can be reduced by some prostaglandins. Conversely, once initiated, cell death is potentiated by AA, LA, some leukotrienes, CB1/2 inhibitors and cytokines that enhance proinflammatory pathways.

Despite these complexities, the data strongly suggest that early intervention via the reduction of intraneuronal Aβ proteotoxicity may reduce AD disease initiation or progression.


posted on Mar, 27 2017 @ 06:25 PM
Adipokines and dementia

The aim of the article is to review the current knowledge of mechanisms linking adipokines, insulin resistance and dementia.

Adipose tissue secretes into the bloodstream a number of hormones named adipokines, which regulate many aspects of the metabolism and energy balance. They also play a role in blood pressure regulation, hemostasis and immunity, and in the development of various pathological conditions which are often accompanied by insulin resistance. Leptin and adiponectin are important adipokines related with dementia. Both diminish insulin resistance, can cross the blood/brain barrier and exert influence on nervous tissue.

It has been found that leptin accelerates beta amyloid disintegration and also decreases tau phosphorylation, thus favoring the removal of two of the main pathological elements of Alzheimer disease and creating future therapeutic possibilities. Adiponectin decreases glucose levels by increasing the oxidation of fatty acids and inhibiting gluconeogenesis. Adiponectin is produced as monomer, which can change into a more active multimeric form. Some of the polymorphic forms of adiponectin favor its multimerization. Other adipokines – resistin and adipokine – like ghrelin are also connected with dementia.

The possibility of using resistin in Alzheimer disease therapy has been raised. Ghrelin's role in neuroprotection, memory consolidation and cognitive functions has been found showing a relationship between ghrelin and Alzheimer disease. Adipokines play an important role in the mechanisms connected with dementia.

Prolonged oral cannabinoid administration prevents neuroinflammation, lowers β-amyloid levels and improves cognitive performance in Tg APP 2576 mice

Indeed, cannabinoids are able to decrease the release of cytokines and nitric oxide in cultured microglial cells induced by lipopolysacharide [19, 20] and Aβ addition [12, 21]

In several in vitro studies cannabidiol (CBD), the major non-psychotropic constituent of cannabis, has shown to be neuroprotective against β-amyloid (Aβ) addition to cultured cells. This action was a consequence of reduction of oxidative stress and blockade of apoptosis [22], tau-phosphorylation inhibition through the Wnt/β-catenin pathway [23] and decreased iNOS expression and nitrite generation [24]

In vivo experiments have shown that several cannabinoids were effective at preventing Alzheimer's disease related changes. In a previous work we have reported that synthetic cannabinoids, such as WIN55,212-2 and JWH-133, prevented the cognitive impairment, glial activation and neuronal marker loss in β-amyloid injected rats [12]. Enhancement of endocannabinoid levels by subchronic uptake inhibition reversed the increase in inflammatory parameters, such as COX-2, TNF-α and IL-1, in Aβ-injected mice, although cognitive impairment was only prevented in early treated mice [25]

Further, we have recently reported that CBD and WIN55,212-2 (WIN) inhibited both glial activation and cognitive deficits, as judged in the water maze test, and by a mechanism involving decreasing microglial activation, as shown in cultured microglial cells [20]

In summary, cannabinoid agonists, in particular CB2 selective agonists, interfere with several interconnected events of importance in the pathophysiology of AD. These compounds by directly interacting with cannabinoid receptors, in particular CB2, decrease microglial activation thereby reducing inflammation and its consequences (eg cognitive deficits). At the same time they may indirectly have beneficial effects on microglial activation (eg decrease cytokine release) by lowering brain Aβ levels

Alzheimer's disease; taking the edge off with cannabinoids?

Certain cannabinoids can protect neurons from the deleterious effects of β-amyloid and are capable of reducing tau phosphorylation

The propensity of cannabinoids to reduce β-amyloid-evoked oxidative stress and neurodegeneration, whilst stimulating neurotrophin expression neurogenesis, are interesting properties that may be beneficial in the treatment of Alzheimer's disease

Δ9-tetrahydrocannabinol can also inhibit acetylcholinesterase activity and limit amyloidogenesis which may improve cholinergic transmission and delay disease progression. Targeting cannabinoid receptors on microglia may reduce the neuroinflammation that is a feature of Alzheimer's disease, without causing psychoactive effects

Thus, cannabinoids offer a multi-faceted approach for the treatment of Alzheimer's disease by providing neuroprotection and reducing neuroinflammation, whilst simultaneously supporting the brain's intrinsic repair mechanisms by augmenting neurotrophin expression and enhancing neurogenesis

Neuronal damage can increase the production of endocannabinoids (Stella et al., 1997; Marsicano et al., 2003), and cells lacking CB1 receptors are more vulnerable to damage (Marsicano et al., 2003). Those studies indicate that neural cannabinoid tone influences neuronal survival and suggest that augmentation of the cannabinoid system may offer protection against the deleterious consequences of pathogenic molecules such as Aβ

Recently, Aβ has been demonstrated to induce hippocampal degeneration, gliosis and cognitive decline, with a concomitant increase in the production of the endocannabinoid, 2-arachidonoyl glycerol, and this may reflect an attempt of the endocannabinoid system to provide neuroprotection from Aβ-induced damage (Van Der Stelt et al., 2006)

Other endocannabinoids, such as anandamide and noladin ether, have been found to reduce Aβ neurotoxicity in vitro via activation of the CB1 receptor and engagement the extracellular-regulated kinase pathway (Milton, 2002). Thus, endocannabinoids can reverse the negative consequences of exposure to Aβ, and such findings suggest that drugs designed to augment endocannabinoid tone, including inhibitors of membrane uptake and fatty acid amide hydrolase inhibitors, may have potential in the treatment of AD

As well, CBD reduces Aβ-induced neuronal cell death by virtue of its ability to scavenge reactive oxygen species and reduce lipid peroxidation; antioxidant properties that occur independently of the CB1 receptor (Iuvone et al., 2004). CBD also reverses tau hyperphosphorylation, a key hallmark of AD, by reducing phosphorylation of glycogen synthase kinase-3β, a tau protein kinase responsible for the tau hyperphosphorylation in AD (Esposito et al., 2006b)

Moreover, since glycogen synthase kinase-3β also evokes amyloid precursor protein processing to increase Aβ production (Phiel et al., 2003), the CBD-mediated inhibition of glycogen synthase kinase-3β is likely to be effective in reducing the amyloid burden


posted on Mar, 27 2017 @ 06:33 PM
The therapeutic potential of the endocannabinoid system for Alzheimer's disease

There is a growing body of evidence that the eCB system is implicated in the regulation of events occurring during the course of AD progression, particularly in the regulation of Ab clearance, inflammation, oxidative stress and ACh homeostasis (for overview see Table 1 and [11,16,32,33,47,71-73])

CB2 appears to mediate at least some of the functions of the eCB system in AD. Increased CB2 expression has been demonstrated in regions of Ab-enriched neuritic plaques [79,80] and neuritic-plaque-associated microglia [76]. Furthermore, CB2 stimulation by synthetic cannabinoids (i.e., JWH-015 and JWH-133) enhanced Ab phagocytosis in vitro [52], blocked Ab-induced activation of microglia [82] and induced removal of Ab by human macrophages [83]. Finally, Ab provoked upregulation of CB2 expression (and 2-AG levels) and selective CB2 antagonism (by SR144528 treatment) blunted Ab-induced reactive astrogliosis [75]

In vitro, anandamide and noladin ether inhibited Ab-induced neurodegeneration by CB1-mediated mechanisms [86]

Animal model research found that WIN55,212-2 was able to prevent Ab- induced cognitive deficits and microglia activation through CB1 and CB2 [82] and THC to decrease AChE-induced Ab aggregation with higher potency than classic drugs such as donepezil [58]

Furthermore, Ab provoked downregulation of CB1 and a reduction in anandamide levels [75] and selective CB1 agonism blunted Ab-induced reactive astroglial cells [87]. In this context it is interesting to note that CB1 antagonism prevented Ab-induced amnesia in mice [88] confirming the complexity of the nature of involvement of CB1 in AD

The few human studies on the effects of cannabinoids on AD patients revealed that THC had a positive effect as an appetite stimulant and antiemetic, increased body weight and improved disturbed behaviours in AD patients [89], although patients also experienced adverse effects such as tiredness and euphoria

Another study found that low-dose THC was effective in improving several clinical parameters including nocturnal motor activity and agitation, without undesired side effects [90]

Finally, a case report suggested the possible usefulness of THC in a 72-year-old woman as THC treatment reduced agitation and aggressiveness. Remarkably, this effect was rapid and dramatic, rendering better results than those observed with other medications [91]. Importantly, no cognitive effects were observed and the role of CB1 and CB2 in mediating the described effects is unknown

Unfortunately, no investigations into the specific effects of FAAH inhibition or CB2 modulations in AD patients have been carried out to date (for overview see Table 1)

There is only limited data regarding the potential therapeutic effects of CBD for AD available (Table 1 and [92-95]). CBD has been shown to increase cell survival of PC12 neuronal cells after exposure to Ab and to decrease ROS production and lipid per- oxidation [111]

Furthermore, CBD inhibited Ab-induced tau hyperphosphorylation as well as expression and production of iNOS and IL-1b in those cells [112,113] thereby attenuating Ab- evoked neuroinflammatory responses (i.e., levels of glial fibrillary acidic protein) [100]

Importantly, a recent study revealed that subchronic administration of CBD promoted microglia migration in vitro and prevented cognitive impairments as well as cytokine gene expression (i.e., IL-6 but not TNF-a) in Ab-injected mice [114]

Finally, in a rat model for Ab-induced neurotoxicity, CBD effects on reactive gliosis and subsequently on neuronal damage were blunted by blockade of PPAR-g, which is involved in the aetiology of AD pathology. Moreover, CBD stimulated hippocampal neurogenesis due to its interaction at PPAR-g [115]

Cannabidiol and Other Cannabinoids Reduce Microglial Activation In Vitro and In Vivo: Relevance to Alzheimer's Disease

Microglial activation is an invariant feature of Alzheimer's disease (AD). It is noteworthy that cannabinoids are neuroprotective by preventing β-amyloid (Aβ)-induced microglial activation both in vitro and in vivo.

All of the cannabinoids decreased lipopolysaccharide-induced nitrite generation, which was insensitive to cannabinoid antagonism.

We have shown that cannabinoids prevent Aβ-induced neurodegeneration by reducing microglial activation (Ramírez et al., 2005), and both CB1 and CB2 receptors in microglia participate in such an action.

More importantly, cannabinoids prevented microglial activation, loss of neuronal markers, and cognitive deficits in Aβ-treated rats (Ramírez et al., 2005).

In vivo, CBD also suppressed neuroinflammation in mice injected with Aβ into the hippocampus by inhibiting the increased glial fibrillary acidic protein and iNOS expression, along with nitrite and interleukin-1β generation (Esposito et al., 2007).

Insulin deficiency exacerbates cerebral amyloidosis and behavioral deficits in an Alzheimer transgenic mouse model

The accumulating evidence that a lower expression of insulin and insulin receptors occurs in the brain of AD suggests a role of impaired insulin signaling pathway in the pathogenesis of AD [27, 28].

In addition, insulin can be partially formed in the hippocampus, prefrontal cortex, entorhinal cortex, and the olfactory bulb [37]. In the brain, insulin exerts its pleiotropic effects through binding to its receptors and forms the insulin/IR complex [38], and triggers the IR to undergo dimerization and autophosphorylation [39].

The phosphorylated or active IR is involved in the activation of two major downstream signaling pathways, the phosphatidylinositol 3-kinase (PI3K) and mitogen-activated protein kinase (MAPK) pathways [20, 40]. GSK3 is one of the key molecules downstream of the PI3K signaling pathway [41], and ERK and JNK are major components of two parallel cascades, respectively, in the MAPK pathways [42]. Importantly, GSK3, ERK and JNK have all been shown to be involved in the formation of pathomorphological AD hallmarks, such as Aβ plaques [43–45], hyperphosphorylated tau [46–50], and cerebral neuronal death [51–53].

The present study provides evidence indicating that insulin deficiency is able to aggravate Aβ-associated neuropathology and memory deficits in APP/PS1 transgenic mouse model. Insulin deficiency could affect the pathogenesis of AD through mechanisms unrelated to Aβ metabolism.

Interestingly, tau hyperphosphorylation at Thr231 and Ser396 sites was significantly increased in insulin-deficient APP/PS1 mice (data not shown). Tau hyperphosphorylation is a key event in the pathogenesis of AD. In vivo and in vitro studies have shown that insulin can affect tau phosphorylation through the activation of GSK3β [18, 73]. In addition, the insulin-degrading enzyme (IDE) plays a critical role in the mechanism related to insulin deficiency and AD [74].

edit on 27-3-2017 by M4ngo because: (no reason given)

posted on Mar, 27 2017 @ 06:48 PM
I can't believe the amount of research that has been done on.

In the articles I am starting to see that Cannabis seems to create homostasis or balancing between dopamine levels and acetylcholine levels somehow. That would be the only way it would be beneficial to both Parkinson disease and Alzheimer disease. It has to be moderating these two. If dopamine levels are too high and acetylcholine is too low, it contributes to alzhiemer disease. The oposite would be parkinsons. Way Too much of both is no good either as is way too little of both.

I wonder what influence cannibinoids have on methylation within the body?

posted on Mar, 27 2017 @ 07:41 PM

originally posted by: rickymouse
I can't believe the amount of research that has been done on.

In the articles I am starting to see that Cannabis seems to create homostasis or balancing between dopamine levels and acetylcholine levels somehow. That would be the only way it would be beneficial to both Parkinson disease and Alzheimer disease. It has to be moderating these two. If dopamine levels are too high and acetylcholine is too low, it contributes to alzhiemer disease. The oposite would be parkinsons. Way Too much of both is no good either as is way too little of both.

I wonder what influence cannibinoids have on methylation within the body?

Parkinson's also represents a deficiency/compromised ECS. The endocannabinoid system regulates motor function.

The Endocannabinoid System in Parkinson's

A series of anatomical, biochemical, and electrophysiological studies have repeatedly demonstrated that the components of the ECB system are highly expressed at different levels in the basal ganglia neural circuit and thus critically modulate motor function [18,19] (Fig. 2).

Cannabinoid receptor agonists inhibit glutamatergic synaptic transmission and reduce the production of tumour necrosis factor-alpha and reactive oxygen intermediates, which are all factors involved in neuronal damage during PD [38,39].

ECBs seem to play a role in prevent excitotoxic cell damage and death [40,41], an event that is thought to mediate, at least in part, the cascade leading to SNpc neuronal death during PD.

In addition to the neuroprotective effects mediated by the modulation of CB1 receptors, some potential beneficial effects might also be exerted by ECBs via their effects on immune system cells such as B cells, NK cells, monocytes, neutrophil granulocytes and T cells [12,42].
Indeed, it has been repeatedly demonstrated that in both patients and experimental models of PD, neuroinflammation is an ubiquitous finding [43] and, apart from the massive loss of dopaminergic neurons, PD brains also show a conspicuous glial reaction together with signs of a neuroinflammatory reaction, manifested by elevated cytokine levels and upregulation of inflammatory-associated factors such as cyclooxygenase-2 and inducible nitric oxide synthase [44,45].
Notably, immune reactions and proinflammatory immune diffusible mediators may be involved in PD pathogenesis not only by directly contributing to neuronal cells damage and loss [46] but also causing an impairment in synaptic transmission and plasticity, two physiological events that are known to be deeply influenced by glial cells [47].

The evidence that ECBs play a central role in regulating basal ganglia physiology and motor function and the profound modifications occurring in ECB signaling after dopamine depletion in both experimental models of PD and patients suf- fering from the disease, provide support for the development of pharmacological compounds targeting the ECB system as symptomatic and neuroprotective therapeutic strategies for PD.

The Endocannabinoid System and Methylation

A preliminary study of endocannabinoid system regulation in psychosis: Distinct alterations of CNR1 promoter DNA methylation in patients with schizophrenia

We here evaluated the transcriptional regulation of ECS components in human peripheral blood mononuclear cells (PBMCs) obtained from subjects suffering from bipolar disorder, major depressive disorder and schizophrenia, focusing in particular on the effects of DNA methylation.

We confirmed the regulation of CNR1in a well-validated animal model of schizophrenia, induced by prenatal methylazoxymethanol (MAM) acetate exposure (N = 7 per group) where we found, in the prefrontal cortex, a significant increase in CNR1expression and a consistent reduction in DNA methylation at specific CpG sites of gene promoter.

Overall, our findings suggest a selective dysregulation of ECS in psychosis, and highlight the evaluation of CNR1 DNA methylation levels in PBMCs as a potential biomarker for schizophrenia.

edit on 27-3-2017 by M4ngo because: (no reason given)

edit on 27-3-2017 by M4ngo because: (no reason given)

posted on Mar, 27 2017 @ 07:56 PM
My uncle suffers from alzheimers.

I've been speaking with my cousin about all this research being done.

Luckily enough he's in Washington state. And he can take his dad up there.

I have a feeling that since Israel has legalized MJ and is doing research. We will get some real good cures for Alzhiemers soon.

posted on Mar, 27 2017 @ 08:15 PM
a reply to: grey580

I am sorry to hear this about your uncle. I know it can dramatically affect the entire family. Unfortunately, I am afraid that once the cascade manifests it is too late. CBD and THC show great promise in treating the symptoms of the disease though. The main thing is, IMO—we have to/need to be incorporating these cannabinoids into our daily diet. Alzheimer's can be prevented. Cured, however, I am not convinced.

Cell death can only be completely prevented by 5-LOX inhibitors, cannabinoids and caspase inhibitors.

However, once the cell death process is underway, death can be reduced by some prostaglandins. Conversely, once initiated, cell death is potentiated by AA, LA, some leukotrienes, CB1/2 inhibitors and cytokines that enhance proinflammatory pathways.

Despite these complexities, the data strongly suggest that early intervention via the reduction of intraneuronal Aβ proteotoxicity may reduce AD disease initiation or progression.
edit on 27-3-2017 by M4ngo because: (no reason given)

posted on Mar, 27 2017 @ 11:17 PM
a reply to: M4ngo

It appears Endocannabinoids maderate things, they even effect the P53 system and trigger our immune system to seek out tumors and discrepancies.

My question is what chemistry that we are consuming is blocking our natural endocannabinoid system. Back in the seventies there was not nearly as many people getting cancer. Disregard their "Cancer deaths have gone down" Because we are not talking about death, we are talking about incidents of cancer which is way up from before. Lots of surgeries being done now, not many before because there was not that much cancer. Back then there was a lot of liver damage from drinking and more heart attacks, but the numbers of no symptom heart attacks has been going down over the years. It has been steadily getting worse for incidents of cancer since the eighties, and recently Alzhiemer disease has been increasing too.

Some chemistry is interfering with the endocannabinoid regulation. Using Cannabis was not needed so much back in the seventies and eighties, the increase in bad health started more in the last thirty years. Now, we can treat this stuff with cannabis, but what is interfering with our bodies natural abilities of endocannabiniod regulation. Cannabis is a treatment, not the cure. Some change is interfering with the bodies natural systems. If the endocannabiniod system is deficient or not properly responding to stimuli, then all sorts of diseases and conditions will possibly happen. I just read about twenty abstracts from the site you had listed, good site. I have to do some research on the cycles involved in the endocannabiniod system to see if anything pops out.

Seems that most of the people are trying to treat the endocannabinoid deficiency and it is hard to find out what is causing it. The money is being spent on treatment options not on avoidance. I have to keep researching this path to find out what is causing it. Actually the endocannabinoids help with arthritis and also slow bone loss. Now, beef cartilage and bone broth soup seem to do a lot of the same things as cannabis, is there a relationship there somewhere. Endocannaboids are lipids and they are utilized in moderating cartilage too. Could there be some in the senovial fluid in the joints and it gets into the soup? I use beef soup as one of my ways to control my epilepsy. But soup made from plain beef has hardly any benefit. Glutamates are one of the worst things for my epilepsy, I have a little but have to avoid high bound and free glutamate foods like the plague. They increase inflammation pretty much. Glutamines also can be a problem too, I have to moderate that chemistry to feel and think right.

I really do not want to be high anymore, that is in my past. It was one of the ways I adopted to dampen my IQ so I could fit in with my friends and coworkers. I learned many ways to dampen my ability to think, I did not want to be considered a nerd. But now many of my friends and relatives seem to be having health issues and it is time to restore my abilities. Even dampened, I still built a business and was in charge of employees most of my life. I really did not need all of the array thinking I am capable of. But now I do.

posted on Mar, 28 2017 @ 12:12 AM
recipe offered in another thread for a topical application (absorbed through the skin)

originally posted by: AnkhMorpork

Topical Solution/Remedy

If anyone wishes to make a medicine for whatever ails you. I have a great recipe that I recently got from someone who's been making it for years.

In this case, it will be absorbed by the skin and there's no intent to get high or to use the medicine for recreational purposes. This is pure medicinal.

Step 1

get a nice large plastic cosmetic type container with a sealable lid, no make that two or three of them, once you get this process going, as it's a type of alchemical fermentation distillery of sorts which requires moving the substance from one container to another as it purifies and ferments and grows stronger (in purer CBD's and CBN's, where any THC present merely relaxes or shocks the cells to receive the cannabinoids - which eat cancer and neutralize toxins).

Step 2

Fill about 1/3 to 1/2 full with very gently melted coconut butter (not on the stove or microwave but maybe above a toaster or over a heater or blow dryer.

Step 3

Add ground indica bud that's been dried and crumbled to dust

Step 4

Add tincture of Frankincense and Myrrh (not sure how much)

Also add a teeny tiny pinch of turmeric as a preservative, but not enough to turn it yellow.

Step 5

Blend and ferment, and then, after a week or whatever, transfer some into the next container as the base and start again, moving it from container to container as it ferments and gets stronger and stronger.


Apply to the skin over the chest (seeps into Adrenal Gland) or any other gland areas like Lymph Nodes.

For lasting absorption choose a location on your chest or arms, and wrap the area in siran wrap and tape it up - continual absorption throughout the day without evaporating or being wiped away by clothing.

Also recommended is altering Ph balance of blood by drinking water that is more alkaline, and adding both Himalayan pink salt sole (pronounced solay), a couple of tablespoons, and food grade hydrogen peroxide, anywhere from a few to 10 drops per 8 ounce glass, to which I would suggest also adding a few drops to 7-10 drops (later on) of nascent iodine, while getting the bad taste removed by adding a little bit of juice powder or fresh juice. Every morning until you start to pee more alkaline, and you're off to the races for a whole new homeostasis of your entire endocrine system since the nascent iodine activates the thyroid.

I would also suggest adding to this remedy the use of various aromatherapy oils (for the molecules) taken via a cool mist diffuser, which can also be used for the food grade H2O2 in the form of oxygen therapy while sleeping. People with Emphysema, after doing the oxygen therapy have coughed it all up and then gotten off their oxygen and out of their wheelchair through the use of H2O2.

As a precaution against the creation of free radicals when doing oxygen therapy, just take alpha lipoic acid before bed, and eat lots of greens and colorful fruits and vegetables, which also aids in the Ph movement to the state of optimal health.

Blood Ph can determine the state of health and homeostasis in the body, which is largely controlled by the endocrine system, and hormonal response. Therefore exercise would also be a vital component to this sort of regimen.

But those CBD's and CBN's, those were made for the body and the body for these "oids".

Then just eat lots of "oids" in your veggies, change your water, add oxygen, and exercise, and you'll be off to the races and even healed of whatever might ail you.

Be blessed,


posted on Mar, 28 2017 @ 07:38 AM
a reply to: M4ngo

Thanks. Unfortunately the process is probably too far gone for him to get better.

However I've been speaking with my cousin so we can try to get things going so he won't get worse.

Things like coconut oil help. Since the coconut oil is a MCT. It's like brain food. Plus reduces inflammation.

I just got hit with IBD myself. And I'm starting to get together all my anti inflammatory supplements together. I'm taking the coconut oil, gotta get krill or algae oil, tumeric and also apple cider vinegar. Also I have to go on a diet because my blood sugar is above average. And that doesn't help alzheimers either.

Great post man. Thanks for the info.

posted on Mar, 30 2017 @ 01:24 AM
a reply to: grey580

Damn I am truly sorry to hear this. I don't know very much about IBD, but the ECS does play a key role in the GI tract.

Differential Expression of Cannabinoid Receptors in the Human Colon: Cannabinoids Promote Epithelial Wound Healing

In the ECS and Skin thread I posted several resouces from an expert on the ECS that covers various sources of food that supports the ECS. The right kind of diet along with moderate exercise and a positive mind can overcome many things. I have witnessed it personally, so I know you can do it too. You can beat this man, just do not give up. I am making a mental note to do some research into this, and if I find something significant I will let you know.

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