Cancer therapy: Is LDN the missing link?

By Pharmacist Michelle Moser
Clinical Liaison — Functional Medicine

Cancer therapies are continually being researched to provide the best patient outcomes. Less side effects, longevity and cure rates are what is sought after. However, the science doesn’t have to be brand new to be accurate. Many older therapies continue to be the best options due to how they invade the cells, decrease abnormal cell growth, enhance natural cell death without many unwanted cytotoxic side effects. After all, like all disease state therapy research, we lean on the science, the studies that are conducted, and the case studies presented in order to make the best recommendations for patients to ponder their medication pathways.

Over the past three decades many scientific articles have been published showing that naltrexone in doses as small as 3-4.5 mg has the potential to reduce tumor sizes in approximately 90% of cancer diagnosis of today. Dr Ian Zagon has published several studies showing how some cancer tumors grow and where LDN can disrupt that pathway. These studies also show where LDN and traditional chemotherapy has decreased cancer cell growth, minimize cytotoxic effects and thereby extend cancer patient's lives. Some patients with breast cancer, head and neck cancers, ovarian cancers, colon cancers as well as several others were treated with LDN and chemotherapy agents with tumor shrinkage when comparing PET scans before and after treatment. Published research showed with chemo, reduced pancreatic cell growth by 46%, tumor volume by 36-85%, tumor size by 75%, and overall incidence of tumors! 

While most of this research has been conducted in the past 20 years, LDN is still not a mainstream therapy with a cancer diagnosis. Low dose naltrexone doesn’t cure anything, but it does reduce inflammation, blocks pain receptors and modulates the immune system.When medications work, they are often explored further to understand how they work, at what doses and at what ages they can be administered. LDN is often used orally, sublingually or transdermally, in the young or those who cannot swallow.  LDN can also be used topically for itching and irritation of the skin. 

Low dose naltrexone also does not interact with many drugs, is low risk, can be compounded to meet the needs of a specific patient and is low cost. 

These, along with many other reasons, have providers saying, "Why not LDN?"

Does low-dose naltrexone pique your interest? If your provider doesn't know much about it, or what the studies have shown, there's a great resource available: your local compounding pharmacist. They would be happy to discuss the potential (and limitations) of LDN with you and your physician to determine if it's something worth trying.

References

Zagon I.S., Combination therapy in Pancreatic Cancer, Cancer Chemother Pharmacology 2005, 56:510

Donahue RN, McLaughlin PJ, Zagon IS, Low dose naltrexone suppresses ovarian cancer and exhibits enhanced inhibition in combination with cisplatin, Exp Biol Med, 2011 Jul; 236(7):883-95

Liu W, Scott K, Dennis J, Kaminsky E, Levett A, Dalgleish A., Naltrexone at low doses up regulates a unique gene expression not seen with normal doses:Implications for it’s use in cancer therapy, Int Jour Oncology, June 7 2016, 793-802

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, Berkson AJ. Integr Cancer Ther. 2009;8:416-22.

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. Berkson BM, Rubin DM, Berkson AJ. Integr Cancer Ther. 2006;5:83-9.

Opioid growth factor - opioid growth factor receptor axis inhibits proliferation of triple negative breast cancer.  Zagon IS. Exp Biol Med 2013;238:589-99

Low-dose naltrexone targets the opioid growth factor-opioid growth factor receptor pathway to inhibit cell proliferation: mechanistic evidence from a tissue culture model.

Donahue RN, McLaughlin PJ, Zagon IS. Exp Biol Med. 2011;236:1036-50.