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 Content preview:  CBD-Gummies CBD-Oil Gummies Now Legal in ALL 50-States! No.Prescrip.tion-Necessary.
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Subject:  ****SPAM****  Newly Legal-CBD Oil Now Comes in Easy to Digest Gummie-Form.

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  <p style=3D"font-size:7.8px; ">=20
   <!-- footer --> Cannabis sativa L. preparations have been used in medici=
ne for millenia. However, concern over the dangers of abuse led to the bann=
ing of the medicinal use of marijuana in most countries in the 1930s. Only =
recently, marijuana and individual natural and synthetic cannabinoid recept=
or agonists and antagonists, as well as chemically related compounds, whose=
 mechanism of action is still obscure, have come back to being considered o=
f therapeutic value. However, their use is highly restricted. Despite the m=
ild addiction to cannabis and the possible enhancement of addiction to othe=
r substances of abuse, when combined with cannabis, the therapeutic value o=
f cannabinoids is too high to be put aside. Numerous diseases, such as anor=
exia, emesis, pain, inflammation, multiple sclerosis, neurodegenerative dis=
orders (Parkinson's disease, Huntington's disease, Tourette's syndrome, Alz=
heimer's disease), epilepsy, glaucoma, osteoporosis, schizophrenia, cardiov=
ascular disorders, cancer, obesity, and metabolic syndrome-related disorder=
s, to name just a few, are being treated or have the potential to be treate=
d by cannabinoid agonists/antagonists/cannabinoid-related compounds. In vie=
w of the very low toxicity and the generally benign side effects of this gr=
oup of compounds, neglecting or denying their clinical potential is unaccep=
table - instead, we need to work on the development of more selective canna=
binoid receptor agonists/antagonists and related compounds, as well as on n=
ovel drugs of this family with better selectivity, distribution patterns, a=
nd pharmacokinetics, and - in cases where it is impossible to separate the =
desired clinical action and the psychoactivity - just to monitor these side=
 effects carefully. Cannabis sativa L. preparations, such as marijuana, has=
hish, and dagga, have been used in medicine for millenia.1 Investigations i=
nto the chemistry of Cannabis began in the mid-19th century, following a ma=
jor trend in chemical research at the time, which centered on the quest for=
 active natural products. Numerous alkaloids were isolated in pure form or =
partially characterized. Morphine, cocaine, strychnine, and many others wer=
e purified and used in medicine. However, most of the terpenoids - a major =
class of secondary plant metabolites, to which the plant cannabinoids also =
belong - were not isolated until the end of the century or even much later,=
 and in many cases their purity was doubtful. </p>
  <p style=3D"font-size:7.8px; ">In 1840, Schlesinger was apparently the fi=
rst investigator to obtain an active extract from the leaves and flowers of=
 hemp.2 A few years later, Decourtive described the preparation of an ethan=
ol extract that on evaporation of the solvent gave a dark resin, which he n=
amed &acirc;??cannabin.&acirc;?=9D 3 For a detailed history of early Cannab=
is research see ref 4. The chemical research on the plant cannabinoids and =
their derivatives over nearly two centuries is described in ref 5. It was, =
however, not until 1964 that ?9-tetrahydrocannabinol (?9-THC), the major ps=
ychoactive component of Cannabis, was isolated in pure form and its structu=
re was elucidated.6 Shortly thereafter it was synthesized and became widely=
 available. These chemical advances led to an avalanche of publications on =
?9-THC, as well as on cannabidiol (CBD), a nonpsychoactive plant cannabinoi=
d.7 However, concern about the dangers of abuse led to the banning of marij=
uana and its constituents for medicinal use in United States and many other=
 countries in the 1930s and 1940s. It took decades until cannabinoids came =
to be considered again as compounds of therapeutic value, and even now thei=
r uses are highly restricted. Here we present an overview of the addictive =
and side effects of cannabinoids vs their therapeutic potential. Marijuana =
may produce mild dependence in humans.8-12 This was shown to depend on the =
personality type of the addicts,13 and can be successfully reversed by abst=
inence or treated by cognitive-behavioral therapy,14 without the occurrence=
 of major withdrawal symptoms. Cannabinoids act on brain reward processes a=
nd reward-related behaviors by a mechanism similar to that found with other=
 addictive drugs. In animal models they enhance electrical brain-stimulatio=
n reward in the core meso-accumbens reward circuitry of the brain and neura=
l firing of a core dopamine (DA) component and thus elevate DA circuit. In =
the reward-relevant meso-accumbens DA circuit. In some animal models they p=
roduce conditioned place preference (CPP) and self-administration.15,16 Oth=
er studies, however, find THC to be a poor reinforcer, with no or little se=
lf-administration.17</p>=20
  <p style=3D"font-size:7.8px; ">The abuse of other substances is influence=
d by the cannabinoids. The cannabinoid system is involved in alcohol-consum=
ption behavior. Cannabinoid CB1 receptor agonists have been found to specif=
ically stimulate alcohol intake and its motivational properties in rats.18 =
The high ethanol preference of young mice is reduced by the cannabinoid rec=
eptor 1 (CB1) antagonist SR141716A (rimonabant) to levels observed in their=
 CB1 knockout littermates.19 Dopamine release induced by ethanol in brain w=
as reduced by SR141716A,20 which can explain in part the antiaddictive effe=
ct of the drug. Cocaine is another substance of abuse in whose acquisition =
and consolidation cannabinoids may be involved. High prevalence of alcohol =
dependence and cannabis dependence can be found in patients with cocaine de=
pendences.21 Marijuana smoking increases plasma cocaine levels and subjecti=
ve reports of euphoria in male volunteers.22,23 Furthermore, a recent genet=
ic study found an association between an n triplet repeat polymorphism in t=
he CB1 encoding CNR1 gene with cocaine addiction in the African-Caribbean p=
opulation.24 In another study it was found that withdrawal from repeated ac=
cess or exposure to cocaine and then a reinstatement of cocaine-seeking beh=
avior or a sensitized locomotor response to a single cocaine challenge, res=
pectively, was potently reduced by pretreatment with rimonabant.25 Similarl=
y, acute administration of rimonabant blocked expression of nicotineinduced=
 conditioned place preference.26 Rimonabant also reduces nicotine self-admi=
nistration, and may be effective not only as an aid for smoking cessation, =
but also in the maintenance of abstinence.27 As the endocannabinoid system =
plays a role in nicotine addiction,28 the potential of cannabinoid antagoni=
sts to treat it is self-evident.29-31 Opiate and CB1 receptors are coexpres=
sed in the nucleus accumbens and dorsal striatum, and the interaction betwe=
en the two systems is well known.32 The reinforcing properties of morphine =
and the severity of the withdrawal syndrome are strongly reduced in CB1-kno=
ckout mice33; this observation opens an opportunity to treat opiate addicti=
on with rimonabant, as noted with alcohol, cocaine, and nicotine addiction.=
</p>=20
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