NOLA Hepper

LDN for Hepatitis C Sept. 2011 Lab Results

2011-09-13T12:54:00.000-07:00

I haven't posted in awhile as nothing really new has been going on - and I hadn't had any new labs done until recently.

ALT: 28 down slightly from 30 it was in the Spring.

AST: 27 down from 33

HCV Viral Load - 36,902 up from 16,500 last time. I am not really concerned about this as

VL does fluctuate - and on the day of the labs, I wasn't really feeling that well - I felt "virusy", if that is a word. It had done that in the past back in December 2009 but went back down to 11,300 in the next test. 36,902 is still very low.

She also ran an AFP test at the request of my Gastro - and it was 5.2, about the same as last time.

I will get back full labs soon and will post those as well. I'm pretty happy with these results considering that I have been out of most supplements for months - just taking Milk Thistle, D3, Lysine and 3 mg. LDN.

March 2011 Hepatitis C Treated with Low Dose Naltrexone (LDN) - Dr. Zagon comments

2011-03-10T10:45:00.000-08:00

Hepatitis C Viral load - 16,500 slightly up from the 14,679 that it was in October 2010.

ALT - 30 up from 24 in October (6-40)

AST - 33 up from 31 in October (10-35)

Basically the same as it has been for the last few lab tests! Normal liver function tests and lower viral load using 3 mg. of Low Dose Naltrexone.

My platelets also went up as did my red blood cell count. However, my IgA was back on the low side again - last labs, it was normal for the first time.

Ferritin was 43, which is down a bit from last. Iron was also down as was total saturation.

I also saw my gastro recently and was pleasantly surprised with his attitude and manner. I had not seen him since 2009 shortly after starting LDN and he had yelled at me for taking it.

I had a new abdominal ultrasound done last week and got back the results. The U/S report used the word unremarkable to describe most things - however, it showed "diffuse fatty infiltration of the liver" DRAT! My last u/s was done about 3-4 months following my appointment with Dr. Berkson in 2009 and my five IV ALA (alpha-lipoic-acid) treatments and it had "normal liver function" with no mention of fattly liver! Every other u/s that I have had since 2001 has had fatty something, but not the one after Dr. Berkson. I do know that Dr. Berkson recommended a course of initial IV ALA treatments, then oral supplementation and then another round of IV ALA. I have never had any more treatments since 2009.

So, maybe that is proof of the power of IV ALA - or as the gastro and I discussed, maybe interpreting ultrasounds is up to whoever reads it. But I would tend to think that the IV ALA did it - back in 2009 during the same time, my AFP (alpha feta protein) test went up to 6.1 (which was slightly above normal) - it had always been normal before. I remember reading at the time that liver regeneration can sometimes cause elevations in AFP. My doctor today told me that I was correct - "You have been reading". My AFP was normal for every test since then.

Fortunately for me, my own CAM doc here does ALA, so I will want to have a few. It'll probably be awhile though as I don't have the money for it now.

Anyway, it was a pleasant gastro visit - probably the only one that I've had since I was diagnosed in 2002.

Dr. Zagon's comments on LDN dosing

For my current labs, I was taking the 3 mg. LDN every other night. In the past, I had tried increasing the dosage and taking it almost every night. Some folks in our Hepatitis Cam group had initial drops in their viral load and liver enzymes on 3 mg. but their levels seemed to go back up down the line. When they increased their LDN dosage, their levels went back down. I wrote to Dr. Zagon about this and this is what he said:

"You are a product of not understanding how LDN works - a classic example I might add. And most of your colleagues on the web share your misinformation.

LDN works through what is called the opioid growth factor - a native peptide (and its receptor) in your body. LDN is a decoy that fills in at the site of the receptor - the body not having the peptide makes more of it in compensation. Now the trick we discovered 30 years ago. A short time of naltrexone - low dose naltrexone is the term lay people use (but really intermittent opioid receptor blockade) increases the peptide. After the naltrexone is metabolized - optimal time is 4-6 hours for around 3 mg, the high levels of peptide and actually an increase in receptors as well can interact. This depresses cell/viral proliferation - and makes you better.

By increasing your dose of LDN you are cutting into the time you need for an optimal reaction. Hence - you feel problems.

My advice - take 3 mg/day. If you have a problem, start taking LDN once every 2 days (many folks are taking it that way - and
some every 3 days).

Dr. Zagon

A story. A lady calls me and says she has breast cancer. She is taking LDN and the cancer is growing more rapidly. I ask her how LDN is being given - she says that since LDN is so good, she is taking it several times a day. Now you know why she had a faster growing cancer - she was not allowing the opioid-receptor interaction to occur because of so much naltrexone.

And, if you block the receptors all day with naltrexone (high dose of naltrexone), we now see that wound healing is accelerated. Why, because the cells are speeding up in replication and healing the wound faster.

Below is what I wrote to Dr. Zagon:

I have been on 3 mg. LDN for over a year for my HCV with terrific results - viral load dropped from 1,400,000 to 11,200 on my April 2010 labs and lft's are normal. I was on 3 mg. every other night,then every night. I recently increased my dosage in an attempt to lower my viral load even more - went up to 3.5 and then to 4 mg. taking it every night. However, I have had small outbreaks of shingles and HHV2 on the 4 mg. dosage. I did not take the LDN for a couple of nights and started again last night at 3.5. I am going togo back to every other night dosing for now.

So after Dr. Zagon's first response, I wrote back to him and explained about our Hepatitis Cam group's database and how most folks lft's and viral load went down when they increased their LDN dosage. This was his reply:

First, science is science. If these individuals are having to go up on dosage to evoke a positive response, that is potentially meaningful. My interpretation is that these patients are exhibiting a tolerance that builds to LDN. Very interesting. Our initial recommendation was 3-10 mg of LDN daily.

Second, your story does not conform to what others may be
seeing - tolerance. If anything, you are encountering a sensitivity. I would certainly try 3 mg every other day and see what happens.

Third, this entire LDN business is empirical right now -
you have to be in the frontier of just plain trying things out. In
your case, lower is the best. It may be that in some individuals
their pharmacology is far different than yours - they might be
building a tolerance and need more. Alternatively, the LDN is either breaking down over time and loses potentcy, or is not or high quality or is being mixed in with "fillers" that are negating the action of the LDN.

That correspondence took place over last summer (2010) - now, I ponder why my viral load seems to be staying the same (though slowly creeping higher) and not getting any lower, or thankfully, not skyrocketing back up to where it was pre-LDN - which was over 1 million. What can I do to get it even lower? So, despite what Dr. Zagon says, I am going to start taking the LDN every night and perhaps slightly increasing the dosage in an attempt to lower my viral load even more. He has added a bit of confusion into the mix, I must say. Or look into TLR's (Toll Like Receptors) - there has been a lot of research of late about them, particularly in HCV. Dosing of LDN 2 x a day is also another possibility - I will update after more research.

Low Dose Naltrexone for Hepatitis C September 2010 Lab Work

2010-09-27T14:34:00.000-07:00

I got back my full September lab results the other day. I have been on 3 mg. LDN since March of 2009 for my Hepatitis C - I also test positive for Sjogren's and RA, though with few symptoms. I have/had an IGA partial deficiency and in these labs, it is normal for the first time. My doctor ( Dr. Kashi Rai) believes that my limited but strict gluten/dairy free diet has been the reason for the result.

I am thrilled that my HCV viral load is still quite low as are my liver enzymes - and that most of my other tests are pretty darn good! After the hellish time I've had of it these past few months, along with Panda's illness and death on October 4th (St. Francis Blessing of the Animals day), and enormous, unrelenting financial and emotional stress, I was prepared for the tests to be terrible. Oh, the power of LDN and DIET!

My liver enzymes are still all within normal levels with ALT (6-40) at 24 from a pre-LDN level of 174 - AST (10-35) at 31 from pre-LDN of 99

HCV viral load went up a tad from the 11,600 it was on my last labs to it's current 14,679. Still a far cry from the pre-LDN 1,280,000 level!

I was also pleased with the overall Lymphocytes - which have all increased.

October 2010 LAB RESULTS

Tests                          09/10            01/09

C-Reactive Protein                   0.10              0.10

Platelet (140-400)                     171               163

Glucose (65-99)                         84                84

BUN (7-25)                               10                 5

Creatinine (.060-1.10)            0.73              0.70

Sodium (135-146)                    138                135

Potassium (3.5-5.3)                  4.3                4.6

Protein total (6.2-8.3)               7.9                 8.9

Albumin (3.6-5.1)                     4.9                 5.2

Globulin (2.2-3.9)                    3.0                 3.7

Bilirubin Total                          1.1                 1.1

Alk. Phos (33-130)                   59                 72

AST (10-35)                             31                 99

ALT (6-40)                               24                174

Cytomegalovirus IGG             2.60                2.36

CMV - IGM                         0.79                0.67

DHEA Sulfate (15-170)         106                  92

Epstein-Barr IGG                1:320                1.320

Estradiol                                  19                   31

Ferritin (10-232)                     53                  115

HCV RNA -                      14,679                 1,280,000

Herpesvirus 6 IGG               1:10                   1.80

HHV6 IGM                          1.20                    1:20

IGF I - ECL                         185

IGF -I                                                            139

Immunoglobulin A (81-463)    95                    72

Immunoglobulin G (694-1618) 1377              1932

Immunoglobulin M (48-271)     93                135

Lymphocytes

CD3 (Mature T cells) ( 57-85) 78                 77

Absolute CD3+ Cells (840-3060) 1441       1008

%CD4 (Helper Cells) (30-61)      57                 52

Absolute CD4+ cells (490-1740) 1067             720

%CD8 (Suppressor T Cells) (12-42) 22            22

Absolute CD8+ cells (180-1170)    405             333

Helper/Suppressor ratio (0.86-5.00) 2.59           2.17

%CD16+CD56 (4-25)                       6               10
(Natural Killer Cells)

Absolute NK Cells (70-760)            102            128
(CD16+CD56 Cells)

%CD19 (B cells) (6-29)                     15             12

Absolute CD19+ Cells) (110-660)     277             189

Absolute Lymphocytes (850-3900)    1857          1577

Progesterone                                        0.5             0.5

Rheumatoid Factor (<14)                      18           31

Sjogren's Antibody(SS-A) (<1.0)          2.8         4.5

T3, FREE (230-420)                             330             337

T4, FREE (0.8-1.8)                               1.0             1.3

TSH, 3RD GENERATION (0.40-4.50) 2.67        1.97

Testosterone Total                                    60            63

Vitamin D, 25-OH Total                            83           62

Also, I wanted to mention that the new 2010 edition of the free LDN book 'Those Who Suffer Much, Know Much' is now available via PDF. My Hepatitis C story is included in this year's edition as well as Joyce's HBV positive daughter's. Also has much more info about using LDN in other disorders as well as more about LDN in general:

LDN Research Trust

Please Help the Cats!

2010-06-30T18:02:00.000-07:00

PANDA RAINBOW BRIDGE - OCTOBER 5, 2010

Panda crossed over at 12:45 AM this morning - up until this past weekend, she had done pretty well. However, the Medicam, while buying her a couple more weeks of life, in the end, affected her liver and kidneys and she began to struggle on Saturday.

I had my own doctor's appointment yesterday but had made arrangements to bring Panda in to be put down that evening. But when I got home from the doctor, she was close to being in a coma. I got her onto the bed where she stretched out on her side - I supported her head with a pillow and also placed one near her paws. Soon, she was kneading the pillows with her paws and breathing deeply, though with her customary purr. I decided to let nature take it's course as she was not suffering.

I awoke at 12:44 to find Panda taking her final breaths - I pet her and kissed her and told her goodbye. That it was okay to go and that I would see her again someday - at the Rainbow Bridge.

Just this side of heaven is a place called Rainbow Bridge.

When an animal dies that has been especially close to someone here, that pet goes to Rainbow Bridge.

There are meadows and hills for all of our special friends so they can run and play together.

There is plenty of food, water and sunshine, and our friends are warm and comfortable.

All the animals who had been ill and old are restored to health and vigor; those who were hurt or maimed are made whole and strong again, just as we remember them in our dreams of days and times gone by.

The animals are happy and content, except for one small thing; they each miss someone very special to them, who had to be left behind.

They all run and play together, but the day comes when one suddenly stops and looks into the distance. His bright eyes are intent; His eager body quivers. Suddenly he begins to run from the group, flying over the green grass, his legs carrying him faster and faster.

You have been spotted, and when you and your special friend finally meet, you cling together in joyous reunion, never to be parted again. The happy kisses rain upon your face; your hands again caress the beloved head, and you look once more into the trusting eyes of your pet, so long gone from your life but never absent from your heart.

Then you cross Rainbow Bridge together....

Author unknown...

Goodbye my love, my heart - you have left the biggest pawprint on my heart and I will never forget you my friend. I love you.

UPDATE - SEPT. 25.

After the last diagnosis of end-stage heart disease, Panda worsened and continued to try and hide. She was struggling to breathe and panting. When I picked her up and put her on the bed, she plopped over onto her side. I called the vet's office again and told them that I was bringing her in to be put down - she was suffering. We got to the vet's office where Panda hobbled around the exam room and seemed to be breathing more normally. Dr. Sagrera watched her and then examined the back of Panda's head - Panda flinched when the area behind her ears was pressed on. Dr. Sagrera said that it was probably due to a tumor in her brain, which was causing her immense pain, which led to her walking about with her head close to the ground. The vet said to try the Medicam, which is a pain killer and analgesic and to see what would happen.

I got Panda home and gave her a small dose of the Medicam - I had some left over from her ear surgery. A couple of hours later, Panda was panting again and trying to push her head under the pillows on the bed. I gave her more Medicam and she eventually went to sleep, breathing easier. Later, after going to bed, I kept reaching over to touch Panda on the bed, to see if she was still breathing. At around 4 AM, I reached over and she was not there - she was at the end of the bed and purring! I got her down and brought her to her litter box, which she used, and took her back to her bed. She demanded breakfast, which I happily gave to her. The rest of the day was uneventful, with Panda dozing for most of it and looking much happier.

That was on the 15th and 16th, and blessedly, Panda has been the same since then! It seems that as long as I can get the right dose of Medicam into her, she is doing okay. And by okay, I mean, getting up and down from the bed on her own, finding her way to the litterbox and water dish. Not bad for a blind cat with a brain tumor and enlarged heart. And not having any more panting or hiding her head episodes. Which is amazing to me that the amount of pain that she must have been in, had led to her symptoms. Whatever the reason, I am blessed that Panda is still with me and happy to be here.

UPDATE - SEPT. 14.

After a hellish night, Panda seemed brighter at 6 a.m. and actually ate some food so I went back to sleep. Upon waking, I couldn't find her and after a 15 minute search, found her wedged in on the side of the fridge. I got her out and she seemed to be having problems walking - she did not want any more food or did not to use her litter box. I called the vet who told me to let her sniff the Vick's vapor rub, which nullifies a homeopathic remedy. I did and left her back on her bed. I had to go out for a bit and when I came back, Panda wasn't on her bed but was in the closet. I got her out and put her on the floor. She seemed to stagger and opened her mouth, panting in a way I had never seen before. So I frantically called the vet back and told the girl who answered the phone that it seemed like it was "time".

I rushed Panda out there where the vet immediately saw her. Panda, meanwhile, had perked up on the way over - she cried most of the trip over - as did I. At Natural Pet Care, the vet has non-traditional exam rooms - just regular rooms with furniture - not the typical little cubicle with the stainless steel table. Panda got up and wandered around the room, getting around much better than she had at home. The vet listened to her chest and suggested a chest x-ray - I was able to check my email on my cell phone and saw that Steve E. had generously made a donation on the blog, so I told the vet to go ahead and do the test. Shortly, the film was ready, and it showed a very enlarged heart - we had known that she had heart problems, but her heart was pushing on her lungs and diaphragm, making it difficult for Panda to breathe. And fortunately, there was no sign of any cancer, at least on the x-ray.

So, for now, we know what we are dealing with! I took Panda back home, where she immediately used her litter box, drank a little water and ate some food - things that she hadn't done in the last two days. She just had a small dinner of wet food and is napping now. The vet also wants me to try and get Taurine and coQ-10 into her as well as the B vitamins and Omega that she is already getting.

Just goes to show you how strong homeopathy can be - those little pellets can pack a wallop! The vet thinks that by tomorrow, any lingering effects of the remedy will be gone. I hope that Panda will perk up even more so that she can enjoy what time she has left with the best quality of life. Thank you Steve E. and to everyone who has donated toward's Panda's veterinary care!

UPDATE - SEPT. 13

Panda has taken a turn for the worse. Last week, she began to get blocked again so she was taken to the vet. The vet felt that Panda's colon was thickened and she also had an ugly ulcer in her mouth - no wonder she seemed so uncomfortable. She has also been waking from her sleep and howling for food, which she would inhale once I'd give it to her. I asked Dr. Sagrera if she thought that the cancer had possibly spread and she said that it was a good possibility - and would explain all of the things that have happened to Panda over the last year. Her original squamous cell carcinoma diagnosis had come a few months following her saga during Hurricane Katrina, which resulted in the loss of her ear.

The vet gave her a homeopathic remedy (Silica 10M) and for the next few days, Panda seemed to spend much of the time sleeping. She ate and used her litterbox regularly. However, starting yesterday and today, she no longer wants to eat and is having problems getting around - not walking, but she will get to her litter box and then just crouch in it and stay in it for hours. She does not seem to be in any pain but is in a fugue like state - she knows me and will purr if I pick her up and talk to her.

I can only hope that this is some kind of "healing crisis" that she will soon pull out of. The vet did say that the Silica can aggravate a problem, or problems, for as long as a week. Today is Monday and she was given the remedy last Thursday.

But I think that she is dying - she is hydrated and looks okay, but so lethargic and out of it that I just don't see how she will pull out of this. I will have to wait until tomorrow to contact my vet as her office is closed on Mondays - but I will call her emergency page number later on tonight it need be - I hope not. I still haven't figured out how to cover the post-dated check that I wrote on Thursday...

I took Panda off of the LDN last week - with the mouth ulcer and her symptoms, it did not seem that it was right to keep giving it to her. She has had almost 5 years since her ear surgery - 4 good years though this last year has been fairly good, even though she lost her sight last October - she has not been in any pain until the impaction problems began and has been able to get around amazingly well.

She is currently on the bed for now, though she will get up every now and then and wander around - but she will run into something and then just sit there - so I am watching her constantly.

I hope that she pulls out of this but I wouldn't be surprised if she just went to sleep on the bed and just never wakes up. If this is her time, then I hope that this is what will happen - I do not want her to suffer any kind of pain. Thankfully, she doesn't seem to be in any - but if she has problems during the night, I will use my vet's emergency number and bring Panda to her - the hell with not having any money. Panda has been my friend since 1996 - one of the longest relationships in my life. We have been through everything together and I do not know what I will do without her.

I really don't want to bury her outside as I probably will be moving in the next year - and I don't want to leave her - though Brooks is out in the garden - I hated to have to bury him as well, but I could not afford to have him cremated, which is what I want for Panda. Regardless, I am heartbroken and the tears are streaming as I type this post.

Please donate if you can. Thank you

UPDATE - JULY 20

Panda is doing great - the extra fatty acids (omega fish oils) have helped her a great deal and she has not had any problems with impaction or constipation - knock on wood. I want to thank everyone who donated towards her veterinary care (and bill)!

But Mom is not doing too well - thankfully, the LDN along with a strict diet and supplements, have restored my health to the point that I can now function. I pray that it stays that way. However, I am struggling to survive here every day and I fear that the unrelenting stress will eventually take a toll.

Though the online book selling and sporadic cat sitting do bring in some income, it is just barely enough to pay the major bills (my credit cards went bye-bye months ago) - utilities, internet, cell phone. The rest goes towards caring for the cats.

I am very small and do not require much food - I have been surviving on potatoes and baked vegetables - with an occassional bit of chicken thrown in. I also still have my fruit smoothie most days though I have been out of the whey protein powder.

If anyone could possibly donate a bit towards the cat care, then I could eat a little more than I have - I've lost 5 pounds in the last couple of weeks and 108 is much too low - I do better around 115 for my 5'4" frame.

Thanks again to all who helped the cats - and thereby helped me!

I haven't been posting too much on the blog lately as I have been struggling to survive here in New Orleans. The cost of living has never gone back to the pre-Katrina days and it's become a lot harder to get by. I just about have my rent money covered and I have paid my utility and car insurance bill. Now, I just have to pay my internet bill - no net, no amazon.com business as a book seller and no blog about LDN and Hep C - and now cats.

My concern is for my cats - the cats are probably the reason that I am here today - they helped bring me back to my childhood roots and my love for all animals - and away from the dark side of the streets.

It was a stray cat that led to my diagnosis of Hepatitis C back in 2002. I took in a stray cat "Oscar" early that year who had a multitude of health problems, including ringworm - and of course, I contracted it. It never would go completely away and I ended up at a doctor, who suggested blood work to "rule anything out". The "anything out" turned out to be Hepatitis C.

Oscar lost his life in early 2004 due to his health problems - but I will never forget him or be able to thank him enough. True, I would have been diagnosed eventually with the HCV, but finding out in 2002 might have saved my liver from additional stress.

Panda needs help - she is my oldest cat at around 15 - no one really knows how old she truly is. She was seen today at the vet and will require many vet visits to keep her comfortable for whatever time she has left. She is a cancer survivor who lost an ear to the disease - she recently went blind and, understandably, does not get around too much - hence, she becomes frequently becomes impacted and needs to see the vet for care.

I first met Panda in early 1996 when I moved into a new apartment following my separation. She was part of a large colony of cats that the former tenant had been feeding (and not spaying and neutering).

Unbeknownst to me, Panda had been adopted as a feral kitten, spayed and vaccinated by the tenant and then left behind when she moved. I kept wondering why Panda kept trying to get inside.

I ended up trapping all of the cats and having them spayed or neutered. In 1998, my landlord decided to sell the house and I was forced to move to another apartment about a mile away. I took Panda and Emerald with me.

Panda kept getting scared and disappearing - she kept going back to her old house, which now had a new owner who did not like cats. For a cat, a mile is not that far away, but she had to cross a major thoroughfare and railroad tracks to do so. I probably went back 5 different times to get her, until one day, she was not there. I went back for almost a month to look for her but never could find her and I feared the worst. However, one day, I got a call from the new owner - there was a black and white cat hanging around the house - could I come look at her. It was Panda! Skinny and scared but ok. I took her back and finally started bringing her inside and she never left again.

During those early years at the new apartment, I had a boyfriend, who had a Min Pin. She had a litter of pups that Panda enjoyed teasing and toying with.

As the years went on, my boyfriend moved away and I returned to cat rescue - and had a house full of cats, as well as caring for the multiple feral cats in the neighborhood. In 2002, I was devastated to learn that I had contracted Hepatitis C, and put me on a health roller coaster for the next several years. (I have detailed this story on my blog, Nola Hepper.

In August of 2005, I found myself with a broke down car, little money and 8 inside cats, along with many feral cats outside. Hurricane Katrina hit New Orleans and the cats and I were trapped inside my apartment with flood waters up to my neck. Emerald did not come in for the storm and was drowned under the floor boards. I was able to get rescued from my roof with 3 of the cats the next morning - Panda, Cayenne and Rosemary. The 5 others were placed up in high closets out of the water - it took me 2 weeks to get back to the house, via a boat, to rescue them - miraculously, they were all still alive!

I detailed our saga on my first post on this blog, here are a few links:

Photos from August 29th, 2005 Katrina

Photos from the LA Times

L.A. Times Sept. 12, 2005 story

Inside, they had a rather unflattering photo of my getting back up into the closet where the cats were - this was the closet that I was in after the water rose...

We spent 6 months in Alabama after Katrina. Panda had suffered an ordeal and ended up with squamous cell carcinoma, which led to surgery to remove her ear. The animal group IMOM (In Memory of Magic) and Best Friends both contributed towards Panda's surgery.

I moved back to New Orleans to a new apartment in early 2006 and became involved with the ongoing cat rescue. My old Lakeview neighborhood had been devastated and most of the feral cats had been killed - either drowned or killed by the ensuing dog packs that roamed the area for many months following Katrina. There were only 3 cats out of the 40 or so in my area that survived. I was able to do this for almost two years until my health took a turn for the worse. I developed shingles, severe IBD and fibromyalgia and at times, could barely get out of bed.

Fortunately, my Social Security appeal ruled in my favor and I soon was on Medicare and receiving a small disability check of $693.00 monthly. The Medicare enabled me to find a good integrative doctor, whose treatment helped me greatly - she also pointed me towards Dr. Berkson, who put me on the Low Dose Naltrexone (LDN). His protocol alone helped restore my liver health to almost normal.

Meanwhile, I lost Brooks, one of the Katrina survivors who had been left in the high closets, due to renal failure. His illness was costly and wiped out the remainder of my savings - though most of the money had gone towards my medical treatment and supplements that were not covered by Medicare.

Right before Brooks passed, Panda suddenly lost her sight! It was first thought that she had an infection but she did not respond to treatment. She was then taken to an eye specialist who thought that her cancer had returned and was causing her blindness. However, her blood work was normal and that diagnosis was later ruled out.

She managed go get around fairly well in the ensuing months, but lately has had a problem with impacted anal glands - which actually abscessed a couple of months back. I took her to the vet a few weeks ago to have them expelled and still owe my vet for that visit. Panda is having problems again and is close to another abscess. Today, my wonderful vet agreed to see Panda again, even though I cannot pay for the visit. I promised the vet's office that I would try and raise the money for payment.

If you can help pay for Panda's vet visit or donate towards the care of the other cats, please go to the "Donate" button which leads to our PayPal account. The DONATE button is on the right menu.

The Others

Cayenne came along in January 1999 - a neighbor found him and put a milk crate over him and called the SPCA. He was still there the next day, so I took him to the vet - and, of course, ended up keeping him.

After Katrina, with Sky:

Rosemary was found in the back alley with her brothers and sisters in 2001:

Now:

Woody was a relative of Rosemary's - found in the same alley - and very, very sick as a baby:

She came close to liver failure following her ordeal after Katrina and flirted with it again last summer.

Tortie Miss was an older feral kitten who was trapped across the street from us - she started following Cayenne home and ended up as an inside cat - lucky for her as all of her outside buddies perished after Katrina.

Mr. Magoo (Goober) showed up in 2002 with Oscar and never left:

Sky and her littermates appeared in the alley in 2004 - they were all trapped, tamed and adopted through PetsSmart. However, Sky got sick and was returned to me - by the time that she healed, she was too old for adoption:

sky kitten trap

After I moved back here in 2006 and was doing cat rescue, I trapped 4 kittens from my old neighborhood - the abandoned house where they were born was being demolished so I could not release them after they were spayed/neutered. The two tamest kittens were taken to ARNO, who later shipped them out of state where they were both adopted. I kept the other two - Velvet and Smoke.

Please help me continue to care for my cats as I have managed to do for many, many years. They saved my life and I am responsible for caring for them to the best of my ability - even with Hepatitis C, Celiac Disease and the multiple other viruses and conditions that I have.

If you are able to contribute to the cat's care, please go to the menu on the right - and either go to the Widget or to the DONATE button. Or, you can help by purchasing a book from Amazon via my account at:

CMBOOKMAKER

If you are in the New Orleans area, I offer a Cat Sitting or Cat Consultant service at:

Nola Catbox

Thank you so much for your help!

Treating Hepatitis C with Low Dose Naltrexone (LDN)

2010-06-05T16:44:00.000-07:00

3 mg. LDN next to Advil

This post is a work in progress..

Treating Hepatitis C with Low Dose Naltrexone (LDN)

Even thought strides are being made for the treatment of the Hepatitis C virus via the newer protease inhibitors used along with traditional combination therapy, overall success rates remain roughly at about 50%. Many people cannot tolerate the treatment or simply cannot undergo it due to other health problems that are contraindicated for Hepatitis treatment. And others, like myself, simply choose not to do the current treatment and are waiting for a less toxic and more successful cure to come along.

I am successfully managing my Hepatitis C virus by using LDN - Low Dose Naltrexone, supplements, diet and exercise and have attempted to share my experiences on my blog, Nola Hepper. Now, I have tried to include all of this information in one place.

I was diagnosed in 2002 with Hepatitis C, genotype 1b. A biopsy revealed minor inflammation with Grade 0-1, Stage 0-1 and my lab work showed slightly elevated liver enzymes. Despite being urged to due interferon/ribavirin treatment back then, I chose to make healthy life style changes instead while waiting for "something else" to come along and learned as much as I could about the HCV virus. My health remained about the same for several years until 2005, when my Hurricane Katrina experience caused me to start having severe side effects. I developed fibromyalgia, shingles, severe chemical sensitivities and terrible IBD. My doctors told me that all of these problems were being caused by the Hep C and again urged me to do treatment.

I was able to get Social Security disability and Medicare and this allowed me to see a very good integrative doctor. She tested me for everything and suggested a course of action for me, which included several new supplements and diet changes. She also gave me a paper written by Dr. Burt Berkson, another integrative doctor who had done extensive work using ALA - Alpha-Lipoic-Acid. His work seemed very promising, so I began to do his protocol of ALA, Milk Thistle (although I had already been taking milk thistle for years), Selenium, and B Complex along with the other supplements that my doctor had recommended for me.

One of the diet changes that my doctor mentioned was to cut down or eliminate wheat - she said that most people cannot really digest it or are sensitive to it. I was a bit skeptical but after researching it, I decided to try it out. And the results were amazing! Within days it seemed that my IBD and bloating had greatly improved. Soon, I noticed that my fibromyalgia had gotten much better as had my chemical sensitivities - I didn't' seem to be quite so sensitive to smells anymore - and you must understand. It had been to the point where going to the grocery was an ordeal - I had to hold my breath going down the detergent or bug spray aisles. This also was much improved! Gluten (one of the proteins found in wheat) is a big problem to most folks with liver disease, particularly those who undergo interferon treatment, as it is a known trigger for celiac disease and can cause elevated liver enzymes.

After researching more about diet and nutrition, which included an appointment with a Certified Clinical Nutritionist, I took things a step further and ordered a food sensitivity/intolerance panel through a company called Alletess as they took my Medicare insurance. This test revealed that I had sensitivities to cow's milk, yeast and some shellfish. Upon eliminating these foods, my IBD really seemed to completely go away and my other health issues got much better as well.

However, my latest liver lab work (January 2009) was frustrating - my HCV viral load test was 1,400,000 - ALT was 174 and AST at 105 - other labs were pretty much in the normal range with a few blips here and there. I had exchange emails with a couple of folks who had seen Dr. Berkson and they said that they liked him and were seeing great improvements in their health - they also mentioned that he had put them both on Low Dose Naltrexone or LDN. So I decided to go out to New Mexico to see him myself.

I started on 3 mg. of LDN in mid-February 2009 while at Dr. Berkson's clinic but after I got back, I started having an upset stomach due to the lactose filler that the pharmacy in New Mexico used in their compounding mixture. I went off of the LDN for about 2 weeks until I got a new prescription mixed with acidophilus - probably March 1st, 2009. I had new labs done in late April 2009 and the results were remarkable. Viral load dropped from the 1,400,000 to 48,000! ALT from 174 to 22 and AST from 105 to 30!. My integrative doctor was amazed as I was but my traditional gastro actually yelled at me, saying that LDN was not "supposed" to treat Hepatitis C and that the labs had to be a mistake. I've never gone back to him.

This is about the time that I became an advocate for LDN and started posting more on my blog and on several LDN yahoo groups and various Hepatitis C, health sites, etc. How could I not with the results that I have had? Since that time, I have played around with the LDN dosage and have used my lab results as a kind of rough guide in doing so. Currently I am back on 3 mg. that I take most every night. My May 2010 lab work showed a viral load of 11,400 - ALT at 25; AST at 30. I'm thinking about increasing the dosage again to see if I can get my viral load even lower or even eliminate it altogether. Someone in my Hepatitis Cam support group increased his dosage to 4.5 and had a viral load at 2,400! We are maintaining a LDN database that records before and after LDN lab results in folks with various kinds of liver problems.

Ideally, it is best to work with a doctor who is familiar with the workings of LDN and who can prescribe it. And to get the LDN from a reputable compounding pharmacy such as Skip's Pharmacy. However, one can also order the 50 mg. tablets and make the solution themselves without a prescription.

If you already have a prescription for LDN, it is probably in a capsule form. If you want to start off at a different dose than whatever your prescription is for, it is better to mix the LDN with water than to simply take a third or half of the capsule alone. The reason being is that one can never be sure where the LDN is in the capsule and if you mix it with water, it is a more accurate dose. For example, I take my 3 mg. capsule and dump it into a dark colored vial (I got a 12 ml (cc) vial at Whole Foods for a couple of bucks). Use a 1 cc (ml) or 3 cc (mg.) syringe and measure in 3 ml. of distilled or bottled water - not tap water. Measure out the needed dose and store the rest in the fridge. For 4.5, simply increase to 4.5 cc's (ml's) of water.

There are slightly different instructions for the 50 mg. tablet but it is the same principal - 50 cc's (ml's) of water mixed with the tablet - obviously you would need a vial large enough for that amount - more detailed instructions are included in one of the links above or here: "How to Obtain Low Dose Naltrexone"

"Once you have a supply of 50 mg Naltrexone tablets, you can convert them as needed to LDN. To do so, fill a graduated cylinder with 50 ml of distilled water (unlike tap or spring water, distilled water contains no impurities that could potentially react with and thus reduce Naltrexone's effectiveness). Pour the water from the graduate into a 4 oz amber glass jar with a tight-fitting lid. Then add a 50 mg Naltrexone tablet. The tablet will mostly dissolve in about five to ten minutes. Since not all of the tablet is soluble in water, instead of yielding a clear solution, the result will be a cloudy suspension. It must be shaken each time before use to evenly disperse all the undissolved particles. One ml of the (shaken) suspension will contain one mg of Naltrexone. Use a graduated baby medicine dropper to measure out the dose you need."

Dosing is very individualized. I am finding that the biggest mistake that doctors are making with LDN is to prescribe the 4.5 dosage in the beginning, particularly to their patients with liver disease - some folks can tolerate this dosage, but in most it is a guarantee of initial side effects - sleep disorders being the most frequent. There are different theories on dosing, depending on what doctor or researcher you listen to. Dr. Berkson starts everyone off at 3 mg. but he prescribes sleep medications in the first month to counteract these sleep problems. Most savvy doctors and LDN veterans know to recommend that people start off at a very low dose such as 1 mg. Start at 1 mg. and stay on it for a week or so then move up to 1.5 or 2 for another week or so until you get to 3 mg. At this point, you can either work your way up to 4.5 or stay at the 3 mg. dosage until you get your first post LDN labs done. Again, dosing is very individual - up to that person's make up, medical problems, etc. - some folks do well on 3 mg and have great results while others need more or less of the Low Dose Naltrexone - some folks take it every other night or less. It really depends greatly on what disorder or multiple disorders the person has along with other factors.

One of the things noted in our LDN Database for Hepatitis C, was a tremendous initial drop in both HCV viral load and liver function tests on the first post-LDN labs done. However, in a few of the patients, their viral load and lfts' would go back up if they stayed on the same initial dose over a 6 month to one year time. But, when they increased their LDN doses, their viral load and lft's would go back down, sometimes tremendously so. This is where having regular labs done is very important to monitor the effect of the LDN on the HCV virus. I have been fortunate in that my levels have remained fairly stable and have even improved since my last labs. However, I am about to jump up to a 4 mg. in an effort to further lower or eradicate the HCV virus.

Why LDN might not work - According to several sites and personal accounts, yeast infections seem to be triggered or made worse when first starting LDN. It is very important to have any candida, or other mold/yeast problems cleared up as having them can interfere with how well the LDN works.

The link below covers this as well as other side effects - note - the site was written by someone with MS, but it is still good info:

Side Effects & Dosing of Low Dose Naltrexone (LDN)

Dr. McCandless ( Children with Starving Brains ) has written about the dietary aspect when using LDN:

Dr McCandless, seldom is LDN stand-alone treatment

There is much more LDN info on other sites:

LDNers.org site - Resouces page

I have covered supplements in another area of the blog - Supplements

a quick recap. The most important supplements for the liver are those that help generate more glutathione, - usually ALA - alpha-lipoic-acid, with NAC - N-acetyl cysteine, SAMe, whey protein (gluten-free) and others.

Silymarin (Milk Thistle) is extremely important as is Vitamin D3 - D3 is better as it is more easily absorbed. A multi vitamin without iron! (capsule form is best and more easily absorbed than tablet), vitamins C & E,

To be continued.....

May 2010 Hepatitis C Labwork with Low Dose Naltrexone (LDN)

2010-05-07T21:41:00.000-07:00

In March, 2009, I started taking Low Dose Naltrexone, or LDN to treat my Hepatitis C. It was initially prescribed to me by Dr. Burt Berkson at his clinic in Las Cruces, New Mexico, in 3 mg. capsules. Since that time, my own doctor writes my LDN refill prescriptions.

Within months, it brought down my viral load and normalized my liver enzymes. And on my most recent lab work (5/2010), my viral load is even lower.

Viral load at 11,300! In December, it was 34,524. September: 18,729. Pre-LDN Jan. 09 - 1,280,000

ALT: 25 December: 34 Sept. 36 Pre-LDN Jan. 09 - 174 (range: 6-40)

AST: 30 December: 31 Sept. 37 Pre-LDN Jan. 09 - 99 (range: 10-35)

My doctor uses Quest lab:

HCV RNA, PCR test result of 11,300 with a log of 4.05. It was the COBAS (R) Ampliprep/COBAS, TagMan (R) RNA Test Kit (Roche)

Will update complete labs soon! Vitamin D at 95 from 53 after taking 5,000-10,000 of NOW Vitamin D3.

Iron, Ferritin and the Liver

2010-04-06T21:53:00.000-07:00

Most doctors only test serum iron levels, while they should always check serum ferritin levels, as this is a more accurate way to gauge iron that is stored in the liver. Elevated serum ferritin can cause oxidative stress, which leads to "fatty liver", fibrosis, elevated liver enzymes and worsening liver health.

Iron’s Role in Hepatitis C Infection

Hepatitis C inflicts most of its damage by latching onto molecules of iron, resulting in free-radical damage to liver cells. In turn, the liver becomes inflamed, which can lead to the formation of scar tissue (fibrosis). If left unchecked, this steady damage will result in cirrhosis or liver cancer.
About 30 percent of people with hepatitis C have very high iron levels. Reduction of serum iron has been shown to normalize liver enzyme levels, which are elevated during periods of active liver damage (Fong TL et al 1998). Iron depletion therapy has also been shown to improve the response to conventional medicines used to treat hepatitis (Fargion S et al 1997). The only effective way to decrease serum iron is to have an iron loss, as occurs when donating blood. Hepatitis C patients cannot donate blood for common use, but their blood can still be removed, although it must be discarded.

Serum ferritin is a measure of the amount of stored iron and is used to guide therapy. A serum ferritin value between 30 and 80 ng/dL is optimal. Many hepatitis C patients have serum ferritin values in excess of 300 ng/dL.

Despite substantial scientific evidence, however, few physicians implement iron-depletion therapy before beginning antiviral therapy. This partially accounts for the high failure rate of conventional drugs in eradicating the virus (Boucher E et al 1997; Martin-Vivaldi R et al 1997; Tsai NC et al 1997.

Hepatitis C Symptoms and Ferritin Levels Video

Other than phlebotomy that can help remove excess iron, I have found the IP-6(Inositol Hexaphosphate) helps lower ferritin levels and keep them down. My serum ferritin was at 176 and after using IP-6, it gradually came down. I switched over to the Jarrow brand of IP-6, which comes in capsules. I had been using a tablet form (Enzymatic Therapy) which was pretty expensive. The capsule form is much cheaper and apparently for me, works much better. My ferritin dropped from 80 to 38 from early September to late December and my lft's normalized.

IP6 Inositol Hexaphosphate

If you use this code: KOV896 you will receive $5.00 off your first order - and I eventually get a discount off of my own order.

Low Dose Naltrexone (LDN) and the Liver

2010-02-19T14:27:00.000-08:00

Low Dose Naltrexone, or LDN, is an FDA approved medication.

"Naltrexone itself was approved by the FDA in 1984 in a 50mg dose for the purpose of helping heroin or opium addicts, by blocking the effect of such drugs. By blocking opioid receptors, naltrexone also blocks the reception of the opioid hormones that our brain and adrenal glands produce: beta-endorphin and metenkephalin."

Although naltrexone itself is an FDA-approved drug, the varied uses of LDN still await application to the FDA after related scientific clinical trials. LDN (in the 3mg or 4.5mg dosage) has not yet been submitted for approval because the prospective clinical trials that are required for FDA approval need to be funded at the cost of many millions of dollars.

Naltrexone is a prescription drug, so your physician would have to give you a prescription after deciding that LDN appears appropriate for you.

http://www.lowdosenaltrexone.org/

Many doctors will not prescribe LDN, as they are not aware that it is FDA approved and that various clinical trials for various disorders have been done or are in progress. The other reason is because of the "Black Box Warning" for full strength Naltrexone due to adverse liver effects on obese patients using 300mg.

Full-dose naltrexone (50mg) carries a cautionary warning against its use in those with liver disease. This warning was placed because of adverse liver effects that were found in experiments involving 300mg daily. The 50mg dose does not apparently produce impairment of liver function nor, of course, do the much smaller 3mg and 4.5mg doses.

Further studies have shown that LDN is actually beneficial to the liver in low doses - however, most of the studies done used much higher doses of Low Dose Naltrexone.

Study of hepatotoxicity of naltrexone in the treatment of alcoholism.

Since a black box warning was issued by the Food and Drug Administration regarding the use of the opiate antagonist naltrexone (NTX), many clinicians have been concerned about current labeling of the potential hepatotoxicity risk of NTX in the treatment of opiate dependence and alcoholism. Despite many reports that demonstrated that the use of NTX did not cause elevation of liver enzymes, controversy concerning whether NTX is hepatotoxic continues. The current study monitored 74 alcoholic patients who received 25mg of NTX daily in the first week and then 50mg of NTX daily for the rest of the 12-week period. After the 12-week treatment, levels of the hepatic enzymes alanine aminotransferase (ALT) and aspartate aminotransferase (AST) did not show any elevation, except in one subject, and the results strongly support that NTX did not induce abnormalities in liver function tests or elevate the liver enzymes. Instead, a statistical significance of decreasing levels of ALT and AST in the liver was shown throughout the study. These findings provide further support that NTX is not hepatotoxic at the recommended daily dose and may be beneficial for patients with elevated liver enzymes.

PMID: 16839858 [PubMed - indexed for MEDLINE]

Effects of long-term treatment with naltrexone on hepatic enzyme activity.

Mean plasma levels of hepatic enzymes did not show significant modification in the course of treatment with naltrexone.

PMID: 1686854 [PubMed - indexed for MEDLINE]

Naltrexone: report of lack of hepatotoxicity in acute viral hepatitis, with a review of the literature.

Many clinicians appear to be concerned about the potential hepatotoxicity of the opiate antagonist naltrexone (NTX) and this may be one reason why it is not used more widely in treating both heroin and alcohol abusers. Some much-quoted early studies noted abnormalities in liver function tests (LFTs) in very obese patients taking high doses, although there was no evidence of clinically significant liver dysfunction.

We describe a heroin abuser in whom clinical and laboratory manifestations of acute hepatitis B and C appeared a few days after the insertion of a subcutaneous naltrexone implant. A decision was made not to remove the implant but the hepatitis resolved completely and uneventfully well within the normal time-scale. A review of the literature indicates that even when given at much higher doses than are needed for treating heroin or alcohol abusers, there is no evidence that NTX causes clinically significant liver disease or exacerbates, even at high doses, serious pre-existing liver disease.

PMID: 15203443 [PubMed - indexed for MEDLINE]

Naltrexone protects against lipopolysaccharide/D-galactosamine-induced hepatitis in mice.

Results demonstrated that post-treatment with naltrexone (20 mg/kg, i.p.) significantly attenuated the deleterious liver function in mice treated with LPS/D-gal. It was also found that naltrexone significantly inhibited the elevation of plasma tumor necrosis factor-alpha (TNF-alpha) caused by LPS/D-gal. The overproduction of nitric oxide (NO) and superoxide anions induced by LPS/D-gal were also significantly reduced by naltrexone. Moreover, infiltration of neutrophils into the liver of mice 12 h after treatment with LPS/D-gal was also decreased by naltrexone. In conclusion, the beneficial effects of naltrexone on LPS/D-gal-induced hepatitis result from its inhibition of pro-inflammatory factors and antioxidant effects. Thus, naltrexone is of therapeutic potential for treating liver injury.

PMID: 19023176 [PubMed - indexed for MEDLINE

Lack of hepatotoxicity with naltrexone treatment.

In summary, chronic administration of naltrexone in doses up to 300 mg/day for periods up to 36 months does not significantly change hepatic function, as measured by SGOT and SGPT levels.

PMID: 7983232 [PubMed - indexed for MEDLINE]

Opioid receptor blockade reduces Fas-induced hepatitis in mice.

PMID: 15389866 [PubMed - indexed for MEDLINE]

Naltrexone, an opioid receptor antagonist, attenuates liver fibrosis in bile duct ligated rats.

CONCLUSIONS: This is the first study to demonstrate that administration of an opioid antagonist prevents the development of hepatic fibrosis in cirrhosis. Opioids can influence liver fibrogenesis directly via the effect on HSCs and regulation of the redox sensitive mechanisms in the liver.

PMID: 16543289 [PubMed - indexed for MEDLINE]

Opioid system blockade decreases collagenase activity and improves liver injury in a rat model of cholestasis.

CONCLUSION: Opioid receptor blockade improved the degree of liver injury in cholestasis, as assessed by plasma enzyme and liver MMP-2 activities. The beneficial effect of naltrexone may be due to its ability to increase liver SAM level and restore the SAM : SAH ratio.

PMID: 17295775 [PubMed - indexed for MEDLINE]

Effect of oral naltrexone on pruritus in cholestatic patients.

CONCLUSION: Naltrexone can be used in the treatment of pruritus in cholestatic patients and is a safe drug showing few, mild and self-limited complications.

PMID: 16534857 [PubMed - indexed for MEDLINE]

Opioid peptides and primary biliary cirrhosis.

Patients with liver disease have increased plasma concentrations of the endogenous opioid peptides methionine enkephalin and leucine enkephalin. As an initial investigation to determine whether opioid peptides contribute to any of the clinical manifestations of hepatic disease nalmefene, a specific opioid antagonist devoid of agonist activity, was given to 11 patients with cirrhosis. They all experienced a severe opioid withdrawal reaction on starting the drug. In the nine patients with primary biliary cirrhosis pruritus was greatly alleviated, fatigue seemed to improve, and plasma bilirubin concentration, which had been rising, showed a modest fall in all except one patient. These results indicate that blocking opioid receptors has an effect on some of the metabolic abnormalities of liver disease.

PMID: 3147046 [PubMed - indexed for MEDLINE]

Pharmacokinetics of long-acting naltrexone in subjects with mild to moderate hepatic impairment.

Long-acting naltrexone is an extended-release formulation developed with the goal of continuous naltrexone exposure for 1 month for the treatment of alcohol dependence. The influence of mild and moderate hepatic impairment on naltrexone pharmacokinetics following long-acting naltrexone 190-mg administration was assessed. Subjects with mild (Child-Pugh grade A) and moderate (Child-Pugh grade B) hepatic impairment (n = 6 per group) and matched control subjects (n = 13) were enrolled. Naltrexone and 6beta-naltrexol concentrations were determined over a period of 63 days following a single intramuscular dose. Naltrexone and 6beta-naltrexol concentrations were detected in all subjects through 28 days. Total exposure (AUC(0-infinity)) of naltrexone and 6beta-naltrexol was similar across all groups. The long apparent half-lives of naltrexone and 6beta-naltrexol (5-8 days) were attributed to the slow release of naltrexone (long-acting naltrexone exhibits absorption rate-limited elimination or "flip-flop" kinetics); elimination was not altered in subjects with hepatic impairment. Based on pharmacokinetic considerations, the dose of long-acting naltrexone does not need to be adjusted in patients with mild or moderate hepatic impairment.

PMID: 16239359 [PubMed - indexed for MEDLINE]

High-dose naltrexone and liver function safety.

Studies have found naltrexone useful in the treatment of diseases other than opiate addiction in which endogenous opioids presumably play a role, such as alcoholism and eating disorders. Some of these studies involve high doses (100-200 mg bid). Because investigational studies with high doses (300 mg/day) reported clinically significant increases in liver enzyme levels, the authors measured a spectrum of liver function parameters in response to high doses of naltrexone in a double-blind, crossover trial (100 mg bid) followed by an open-label period (200 mg bid). They observed no adverse clinical or laboratory changes in liver function in association with high-dose naltrexone therapy in eating disorders.

PMID: 9097868 [PubMed - indexed for MEDLINE]

Effect of liver cirrhosis on the systemic availability of naltrexone in humans.

CONCLUSIONS: Our data suggest the occurrence of important changes in the systemic availability of naltrexone and 6 beta-naltrexol in liver cirrhosis; such alterations are consistent with lesser reduction of naltrexone to 6 beta-naltrexol and appear to be related to the severity of liver disease. This must be considered when administering naltrexone in conditions of liver insufficiency.

PMID: 9314128 [PubMed - indexed for MEDLINE]

Hepatic safety of once-monthly injectable extended-release naltrexone administered to actively drinking alcoholics.

RESULTS: There were no significant differences in alanine aminotransferase, aspartate aminotransferase, or bilirubin levels between the study groups at study initiation or at subsequent assessments. Gamma-glutamyltransferase in the XR-NTX 380 mg group was lower compared with placebo at weeks 4, 8, 12, and 20. Both high (>3 times the upper limit of normal) liver chemistry tests (LCTs) and hepatic-related adverse events were infrequent in all study groups. In patients who were drinking heavily throughout the study, obese subjects, or those taking nonsteroidal anti-inflammatory drugs, there was no increase in frequency of high LCTs or hepatic-related adverse events in patients receiving XR-NTX (either dose) compared with placebo. CONCLUSION: Extended-release formulation of naltrexone does not appear to be hepatotoxic when taken at the recommended clinical doses in actively drinking alcohol-dependent patients.

PMID: 18241321 [PubMed - indexed for MEDLINE]

Changes in transaminases over the course of a 12-week, double-blind nalmefene trial in a 38-year-old female subject.

A gradual return to normal in ALT and AST, while treatment with nalmefene continued, does not support the role of nalmefene as an hepatotoxin. Relapse to drinking was excluded because of normal values for the gamma-glutamyltransferase, and verification of sobriety by self-report, significant other, and breathalyzer. A virology panel ruled out the presence of viral hepatitis. Dietary intake before the elevation in LFTs contained elements that have established association with hepatocellular changes. The routine prescription of serial LFTs in alcoholism pharmacotherapy trials may be expected to reveal clinically nonsignificant elevations that could potentially be related to exogenous factors, such as dietary composition and should not be reflexively attributed to medication under investigation and/or drinking.

PMID: 7847604 [PubMed - indexed for MEDLINE]

Effects of long-term treatment with naltrexone on hepatic enzyme activity.

The influence of naltrexone on liver function in heroin addicts was studied, with respect to the metabolizing function by using the antipyrine clearance and to cellular damage by monitoring plasma levels of hepatic enzymes. The clearance of antipyrine was not affected by naltrexone treatment, and, during the study period, the use and withdrawal of benzodiazepines and alcohol did not change this parameter; moreover, there was no relationship between changes in plasma hepatic enzymes and antipyrine half-life. Mean plasma levels of hepatic enzymes did not show significant modification in the course of treatment with naltrexone.

PMID: 1686854 [PubMed - indexed for MEDLINE]

Effects of acute administration of naltrexone on cardiovascular function, body temperature, body weight and serum concentrations of liver enzymes in autistic children.

The effects of acute, orally administered naltrexone (0.5, 1.0, 1.5 and 2.0 mg/kg), a potent opiate receptor antagonist, on auscultated heart rate, systolic blood pressure and axillary body temperature were investigated before and about 1 h postdrug in 5 autistic children (4-12 years of age). In addition, an electrocardiogram was recorded on each child before and about 3 h after placebo or 2.0 mg/kg of naltrexone. Finally, the serum concentrations of the liver enzymes glutamic-oxaloacetic transaminase (SGOT) and glutamic-pyruvic transaminase (SGPT) were measured 24 h following placebo or naltrexone administration. Naltrexone had no statistically significant effects on any of these measures in comparison with baseline or placebo levels. Thus, these data provide preliminary evidence for the safety of acute administration of naltrexone in children.

PMID: 2721334 [PubMed - indexed for MEDLINE]

Naltrexone hydrochloride (Trexan): a review of serum transaminase elevations at high dosage.

In summary, evidence is presented associating typically asymptomatic and reversible elevations of serum transaminase values with high daily dosages of naltrexone. Statistical significance was found only between placebo and the 300 mg dosage. Subjects aged 40 years and over were significantly more likely to develop this finding than younger subjects. All subjects with significant elevations of transaminase values in these studies took daily naltrexone dosages higher than recommended for opioid addiction. The daily dosage of naltrexone recommended for opioid addiction did not cause abnormalities of serum transaminase values in these studies.

PMID: 3092099 [PubMed - indexed for MEDLINE]

Opioid receptor blockade improves mesenteric responsiveness in biliary cirrhosis.

The maximum pressure response to phenylephrine was decreased significantly in cirrhosis while chronic naltrexone treatment completely improved it (P <>

PMID: 18465246 [PubMed - indexed for MEDLINE]

[Antipruritic therapy with the oral opioid receptor antagonist naltrexone. Open, non-placebo controlled administration in 133 patients]

CONCLUSIONS: The oral opiate antagonists may well be an effective, well-tolerated therapy for intractable pruritus in many diseases.

PMID: 15517116 [PubMed - indexed for MEDLINE]

Endogenous opioids modulate hepatocyte apoptosis in a rat model of chronic cholestasis: the role of oxidative stress.

CONCLUSION: Our findings demonstrate that the administration of opioid antagonist is protective against hepatic damage in a rat model of chronic cholestasis. We suggest that increased levels of endogenous opioids contribute to hepatocytes apoptosis in cholestasis, possibly through downregulation of liver anti-oxidant defense.

PMID: 17403194 [PubMed - indexed for MEDLINE]

Involvement of endogenous opioid peptides and nitric oxide in the blunted chronotropic and inotropic responses to beta-adrenergic stimulation in cirrhotic rats.

Concurrent administration of naltrexone and L-NAME also restored to normal the basal abnormalities and the blunted responses to isoproterenol in cirrhotic rats, and did not show any antagonistic effect. Based on these findings, both the endogenous opioid peptides and NO may be involved in the attenuated chronotropic and inotropic responses to beta-adrenergic stimulation in cirrhosis. It seems that the iNOS activity results in NO-induced hyporesponsiveness to beta-adrenergic stimulation in cirrhosis.

PMID: 16968416 [PubMed - indexed for MEDLINE]

Low Dose Naltrexone January 2010 Lab Results for Hepatitis C

2010-01-05T19:54:00.000-08:00

I started Low Dose Naltrexone (LDN) last March for Hepatitis C. I also test positive for Sjogren's Syndrome and Rheumatoid Arthritis (RA). These are my latest lab results.

I was a bit apprehensive as I didn't feel too well on the morning of my labwork - I had that "virusey" feeling and was also a bit stressed as they couldn't find the tests that they needed to run in the Quest Lab computer - so I sat for 45 minutes fuming. I had been feeling great except for that day (of course).

My HCV viral load crept up a bit from 18,729 in September to 34,524 - not too bad considering how I felt that day. Last January, pre-LDN, it was 1,280,000 and had dropped to 49,400 in June after being on LDN for 3 months. So I'm staying pretty stable - better than skyrocketing back up but not going down as I had hoped. For awhile, I was taking the 3 mg. LDN every other night, but for the last month or so, I went back to every night dosing. I will discuss with my doctor about possibly increasing the LDN dosage.

My ALT/AST were back to normal range though they weren't that high last time. In January last year, my ALT was 174, in May it dropped to 23, in Sept. it was 36 (range 6-40) and now is 34. My AST was 99 in January, 30 in May, 37 in Sept.(range 10-35) and 31 now.

Albumin (range 3.6 - 5.1) 4.8 - was 4.9 - it was 5.2 last January

Globulin (range 2.2 - 3.9) 2.9 from 3.0 - it was 3.7 last January

Bilirubin total (range 0.2 - 1.2) 0.7 from 1.1

Alkaline Phosphatase (range 33-130) 66 from 57

Total Protein - (range 6.2 - 8.3) 7.7 from 7.9 - it was 8.9 last January

Alpha Fetoprotein - 5.0 same as last time - was 6.1 which was high earlier last year.

My ferritin dropped from 80 to 38 which might be pushing it a bit - I'd been religiously taking the IP-6 along with a product called Chelaco (which my doc sells). My total iron is 136 (range 40-160) down from 165 and iron binding capacity is 373 from 352 (range 250-450)

Sjogren's level - 3.3 from 3.5 - it was 4.5 in January, pre-LDN

RA - 21 from 24 - it was 31 in January - pre-LDN

Vitamin D (range 20-100) - 59 from 49 but had been 62

Most of my other blood counts are the same - I need to talk to my doc before I try and interpret them - nothing really out of range but some of the ones that we were trying to change, via the methyl B vitamins are the same as they were in 2007. (MCV, MCH) red blood cell count, etc. I might talk to her about being tested for IF - Intrinsic Factor which can inhibit your body from absorbing B-12.

My red blood cell counts have always been on the low end - which was another argument on my part whenever a doc would try and push HCV treatment on me - ("how long before I'd be on Procrit? I'd ask them)

Slight decrease in platelets (range 140-400) 163 from 172 (186 last January)

Slight drop in red blood cell count (range 3.80-5.10) 3.84 from 3.95 (4.21 last January but 3.78 prior to that)

White blood cell count (range 3.8-10.8) 6.1 from 4.6 (6.0 from last Jan.)

Neutrophils - (range 1500-7800) 4111 from 2585 (3750 last jan.)

Eosinophils (range 15-500) 140 from 120 (102 last jan.)

Basophils (range 0-200) 24 from 14 (12 last Jan)

The LDN isn't really affecting my lymphocytes overall - some are better, some are worse.

CD3 (Mature T cells) (range - 57-85) 80 from 77

Absolute CD3+ Cells (range 840-3060) 1122 from 1008

%CD4 (Helper Cells) (range 30-61) 58 from 52

Absolute CD4+ cells (range 490-1740) 817 from 720

%CD8 (Suppressor T Cells) (range 12-42) 19 from 24

Absolute CD8+ cells (range 180-1170) 269 from 333

Helper/Suppressor ratio (range 0.86-5.00) 3.05 from 2.17

%CD16+CD56 (Natural Killer Cells) (range 4-25) 7 from 10

Absolute NK Cells (CD16+CD56 Cells) (range 70-760) 99 from 128

%CD19 (B cells) (range 6-29) 10 from 11

Absolute CD19+ Cells) (range 110-660) 139 from 134

Absolute Lymphocytes (range 850-3900) 1404 from 1308

Absolute CD3+ cells (range 840-3060) 1122 from 1008

Absolute CD4+ cells (range 490-1740) 817 from 720

Absolute CD8+ cells (range 180-1170) 269 from 333

Absolute NK Cells (CD16+CD56+ cells) (range 70-760) - 99 from 128

Absolute CD19+ cells - (range 110-660) 139 from 134

My doc also tests all of my adrenals (4 thyroid tests, progesterone, testosterone, etc.) Immunoglobulins, HHV 1-6 viruses, along with the standard CBC's, etc. All are pretty much the same as they were 2 years ago.

Overall, I'm pretty happy with the results especially as my viral load did not really increase as I had feared it might - and my LFT's have stabilized.

Hepatitis Supplements and Diet

2009-11-22T17:01:00.000-08:00

These are the supplements, diet and exercise regimen that I am on, along with taking 3 mg of Low Dose Naltrexone for controlling my Hepatitis C virus. It is based on Dr. Berkson's original protocol of using ALA (Alpha-Lipoic-Acid), Selenium, and Silymarin (Milk Thistle) to treat his patients with liver disease.

The 3 basic antioxidants there were used in this report are Alpha-Lipoic Acid (thioctic acid), Silymarin (milk thistle) and Selenium (selenomethionine). The Alpha-Lipoic Acid product was manufactured by Asta Medica at Frankfurt Am Main, Germany. The Silymarin was a product distributed by NOW Foods of Bloomingdale, Illinois, and the Selenium was encapsulated by Metabolic Maintenance Products Inc., of Sisters, Oregon.

Berkson Clinical Study

Dr. Berkson put me on 3 mg. of Low Dose Naltrexone back in February of 2009. I am also taking the "triple antioxidants" along with other supplements that he and my own CAM doctor believe is right for me. I use primarily Metabolic Maintenance, BlueBonnet Nutrition and Now Brands, especially for the ALA, as the best source is European.

DOSAGES

ALA - I take 300 mg. two times daily with food - some folks take it without food but if you have problems with your blood sugar levels, ALA can lower them, so it is probably better to take with food. At Dr. Berkson's clinic, they would make sure that you had eaten something prior to the IV ALA treatments - which are, of course, different than oral supplementation.

B-Complex - It is also very important to take a B Complex along with ALA as the ALA will use up the B vitamins in the body. I use Bluebonnet B Complex - I also take additional Biotin, B-12, and Pantothenic Acid (B5) as a vitamin diagnostic test showed that I have low levels of those 3 B vitamins.

From Dr. Berkson's book "

"User's Guide to the B Complex Vitamins"

"Both ALA and the B vitamins are essential in helping the cells miochondria make energy. When mitochondria function correctly, they require a number of enzymes.

ALA is the major key that turns on these enzymes. thiamine, niacin, riboflavin, biotin, and other B-complex vitamins are also involved in this system of enzymatic processes and becove depleted as the mitochondria produce energy. Therefore, if a person supplements with ALA, he or she must also take at least on B-complex capsule with it. In other words, since ALA revs up mitochondrial activity and uses up B vitamins in the process, there's a chance a person can become deficient in many key B vitamins without proper supplementation."

Selenium - 200 Mcg. in two doses - and try not to exceed 400 Mcg. daily - take into consideration if any of your other supplements contain Selenium as well. Also, foods such as brazil nuts contain high amounts of selenium, so use caution if you eat a lot of foods that contain selenium.

Silymarin (milk thistle) - 600-900 mg daily I have been using the Jarrow brand lately - very cost efficient and works well.

Vitamin D-3 is very important as well. My doctor regularly tests me and says that levels should be at least above 50 and optimally around 75. I am taking from 2,000 to 8,000 IU daily as my levels are not ideal. Most people with liver disorders, particularly with Hepatitis C, are deficient in Vitamin D.

Ideally, I like to take other supplements that help support the methylation cycle, which in turn helps boost glutathione levels that are crucial for the liver and overall cellular growth. NAC, SAMe, Taurine, Whey protein (mixed in a daily fruit smoothie), help the cycle. I can't always afford all of these supplements, but always try and have the "triple antioxidant's and B Complex on board, as well as an iron-free daily vitamin. Digestive enzymes are also very beneficial and help the entire digestive cycle.

I also use a great deal of L-Lysine, an amino acid, which helps control the various Herpes viruses that I have. Grapefruit seed extract is very beneficial for viral infections and yeast - I take the GSE for a couple of months and then switch over to Olive Leaf extract.

IP-6 is important as it helps keep ferritin levels down. I usually take one or two 500 mg. capsules twice daily - note, it is very important to take IP-6 away from any other supplements or food for at least a half hour to an hour. I find that if I wake up during the night to use the restroom, I will take one dose then. The Jarrow formula works very well and is very inexpensive compared to others.

I've found that iHerb has very inexpensive prices on most supplements (but not Metabolic Maintenance) - Use this code to get $5.00 off your first order: KOV896

iHerb

This site has Metabolic Maintenance products at lower prices - but they do not ship as fast:

My Health-Store

Diet is very important with any type of liver disease. When you consider that everything that you eat is processed by the liver, it makes all the more sense to pay attention to your diet. Organic foods contain a lot less harmful elements than those produced in mass, or those that have been genetically engineered. Avoid processed foods, particularly those with gluten (the protein found in wheat and barley), and fried, greasy foods. Many people with immune disorders also cannot tolerate dairy products or are lactose intolerant. Avoid "fake" foods - like margarine or MSG. I like to use Stevia instead of sugar or any of the artificial sweeteners like Splenda.

One of my favorite bloggers is George Henderson and one of his best posts is:

Hepatitis C in 5 Words or Less

A Hep C protocol should protect against the following aspects of HCV infection:

Oxidative stress (liver damage, diabetes, inflammation) – Hep C depletes antioxidants, low antioxidant levels are associated with poor outcomes. The combination of oxidative stress and hypomethylation is the preventable cause of hepatitis, fibrosis, and cirrhosis.

Some genotypes also promote the accumulation of iron, which increases oxidative stress exponentially. Genetics, iron fortified foods, and poor liver function can also add to iron loads, which should be kept in the 30-80 ferritin range.

Treatment – mixed antioxidants, silymarin, polyphenols.

Hypomethylation (steatosis, fatigue, depression) – Hep C depresses methylation, which allows fats to accumulate and decreases energy output. Methylation is the process needed to supply creatine, phosphatidylcholine, carnitine, co-enzyme Q10, glycine, melatonin, adrenaline, cholesterol and steroids; methylation also inactivates histamine and niacinamide, and helps with detoxification. Methylation also plays a role in DNA synthesis and in regulating the expression of genes and the activity of proteins. All methylation in the body is carried out by the SAMe form of methionine, except for the methylation of methionine itself, which requires B12, folic acid, and betaine. Hypomethylation (deficient methylation) in Hep C is largely due to inhibition of vitamin B12 by oxidative stress, the poor absorption of B12 and folate when stomach acid is inadequate, and anorexia and nausea limiting intake of foods rich in methionine. So-called low fat foods that are low in high-quality protein and essential fats and high in carbohydrates are especially problematic - the liver synthesises fats from carbohydrates in any case. Cooked fats and hydrolysed fats should be avoided, omega-6 EFAs and PUFAs - most vegetable oils - and saturated fats minimised, while fatty fish (omega 3 EFAs) and extra virgin olive oil (monunsaturated omega 9 fatty acid) should be eaten whenever possible.

Treatment – l-methionine, B12, folic acid, phosphatidylcholine (lecithin), carnitine.

Immunosuppression (HCV replication, co-infections, allergies) – Hep C interferes, both directly, and via oxidative stress, with immune function, allowing co-infections and autoimmune syndromes to develop. Increased levels of interferons during illness can bring about gluten and other allergies in previously tolerant individuals.

Treatment – selenium, zinc, vitamin A, vitamin C, cordyceps, astragalus, garlic.

Inflammation (other inflammatory conditions, liver damage, mood disorders) – Hep C increases production of pro-inflammatory cytokines, which can promote fibrosis, and prostaglandins, which strip essential fatty acids from cell membranes, causing pain and mood changes. Inflammation and oxidative stress are closely related. Similar processes are involved in PMS, bipolar disorders, psychosis etc. so it is not surprising that moods, emotions and perceptions can be affected by Hep C. Inflammatory cytokines can also trigger sensitivity to complex proteins such as gluten (wheat, rye, barley) and casein (cow's milk), which then become an additional cause of inflammatory disease.

Treatment – magnesium, vitamin D, ginkgo, EPA and DHA, evening primrose oil.

Coagulation (liver damage, inflammation) – rapid coagulation (clotting time) is associated with fibrosis, thinner blood with better outcomes. Blood clots often become a focus of inflammation, leading to fibrosis. Most anti-fibrotics and anti-inflammatories are anticoagulants; for example:

Treatment – ginkgo, vitamin E, fish oil, garlic

Detoxification (liver damage) - Exotoxins and endotoxins requiring phase 1 and phase 2 detox – drugs, toxins, pollutants, cholesterol and steroids - must be processed by liver and kidneys. Many of the phase 2 reactions use glutathione, glycine and taurine, levels of which are reduced in Hep C, and pantothenic acid (B5) as acetylCoASH, which instead becomes tied up with unprocessed fats in steatosis. Glycine production is inhibited by hypomethylation. Improperly metabolized toxins can add to oxidative stress, damaging the liver, or inhibit enzymes, impairing liver function.

Treatment – sulfur amino acids, B vitamins, broccoli sprouts, whey protein

Nutrition

Fresh vegetables and fruits - lean meats - brown rice, gluten-free grains such as quinoa - avoidance of processed or "fast food". Eat several small meals as opposed to a few heavy ones as it is easier for the liver to digest. Here is more:

DIET AND NUTRITION FOR LIVER DISEASE AND HEPATITIS

Nutrition And The Liver

Video - Foods to avoid when living with Hepatitis C

Easy Fruit Smoothie
Fresh fruit - strawberries, pineapple, banana - half fresh and half frozen - add juice - Goji or other juices are great! - Add whey protein(gluten-free!) for more punch

GLUTEN FREE DIET

I maintain a strict gluten and dairy free diet - most folks with Hep C or liver disorders (or really just about any disease) have problems or sensitivities to the proteins in these food sources. A great resource is called
"The Gluten File" Check out the page on "Liver Disease" for many studies and abstracts. One study is:

Celiac disease in patients with severe liver disease: gluten-free diet may reverse hepatic failure.

BACKGROUND & AIMS: Mild liver abnormalities are common in patients with celiac disease and usually resolve with a gluten-free diet. We investigated the occurrence of celiac disease in patients with severe liver failure.

METHODS: Four patients with untreated celiac disease and severe liver disease are described. Further, the occurrence of celiac disease was studied in 185 adults with previous liver transplantation using serum immunoglobulin A endomysial and tissue transglutaminase antibodies in screening.

RESULTS: Of the 4 patients with severe liver disease and celiac disease, 1 had congenital liver fibrosis, 1 had massive hepatic steatosis, and 2 had progressive hepatitis without apparent origin. Three were even remitted for consideration of liver transplantation. Hepatic dysfunction reversed in all cases when a gluten-free diet was adopted. In the transplantation group, 8 patients (4.3%) had celiac disease. Six cases were detected before the operation: 3 had primary biliary cirrhosis, 1 had autoimmune hepatitis, 1 had primary sclerosing cholangitis, and 1 had congenital liver fibrosis. Only 1 patient had maintained a long-term strict gluten-free diet. Screening found 2 cases of celiac disease, 1 with autoimmune hepatitis and 1 with secondary sclerosing cholangitis.

CONCLUSIONS: The possible presence of celiac disease should be investigated in patients with severe liver disease. Dietary treatment may prevent progression to hepatic failure, even in cases in which liver transplantation is considered.

PMID: 11910339 [PubMed - indexed for MEDLINE]

If you have undergone interferon treatment, chances are that it triggered gluten intolerance or full blown celiac disease:

Silent celiac disease in chronic hepatitis C: impact of interferon treatment on the disease onset and clinical outcome.

http://www.ncbi.nlm.nih.gov/pubmed/15492610

Unmasking of coeliac disease on interferon treatment for hepatitis c

A 45-year-old woman with chronic hepatitis C, contracted 25 years previously from intravenous drug use, was referred to our hepatitis C clinic by her general practitioner. She was noted to have persistently elevated serum transaminases, with alanine transaminase of 158 U/L (normal < 34) and aspartate aminotransferase of 92 U/L (normal < 31), but was clinically well. She had an albumin of 34 g/L (normal 36–48), bilirubin of 17 µmol/L (normal < 18) and International Normalized Ratio of 1.3. A normal sized liver but coarse echotexture with no mass lesions was noted on abdominal ultrasound. There were no signs of portal hypertension on examination or on ultrasound.

She had an upper gastrointestinal endoscopy done 4 years prior to investigate transient mild diarrhoea in which small bowel biopsies were taken. On histological examination, the villi appeared slightly short and broad, and there was some branching of crypts, but no characteristic degenerative or inflammatory changes of coeliac disease was seen.

As there were no contraindications to anti-viral therapy, she was commenced on pegylated interferon alpha (180 µg subcutaneously, weekly) and ribavirin (400 mg twice a day). She initially tolerated treatment well, but after 12 weeks developed abdominal pain and bloating, nausea, vomiting and watery diarrhoea. She was provided a course of oral metronidazole, which did not improve her symptoms. As it was felt that these symptoms were due to the interferon treatment, her interferon dose was gradually reduced to 90 µg/week, and she was provided with loperamide.

Despite this, her symptoms progressively worsened and by week 20 of treatment, she was noted to be anaemic with a haemoglobin level of 97 g/L (normal 115–165) and ferritin of 7 µg/L (normal 18–464). She was also folate deficient with a serum folate of 4.5 nmol/L (normal > 6.8) and had a bilirubin of 17 µmol/L and albumin of 30 g/L. As she had genotype 1 with evidence of cirrhosis and was managing treatment relatively well, we decided to continue antiviral treatment despite her symptoms to complete a 48-week course. She continued to have four to six episodes of watery diarrhoea a day and by completion of therapy, her weight had dropped from 67.2 to 57.8 kg. Of note there was no fever, no haematemesis, no melaena and no per rectum bleeding.

She was reviewed 12 weeks post treatment, when she was noted to have a negative hepatitis C RNA PCR, but her liver function tests remained abnormal with alanine transaminase of 51 U/L and aspartate aminotransferase of 81 U/L. As abdominal bloating, nausea, lethargy and diarrhoea were persistent, she had a repeat upper gastrointestinal endoscopy. Small bowel biopsies this time revealed striking total villous atrophy and marked crypt elongation with prominent epithelial lymphocytosis consistent with untreated coeliac disease. Her anti-gliadin and anti-endomysial IgA were also positive.

She was commenced on a gluten-free diet with resolution of both symptoms and liver function tests over 3 months. Further small bowel biopsies were taken 9 months after commencement of gluten-free diet showed preserved villous architecture with no significant acute inflammatory process. Repeat anti-gliadin and anti-endomysial antibodies at this time were also negative. Twelve months after completion of interferon and ribavirin treatment, she remains hepatitis C PCR negative.

Hepatitis C is associated with a myriad of autoimmune conditions including autoimmune thyroiditis1 and Sjogren's syndrome.2 More recently, coeliac disease as well as dermatitis herpetiformis have also been associated with hepatitis C.3 In addition, hepatitis C is associated with autoantibody production. Antinuclear antibodies, rheumatoid factor, anti-cardiolipin antibodies, smooth muscle antibodies, or anti-thyroid antibodies are detected in 40–65% of patients, but usually in low titre.4 Additionally, both coeliac disease and hepatitis C are common and so any coexistence may simply be a conjunction of two common conditions.

In this patient, the chronic hypertransaminaesemia was attributed to hepatitis C. However, the alanine aminotransferase remained high despite the clearance of hepatitis C, and did not normalize until a gluten-free diet was instituted. Thus occult coeliac disease may have been the cause. She probably had pre-existing subclinical coeliac disease, which only became symptomatic upon treatment with interferon. It has been noted that coeliac disease may be associated with nonspecific mild chronic elevation in serum aminotransferase levels in 40% of patients,13 and adherence to a gluten-free diet results in normalization of these abnormalities. Coeliac disease can cause progressive hepatitis and hepatic steatosis without apparent reason. Even if a patient has severe liver disease as a result of untreated coeliac disease, a gluten-free diet may reverse liver failure.14

We recommend that all patients be screened for coeliac disease prior to anti-viral treatment. The coeliac autoantibodies should be checked and if any suggestive symptoms are present or if antibodies are positive, upper gastrointestinal endoscopy with small bowel biopsies should be considered.

Weight loss and diarrhoea are common side effects of interferon therapy, but marked weight loss or excessive diarrhoea should prompt a search for coeliac disease, as the activation of silent coeliac disease during interferon treatment is common. Symptoms often subside after interferon withdrawal.

The investigation of chronic transaminitis should include coeliac serology as coeliac disease can cause liver disease.

http://onlinelibrary.wiley.com/doi/10.1111/j.1445-5994.2009.02087.x/full

The prevalence of celiac autoantibodies in hepatitis patients

Celiac disease has been associated with other autoimmune disorders such as autoimmune hepatitis, moreover it is known that T cell mediated immune response to dietary gluten and released cytokines are important for the entheropathy seen in celiac disease. We investigated celiac autoantibodies in patients with autoimmune hepatitis (AIH), and chronic hepatitis B (CHB).Sera from 84 patients with Autoimmune Hepatitis (AIH) type 1 and 88 patients with Chronic Hepatitis B (CHB) were tested for Immunoglobulin A and G antibodies to Gliadin, Immunoglobulin A antibodies to tissue transglutaminase using enzyme immunoassay, and Immunoglobulin A anti-endomysial antibodies by both indirect immunofluorescence, and enzyme immunoassay. The patients positive for anti-endomysial antibodies and/or anti tissue transglutaminase antibodies were considered for deuodenal biopsy. The study was approved by Research Center for Gastroenterology and Liver Disease Ethics Committee and all patients gave their written informed consent to participate.Immunoglobulin A anti-endomysial and Immunoglobulin A anti-gliadin antibodies were positive in two out of 84 patients with AIH. Moreover, Immunoglobulin A anti-gliadin antibodies were positive in another patient who was also positive for anti tissue transglutaminase antibodies. Tissue transglutaminase antibodies were positive in eight (9.1%) of 88 patients with CHB, two of which were also positive for anti-endomysial antibodies. One of the patients with CHB was only positive for anti-endomysial antibodies.

Compared with the general population, the prevalence of celiac autoantibodies in CHB and AIH patients is relatively high, and it is noteworthy that most positive patients were asymptomatic for celiac disease. We suggest screening for celiac disease before and during treatment in patients with viral and autoimmune hepatitis.

PMID: 20952805 [PubMed - in process]

http://www.ncbi.nlm.nih.gov/pubmed/20952805

I'll also reference George Henderson again here - he says it so well - thank you George!

Gluten and Casein as Factors responsible for the Characteristic Diseases of Chronic Hepatitis C

Not everyone exposed to HCV develops a chronic infection. The rate of natural clearance is unknown, because most people are not aware they are infected until the condition becomes chronic. One known factor in chronic infection with viral hepatitis (A&B) is selenium deficiency in malnourished populations. Celiac disease, the most easily diagnosed form of gluten toxicity, is known to cause selenium deficiency in well-fed populations. Celiac also causes a general deficiency of many antioxidants, protein, and minerals and vitamins. There is a strong association between HCV and celiac disease in many populations tested. There is an even stronger association between interferon-alpha treatment and celiac disease. Interferon-alpha is the cytokine that triggers celiac disease naturally.

Celiac disease is only the easiest to diagnose of the gluten sensitivity syndromes. It results in destruction of the intestinal cell vilii, damage which can be detected on biopsy.

Even so celiac is seriously underdiagnosed. It is likely that anyone in New Zealand with the symptoms of celiac disease, who is HCV positive, will be told that their symptoms are due to hepatitis C. Testing for Celiac will happen slowly and most likely not at all, unless the patient insists, and testing for other forms of gluten sensitivity is unlikely. Milder forms of gluten sensitivity might only disrupt those gut receptors responsible for functions such as immune regulation (especially endorphin receptors), mineral transport, or absorption of specific vitamins. Antibodies may form to the proline-rich gluten, gliadin and casein sequences released by peptide digestion which enter the bloodstream, which then attack the proline-rich collagenous tissues, promoting diseases such as liver fibrosis and rheumatoid arthritis.

It so happens that the auto-immune symptoms associated with celiac and gluten sensitivity diseases, including liver and gall-bladder disease, and which usually resolve slowly on a strict gluten and dairy-free diet, are essentially identical to the various syndromes seen in chronic Hep C, especially during or after interferon-alpha treatment.

Syndromes caused by gluten in celiac disease include:

- fibrosis and cirrhosis of the liver
- gall bladder obstruction
- insulin resistance
- thyroiditis
- sicca syndrome (dry eyes and mouth)
- vasculitis
- brain fog (poor memory, confusion)
- depression
- fibromyalgia
- fatigue
- optic neuritis
- deficiencies of selenium, magnesium, zinc, chromium
- deficiencies of fat-soluble vitamins (A, D, E, K)
- deficiency of those vitamins converted in the intestines (including folate, B6)
- anaemia
- thrombocytopenic purpurea (low platelets due to autoimmunity)
- GI disturbance; diarrhea, steatorrhea

These symptoms are aggravated by the nutrient deficiencies, especially antioxidant, magnesium, and chromium deficiencies, associated with gluten sensitivity. In fact, the symptoms of both Hep C and celiac disease are often partially, but significantly, relived by supplementation of these nutrients, especially when anti-inflammatory botanicals (curcumin, grape seed, ginkgo, milk thistle etc) are added. Other treatments effective against Hep C have obvious links to gluten sensitivity; for example, low dose naltrexone may exert its beneficial effects on cancer, autoimmune disease, and viral immunity by repairing damage done to endorphin receptors by gluten and casein digests. Similarly, enzyme therapy for cancers may work by promoting the complete digestion of gluten and casein exorphins, and the ketogenic diet for cancer may work by eliminating grains and lowering insulin levels (and hence inflammation), rather than merely by depriving cancer cells of glucose.

Exorphins are chemicals found in protein digests (the peptides produced by pepsin digestion of food proteins) which have an affinity for endorphin receptors. Endorphins are the messengers of emotion, and gluten sensitivity is very often found in schizophrenia, autism, ADHD, Aspergers, and the various mood disorders. However, the endorphin system also regulates the immune system, and defects of endorphins and endorphin receptors are associated with cancers and autoimmune disease, as well as AIDS. Endorphins also regulate gut motility; the well-known constipating effect of cheese is an opioid effect. Even people who have no gluten antibodies and no leaky gut (which allows gluten digests to enter the bloodstream in especially large doses) are influenced by the opioid effect of exorphins at the local, gut level.

Diagnosing non-celiac gluten and casein sensitivity without exclusion diets is difficult, if not impossible. Commonly in New Zealand a scratch test for gluten is the doctor’s first choice. This is worse than useless, because we are not talking about an allergy to gluten at all (though these do exist). When gluten, milk and maize are digested in the stomach (by pepsin and hydrochloric acid) a variety of peptides are released. The exact combination of peptides that might appear in the gut varies with the individual, the state of his digestion, and the strain of wheat, milk or maize consumed. Gliadomorphin is a characteristic wheat exorphin; beta-casomorphin-7 is thought to be the most toxic milk exorphin; and the maize exorphins have not yet been identified.

Autoimmune reaction to antigenic peptides is not the only way in which exorphins can harm us, so the current insistence on immunological testing seems limited. Also, current tests do not include antibodies to every possible peptide digest of gluten; this would probably be impossible.

Luckily, no-one needs to eat grains. Our ancestors got along in better health without them for millions of years. Grain consumption is a comparatively recent phenomenon in human history; very recent indeed in some cases; in Northern Europe and in colonized Oceania it is a habit of mere centuries, if that. In parts of the world where grain-eating goes back longest, for example the eastern Mediterranean, there is a higher rate of adaptation. This does not mean that individuals adapted to grains; individuals died young or became sterile if they lacked the more grain-adapted genes, in order that the race might adapt. But this still does not rule out the diseases of later life. Study of remains of grain-dependent societies, such as Rome and ancient Egypt, show that so-called “modern” diseases such as arthritis and cancer were prolific there. It is trendy to think that such disease results from technology; radiation, pesticides, food processing; and that it can be prevented with an organic vegetarian diet. The sad truth is that in most cases wheat and milk - even organic wheat and milk – products of the older agricultural revolution – are doing more harm than those traces of the modern industrial revolution that we cannot avoid. If our immune systems and our detox enzymes cannot cope with some new agricultural chemical, the most likely reason is the disruption they have received from the old agricultural chemicals – gluten and casein. It was also agriculture, not food processing, that first placed man in a guilty relationship with his food. Pre-agricultural man killed to eat and took from the forest, and had rituals that made peace with the animals and the plants. He took from these bounteous gods, not from captive creatures. Agricultural man kills for money, pays others to kill for him, and burns down the forest to plant his cash crops. If this was original sin, then the wages of sin have indeed been death.

It is customary to blame lead piping for the decline of Rome. The Roman people were highly wheat-addicted; they would riot for bread; “Bread and Circuses” was the formula for keeping them happy; they were so addicted that the state found it more convenient to supply bread for free (like a methadone clinic for the opiate of the people). Today the state oversees the addition of gluten, milk and maize to an ever-widening range of foods, so that a mere bread shortage is not likely to cause withdrawals. This is probably not intentional; addicts tend to assume that everyone wants to share their habit. In the case of Rome, wheat and lead may have had a synergistic toxicity. Both lead poisoning and wheat consumption tend to reduce iron and zinc absorption. This is why celiac children are often of short stature. The Romans would have become increasingly incapable of sensible planning and come to lack the stern old Roman self-control. We know that a decreasing birthrate of “true born” Romans eventually led to the conscription of barbarian armies and the opening up of Roman citizenship. Today gluten, and the antioxidant deficiency it causes, is a major cause of infertility.

Research has been done into the links between gluten sensitivity and Hep C, showing a strong association (especially after interferon therapy). There is also a strong association between Hep C and lymphoma (a cancer of the lymph glands). Lymphoma is the characteristic cancer caused by gluten; celiacs have a 30x elevated risk of lymphoma. To date no-one seems to have tested a strict gluten- and dairy-free diet for chronic Hep C or post-interferon toxicity, but a great many people with Hep C who take their health seriously have gone gluten free, often without knowing of the links between the two conditions, but motivated by their own well-being when avoiding gluten. There is no nutritional need that can only be met by grains; nuts and seeds, for example, supply the same amino acids, fats and vitamins in greater concentration (for example, sunflower and sesame seeds are superior sources of methionine and vitamin E), while legumes are rich in complex carbohydrates.

Gluten is also a cause of insulin resistance, and everyone who develops liver fibrosis has some degree of insulin resistance. Gluten itself causes a four-fold rise in insulin levels (unusual for a protein). The cure for insulin resistance is two-fold; a high-protein, low-carb diet (the Paleolithic diet is the most natural version of this diet) and replacement of the nutrients depleted by gluten which are essential for the function of insulin receptors; chromium, magnesium and the antioxidant minerals and vitamins.

Gluten also seems to cause amino acid deficiencies, including some of the very amino acids which wheat is supposed to supply, methionine and cysteine. Gluten is very much an anti-nutrient once one is sensitive to it.

Dangerous Grains by James Braly M.D. and Ron Hoggan M.A.

On milk, exorphins, and beta-casomorphin-7 (BCM7):

The Devil in the Milk by Keith Woodford

On endorphin receptors and AIDS:

Molecules of Emotion by Candace B. Pert

Read more: http://blogs.myspace.com/georgedhenderson#ixzz13Qu2vFF4

Dr. Berkson's 2009 Videos - Pancreatic Cancer, RA, Lupus, Lymphoma, more

2009-11-10T10:22:00.000-08:00

Dr. Berkson was the keynote speaker at the recent Low Dose Naltrexone Conference held in Bethesda Md. at the NIH - National Institute of Health. There, he presented a 2 hour presentation detailing his successful treatments of various disorders, including pancreatic cancer, b-cell lymphoma, RA, Lupus, breast cancer, liver cancer and cirrhosis, among other diseases.

Newly published abstract about Dr. Berkon's use of ALA and LDN in treating 3 pancreatic cancer patients:

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.

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

The authors, in a previous article, described the long-term survival of a man with pancreatic cancer and metastases to the liver, treated with intravenous alpha-lipoic acid and oral low-dose naltrexone (ALA/N) without any adverse effects. He is alive and well 78 months after initial presentation. Three additional pancreatic cancer case studies are presented in this article. At the time of this writing, the first patient, GB, is alive and well 39 months after presenting with adenocarcinoma of the pancreas with metastases to the liver. The second patient, JK, who presented to the clinic with the same diagnosis was treated with the ALA/N protocol and after 5 months of therapy, PET scan demonstrated no evidence of disease. The third patient, RC, in addition to his pancreatic cancer with liver and retroperitoneal metastases, has a history of B-cell lymphoma and prostate adenocarcinoma. After 4 months of the ALA/N protocol his PET scan demonstrated no signs of cancer. In this article, the authors discuss the poly activity of ALA: as an agent that reduces oxidative stress, its ability to stabilize NF(k)B, its ability to stimulate pro-oxidant apoptosic activity, and its discriminative ability to discourage the proliferation of malignant cells. In addition, the ability of lowdose naltrexone to modulate an endogenous immune response is discussed. This is the second article published on the ALA/N protocol and the authors believe the protocol warrants clinical trial.

PMID: 20042414 [PubMed - in process]

Even though I have provided these links in an older post, "Dr. Berkson & LDN" , these videos have just been made available and contain crucial information that might save countless numbers of people. His successful treatment of a patient with pancreatic cancer will be published in December, along with 2 other cases.

Introductory remarks - ALA - Hepatitis C

1) http://www.youtube.com/watch?v=WHyUfHqR4PA

Pet Scans - Treatment Protocol - ALA Explanation - Pancreatic Cancer with Mets to Liver (case to be published in December)

2) http://www.youtube.com/watch?v=xy65UGsVMac

Pancreatic Cancer with Mets to Liver - Hepatitis C with Liver Cancer -

3) http://www.youtube.com/watch?v=dRf8Xuqhb5Q

RA with Lymphoma from Humira - B Cell Lymphoma - Breast Cancer - Rheumatoid Disorders - Dermatomyositis -

4) http://www.youtube.com/watch?v=RXz3VIuyHHk

RA - SLE (Lupus) -

5) http://www.youtube.com/watch?v=nttilGKpJvU

ALA and purity; Asian products vs European - ALA discussion - Epstein-Barr Virus -

6) Dr Berkson Q & A Part One

http://www.youtube.com/watch?v=RsBN78Cl1s4

Lab Tests - Dosing of LDN and ALA - R Form Lipoic Acid - B Complex -

7) Dr Berkson Q & A Part Two:

http://www.youtube.com/watch?v=c29DAE4MGmo

Pancreatic Cancer & Thoughts on Treatment - ALA Gene Expression - Misc.

8) Dr. Berkson Q & A Part Three:

http://www.youtube.com/watch?v=nYxzDuKAdfI

http://www.drberkson.com/

Low Dose Naltrexone for Hepatitis C Lab Results

2009-11-02T16:43:00.000-08:00

I had new labs done last month and they were even better than the first ones! My viral load dropped down to 18,700! In January, it was over a million - it had dropped down to 49,000 in May and keeps dropping! How low can it go? I hope to 0!!!!!

I feel pretty good now too. Much more energy. The Low Dose Naltrexone is really doing a number on my Hepatitis C virus. I had started at 3 mg. a night but now take it every other night and it still seems to be working......for me, it seems that less is more with the LDN.

I belong to a Yahoo support group called:

Hepatitis Children and CAM Alternatives

Click to join Hepatitis_Children_and_CAM_Alternatives

Despite it's name, there are a great many adults who have various forms of Hepatitis. C, B or autoimmune. Many of the members are also using LDN for their conditions and all are having great results.

If you are considering using the combo treatment of interferon and ribavirin to treat your Hepatitis C, or have tried it and failed treatment or had to stop because of the side effects, please consider using Low Dose Naltrexone instead. Other than initial sleep disturbances, there are very few, if any, side effects. It is very inexpensive as well. My 3 month supply costs about $50.00 and I get it from Skip's Pharmacy through the mail. Their site is here:

Skip's Pharmacy

On another note, my fibromyalgia, IBD, and chemical sensitivities are much, much better as well. The combination of a gluten/dairy free diet and the LDN has made all the difference in the world.

Dr. Burt Berkson and Low Dose Naltrexone

2009-06-28T17:21:00.000-07:00

When I first started this blog, it was to detail my life in New Orleans with Hepatitis C and my daily struggles in post-Katrina New Orleans. However, after having such wonderful results with Low Dose Naltrexone after visiting Dr. Berkson in his clinic in New Mexico, it has become more about promoting LDN than anything else.

Indeed, 95% of the visitors here google "Dr. Berkson" in some form and my blog comes up more than his own site - I wonder what the poor man has to think about this...? At any rate, I am happy that so many folks are visiting here and learning more about LDN - and Dr. Berkson.

My own integrative doctor told me about Dr. Berkson and his work with Hepatitis C and Alpha-Lipoic-Acid a few years back.

I began taking his regimen of ALA, milk thistle and selenium in his recommended dosage - my liver function tests did improve overall but the inflammation and fatty liver continued.

A couple of people that I knew through various Hepatitis C forums went to see Dr. Berkson and both had good experiences with him, so I decided to go. I still had a little money left from the settlement that I had gotten after losing my house and possessions due to the flooding after Katrina. Not much, but enough to cover the air fare, rental car, IV ALA treatments and misc.costs.

I called his clinic and was told to fax them a few medical test results - a PT (Prothrombin time - which tells how long it takes your blood to clot), platelet count, LFT'S (liver function tests) and I believe, HCV viral load test - I can't really remember exactly. I ended up sending a lot of stuff - to the point that it cost me 27.00 at Office Max to do so - I don't have a fax machine.. The woman on the phone was very nice, though a bit rushed, and she took down other information.

They called me back the next day and set up an appointment several months away, but later in the day, they called me back and said that Dr. Berkson had reviewed my lab work. Could I come in two weeks? Well, this unnerved me because I thought that he had seen something really horrible in my labs. But, it turned out that they had a cancellation and were just trying to fill it. I couldn't make it on such short notice, so they made another appointment for six weeks later - which was fine for me and months earlier than what they had originally told me. I've since heard that this is common with Dr. Berkson's office so don't get discouraged it they tell you that it will be six months before you can get in - if they have a cancellation, they will try and get you in earlier.

I flew into El Paso, Tx. on a Saturday in mid-February, 2009 as my appointment with the doctor was on a Monday and the place that I was staying at's office was closed on Sunday - I didn't want to rush it by flying in Monday morning. From there, I drove the 40 miles to Las Cruces, New Mexico. I had booked a room at Value Place as they offered kitchenettes. - plus it was fairly cheap compared to staying at a regular hotel - about $225.00 for the week. With my gluten/dairy free diet, I needed a place where I could prepare my own meals and save money. The motel offered for sale a cooking set, but I bought what I needed from a nearby Big Lots.

Dr. Berkson's office was two exits from my motel and easy to find. I was surprised that it was a "regular" doctor's office and not an enormous clinic - actually kind of on the small side. After about 45 minutes wait time (I chatted with Dr. Berkson's lovely wife, who worked in the office) ,I met with Dr. Berkson. I told him that it was an honor to meet him. He reviewed my labs which my own doctor had recently ordered and seemed satisfied with what I had with me, otherwise, he would have ordered others. After taking my history and examining me, he told me what he wanted me to do while I was there as well as follow-up instructions, which mostly centered around diet. He went over which foods to eat and which to avoid and stressed too, the importance of exercise every day.

for more on supplements and nutrition

He wrote me a prescription for 3.0 mg. of Low Dose Naltrexone, as well as a prescription for valium as he said that the LDN usually caused initial sleep disturbances. Our time seemed very short, although it was close to an hour appointment, but I wanted to ask more questions - he told me that we would meet again later on in the week. I might add that I had originally planned on a two week visit instead of the one week that I ended up staying due to one of my beloved cats going into renal failure right before I left town.
I was whisked immediately into the "treatment room" - a small comfortable room that probably had about 8 chairs with IV poles next to them. They asked me if I had eaten something as they insist that you do so prior to getting any ALA treatments. The nurse was very nice and matter of fact - she was great with her IV (btw - they use the "butterfly" set up's that was placed into my hand) - it took about 30 minutes and near the end, I was given a B-12 injection in my upper arm. I've since heard that they might have changed this over to a B Complex injection but I am not sure. At any rate, I felt fine and had no ill effects. Afterwards, I went to the front desk and checked out and was told the office schedule - they wanted me to come two times a day for IV's. I was also given directions to the Rexall drugs that provided the LDN and sleep aid prescription - I think that it was about $63.00 for a 90 day supply.

In the next week, I received 4 IV Alpha-Lipoic-Acid treatments and Vitamin B injections while I was receiving the IV treatment. The ALA uses up the B vitamins and it is important to take a good B complex while taking any ALA. The clinic also stressed that one must eat prior to getting the IV treatment, as the ALA can also lower blood sugar.

The treatment room was always full, with a variety of people getting treated for various disorders. Everyone was very nice and pretty cheerful for a medical clinic! I thought back to my years of being treated at a teaching hospital and the hours of waiting miserably in the waiting rooms. This was more like it!

They were disappointed that I could only stay for the week, but I told them that one of my beloved cats, Brooks, had just been diagnosed with end stage renal failure and that I had to get back to care for him. I had my last treatment on Friday morning and flew back to New Orleans the next day.
During the months that passed, I really didn't feel much better and thought that the LDN wasn't working. However, this was a period when I was so stressed out over my cat, Brooks, and his renal failure disease, that all I could concentrate on was his care, as well as caring for the other cats - taking Brooks to the vet every 2 days for sub-q fluids and almost losing him a couple of awful times. Fortuntately, Brooks finally allowed me to do the fluids on him myself and he stabilized after awhile. But the stress of his illness was having a toll on my well being.

Until..... I had my 4 month blood work results and doctor's appointment in early June and was floored by the results. My liver function tests were completely normal! My ALT/AST fell from 174/90 to 23/30 in 4 months - normal levels for the first time ever! And my viral load test went from over a million to 49,400! Amazing!

On a side note, check this out - back in 1986, a friend and I went to a road side garage sale and we bought a strange wall hanging for $1.00 - it "spoke to us":

It's still hanging on my wall - so when I got out to New Mexico, I saw nothing but red fire hydrants and took this picture:

Far out - maybe that poster wall hanging in 1986 was an omen of things to come - I just found it weird... ok, back to LDN and Dr. Berkson.......

I began to read more about LDN and joined several online LDN support groups, including "Hepatitis Children and Cam Alternatives", where several members were also using naltrexone to treat their various liver disorders. One member had treated her adopted daughter for Hepatitis B and eventually achieved sero-conversion - her liver enzymes also returned to normal and her viral level was undetectable.
Here is her story:

Treating Hepatitis B With Low Dose Naltrexone

Updated LDN May 2010 Labs

Updated Lab Results September 2010

More info about Low Dose Naltrexone:

LDN info

LDN Database

LDN SCIENCE

The Promise of Low Dose Naltrexone

From the recent 2009 Low Dose Naltrexone Conference where Dr. Berkson was the keynote speaker - he talks about ALA with LDN for treating Hepatitis C, Liver Cancer, Pancreatic Cancer, Lymphoma and many other disorders:

Introductory remarks - ALA - Hepatitis C

1) http://www.youtube.com/watch?v=WHyUfHqR4PA

2)Pet Scans - Treatment Protocol - ALA Explanation - Pancreatic Cancer with Mets to Liver (case to be published in December)

2) http://www.youtube.com/watch?v=xy65UGsVMac

Pancreatic Cancer with Mets to Liver - Hepatitis C with Liver Cancer -

3) http://www.youtube.com/watch?v=dRf8Xuqhb5Q

RA with Lymphoma from Humira - B Cell Lymphoma - Breast Cancer - Rheumatoid Disorders - Dermatomyositis -

4) http://www.youtube.com/watch?v=RXz3VIuyHHk

RA - SLE (Lupus) -

5) http://www.youtube.com/watch?v=nttilGKpJvU

ALA and purity; Asian products vs European - ALA discussion - Epstein-Barr Virus -

6) Dr Berkson Q & A Part One

http://www.youtube.com/watch?v=RsBN78Cl1s4

Lab Tests - Dosing of LDN and ALA - R Form Lipoic Acid - B Complex -

7) Dr Berkson Q & A Part Two:

http://www.youtube.com/watch?v=c29DAE4MGmo

Pancreatic Cancer & Thoughts on Treatment - ALA Gene Expression - Misc.

8) Dr. Berkson Q & A Part Three:

http://www.youtube.com/watch?v=nYxzDuKAdfI

Dr. Berkson interviews - must listen to or read!

Honest Medicine

Cancer Treatment Combining Lipoic Acid and Naltrexone, and,Lipoic Acid's Use As An Effective Cure for Severe Liver Disease

Not Ready For Any Support Group

2008-06-04T12:48:00.000-07:00

For many years, I have sought alternative or natural solutions to treat my Hepatitis C virus and have basically learned to "take charge of my health". and to question my doctors and whatever pharmaceuticals that they prescribe (or try to prescribe) to me.

I have refused the current interferon/ribavirin "treatment" for Hep-C for many reasons. The main reason is that it doesn't really work, particularly on my genotype (kind of strain) of 1b, and it is horrendously toxic and damaging to the immune system. I was fortunate that my biopsy done in 2003 showed only minor inflammation at Stage 1/Grade 1 and the virus has not really progressed - thankfully.

My initial information about hep-c (and most other disorders) came from the wonderful book, "Prescription for Nutritional Healing" - which I credit for saving my life. I had seen the book at Whole Foods Market sometime in the 90's and bought one at a garage sale around 1997-98. I learned about Milk Thistle and began taking it as I thought that it might provide my liver some kind of protection against my drinking - I had pretty much quit doing any kind of hard drugs by then, but I still loved my beer. At any rate, I found out that I had the virus in 2002 and my 2003 biopsy revealed (amazingly enough) little damage. What was also extremely amazing to me was that my liver was still functioning at all as I had several decades of extensive drug/alcohol use/abuse as well. And I mean serious, hard drugs too. I can only surmise that the milk thistle might have protected and repaired my liver enough to prevent anything worse.. But who knows? Matthew Dolan's great book, The Hepatitis Handbook is another great souce - I hope that he updates it someday.

I'm doing great with my own research and with the help of my great doctor, Dr. Kashi Rai. I will attempt to chronicle my battle with the Hep-C dragon, as well as my 7 herpes viruses, (HHV-1, HHV-2, Herpes Zoster, EBV (epstein barr), CMV, and the newly emerged HHV-6) as well as my gluten, dairy, nut, most seafood food intolerance. My favorite book about Celiac/Gluten intolerance is Dangerous Grains by James Braly and Ron Hoggan.

I share my life with 10 cats, now 9 since Brooks died in October.. ( of which 8 of them and I lived through the flood after the levee breaches following Hurricane Katrina) while I continue with the daily juggling act of surviving in post-Katrina New Orleans. Brooks had been battling end stage renal failure and I did the best that I could to help make his last bit of time, good time.

New Orleans is still recovering from Hurricane Katrina, or more accurately, the flooding caused by the breaches in the levees and floodwalls that were constructed by the Federal Government's U.S. Army Corps of Engineers. To learn why New Orleans flooded - and it was not due to a "natural disaster" but due to the "Worst Engineering Disaster in History" as cited by The American Society of Civil Engineers, check out Levees.org

I should know. My car broke down 2 days before Katrina - which was up until that Friday, still supposed to hit the panhandle of Florida. I had 8 cats and took care of dozens of feral cats in my neighborhood. I was broke and I refused to leave the cats behind.

The storm on Monday, August 29th, 2005, was pretty scary but afterwards, I was able to use my cell phone to call up friends to let them know that everything was ok. There were trees down and wind damage but really, not much rain at all. Then, the water started gradually coming up - and kept rising. Soon, I could hear dogs up and down the block barking and yelping until I didn't hear them anymore. My feral porch cat, Emerald, had ridden out the storm underneath the house, as did most of the feral cats in New Orleans - a city of raised homes. I heard her crying and I tried to get to her through the floor furnace - but when I got it opened , water gushed in........and I never heard or saw Emerald again.

The rest of the day and night are a blur to me now - my mind fractured off into the surreal - like watching a movie of someone else. I managed to climb up into a 7 foot high closet before passing out from shock, exhaustion and hyperthermia. But I woke several times during that long night and could hear my cats crying in terror.

The next morning, I woke and could hear what sounded like copters flying overhead. But all that I wanted to do was to lie there and never move again. One of the cats started crying pitifully from the front room and I opened my eyes to see her clinging to the curtains. This got me moving and out of the closet and down into the water that came up to my neck.

During the next hour, I was able to break out my back windows and swim 3 of the cats out to the carport roof - I could only find 2 carriers as they had sunk down somewhere on the floor in the murky water. The 5 others were placed up into the same closet that had given me refuge and another feral cat swam outside to cling onto the limbs of a tree.

I was rescued by a first responder in an airboat and taken to the railroad tracks nearby. Soon, the Missouri Coast Guard picked me and the 3 cats up and took us out to the Interstate. Eventually, a school bus took us, and other rescued folks and their pets to a shelter in Thibodaux, La. - about 40 miles west of New Orleans. I spent several days there in pretty primative conditions - no electricity, no phones, no email.

Family members were finally contacted and they came to get me 5 days later. It took another 2 days to get to where my Mom had evacuated to - in Birmingham, Alabama, where we had relatives. But throughout this ordeal, I was obsessed about the poor cats that I left up in that closet and I contacted every rescue group listed to try and get someone, anyone to go save them.

Finally, after getting no responses, I decided to go back to New Orleans to get them myself. Everyone told me that it would be impossible - the city was under lock down and no one was being allowed back in. Huh. Through an internet chat room, I met a man named Steve Vicknair who was in Houston, Texas. He had a boat and he wanted to help people like me rescue their pets.

And that is what we did. On September 11th, 2005 - two weeks! after Katrina, we got back to my still flooded apartment to find all cats still alive!!!! They had no food or water for all of that time - but they survived!!!!!

I stayed in Birmingham with my Mom (and the 8 cats) for 6 months until her health declined and she moved into an Assisted Living facility. Her house (and my inheritance) had taken in 11 feet of water and was very underinsured. She did have flood insurance as did most of the families in New Orleans - but the very minimum. We fought with Traveler's home owner's insurance for almost 2 years before they paid my Mom what she was owed. But the house could not be repaired.

I moved back to New Orleans in March of 2006 into an apartment in the Mid-City area - an area that had not gotten too much flooding compared to the 80% of the rest of the city. I got back involved with animal rescue, cats in particular...it was still a hairy time, with packs of dogs running wild in the streets and many, many starving animals. Things have somewhat improved but the animals of New Orleans still need so much help.

ARNO - Animal Rescue New Orleans - is still here. It is an all volunteer group that was formed shortly after Katrina - and has probably done the most out of all of the rescue groups:

The Katrina pictures that I managed to take when the water came up......and months later:

Katrina

The Cat Rescue pics:

Cat Rescue

Mom's House

My health gradually deteriorated in those first years back - my health care had been provided at Charity Hospital for about 3 years before Katrina, but it had to close - and is still closed. However their clinics still remained open - an emergency one had been set up at the Lord & Taylor department store near the devastated Superdome - that was so strange to go there for medical treatment, when a year earlier I had shopped for shoes.....

I developed shingles, and a strong chemical sensitivity - possibly due to the stress and perhaps being in the water during and after Katrina. I was in constant pain from fibromyalgia and my IBD often prevented me from leaving the house.

Thankfully, I was able to get Social Security disability - 3 years in the making - it only provides $693.00 a month but I do get Medicare, which enabled me to find Dr. Rai - the doctor who led me to Dr. Berkson - who changed my life.

I could never live anywhere else - New Orleans is and forever will be - the center of the universe!