Journal of Immunity

Vol 3 No 3 July-Sept 2005

Low-dose Prednisolone increased or stabilized CD4 counts and slowed or stopped HIV progression in two long-term studies in Germany (Eur J Med Res 2005)

Definitions:

HAART Highly Active Anti-Retroviral Therapy This is usually a combination of 3 or more drugs to treat HIV infection.

CD4 A type of white blood cell that is a master control cell of the immune system. Activated CD4 helper cells are targeted by the HIV virus.

Prednisolone and Prednisone are synthetic hormones that act in the body like natural cortisol (hydrocortisone) produced by the adrenal glands. They are anti-inflammatory, normalizes overactive components of the immune system like interleukin 6 and tumor necrosis factor that feed HIV progression to AIDS and cancer progression as well.

STI Structured Treatment Interruptions. Not to be confused with drug holidays that are taken at random, STI's are planned by doctors and patients to test the patients immune response to HIV without the intervention of anti-viral drugs. STI's are also used to reduce the side effects of prescription drugs and as interim periods to consider other treatment options.

Immune-based therapies do not target the virus directly, therefore, no viral resistance ever occurs. Immune-based therapies seek to balance the immune response in AIDS by reducing overactive humoral (antibody) response and promoting cell-mediated immune (CMI) responses that target infected cells.

The HIV virus actually promotes an ineffective humoral immune response to its presence and eventually wears out the immune system. Deficiency of immune response in not the problem in early stages of AIDS; dysfunction and imbalance of the immune system are the problem. You could say that immune based therapies seek to quiet an overactive and ineffective immune response and put the virus in a state of low activity or dormancy.

Low-dose prednisolone treats HIV-patients during structured therapy interruptions (STIs)

June 22, 2005 Eur J Med Res

Albrecht Ulmer, Bertisch-Mollenhoff, Frietsch B, Muller M., Eur J Med Res.2005 Jun 22;10(6):227-32. Schwerpunktpraxis, Stuttgart, Germany. albrecht.ulmer@gmx.de

BACKGROUND: A favorable development of CD4+ T cells was firstly noticed in therapy-naive HIV-patients without antiretroviral therapy (ART) taking 5 mg prednisolone daily. This observation led to the prescription of prednisolone during structured therapy interruptions (STI).

OBJECTIVE: To evaluate the effect of low dose prednisolone on pre-treated patients during STI.

METHODS: A retrospective analysis including all pre-treated patients with prednisolone therapy for > or =6 months during STI has been conducted. The patients with prednisolone onset right at the beginning of STI (n = 95) were compared with all patients without Prednisolone therapy during their first 6 months of STI (n = 49). Patients with prednisolone were divided into two subgroups: the ongoing STI-group and the patients with ART-restart.

Additionally, the development of all 33 patients from the control group having started prednisolone later during STI was documented. Irrespective of the time of initiation of prednisolone therapy during STI, the development of CD4+ T cells in all patients with prednisolone for >12 months during STI was analyzed. (n = 108)

RESULTS: The mean daily CD4+ T cell decrease during STI was significantly less pronounced in the prednisolone-group (-0.50 vs. -0.74 cells/day; p = 0.0361). The daily CD4+ T cell decline of the 33 patients from the control subgroup including patients with a later onset of prednisolone therapy was only -0.11 during a mean time of 715 days under prednisolone.

The CD4+ T cell count of the STI-patients treated with prednisolone for >12 months (n = 108; mean: 837 days +/- 64.6 (366-1,756 days)) decreased from 677/microl to 504/microl. - 51 of 81 patients (63%) included in 2-year-analysis showed stable CD4+ T cell counts (mean daily CD4+ T cell decrease: 0.08) and continued ART interruption.

CONCLUSION: This retrospective evaluation provides evidence that low dose corticosteroids are associated with less decrease of CD4+ T cell count in pre-treated HIV patients resulting in prolongation of the potential time of structured treatment interruptions for many HIV patients.

Low dose prednisolone reduces CD4+ T cell loss in therapy-naive HIV-patients without antiretroviral therapy.

Albrecht Ulmer, Bertisch-Mollenhoff, Frietsch B, Muller M., Eur J Med Res. 2005 Mar 29;10(3):105-9. Stuttgart, Germany. albrecht.ulmer@gmx.de

BACKGROUND: A favorable development of CD4+ T cells was noticed in therapy-naive HIV-patients without antiretroviral therapy (ART) taking 5 mg prednisolone daily. Based on these encouraging observations, prednisolone therapy in further HIV-patients without antiretroviral therapy was initiated.

OBJECTIVE: To evaluate the effect of low dose prednisolone on therapy-naive HIV patients without antiretroviral therapy.

METHODS: A retrospective analysis has been conducted comparing the development of CD4+ T cells, viral load and clinical outcome in all therapy-naive HIV-patients with (n = 65; CD4 > or =300/microl) or without (n = 136; CD4 > or =300/microl) prednisolone treatment for > or =6 months.

RESULTS: After 3 years, therapy-naive patients on prednisolone therapy showed a CD4+ T cell increase of +50.1/microl whereas in the untreated group a decrease of -186.1/microl (p = 0.0021) was noted. After 12 months, nearly twice as much untreated patients experienced a first-time CD4+ T cell loss of >100/microl or initiation of HAART due to clinical development compared to prednisolone-treated patients (64.1% vs. 35.0%).

CD4+ T cell increase was associated with viral load at baseline: Patients with lower viral loads at baseline (<30,000 copies/ml) showed a favorable development with statistically significant less drop-outs (defined as HAART-onset and/or prednisolone discontinuation for the prednisolone group) than patients with higher viral loads at baseline in the first 3 years in the prednisolone group.

Conclusion: Low dose prednisolone seems to be associated with a stabilization of CD4+ T cell count in therapy-naive HIV patients resulting in a pronounced prolongation of the potential time without HAART for many HIV patients.

Significant viral load reduction for HIV (posted on Keep Hope Alive Message Board by Dan on 6/12/05)

Last fall after testing positive for HIV my viral load was 33,600 (PCR). Four months ago it dropped to 7,180. Recently, it is down again to 3,850. My CD4's have gone from 370 to 687. I am on no HIV meds. My work and much expense has apparently paid off. I was so elated at the news. My doc wanted to know what I'm doing and said half jokingly that it should be patented. I told him what I do is complex and varies, and that I'm not really sure what is primarily responsible for the improvement. But he wanted me to tell him what I'm taking so I said mushrooms and selenium. He was in a hurry as usual so I left it at that.

I have been on a journey to improve my health for many years. Long story....short version, I have another chronic illness, genetic, that I battle on a daily basis, similar to Cystic Fibrosis. I am prone to severe lung infections and lowered immunity. Though not as lethal as HIV can be, it is an immense daily struggle. That is why the results of the recent testing is nothing short of miraculous. I think there is a cross over effect with the supplements I take...it improves immunity therefore it helps both conditions. Excuse me for going on, but I felt I should give some relevant background info. How I (seemingly) stopped the progression of HIV: Mushrooms, many kinds, but primarily Maitake, Shitake, Reishi, Royal Agaricus. I take so many other things but let me highlight a few- NAC, plant based selenium, large doses of Vitamin A and Beta carotene, 5 mg of prednisone, oxygen supplements, including ozone, hydrogen peroxide, etc., probiotics, lots of vitamin C in the form of Rosehips powder and fresh fruits and veggies.

I often take herbs such as licorice, heal-all (prunella vulgaricus) lots of cayenne and fresh, raw ginger, ginseng, oregano, eleuthero. That is just some of the things I have tried consistently. I tend to rotate things and eat as much fresh, organic food as possible. My gut feeling is that the mushrooms were probably the biggest boost to my immune system, but I really can't be certain. I have worked hard, prayed, studied, spent so much money, but I made up my mind that I was going to beat this virus without meds! ( Well, maybe a little prednisone)

Thanks to all of you for sharing and thanks especially to Mark. You have helped me more than you will ever know. Dan

Note: To access the posting and Dan's email go to the Message Board at keephopealive.org

Since 1990 Albrecht Ulmer has treated over 200 HIV+ patients using low-dose Prednisolone

M Konlee / C LeBeau

With 166 articles published in peer reviewed medical journals, Albrecht Ulmer is a clinician and researcher who is well known worldwide. His first experience using prednisolone for HIV started in 1990 and his views, based on his clinical experience and more recently controlled studies, is that low dose prednisolone helps persons with HIV or AIDS to increase or maintain higher CD4 counts and can delay the onset of anti-retroviral therapy and in some instances may eliminate the need for it for several years.

Persons taking a break from anti-retroviral therapy could delay the return to HAART therapy by several months or years. This treatment has broad implications worldwide as it is very low cost, is a simple once a day pill and is so low a dose, just 5 mg a day, as to have no adverse side effects. None of the lipodystrophy, heart disease or other conditions associated with protease inhibitors.

WOW! Why isn't this story making headlines? Probably because many publishers cannot make sense out of using an immunosuppressive drug for an immune deficiency disease. This is because the earliest experts defined AIDS as an immune deficiency disease at the time (opportunistic infections and CD4 decline).

The truth about HIV infection and AIDS is that it is not a deficiency disease at all but an illness of immune system over-activity (TH2 type cytokines), B cell and excess antibody production.

HIV infection leads to AIDS not because of under-activity of the immune system but because of over-activity and specifically over-activity of certain immune messengers like interleukin 6 (IL-6) and tumor necrosis factor (TNF) that are inflammatory in nature.

Low dose prednisolone, prednisone or hydrocortisone have anti-inflammatory effects and reduce IL-6 and TNF, antibody production that is not effective against the virus and lowers humoral immune system activity. HIV needs an agitated and active immune system, especially the humoral arm - B cells and Plasma cells that produce endless ineffective antibodies in order to keep replicating. Essentially, HIV stimulates the immune system into over-activity, eventual exhaustion and self destruction. Due to rapid mutations and quirks in the design of HIV, the humoral antibody response is not effective because it can only target the virus outside the cells, not inside.

What is effective is cell mediated immune responses and CD8 cytotoxic lymphocytes that target HIV infection inside the cells. Unfortunately, elevated IL-6 and TNF suppress these responses. Where low dose prednisolone (PRD) et al are effective is that they reduce the gasoline the IL-6 and TNF that drives HIV activity.

Prednisolone also deactivates receptors on the CD4 cells making them less vulnerable to HIV infection. Low dose prednisolone is a significant low cost breakthrough in treating HIV and AIDS with worldwide implications. Because it is low cost, pharmaceutical companies could stand to lose billons of dollars in sales of anti-retroviral drugs.

As a treatment for HIV, low dose prednisolone may get the attention it deserves when "experts" finally realize that is immune balancing and stabilizing and that describing it as immunosuppressive is a half-truth. This is because broad immune suppression occurs primarily at high doses and when used long term. (Example: 30 to 100 mg daily). Serious side effects can also occur at high doses including excessive weight gain. High dose prednisolone will totally suppress the antibody response leaving a person vulnerable to colds and flu's and other common infections. That is why more is not better when it comes to using prednisolone, prednisone or hydrocortisone. You could say "a little dab will do ya."

None of these adverse effects occur at the very low dose of 5 mg daily. Low dose prednisolone is a totally different treatment than high dose prednisolone. The time is due to report these differences responsibly as the correct dose could someday be a matter of life or death for millions of people worldwide.

Response to levamisole and low-dose prednisolone in 41 patients with chronic oral ulcers: a 3-year open clinical trial and follow-up

Lu, S Y; Chen, W J; Eng, H L. Lu SY, Chen WJ, Eng HL. Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 1998 Oct;86(4):438-45. [Article in English] Department of Dentistry, Chang Gung Memorial Hospital, Kaohsiung, Taiwan, Republic of China.

OBJECTIVE: The purpose of this open clinical trial and follow-up study was to evaluate the short-term and long-term clinical efficacy of levamisole used with low-dose prednisolone in 30 patients with oral lichen planus, 6 patients with erythema multiforme, 3 patients with mucous membrane pemphigoid, and 2 patients with early pemphigus vulgaris.

STUDY DESIGN: All patients were given 150 mg/day of levamisole and 15 mg/day of prednisolone for 3 consecutive days each week, along with topically applied dexamethasone orobase (dexaltin).

RESULTS: Twenty-three patients showed dramatic remission of signs and symptoms within 2 weeks; 18 patients experienced partial remission. Forty patients reported significant pain relief, and almost none showed evidence of oral ulcerative lesions after 4 to 8 weeks of treatment. In contrast, 1 patient with oral lichen planus with allergy to levamisole reported a partial response from prednisolone alone. All 29 patients with oral lichen planus remained free from symptoms for more than 6 months. All 6 patients with erythema multiforme, all 3 patients with mucous membrane pemphigoid, and both patients with pemphigus vulgaris also remained free from symptoms for 2 to 3 years.

There were few side effects from the treatment; there was minor skin rash from levamisole in 1 case of oral lichen planus. We also designed a flexible plastic carrier for topically applied dexaltin in the treatment of diffuse atrophic or ulcerative gingivitis.

CONCLUSIONS: The addition of levamisole to prednisolone may produce improved results in the management of erosive lichen planus, erythema multiforme, mucous membrane pemphigoid, and early pemphigus vulgaris.

Alopecia universalis treated with oral cyclosporine A and prednisolone: immunologic studies.

Teshima, H; Urabe, A; Irie, M; Nakagawa, T; Nakayama, J; Hori, Y. Teshima H, Urabe A, Irie M, Nakagawa T, Nakayama J, Hori Y. Int J Dermatol. 1992 Jul;31(7):513-6. Department of Psychosomatic Medicine, Faculty of Medicine, Kyushu University, Fukuoka, Japan.

Alopecia universalis is a refractory condition. Although the cause of this disease is unknown, immunologic abnormalities have recently been suspected. Thus, we treated six cases of refractory alopecia universalis with immunotherapy.

Oral administration of cyclosporine A (2.5 mg/kg) and prednisolone (5 mg/day) resulted in marked symptomatic improvement. Cyclosporine A did not produce any side effects because the administered dosage was relatively low. At present, more than 6 months after the cessation of treatment, recurrence of alopecia has not been seen.

Oral administration of low-dose cyclosporine A and prednisolone is considered to be an effective treatment for this disease. Immunologic examination of peripheral blood demonstrated improvement of immunologic function.

In particular, CD8-positive T cells, NK cells, and C3, which had been reduced, were increased. A reduction in active CD4 cells, eosinophils, and circulating immune complexes was observed.

Histology with fluorescent antibodies showed T-cell infiltration around the hair matrixes. This phenomenon was no longer observed after treatment. These improvements in immunologic function were seen in parallel with the resolution of the clinical symptoms, indicating that immunologic abnormalities are related to this disease

Rwandan women's CD4 count increased on Prednisone therapy

An article dated August 2004 and published by www.amfar.org (American Foundation for AIDS Research) by Gunjan Sinha is titled "A Place in the Sun for Immuno suppressants. "

The article discusses the past 14 years experiences of Albrecht Ulmer in using prednisone or prednisolone to treat persons with HIV or AIDS. His first experience with prednisone was in 1990 when an HIV positive patient with recurrent fevers and fatigue could barely get out of bed although using AZT for HIV at the time. In desperation, he tried an anti-inflammatory drug prednisione that he added to his regimen. The patient quickly improved and that was Ulmer's first clue that Prednisone might help people with HIV.

Sinha reports that 7 years later, an HIV-positive Rwandan women walked into Ulmer's large Stuttgart practice complaining of fatigue and depression. Her CD4 count was not low enough to start her on HIV meds, so he prescribed prednisone. She began to feel better and her CD4 counts inched higher. In a few years, they had nearly doubled.

Since 1997, Ulmer has prescribed prednisone to over 200 of his HIV patients, some not yet on the HIV meds and some no longer taking the HAART medications. Ulmer reports that CD4 counts have stabilized or increased in up to 70% of his patients. He states he has had the best success in persons with CD4 counts of 300 of higher and viral loads of 30000 or less.

For several years, his colleagues at J.W. Goethe University in Frankfurt have ignored him. Now with two published studies in the European Journal of Med Research in 2005, the time is overdue for the both the media and the medical establishment to start paying attention to his work.

With growing numbers of deaths from heart attacks in persons using protease inhibitors and drug cocktails, the time is overdue for new non toxic treatments that prevent opportunistic infections and HIV progression to AIDS.

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From ACRIA Winter 2001/02 - Vol. 11 No. 1 Wondering Aloud: Theories of One Long Term Non Progressor

by Mark Milano<

/H4>

The following article is reprinted with permission of the author and can be found online at http://www.acria.org/treatment/treatment_edu_winterupdate2001_2002_wondering.html

Speculation abounds as to what makes a long-term non-progressor (LTNP), as do definitions of exactly what a LTNP is. Some have looked at the maintenance of HIV-specific CD4 cells, others at cytokines like IL-10, and still others hope to create LTNPs by using therapeutic vaccines. In my own case, I've wondered for years if I may have stumbled on a way to slow disease progression by the use of a simple, cheap and non-intuitive treatment.

I trace my infection back to 1981 or earlier, based on frozen blood from 1984 and a CD4 count below 500 in March of 1982. Though I'm still healthy twenty years later and have never taken antiretrovirals, I don't really fit into the category of LTNPs, who have normal CD4 counts around 1,000. My CD4 count has hovered around 300 for years, and my only clear-cut symptom of HIV disease has been occasional thrush (though I do struggle to maintain my pre-HIV bodyweight).

My personal theory has to do with a fortunate hospitalization in 1985. After months of flu-like symptoms and a drop in weight of thirty pounds, I was hospitalized due to extremely high calcium levels. I was finally diagnosed with sarcoidosis, an autoimmune disorder not associated with AIDS in which the immune system attacks one's own tissues. Prednisone, a corticol steroid, cleared up my symptoms immediately. A year later I stopped the prednisone, but I eventually went back on it when my symptoms returned. The trick was moving to alternate-day dosing, which eliminated all side effects but still controlled the sarcoidosis.

I thought my body was controlling HIV on its own, but I was surprised to learn years later that there was some evidence the prednisone might actually be the cause of my good health. HIV chronically stimulates the immune system, causing the over-production of a number of immune system components such as immunoglobulins, tumor necrosis factor and alpha-interferon. It also increases activation of T-cells, which leads to greater HIV replication. Using immune-suppressants to dampen some of this over-stimulation has been proposed, and some small studies have shown benefits for prednisone in people with HIV, but the data is far too sketchy to suggest using this approach in clinical practice.

The National Institutes of Health (NIH) began a study in 1999 to specifically look at the benefits of prednisone in people with HIV. Unfortunately, they took the "more is better" approach, using 40 mg a day - far too high to take on a long-term basis (I'm currently on 15 mg every other day). When pre-clinical indications of bone loss were found, the study was stopped. Since the NIH rarely re-visits failed hypotheses, we'll most likely never find the answer as to whether a drug like prednisone could be beneficial if started early in disease.

Now, my lack of progression could be due to the sarcoidosis itself - the theory being that the sarcoidosis is creating excess CD4 cells and HIV is killing them off, leading to a steady state. But since my sarcoidosis is so well-controlled by the prednisone, I don't think that's the case. One could also say that I'm just a very slow progressor, but whenever I stop the prednisone I feel far less healthy, and HIV-related symptoms like sinusitis and rash start appearing.

It bothers me that I may have chanced on an effective way to slow HIV disease, but that no one else will benefit. If low-dose prednisone actually works to slow progression, it would be the answer for people who don't have advanced HIV disease, particularly for those in developing nations who can't afford combination therapy which costs over $10,000 a year. Prednisone is one of the cheapest drugs in the world, and a regimen of one pill every other day is feasible in even the most resource-poor settings.

Of course, the very fact that prednisone is cheap and off-patent makes it extremely difficult to find funding for the controlled studies needed to prove its benefit. And the necessary trial would be considered unethical by many, since it would need to randomize people to either prednisone or placebo, with no other antiretrovirals to mask disease progression. But with the new U.S. recommendations that treatment can be delayed until CD4 counts drop below 350, and with the British recommending people wait until 200, a trial could be designed for those with higher CD4 counts.

So here I sit, wondering if it is the prednisone that's keeping me healthy, wondering if there will ever be a way to prove it, wondering what would have happened to me if I hadn't started the drug sixteen years ago, and wondering if we aren't missing entirely different ways to control HIV disease, since almost all research focuses on antiretrovirals and not on treatments that support the immune system.

Mark Milano is a treatment educator at ACRIA and a longtime AIDS activist. He can be reached at ACRIA, 230 W 38th St, 17th Flr, NY, NY 10018 212-924-3934 or at mmilano@acria.org

20 yr Case Report Mark Milano's use of Prednisone to treat HIV

by Conrad LeBeau

POZ magazine reports in August, 2005, in an article called "haart-less and healthy" about New Yorker Mark Milano who began using prednisone to treat Sarcoidosis in 1985. Mark Milano is a New York HIV-Treatment educator who has never used anti-viral HIV drugs to treat his condition. The Prednisone cleared up the Sarcoidosis in 1985 and he found that as long as he used the prednisone, his CD4 counts also held up.

Milano states he was first infected with HIV in 1982 and that his CD4 count was as low as 74 at one point. Since 1985, he has kept his CD4 count up using a low dose of Prednisone. The dose he currently uses is 15 mg every other day which averages out to 7.5 mg daily. His current stats are CD4's - 400 and viral load 475K. He has and continues to remain free of opportunistic infections.

He states: "Dosing is the key..I take 15 mg every other day, with only minor muscle loss and fat gain (which may be just be my age). " His theory is that HIV needs activated CD4 cells to reproduce, and low dose prednisone reduces immune activity just enough to slow down HIV. He adds that if his CD4's drop to 200 or less he would go on the HIV meds.

What makes Milano's case interesting is that in spite of the high viral load, his CD4 counts stay up high enough to prevent the opportunistic infections that are the hallmark of AIDS. That this happens in spite of a viral load of 475,000 is amazing. What this suggests is that the viral load is neutered or made ineffective by the presence of the low dose prednisone.

Prednisone, like its counterparts, methyl-prednisolone and hydrocortisone, lower interleukin 6 and TNF levels, two TH2 cytokines that are overactive in both cancer and AIDS progression. Normalizing these two cytokines holds great promise in stopping both HIV progression to AIDS and cancer progression.

Unfortunately, development of low cost treatments for HIV/AIDS, cancer and other life long illnesses are not top priorities for pharmaceutical companies where Wall Street stockholders looks at the bottom line of profits as the essential priority. Nor has the US Congress or the White House directed the National Institute of Health to use its resources to find low cost treatments for AIDS and cancer. The time for change is long overdue.

Combining Immune Modulators during Strategic Treatment Interruptions

It appears from the published research of Ulmer A et al in Germany that low dose prednisolone could eliminate the need for protease inhibitors and drug cocktails in about two-thirds of the HIV + population taking drug cocktails. This would not only save taxpayers billons of dollars it would reduce and eliminate the side effects of drugs that affect a significant number of persons taking using them - effects including heart disease and osteoporosis.

Taking one pill a day (5 mg of prednisolone) most likely in the morning but with no rigorous or strict dosing schedule will also reduce a lot of stress on the population affected with HIV. Based on current published research the best candidates are those with viral loads of 30000 or less and a CD4 count of 300 or more.

These candidates could opt to try low dose prednisolone alone or in combination with other immune modulators like low dose Naltrexone (4.5 mg taken before bedtime once a day), raw mushrooms, garlic, plant based selenium, licorice root tea (increases adrenal cortisol output) and fish oil supplements and to consider thymic proteins if an increase in platelet counts is desired.

Persons with HIV should do their own online research at the National Library of Medicine, medical libraries and bring these articles to their physicians attention. Discuss with your doctor the merits of a strategic treatment change using an immune-based treatment for HIV like 5 mg of prednisolone daily. By monitoring CD4 counts, you can determine if you will need stronger medicine at some future time such as when your CD4 count gets close to 200 as you do not want it to fall below that number. Taking a year or two off drug cocktails should reduce the risks of viral resistance and increase the useful shelf life of these same drug combinations. As in all matters, your physician may agree or may have a different opinion.

Chronic immune activation and inflammation in the pathogenesis of AIDS and cancer.

Dalgleish AG, O'Byrne KJ. Adv Cancer Res. 2002;84:231-76. Department of Oncology, St George's Hospital Medical School, London

Infection with the human immunodeficiency virus (HIV) invariably leads to the development of acquired immunodeficiency syndrome (AIDS) in most infected humans, yet does so rarely, if at all, in HIV-infected chimpanzees. The differences between the two species are not due to differences in cellular receptors or an inability of the chimpanzee to be infected, but rather to the lack of pan-immune activation in the infected primate. This results in reduced apoptotic death in CD4+ T-helper lymphocytes and a lower viral load.

In humans the degree of chronic immune activation correlates with virus load and clinical outcome with high immune activation leading to high viral loads and the more rapid progression to AIDS and death. The type of immune perturbation seen in HIV-associated AIDS is similar to that of chronic graft-versus-host disease (GVHD) where reduced cell-mediated immune (CMI) responses occur early in the course of the disease and where humoral responses predominate.

A reduced CMI response occurs in a number of chronic infectious diseases, including tuberculosis and leishmaniasis. More recently, it has become increasingly apparent that the CMI response is suppressed in virtually all malignant diseases, including melanoma and colorectal and prostate cancer. This raises the possibility that, as the malignant process develops, the cancer cells evolve to subvert the CMI response. Moreover, the reduced CMI response seen in colorectal cancer (CRC) patients is completely reversed following curative surgery strongly supporting the hypothesis that CRC can suppress the systemic immune response.

Wound healing, ovulation, embryo implantation, and fetal growth are all associated with suppressed CMI and neovascularization (the formation of new blood vessels) or angiogenesis (the formation of new blood vessels from an existing vasculature). If unresolved, wound healing results in chronic inflammation, which can give rise to the phenomenon of "scar cancers."

Indeed all the chronic inflammatory conditions known to be associated with the subsequent development of malignant disease, including chronic obstructive airway disease (COPD), ulcerative colitis (UC), and asbestosis, give rise to similar proangiogenic, suppressed CMIIn keeping with this CMI-associated cytokines such as interleukin (IL)-2 and interferon (IFN)-gamma tend to be antiangiogenic, whereas humoral cytokines such as IL-6 tend to be proangiogenic. ..If the observed association is relevant to carcinogenesis, then treatments aimed at reducing the components of these inflammatory conditions may be useful both in the setting of chemoprevention and the therapeutic management of established disease.

Note: Anti-inflammatory treatments for overactive humoral immune responses (i.e. antibody production / Il-6/ TNF) include hydrocortisone and pharmaceutical equivalents like prednisolone and prednisone. Five mg of prednisolone or prednisone is the equivalent of about 20 mg of natural hydrocortisone, an anti-stress adrenal hormone.

Case report: Beets may have helped reduce Hepatitis (HCV viral load)

C LeBeau

July 31st. Today I talked to a person in Milwaukee (H.H.) who has been dealing with hepatitis C for several years. H.H. has been taking interferon prescribed by his doctor for over 8 years on and off. About 2 months ago, I told H.H. that methyl donors in beets should help protect his liver and might help lower the HCV viral load. In May, H.H. began to eat a serving of beets daily while continuing on the interferon.

He told me he ate one 15 ounce can of beets daily and drank the juice in the can also. He did this for 2 months. He did not juice raw beets. Today, 7/31/05, he reports his last lab results since adding beets to his daily diet for the past two months. The latest test results showed the HCV virus is now non-detectable. The doctor told him he thinks he is cured and has stopped the interferon but will monitor his blood for the next several months to see if the virus comes back.

H.H. however, does not give special credit to the beets which he said he ate tons of, but to God. He said several people prayed for him and that God has answered his prayers. I will continue to follow this case and report any new findings. To his thoughts I might add: God created beets.

Update: The significance of this case is that H.H. are canned beets and did not even try to make raw beet juice. This also raises the question of what a can of cooked beets might do to treat cancer and a wide range of other conditions linked to elevated levels of interleukin 6. Early in September, H.H. reported the HCV viral load had returned after he had stopped the daily beet serving and had also stopped using the interferon. He has again resumed eating the beets and his doctor is giving him interferon at half the regular dose. While on the interferon treatments for the past 8 years, his HCV viral load never reached non-detectable levels until he started on the beet regimen. It is evident he stopped the beet therapy too quickly to have a cure. He can always retry. It should be noted that the cases of cures for hepatitis C are few and far between. In view of his results the use of beets and most certainly plant based selenium should be part of a treatment protocol.

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