Low Dose Naltrexone and Alpha Lipoic Acid : The nutrient/drug combination that cures incurable cancer
As you may know, pancreatic cancer is one of the hardest cancers to cure. Traditional oncologists have nothing to offer to treat it. In fact, the honest ones won’t even treat you because they know nothing in their arsenal will work. But I’ve just found out about a very simple treatment on terminal pancreatic cancer that’s just astounding.
I have the case reports of three patients with stage-4 pancreatic cancer. Every one of the patients’ cancer had spread to the liver or beyond. Traditional oncologists would consider each of these cases as terminal. But what you’re about to read is astonishing.
Each of these patients had intravenous alpha-lipoic acid (ALA) and low-dose Naltrexone. Their cancers disappeared and didn’t return, even on long-term follow-up. It sounds too simple, doesn’t it? But it’s not.
Here’s why it works: ALA reduces oxidative stress. It stabilizes NF(k)B, a potent inducer of inflammation. It encourages apoptosis in cancer cells (cell suicide), and discourages their proliferation.
Naltrexone is a narcotic antagonist. When you take low doses (say 4.5 mg at bedtime), it blocks your production of endorphins (your own self-made narcotics). When it wears off, your brain makes an explosion of endorphins. These molecules directly talk with your immune cells. When this happens, your brain and immune system actually become part of a greater unified organ. This activation of your immune system may enable it to overcome the defenses cancer puts up to immune cell activity.
If you have incurable cancer, never give up hope. This could be the miracle you’re looking for. This is a very easy to do treatment that’s quite safe. Take it to any alternative physician. It’s not going to help everyone. But it sure beats the poisons the conventional pundits will pump into you.
The dose of Naltrexone is only 4.5 mg. Any compounding pharmacy can make it for your doctor. The dose of the intravenous ALA starts at 100 mg per treatment and works up to 600 mg if well tolerated. And you have to do it just twice weekly.
Yours for better health and medical freedom,
Robert J. Rowen, MD
Ref: “Revisiting the ALA/N (alpha-lipoic acid/low-dose naltrexone) protocol for people with metastatic and nonmetastatic pancreatic cancer: a report of 3 new cases,” Berkson BM, Rubin DM, et al, Integr Cancer Ther, 2009; 8(4): 416-22.
#2: From: Terry Vanderheyden
Society for Experimental Biology and Medicine
Public release date: 12-Jul-2011
Ovarian cancer: low dose naltrexone (LDN) has potent antitumor effect
Researchers at The Pennsylvania State University College of Medicine, Hershey, Pennsylvania have discovered that a low dose of the opioid antagonist naltrexone (LDN) has an extraordinarily potent antitumor effect on human ovarian cancer in tissue culture and xenografts established in nude mice. When LDN is combined with chemotherapy, there is an additive inhibitory action on tumorigenesis. This discovery, reported in the July 2011 issue of Experimental Biology and Medicine, provides new insights into the pathogenesis and treatment of ovarian neoplasia, the 4th leading cause of cancer-related mortality among women in the United States.
The strategy of LDN therapy in repressing cancer was first reported over 30 years ago by Drs. Zagon and McLaughlin (Science 221:671-673). Naltrexone (NTX) is a general opioid receptor antagonist devoid of intrinsic activity that results in a compensatory elevation in endogenous opioids and opioid receptors. Blockade of opioid peptides from opioid receptors for a short time each day (4 to 6 hr) with LDN provides a sufficient window of time (18-20 hr) for the elevated levels of endogenous opioids and opioid receptors to interact and elicit a response: inhibition of cell proliferation. Thus, LDN acts as a decoy to upregulate native opioids and opioid receptors. When NTX is metabolized and no longer present, an enhanced opioid-receptor effect is permitted to occur. The endogenous opioid peptide, opioid growth factor (OGF) (chemical term = [Met5]-enkephalin) and its receptor (OGFr) is related to LDN action, and constitutes a tonically active inhibitory axis that suppresses cell proliferation through a depression in DNA synthesis by way of cyclin-dependent kinase inhibitory pathways. In the case of human ovarian cancer, this laboratory (Amer. J. Physiol. 296:R1716-1725, 2009) previously found that the OGF-OGFr axis is present and functional in human ovarian cancer.
The present study addressed the question of whether modulation of the OGF-OGFr axis by LDN could alter the progression of established ovarian tumors. Moreover, the authors asked whether LDN can be combined with standard chemotherapy to invoke an even greater effect on ovarian cancer. A model of LDN in tissue culture was established that exposed human ovarian cancer cells to NTX for 6 hr every two days, resulting in reduced DNA synthesis and cell replication from vehicle subjected controls. When a short term exposure to NTX was combined with standard of care chemotherapeutic agents, taxol or cisplatin, an enhanced anticancer action relative to either drug was observed. The effects of LDN, but not taxol or cisplatin, could be reversed, indicating the non-toxic nature of LDN. Although favorable results with LDN alone and in combination with chemotherapeutic drugs were recorded in a tissue culture setting, this begged the question of whether LDN was effective on tumors transplanted into mice. Using nude mice with established xenografts of human ovarian cancer, LDN was found to repress tumor progression, reducing DNA synthesis and angiogenesis but not altering cell survival. LDN’s repression of cancer progression was comparable to that of cisplatin or taxol. However, the combination of LDN with cisplatin, but not taxol, had an even greater antitumor effect than LDN or taxol alone. Moreover, cisplatin was toxic to the mice, as detected by weight loss. However, LDN in combination with cisplatin attenuated the toxicity of this chemotherapeutic agent, indicating that LDN was protective of the adverse events elicited by a chemotherapeutic drug. Finally, LDN was discovered to upregulate the expression of both OGF and OGFr, indicating that this endogenous opioid system, which inhibits cell proliferation, was activated by LDN.
The research team was comprised of Dr. Ian S. Zagon, Distinguished University Professor, and Dr. Patricia J. McLaughlin, Professor, along with a doctoral student, Dr. Renee N. Donahue, in the Department of Neural & Behavioral Sciences. Drs. Zagon and McLaughlin have extensive collaborations focused on demonstrating the remarkable properties of LDN and OGF in a variety of preclinical and clinical studies. LDN has proven successful in Phase I and II clinical trials in the treatment of Crohn’s disease, and OGF has been found to be safe and efficacious for pancreatic cancer. Co-author Dr. McLaughlin states: “Given the extraordinary biological control of the OGF-OGFr axis with respect to cell proliferation, and the unique modulatory capability of LDN to enhance opioid-receptor response by way of native biological processes, this is particularly attractive as a biological-based treatment in arresting the progression of ovarian cancer.” Dr. Zagon adds that “More than 75% of women are diagnosed with ovarian cancer in advanced stages because of a lack of diagnostic biomarkers. Although the initial clinical response to cytoreductive surgery and adjuvant chemotherapy is excellent, nearly 65% of advanced-staged patients relapse within 2 years. All subsequent treatments are pallative. Thus, the clinical implications of our study speak to the urgency for initiating clinical trials using LDN in the treatment of advanced ovarian cancer.”
Steven Goodman, Ph.D. Editor-in-Chief of Experimental Biology and Medicine said “Researchers at The Pennsylvania State University College of Medicine have discovered that a low dose of the opioid antagonist naltrexone markedly suppresses progression of human ovarian cancer transplanted into mice. Low dose naltrexone combined with cisplatin, but not taxol, had an additive inhibitory action on tumorigenesis. Therefore low dose naltrexone offers a non-toxic and efficacious biologic pathway-related treatment that may benefit patients with this ovarian cancer.”
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