Activity of Cholestyramine, Activated Charcoal, and Super Activated Charcoal Compared

One of the discussions over the years has been the use of binding agents to soak up fat-soluble porphyrins dumped into the digestive tract by the liver, and keep them from getting re-absorbed on their way through the digestive tract. This not only lowers the immediate porphyriai [2] reactions, but helps over time to lower the total body load of fat-stored porphyrins. Some people with Cpni [3] don't appear to be bothered much by porphyria and find binding agents not at all helpful, others find it life saving as porphyria is a big component of their distress from Cpn. Since some tissues like the liver and bone marrow are bigger producers of hemei [4], it stands to reason that Cpn infectionsi [5] in these tissues would probably create the worst secondary porphyriai [6]. If your primary infection site is in tissues not productive of heme you will likely not have as much porphyria.

Anyway, anecdotal reports on www.cpnhelp.org [7] are that some people find prescription cholestyramine (Questran) to be more effective than the cheaper OTC activated charcoal, while others find the charcoal to be just the ticket. There is even a pricey but flavored choco-mint powdered form of activated charcoal!  [8] I have likened this to taking choco-mint flavored  xerox toner, but it is a way to get a bigger dose of charcoal without capsules.

Then I read that there is a "Super charcoal" which has double to triple the absorbtive capacity of the regular stuff, meaning that less is needed for the same effect. In trying to find out more, I came upon a page [9] that listed a bunch of medline comparisons between cholestyramine and activated charcoal. I've copied these below and highlighted the conclusions. There may be some newer studies to add as this has not been updated in a while. It is my impression that some of these studies were done to test a specific brand of super charcoal, and so keep that in mind. The general conclusion is that the activated charcoals are as effective as cholestyramine in lowering cholesteroli [10], and binding with Fats, and (this should generalize to porphyrins as well). It does appear that the superactivated versions are more effective at binding some of the porphyrins than regular AC's.

TI: Sorbent therapy of the porphyrias. IV. Adsorption of porphyrins by sorbents in vitro.
AU: Tishler-PV; Winston-SH
SO: Methods-Find-Exp-Clin-Pharmacol. 1985 Sep; 7(9): 485-91
ISSN: 0379-0355
PY: 1985
LA: ENGLISH
CP: SPAIN
AB: The adsorption capacities (Qm's) of the ion exchange resin cholestyramine and 8 activated charcoals for uroporphyrin, protoporphyrin and coproporphyrin, porphyrins that accumulate within tissues or vasculature in certain porphyrias, have been determined. Qm's (mg porphyrin/gm dry sorbent) were derived from Langmuir isotherms, which were constructed from experiments that assessed the amount of porphyrin adsorbed after the addition of varying amounts of porphyrin in solution to a constant amount of sorbent. These experiments were carried out at pH 8.2 in 0.5% desoxycholate, to simulate conditions of the small intestine. For uroporphyrin I, the Qm for Amoco Supersorb PX-21 highly activated charcoal was greater than that for cholestyramine (mean +/- SD of 26.5 +/- 12.7 vs. 17.0 +/- 2.6; t'32 = 2.46, P less than 0.025) and highly significantly greater than those of the other charcoals. For protoporphyrin IX, cholestyramine and Amoco Supersorb PX-21 charcoal had the highest Qm's (32.4 +/- 8.6 and 30.9 +/- 9.2), but these were not significantly greater than the Qm's of 5 other charcoals. Little difference was found among sorbents in the rate of adsorption of either porphyrin. For coproporphyrin III, the Qm's of cholestyramine and Amoco Supersorb PX-21 charcoal were not significantly different (39.2 +/- 13.7 vs. 35.1 +/- 4.0) but they were greater than that of Norit USP XX (20.0). Virtually no desorption of porphyrin from either cholestyramine or Amoco Supersorb PX-21 charcoal was detected. Both cholestyramine and Amoco Supersorb PX-21 charcoal appear to be highly avid sorbents for porphyrins of varied states of carboxylation.(ABSTRACT TRUNCATED AT 250 WORDS)
MESH: Adsorption-; Human-; In-Vitro; Liver-Diseasesi [11]-etiology; Liver-Diseases-therapy; Porphyria-complications; Porphyrins-; Support,-U.S.-Gov't,-Non-P.H.S.
MESH: *Charcoal-therapeutic-use; *Cholestyramine-therapeutic-use; *Porphyria-therapy; *Skin-Diseases-therapy
RN: 11041-12-6; 16291-96-6
NM: Cholestyramine; Charcoal
AN: 86090956
UD: 8604

TI TITLE: Sorbent therapy of the porphyrias. V. Adsorption of the porphyrin precursors delta-aminolevulinic acid and porphobilinogen by sorbents in vitro. AU AUTHOR(S): Winston-SH; Tishler-PV SO SOURCE (BIBLIOGRAPHIC CITATION): Methods-Find-Exp-Clin-Pharmacol. 1986 Apr; 8(4): 233-7 PY PUBLICATION YEAR: 1986 LA LANGUAGE OF
ARTICLE: ENGLISH CP COUNTRY OF PUBLICATION: SPAIN
AB ABSTRACT: The acute attacks of the acute hepatic porphyrias may be precipitated by the excessive intracellulari [12] accumulation of the porphyrin precursors delta-aminolevulinic acid (ALA) or porphobilinogen (PBG). Sorbents that bind porphyrin precursors in the gastrointestinal tract may interrupt their enterohepatic circulation, thus reducing the body burden of these materials and minimizing the frequency or severity of acute attacks. We have determined the adsorption capacities (Qm's) of several activated charcoals and the ion exchange resin cholestyramine for ALA and PBG. Qm's (mg ALA or PBG adsorbed/gm dry sorbent) were determined from Langmuir isotherms, which were derived from studies of the amount of porphyrin precursor adsorbed after the addition of a constant amount of ALA or PBG to varying amounts of sorbent. These experiments were carried out pH 8.2 in 0.1% desoxycholate, to simulate conditions of the small intestine. Extremely high Qm's were obtained for all charcoals and both porphyrin precursors; those for cholestyramine were one or several orders of magnitude lower. For ALA, the Qm of Gulf Bio-Systems Super Char charcoal (110 +/- 35 [SD]) was not significantly greater than that of Med-Corp Acta-Char charcoal (95 +/- 20), but it did exceed those of all other charcoals by a statistically significant amount. For PBG, the Qm of Super Char (68 +/- 14) was marginally greater than that of Mallinckrodt USP charcoal (42 +/- 21, t8 = 2.18, p approximately equal to 0.06), but it was significantly greater than that of Acta-Char charcoal (27 +/- 12). All sorbents adsorbed ALA or PBG at comparable rates, and the complex of sorbent and porphyrin precursor appeared to be undissociable.(ABSTRACT TRUNCATED AT 250 WORDS) MESH MEDICAL SUBJECT HEADINGS: Adsorption-; Kinetics-; Support,-U.S.-Gov't,-Non-P.H.S. MESH MEDICAL SUBJECT
HEADINGS: *Aminolevulinic-Acid; *Charcoal-; *Cholestyramine-; *Levulinic-Acids; *Porphobilinogen- RN CAS REGISTRY NUMBER OR EC
NUMBER: 106-60-5; 11041-12-6; 16291-96-6; 487-90-1
NM NAME OF SUBSTANCE: Aminolevulinic-Acid; Cholestyramine; Charcoal; Porphobilinogen ISSN INTERNATIONAL STANDARD SERIAL NUMBER: 0379-0355 AN MEDLINE ACCESSION NUMBER: 86255821 UD UPDATE CODE: 8610

TI TITLE: Correlative studies of the hypocholesterolemic effect of a highly activated charcoal. AU AUTHOR(S): Tishler-PV; Winston-SH; Bell-SM AD ADDRESS OF AUTHOR: Brockton/West Roxbury Veterans Administration Medical Center, MA. SO SOURCE (BIBLIOGRAPHIC
CITATION): Methods-Find-Exp-Clin-Pharmacol. 1987 Dec; 9(12): 799-806 PY PUBLICATION YEAR: 1987 LA LANGUAGE OF ARTICLE: ENGLISH CP COUNTRY OF PUBLICATION: SPAIN AB ABSTRACT: We have carried out in vitro and animal studies to determine the cholesterol lowering efficacy of activated charcoals vs. cholestyramine. In the in vitro studies, we determined the adsorption capacity (Qm) of cholestyramine and activated charcoals for cholesterol in glacial acetic acid. Mean (+/- SD) Qm's (mg cholesterol adsorbed/gm dry sorbent) decreased in the order Super Char highly activated charcoal (277 +/- 121), Norit USP XX charcoal (33 +/- 10), Acta-Char charcoal (26 +/- 4), Mallinckrodt USP charcoal (26 +/- 10), Norit A charcoal (22 +/- 4) and cholestyramine (0). For the bile salt sodium desoxycholate in ammonia: sodium bicarbonate, pH 8.2, the Qm with cholestyramine was 4641 +/- 2669 and with Super Char was 2814 +/- 667 (p = 0.11). We then contrasted the effect of cholestyramine (1%, added to the diet) and Super Char (1% or 2%) on plasma cholesterol concentrations in rabbits made hypercholesterolemic with a diet containing casein. The percent reductions were 61 in one rabbit fed chole styramine, 61 and 67 in two rabbits fed 1% Super Char, and 90 in one rabbit fed 2% Super Char. In WHHL homozygous rabbits, reductions in plasma cholesterol from pre-treatment and post-treatment levels, respectively, averaged 52% and 38% with 2% cholestyramine (2 animals), 70% and 43% with 2% Super Char (2 animals), and 70% and 63% with 4% Super Char (3 animals). The effectiveness of cholestyramine in animals that lack functional cellular receptors for low density lipoprotein was unexpected. Super Char charcoal appears to be an effective hypocholesterolemic agent, warranting study in man. MESH MEDICAL SUBJECT HEADINGS: Animal-; Cholestyramine-therapeutic-use; Comparative-Study; Deoxycholic-Acid-pharmacology; In-Vitro; Rabbits-; Support,-U.S.-Gov't,-Non-P.H.S. MESH MEDICAL SUBJECT HEADINGS: *Anticholesteremic-Agents-therapeutic-use;
*Charcoal-therapeutic-use; *Hypercholesterolemia-drug-therapy
RN CAS REGISTRY NUMBER OR EC NUMBER: 11041-12-6; 16291-96-6; 83-44-3 NM NAME OF SUBSTANCE: Cholestyramine; Charcoal; Deoxycholic-Acid ISSN INTERNATIONAL STANDARD SERIAL NUMBER: 0379-0355 AN MEDLINE ACCESSION NUMBER: 88156426 UD UPDATE CODE: 8806

TI TITLE: Superactivated charcoal versus cholestyramine for cholesterol lowering: a randomized cross-over trial. AUTHOR(S): Park-GD; Spector-R; Kitt-TM AD ADDRESS OF AUTHOR: Department of Internal Medicine, College of Medicine, University of Iowa, Iowa City. SO SOURCE (BIBLIOGRAPHIC CITATION): J-Clin-Pharmacol. 1988 May; 28(5): 416-9 ISSN INTERNATIONAL STANDARD SERIAL NUMBER: 0091-2700 PY PUBLICATION YEAR: 1988 LA LANGUAGE OF ARTICLE: ENGLISH CP COUNTRY OF PUBLICATION: UNITED-STATES AB ABSTRACT: To evaluate the relative abilities of superactivated charcoal (20 g twice daily) and cholestyramine (8 g twice daily) to lower plasma cholesterol concentrations acutely, six hypercholesterolemic patients were studied using a randomized cross-over design. After a 1-week dietary control period, each subject received 3 weeks of each treatment regimen on separate occasions. Superactivated charcoal and cholestyramine reduced total plasma cholesterol by 21.8 +/- 3.8% and 16.2 +/- 2.4%, respectively. Side effects were mild and similar for both treatments. At the dosage regimens studied, superactivated charcoal and cholestyramine have comparable ability to lower plasma cholesterol concentrations. MESH MEDICAL SUBJECT HEADINGS: Adult-; Charcoal-adverse-effects; Cholestyramine-adverse-effects; Clinical-Trials; Diet-; Female-; Human-; Male-; Middle-Age; Random-Allocation; Support,-Non-U.S.-Gov't; Support,-U.S.-Gov't,-P.H.S.; Time-Factors; Triglycerides-blood MESH MEDICAL SUBJECT HEADINGS: *Anticholesteremic-Agents; *Charcoal-pharmacology; *Cholesterol-blood; *Cholestyramine-pharmacology PT PUBLICATION TYPE: CLINICAL-TRIAL CN CONTRACT OR GRANT NUMBERS: RR59 RN CAS REGISTRY NUMBER OR EC NUMBER: 11041-12-6; 16291-96-6; 57-88-5 NM NAME OF SUBSTANCE: Cholestyramine; Charcoal; Cholesterol AN MEDLINE ACCESSION NUMBER:88273727 UD UPDATE CODE: 8810

TI TITLE: Activated charcoal in the treatment of hypercholesterolaemia: dose-response relationships and comparison with cholestyramine. AU AUTHOR(S): Neuvonen-PJ; Kuusisto-P; Vapaatalo-H; Manninen-V AD ADDRESS OF AUTHOR: Department of Clinical Pharmacology, University of Helsinki, Finland. SO SOURCE (BIBLIOGRAPHIC CITATION): Eur-J-Clin-Pharmacol. 1989; 37(3): 225-30 ISSN INTERNATIONAL STANDARD SERIAL NUMBER: 0031-6970 PY PUBLICATION YEAR: 1989 LA LANGUAGE OF ARTICLE: ENGLISH CP COUNTRY OF
PUBLICATION: GERMANY-WEST
AB ABSTRACT: The dose-response relationship of activated charcoal in reducing serum cholesterol was determined and the effects of charcoal and cholestyramine were compared in patients with hypercholesterolaemia. In a cross-over study 7 patients ingested charcoal 4, 8, 16 or 32 g/day, and finally bran, each phase lasting for 3 weeks. Serum total and LDL-cholesterol were decreased (maximum 29% and 41%, respectively) and the ratio of HDL/LDL-cholesterol was increased (maximum 121%) by charcoal in a dose dependent manner. Ten further patients with severe hypercholesterolaemia ingested daily for 3 weeks, in random order, activated charcoal 16 g, cholestyramine 16 g, activated charcoal 8 g + cholestyramine 8 g, or bran. The concentrations of total and LDL-cholesterol were reduced by charcoal (23% and 29%, respectively), cholestyramine (31% and 39%) and their combination (30% and 38%). The ratio of HDL/LDL-cholesterol was increased from 0.13 to 0.23 by charcoal, to 0.29 by cholestyramine, and to 0.25 by their combination. Serum triglycerides were increased by cholestyramine but not by charcoal. Other parameters, including the serum concentrations of vitamin A, E and 25(OH)D3 remained unaffected. The changes in lipids only partly subsided during the 3-week bran phase. In general, the acceptability by the patients and the efficacy of activated charcoal, cholestyramine and their combination were about equal, but there were individual preferences for particular treatments. MESH MEDICAL SUBJECT HEADINGS: Adult-; Cholesterol-blood; Comparative-Study; Dose-Response-Relationship,-Drug; Drug-Therapy,-Combination; Female-; Human-; Hypercholesterolemia,-Familial-blood;
Lipoproteins,-HDL-Cholesterol-blood;
Lipoproteins,-LDL-Cholesterol-blood; Male-; Middle-Age; Support,-Non-U.S.-Gov't; Triglycerides-blood MESH MEDICAL SUBJECT
HEADINGS: *Charcoal-therapeutic-use; *Cholestyramine-therapeutic-use; *Hypercholesterolemia,-Familial-drug-therapy
RN CAS REGISTRY NUMBER OR EC NUMBER: 11041-12-6; 16291-96-6; 57-88-5 NM NAME OF SUBSTANCE: Cholestyramine; Charcoal; Cholesterol AN MEDLINE ACCESSION NUMBER:

So far, the only super charcoal sources I've seen are for fish tank filters and for soaking up household or chemical spills. If anyone finds pharmaceutical grade versions, please post. I'll enable comments on this even though it's a handbook page.

Antibiotic Susceptibility Tests for Three Phases of Cpn

The following is from the indicated patent.

Editor: In reading the table, "positive" means that the signal for Cpni [3] still could be detected. "Negative" means that no signal for Cpn was detected, i.e. Cpn was eradicated in all of it's forms. The MOMP gene detected by the Vanderbilt tests is present if any of the three phases of Cpn are present. The table demonstrates the faster erradication using the INHi [13]/Metronidazolei [14]/Penicillamine combo with the particular cell culture being tested, and that other combinations were also effective given longer time. Please remember that this is a laboratory cell culture test, not a clinical trial.

"Two week exposure of single agents including the fluoroquinolone, ofloxacin, and the macrolide, clarithromycin, at 1 .mu.g/ml failed to clear HeLa cells in culture of a detectable PCRi [15] signal for the MOMP gene of Chlamydia pneumoniae. In contrast, triple agents consisting of isoniazid (INH), metronidazole, and penicillamine (1 .mu.g/ml each) resulted in no detectable PCR signal (Table 9). None of these agents, effective in the triple combination, is currently recognized as an anti-chlamydial agent.

Table 10 provides the results of an expanded study of antimicrobial susceptibilities at two different concentrations of antimicrobial agents, used alone and in combination, when exposed to the antimicrobial agents for two weeks. In addition to the agents already mentioned, minocycline, doxycycline, rifampin and sulfamethoxizole/trimethoprim, at all concentrations tested, failed to clear the PCR signal for chlamydia MOMP. Only the triple combination of isoniazid, metronidazole and penicillamine cleared the PCR signal. The triple combination was effective at both low and high concentrations. Table 10 also demonstrates the effect of a 4 week exposure with the same expanded series of antimicrobial agents alone and in combination. A number of triple combinations of antimicrobial agents resulted in cell cultures in which the PCR signal for the chlamydial MOMP gene could not be detected."

Candida

Candida is a ubiquitous human pathogen which is well known, understood and researched by traditional medicine. However alternative practitioners have put forth a new understanding about how it may function in the body and though this theory is not well established or well supported in research yet, some people find that addressing "candida" in the alternative paradigm helps them reach their goals.

With this in mind, and with the experience of a few of our members who have in fact felt they have done better by embracing this alternative approach along with the CAPi [1], we offer here this information to give you a brief overview of what the theory is and how it may possibly be helpful. We have also compiled a list of the anti candida supplementsi [16] our members have found helpful for relieving their symptoms. This is in no way part of any CAPS protocol endorsed by either Dr Wheldon, Dr Stratton or used at all at Vanderbilt, although any competent physician will address candida in the symptomatic patient experiencing traditional candida (ie a vaginal infection)

The inclusion if this page should not be interpreted as an endorsement of the relatively unproven alternative form of candidiasis, nor should it cause you to think that all people using CAP have this issue because our experience has been that few people do. This is assumed to be because the CPn is an immune system pathogen and as the system is freed of it's pathogenic load, the improved function allows any other secondary or opportunistic infections to be cleared up as well. That having been said, it is also true that antibiotics, especially long term ones, are known to disrupt the balance of bacteria and yeast normal to the gut and therefore yeast issues are, to a certain extent, considered a possibility by any practitioners prescribing these drugs.

Please be aware that this page is not intended to be an exhaustive review of the theories and possibilities, it is just to give you a brief overview of what it is and how it might be an issue for our members and give you enough information to decide if you need to pursue it further.

The wewll established view of traditional medicine:

Candida Albicans is a yeast that lives in all human beings and it is part of what is considered normal flora for the body (normal germs). It thrives in dark moist places on the body such as the intestinal tract, the mouth, the vagina and the moist crevices of the skin. Ordinarily, there is also other normal flora in these places that keeps the yeast in check and stops it from overgrowth.

When something upsets this natural balance, then pathogenic numbers of candida can be allowed to grow. Taking antibiotics is one of the primary things that allows this over growth to occur because the "other normal flora" that keeps candida in check are reduced by the antibiotic. People then may experience monilial vaginosis (vaginal yeast infection), thrush [17],skin infections or dysbiosis (intestinal imbalance in the yeast population resulting in diarrhea or constipation). According to traditional medicine, these are temporary problems that are easily fixed with probiotics and/or antifungals and a little time, as the body and immune system straightens this issue out without too much difficulty in the normal person.

In the immunocompromised person, such as an AIDS patient whose immune system is severely impacted, the yeast can overgrow and actually become systemic (in the blood, body wide). This is a grave emergency requiring ICU care and IV antifungal drugs. This systemic version of yeast in the immunocompromised patient is very obvious, severe and potentially fatal.

The traditional view is very black and white on this. Either candida is a minor non issue that your body can handle with minor assistance or it is very, very grave and life threatening due to some kind of profound immune dysfunction. An example of the traditional view on candida can be found HERE [18].

The alternative view:

Alternative practitioners agree with all that is stated above as it is well documented. But they also believe that there can be a subacute version of candida dysbiosis that the body does not correct on it's own.

This is the theory: the person takes an antibiotic and intestinal dysbiosis in the traditional sense occurs. The body for some reason does not get back into balance and the yeast remains the dominant organism in the intestines. It changes forms into a mycelic type (it puts out tendrils) that penetrate the intestinal walls causing the barrier to be compromised so that foods and other things the person eats are allowed to "leak out" as undigested proteins into the person's blood stream (ordinarily food is broken down thoroughly into generic components like simple carbohydrate). This "leaky gut" creates havoc system wide as the person will react to these foreign proteins as if they were bacteria, causing the immune system to react and creating antibodies and inflammation. This results in a multitude of symptoms in the patient in nearly every organ and system in the body. Some authors suggest there is even molecular mimicry involved, meaning that these foreign proteins that do not belong in the blood may cause the immune system to create immune cells that cross react (attack the foreign protein of the food that leaked out as well as accidentally attacking some of your own tissues). In this paradigm, this is theoretically seen as the cause of "autoimmunity".

In the US, the assessment of this type of candidiasis is largely done by naturopaths (ND's), who are responsible for the wide spread awareness/concern of this possible issue as they have embraced the model in spite of it's lack of scientific support. For many, treatment and diagnosis of candidiasis comprises the bulk of their practice and is their first treatment and diagnosis of choice in many, if not most, illnesses. In their view, it is seen as a widespread and common illness requiring lots of time (years), effort (including a very stringent and difficult diet) and naturopathic assistance (endless prescriptions for supplements and or antifungals like nystatin) to recover. This is an expensive as well as involved treatment. Chronic illnesses like MSi [19] are seen as a "candida leaky gut" causing molecular mimicry and the theory says if you treat the candida, the MS goes away as the chronic immune stimulation is relieved. Diseasesi [11] like CFSi [20] are likewise seen as being foreign proteins system wide and exhaustion caused by the constant battle against this pathogen.

In the case of MS, some practitioners have gone even further and stated in no uncertain terms that MS is caused by candida and/or fungus. An example of this may be seen here [21]. Dr Wheldon has addressed this issue from his extensive background as a microbiologist and recognized immediately that the authors made a critical error in their thinking: the word gliotoxin is descriptive, not specific, and like the word "antibiotic" refers to many things. He notes that the "gliotoxin" found in the brain of MS patients is compeletely different chemically and structurally than the gliotoxin created by candida. You may read about this from Dr Wheldon himself HERE [22] One need not worry that perhaps MS can be triggered by candida; there is no evidence of fungus or fungal byproducts in the brains of MS patients. The "gliotoxin" found in MS brains is a protein, the gliotoxin made by candida is not, and utterly different. There are however a number studies finding the DNA fingerprint of CPn in MS brains many of which we reference in our archives.

There is little in the way of hard science (ie peer reviewed studies that are generally accepted) directly supporting the alternative candidiasis model in any of it's versions. Its treatment and diagnosis instead rely heavily on anecdotal evidence and the proposed theory. Yet, it is not unreasonable to imagine that candida might become problematic in the gut as it certainly can become a problem in the mouth or vagina and these well known types of infections do need treatment. So, while it is not implausible that the intestines also might be infected in the same way as these other areas, it is as yet still theoretical. What would be needed is for many people who had a specific set of symptoms to have a biopsy or some other incontrovertible proof of the proposed mycelic intestinal candida infection, allow half to be treated for the candida and the other half to be given a fake medicine, and for those persons who got actual anti candida medicine to recover normal health with relief of those symptoms as well as demonstrating a normal candida free biopsy after the treatment.
Such a double blind study has not been done and thus treatment remains a kind of empirical treatment for a kind of infection we have no proof exists in the mycelic form in the guts of such individuals.

From the traditional medicinal point of view the theory and treatment borders on quackery and the diagnosis 'candidiasis' in the alternative paradigm tends to be viewed with extreme skepticism. The lack of good studies supporting the diagnosis and the commercially driven candida supplement market do not help. A few conventional MD's who were treating candidiasis in the alternative paradigm have had their practices and licenses scrutinized by their local medical boards for endorsing scientifically unproven and unsupported practices and some have even had their licences suspended. While there are some forward thinking MD's for whom such as yet unproven but anecdotally supported paradigms are a reasonable approach, especially for patients struggling with issues not helped by conventional approaches, by and large you will not find support for this paradigm in the conventional medical community.

So, how does anyone know they have candidiasis issues that possibly might be helped by the alternative approach? When might one consider it?:

The evidence for this is largely anecdotal, meaning that if alternative practitioners treat using anti yeast supplements people seem to feel better, rather than there being some kind of objective measure of improvement, like a clear lab result. There are some labs that test for this form of candidiasis and some patient directed tests to do(like the home saliva test seen HERE [23]) but none of these are generally accepted so you cannot go to your regular medical doctor and ask for a candida test other than the traditional type of smear, such as that used to detect monilial vaginosis. If you have not done it yet, find the clickable word 'thrush' earlier in this document and see the pictures of what a candida infection looks like in the mouth. It is much more than a "white tongue", but one can imagine theoretically if such an infection were in the intestines it could be a problem as it is outlined by the alternative theory.

The symptoms of candidiasis in the alternative paradigm may be seen HERE [24]. It includes a very long list of symptoms that presumably may be related to candida overgrowth.

In addition to the above list of symptoms, the people on CAP who feel they are having an issue with candida overgrowth along with treatment have complained of such symptoms as brain fog, a stall or plateau in their treatment progress, intestinal symptoms like bloating, diarrhea or constipation, thrush, skin infection confirmed as yeast, and typical vaginal candida. If you have these symptoms talk to your doctor about possible treatment as some of our members have had candida issues (like candida skin infections or monilial vaginitis) that were easily diagnosed by their regular doctor and well treated using conventional medicine and prescription medication. If your symptoms are vague and your doctor finds nothing unusual, then you might try using some of the anti candida supplements listed in Michele's chart (link below )working from the alternative theory or seek the help of a competent Naturopath.

Of course do note that taking antibiotics long term even in the conventional medical paradigm results in a person being at risk for candida issues, especially dysbiosis. The CAP supplements include daily doses of probiotics to help keep yeast overgrowth at bay. Since the CPn is an immune system infection and the immune system gets repaired by treatment, the model includes the idea that the body will be able to handle yeast effectively as any normal person would without difficulty as treatment progresses. NAC is also anti yeast as it breaks up the gliotoxin made by candida (reference David Wheldoni [25], link above).

If you, however, feel that you might personally be benefitted by treating for yeast issues via supplements along with CAP, then this brief background of the issue and its various aspects will get you started. Please study further for more information as this is intended as an overview, but be aware that this is an area that has many commercially driven claims. Be cautious and note that the claims in this arena are often not supported by the rigerous scientific standards that would be ideal. As an example, if one company claims that their product is the only one that actually gets rid of candida, one wonders how they can make this statement given that there are no standard tests for this issue, no standardized objective diagnostic criteria and no hard evidence for evaluating whether or not candida is gone. Perhaps what they mean is that all the people we talked to thought they were better after using our product. I personally do not mind using such a product to see if it helps me in some way but I resent weak evidence being presented as if it were real "research".

I personally have used Candex and Candida cleanse in addition to Primal defense and saccaromyces boulardii as probiotics and found the addition of the "anti candida" supplements regulated my elimination back to normal where the probiotics alone (several brands) did not do that, so I use them for a specific symptom because they work for that symptom in me.

Briefly, the kinds of treatments for this issue fall into several catagories:
1 Prescription anti-fungals, such as nystatin, which interfere with replication of the yeast which your regular MD will prescribe if you have a traditional yeast infection recognized by the traditional paradigm.
2 Probiotics which are "healthy" normal bacteria that crowd out the candida overgrowth and return the bowel to balance and which are also killed off themselves by the antibiotics taken in CAP, thus constant doses are needed. These are included in the CAP as they are well known to help reduce the incidence of dysbiosis and possibly even clostridium difficile (s boulardii especially)
3 enzymes which break down the walls of the candida thus killing it and which must be taken on an empty stomach (or it'll just break down the food that is there instead)

The next page on this subject is a list of such items compiled by Michele of all the supplements members of this site have discussed for this issue. We are not endorsing any of these products specifically, just providing a list so people can see what we discussed and the comments made by people about those products...
nor are we offering medical advice or diagnosing any health issue. Only your doctor can do that. And finally, a repeat that these kinds of supplements are not part of the CAPs protocols nor are they viewed as necessary for the ordinary person on CAP. Most people will find they have no problems with candida.

Candida Supplements

This page will continually be revised! As will the Antifungal and Probiotic chart.  If you'd like to add something to the list or make some contribution in terms of your practice, please pm Michele [26] and give me your ideas.

We are looking for people to give us a protocol of antifungals/probiotics that works for them.   It might be useful also if you include the symptoms your are trying to eradicate.   No more than a paragraph would be good.

Cpn "Quick Survey's" of Treatment Results

These are two informal surveys done a couple of months ago to get some quick answers about treatment response. They are both small numbers, hence called informal.

We had done larger surveys in prior years but the last one was too ambitious in scale and too difficult to analyze and correct errors in. I'll try again eventually with a more modest survey.

These were done as "quick and dirty" polls to get some sense of responses to CAPi [1]i [29] from those active on the site at the time. Note that both are small numbers, so any individual's extreme responses will affect the percentages a lot. Keep that in mind. I'm always cautious about poll results on websites because the sampling is not at all random (we are a self-selected group) and results are easily distorted by numbers, errors in reporting, e-vandalism, etc.. i.e. lack of scientific controls.

Having viewed posts on this site longitudinally over quite a period of time, as I started the site, I can say that the majority of people who have done the CAP for Cpni [30] have reported improvements in their disease condition. Mileage varies. Improvement for some means being able to work or write again, and for others... that they are not dead. Hard to assess the scale of it, so the surveys leave it subjective.

The time needed on treatment needed to have appreciable improvements appears to be dependent on bacterial loadi [31]i [31] (indicated by strength of initial negative reactions to CAP antibioticsi [27]i [27]/agents): the more severe the reactions the longer it takes as well as the slower one must go. As the course of treatment appears to be on the order of 2-5 years, and Cpnhelp is only 2 years 31 weeks (really!) old we don't have many who have completed treatment altogether (although there are quite a few who have been treated by Dr. Wheldon, Dr. Stratton, Dr. Powell, etc who have completed treatment and were never involved in this site). 

We have only had one definitive report of someone with MS (who I believe was around for this survey) who did a full CAP for over a year, and whose MS continued to worsen with no apparent effect on the course. There probably have been others who we don't have reports on. I think we have at least two "Former MS patients" (Sarah and LifeontheIce) who have completed CAP treatment and are medically considered free of their original disease. I report these so you have some sense of the range of responses. 

The results for the MS group:

Followed by the CFSi [20]/FM group results:

Cytochrome P450, Drug Interactions, & Secondary Porphyria

I’ve read a good deal of discussion about these issues since starting on CAPi [1]. Perhaps I’ve overlooked something in the archives, but I’ve read some recent sources that have given me new information about this complex topic.

Cytochrome P450 (CYP) is an isoenzyme, so called because it is closely related to other variants by homologous genesi [32]. They are named by a root (CYP), family (a number), a subfamily (a letter), and then the gene (another number). So, for example, one isoenzyme goes by the name of CYP2D6. CYP isoenzymes in the same family and subfamilies share structural similarities. The name comes from the fact that the cellular proteins in these enzymes have pigments that absorb light at wavelengths near 450 nm. These enzymes metabolize drugs, toxins and other substances, so they can be safely eliminated from the body. They are critical to the first phase of metabolism that makes a substance (or substrate) water soluble through an oxidation process. If the substrate is not transformed into a form that can be rapidly eliminated, then a second metabolic phase is undertaken (conjugation reaction) that adds a small endogenous molecule to make the substrate water soluble. As previously discussed here, most of the CYP metabolization occurs in the liver. Here’s a site [33] listing all the different genetic expressions of CYP, but 90% of the processing is done by six: 1A2, 2C9, 2C19, 2D6, 2E1, 3A4,5,7. 50% of all drugs are metabolized by CYP3A4,5,7. 

Each CYP isoenzyme has a list of substrates [34] that it can process. Some substrates can be processed by more than one enzyme. Each enzyme also has a list of substrates that can inhibit or induce metabolization. If metabolization is inhibited, all substrates that are processed by that enzyme stick around longer and at higher concentrations and therefore are more potent. When metabolization is induced, then all the substrates processed by that enzyme are eliminated more rapidly and so they are less potent. Many of the new drugs that are more potent (or have a longer half-life) achieve that effect by inhibiting the enzyme that processes them. 

You have to watch out for interactions between substrates. For example, if you take Lovastatin for high cholesteroli [10], you are advised not to eat grapefruit or drink grapefruit juice. This is because Lovastatin is processed by CYP3A4,5,7 but grapefruit juice is a moderately strong inhibitor of this enzyme. The interaction would increase the potency of Lovastatin and any other any other drug you take that is processed by CYP3A4,5,7. 

Several other factors can affect CYP isoenzyme activity. Genetic and age differences are modulators for some enzymes. 5-10% of Caucasians are slow metabolizers for the 2D6 enzyme, and 20% of Asians are slow for the 2C19 enzyme. The activity of the isoenzyme 3A4,5,7 declines with age, so drugs that are processed by this enzyme become more potent as you get older. However, 2D6 does not change with age. Bacterial endotoxinsi [35] (lipopolysaccharides - LPSi [36]) and inflammationi [37] from cytokinesi [38] also decrease CYP enzyme activity. 

CYP enzymes contain a hemei [4] iron center which is why they can induce secondary porphyriai [6]. When CYP substrates are ingested, the liver produces more heme precursors to process them. Too much demand can lead to secondary porphyria, particularly as suggest by Dr. Stratton, when the liver is infected with C. pneumoniae.

Here is a list of some of the medications and supplementsi [39] prescribed by both the Stratton and Wheldon protocolsi [40] and their effects on the some of the main CYP enzymes, as described by Flockhart DA. Drug Interactions: Cytochrome P450 Drug Interaction Table. Indiana University School of Medicine (2007). [34] Accessed June 5, 2008. 

Substance                  Substrate                        Inhibit                                    Induce

Azithromycin                                   

Cimetidine                                                    1A2 (Weak)

2C19, 2D6 (Weak),

                                                                        3A4,5,7 (Weak)           

 Clarithromycin            3A4,5,7                   3A4,5,7 (Strong)           

Doxycycline                                   

Duloxetine                    2D6                         2D6 (Mod)           

Glucocorticoids                                                                                                3A4,5,7

Ibuprofen                       2C9                       

Isoniazid (INH)                                              2C9, 2C19,                              2E1

                                                                         3A4,5,7           

Levaquin                                   

Methronidazole                                   

Omeprazole                 2C19                        2C19 (strong)                         1A2

Prednisone                                                                                                      2C19

Quercetin                                                       2C8           

Rifampin                                                                                                         2B6, 2C8,

                                                                                                                         2C19, 2C9,

                                                                                                                         2D6, 3A4,5,7

Table 1. CAP drugs, their CYP enzyme substrate, and modulatory CYP effects.

So, what can you conclude from this information? First, pay attention to interactions among drugs and supplementsi [16] that are metabolized by CYP enzymes. Early in my treatment for CFSi [20], my doctor prescribed both Cymbalta (duloxetine) and Wellbutrin (bupropion). Although not listed in this table, you can find from Dr. Flockhart’s tables that bupropion is a strong inhibitor of the 2D6 enzyme used to metabolize duloxetine. Combine this interaction with the possibility that I am one the 10% of Caucasians who are slow 2D6 metabolizers, and you have a plausible explanation why after a few months duloxetine became toxic for me to take. Recently on the cpnhelp.org site, there was some discussion [41] about rifampin. It induces metabolization in most of the major CYP enzymes, so the potency of other concomitant drugs or supplements processed by CYP might be weakened. Jim reported on a article that showed Vitamin Di [42] depletion by rifampin. Vitamin D is degraded by CYP24A1, so apparently rifampin can speed up metabolization in many different forms of CYP. Probably a good idea, as Daisy suggested, to take rifampin at a different time from your other medications and supplements. 

Second, to reduce secondary porphyria cut down on substances that require CYP metabolization. Here’s a list of drugs [43] that can create problems. You also can look at Flockhart’s table for other CYP substrates. 

Finally, note that not all the antibioticsi [27] we use are metabolized by CYP. About a month ago, I started on the revised Stratton protocol, changing from azithromycin to clarithromycin. I’ve had a much harder time with porphyria symptoms since making the change. Clarithromycin is processed by the CYP 3A4,5,7 enzyme and also is a strong inhibitor of it as well, which is why the antibiotic is potent. Azithromycin is metabolized by biliary elimination and not CYP. This change in medication has increased the demand for CYP in my system, and perhaps produced more heme precursors that cause porphyria. 

-------------------

CFS since 1/07. Pall anti-oxidant protocol since 8/07 with IM hydroxo-B12. Dx 3/08: Cpn, EBVi [44], CMV. Valtrex since 3/08. CAP since 4/08: Biaxin 500 mg BID, NAC 1200 mg BID, Flagyli [14] 500 mg BID pulse every 3 weeks.  

___________________________________________________________
CFSi [20] since 1/07. Pall anti-oxidant protocol since 8/07 with IM hydroxo-B12. Dx 3/08: Cpni [3], EBVi [44], CMV. Valtrex since 3/08. CAPi [1] since 4/08: Biaxin 500 mg BID, NACi [45] 1200 mg BID, Flagyli [14] 500 mg BID pulse every 3 weeks. 

INH

Some patients are prescribed Isoniazid (INHi [13]) in their CAPi [1]. I thought it would be helpful to have an extract from the patent materials which explains this "novel class of antichlamydial agents." INH has the potential for liver toxicity, so should always be used with regular blood tests for liver function.

Some things of note:

• In vitro (in the test tube) INH is effective against both the replicating and cryptic stationary phase of Cpni [3] but in vivo needs to be used along with other agents such as metronidazolei [14] and NACi [45].
• It is effective also against mycobacterial infectionsi [5], which can be a co-infection along with Cpn, causes similar inflammatory action in the body to Cpn infection, and is even more difficult to test for.
• It is particularly effective in clearing immunei [28] cells, macrophages and monocytes, of Cpn helping to empower the immune system. It is also noted as particularly suitable to clear Cpn from human blood vessels.
• It is not noted to what degree INH is effective in other tissues (e.g. nervous system tissue, crossing the BBBi [46], etc). Readers, please post any references to these questions in the forums.
• Niacini [47], a vitamin, is also effective (INH is a niacin derivative compound)
  

From patent 6,756,369 June 2004 (underlines added):

A unique class of antichlamydial agents that is effective against the replicating and cryptic stationary phases of Chlamydia (and possibly against some other stages of the cryptic phase) have been identified using the susceptibility tests described herein. This novel class of agents comprises ethambutol and isonicotinic acid congeners which include isoniazid (INH), isonicotinic acid (also known as niacin), nicotinic acid, pyrazinamide, ethionamide, and aconiazide; where INH is most preferred. Although these are currently considered effective only for mycobacterial infections, due in part to currently available [susceptability] susceptibility testing methodologies, it has been discovered that these agents, in combination with other antibioticsi [27], are particularly effective against Chlamydia. It is believed that the isonicotinic acid congeners target the constitutive production of catalase and peroxidase, which is a characteristic of microorganisms, such as mycobacteria, that infect monocytes and macrophages. Chlamydia can also successfully infect monocytes and macrophages.

Using INH to eradicate Chlamydia from macrophages and monocytes subsequently assists these cells in their role of fighting infection. However, these agents appear to be less effective, in vitro, against the cryptic phase. Thus, ethambutol, INH and other isonicotinic acid congeners ideally should be used in combination with agents that target other phases of the chlamydial life cycle. These isonicotinic acid congeners are nevertheless excellent agents for the long term therapy of chronic/systemic chlamydial infection generally, and in particular to chlamydial infection of endothelial and smooth muscle cells in human blood vessels.

INH and its congeners can be used to clear infection from monocytes and/or macrophages. When monocytes and macrophages are infected by Chlamydia, they become debilitated and cannot properly or effectively fight infection. It is believed that, if the chlamydial infection, per se, is cleared from these cells, then the monocytes and macrophages can resume their critical roles fighting chlamydial or other infection(s). Thus, patient responsiveness to combination therapy can be optimized by the inclusion of isonicotinic acid congeners. Accordingly, one aspect of the invention provides a specific method for reempowering monocytes or macrophages that have been compromised by a Chlamydia infection and, in turn, comprise treating the infection in other sites. Such compromised macrophages or monocytes can be activated by treating the chlamydial infection by contacting the infected macrophages and/or monocytes with an antichlamydial agent.

Patient Info - CAP medications