Alpha-Lipoic Acid for cancer

Alpha-Lipoic Acid--is a powerful antioxidant that regulates gene expression and preserves hearing during cisplatin therapy

Lester Packer, Ph.D. (scientist and professor at the Berkeley Laboratory of the University of California), refers to lipoic acid as the most powerful of all the antioxidants; in fact, Packer says that if he were to invent an ideal antioxidant, it would closely resemble lipoic acid (Packer et al. 1999). Alpha-lipoic acid claims anticarcinogenic credits because it independently scavenges free radicals, including the hydroxyl radical (a free radical involved in all stages of the cancer process and linked to an increase in the likelihood of metastasis).

Lipoic acid increases the efficacy of other antioxidants, regenerating vitamins C and E, coenzyme Q10, and glutathione for continued service. In fact, lipoic acid boosts the levels of glutathione by 30-70%, particularly in the lungs, liver, and kidney cells of laboratory animals injected with the antioxidant. In addition, glutathione tempers the synthesis of damaging cytokines and adhesion molecules by influencing the activity of nuclear factor kappa B (NF-kB), a transcription factor (Exner et al. 2000). 

Lipoic acid can down-regulate genes that accelerate cancer without inducing toxicity. So responsive are cancer cells that laboratory-induced cancers literally soak up lipoic acid, a saturation that increased the lifespan of rats with aggressive cancer by 25% (Karpov et al. 1977).

Alpha-lipoic acid was preferentially toxic to leukemia cells lines (Jurkat and CCRF-CEM cells). The selective toxicity of lipoic acid to Jurkat cells was credited (in part) to the antioxidant’s ability to induce apoptosis. Lipoic acid activated (by nearly 100%) an enzyme (caspase) that kills leukemia cells (Pack et al. 2002). Other researchers showed that lipoic acid acted as a potentiator, amplifying the anti-leukemic effects of vitamin D. It is speculated that lipoic acid delivers much of its advantage by inhibiting NF-kB and the appearance of damaging cytokines (Sokoloski et al. 1997; Zhang et al. 2001).

 Finding that lipoic acid can differentiate between normal and leukemic cells charts new courses in treatment strategies to slow or overcome the disease (Packer et al. 1999).

As with all antioxidants, the appropriateness of using lipoic acid with chemotherapy arises. Animal studies indicate that alpha-lipoic acid decreased side effects associated with cyclophosphamide and vincristine (chemotherapeutic agents) but did not hamper drug effectiveness (Berger et al. 1983). More recently, a combination of alpha-lipoic acid and doxorubicin resulted in a marginally significant increase in survival of leukemic mice (Dovinova et al. 1999).

 Nonetheless, the definitive answer regarding coupling antioxidants with conventional cancer therapy is complex. Factors, such as type of malignancy, as well as the nature of the cytotoxic chemical and even the time of day the agents are administered, appear to influence outcome some.

I GIVE LUCY A 90# LAB Alpha-Lipoic Acid in her AM meal. One 300mg cap.

Another article on Artemisinin - Wormwood for Cancer

Artemisinin (Wormwood) for Cancer

Recently, another ancient herb called artemisinin was discovered. History documentation showed that it was used to treat intestinal  parasitic infections, hemorrhoids (its an anti-inflammatory) and malaria as early as 2000 years ago. 


THE USE FOR MALARIA

This treatment for malaria was, however, lost over time. It was only rediscovered in an archeological dig in the 1970s where its medicinal use was found in a recipe inside a tomb. The formula was dated back to 168 B.C. where the Chinese chemist isolated the primary active ingredient from the leafy portion of plant called A. annua L.

In 1972, scientists in the West called this crystalline compound "qinghaosu" or "artemisinin". Since then, studies in China and Vietnam have confirmed that artemisinin is a highly effective compound with close to 100 percent response rate for treating malaria. It has the ability to destroy the malaria parasite by releasing high doses of free radicals that attack the cell membrane of the parasite in the presence of high iron concentration. In fact, over one million malaria patients have been cured via this method. Their symptoms also subsided in a matter of days.

However, the treatment using this herb to treat malaria is not approved for use in the U.S.A due to the concern that it has a 21 percent recrudescent rate. Scientists believe that this is more likely due to patients not taking the compound for a long period. Many of them actually stop taking it as soon as their symptoms subside. 

It has been shown that this herb works via highly reactive oxygen-based free radicals that becomes activated in the presence of iron. Iron is an oxidant, and our body tries to protect us from excessive iron moving it to a binded state such as hemoglobin and enzymes. The malaria parasite accumulates iron by infecting iron-rich red blood cell. Excessive iron that is spilled onto the surrounding tissues will activate the artemisinin to generate a burst of free radicals that attack the iron rich cells, killing the parasite in the process.
 In other words, this compound works well in an iron rich environment (remember that malaria lives in the red blood cell rich in iron) through the release of free radicals that serve to damage the malaria organism. It is also interesting to note that drugs known to work by enhancing oxygen radical effects such as doxorubicin can enhance the effects of artemisinin.

For malaria, there is no resistance nor toxicity at the dosage of 3 grams, (about 50mg/kg) administered over a 3 to 5 day period. It is especially useful in the treatment of drug resistant malaria.

Outside of the United States, artemisinin is the number one natural herb used for malaria treatment.


THE USE FOR CANCER

So far, the most extensive study on the use of Artemisinin as an anti-cancer agent was carried out by bioengineering scientists Drs Narenda Singh and Henry Lai of the University of Washington. This study was reported in the Journal Life Science (70 (2001): 49-56).

Iron is required for cell division, and it is well known that many cancer cell types selectively accumulate iron for this purpose. Most cancers have large number of iron attracting transferring receptors on their cell surface compared to normal cells. In laboratory studies of radiation, resistant breast cancer cells that has high propensity for accumulating iron revealed that artemisinin has 75 percent cancer cell killing properties in a 8 hours and almost 100 percent killing properties within 24 hours when these cancer cells are "pre-loaded" with iron after incubation with holotransferrin. On the other hand, the normal cells remained virtually unharmed. Another study showing the effectiveness of artesunate in treatment of cancer was also published in Oncology (April 2001: 18(4): 767-73).

Artemisinin is effective against a wide variety of cancers as shown in a series of successful experiments. The most effective is leukemia and colon cancer. Intermediate activities were also shown against melanoma, breast, ovarian, prostate, CNS and renal cancer. Although artemisinin is insoluble in water, it is able to cross the blood brain barrier (the water soluble artesunate is the weakness among the derivates) and may be particularly suitable for curing brain tumors, together with Poly-MVA (an metalo-vitamin)

In laboratory studies, iron needs to be added to enhance the effects of artemisinin. Within the human body, no such addition is necessary, as iron already exist in the body. Animals get plenty in their diet. It can also be taken orally and therefore high doses are not required. Some people believe that as nitrogen (tertiary amine) is absent in ART, cancer cells cannot get rid of it once it enters into the cancer cell. As a result, ART stays in the cell much longer.

In addition to the high affinity for iron in aggressive cancer cell types, most cancer cells also lack the enzyme catalayse and gutathione peroxidase. Catalayse breaks down hydrogen peroxide. A low catalayse content means a higher hydrogen peroxide load, which can release superoxide free radicals when properly stimulated to do so. This is in fact one common mechanism among chemotherapeutic agents. These traits make cancer cells more susceptible to oxidative damage as compare to normal cells in the presences of hydrogen peroxide.  

According to Dr Rowen , a naturally oriented medical doctor and editor of the medical newsletter " Second Opinion" , the Hoang family of physicians in Vietnam had used arteminisin in the treatment of cancer for years. They have reported that, over a 10-year period, more than 400 patients were treated with artemisinin in conjunction with a comprehensive anti-cancer program with 50 to 60 percent long-term remission rate. The safety record of artemisinin has well been studied for over 25 years. No significant toxicity in short-term use for malaria at high dose of up to 70 mg/kg per day has been reported.

Artemisinin is not a stand-alone chemotherapeutic agent. A combination of nutritional supplements as well as a good anti-cancer diet is required.



TOXICITY AND SIDE EFFECTS 


When ART is tested with monkeys, they showed no toxicity when they received up to 292 mg/kg of artemether over 1 to 3 months. This is equal to a human dose of 20,000 mg for a 70 kg male (Journal of Traditional Chinese Medicine 2(1):31-36 1982). In another study, there was also no sign of toxicity in over 4000 patients. This does not exclude possible cases of long-term cumulative toxicity which is unknown at this time. 




(my 80 pound dog takes 200mg)


CAUTIONS

a. No artesminin should be taken within 30 days of radiation therapy because of possible free iron leaks to the surrounding tissues after radiation therapy.


DOSAGE

The therapeutic dose ranges from 200 mg a day  up to 1,000 a day (in divided doses ) depending on cancer types and the source of the herb.In laboratory studies, significant CANCER cell toxicity is shown to have been effected at dosage as little as 1-2 mg/kg body weight.
The exact dosage is highly controversial. In addition to the lack of clinical trials and individual variations, the dosage is highly dependent on the purity and potency of the herb itself. 


(my 80 pound dog takes 200mg)

Artemisinin  should always be taken with food. Flax oil, cottage cheese, or fish oil mixed may be administered at the same time to enhance absorption.
Always take artesminin at least 2-3 hours aside from antioxidants. 



Despite its seemingly high degree of effectiveness, it is important to note that artemisinin is not a stand-alone compound. Concurrent use of liver detoxification, immune enhancement, and periodic laboratory measurement should also be considered as part of an overall aggressive anti-cancer program.

Low Dose Naltrexone News Article

"Naltrexone is the generic name for a drug, approved by the FDA in 1984, used to treat alcohol and opioid addiction. Opioids are generally pain-management agents such as morphine, codeine, oxycodone, and fentanyl. Opioids also include heroin and methadone, as well as our own naturally occurring endorphins.

Endorphins are a type of neurotransmitter, released when we are subject to pain or stress, which have the effect of reducing these sensations. More than that, endorphins promote modulation of the appetite, release of sex hormones, feelings of euphoria, and enhancement of immune response. Some foods—such as chili peppers (the hotter the better) and chocolate—are said to promote endorphin release. Acupuncture, sex, massage, and exercise have also been shown to activate endorphin release.

Naltrexone is an opiate receptor antagonist; that is, it blocks cellular opiate receptors. As such, it removes the pleasurable feelings associated with alcohol and opioid abuse. In fact, the drug does such a good job of blocking the receptors that many heroin addicts would stop taking naltrexone, since it simply made them feel terrible all the time. As such, methadone became the drug of choice in the treatment of heroin addiction.

A Neurologist, Bernard Bihari MD, who at the time was treating heroin addicts with naltrexone, discovered that a substantial number of them—who also suffered from AIDS—had extremely low levels of endorphins. He postulated that this may have been the reason they turned to heroin in the first place. While opioid (and thus endorphin) receptors are found throughout the body, they are especially prevalent on immune system related cells.

Since many diseases stem from some sort of immune dysfunction, Bihari wondered if low endorphin levels were a factor. In 1985, Bihari discovered that simply using a low dose of naltrexone (LDN) blocks the endorphin receptors for only about an hour, the net result being that the body responds by secreting much more of the endorphins—often by a factor of five. 

Within a few years, he was seeing the therapeutic benefits of LDN in patients with such varied conditions as lymphoma, lupus, and pancreatic cancer. 

The first study of LDN published in a US-based medical journal would come in 2007, with Dr. Jill Smith's article in the American Journal of Gastroenterology entitled "Low-dose naltrexone therapy improves active Crohn's disease" (e-published in January, print published in April). Smith and her team found that 67% of the patients went into remission and fully 89% showed some therapeutic benefit. This encouraging work led to an NIH grant and a Phase II placebo-controlled clinical trial, currently in progress. 

In September, 2008, results were published for a Phase II clinical trial in Italy in which LDN was used to combat multiple sclerosis (MS). Again, the results were highly promising. Since MS is thought to result from an autoimmune process whereby T cells mistake myelin—the coating around nerve cell fibers in the brain and spinal chord—for a foreign invader and attack it, many assumed that MS was the consequence of an overactive immune response. These results, though, would argue against that theory.

In 2007, Burton Berkson MD, PhD and associates published an article in Integrative Cancer Therapies entitled "Reversal of signs and symptoms of a B-cell lymphoma in a patient using only low-dose naltrexone." Berkson's 2006 article in the same journal entitled "The long-term survival of a patient with pancreatic cancer with metastases to the liver after treatment with the intravenous alpha-lipoic acid/low-dose naltrexone protocol" described the incredible turnaround of a patient previously diagnosed as terminal in 2002.

LDN is inexpensive with virtually no harmful side effects. However, since it is no longer a proprietary drug, the pace of rolling out clinical trials for the off-label effects described in this article will probably be slow, as will its acceptance by mainstream medicine. Still, there is nothing to prevent a patient from taking an FDA approved drug for an off-label indication, and this practice goes on all the time."

Certainly, there is much appeal in a naturally-acting immune modulator that is cheap and effective. We await vets and doctors to get around to seeing the light. No, we can't wait! Help them and show them gently the data. Probably again. And again. Nope? Then you probably have to find another doctor, then try again and again....

Low Dose Naltrexone Studies and References

References:
(1) http://www.ldninfo.org/index.htm
Web site for low dose nalotrexone information. 

(1A) http://www.ldninfo.org/bbihari_cv.htm
Curriculum Vitae, BERNARD BIHARI, M.D. 29 West 15th Street New York, N.Y. 10011, (212) 929-4196 retired as of March 2007.

(2) http://www.ncbi.nlm.nih.gov/pubmed/17222320
Low-dose naltrexone therapy improves active Crohn's disease.Smith JP, Stock H, Bingaman S, Mauger D, Rogosnitzky M, Zagon IS. Am J Gastroenterol. 2007 Apr;102(4):820-8. Department of Medicine, Pennsylvania State University College of Medicine, Hershey, Pennsylvania 17033, USA. 

OBJECTIVES: Endogenous opioids and opioid antagonists have been shown to play a role in healing and repair of tissues. In an open-labeled pilot prospective trial, the safety and efficacy of low-dose naltrexone (LDN), an opioid antagonist, were tested in patients with active Crohn's disease. METHODS: Eligible subjects with histologically and endoscopically confirmed active Crohn's disease activity index (CDAI) score of 220-450 were enrolled in a study using 4.5 mg naltrexone/day. Infliximab was not allowed for a minimum of 8 wk prior to study initiation. Other therapy for Crohn's disease that was at a stable dose for 4 wk prior to enrollment was continued at the same doses. Patients completed the inflammatory bowel disease questionnaire (IBDQ) and the short-form (SF-36) quality of life surveys and CDAI scores were assessed pretreatment, every 4 wk on therapy and 4 wk after completion of the study drug. Drug was administered by mouth each evening for a 12-wk period. RESULTS: Seventeen patients with a mean CDAI score of 356 +/- 27 were enrolled. CDAI scores decreased significantly (P= 0.01) with LDN, and remained lower than baseline 4 wk after completing therapy. Eighty-nine percent of patients exhibited a response to therapy and 67% achieved a remission (P < 0.001). Improvement was recorded in both quality of life surveys with LDN compared with baseline. No laboratory abnormalities were noted. The most common side effect was sleep disturbances, occurring in seven patients. CONCLUSIONS: LDN therapy appears effective and safe in subjects with active Crohn's disease. Further studies are needed to explore the use of this compound. 

(3) http://www.ncbi.nlm.nih.gov/pubmed/6640516
Cancer Lett. 1983 Nov;21(1):89-94. Opioid antagonists inhibit the growth of metastatic murine neuroblastoma.Zagon IS, McLaughlin PJ. 

Naltrexone (NTX), an opiate antagonist, had an inhibitory effect on the growth of S20 Y neuroblastoma in A/Jax mice. Daily injections of 0.1 mg/kg NTX resulted in a 69% tumor take, 70% delay in time prior to tumor appearance, and a 60% increase in median survival time. Inoculation of NB in control mice resulted in 100% tumor take within 15 days. The pattern and incidence of metastases of NTX and control mice were similar. These results show that NTX has antineoplastic activity, and suggests a role for the endogenous opioid system in neuro-oncogenic events. 

(4) http://www.ncbi.nlm.nih.gov/pubmed/6316064
Life Sci. 1983 Dec 12;33(24):2449-54. 
Naltrexone modulates growth in infant rats.Zagon IS, McLaughlin PJ. 

Naltrexone, a potent opiate antagonist, had both stimulatory and inhibitory effects on somatic growth in preweaning rats depending on dose. Daily injections of 50 mg/kg naltrexone, which blocked morphine-induced analgesia for 24 hr/day, resulted in increased body and organ weights, and acceleration in the appearance of physical characteristics and maturation of spontaneous motor activity. Naltrexone in a dosage of 1 mg/kg, which blocked morphine-induced analgesia for 4 hr/day, had the opposite effects. These results show that naltrexone can modulate growth, and suggest a role for the endorphins and opiate receptors in developmental events. 

(5) http://www.ncbi.nlm.nih.gov/pubmed/10592296
Brain Res. 1999 Dec 4;849(1-2):147-54. Cloning, sequencing, expression and function of a cDNA encoding a receptor for the opioid growth factor, [Met(5)]enkephalin. 
Zagon IS, Verderame MF, Allen SS, McLaughlin PJ. Department of Neuroscience, The Pennsylvania State University, College of Medicine, 500 University Drive, Hershey, PA, USA. 

The native opioid growth factor (OGF), [Met(5)]enkephalin, is a tonic inhibitory peptide that modulates cell proliferation and tissue organization during development, cancer, cellular renewal, wound healing and angiogenesis. OGF action is mediated by a receptor mechanism. We have cloned and sequenced a 2.1-kilobase (kb) cDNA for a receptor to OGF (OGFr). The open reading frame was found to encode a protein of 580 amino acids, and eight imperfect repeats of nine amino acids each were a prominent feature. The protein encoded by this cDNA exhibited the pharmacological, temporal and spatial characteristics of the OGFr. Functional studies using antisense technology demonstrated an enhancement in cell growth. The molecular organization of the OGFr has no homology to classical opioid receptors. These results provide molecular validity for the interaction of OGF and OGFr in the regulation of growth processes. 

(6) http://www.ncbi.nlm.nih.gov/pubmed/11029512
Opioid growth factor regulates the cell cycle of human neoplasias.Zagon IS, Roesener CD, Verderame MF, Ohlsson-Wilhelm BM, Levin RJ, McLaughlin PJ. 

Department of Neuroscience and Anatomy, H-109, The Pennsylvania State University, College of Medicine, Hershey, PA 17033, USA. 

The native opioid growth factor (OGF), [Met5]-enkephalin, is a tonic inhibitory peptide that modulates cell proliferation and migration, as well as tissue organization, during development, cancer, homeostatic cellular renewal, wound healing, and angiogenesis. OGF action is mediated by the OGF receptor (OGFr). To investigate the target of OGF as to cell proliferation, the effects of excess OGF, and a deprivation of OGF-OGFr interaction by an opioid antagonist, naltrexone (NTX), were examined in 3 human cancer cell lines: pancreatic (BxPC-3), colon (HT-29), and head and neck (CAL-27). OGF exposure decreased growth, DNA synthesis, and mitosis, and increased the doubling time from control levels. FACS analysis revealed a marked increase in cells in the G0/G1 phase and compensatory reduction in cells in S and G2/M phases. Consistent with this observation, the percentage of labeled mitosis (PLM) analysis showed a notable increase in the time of the G0/G1 phase. Receptor blockade with NTX increased the rate of growth, length of DNA synthesis and mitotic phases, and decreased doubling time from control values. FACS analysis indicated an increase in the proportion of cells in S and G2/M phases, and a decrease in the number of cells in the G0/G1 phase. PLM evaluation demonstrated a shortening of the length of the S and G2 phases in the 3 cell lines, and decreases in the M and G0/G1 phases in some cancers. These results indicate that OGF action is directed at the G0/G1 phase, but interruption of OGF-OGFr interfacing has widespread repercussions on the cell cycle. The data on blockade of OGF-OGFr during log phase growth suggest a requisite escorting of the growth peptide and its receptor through the cell cycle. 

(7) http://www.ncbi.nlm.nih.gov/pubmed/8620464
Cancer Lett. 1996 Mar 29;101(2):159-64. 
Inhibition of human colon cancer by intermittent opioid receptor blockade with naltrexone.Hytrek SD, McLaughlin PJ, Lang CM, Zagon IS. 

Nude mice inoculated with human colon cancer (HT-29) and receiving 0.1 mg/kg naltrexone (NTX) beginning immediately after tumor cell injection exhibited a marked retardation in tumorigenicity. This dosage of NTX, which blocked opioid receptors for 6-8 h/day, resulted in a delay of 2.4-fold in tumor appearance compared to control subjects. At the time (10 days) when all control mice had tumors, 80% of the mice in the 0.1 mg/kg NTX group had no signs of neoplasia. Binding capacity, but not affinity, of [3H][Met5]-enkephalin was reduced 85% of control levels in tumor tissue from mice of the 0.1 NTX group. Plasma, but not tumor tissue levels of [Met5]-enkephalin were elevated (2.5-fold) in contrast to control values. These results suggest that daily intermittent opioid receptor blockade with NTX provokes the interaction of opioids and receptors in the interval following drug availability, with opioids serving to inhibit tumorigenicity of human colon cancer. 

(8) http://www.ncbi.nlm.nih.gov/pubmed/9066724
Cancer Lett. 1997 Jan 30;112(2):167-75. Opioid growth factor (OGF) inhibits human pancreatic cancer transplanted into nude mice.Zagon IS, Hytrek SD, Smith JP, McLaughlin PJ. 

Nude mice inoculated with human pancreatic cancer (BxPC-3) cells and receiving 5 mg/kg of opioid growth factor ([Met5]enkephalin; OGF) three times daily exhibited a marked retardation in tumorigenicity compared to animals injected with sterile water (controls). OGF-treated animals had a delay of 43% in initial tumor appearance compared to control subjects (10.6 days). At the time when all of the control mice had tumors, 62% of the mice in the OGF group had no signs of neoplasia. Tumor tissue excised from mice after 30 days was assayed for levels of [Met5]enkephalin and zeta opioid receptors. Tumor tissue levels of [Met5]enkephalin were 24-fold greater in OGF-treated mice than controls, but plasma levels of OGF were 8.6-fold lower in animals receiving OGF. Specific and saturable binding of radiolabeled [Met5]enkephalin to nuclear homogenates of pancreatic tumor tissue was recorded, with a binding affinity (Kd) of 10 nM and a binding capacity (Bmax) of 46.8 fmol/mg protein. Binding capacity, but not affinity, of [3H-Met5]enkephalin was reduced by 58% of control levels in tumor tissue from mice of the OGF group. OGF and the zeta (zeta) opioid receptor were detected in human pancreatic tumor cells by immuno-cytochemistry. These results demonstrate that an endogenous opioid and its receptor are present in human pancreatic cancer, and act as a negative regulator of tumorigenesis in vivo. 

(9) http://www.ncbi.nlm.nih.gov/pubmed/6867737
Science. 1983 Aug 12;221(4611):671-3. Naltrexone modulates tumor response in mice with neuroblastoma.Zagon IS, McLaughlin PJ. 

(10) http://www.ncbi.nlm.nih.gov/pubmed/6300232
Matthew, PM, Froelich CJ, Sibbitt WL, Jr., Bankhurst AD, Enhancement of natural cytotoxicity by beta-endorphin, J Immunol 130, pp.1658-1662, Apr 1983. 

(11) http://www.ncbi.nlm.nih.gov/pubmed/6867737
Zagon IS, McLaughlin PJ, Naltrexone modulates tumor response in mice with neuroblastoma, Science 221, pp.671-3, Aug 12, 1983. 

(12) http://www.ncbi.nlm.nih.gov/pubmed/6867737
Hytrek SD, McLaughlin PJ, Lang CM, Zagon IS, Inhibition of human colon cancer by intermittent opioid receptor blockade with naltrexone, Cancer Lett 101(2), pp. 159-64, Mar 29, 1996. 

(13) http://www.ncbi.nlm.nih.gov/pubmed/8853403
Zagon IS, Hytrek SD, Lang CM, Smith JP, McGarrity TJ, Wu Y, McLaughlin PJ, Opioid growth factor ([Met5]enkephalin) prevents the incidence and retards the growth of human colon cancer, Am J Physiol 271(3 Pt 2), pp.R780-R786, Sep 1996 

(16) http://www.ncbi.nlm.nih.gov/pubmed/6087062
Zagon IS, McLaughlin PJ, Duration of opiate receptor blockade determines tumorigenic response in mice with neuroblastoma: a role for endogenous opioid systems in cancer, Life Sci 35, pp. 409-416, 1984. 

(17) http://www.ncbi.nlm.nih.gov/pubmed/6087062
Zagon IS, McLaughlin PJ, Opioid antagonist modulation of murine neuroblastoma: A profile of cell proliferation and opioid peptides and receptors, Brain Res 480, pp. 16-28, 1989. 


 


(20) http://en.wikipedia.org/wiki/Naltrexone
wikipedia:"Naltrexone is an opioid receptor antagonist used primarily in the management of alcohol dependence and opioid dependence. It is marketed in generic form as its hydrochloride salt, naltrexone hydrochloride, and marketed under the trade names Revia and Depade. In some countries including the United States, an extended-release formulation is marketed under the trade name Vivitrol. It should not be confused with naloxone, which is used in emergency cases of overdose rather than for longer-term dependence control."

(21) http://commons.wikimedia.org/wiki/Image:Southworth_&_Hawes_-_First_etherized_operation_(re-enactment).jpg
Re-enactment of the first operation under anesthesia (ether). The actual operation took place on October 16, 1846; Daguerrotype TITLE: Operating room of the Massachusetts General Hospital, Boston.   Mr. Holman with surgeons: John Mason Warren, George Hayward, Solomon D. Townsend, John Collins Warren and James Johnson around man on operating table. Daguerreotype by Southworth & Hawes, ca. 1850. No known restrictions on publication.

(22) http://www.thecompounder.com/index.php
The Compounder Pharmacy 340 Marshall Ave Unit 100 ~ Aurora, IL 60506-2956
Phone: 630-859-0333 Fax: 630-859-0114

(23) http://wcbstv.com/topstories/lo.dose.naltrexone.2.732830.html
Drug Addiction Medication May Treat Other Diseases Dr. Max Gomez NEW YORK (CBS)
MAy 2008.

(24) http://www.skipspharmacy.com/sppress/?cat=8
Skip's Pharmacy LDN PAGE 21000 Boca Rio Rd Suite A-29 Boca Raton, Florida 33433 
561-218-0111 800-553-7429 Fax: 561-218-8873

Low Dose Naltrexone in the treatment of dogs, cats, horses and other pets

Information on the use of Low Dose Naltrexone in the treatment of dogs, cats, horses and other pets. Known by the acronym LDN, this is a "low dose" form of therapy utilizing the FDA approved drug Naltrexone for the "off label" treatment of immune related disorders. The mechanism of action appears to involve an immune modulating or balancing effect of various components of the immune system mediated through an effect on Endorphin levels. Naltrexone was approved by the FDA in 1984. It is legally available to be prescribed by physicians and veterinarians for any purpose. When given to humans in low doses, Naltrexone increases the body's production of endorphins. Endorphins are hormones, produced by the body, which help maintain and regulate the immune system. There is a growing body of information reporting the effectivness of LDN in the treatment of a wide range of immune related and auto-immune disorders. It has been in use in this manner for over 20 years. LDN Has Virtually No Side Effects: Occasionally, during the first week's use of LDN, patients may have some difficulty sleeping. This rarely persists after the first week. Should it do so, dosage can be temporarily reduced from 4.5mg to 3mg nightly for humans or for most dogs from 3mg to 2mg. Remember regular dosages are 50mg and up. So this really is LOW DOSE Naltrexone usage. In developing Naltrexone for full dose use toxicity testing in rats, rabbits, dogs and monkeys determined that at therapeutic levels Naltrexone was non-toxic and had very few side effects. However obtaining FDA approval for the Low Dose regimen will require funding that due to the present out of patent or generic status of the drug will be difficult to obtain from any pharmaceutical company. Some privately funded pilot studies have been conducted and show much promise. More extensive studies are needed and funding continues to be sought by advocates of LDN.

Low Dose Naltrexone Alternates

I know it can be difficult, if not impossible, to get the vet to prescribe Low Dose Naltrexone for your dogs cancer due to them knowing nothing about this stuff and used this way, so I found a link to a LDN site where a person has found some 'alternate' sources..... I have nothing to do with this, as always buyer beware.
I was lucky enough to finally get my dogs holistic vet to do it, but my regular vet was not willing at all till they could see, a year later, the dog is still around and fine. Oh, now it's ok....! The dog has cancer, the law says vets are allowed to prescribe ANYTHING they want as they see fit, and it's used in very very low dosages compared to normal, has low side effect profile even at HIGH doses, and the vet still gives grief!


http://ldn.proboards.com/index.cgi?board=forum&action=display&thread=2609


http://www.lowdosenaltrexone.org/ is a great info site

Treating Dog Cancer with Chinese Herbs

Studies have shown that about 90% of cancer patients have sub clinical thyroid deficiency. DHEA and melatonin are also low in most cancer patients and many others with chronic diseases.
Proper nutrition is essential in successful cancer therapy. Cancer is a wasting disease. Forty percent of cancer patients actually die from malnutrition. You cannot fight a life-threatening disease while malnourished.


TCM (TRADITIONAL CHINESE MEDICINE)


According to the Animal Cancer Center at Colorado State University (CSU), cancer is the No. 1 cause of death in geriatric dogs and cats. Nearly half the deaths of companion dogs and cats are from cancer. Roughly half of all dogs and cats will develop cancer if they live to be 10 or older. A recent CSU oncology study involving 254 clients showed that 76 percent of clients used complementary and alternative medical (CAM) therapies, with nutritional supplements the most commonly used. More than half the clients indicated strong interest in CAM; 40 percent expressed average interest, and 3 percent reported no interest. Keum Hwa Choi, Associate Professor at the University of Minnesota, College of Veterinary Medicine, reported that patients receiving both conventional and Traditional Oriental Medicine therapies had better survival rates, longer duration of remission and quality of life than those patients who did not utilize both systems of medicine.

While the ultimate goal in treating neoplasia is complete and permanent remission, that is sadly unattainable with Western medicine, alternative modalities, or various combinations thereof.

Using chinese medicinal herbs data I have found shows you can achieve:

Goal 1: Stabilization—Achieved in 90% cases
Goal 2: Shrinkage of mass—Achieved in 30% cases
Goal 3: Disappearance of mass—Achieved in 5-10% of cases

Minimally, improved quality of life is achieved with TCM treatment.

Chronologically, TCM has a 3-6-1-3 goal when dealing with oncology patients. The first goal is for the patient to live 3 months post-diagnosis. If the patient succeeds, then the expectation is for 6 months, then 1 year and finally 3 years.



Treatment Strategies for Treating Neoplasia with TCM

Strengthen the Body's Resistance and Tonify Zheng Qi (IMMUNITY)
a. Tonify Qi and strengthen Spleen

Herbal Formulas: Si Jun Zi Wan. Bu Zhong Yi Qi Wan, Liu Jun Zi Wan, Wei Qi Booster

b. Nourish Blood and Yin
Herbal Formulas: Si Wu Tang, Shi Quan Da Bu, Ba Zhen Tang, Dang Gui Bu Xue Wan

c. Nourish Yin and Body Fluids:
Herbal Formulas: Sha Shen Mai Dong, Sheng Mai Yin

d. Tonify Kidney Yang
Herbal Formulas: You Gui Wan, Shen Qi Wan


The physiological effects of tonic herbs include enhanced immune system; inhibition of tumor growth, metastasis and mutation; protection of bone marrow and the hematopoietic system; decreased side effects of chemotherapy and radiation therapy; improved quality of life. Proposed mechanisms of these herbs includes stimulation of NK cell activity, synthesis of cytokines to restrict tumor cell growth, and regulation of neoplastic cell growth cycle.
Move Qi and Blood

Stagnation of Qi and Blood is the basic pathologic change seen in the development of cancer. Physiological effects of herbs that move Qi and Blood include destruction of tumor cells, immune system regulation, enhanced effects of primary therapy (radiation, chemotherapy), neuroendocrine regulation, prevention of post-radiation fibrosis and other side effects, and the alleviation of pain.

Herbal Formulas: Xue Fu Zhu Yu Tang, Stasis Breaker or Max's Formula (Jing Tang), Chihko and Curcuma (ITM). Should use in conjunction with herbals that nourish Qi and Blood since we need to ensure that there is adequate Qi and Blood to move (e.g., Wei Qi Booster).

Clear internal toxins

Infection and chronic inflammation are predisposing factors in the development of cancer. Herbs that eliminate toxic heat may have direct anti-tumor effects via regulation of the body's immune system, cAMP levels and DNA/RNA synthesis by tumor cells, and growth inhibition of tumor cells. In addition to being antitoxic and stimulating immune function, some of these herbs have antibiotic and anti-inflammatory properties. 



Herbal Formula: Viola Clear Fire (Golden Flower), Zhong Gan Ling (Golden Flower)

Soften hard masses, dissolve aggregations

Herbs in this category soften and shrink masses; they are typically used in combination with tonic herbals to prevent the reformation of Qi/Blood/ Phelgm entanglement. There herbs may also alleviate pain from the tumor mass and help to control metastasis.

Herbal Formulas: Stasis Transforming Formula (Golden Flower), Stasis Breaker (Jing Tang), Max's Formula (for weaker animals; Jing Tang), Chihko and Curcuma (ITM).

Herbal Formulas: Max Formula (Jing Tang), Phlegm Transforming Formula (Golden Flower)

Bring the body back to balance

The fundamental basis of TCM is balance and harmony. When the body is out of balance, there is disharmony and disease is manifested. Treatment therefore seeks to help the body to come back into balance, eliminating excesses and supplementing deficiencies.
Manage clinical signs and symptoms
a. Anorexia, nausea, vomiting

Herbal Formulas: Eight Gentlemen, Happy Earth (Jing Tang)

b. Diarrhea
Herbal Formula: Shen Ling Bai Zhu San

c. Constipation
Herbal Formula: Ma Zi Ren Wan

d. Inflammation, oral ulcers
Herbal Formula: Wu Wei Xiao Du Yin

e. Anemia, pancytopenia
Herbal Formulas: Marrow Plus (Health Concerns), Gui Pi Tang, Si Wu Tang, Chemo Blood Support Formula (Golden Flower)

f. Hemorrhage
Herbal Formula: Yunnan Baiyao, topically to bleeding lesions or orally. May be used preventatively or in acute hemorrhage due to hemangiosarcoma.

If no improvement is seen after 1 month of herbal administration, reevaluate and switch herbal formulas.


Food Therapy for Cancer Patients

The nutritional status of cancer patients is often suboptimal due to the effects of cancer itself and nutrient loss via vomiting, diarrhea, effusion/exudate production, GI obstruction and blood/body fluid loss. Additionally, tumors preferentially utilize glucose for metabolic energy and trap nitrogen from glutamine and other amino acids for protein synthesis. Anorexia and insulin resistance may also result from tumor secretions and the secondary production of cytokines.

There is a synergism of treatments when utilizing TCM. Food therapy is critical to the treatment of cancer as most of our commercially available pet foods promote root causes of cancer in TCM.

As cancer cells seem to utilize simple carbohydrates, complex carbohydrates, protein and fat in descending order, the knee jerk reaction is to feed a no to low carbohydrate diet.  Some believe that increased glycemic load (glycemic index multiplied by grams of carbohydrate per serving size) results in the increased of certain forms of cancer. Although we are all hesitant to recommend any radical diet change without thoughtful and educated consideration, clinical results in this area can speak volumes.  In general, when feeding a cancer patient, a ratio of 50-60:15-30:25-35 (protein: mostly low glycemic index carbohydrates: lightly cooked vegetables) is followed. Supplementation with fish oil, digestive enzymes, probiotics and vitamin-minerals is also recommended. The patient's nutritional status should be followed closely as ration adjustments or supplementation with more oil/substitution with olive oil, flax seed oil or borage oil may be required due to weight loss or intolerance of fish oil.



Here are some other Chinese herbal patent formulas as more examples



Eight Gentleman

Used to treat chronic gastro intestinal disorders, vomiting and poor appetite.





Lilium

Used to treat upper and lower respiratory infections.





Di Tan Tang

Clears out phlegm and open the orifices while tonifying Qi. This TCM Herbal formula is best suited for conditions of internal obstruction due to severe phlegm where the smoothe circulation of fluids has stopped creating more phlegm.





Cervical Formula

Cervical disc, injuries and stiffness.





Yin Qiao San

For influenza, respiratory infections, early in the course of disease when symptoms are first felt, good for animals going to kennel for boarding.





Yunnan Bai Yao

For carcinoma, stops bleeding.





Ba Zheng San

Used to treat cystitis, stone and or crystals in urine, acute urinary tract infection, and bloody urine.





Nei Xiao Wan

Stasis Breaker – For lumps, nodules and internal abnormal masses, for blood stagnation / stasis.





BuQi Zi Yin Tang

Hindquarter weakness formula for cervical disc, injuries and stiffness.





Great Windkeeper

Used for treating skin allergies usually found in the spring and fall when the winds are active.





Long Dan Xie Gan Wan

For ear infection, otitis, dermatitis and epilepsy.





Wei Qi Booster (Immune Booster)

Immune system boost, general weakness, fatigue, apathy, poor appetite, weight loss in old animals, chronic viral infections, post-chemo or radiation, anemia, hyperthyroidism, chronic arthritis or renal failure in aged dogs.


Ingredient Actions
Bai Hua She
She Cao
Inhibit cell mutation and tumor growth
Ban Zhi Lian Inhibit cell mutation, inhibit tumor
growth
Chen Pi Move Qi and transform phlegm
Dang Gui Tonifies Blood
Dang Shen Tonify Qi and boost Wei Qi
Huang Qi Tonifies Qi in whole body and Wei Qi
Wu Yao Move Qi and clear stagnation
Xuan Shen Cool Blood and nourish Yin
Contraindication:
Do not use in conditions with Excess Heat
(Acute inflammation or infection, high fever)


Stasis Breaker (A tumor buster)
General Dosage:
Horse: 15 g BID as top dressing on feed
Dog/Cat: 0.5 g per 10 to 20 lb body weight BID
“In TCVM, the main
pattern of tumor and
cancer masses is
Blood stasis.”
Contraindication: Do not use in pregnant or weak animals.
Use as needed up to 3 months. May be used
with Wei Qi Booster.
In TCVM, tumor tissues and nodules are classified as
Blood stasis and stagnation. The key treatment strategy
is to remove Blood stasis. Both Stasis Breaker and Max
Formula are designed for the treatment of neoplasia,
tumors and nodules. The difference is that Stasis Breaker
has a strong action while Max Formula has a milder
effect. Thus, Stasis Breaker is used for excess enlargement
in strong animals.

ALTERNATIVE OPTIONS FOR
CANCER PATIENTS
Ingredient Actions
Bai Hua She
She Cao
Inhibit cell mutation and tumor growth
Ban Zhi Lian Clear Heat-toxin, inhibit cell mutation,
inhibit tumor growth
E Zhu Purge the interior, break Blood stasis
and clear mass
Mu Li(Shu) Soften hardness and clear mass
San Leng Purge the interior, break stasis and
clear mass
Zhe Bei Mu Soften harness and clear nodules

Lucy Dog Nasal Cancer 1 year 3 months still in remission

Nasal Cancer still in remission 1 year 3 months after diagnosis.Proof of Life photo given to show current TIME Magazine. Please help your dog and review my blog. I am not selling anything. I am just sharing everything I found researching and used it on her. No rad or chemo used.