CBRM-OX - A Scientifically Engineered Cannbinoid-Receptor Modulator (CB1 / CB2 Partial Agonist)

This article has been exclusively written for TrueLIFE Research - TeamTLR.com and to foster further progress within Cannibinoid Receptor Research and in reinforcing the significance of the CB1/2 system in current & future medical/scientific applications. 

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Until now, there has been no real suitable alternative to marijuana or cannabis; no alternative that is broadly available and is characterized with nearly the same properties and mechanism of action. Moreover, there isn't a formally announced cannbinoid acting substance that does not also relay the imperfections of cannabis itself (despite it being a solid and medically useful substance itself, it has drawbacks). While there are many ligands in existence under fairly obscure scientific conductions (to the common eye at least), most of these aren't plausible for human use or activity or they lack the proper ratio of oral bioavailability:CNS penetration(1). There are also quite many ligands which are later found to have additional, formerly unannounced properties and properties that may actually have a totally contrary (opposing) effect relative to the main direction in which the study is aiming to make progress from.

Therefore there is (or would have been) quite a pause on some ends of the scientific and research community - and a dilemma imagined within the possibility for 'later-phase' trials which may not be thwarted until more suitable ligands are developed and tailored for larger mammals and.. humans.

However, Project TLR has developed a highly potent active agonist at the human cannbinoid receptors 1 & 2.

A new optimized substance that displays remarkable bioavailability and...                             

                          Is  a  Natural   Extract

Source: Proprietary sources
(non-Cannabis genus)

Animal Research:

Research within animal models has been conducted that has shown potent in vivo CB1/CB2 partial agonist activity. Modulation of other cannabinoid pathways is present with lesser potencies and affinities. Evaluation displays a potency equivalence within CB1 partial agonist effects approximately at 72% of the standard D9-THC. No toxicity or adverse effects were observed at 10x the maximal effective dosing, as a maximal dose assayed.

This remarkable efficiency is suitable for higher level studies and the lack of toxicity and adverse events as well as near total selectivity is able to usher in these "higher ground developments". Within this research, it will be necessary to go over the reasoning for such emphasis (and devotion) upon this neuronal and bodily system, known as the  Cannibinoid-Receptors, a powerful G-Protein-Coupled Receptor family with very broadly distributed actions.

As explained in the Rimonabant piece, cannibinoid antagonists tend to have appetite suppressant and anti-obesity (anti-lipogenic) effects. Agonists on the other hand, are similar to marijuana and its reported appetite stimulant effects, however, they do not overtly produce an obese phenotype nor do they necessarily distort insulin function. This creates quite a paradox -in study- as fatal opposites at the receptor seem to have a fair amount of leverage in their contrasting effects; outlined by an apparent lack of adverse effects or 'extreme opposite' paradigms. 

CBRM-OX is a partial agonist at both CB1R/CB2R and thus displays the typical appetite stimulant effects and thus has indications for anorexia, chronic pain (displays anti-nociceptive effects), S.A.D (Seasonal Affective Disorder), anxiety and also acute pain as with a recent injury. The mood-lifting affects are assessed as serene & applicable (motivated but calm) and effects against anxiety seemed elongated as use continues. Effects against acute pain were transient on a one-time use but were extensive upon continuous use. The smooth arousing effect is assayed as improving sensory and social qualities as well as increased enjoyment of food and other activities. 

CBRM-OX demonstrates remarkable relief of pain but may not be attested directly within MS or autoimmune disorders and such until more volunteers step in , however, in sports injuries it provides substantial relief and is actually surprisingly void of any psychogenic side-effects or any other side-effects. Constipation was not noted nor were there any reported gastrointestinal problems throughout the course of the initial study. This may be representative of the neuronal selectivity or perhaps with the rate of binding/displacement and / or the fact that the propietary compound has equipotent affinity for both CB1 & CB2 as opposed to many other ligands which are imbalanced by contrast or are only affinitized to one receptor. Because CB2 receptors are noted to be of particular high density in periphery, it could also be that the activation of this receptor plays a mediating role on the actions sustained by CB1 activation. Either way, it has become a humongous resolve for cannbinoid receptors research!!!!


WwW: Projected writers assessment will be as well with CoRaGeOn and AMx ReBorN as they do , additional logs will be committed. 

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Rimonabant (CB1 Antagonist) - Opening up the Field for Intense Cannibinoid Receptor Research And Reactions (Discussion on Weight Loss Effects & Benefits Included)

This article has been exclusively written for TrueLIFE Research - TeamTLR.com and to foster further progress within Cannibinoid Receptor Research and in reinforcing the significance of the CB1/2 system in current & future medical/scientific applications. 

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                                                    ~SHORT OVERVIEW~


Rimonabant is a potent Cannibinoid-Receptor ligand used in a variety of medical and scientific applications. Specifically it is a potent CB1 Antagonist/Inverse Agonist, it is orally active and the first agent in this class to demonstrate such selectivity. It also crosses the blood-brain-barrier very well and hits CNS receptors with a high rate of binding; displaying nanomolar affinity for central sites(1).

Rimonabant has shown robust reductions in body fat mass and appetite; and as such is further characterized soon-after approval as an anorectic anti-obesity drug(2)(3), in which it's major clinical use began. The compound further was studied based on it's CNS effects for anti-addictive potential; including in cocaine craving and withdrawal(4), but even more so, for smoking cessation and in the context of nicotine withdrawal(5)(6).

Other potential uses investigated and studied with rimonabant are the improvement of short-term memory and / or the blockade of THC-related impairment of short-term-memory(7).

                      DETAILED OVERVIEW & EFFECT EXPLORATION


The cannabinoid receptor type 1, often abbreviated as CB₁, is a G protein-coupled cannabinoid receptor located primarily in the central and peripheral nervous system. It is activated by the endocannabinoid neurotransmitters anandamide and 2-arachidonoylglycerol (2-AG); by plant cannabinoids, such as the compound THC, an active ingredient of the psychoactive drug cannabis; and by synthetic analogues of THC.

CB_{1  Receptors are negatively coupled to adenylate cyclase; as a result, when activated, they metabatropically inhibit neurotransmitter release as well as cortisol and ACTH secretion(8)(9)(10)(11).}

The appetite suppressant effects of Rimonabant are the result of direct hypothalamic actions and as well the large increases in noradrenaline and serotonin resultant from central cannibinoid receptor 1 blockade(12)(13)(14). Additionally, rimonabant may make sweet foods less palatable and decrease the food-reward behavioral response(15), of course, having opposite effects of THC in many ways (including chemically), would further reinforce this paradigm.

Rimonabant also acts directly in fat cells and decreasing their synthesis, thereby extending it's weight loss potentials(16).

As the second messenger cyclic adenosine monophosphate (cAMP) has a very broad distribution throughout much of every cell in the body and in the nervous system...the additional effects of Rimonbant in increasing energy expenditure (17) would likely be via this route; CB1 receptors being primarily negatively coupled to adenylate cyclase would maintain this assertion(18). Thus rimonabant can be seen as a receptor-based-adenylate cyclase stimulator or cAMP secretagogue(19). 

Rimonabant is also shown to improve insulin sensitivity thereby leading to stable blood sugar levels and from this facet , the resulting weight loss or weight stabilization(20)(21). Thus , Rimonabant can technically be classified as a multi-modal weight loss agent and an ideal candidate for weight loss especially in circumstances where other medications have failed or to where the hypothalamus/pituitary appears to be malfunctional or under-active in the patient.

<sub>Effects at the mu-Opioid receptor may also underlie some of Rimonabant's effects on appetite and on energy expenditure, as it appears to be a strong property and a shared interaction with some of the 'later' CB1 ligands(22).
Mu-Opioid receptors are proven to play a huge role in hypothalamic function and in the release of neurotransmitters centrally(23). Given the similarity in mu-opioid and CB1 receptors (they both functionally inhibit cAMP production) - this would be a plausible hypothesis in the overall therapeutic effects of Rimonabant and on it's extravagant cAMP boosting effects.



To further reiterate this effect; take the rimonabant-forskolin excerpt from this study - the rationale section elucidates this effect and also correlates (but doesn't confine) it to the prefrontal cortex and cerebellum; further re-confirming it's central effect on the second messenger concentration. Additionally, in studies with the SSRI fluoxetine, it shows there is a direct serotonin-cannibinoid interaction and also demonstrates the CB1 inhibition of adenylate cyclase in overall CNS activity is an essential prospect in the study of depression and other mental disorders.</sub>


Rimonabant has also been shown to have some GABA-ergic activity  (potentiation), which may contribute to it's overall therapeutic effect on satiety and on lipogenic circumstances(24)(25).

The compound is also shown to improve spatial memory , object recognition, social-short-memory and to potently reverse / block THC-related impairment of short-term memory. It is demonstrated to have this effect in both young and old patients/subjects; leading to it's interest in treating neurodegenerative disorders such as Alzheimer's and Dementia.<see here>. (!)_(!)

Rimonabant can reverse slowed-intestinal transit caused by THC- and thus potentially alleviate constipation and other bowel issues associated with use of agonists to the CB1R's(26)(27)(28). On the flip side however, it may produce anxiety-related gastrointestinal pathology in sensitive individuals and may be counter-productive in those with an existing gastrointestinal disorder that is highlighted by diarrhea(29)(30). 

These effects however are fairly rare occurrences within the majority of users of Rimonabant. 

Rimonabant has the ability to increase male fertility by increasing spermatogenesis in the human male and sperm motility(see here).

Rimonabant has been shown to improve anxiety and hostility in patients with schizophrenia according to a huge statistical analysis and double-blind placebo controlled study conducted in 2011(31). Accordingly, schizophrenics have been shown to have an altered (increased) CB1 receptor density in multiple brain regions, thus producing more than just psychological effects but also contributing to a schizophrenics overall quality of life(32).

Of notability, Rimonabant may be the only publicly available compound that has been shown to specifically reduce the craving for chocolate and it's reinforcing properties; mainly but not solely concerning the flavor/palatibility(33)(34). 

Finally, rimonabant has shown to be effective reducing cue-induced cocaine reinstatement and thus may have mediating effects but not necessarily directly suppressing effects in primary cocaine addiction(35)(36)(37)
CB1 receptors seem to play a huge role in forming accumbal encoding and thus [promote] dopamine release in the nucleus accumbens. CB1 receptor activation is essential for addiction and reward related behavior.(38). 

Despite all of this , CB1 activation may be ideal in some conditions characterized by lack of motivation to reward, in contrast, antagonism doesn't necessarily reduce motivation per se, and in normal persons side-effects such as depression can occur as a result of both agonists and antagonists - but are not very common(!)(!).

The benefits of Rimonabant can be concluded as.

• Rimonabant can improve Insulin Sensitivity and can increase fat loss.
• Rimonabant markedly suppresses appetite.
• Rimonabant may help avert cue-related cocaine reinstatement.
• Rimonabant is a superb smoking cessation aid.
• Rimonabant may help antagonize Cannibinoid-related responses.
• Rimonabant may potentiate GABA-A and many other neurotransmitters.
• Rimonabant provides robust increases in cyclic AMP (cAMP) and enhances Forskolin's effects by amplifying cAMP increases.
• Rimonabant increases spermatogenesis and sperm motility.
• Rimonabant can alleviate constipation induced by THC and other agonists of the CB1 receptor.
• Rimonabant blocks THC-related impairment of short-term memory and may promote memory acquisition/retention in general .
• Rimonabant specifically may also improve spatial memory, object recognition and social short-term memory; may have significant application in neurodegenerative disorders.

                                     

***SOURCES/CITATIONS***

http://www.ncbi.nlm.nih.gov/pubmed/23562616

https://www.ncbi.nlm.nih.gov/pubmed/15864349

https://www.ncbi.nlm.nih.gov/pubmed/22063718

http://www.ncbi.nlm.nih.gov/pubmed/21797816

http://www.ncbi.nlm.nih.gov/pubmed/18410553

https://www.ncbi.nlm.nih.gov/pubmed/20439721

https://www.ncbi.nlm.nih.gov/pubmed/19597516

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SFME-OX -A Ploy to Re-Engage the Efficiency of the Mu-Opioid System; Tolerance Uncovered! (Enhancing / Re-Sensitizing mu-Opioid Receptor System)

This article has been exclusively written for TrueLIFE Research - TeamTLR.com and to foster further progress within opioid system research and in reinforcing the significance of the system in current medical dilemmas. 

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Since the late 1990's to early 2000's a predictable problem in those needing strong pain medication has been the eventual tolerance(1)(2) and, when looking 'under the microscope' ; neural de-sensitization of the receptors was uncovered(3). This has provoked much research and has created a dilemma in the medical profession, forcing caregivers and Doctors alike, to adjust or augment the dose of opioid-like painkillers, often unexpectedly(4)(5). 

In severe trauma and other debilitating conditions such as multiple sclerosis, cerebral palsy co-existing with injury, and in many other circumstances where severe , neurological or muscular pain endures, there aren't many alternatives to narcotics(at least equivalently effective ones)(6)(7). In dentistry, after a surgery or operation the same is true regarding alternatives, limited indeed(8)(9). The difference between dentistry and GP complaints?  : frequency. People usually go to their primary doc's more than their dentist, and more severe cases of pain are referred to specialists where much testing is completed. Still, in all of this, the pain has to be taken care of in order for the patient to fully cooperate with his/her medical advisory - one isn't likely going to be very motivated to go anywhere if they are in so much pain irrespective of tried remedies and such(10)(11).

Now imagine a scenario in which a severe sports complication or an elderly falls or has some other traumatic event causing injury, and their opioid pain medication which is supposed to do the trick - starts whittling down in effect, and to worsen the ordeal - higher doses are creating increased side-effects! Maybe even as intolerable as the pain itself...
Or consisting of increased pain due to the med losing it's effectiveness!!

What's the solution? Because the bridge certainly doesn't look too sturdy from here.

We need something that will allow victims of debilitating illness or severe injuries to utilize at maximum efficiency, the lowest possible therapeutic dose of their opioid pain medication...else , we are just lost and heavily restricted with worry , fear, and limited options. We need something that can act as a regulator of the entire system it works on, or at least the part that contracts to the alleviation of pain.

Now while some preliminary research was done a few years ago regarding re-sensitizing the responses to opioid pain medications, it was just that, very VERY preliminary..(12)(13).and probably not the best case made in favor of overall efficacy. However, new research is being presented by TeamTLR which aims to elucidate the root problem, and provide a potential solution that will provoke a new awakening in the pinnacle of medical research with regard to these issues.

The research compound is valuable and a huge step forward and goes by the name SFME-OX.
SFME-OX:Selective Filamin A MOR-System Enhancer Optimized Xtract binds Filamin A in a highly selective manner that demonstrates the effect of markedly reducing Mu-Opioid Receptor System (MOR-S) tolerance.  

SFME-OX further demonstrates a marked reduction in inflammatory cytokine production.

(Cytokine's are small proteins involved in cell-signaling and a collection of them are involved in specific growth related processes as well as with inflammatory modulation. However, abundance of them relates to their significance and too many or too much production of them often leads to inflammatory responses which can lead to brain and joint inflammation.) 

Most NSAID's don't directly antagonize but indirectly reduce cytokine mediated responses and other pain relievers may offer some relative protection but usually do not go against the grain and reduce the source of the issue(!).

Source Plant:  Proprietary Lobelia species.

Animal Data:

In vitro data shows selective pM affinity binding at the Filamin A protein pocket that produces an marked enhancement MOR tone within an upregulation of MOR expression.  In vivo efficacy in murine models has been demonstrated eliciting a reversal of downregulation created via mu-opiate administration thus potently reducing tolerance to mu-opioid receptor agonist agents as demonstrated.

(This is revolutionary, by preventing or reversing the mu-opioid related downregulation, sensitivity to the medications are maintained or re-instated, and so by doing this, we have caught a major 'therapeutic break' - finally making our way into solutions that will lead to even more groundbreaking solutions for trauma, injury and autoimmune disease management.)

Future Human Clinical Trial Protocol and Projections:

SFME-OX is anticipated to provide potent upregulation of the Mu-Opioid Receptor sensitivity/expression at dose arms of 10mg and 20mg to be administered once daily.  Said administration is projected to provide a rapid restoration of sensitivity to opiate therapeutic agents and allowing a marked reduction in dosage to provide superior positive effects with reduced adverse effects.  An optimum course is anticipated to be via a 1 week of usage followed by 1 week of discontinuance alternating schedule. 


As you can see with the overview above, this is more than just evidence, but rather; an active trial that is long over-due - and the human trials will become the brew for the future insights and management of chronic pain and other disorders where opioid-systems or their malfunction plays a critical role. This may expand to even mental disorders such as depression and anxiety, to which mu-opioid receptors also play a huge role(14)(15)(16)(17).


Which brings me to my last point, because we have already seen the devil of de-sensitization with many anti-depressants (although in these cases, de-sensitizationd is often postulated to be beneficial) - the worry that would come with developing mu-agonists for depression or anxiety would stem from the possibility (or even probability) of fairly quick tolerance(18)...where most anti-depressants on the market now increase in effect the longer you take them (19) - an agonist at the mu-receptor would most likely be the opposite(20)..given they are a major GPCR (G-Protein-Coupled-Receptor).

So SFME-OX represents a future and present research tool for these dilemmas as well and the progress we make now will be as vast considerations for the future developments and even as a course of augmentation not prior seen...the unprecedented value in MU-SYSTEM SPECIFIC re-sensitization will parallel the benefits (but stand as the respective equivalent thereof) of 5-HT1AR desensitization in anti-depressant therapy(21)(22).

So both on a Central Nervous System and on a peripheral level, this critical method of re-sensitizing and enhancing the mu-opioid-complex function will prove to be a novel but long over due approach to the current treatment regimens or augmentation of current treatments in which will provide a better outcome for patients with a multitude of health complications sensitive to opioid-receptor function.

Baclofen! - Not just a Muscle Relaxant. (Therapeutic Uses Explored)

This article has been exclusively written for TrueLIFE Research - TeamTLR.com and to foster further progress within anxiolytic/s research and in reinforcing a scientific basis for GABA-ergic compounds such as Baclofen. 

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A. Baclofen as a full agonist at the GABA-B receptor acts as a centrally-acting anxiolytic and skeletal muscle relaxant.  As well, it shows efficacy in treatment of alcohol cessation.


Though baclofen isn't exactly a 'new' drug - it is a very effective medication that is often overlooked. The chemical has incredibly unique properties, and unlike GABA-A selective agonists, it can actually increase/potentiate dopamine release(1). Acknowledging the striatal occupancy of baclofen and the enduring dopaminergic effects(2)(3) has led to the proposal of it's use in cocaine addiction as an anti-craving medication(4) as well as a utility in opioid and alcohol dependence(5)(6)(7). It also runs a lower risk of dependency than benzo's, and withdrawal, though a possibility, is on average less frequent than benzo's - and usually not a concern in short-term (acute) therapeutic use of the drug(8)(9).

Baclofen has significant anxiolytic properties; that is it alleviates anxiety - and it seems to be applicable in a wide array of stress related conditions such as PTSD(10), alcoholism & withdrawal  (11), and repeated social stress(12).

                           BACLOFEN AND YOUR GUT

Additionally, baclofen has been shown to decrease serotonin release in the gut(13), as opposed benzo's and selectice GABA-A agonists which may increase it. The implications of this are that baclofen may have the ability to affect the outcome of irritable bowel syndrome and may decrease the incidence of diarrhea and abdominal pain(14)(15). Although not strictly by a serotonergic mechanism, baclofen has shown current use in the treatment of spastic colon (IBS) as evidenced by positive experiences and treatment outcomes. 
Additionally, baclofen is often prescribed as part of a regimen to counteract Gastro-Oesophageal-Reflux-Disease (G.E.R.D) and is shown to be quite effective(16)(17).



So baclofen is not your typical muscle relaxant, as it seems to have these effects inward as well. With anti-contractile effects in the gut and in regards to neurons secreting PH efflux toward the esophagus, baclofen is effective. These all point to a very diverse substance with minimal peripheral / systemic side-effects. The additional uses with regard to psychosomatic worries and stimulant dependence also seem to be quite promising(18)(19)(20)(21)!

      BACLOFEN - A scientific Utility unveiling the Biological Relevance & Differentiation of GABA-B Receptors

Baclofen is also an efficient tool in scientific study and has nearly made a revolution in terms of actively demonstrating the function of the GABA-B receptor with relation to behavioral, neurological and adrenal role's(22)(23)(24). Due to specific studies involving hypothalamic slices/cultures (in vitro) - we now can characterize and differentiate the roles of each GABA receptor, helping us to understand more the specific inhibitory and / or stimulatory actions of the pathway(25).

The endocrine actions of Baclofen reveal a site-interaction and modulation between GABA-B receptor complex and opioid-receptor signaling(26)(27). Baclofen is demonstrated to yield robust reductions in cortisol secretion during hypoglycemia and in response to stress(28).

This may underlie the potential for it in managing blood sugar and delaying onset of diabetes shown in this study.

 REITERATING THE MUSCLE RELAXANT EFFECTS OF BACLOFEN

Restless Legs Syndrome is a common complaint in the USA, and baclofen seems to be one of the most efficacious treatments next to dopaminergic drugs and GABApentin(29)(30).

Baclofen's steady use is most associated with tension in sports injuries and in some autoimmune disorders, and it is also widely studied in spinal cord injuries(31)(32)(33). 

Intrathecal Baclofen administration is a common course of action in MS patients and is well-tolerated . The attenuation of spasticity in MS patients with baclofen is remarkable and the low-side-effect profile contributes to the overall appeal in MS with the drug(34)(35).

Additionally, baclofen has been found to remedy and attenuate some side-effects associated with anti-psychotic drugs, notably the akathisia (Inner Restlessness) and muscular restlessness(36)(37)(38).

Finally, baclofen is a distinct Anti-HICCUP agent, and as such may be a most valuable lesson in the neuro-physiology of muscular function relating to the digestive system. Because baclofen effectively alleviates hiccups of idiopathic origin, this has long-standing implications in how we go about medicating those patients who present with both gastrointestinal and muscular complaints(39)(40)(41)(42).


In conclusion, Baclofen is useful and has shown efficacy for the following .

• Spasticity in Multiple Sclerosis.
• Restless Legs Syndrome.
• Muscle Tension after Spinal Injury.
• G.E.R.D Complaints.
• Hiccups.
• Some features of I.B.S; diarrhea.
• PTSD and chronic Stress.
• Anxiety**
• Alcoholism, Stimulant Dependence and Reducing Cocaine Cravings.
• Alleviation of Anti-Psychotic Induced Akathisia.**

** = some evidence, better results when co-administered with another drug or as an augmentive therapy. May not apply to all cases.

Good People Can Appreciate the Darkness, Too (Dispelling the Myths, Biblical & Logical Reinforcements Included)

It has come to my attention that some people have, erroneously, assumed that darkness is only a place for evil to lie (as in lay), or that darkness is always referred to as that which is owned by evil or such...but it should be known that logically and biblically, this is a fatal oxymoron. God has created the darkness as well, and light can not exist without darkness - they are both essential instruments/elements to our existence. (I say instruments because they are in a collaboration, and yet technically not separate entities)

Furthermore, even if you do see 'darkness' as the 'ways of' ; what you see as dark (immoral ways and methods) - I would say this.

In order to fully appreciate the light, we must have once dwelt in darkness - because that is when light is truly distinguished. ~AMxReBorN~ 

So from a philosophical or spiritual standpoint - this can be fully absorbed. But this post isn't about me, it's about clarification. It's about allowing people to have their peace. Giving re-assurance. Comfort; knowing the ideals and de-stabilization tactics used by unscrupulous organizations can be set aside by the truth.

But let us not define darkness as one thing or another.

 There was value in knowledge then, there is now, and God speaks the same.

                                           
This proves that God sees darkness and light as Alike; both are necessary, and though he is cited as being "of light, where there is no darkness" , God has created the darkness for a reason - and we, each of us, we are not God.  We are born from and to co-exist with both light and darkness - this does not mean to appreciate one 100% over the other, or 90% one and 10% another - but it also does not mean that appreciating each equally means we are neutral , neither good nor evil, it simply means we acknowledge the truth from the very beginning..something that we must come to terms with in order to understand ourselves and the life we were given...if we can not appreciate the darkness as well - and if we underestimate it - we are not filled with knowledge, we are ignorant, and choosing to live in ignorance. 

This also does not mean we should act as if darkness is the Superior entity, and it ABSOLUTELY should not mean that darkness should be deemed an inferiority, nor should it be erroneously presumed to be relating to evil, because this is not the case.

So draw your sword to fight for what is right, but understand that you must be in harmony with both elements, appreciate both....in order to understand and continue Wisely in life.

So does God say it is O.K to appreciate the darkness, well of course! But in the terms of darkness as night, and as what exists in darkness we are encouraged to understand, for in him the hidden treasures and knowledges are revealed. 

God understands and appreciates night-owls , because they can appreciate what others are so quick to be afraid of. Only because they (the others) do not understand it, they fear what they do not understand...once you have been conditioned to believe in such a blind phenomenon, the only reversal is understanding...and once you see both sides of the Same Coin - you will have to dismiss what others have been so quick to hold on to....damage comes from blindness, and re-conditioning is the key to reverse the incorrect gestures pushed upon us.

NOW, Let's talk about Health. (Including Mood)

We can utilize darkness, and it does not equate to sacrificing serenity !!

Onyx is a special stone that is regarded as Symbolizing a happy life with a Great companion (!) - and contrary to the people who criticize it for being 'dark' and thus of despair, it actually is said to help block negative energies and negative thoughts of others, and to actually promote serenity and peace(!).

Now I didn't come here as a salesman, I am simply showing you that there is more to black, darkness, and anything of that nature than what most will tell you .

Stop hoarding light as if it is the cure to everything. 

But certainly, do not bathe yourself in darkness 100% and don't utilize it at all - if you don't know what it means...darkness doesn't mean to rip up the flesh of another, or to practice in deceit, darkness is just another element, a subtle, but profuse, proliferated, and consistent entity. 

DARKNESS IS NOT GLOOM, If you feel horrible in darkness, it may be some sort of biological issue where your body responds with chemicals, but then YOU have to truly search yourself to find if this RESPONSE, is based on the fear of the unknown, or fear that darkness is some consuming entity, perhaps, if you expect darkness to consume you - it will...but if you live in harmony with it...perhaps then, it is something else entirely, it's true nature revealed to you.

Now OF COURSE, if your power goes out as if someone snipped the power core, breaker links etc - and no other house is like that - then maybe it's worth a check and some extra vigilance, and maybe a little fear, but maybe not...indeed, people who become victims of people who UTILIZE darkness for malicious acts DOESN'T MEAN that darkness is to blame - but rather, it is the person who utilized it that hopes to work on your fears..again, because you do not understand it. 

To become a fully wise, and diverse individual, come prepared, but do not live in fear - be vigilant, but do not assume , especially not based on something as trivial, but yet significant as darkness and light...good or evil .

Because really when we say we 'see' we really only perceive, and perception is subject to many faces.
~AMx ReBorN~