Inhibiting Babesia ARTICLE IS ONLY PARTIALLY QUOTED Take a look at the whole thing
"We examined the inhibitory effects of three heparins on the growth of Babesia parasites. The multiplication of Babesia bovis, B. bigemina, B. equi, and B. caballi in in vitro cultures and that of B. microti in vivo were significantly inhibited in the presence of heparins, as determined by light microscopy. Treatment with various concentrations of heparin showed complete clearance of the intracellular parasites. Interestingly, a higher percentage of abnormally multidividing B. bovis parasites was observed in the presence of low concentrations of heparin. Furthermore, fluorescein isothiocyanate-labeled heparin was preferably found on the surfaces of extracellular merozoites, as detected by confocal laser scanning microscopy. These findings indicate that the heparin covers the surfaces of babesial merozoites and inhibits their subsequent invasion of erythrocytes.
Babesia parasites are tick-transmitted intraerythrocytic protozoa of the phylum Apicomplexa. They affect a wide variety of wild and domestic animals and are responsible for enormous economic losses to the livestock industry worldwide (25). Moreover, some are major etiologic agents of human babesiosis (20). During the asexual growth cycle in a natural host, merozoites internalize the host erythrocytes (RBCs) via multiple adhesive interactions of several protozoan molecules with the host cell surface (45). Thus, the parasites destroy the infected RBCs, which results in severe clinical symptoms, such as high fever, anemia, hematuria, and hemoglobinuria, in the infected hosts. Therefore, understanding of the basic molecular mechanism(s) of the asexual growth cycle, particularly the process of merozoite invasion into the host RBC, may accelerate the development of effective therapeutic methods and methods for the prevention of babesiosis. Heparin is a highly sulfated form of heparan sulfate (HS) (36) and is known to be an inhibitor of the blood coagulation system (19, 23) or as a coreceptor in the binding of fibroblast growth factor to its receptor (29). HS and heparin are complex entities composed of anionic, linear mucopolysaccharides with alternating uronic acid and hexosamine residues in which a limited set of monosaccharide units gives rise to a number of complex sequences by variable substitution with O-sulfate, N-sulfate, and N-acetyl groups (28), rendering the heparin polydisperse (26). While HS is produced in most cell types, heparin is a biosynthetically derived component of mast cells and basophils (16) and has a molecular weight (MW) of approximately 3,000 to 37,500, with an average MW of 13,000 (26). Due to the sulfate and carboxylate residues, heparin is highly negatively charged (9) and, moreover, is often used as a model glycosaminoglycan (GAG) to study the HS interaction with proteins (29).
Heparin has also been used for the treatment of patients affected by the cerebral form of Plasmodium falciparum infection (27, 30, 39). The therapeutic effect of heparin was demonstrated in rhesus monkeys experimentally infected with Plasmodium knowlesi (11). The growth-inhibitory effects of heparin were also described in in vitro studies with P. falciparum (7, 24, 38) and Theileria sergenti (14). However, the precise mechanisms of its inhibitory capacity against these hemoprotozoa are not fully understood.
In the present study, we examined the inhibitory effects of three kinds of heparin preparations on the in vitro growth of Babesia bovis, B. bigemina, B. equi, and B. caballi and characterized the inhibitory properties by light microscopy and confocal laser scanning microscopy. Additionally, the in vivo inhibitory effect of one heparin preparation against the rodent species B. microti was confirmed in mice, which has been successfully established as an experimental model for babesioses of many other animals (20, 32, 46). Finally, the mechanisms by which heparin interferes with the asexual growth cycle of Babesia parasites are discussed.
Effect of heparin on the course of B. microti infection in mice. Sixty 8-week-old female BALB/c mice were divided into six groups (n = 10 mice in each group) and were intraperitoneally inoculated with 107 B. microti-infected RBCs. From days 1 to 10 postinfection, 500, 250, 100, 20, or 4 U of heparin 1 (dissolved in 100 μl of phosphate-buffered saline [PBS]) was administered to each mouse in groups one to five, respectively, and 100 μl of PBS was injected into the mice in the sixth group as a placebo control. All injections were via the subcutaneous route. The levels of parasitemia in all mice were monitored daily until 13 days postinfection by observing stained thin blood smears prepared from venous tail blood. All animal experiments were conducted in accordance with the Standard Relating to the Care and Management of Experimental Animals promulgated by the National Research Center for Protozoan Diseases, Obihiro University of Agriculture and Veterinary Medicine, Hokkaido, Japan.
Effects of heparins on in vitro growth of cultured parasites. The in vitro growth of B. bovis was entirely arrested in the presence of 500 or 100 U of heparin 1 per ml, and a subsequent viability test revealed complete destruction of the parasite (Fig. 1A). Twenty units of heparin 1 could suppress growth but not clear the parasites from the host RBCs. The IC50 was determined to be 7 U/ml (35 μg/ml) (Table 1). The morphological phenomena observed by light microscopy showed that the parasites exposed to different concentrations of heparin showed a gradual increase in the number of abnormally multidividing forms (Fig. 1B and Fig. 2B). In particular, 20 U of heparin per ml was found to significantly increase the proportion of abnormally multidividing forms to 32% of the entire population within 3 days (Fig. 1B). On the other hand, the multidividing form was rarely observed in the control culture of B. bovis, in which a maximum of only about 4% multidividing forms was detectable. Additionally, concentrations of 20 U of heparin per ml and greater caused significant increases in the number of extracellular (free) merozoites (Fig. 2C) compared to the number in the untreated control groups (Fig. 2A). The apparent percentage of free merozoites reached a peak of 51.4% of the entire population on day 2 of culture in the presence of 20 U of heparin per ml, whereas the peak was 7.8% for the control group (data not shown)."
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I am back on heparin now. I know that many are VERY fearful about having bleeding complications from it, but unless you are a genetic bleeder this is not likely to be a problem.
The dose given to us is SO MINUT, it is beyond not dangerous. My doc didn't even check my blood this time around. Mind you, if this is your first time, you need to have your blood checked, but I was on heparin for over 3 years with no problems.
I had 2 minor surgeries while on it. Neither doctor even batted an eye. My daughter gave birth to her first child while on it, with absolutely no problems.
Babesia may be a lot easier to get rid of then we think. Is this possibly the missing reason I got such a high state of remission WITHOUT the massive ABX?
Posted by lou (Member # 81) on :
Wonder if those people who are taking heparin for hypercoagulation have noticed any effect on their babesia?
I notice that most of this article has to do with in vitro testing, except for one mouse study. Says heparin has been used with falciparum malaria....would be interesting to read a journal article on such treatment.
Posted by Jellybelly (Member # 7142) on :
Lou, take a look at the whole article, it is rather long, so I didn't post the whole thing. I'm still reading it myself.
It does say:
quote:Additionally, the in vivo inhibitory effect of one heparin preparation against the rodent species B. microti was confirmed in mice, which has been successfully established as an experimental model for babesioses of many other animals (20, 32, 46). Finally, the mechanisms by which heparin interferes with the asexual growth cycle of Babesia parasites are discussed.
The results of the mice testing:
quote:When the infected mice showed about 1% parasitemia, they received subcutaneous injections of either 500, 250, 100, 20, or 4 U of heparin for 10 consecutive days. In the treated group, the levels of parasitemia increased significantly more slowly, achieving peak parasitemias of 10% (in the presence of 500 U), 15% (250 U), 17% (100 U), and 34% (20 U) on day 8 after inoculation. In contrast, in the control group, the peak parasitemia of more than 72% occurred on day 7 after inoculation.
Heparin is something we all produce naturally. I am on 8000 units per day, way more then was used in these tests, yet it is still considered extremely low dose.
Posted by 5dana8 (Member # 7935) on :
hey Jellybean
Interesting article,
thanks for posting
blessings dana
Posted by david1097 (Member # 3662) on :
This info has been around for a number of yeeears now It is not the solution that was hoped for although it seems to help some people.
I tried it with no effect.
Posted by Jellybelly (Member # 7142) on :
Hasn't been around that long, cuz the study only came out in 2004. In the medical world that is barely a blip on the radar.
If you tried heparin and were looking for positive results in a few days, you probably weren't going to see that happen. Although I did see some positive results, but not remission. Remission came over the course of several years, and with nearly NO ABX, some but very little, microscopic compared to most of you.
While you may hve tried it, I would venture a guess, that 98% here have not. Many are fearful of it, which seems to be unwarranted. Osteoperosis doesn't seem to be a concern either, especially with the low molecular form.
Scared of shots like me? That can be manuvered around as well. I have not had even one shot for heparin. I spray it into my nose, and have never had a nose bleed from doing that either.
There are a few of us here who have used heparin "long" term and we have enjoyed some fairly long remissions. Mine lasted for over 4 1/2 years. I am in what seems like an early relapse now, but, I am back to business, which includes heparin and hoping to knock it right back down.
Heparin will make you herx as well, and so if you got worse while on, may just be an indicator it is working.....now where have I heard that before?
Posted by Jellybelly (Member # 7142) on :
I was on heparin originally for hypercoagulation only, tested through Hemex and had sky high indicators. Didn't know I had Lyme then and had never heard of babesia.
Several months after starting heparin, I started Doxy for 2 Mycoplasma infections. Herxed so severely at a normal dose, I ended up in the ER.
Later found out heparin makes abx more potent, thus you may need less, and that is a good thing......I would think.
Learned about low dose Mino usage through the Road Back Foundation and proceeded with micro doses as I could tolerate them.
I found out just about 2 1/2 years ago I had Lyme and very likely Babesia as numerous "past" and a few present symptoms pointed right at it.
Fast forward about 10 months later when in remission, I stumble on a study about heparin inhibiting Babesia and other information suggests it does the same for Lyme.
I would really implore you to speak with your your LLMD about giving heparin a closer look. Educate yourself first. There is plenty of information in the CFS/FM forums as it has been used for many years already, with excellent success.
Posted by kelmo (Member # 8797) on :
My daughter started on a lozenge form of heparin.
What we found by using that method is it also dissolves the mucus layer of the stomach.
She had to discontinue it. Her blood used to be like fudge, but now it's nice and red.
We would like to sometime pick heparin back up in the protocol. From what I hear, it keeps the bacteria from sticking to the red blood cell.
Kelly
Posted by Parisa (Member # 10526) on :
Okay, here's my post that somehow ended up in Senator Kennedy's thread:
Dr. Schaller brings it up in his book and says that (in the study) treatment showed complete clearance however his concern was that some mice died from the higher doses used and the ideal human dose was not known.
I know quite a few people are taking it for hypercoagulation. Do you know if it has helped your babesia?
Posted by Boomerang (Member # 7979) on :
Hubby was tested for hypercoagulation, but he was okay.
Posted by Ruth Ruth (Member # 11059) on :
duplicate post. sorry!
[ 16. August 2007, 09:25 PM: Message edited by: Ruth Ruth ]
Posted by Ruth Ruth (Member # 11059) on :
duplicate post. sorry!
[ 16. August 2007, 09:24 PM: Message edited by: Ruth Ruth ]
Posted by Ruth Ruth (Member # 11059) on :
I haven't had any problems with hypercoagulation and I have been diagnosed with babs.
I think that a couple years of taking systemic enzymes to keep the blood "slippery" may be why. I used to take 6-10 capsules of Vitalzym a day. I was doing that to help with inflammation, but I guess it was good for my blood too.
Too bad no one will ever fund a study to compare effects of Heperin against something like that.
{edit: to add a missing word!} Posted by HaplyCarlessdave (Member # 413) on :
Interesting. But unless other factors call for treatmwnt with heparin,artimesia and atovaquone are much safer, in many respects.
For instance, yours truly had a really close call with heparin-like treatments for blood clots (result of injuries-- way before I had Lyme, etc.) DaveS
Posted by tailz (Member # 10014) on :
Will heparin kill malaria? Mine was equivocal (they aren't sure).
One of the girls who drew my blood last summer commented on how quickly my blood clotted in the tube. I used to be a phlebotomist myself - it did clot extra fast.
Posted by Jellybelly (Member # 7142) on :
Parisa, It is true that 4 mice did die at the highest heparin doses which were really high for a mouse. 3 out of 10 died when given a whopping 500U and 1 died out of 10 given the 250U.
Those are incredibly high doses considering the size of a mouse. When my coagulation was at it's worst, I was at 12,000U, that is nothing when compared to the ratio given the mouse.
The good thing is that even though with the lower doses clearing of Babesia was slower, it still worked! We don't want a massive die off anyways. Who knows the mice may have died from a massive herx and anaphalactic shock rather then from the heparin directly. The article doesn't say.
Posted by nikkib (Member # 10016) on :
Does anyone use a LLMD in NY, NJ, or CT area that uses Heparin? Mine wont and I am thinking of switching from him shortly! Thanks, Nikki
Posted by lou (Member # 81) on :
Here is one article on heparin and falciparum malaria:
PLoS Pathog. 2006 Sep;2(9):e100.
Release of sequestered malaria parasites upon injection of a glycosaminoglycan.
Vogt AM, Pettersson F, Moll K, Jonsson C, Normark J, Ribacke U, Egwang TG, Ekre HP, Spillmann D, Chen Q, Wahlgren M.
Department of Microbiology, Tumor, and Cell Biology, Karolinska Institutet, Stockholm, Sweden.
Severe human malaria is attributable to an excessive sequestration of Plasmodium falciparum-infected and uninfected erythrocytes in vital organs. Strains of P. falciparum that form rosettes and employ heparan sulfate as a host receptor are associated with development of severe forms of malaria.
Heparin, which is similar to heparan sulfate in that it is composed of the same building blocks, was previously used in the treatment of severe malaria, but it was discontinued due to the occurrence of serious side effects such as intracranial bleedings.
Here we report to have depolymerized heparin by periodate treatment to generate novel glycans (dGAG) that lack anticoagulant-activity. The dGAGs disrupt rosettes, inhibit merozoite invasion of erythrocytes and endothelial binding of P. falciparum-infected erythrocytes in vitro, and reduce sequestration in in vivo models of severe malaria. An intravenous injection of dGAGs blocks up to 80% of infected erythrocytes from binding in the micro-vasculature of the rat and releases already sequestered parasites into circulation.
P. falciparum-infected human erythrocytes that sequester in the non-human primate Macaca fascicularis were similarly found to be released in to the circulation upon a single injection of 500 mug of dGAG. We suggest dGAGs to be promising candidates for adjunct therapy in severe malaria.
PMID: 17009869 [PubMed - indexed for MEDLINE]
Posted by oxygenbabe (Member # 5831) on :
Okay lou that is interesting. We need a GAG that won't thin the blood. This *can* be dangerous for some and we *don't* know the human levels required. But many with chronic lyme/babesia have been on heparin and have not reported a cure, though it was very helpful for jellybelly.
You are not killing the babesia, just distracting it and getting rid of it that way. I wonder though if you permanently get rid of it. Probably not. This is akin to what cranberry does to e. coli, takes away the ability of its fingers to bind to epithelial lining such as bladder. You don't develop bug resistance in these instances because the bug is not fighting for survival. Its binding to something. I thought fucoidan might help. I'll find the actual study here and contact the scientists.
Posted by tailz (Member # 10014) on :
I really think I need heparin.
Here's a strange question - doesn't heparin come from a pig?
Posted by Jellybelly (Member # 7142) on :
Oxygenbabe, We may already have one. Take a look at Nikkib's post about Levonox or low molecular weight heparin/LMWH. It appears that depolymerized heparin and LMWH are the same.....I think.
LMWH still thins the blood because they are beginning to send people home who have had deep vein thrombosis with LMWH.
Posted by oxygenbabe (Member # 5831) on :
I'll search but the abstract lou posted says they lack anticoagulant activity, so how could it be the same thing, I'm confused. Where is the post by nikkb?
Posted by Jellybelly (Member # 7142) on :
Is Lou's post saying that dGAG were generated by the depolymerized heparin. Is it the dGAGs that do not have anticouglulant activity?
How do you get just the dGAGs. I googled "glycans dGAG glycosaminoglycan" and got nothing that was making any sense to me. What are they?
Posted by nikkib (Member # 10016) on :
Lovenox does thin the blood....I was on it for my pregnancies. I also have to take it whan i fly to decrease the chances of bloodclots. Interestingly, we went on a trip about 2 months ago at which point I was having a horrible vertigo herx. I had to take Lovenox when I was on the plane and suddenly the vertigo was gone? I was so relieved I did not stop taking the Lovenox for the entire week (but did stop my abx that week) and I had almost no symptoms! I havent been on the Lovenox since that last day and have felt like crap since the minute we arrived in NY. Coincidence? -Nikki
Posted by randibear (Member # 11290) on :
is herparin a prescription?
Posted by D Bergy (Member # 9984) on :
For those using Rife devices, you may want to use the Babesia frequencies. While co-infections are generally not reported to respond well to frequency treatments, Babesia seemed to be rather easily eradicated in our case. I am just going by lack of symptoms and lack of later reactions to the frequencies. Not iron clad proof by any means.
I believe I mentioned this in another thread but thought it would be a good reminder since someone asked me about this privately.
Best Regards
D Bergy
Posted by jasonsmith (Member # 10914) on :
I've read that since heparin thins the blood, the abx penetrate deeper in the tissue.
I've also read heparin is anti-viral, anti-inflammatory, and anti-bacterial.
Posted by AndrewInCA (Member # 2010) on :
Would the amount of heparin used when on IV Rocephin at every infusion be enough to have any effect, or are we talking about much larger doses?
Posted by Jellybelly (Member # 7142) on :
Do you know how many units go into the IV?
Posted by lou (Member # 81) on :
Think he is talking about the heparin flush at the end of the infusion, and that is a very small amount, like 5 ml.
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