Re: info for my doc on LDN

[Guest guest]

Hi All,

I would like to get my doc to prescribe LDN for me. I did forward

him two sites, ldn.org + another....he wasn't too impressed and said

he would need a lot more information before he would prescribe. I've

gone to Gazorpa.com and I am unable to access the " Doctor's Folder "

which I was hoping to read and forward to him.

I do have one study on lymphoma from sage.com to forward to him but

don't think that will do it. Can anyone help with this or have the

info stored in another way on their own computer? I emailed

Gazorpa.com but haven't received a response.

Also, the other doc in my area--well the new patient coordinator will

take at least two weeks to get back to me. The doctor has a long

waiting list for new patients and doesn't take insurance. I would

prefer to have my own doc or oncologist work with me on it, if possible.

I have stage 0 Chronic Lymphocytic Leukemia (CLL). Thanks for your

help.

Best regards,

Lynn C.

[Guest guest]

Hi Lynn,

This site will tell you how to obtain LDN:

http://tinyurl.com/2dfbvd

For more information about LDN, visit

http://tinyurl.com/2boot2

With best wishes,

Dudley Delany

dudley_delany

[low dose naltrexone] Re: info for my doc on LDN

Hi All,

I would like to get my doc to prescribe LDN for me. I did forward

him two sites, ldn.org + another....he wasn't too impressed and said

he would need a lot more information before he would prescribe. I've

gone to Gazorpa.com and I am unable to access the " Doctor's Folder "

which I was hoping to read and forward to him.

I do have one study on lymphoma from sage.com to forward to him but

don't think that will do it. Can anyone help with this or have the

info stored in another way on their own computer? I emailed

Gazorpa.com but haven't received a response.

Also, the other doc in my area--well the new patient coordinator will

take at least two weeks to get back to me. The doctor has a long

waiting list for new patients and doesn't take insurance. I would

prefer to have my own doc or oncologist work with me on it, if possible.

I have stage 0 Chronic Lymphocytic Leukemia (CLL). Thanks for your

help.

Best regards,

Lynn C.

[Guest guest]

Lynn wrote: " I've gone to Gazorpa.com and I am unable to access the

" Doctor's Folder " which I was hoping to read and forward to him. "

Dear Lynn:

I'm so sorry... there seems to be something wrong with the " Doctor's

Folder " .

I will fix it tomorrow and post again...

--Maureen

(Gazorpa)

[Guest guest]

Hello Lynn,

In my opinion, if you can provide the proven clinical trials where

low dose naltrexone have successfully helped cancer, then it may help

your doctor in feeling more comfortable trying something 'cutting

edge'.

The below published medical studies can be located on the National

Institutes of Health / National Library of Medicine / PubMed

website

(http://www.ncbi.nlm.nih.gov/sites/entrez?db=pubmed)

Since the below are only excerpts, you will probably want to go to

the PUBMED website, pull up the Article (using the ID number that's

included below) and print each of the abstracts (that way it will

reflect the NIH/NLM/PUBMED originating website).

The first two studies are from Dr. Berkson's work actually

treating cancer patients and the other two articles are from Dr.

Zagon and others researchers at the Hershey Medical School. Dr.

Zagon has been one of the researching pioneers (and experts) in the

area of low dose naltrexone and opioid growth factor.

Also, you may want to print out a couple of links from the Hershey

Medical School about Dr. Zagon's and his work in the area of opioid

receptors.

http://fred.psu.edu/ds/retrieve/fred/investigator/isz1

http://www.hmc.psu.edu/neuroscienceresearch/admin/facultybiopages/zago

n.htm

(*note: this article lists some of the cancers helped as part of Dr.

Zagon's research - including colon, pancreatic, head/neck, etc.)

The above and below may be helpful to your doctor to see that a

well respected Medical School is conducting the research in this

area, as well as a very respected doctor (BM Burkson) is actually

using LDN to help different patients with different cancers.

God bless you in your journey of healing!

Joyce

*******************************

Integr Cancer Ther. 2007 Sep;6(3):293-6.

Reversal of signs and symptoms of a B-cell lymphoma in a patient

using only low-dose naltrexone.

Berkson BM, Rubin DM, Berkson AJ.

Integrative Medical Center of New Mexico, Las Cruces, USA.

PMID: 17761642 [PubMed - indexed for MEDLINE]

***************************************************

Integr Cancer Ther. 2006 Mar;5(1):83-9.

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.

Integrative Medical Center of New Mexico and New Mexico State

University, Las Cruces.

The authors describe the long-term survival of a patient with

pancreatic cancer without any toxic adverse effects. The treatment

regimen includes the intravenous alpha-lipoic acid and low-dose

naltrexone (ALA-N) protocol and a healthy lifestyle program. The

patient was told by a reputable university oncology center in October

2002 that there was little hope for his survival. Today, January

2006, however, he is back at work, free from symptoms, and without

appreciable progression of his malignancy. The integrative protocol

described in this article may have the possibility of extending the

life of a patient who would be customarily considered to be terminal.

The authors believe that life scientists will one day develop a cure

for metastatic pancreatic cancer, perhaps via gene therapy or another

biological platform. But until such protocols come to market, the ALA-

N protocol should be studied and considered, given its lack of

toxicity at levels reported. Several other patients are on this

treatment protocol and appear to be doing well at this time.

PMID: 16484716 [PubMed - indexed for MEDLINE]

***********************************************

Neuropeptides. 2007 Dec;41(6):441-52. Epub 2007 Oct 1.

Opioids and migration, chemotaxis, invasion, and adhesion of human

cancer cells.

Zagon IS, Rahn KA, McLaughlin PJ.

Department of Neural and Behavioral Sciences, The Pennsylvania State

University, College of Medicine, Hershey, PA 17033, United States.

This study was designed to examine the role of opioids on cell

migration, chemotaxis, invasion, and adhesion, with an emphasis on

whether the opioid growth factor (OGF, [Met(5)]-enkephalin) or the

opioid antagonist naltrexone (NTX) impacts any or all of these

processes. Drug concentrations of OGF and NTX known to depress or

stimulate, respectively, cell proliferation and growth were analyzed.

Three different human cancers (pancreatic, colon, and squamous cell

carcinoma of the head and neck), represented by seven different

cancer cell lines (PANC-1, MIA PaCa-2, BxPC-3, CAL-27, SCC-1, HCT-

116, and HT-29), were evaluated. In addition, the influence of a

variety of other natural and synthetic opioids on cell motility,

invasion, and adhesion was assessed. Positive and negative controls

were included for comparison. OGF and NTX at concentrations of 10(-4)

to 10(-6)M, and dynorphin A1-8, beta-endorphin, endomorphin-1,

endomorphin-2, leucine enkephalin, [D-Pen(2,5)]-enkephalin (DPDPE),

[D-Ala(2), MePhe(4), Glycol(5)]-enkephalin (DAMGO), morphine, and

U69,593 at concentrations of 10(-6)M, did not alter cell migration,

chemotaxis, or invasion of any cancer cell line. OGF and NTX at a

concentration of 10(-6)M, and incubation for 24 or 72h, did not

change adhesion of these cancer cells to collagen I, collagen IV,

fibronectin, laminin, or vitronectin. Moreover, all other opioids

tested at 10(-6)M concentrations and for 24h had no effect on

adhesion. These results indicate that the inhibitory or stimulatory

actions of OGF and NTX, respectively, on cell replication and growth

are independent of cell migration, chemotaxis, invasion, and adhesive

properties. Moreover, a variety of other exogenous and endogenous

opioids, many specific for the mu, delta, or kappa opioid receptors,

also did not alter these biological processes, consonant with

previous observations of a lack of effects of these compounds and

their receptors on the biology of cancer cells.

PMID: 17910895 [PubMed - in process]

******************************************************

Cancer Res. 2007 Nov 1;67(21):10511-8.

The opioid growth factor (OGF)-OGF receptor axis uses the p16 pathway

to inhibit head and neck cancer.

Cheng F, Zagon IS, Verderame MF, McLaughlin PJ.

Department of Neural and Behavioral Sciences, The Pennsylvania State

University College of Medicine, Hershey, PA 17033, USA.

Head and neck squamous cell carcinoma (HNSCC) represents 5.5% of

malignancies worldwide, with approximately 30,000 new cases and

approximately 11,000 deaths reported in the United States annually.

The opioid growth factor (OGF; [Met(5)]-enkephalin) and the OGF

receptor (OGFr) form an endogenous growth regulating system; the OGF-

OGFr axis influences the G(0)-G(1) phase of the cell cycle in HNSCC.

Cells treated with small interfering RNA (siRNA) for OGFr no longer

responded to the growth inhibitory effects of OGF or the growth

stimulatory effects of naltrexone, indicating that these activities

are entirely mediated by OGFr. In this investigation, we examined the

precise target of OGF in the cell cycle. Using SCC-1 cells, OGF

decreased the phosphorylation of retinoblastoma protein. This change

was correlated with reduced Cdk4, but not Cdk2, kinase activity. OGF

treatment increased cyclin-dependent kinase inhibitor p16 protein

expression. Importantly, p16 complexed with Cdk4 was increased by OGF

treatment at all time points, consistent with the hypothesis that OGF

mediated growth inhibition through p16. Blockade of OGF-OGFr

interactions with naloxone abolished the increased expression of p16

protein by OGF. Inhibition of p16 (INK4a) activation by p16-specific

siRNA blocked OGF's repressive action on proliferation of SCC-1, CAL-

27, and SCC-4 HNSCC cells. These data are the first to reveal that

the target of cell proliferative inhibitory action of OGF in human

HNSCC is a cyclin-dependent kinase inhibitory pathway, and this may

be useful in the diagnosis and treatment of HNSCC.

PMID: 17974995 [PubMed - indexed for MEDLINE]