• Welcome to Phoenix Rising!

    Created in 2008, Phoenix Rising is the largest and oldest forum dedicated to furthering the understanding of and finding treatments for complex chronic illnesses such as chronic fatigue syndrome (ME/CFS), fibromyalgia (FM), long COVID, postural orthostatic tachycardia syndrome (POTS), mast cell activation syndrome (MCAS), and allied diseases.

    To become a member, simply click the Register button at the top right.

Natural Alternatives to Rituximab?

Messages
3
I'm wondering if there's a substance or combined substances in the natural world (non-synthetic) that would mimic Rituximab's effects? I think many of us are excited about Rituximab but don't see it as being widely available to ME/CFS patients in the near future. I just want to live a normal life again.
 

LisaGoddard

Senior Member
Messages
284
Hi, There is a component called halofuginone in the chinese herb chang shan which is being studied for its use in autoimmune diseases but not sure that it works like rituximab. I've tried chang shan but the whole herb must have some immune stimulating properties as I got very bad inflammation symptoms (as I do now with even mild immune stimulants) and had to stop.
I would be really interested to know is anyone has any suggestions on a rituximab alternative so will be checking this thread. Hopefully, someone has some ideas.
Lisa
 

kday

Senior Member
Messages
369
http://www.ncbi.nlm.nih.gov/pubmed/10726985
The agents found to induce programmed cell death (measured either morphologically or flow cytometrically) included extracts of plants like mistletoe and Semicarpus anacardium. Isolated compounds like bryonolic acid (from Trichosanthes kirilowii var. Japonica, crocin (from saffron) and allicin (from Allium sativum) have also been found to induce programmed cell death and therefore arrest proliferation. Even Chinese herbal medicine "Sho-saiko-to" induces programmed cell death in selected cancerous cell lines. Of considerable interest is the finding that Panax ginseng prevents irradiation-induced programmed cell death in hair follicles, suggesting important therapeutic implications. Nutraceuticals (dietary plants) like soya bean, garlic, ginger, green tea, etc. which have been suggested, in epidemiological studies, to reduce the incidence of cancer may do so by inducing programmed cell death. Soy bean extracts have been shown to prevent development of diseases like polycystic kidneys, while Artemisia asiatica attenuates cerulein-induced pancreatitis in rats.
Not sure if that helps.
 

Snow Leopard

Hibernating
Messages
5,902
Location
South Australia
I'm pretty sure there is nothing 'natural' out there that will have the specificity of a monoclonal antibody. (Unfortunately).

There might be 'natural' compounds that target b-cells, but anything with a strong effect will also have strong side-effects due to lack of specificity.
 

Tia

Senior Member
Messages
247
I've heard theres a thing called "Devils claw" that is some kind of plant from the deep djungle that's supposed to allieve inflammatory diseases and so should work for me, but the trick is to be VERY careful with it since if you use too many drops, it sets the nervous system going which gives major anxiety so one should go up in dosage slowly and carefully..
 

Hip

Senior Member
Messages
17,824
• Low-dose naltrexone (LDN) depresses B cell production, which might explain why LDN is of benefit for ME/CFS.
QUOTING: Kofi, from the Usenet newsgroup alt.support.ibs:

"Another interesting paper from Bonneau.
Since low-dose naltrexone stimulates the opioid growth factor axis, this indicates that LDN acts as a B-cell depletion agent similar to much more expensive specialty drugs like Rituxan/Rituximbab and the recently approved BLYS/BAFF inhibitor for lupus (Benlysta?). Thus LDN may be broadly appropriate not just for cancer but also for autoimmunity because of its broad actions on the Opioid Growth Factor Receptor system."

Source: Low-dose naltrexone depresses B cell production; implications for autoimmunity.

The Bonneau paper: B lymphocyte proliferation is suppressed by the opioid growth factor-opioid growth factor receptor axis: Implication for the treatment of autoimmune diseases.


• Kava kava herb (Piper methysticum) if used long-term can deplete lymphocyte cells (lymphocytes comprise B-cells, T-cells and NK cells), so kava kava might deplete B-cells, but also indiscriminately deplete T-cells and NK cells.

Thus low-dose naltrexone plus kava kava could be an interesting experiment in treating ME/CFS, as this combo might provide some rituximab-like effects.

The only thing of concern with kava kava is that some forms can be toxic to the liver (hepatotoxic), but it is kava leaf or kava stem that is toxic, not kava root, I understand, so make sure you get the root. Acetaminophen / paracetamol should not really be taken with kava.
 
Messages
445
Location
Georgia
Kava kava is really hard to drink. I tried it in Hawaii and it tasted like boiled mud. I didn't get much of an effect, except my lips turned numb. I also took Ldn for several months and didn't notice any change.
 

alex3619

Senior Member
Messages
13,810
Location
Logan, Queensland, Australia
I'm pretty sure there is nothing 'natural' out there that will have the specificity of a monoclonal antibody. (Unfortunately).

There might be 'natural' compounds that target b-cells, but anything with a strong effect will also have strong side-effects due to lack of specificity.

Hi Snow Leopard, this is substantially my understanding. Due to the mechanism of action of Rituximab, any "natural" therapy that mimics it would be more dangerous than Rituximab, with one important exception.

Rituximab is a natural antibody. Its just isolated and purified. Its not a synthetic drug, though it was tested and marketed as one. The only equivalents would be alternative B cell targeting antibody based drugs.

Bye, Alex
 

Dolche

Dolche
Messages
25
I'm wondering if there's a substance or combined substances in the natural world (non-synthetic) that would mimic Rituximab's effects? I think many of us are excited about Rituximab but don't see it as being widely available to ME/CFS patients in the near future. I just want to live a normal life again.
All you have to research is iv nutraceuticals protocols for cfs. It falls under orthomolecular medicine many have been help by highdose iv vitamin c and hydogenperoxdide iv,myers cocktail iv, gluthathione, plant sterols. They are extremely beneficial if you stick to them for months based on your needs and keep the ante. They guaranteed and improvement in functionality. In addition to vegetable, fruit, good fats, fish, organic chicken, noooo sugar , nooo bread. And juicing at least twice a day. Take daily vitamimns , cq10, omega 3,probiotics,b12 complex, niacin, goji berry juice,coconut oil .

Rordon clinic is helpful?....Research vitam c it's a miracle antioxidant our body needs and it's not produced by our bodies. Cfs people need loooooots of it. Kills viruses, but only makes you tired ...herx is more tolerable no pain??? Vitamin c is antimmlamatory!

http://www.riordanclinic.org/patient-care/testimonials/

you need a good doctor holistic immunologist, oncologist , or endocrinologist or orthomolecular, they need to understand our immune panels.

Blessings


Julia
 

Hip

Senior Member
Messages
17,824
Here is something that I just ran across that might be as close as we can get as a natural alternative, but it still appears to have unforseen drawbacks.

http://www.lifescript.com/health/ce...native_treatments/tripterygium_wilfordii.aspx


This Tripterygium wilfordii herb looks interesting.

"Preparations of Tripterygium wilfordii hook have been used in the treatment of a number of autoimmune and inflammatory diseases since the 1960s. Accumulated data from the clinical trials suggest efficacy of this treatment in a number of rheumatic diseases, including rheumatoid arthritis and systemic lupus erythematosus." 1

"Extracts of Tripterygium wilfordii hook are effective in traditional Chinese medicine for treatment of immune inflammatory diseases including rheumatoid arthritis, systemic lupus erythematosus, nephritis and asthma." 1
 

August59

Daughters High School Graduation
Messages
1,617
Location
Upstate SC, USA
Hip & @ SL - It's those adverse effects that almost had me comeback and delete this post. I know that the majority of us would be very cautious and do our homework, but it's that one that didn't and just by luck found it available on the net, order it and ended up in hospital.

I almost wish there was a "Senior Thread", but you know how that goes as it would not take long to get pm'd to someone. If either one of you wants to move it to a 3-way conversation or just 2 is fine.

We can leave it there and I can edit with a strong precautionary statement. It was interesting to me because I was planning on looking at it much further and see how the adverse effects held up through more research, but I haven't been able to do dit due to my disability hearing popping up at the last minute.
 

Hip

Senior Member
Messages
17,824
I know that the majority of us would be very cautious and do our homework, but it's that one that didn't and just by luck found it available on the net, order it and ended up in hospital.

You took thunder god vine (Tripterygium wilfordii) and ended up in hospital?

Very sorry to hear that. What exactly happened? What side effects did you experience that needed hospital treatment?

(I put the above in red, in order make sure everyone sees it. Perhaps you might add the same sentence in red to your above original post about Tripterygium wilfordii, just to be on the safe side.)

It is true that people with ME/CFS can sometimes be very sensitive to even innocuous, safe supplements that cause no problems in anyone else. But Tripterygium wilfordii does seem to have a high rate of significant side effects. See here:

Thunder god vine (Tripterygium wilfordii) side effects:

Thunder god vine can cause severe side effects and can be poisonous if it is not carefully extracted from the skinned root. Other parts of the plant—including the leaves, flowers, and skin of the root—are highly poisonous and can cause death.

There are no consistent, high-quality thunder god vine products being manufactured in the United States. Preparations of thunder god vine made outside the United States (for example, in China) can sometimes be obtained, but it is not possible to verify whether they are safe and effective.

A number of participants in the NIAMS study experienced gastrointestinal adverse effects such as diarrhea, indigestion, and nausea, as well as upper respiratory tract infections. Reference: 1

A small molecule, Triptolide, derived from Tripterygium wilfordii has been shown to disrupt mitochondrial function in cells and is under investigation as an anti-tumor agent or to suppress auto-immune disorders. Reference: 1
 

August59

Daughters High School Graduation
Messages
1,617
Location
Upstate SC, USA
I didn't take it and end up i the hospital.

I said it would be my luck for putting it up on the forum that someone will go buy some without researching it really good and end up in the hospital.

That's why I thought very hard after I put it up there that I should go back and delete it because I am a little scared someone "in a desperate attempt" to find relief may finf some and end up hurting themselves.

Very sorry for the confusion!
 

beaverfury

beaverfury
Messages
503
Location
West Australia
Plasmapheresis

An important use of plasmapheresis is in the therapy of autoimmune disorders, where the rapid removal of disease-causing autoantibodies from the circulation is required in addition to other medical therapy. It is important to note that plasma exchange therapy in and of itself is useful to temper the disease process, where simultaneous medical and immunosuppressive therapy is required for long-term management. Plasma exchange offers the quickest short-term answer to removing harmful autoantibodies; however, the production of autoantibodies by the immune system must also be suppressed, usually by the use of medications such as prednisone, cyclophosphamide, cyclosporine, mycophenolate mofetil, rituximab or a mixture of these.

Sounds feasible. Wonder if its been tried for me/cfs?
 

user9876

Senior Member
Messages
4,556
An important use of plasmapheresis is in the therapy of autoimmune disorders, where the rapid removal of disease-causing autoantibodies from the circulation is required in addition to other medical therapy. It is important to note that plasma exchange therapy in and of itself is useful to temper the disease process, where simultaneous medical and immunosuppressive therapy is required for long-term management. Plasma exchange offers the quickest short-term answer to removing harmful autoantibodies; however, the production of autoantibodies by the immune system must also be suppressed, usually by the use of medications such as prednisone, cyclophosphamide, cyclosporine, mycophenolate mofetil, rituximab or a mixture of these.

Sounds feasible. Wonder if its been tried for me/cfs?


ECP (extracorporeal photochemotherapy) is now being used to treat GVHD as an alternative to Prednisone. I think there has been some sucess in treating auto immune disease in the past. It seems to work by performing chemo using drugs and light on the t cells. Side effects seem low but it is very expensive.
http://www.nature.com/leu/journal/v17/n11/full/2403114a.html

The ECP process consists in the withdrawal by apheresis, of peripheral blood mononuclear cells (MNC) of the patient, the ex vivo incubation of MNC with the photoactivable drug 8-methoxypsoralen (8-MOP), followed by UV-A irradiation, and, finally, the infusion of photoinactivated cells to the patient. Between 10 and 15 billions of MNC containing the pathogenic T cells are treated in one ECP procedure.
The mechanism seems unclear but they talk about downregulation of the activity of T-cell clones in auto immune diseases (http://www.ncbi.nlm.nih.gov/pubmed/15214889)


http://www.ncbi.nlm.nih.gov/pubmed/19369039
Recent studies demonstrated that ECP downregulates the immune response and induces tolerance by regulatory T cells. Other studies suggest that the mechanism of ECP also involves the recruitment and involvement of additional immune cells. Although immune tolerance induced by ECP is the most likely mechanism of the clinical efficacy of ECP it is not clear how ECP, both activates tumor immunity against cutaneous T-cell lymphoma and induces tolerance in autoreactive disorders. Further studies are necessary to determine the details of the underlying mechanisms of action.