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QUESTION:  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
Colchicine
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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."[1] 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."[1] 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[2].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.[3] The absolute configuration was determined by Corrodi and Hardeggerin 1955.[4] 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.[1] 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.[5] 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 axial chirality.  
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)[9]. The designation of this asymmetry is "S or R" according to the rules of molecular asymmetry, in which the "a" stands for axial chirality.[10] 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 [8], 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 [8]. (+)-(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[15]. These analogs may moresuccessfully treat diseases in which colchicine is presently used, such asfamilial Mediterranean fever (FMF)[16], chronic constipation [17],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

References
1)Weede, R.P. Poison in the Pot: The Legacy of Lead Southern Illinois UniversityPress: Carbondale and Edwardsville, 1984, 83.
2)Singer, C. A History of Scientific Ideas Barnes and Nobles, 1996.
3)Pelletier, P.S.; Caventon, J. Ann. Chim. Phys. 1820, 14, 69.
4)Corrodi, H.; Hardegger, E. Die Konfiguration des Colchicins und verwandterVerbindungen Helv. Chem. Acta 1955, 38, 2030-2033.
5)Katzung, B.G. Basic and Clinical Pharmacology; B.G. Katzung, Ed.; Apleton andLange: Norwalk, 1995, 536-559.
6)Voet, D.; Voet. J.G. Biochemistry John Wiley and Sons, Inc.: New York, 1990,758-762.
7)Capraro, H. G.; Brossi, A. The Alkaloids; Brossi, A., Ed.; Academic Press: NewYork, 1984; Vol. 23, 1-70.
8)Boye, O.; Brossi, A. The Alkaloids; Brossi, A., Cordell, G.A., Eds.; AcademicPress: New York, 1992; Vol. 41, 125-178.
9)Kuhn, R. "Molekulare Asymmetrie" in Stereochemie; Frendenberg, K.Ed.; Franz Deutike: 1933, p.803.
10)Eliel, E.L.; Wilen, S.H. Stereochemistry of Organic Compounds; John Wiley andSons, Inc.: New York, 1994, 1119-1122.
11)Brossi, A. Bioactive Alkaloids. 4. Results of Recent Investigations withColchicine and Physostigmine. J. Med. Chem. 1990, 33, 2311-2319.
12)Wildman, W.C. The Alkaloids; Manske, R.H.F., Holmes, H.L., Eds.; AcademicPress: New York, 1968; Vol. 11, 407-456.
13)Cook, J. W.; Loudon, J. D. The Alkaloids; Manske, R.H.F., Holmes, H.L., Eds.;Academic Press: New York, 1952; Vol.2, 261-330.
14)Wildman, W.C. The Alkaloids; Manske, R.H.F., Ed.; Academic Press: New York,1960I>; Vol.6, 220-246.
15)Chen, K.; Kuo, S.C.; Hsieh, M.C.; Mauger, A.; Lin, C.M.; Hamel, E.; Lee, K.H.Antitumor Agents. 178. Synthesis and Biological Evaluation of Substituted2-Aryl-1,8-naphthyridin-4(1H)-ones as Antitumor Agents That Inhibit TubulinPolymerization. J. Med. Chem. 1997, 40, 3049-3056.
16)Buskila, D.; Zaks, N.; Neumann, L.; Livneh, A.; Greenberg, S.; Pras, M.Langevitz, P. Quality of life of patients with familial Mediterranean fever.Clin. Exp. Rheumatol. 1997, 15, 355-360.
17) Verne,G.N.; Eaker, E.Y.; Davis, R.H.; Sninksy, C.A. Colchicine is an effectivetreatment for patients with chronic constipation: an open-label trial. Dig.Dis. Sci. 1997, 42, 1959-1963.


QUESTION:
  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 situation.

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


HERNIATED DISK
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.