BACK TO ASK THE HERBALIST
I'm a 42 yr. old male who has had a history of disc
problems in the L-4, L-5area.
I have used chiropractic care which has worked after one
or two sessions. Recently, my discs herniated. The
swelling was so great my Dr. couldn't adjust me. A
friend of mine suggested seeing a retired back surgeon
who has been using Colchicine injections with fantastic
results. Even though this medicine has been used for
gout, it has reduced swelling in discs. I went and after
the first visit it began to work. I also take a low
dosage orally twice a day. My question, to cut down on
the costs can I go to my local health food store and get
anything and get the same results?
ANSWER: For thousands of years this plant has
been used for gout pain, they did not have injectables
then, look for a OTC preparation of the plant meadow
saffron Latin named: Colchicum autumnale or other pain
reliever such as California poppy, Jamaican Dogwood and
anti-inflammatory herbs such as Turmeric and Sarsaparilla.
From the net
Matthew J. Dowd, Graduate Student
Department of Medicinal Chemistry
Medical College of Virginia Campus
Virginia Commonwealth University
"No other pain is more severe than this, not iron
screws, nor cords, not the wound of a dagger, nor
burning fire." Imagine feeling this pain, as
described by Aretaeus, the Greek physician of the second
century. Thomas Sydenham, a 17th Century physician,
described the pain as "a violent stretching and
tearingof the ligaments - now it is a gnawing pain, like
that of a dog." The disease gout is the source
of these vivid descriptions. Through the centuries, gout
has been a debilitating affliction most associated with
a decadentlifestyle, middle-aged men, and alcohol. The
major symptom is an intense, burning pain of the joint
of the big toe. Because of its long history, gout has
been the target of a number of effective and some
not-so-effective treatments. Some of the less
beneficial treatments include rest and relaxation until
the pain subsides, consumption of wine or alcoholic
punch, and even vibration-generated heat from a glass
boot. With the age of modern medicine came also more
effective treatments for gout, such as the drugs
probenecid,allopurinol, cortisone, and nonsteroidal
anti-inflammatory drugs (NSAIDS) such as ibuprofen and
indomethacin. Clearly, the anti-gout agent with the
longest history is colchicine.
(-)-Colchicine(1), which was first used over 2000 years
ago in the form of preparations of the meadow saffron
Colchicum autumnale (Fig. 1), is still one of the more
effective treatments for the intense pain associated
with a gout attack.Padanius Dioscorides, a Greek surgeon
in the Roman Army during the rule of Nero(AD 54-68),
first described the meadow saffron in his influential De
Materia Medica, a pharmacopeia which systematically
described about 600 plants.Throughout the years, many
historians, physicians, and pharmacopeias have noted the
beneficial effects of Colchicum extracts for the
treatment of gout.
It was not until 1820 when (-)-colchicine, the
pharmacologically activec onstituent of the plant, was
isolated by the French chemists Pelletier and Caventon.
The absolute configuration was determined by Corrodi and
Hardeggerin 1955. As can be seen, colchicine is a
tricyclic alkaloid, the main features of which include a
trimethoxyphenyl ring (A ring), a seven membered ring
(Bring) with an acetamide at the seven position, and a
tropolonic ring (C ring).
Thegoal of most colchicine research is a more thorough
understanding of the cause of gout, which is often
thought of as a disease of rich living. However, as many
victims will testify, the affliction does not limit
itself to thislifestyle. Gout, from the Latin gutta,
meaning drop, was used to describe the symptoms because
physicians presumed the disease was caused by the
dropping of phlegm into the big toe. Hyperurecosia,
or elevated blood levels of uric acid, causes the
common symptoms of gout[5,6]. In humans and other
primates,uric acid is the final metabolite in the
breakdown of purines. When thismetabolic pathway becomes
overwhelmed, from either an enzymatic deficiency or an
increase in dietary purines, uric acid cannot be
efficiently elimated from the body. The poorly soluble
uric acid crystalizes, initiating a response
frommacrophages and leukocytes. The phagocytosis of
urate crystals by the macrogphages and leukocytes
stimulates the release of cytokines and interleukins,
leading to inflammation and the distinctive symptoms.
The precise mechanism by which colchicine relieves the
intense pain of gout is not known. However, it is
believed that the major relief of pain involves
colchicine's major pharmacological action: binding to
tubulin dimers. Tubulin (MW approximately 10,000 Dalton)
is a protein consisting of two forms, alpha and beta.
Alpha and beta tubulin form dimers, and these dimers
polymerize to form long filaments of microtubules.
When colchicine binds to the tubulin dimers, the dimers
are unable to form the microtubules. The microtubules
are vital for formation of spindle fibers during mitosis
and meiosis, intracellular transport of vesicles and
proteins, flagella reassembly, ameboid motility, and
other cellular processes. Inhibition of ameoboid
motility prevents macrophage and leokocyte migration and
phagocytosis, thereby presumably preventing the
inflammation and pain of gout. Becausecolchicine
disrupts mitosis, halting the process at metaphase,
scientists have also evaluated colchicine as an
anticancer agent. However, serious toxicities prevent
the use of colchicine in antineoplastic therapies.
Oneinsight into the molecular action of colchicine has
been the determination of the biologically active
conformation [7,8]. (-)-Colchicine has only one
stereogenic center: carbon -7. The designation of this
carbon is S, according to the common Cahn-Ingold-Prelog
rules. However, colchicine is also asymmetricdue to
Thesingle bond between the A and C rings is rotationally
restricted, in a similar manner to certain substituted
biphenyls (Figure 2). This restriction adds adegree of
asymmetry to the molecule. In 1933, Kuhn designated this
type ofstereoisomerism as atropisomerism (from Greek -
"a" meaning not; "tropos"; meaning
turn). The designation of this asymmetry is "S
or R" according to the rules of molecular
asymmetry, in which the "a" stands for axial
chirality. In colchicine, the C-C bond between the
aA and aC rings is the chiral axis.
In light of this molecular asymmetry, colchicine has
four stereoisomers, as shown in Figure 3. Each pair has
either the R or S configuration at
C-7.(-)-(aS,7S)-Colchicine, the natural isomer, can
interconvert between the two conformational isomers aR
and aS, given enough energy. The energy barrier of
rotation in colchicine, approximately 22-24 kcal/mol
, is large enough to allow the synthesis and
isolation of the conformations as stereoisomers. The
research of many medicinal chemists, in particular
Arnold Brossi, has led to the conclusion that the
counterclockwise as conformation is that of the
naturally occurring alkaloid.[7,8,11-14] Shown in Figure
4 are energy-minimized models of the atropisomers of
(7S)-colchicine (Constructed using Sybyl 6.4,Tripos,
Inc). Note the very different arrangement of the
acetamide group in thetwo conformations.
In the search for more effective agents than those
provided by Mother Nature, medicinal chemists have
synthesized hundreds of analogs of colchicine and
colchicine-like compounds. Analysis of these data has
yielded information about the optimal structural
requirements for binding to tubulin and
inhibitingtubulin polymerization. The basic, although
not comprehensive, structure-activity relationships (SARs)
are summarized in Fig 5, adapted fromBoye and Brossi
. (+)-(aR,7R)-Colchicine (see Figure 4), the
unnatural enantiomer of (-)-colchicine, is devoid of
tubulin binding activity. Theappropriate torsion angle
(about 53 degrees) between rings A and C is requiredf or
tubulin binding ability. Removal or demethylation of the
methoxy groups decreases potency. On the B ring, the
acetamide can be replaced by other alkylamides with
retention of potency; however, the free amine has
decreased antitubulin activity. The acetamide can be
eliminated altogether, and activity isretained. On the C
ring, demethylation to the 10 -OH (i.e., colchiceine)
destroys activity. Replacement of the 10-methoxy with
SCH3 or NR2 leads toincreased potency. Reversal of the
oxygen pattern (i.e., 9-methoxy and 10-keto)produces
isocolchicine, which is inactive. It is apparent that
the tropolonicfunctionality contributes to activity.
This seven membered C ring can, however,be replaced with
a an anisole ring, producing a bridged biphenyl, which
retainstubulin binding activity, as long as the torsion
angle between the rings A andC is acceptable.
Presentand future work in the design of colchicine
analogs and other agents thatinhibit tubulin
polymerization will attempt to make agents wth
reducedtoxicities and a larger therapeutic window.
These analogs may moresuccessfully treat diseases in
which colchicine is presently used, such asfamilial
Mediterranean fever (FMF), chronic constipation
,immunosuppresion, and several other
pathophysiological processes. Another majorgoal is to
determine the precise interaction between colchicine and
tubulin dimers.Knowledge of the tubulin-colchicine
interactions at the atomic level may leadto the design
of better drugs, preventing future generations from
experiencingthe pain "more severe than iron
screws and burning fire."
Dateposted: April 30, 1998
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Hello I have a central herniated disk which occurred
approx 31/2 months ago. Most of my pain is gone away but
I have a little numbness in my right foot around the
large toe and one along side it. I also have tightness
in my thigh muscle especially after walking for a
extended period of time. I am on vioxx and have been for
about a month now is there anything that could help my
ANSWER: If this were my issue
For antiinflammantion I would try Turmeric
For increased peripheral circulation Gingko
For Nerve issues Saint Johnswort and Fresh Oats
Taken all as a alcohol extract
QUESTION: I herniated a disk 3 months ago and though the
pain has greatly gone down the aftermath still lives on. My left
peck,tricep,and bicep don't flex and the strength is 1/3 of what it
was 3 months ago. Beside vitamins I'm taking glucosmine,msm,and
valerian. Is there anything I can take to help speed up the
healing of the nerve and disk that was damaged and causing the muscle
not to flex or pump up after a work out?
ANSWER: Herbal antiinflammatory agents such as Turmeric
and Sarsparilla internally and to help with nerve damage St Johnswort
tincture internally and St Johnswort oil externally rubbed into the
area. You may want to slow down or cut back on your work outs
until things heal properly.