A Case of Remission from Crohns Disease with Low Dose Naltrexone LDN
by Jeffrey Dach MD
Tom came into my office about 6 months ago. He is a 32 year old male with a long history of inflammatory bowel disease. He has been evaluated and treated by many gasteroenterologists over the years, and was told he has Crohn’s Disease, and will never fully recover.
Upper Left Image: Crohn’s with typical ulceration of distal ileum on barium xray courtesy of jeffrey dach md.
Tom had seen my previous article on Low Dose Naltrexone, and he was interested in using it for his Crohn’s Disease. None of his other doctors would give it to him. I started him on the drug immediately. LDN is safe with virtually no adverse side effects, and has been shown effective for Crohn’s Disease in a publication by Jill Smith MD at Penn State University.(2)
Crohn’s Disease is a chronic inflammatory condition of the small bowel, and complete recovery is very rare.
The following is the email from Tom describing his experience after 6 months of treatment with LDN:
Thank you for helping me get rid of symptoms of one of the most problematic and debilitating diseases. For more than 10 years I had been struggling with Crohn’s disease and fighting a losing battle. For a lot of people, Crohn’s disease doesn’t respond well to traditional methods of treatment.,
The anti-inflammatory drugs I was taking before I saw Dr. Dach had very little effect and the prednisone was such a destructive drug, I could only be on it for short periods of time. I gained 85 pounds on my last round of prednisone and as soon as I came off, the bleeding and intestinal pain resumed and I started worrying about long car rides and being far from bathrooms. This had a big impact on my personal and professional life. I knew that if I ever wanted to get rid of the disease it would be with an unconventional treatment.
I first heard of LDN from doing a search on the internet and made an appointment with Dr. Dach. I had exhausted every possible option before and felt like I had no where else to turn. When I went to my appointment, Dr. Dach spent a lot of time with me and it felt very different than the “assembly line approach” that I was used to.
My first visit was in the summer of 2008 and I’ve been symptom-free ever since. I could feel my body healing almost immediately after starting treatment. For me, low-dose naltrexone has been a miracle drug. I can now lead a normal life and do all kinds of things Crohn’s disease would have prevented me from doing, like sitting through a movie or taking a long car trip. This has changed my life and I hope more people can benefit.
Regards, from Tom
For more information on LDN for Crohn’s: Click Here: Low Dose Naltrexone LDN Part One
Links and References:
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.
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.
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.
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.
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.
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.
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.
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.
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
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.
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.
Duane Hanson’s sculpture “Drug Addict” from 1974 (together with an unidentified museum guest). Picture taken at an exhibition at the Louisiana Museum of Modern Art, Denmark. Source Own work Date Spring 1975 Public domain.
Wikipedia: “Naloxone is a drug used to counter the effects of opioid overdose, for example heroin or morphine overdose. Naloxone is specifically used to counteract life-threatening depression of the central nervous system and respiratory system. It is marketed under various trademarks including Narcan, Nalone, and Narcanti, and has sometimes been mistakenly called “naltrexate.” It is not to be confused with Naltrexone, another opioid receptor antagonist with qualitatively different effects, used for dependence treatment rather than emergency overdose treatment.”
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.”
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.
Drug Addiction Medication May Treat Other Diseases Dr. Max Gomez NEW YORK (CBS) MAy 2008.
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