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» LymeNet Flash » Questions and Discussion » Medical Questions » Mepron and CO-Q10 per Dr. B's guidelines?

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Author Topic: Mepron and CO-Q10 per Dr. B's guidelines?
jloisu
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Was just looking at Dr. B's guidelines (see below) for nutritional supplements and he says that CO-Q10 is not required while on Mepron. Is that because Mepron takes the place of CO-Q10, or because there is an interaction?

http://www.ilads.org/burrascano_1102.htm#choices

Anyone know?

Thanks,

jloisu

--------------------
jloisu

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WildCondor
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There is an interaction. Do not take COQ10 while taking Mepron or malarone.
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liz28
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I actually called Dr. B's office on this one. The two cancel each other out. Since mepron costs $600 a bottle, you probably don't want to waste it.

Although you should know that once my babesia was greatly reduced, I started taking CoQ10 in the morning and mepron (which my insurance covers, thank God) at night, and both worked fine. And also, I've been on mepron and artemisinin for almost a year. The babesia still flares if I go off the abx, but is symptomless if I stay on them. So don't despair if you get little relapses, just keep your abx handy.

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ImLymed
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Thanks for the info on Co-Q10. I told my LLMD
I was taking that once aday and wasn't told to stop when I started the Mepron.

Thanks ImLymed

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Lonestartick
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It is my understanding that you want to avoid taking Co-Q10 (known as ubiquinone) with Mepron (Atovaquone) because their structures are very similar. Atovaquone is a structural analog of ubiquinone.

Ubiquinone is just the proper name for Co-Q10, which acts as a respiratory chain electron carrier in the mitochondria of the protozoa.

Bc1 complex (via ubiquinone) plays a central role in the electron transport chains of mitochondria, chloroplasts and bacteria by converting redox free energy into a proton gradient that is used to drive the cell's metabolism through ATP synthesis.

Atovaquone (Mepron) targets the cytochrome bc1 complex in protozoans to short circuit the cell's metabolism. Co-Q10 competes for one of the important sites where Mepron needs to bind in order to inhibit this electron transport and stop Babesia's production of energy (ATP). Co-Q10 also appears to act to promote the very electron transport that Mepron is trying to inhibit.

If I recall, something I read once seemed to suggest that Co-Q10 might even contribute to Mepron resistance, but I'm not sure if I remember that part correctly at this point. It's been so long since I have felt any need for this type of knowledge.

It is important to understand that Co-Q10 is contraindicated with Mepron even if you are careful to separate these medications by a number of hours. According to Dr. B, you should not take these two together at all.

That's probably more than you wanted to hear about the interaction, but I have always found that the more I understand about the reasons why things are contraindicated, the easier it is for me not to tempt fate just to see a natural remedy helps to control symptoms.

Just remember, Co-Q10 competes with Mepron and it also acts to fuel the metabolism that is crucial to Babesia's survival, so it's doubtful that you will want to add fuel to the fire while you are treating the infection.
[Cool]

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liz28
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Yeah, I should say that I'm not on mepron anymore, just maintenance artemisinin.
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Lonestartick
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I'm topping this old topic and adding to it for the Lyme & Babs patient who contacted me last week.

This is what a pharmacist wrote on another website about the interaction between CO-Q10 and Mepron. Basically, they counteract one another and that's why Dr. B's guidelines recommend that patients do not take them together because their affects cancel each other out.
------------------------------------

Mepron is a medication used to treat protozoan infections that commonly accompany Lyme disease and HIV infection. This class of medication is called an "ubiquinone analog" which means it interferes with coQ10 in the organism that you are trying to kill. This effect results in the death of the organism as the mitochondria is unable to produce energy to fuel important cellular processes such as DNA replication. People who are prescribed this medication should not use coQ10 simultaneously due to the potential counteracting effect of the coQ10. This effect would be similar to taking excess vitamin K while taking Coumadin (warfarin) a blood thinner. Until we have definitive data showing coQ10 (ubiquinone) to be safe when taken along with Mepron, we advise against it.
Reference:
Ray Hinish, Pharm.D., CN, C.P.T. - 06/30/2007
http://forum.lef.org/default.aspx?f=35&m=36801


quote:
Originally posted by Lonestartick:
It is my understanding that you want to avoid taking Co-Q10 (known as ubiquinone) with Mepron (Atovaquone) because their structures are very similar. Atovaquone is a structural analog of ubiquinone.

Ubiquinone is just the proper name for Co-Q10, which acts as a respiratory chain electron carrier in the mitochondria of the protozoa.

Bc1 complex (via ubiquinone) plays a central role in the electron transport chains of mitochondria, chloroplasts and bacteria by converting redox free energy into a proton gradient that is used to drive the cell's metabolism through ATP synthesis.

Atovaquone (Mepron) targets the cytochrome bc1 complex in protozoans to short circuit the cell's metabolism. Co-Q10 competes for one of the important sites where Mepron needs to bind in order to inhibit this electron transport and stop Babesia's production of energy (ATP). Co-Q10 also appears to act to promote the very electron transport that Mepron is trying to inhibit.

If I recall, something I read once seemed to suggest that Co-Q10 might even contribute to Mepron resistance, but I'm not sure if I remember that part correctly at this point. It's been so long since I have felt any need for this type of knowledge.

It is important to understand that Co-Q10 is contraindicated with Mepron even if you are careful to separate these medications by a number of hours. According to Dr. B, you should not take these two together at all.

That's probably more than you wanted to hear about the interaction, but I have always found that the more I understand about the reasons why things are contraindicated, the easier it is for me not to tempt fate just to see a natural remedy helps to control symptoms.

Just remember, Co-Q10 competes with Mepron and it also acts to fuel the metabolism that is crucial to Babesia's survival, so it's doubtful that you will want to add fuel to the fire while you are treating the infection.
[Cool]


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Marnie
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ONCE MORE!


Check Interactions

No interactions were found for the drugs you selected.

You searched for interactions between the following drugs and herbs:

Coenzyme Q-10 � Mepron

Add or Delete DrugsStart Over with a New List of

Drugs Note: Herbal products are not subject to review or approval from the FDA. Not all of the risks, side effects, or interactions associated with the use of herbal products have been studied. Not all drug interactions are known or reported in the literature, and new drug interactions are continually being reported. This information is provided only for your education and for you to discuss with your personal healthcare provider.


http://www.drugdigest.org/DD/Interaction/InteractionResults?drug=&drugList=4021&cD=4021&cD=56&dN=%22Coenzyme+Q-10%22+%22Mepron%22+&CheckFDA=1

Furthermore:

Also, the anti-parasitic agent atovaquone - Mepron - used against Pneumocystis Carinii Pneumonia is a CoQ10 analogue .

http://www.hivresources.com/Newsletter/Issue43/Iss43p10.html

Definition of: analog

A representation of an object that resembles the original.

"Atovaquone - also called Mepron, or 566C80 - is a napthoquinone used for the treatment of infections caused by pathogens such as Plasmodium spp. and Pneumocystis carinii.

The mechanism of action against the malarial parasite is the ***inhibition of dihydroorotate dehydrogenase - DHOD -***, a consequence of blocking electron transport by the drug.

As an analog of ubiquinone - coenzyme Q - CoQ , atovaquone irreversibly binds to the mitochondrial cytochrome bc1 complex; thus,

electrons are not able to pass from dehydrogenase enzymes via CoQ to cytochrome c.

Since DHOD is a critical enzyme in pyrimidine biosynthesis, and because the parasite cannot scavenge host pyrimidines, the drug is lethal to the organism.

Oxygen consumption in P. carinii is inhibited by the drug;

thus, electron transport has also been identified as the drug target in P. carinii.

However, unlike Plasmodium DHOD, P. carinii DHOD is inhibited only at high atovaquone concentrations , suggesting that the organism may salvage host pyrimidines and that atovaquone exerts its primary effects on ATP biosynthesis....

Antimicrob Agents Chemother. 2000 March; 44 - 3: 713-719

We normally MAKE CoQ10 when we exercise...IF we have enough of the nutrients to MAKE this enzyme!

It appears hydrogen and the hydroxyl radical INactivates dihydroorotate dehydrogenase.

(not allowed to link)

We make hydrogen all the time...it goes into the cells and to carry it INTO the mitochondria -powerhouses - requires CoQ10.

This looks to target the parasite mitochondria while leaving our own alone.

"collapsing the charge characteristic of the

parasite mitochondria."

http://www.lymenet.de/literatur/atovaquone.htm

I had to edit out parenthesis in order to post.

It appears to uncouple oxidative phosphorylation.

[ 02. August 2007, 05:56 PM: Message edited by: Marnie ]

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Lonestartick
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Marnie,

I'm not sure what you meant by ``ONCE MORE!'' I see that your first source does not list any known interactions. That said, I do not think Dr. B and my own LLMD are wrong about their advice that Mepron and CO-Q10 are not to be taken together.

As expensive as Mepron is and as resistant as Babesia can be, I would strongly encourage patients to listen to our LLMD experts on this very important topic, since Babesia is a serious co-infection that is implicated in many Lyme disease treatment failures.

Furthermore, although your first source says that there is no known interaction, you go on to cite another source further down, which clearly explains the reason for such an interaction where it says...


quote:
Originally posted by Marnie:

As an analog of ubiquinone (coenzyme Q [CoQ]), atovaquone irreversibly binds to the mitochondrial cytochrome bc1 complex; thus, electrons are not able to pass from dehydrogenase enzymes via CoQ to cytochrome c.
!

You might reread your citation again, since it is explains why there would be an interaction. It clearly supports my explanation above.
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RoadRunner
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Lonestartick

I would go with DR. B. and your llmd on this one because they think the same way as three llmd's in CT. do.

don't take together....


RR

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Marnie
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I said once more because I posted the same another thread.

Here are some additional points:

Atovaquone (mepron) is a highly lipophilic drug that closely resembles the structure ubiquinone (CoQ10).

Its inhibitory effect being comparable to ubiquinone , in sensitive parasites atovaquone can act by selectively affecting mitochondrial electron transport and parallel processes such as ATP and pyrimidine biosynthesis.


For illustration, cytochrome bc1 complex (complex III) seems to serve as a highly discriminating molecular target for atovaquone in Plasmodia atovaquone has the advantage of not causing myelosuppression, which is an important issue in patients who have undergone bone marrow transplantation.

http://redpoll.pharmacy.ualberta.ca/drugbank/cgi-bin/getCard.cgi?CARD=APRD00805.txt

Some pathogens MAKE CoQ10. IF we instead give ENOUGH CoQ10, perhaps the fatty acids the pathogen needs to make it will not be needed and transported into the cells.

"Hence, it was concluded that CoQ[10] (if not both CoQ[10] and CoQ[9]) in P. carinii was not scavenged from the host but was synthesized by the organism.

Although lung tissues contained substantial free fatty acids, the organism was enriched in these lipids.

The high concentration of free fatty acids and relatively low level of triglycerides in P. carinii suggest that fatty acids may represent major carbon sources for ATP production by the organism.

cat.inist.fr/?aModele=afficheN&cpsidt=3090596

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Vanilla
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My LLMD said if you are on Mepron or Malarone do not take CO Q 10 period even hours apart.
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jasonsmith
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Does anyone know if Whelcol interacts with Mepron? I take them 4 hours apart.
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Marnie
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Vanilla, please ask your LLMD why. Are they antagonists or agonists?

I am curious as to what reasons he will give especially since the drug digest did not indicate any interactions and all the research seems to point to they are pretty much the same.

Not cost wise.

BTW...from what I have read, the liquid form far surpasses (effectiveness) the pill form of Mepron. That seems odd.

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Lonestartick
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It seems that the confusion here stems from the fact that the term Analog does NOT mean that these two things "are pretty much the same" or that they can be substituted for one another.

Analogs are things whose physical structures are related to one another, but even though they might share similar physical structures, they do not necessarily share physical or biological properties. Indeed, their actions can be very different and, in this case, they are opposing.

In this circumstance, the similarity here means they can compete with one another, but just because they are analogs, they do not actually function the same way.

Furthermore, we know this for certain, because Mepron blocks the transport of electrons, directly short circuiting the parasite's metabolism; whereas CO-Q10 functions to transport electrons, facilitating the parasite's metabolism.

That means that these analogues work in entirely opposite ways and the CO-Q10 can block and counteract the very mechanism by which Mepron attacks the parasitic infection. That's why our LLMDs caution against their concomitant use.


Please note, the research does NOT point to them being "pretty much the same" at all if one reads it carefully.

http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=89752
http://www.lymenet.de/literatur/atovaquone.htm
http://www.emedicine.com/ped/topic193.htm
http://aac.asm.org/cgi/content/full/44/3/713

It is very important NOT to take Mepron and CO-Q10 together and there are multiple warnings on this site about those interactions based on research as well as clinical experience treating Lyme and Babesia co-infections.

Please listen to your LLMDs on this one! Advice that is contrary to theirs could lead to treatment failure.


Thank you Roadrunner - I remember you!!! It's so good to a familiar face from the old days at Lymenet. Take care and be well. Hope you're still running. Now that I'm healthy, I jog - it's not really running, but I love it.

edited to put important text in bold

[ 05. August 2007, 08:05 PM: Message edited by: Lonestartick ]

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Lonestartick
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quote:
Originally posted by Marnie:
BTW...from what I have read, the liquid form far surpasses (effectiveness) the pill form of Mepron. That seems odd.

The liquid form of Mepron has pretty much replaced the old poorly water-soluble atavaquone tablets, which were plagued with erratic systemic absorption. The introduction of the liquid suspension is also more preferable because it allows for twice daily dosing as a result of its superior bioavailability as opposed to the old tid dosing with the pill form.

Marnie, could you please go back and correct your post under your other topic to state clearly that patients should NOT take CO-Q10 together with Mepron, because your advice goes against research and clinical experience treating Lyme and co-infections. Please correct that ASAP. Pretty please. It's really important.

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EWT1638
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Mepron for $600? It costs $789 here! Anyway, be careful not to spill it on ANYTHING, it will NOT come out....I used OXYclean and it made the stain look like blood!

Funny, both Mepron and CO Q10 are weird yellow colors.

--------------------
When you reach your "wits-end" remember this: "Peace I leave with you, my peace I give you. I do not give as the world gives. Do not let your hearts be troubled and do not be afraid." John 14:27

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RoadRunner
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lonestartick thank you yes it is always nice to see old members.

here is some more

Citations 1 to 5 of 5 from MEDLINE

TITLE: Characterization of cytochrome b from Toxoplasma gondii and
Q(o) domain mutations as a mechanism of atovaquone-resistance.
AUTHORS: McFadden DC, Tomavo S, Berry EA, Boothroyd JC
SOURCE: Mol Biochem Parasitol. 2000 Apr 30;108(1):1-12.
CIT. IDS: PMID: 10802314 UI: 20264021

TITLE: Effects of atovaquone and diospyrin-based drugs on the
cellular ATP of Pneumocystis carinii f. sp. carinii.

AUTHORS: Cushion MT, Collins M, Hazra B, Kaneshiro ES

SOURCE: Antimicrob Agents Chemother. 2000 Mar;44(3):713-9.

CIT. IDS: PMID: 10681344 UI: 20145395


TITLE: Effects of atovaquone and diospyrin-based drugs on ubiquinone
biosynthesis in Pneumocystis carinii organisms.
AUTHORS: Kaneshiro ES, Sul D, Hazra B

SOURCE: Antimicrob Agents Chemother. 2000 Jan;44(1):14-8.

CIT. IDS: PMID: 10602716 UI: 20068669


TITLE: Resistance mutations reveal the atovaquone-binding domain of
cytochrome b in malaria parasites.
AUTHORS: Srivastava IK, Morrisey JM, Darrouzet E, Daldal F, Vaidya
AB
SOURCE: Mol Microbiol. 1999 Aug;33(4):704-11.

CIT. IDS: PMID: 10447880 UI: 99377123


TITLE: Sequence polymorphisms in the Pneumocystis carinii
cytochrome b gene and their association with atovaquone prophylaxis failure.

AUTHORS: Walker DJ, Wakefield AE, Dohn MN, Miller RF, Baughman
RP, Hossler PA, Bartlett MS, Smith JW, Kazanjian P, Meshnick SR

SOURCE: J Infect Dis. 1998 Dec;178(6):1767-75.

CIT. IDS: PMID: 9815231 UI: 99034664
Atovaquone (also called Mepron, or 566C80) is a napthoquinone used for the treatment of infections caused by pathogens such as Plasmodium spp. and Pneumocystis carinii. The mechanism of action against the malarial parasite is the inhibition of dihydroorotate dehydrogenase (DHOD), a consequence of blocking electron transport by the drug. As an analog of ubiquinone (coenzyme Q [CoQ]), atovaquone irreversibly binds to the mitochondrial cytochrome bc(1) complex; thus, electrons are not able to pass from dehydrogenase enzymes via CoQ to cytochrome c. Since DHOD is a critical enzyme in pyrimidine biosynthesis, and because the parasite cannot scavenge host pyrimidines, the drug is lethal to the organism. Oxygen consumption in P. carinii is inhibited by the drug; thus, electron transport has also been identified as the drug target in P. carinii. However, unlike Plasmodium DHOD, P. carinii DHOD is inhibited only at high atovaquone concentrations, suggesting that the organism may salvage host pyrimidines and that atovaquone exerts its primary effects on ATP biosynthesis. In the present study, the effect of atovaquone on ATP levels in P. carinii was measured directly from 1 to 6 h and then after 24, 48, and 72 h of exposure. The average 50% inhibitory concentration after 24 to 72 h of exposure was 1.5 microgram/ml (4.2 microM). The kinetics of ATP depletion were in contrast to those of another family of naphthoquinone compounds, diospyrin and two of its derivatives. Whereas atovaquone reduced ATP levels within 1 h of exposure, the diospyrins required at least 48 h. After 72 h, the diospyrins were able to decrease ATP levels of P. carinii at nanomolar concentrations. These data indicate that although naphthoquinones inhibit the electron transport chain, the molecular targets in a given organism are likely to be distinct among members of this class of compounds.


RR

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Marnie
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RR...do you see the word, "resistance"? As well as: "atovaquone prophylaxis failure" that YOU posted?

Lonestar....I ran a drug-supplement interaction check and it did NOT indicate Mepron-CoQ10 interact.

It does not appear they are antagonists, but I wonder if instead, they MIGHT be agonists?

Do you know the difference?

Yes, unfortunately the malaria parasite has mutated to become resistant to Mepron.

Please take note of the following:

"In one experiment, three groups of mice were infected with the parasite that causes malaria.

All of the untreated mice died within three weeks. During the same time, even 80 percent of the mice treated with antimalarial drugs died.

But when CoQ10 was combined with the antimalarial drug , only 42 percent of the mice died.

Similar benefits were observed in laboratory animals infected with E. coli, Pseudomonas, and Klebsiella (one type of pneumonia) infections."

http://www.holisticonline.com/Remedies/Biot/biot_anthrax-coQ10-nat-rem.htm

Oxidative stress damages not only the cells which are infective, but also looks to damage our IMMUNE fighting cells as well.

Dr. B "had" lyme which is why he got interested in treating this disease (according to a post by Scott). I have tremendous respect for Dr. B and feel he was waaaaaaay ahead of his time re: supplements, physical therapy, etc. I often wonder how he figured that all out without knowing Bb's genetic codes (pretty recent research!).

However, he is/was recently fighting prostate cancer.

The diseases are very closely linked!

It takes TIME for this to happen!!!

Bb infects epithelial cells that line our blood vessels first and then the Langerhans cells and other immune cells. Bb causes DNA damage when it locks on and triggers oxidative stress which impacts the mitochondria. Those cells rely on glucose only. Cells are "undermethylated".

Those are cancerous cells i.e., they gobble up sugar, have DNA damage, few mitochondria left, undermethylated, originate as epithelial cells and then infected lymph cells that have migrated...

Why would those cells migrate to cells containing estradiol (one of 3 forms of estrogen)?

"Reports on PKC delta function in estrogen-responsive tissues are contradictory.

PKC delta was upregulated by estradiol

in corpus luteum (Maizels et al., 1996), while it was downregulated in MCF-7 cells in a time- and dose-dependent manner (Shanmugam et al., 1999). PKC delta increased mammary tumour cell growth and metastasis by activation of the Ras/Erk1/2 pathway (Keshamouni et al., 2002).

Bb has a PKC inhibitor. These NORMALLY cause cell death. I think Bb's PKC inhibitor is PKC DELTA.

But we have a cell that is UPREGULATING PKC delta. It is Il 1 beta.

The man-made drug, Tamoxifen, is a PKC inhibitor. It is used to kill "estrogen dependent" breast cancer cells.

Gals only? Nope.

These results demonstrate for the first time that 1) endogenous testosterone is a primary modulator of coronary PKC delta protein and activity in males and 2) Testosterone increases Cav1.2 protein expression in a PKC delta-dependent manner.

Testosterone levels are implicated in prostate cancer, but estradiol even moreso:

"Men produce estrogen (Estradiol) but in much lower amount than women. Men also produce progesterone, but about half the amount from that of females.

Progesterone is made in men by the adrenal glands and testes. Progesterone is vital to good health in both women and men.

It is the primary precursor of our adrenal cortical hormones and testosterone.

The male hormone, testosterone, is an antagonist to estradiol (E2).

It is made from progesterone. Men normally continue to produce relatively normal level of testosterone for their age and well into the seventies.

Contrary to common perception, testosterone does not cause prostate cancer. Young men have high levels of testosterone and old men low levels.

If testosterone were the cause of prostate cancer, young men would be dying of prostate cancer.

Studies had shown that men with the highest level of testosterone have the least prostate enlargement. Conversely, men with the highest level of estrogen have enlarged prostates.

Declining testosterone from aging, together with increasing level of estrogen, is the most likely reason for prostate enlargement and cancer in men.

The prostate is embryologically the same as the uterus in the female. Research Studies (Listed at the end of this newsletter) have shown that when prostate cells are exposed to estrogen, the cells proliferate and become cancerous.

When progesterone or testosterone was added, cancer cell dies.

During the aging process, progesterone level falls in men, especially after age 60. Progesterone is the chief inhibitor of an enzyme called 5-alpha reductase that is responsible for converting testosterone to dihydrotestosterone (DHT), a much more potent derivative that is linked to prostate cancer.

When the level of progesterone falls in men, the amount of conversion from testosterone to DHT increases. Unfortunately, DHT is not as powerful an inhibitor of cancer cell compared to testosterone.

When the level of testosterone decreases, the relative level of estradiol in men increases. Estradiol, turns on BCL2 oncogene (Onco means cancer) and increases the risk of prostate cancer if adequate amount of progesterone is not there to counteract its effect by stimulating the P53 cancer protection gene."

http://tsangenterprise.com/news75.htm

Bb triggers NFkB, a cell nucleus call to alarm, so to speak. This triggers TNF alpha and bad boy Il 1 Beta ...interleukin 1 beta.

ONGOING.

NOT GOOD.

NFkB triggers IKKA which turns OFF a tumor suppressor gene. That gene makes a protein called maspin which prevents metastasis in prostate cancer. If that gene is turned OFF = hello cancer metastasis.

We must INactivate NFkB...get TNF alpha AND IL 1 beta down simutaneously.

"Stimulation with IL-1beta activated PKC-alpha and -delta" :...

There is much we have learned in the past few years and continue to learn!

[ 04. August 2007, 05:52 PM: Message edited by: Marnie ]

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Lonestartick
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quote:
Originally posted by Marnie:
Lonestar....I ran a drug-supplement interaction check and it did NOT indicate Mepron-CoQ10 interact.

It does not appear they are antagonists, but I wonder if instead, they MIGHT be agonists?

Do you know the difference?

Yes, unfortunately the malaria parasite has mutated to become resistant to Mepron.

Yes, Marnie. I understand that those terms can be a bit confusing. Nevertheless, despite your search at the drug interaction site, we do know there is an interaction because the medical literature clearly states how and why that is as it pertains to the treatment of the Lyme co-infection Babesia. (see my posts above)

That should no longer be up for debate. Please correct your mistake under your other topic now because to fail to do so would be irresponsible at this point when you are dispensing medical advice that contradicts the medical advice of our very best LLMDs.

Such confusing advice could even be considered negligent and might possibly even get Lymenet in trouble.

CO-Q10 might be considered an ``Agonist,'' even though it doesn't really activate a cell membrane receptor and affect a response so much as it sits there itself and functions to transfer electrons facilitating the parasite's metabolism. Mepron doesn't activate the receptor, so much as it binds there and does not allow the transfer of those electrons that normally occurs in the presence of CO-Q10, so it would act as an ``Antagonist''.

However, what exists here is a case of ``Antagonism'' pharmacologically speaking, because there is an interaction between two agents that is less than the sum of the two drugs acting separately, since they both compete with one another to cancel each other out.

If you pay attention to Malaria's ability to develop resistance, I'm sure you will understand why it is unwise to continue to advise patients to take CO-Q10 with Mepron against the advice of our most experienced LLMDs, because using them together may increase the risk for Mepron resistant Babesia, which is known to be a complicating factor in Lyme treatment failures.

Marnie, please remember Dr. B didn't need to know anything about Bb's genetic codes in order to determine that CO-Q10 and Mepron cannot be taken together while treating Babesia, based on their documented effects on Babesia and other similar parasitic infections.

Remember also that he was treating the Lyme co-infection Babesia with Mepron. This had NOTHING to do with the patient's Borrelia infection, other than clinical experience had shown that patients do not successfully recover from Borrelia in the presence of untreated Babesial co-infections.

Yes, I too admire Dr. B greatly. I have had the chance to hear him speak at several conferences, most recently at ACAM. The man is a brilliant clinician and researcher. I had goose bumps when I saw some two hundred non-Lyme doctors leap to their feet to give him a standing ovation and an award. He is truly in a league of his own, even among his medically educated peers.

The rest of your discussion is NOT applicable to this topic on CO-Q10 being incompatible with Mepron for the treatment of Babesia, so I will refrain from commenting.

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Marnie
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1. There are NO MITOCHONDRIA IN RED BLOOD CELLS.

2. CoQ10 carries hydrogen into the mitochondria of cells that HAVE mitochondria.

3. Mepron deals with complex 3. CoQ10 deals with other complexes :

"Within the mitochondrial membrane, CoQ10 acts as a hydrogen electron shuttle that literally escorts the hydrogen electrons from one cytochrome to the next (from one step in the staircase to the next).

It specifically functions as an electron acceptor for complex I and complex II within the mitochondrial membrane.

As such, a decline in CoQ 10 levels within the mitochondrial membrane results in a decreased ability to synthesize ATP, resulting in development of the type of cellular dysfunction and death found in Parkinson's disease."

http://findarticles.com/p/articles/mi_qa3987/is_200301/ai_n9211374

"Mechanism of Action: Atovaquone is a hydroxy-1,4-naphthoquinone, an analog of ubiquinone, with antipneumocystis activity. The mechanism of action against Pneumocystis carinii has not been fully elucidated. In Plasmodium species, the site of action appears to be the cytochrome bc1complex (Complex III)."

http://us.gsk.com/products/assets/us_mepron.pdf.



Some pathogens MAKE CoQ10 from nutrients.

Blocking them from making it is not the same as giving CoQ10 which is already MADE.

The pathogen may not be able to USE the "already made" form.

Just like Bb having a gene for the enzyme C-acetyltransferase. We need that enzyme to MAKE acteylcholine. If that enzyme drops, we make LESS acetylcholine. But Bb cannot USE, cannot BREAK down acetylcholine. What Bb is really after are the OTHER nutrients that make up acetylcholine.

I am aware that ONE pharmacist said the following:

"Until we have definitive data showing coQ10 (ubiquinone) to be safe when taken along with Mepron, we advise against it.

Reference:
Ray Hinish, Pharm.D., CN, C.P.T. - 06/30/2007
Pharmacist/Certified Nutritionist/Personal Trainer
0210 S. Dolfield Road * Owings Mills, MD 21117"

Bacically they don't KNOW.

Consider the following:

"Some people recommend that if you are using graviola, which reduces cellular energy, you don't want to use CoQ10, which helps cells produce energy aerobically , because it may increase a cell's energy production.

On the face of it, this makes sense - until you consider that we want to help all the cells in our body produce energy aerobically, to make them more resistant to cancer which primarily used anaerobic energy production. The benefits of CoQ10, Oxy E and other oxygenators more than offsets any possible decrease in the effectiveness of graviola."

Mepron INCREASES T cells.

During pregnancy, our bodies go into "immune suppression" so we don't attack the fetus.

Researchers have given cows during the (immunosuppressive) lactation time, Mepron,to INCREASE T cells so they don't deveolp mastitis (a painful breast inflammation which can happen in women who are breast feeding too).

It APPEARS increased T cells maybe contributing to a DECREASE in NK cells (which are few to begin with).

There is already an overabundance of T cells in lyme and too few NK cells.

"Lyme arthritis synovial fluid contains a large proportion of gamma and delta T cells that proliferates upon stimulation with the causative spirochete, Borrelia burgdorferi

Even in the absence of an appropriate model or direct evidence, T cells have been hypothesized to exacerbate the manifestations of Lyme disease.

To define definitely the role of T cells in Lyme disease, the course of disease in immunocompetent and B cell-deficient mice was compared.

By 8 wk postinoculation, immunocompetent mice resolved both carditis and arthritis, whereas foci of myocarditis and severe destructive arthritis characterized disease of B cell-deficient mice. Cell transfer experiments using infected B6-Rag1 knock out mice demonstrated that: 1) innate immunity mediated the initial sequelae of infection, 2) transferring both naive T cells and B cells induced resolution of carditis and arthritis, 3) infected mice reconstituted with T cells developed myocarditis and severe destructive arthritis, and 4) CD4+ T cells were responsible for the observed immune-mediated pathology.

These data demonstrate directly the deleterious effect of T cells in Lyme disease."

The Journal of Immunology, 2000, 164: 6096-6099.

To simultaneously treat BOTH infections, it maybe better to focus on Artemisinin.

Besides ROS (how that herb works...releases reactive oxygen species), NO...

watch for the words "alkylate" and "histidine" (Bb has histidine it its zinc fingers) in the following link:

http://www.rsc.org/delivery/_ArticleLinking/DisplayArticleForFree.cfm?doi=a827273z

[ 06. August 2007, 10:51 AM: Message edited by: Marnie ]

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Lonestartick
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quote:
Originally posted by Marnie:
1. There are NO MITOCHONDRIA IN RED BLOOD CELLS.

This is a NOT pertinent to the discussion, because even though our Red Blood Cells do NOT have mitochondria, the Babesia parasite has mitochondria and continues to have mitochondria even when it is residing inside our infected Red Blood Cells.

quote:
Originally posted by Marnie:
2. CoQ10 carries hydrogen into the mitochondria of cells that HAVE mitochondria.

Again, Babesia have mitochondria. CO-Q10 (ubiquinone) accepts not only electrons, but also accepts protons when it is reduced and releases both when oxidized. It is also an important part of respiratory complex 3.

quote:
Originally posted by Marnie:
3. Mepron deals with complex 3. CoQ10 deals with other complexes :

Not quite Marnie... This is where you are confused because your understanding of complex 3 is incomplete. Complex 3 is called the coenzymeQ-cytochrome c oxidoreductase complex and it is the same thing as cytochrome bc1 complex (see my other posts above)

Your statement above is also misleading because CO-Q10 shifts readily from ubiquinone to semiquinone to its dihydroquinone as it is reduced and oxidized within the ETS. There are many electron carriers involved in the ETS and these are thought to be organized within the inner mitochondrial membrane into four different types of respiratory complexes.

Complex 3 is called the coenzymeQ-cytochrome c oxidoreductase complex because it accepts electrons from coenzyme Q and passes them to cytochrome c. This complex is also referred to as cytochrome b/c1 complex, because those two cytochromes are its most prominent components.

So, if Mepron deals with Complex 3 we know that it also deals with CO-Q10 to transfer electrons and facilitate the parasite's metabolism. This is why, based on current science, our doctors tell us not to take CO-Q10 together with Mepron, because there is compelling evidence which suggests they compete to cancel each other out.

Remember, ``Atovaquone (Mepron) -- A hydroxynaphthoquinone that inhibits the mitochondrial electron transport chain by competing with ubiquinone at the ubiquinone-cytochrome-c-reductase region (complex III). Inhibition of electron transport by atovaquone results in inhibition of nucleic acid and ATP synthesis in the parasites.''
http://www.emedicine.com/ped/topic193.htm

Enough said!

Marnie, the rest of your discussion is not really applicable to this particular topic and is rather distracting, so I will refrain from commenting.

Now Marnie, could you quit debating and correct your posts advising that patients should take CO-Q10 with their Mepron because your advice disagrees with that of our very best LLMDs's instructions and it could lead to treatment failure. Not to correct your advice now would be both irresponsible and inexcusable.

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bejoy
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Thanks for the discussion. Very interesting and enlightening. I value all input. There are lots of unknowns out here in lymeland, and I enjoy opportunities to use my head and make up my mind.

I do find it easiest to read information that is presented in a respectful and supportive manner to all involved. Thanks to all who take their time to keep us up to date and informed.

--------------------
bejoy!

"Do not go where the path may lead; go instead where there is no path and leave a trail." -Ralph Waldo Emerson

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Michelle M
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I'm pretty sure I'm having a flashback.

"When will this end?"

It is hard enough for me to process information. However, it is virtually impossible when it is delivered in an exasperated and condescending tone.

My LLMD advises against the combination.

[Roll Eyes]

Michelle

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RoadRunner
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I know of about six LLMD is my area that say don't take mepron with Q10 if you email me I will give names of all of them.

would you listen to a LLMD or some nurse who doesn't have lyme.

RR

--------------------
"Beep Beep"

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Marnie
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This is a discussion about whether or not Mepron and CoQ10 have any interactions, it is NOT "advice".

CoQ10 has PRO-OXIDANT AND ANTI-OXIDANT effects. BOTH.

Mepron, however, has ONLY a "pro-oxidant" effect working at ONLY the complex III level (block) to increase the powerful superoxide free radical to destroy babesia.

I believe low levels of CoQ10 - due to several nutrient deficiencies (17 steps and many nutrients are needed to MAKE CoQ10) - allow babesia to survive .

In healthy individuals, this infection usually disappears on its own.

Pro-oxidant (to destroy babesia)...anti-oxidant to recover...pro-oxidant (to destroy babesia)...anti-oxidant to recover = CoQ10.

Same with H2O2 (a mild acid) that we are making inside of our cells every split second before the anti-oxidant enzymes kick in.

NORMALLY H2O2 is able to destroy many pathogens too, but the cells can't stay acidic, so we have to break H2O2 down.

Hit the pathogen (via H2O2)...recover...hit the pathogen (via H2O2)...recover. (Unfortunately Bb has figured out how to sabotage that system.)


Three DIFFERENT large enzyme complexes catalyze the flow of electrons between CoQ, Cytochrome C, and oxygen

1) NADH-CoQ reductase (oxidoreductase)(NADH dehydrogenase) catalyzes electron flow between NADH and CoQ = Complex I

2) Cytochrome reductase (oxidoreductase) catalyzes electron flow between CoQ and cytochrome C = Complex III

3) Cytochrome oxidase catalyzes electron flow between cytochrome C and O2 to form H2O = Complex IV

Mitochondrial inner enzyme complexes I and V are important sites of cellular injury in myocardial ischemia.

Mepron ONLY works by blocking complex III.

No "recovery".

I have been unable to find any "interactions" between Mepron and CoQ10.

Please ask your LLMD WHY he/she feels they should NOT be taken on the same day.

Since CoQ10 also functions as a PRO-OXIDANT, this is very strange.

Even GlaxoSmithKline (1-888-825-5249) has no information available about any potential interaction between that drug and that supplement.

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RoadRunner
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GlaxoSmithKline they will never say anything bad about there products.... it would cost them money.
wake up!!

from DR B. to DR J and about four or five others LLMD say not to use together is enough for me.


I don't have to ask anyone if you aren't listening to your LLMD why go to him? just go to a IDSA duck if that is what you want to do and be sick the rest of your life.


A discussion is advice....

I listened to my LLMD and I am better because I did what he told me too do and on no meds over two and half years.

RR

--------------------
"Beep Beep"

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RoadRunner
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lonestartick said it all


Originally posted by Marnie:
1. There are NO MITOCHONDRIA IN RED BLOOD CELLS.

This is a NOT pertinent to the discussion, because even though our Red Blood Cells do NOT have mitochondria, the Babesia parasite has mitochondria and continues to have mitochondria even when it is residing inside our infected Red Blood Cells.

quote:Originally posted by Marnie:
2. CoQ10 carries hydrogen into the mitochondria of cells that HAVE mitochondria.

Again, Babesia have mitochondria. CO-Q10 (ubiquinone) accepts not only electrons, but also accepts protons when it is reduced and releases both when oxidized. It is also an important part of respiratory complex 3.

quote:Originally posted by Marnie:
3. Mepron deals with complex 3. CoQ10 deals with other complexes :

Not quite Marnie... This is where you are confused because your understanding of complex 3 is incomplete. Complex 3 is called the coenzymeQ-cytochrome c oxidoreductase complex and it is the same thing as cytochrome bc1 complex (see my other posts above)

Your statement above is also misleading because CO-Q10 shifts readily from ubiquinone to semiquinone to its dihydroquinone as it is reduced and oxidized within the ETS. There are many electron carriers involved in the ETS and these are thought to be organized within the inner mitochondrial membrane into four different types of respiratory complexes.

Complex 3 is called the coenzymeQ-cytochrome c oxidoreductase complex because it accepts electrons from coenzyme Q and passes them to cytochrome c. This complex is also referred to as cytochrome b/c1 complex, because those two cytochromes are its most prominent components.

So, if Mepron deals with Complex 3 we know that it also deals with CO-Q10 to transfer electrons and facilitate the parasite's metabolism. This is why, based on current science, our doctors tell us not to take CO-Q10 together with Mepron, because there is compelling evidence which suggests they compete to cancel each other out.

Remember, ``Atovaquone (Mepron) -- A hydroxynaphthoquinone that inhibits the mitochondrial electron transport chain by competing with ubiquinone at the ubiquinone-cytochrome-c-reductase region (complex III). Inhibition of electron transport by atovaquone results in inhibition of nucleic acid and ATP synthesis in the parasites.''
http://www.emedicine.com/ped/topic193.htm

--------------------
"Beep Beep"

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Lonestartick
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I am sorry about my tone earlier. I really should have waited to edit my topic before posting until I was able to have the distance to read that my frustrations and worries were coming through in a rather harsh manner. (Thank you for pointing that out so kindly.)

Please understand my firm tone was only because I feel this is so important. I have been in the Lyme community long enough to have personally seen patients end up as treatment failures and so many of them lose everything.

I do not wish for that to happen to any one of you because you didn't follow your doctor's advice.

Especially when our most respected LLMDs all agree that CO-Q10 should NOT be taken with Mepron while treating the Babesia co-infection, because it is implicated in treatment failures. I have seen this presented at conferences.


I hope and pray my previous tone will not detract or prevent any patients who have questions from printing the entire topic and asking their LLMD's to help them understand the interaction.

(Once you are no longer taking Mepron I'm sure your LLMD will reassure you that you can resume CO-Q10 for mitochondrial support, but please ask first.)

Please remember that your LLMDs have thorough and complete backgrounds in chemistry and biochemistry. They also have the most clinical experience treating Lyme and co-infections.

Your LLMDs are the ones who are most capable of understanding and interpreting the research as it pertains to Lyme disease and the complicating co-infection Babesia.


Our LLMD's have all participated in many treatment successes, unfortunately almost all of us who have recovered leave the forums, myself included.

Please remember, your LLMDs are the best ones to advise you what works and what doesn't while treating Lyme & co-infections. So if you are on Mepron, please, please, please check with your LLMD before you take these two things together.

I cannot in good conscience continue to debate any further, because I feel this important topic is one for Lyme patients to decide with the LLMDs who are responsible for treating them.

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