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Hab ich dir ja schon einige male empfohlen – L-Lysin, zusätzlich Omega 3, Vit D ( nimmste eh) , am besten noch colostrum…
aber alles halb so wild – die viralen CoInfekte haben wir fast alle…. ich auch
hatte valtrex, interferon und Co. – ging mir kein stück besser – Ergo intrazelluläre erreger beseitigen – und dann wirds wieder …
schau mal was david wheldon dazu sagt …
LG
Again, might these inner aliens return to a state of dormancy when the primary cause of cytokine disturbance is removed? It seems likely: we have been living with these beings, their genome trapped within ours, for untold time.
Human Herpes Virus 6, Epstein-Barr Virus
and Endogenous Retroviruses: an input into Multiple Sclerosis?A Brief Note
Human Herpes Virus 6 (HHV6), discovered in 1986, is a very common virus of early childhood, establishing itself in most children around the age of two and often causing a fever lasting for about three days. This age is too early in a person’s life to fit the epidemiological data for the acquisition of a primary pathogen in MS, although rare late primary infection, which might result in chronic active disease, cannot be completely ruled out. The virus is neurotropic, but primary infection seldom causes serious disease. It ordinarily remains dormant in the CNS for life.
Several studies have found elevated indicators of HHV6 in persons with MS. Challoner and co-workers found HHV6 DNA to be very common in the adult human brain; using immunohistochemical methods they found viral protein expression within the nuclei of of oligodendrocytes adjacent to MS lesions. [Challoner PB, Smith KT, Parker JD et al., Plaque-associated expression of human herpesvirus 6 in multiple sclerosis. Proc Natl Acad Sci U S A. 1995 Aug 1;92(16):7440-4.] On the face of it this seems like strong evidence of a primary causal connection. But is it? Let us look at at a parallel situation. Active ongoing infection with HHV6 is generally universal in persons with end-stage AIDS. [Corbellino M, et al. Disseminated human herpesvirus 6 infection in AIDS. Lancet 1993; 342:1242; Knox KK, Carrigan DR. Disseminated active HHV-6 infections in patients with AIDS. Lancet. 1994 Mar 5; 343(8897): 577-8.] The latter workers, using immunohistochemistry, found that in biopsied lymph nodes from AIDS patients the densities of HHV6 infections were significantly (p<0.016) higher in areas undergoing active HIV destruction than in areas free of destructive changes. [http://www.wisconsinlab.com/hiv.htm last viewed 13th Nov 2005.] An increased HHV6 load has been found in the lesions of AIDS-associated Progressive Multifocal Leukoencephalopathy, suggesting a cascade of pathogens (HIV, JC polyoma virus and HHV6.) [Blumberg BM, Mock DJ, Powers JM, et al., The HHV6 paradox: ubiquitous commensal or insidious pathogen? A two-step in situ PCR approach. J Clin Virol. 2000 May; 16(3): 159-78.]
Active HHV6 infection has been found superimposed on Legionnaire’s Disease. [Russler SK, Tapper MA, Knox KK et al., Pneumonitis associated with coinfection by human herpesvirus 6 and Legionella sp. in an immunocompetent adult. Am J Pathol. 1991; 138(6): 1405-11.] 2 of 3 patients with viral encephalitis, in whom both HHV6 and Herpes Simplex Virus (HSV) were isolated, died, a much higher proportion than in encephalitis due to HSV alone, where 1 of 19 died. [Tang YW, Espy MJ, Persing DH, Smith TF. Molecular evidence and clinical significance of herpesvirus coinfection in the central nervous system. J Clin Microbiol. 1997 Nov;35(11):2869-72.]
It seems that HHV6 is what might be termed a ‚henchman‘. That is, an organism widely present in human tissues and which is roused from a state of inactivity to cause gross pathology in areas that are already compromised by a primary intracellular pathogen. (It will be noted that Legionella pneumotropica is a strongly intracellular bacterium.) One might hypothesize that HHV6 may act as a ‚henchman‘ in chronic infections with Chl pneumoniae, which is of course also an intracellular pathogen. One might further speculate that eradication of the chlamydial infection, support of mitochondrial fatigue and restoration of normal immune function might return HHV6 to a state of dormancy.
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Epstein-Barr Virus (EBV) is another possible henchman. Usually acquired in childhood, late adolescence, or early adulthood, this common herpesvirus causes infectious mononucleosis and then establishes life-long latency in B lymphocytes; reactivations occur sporadically, with shedding of the virus in the saliva. Antibodies to EBV nuclear antigen-1 slowly rise after infection in the blood, and remain elevated for life. Antibodies to EBVNA-1 are found in oligoclonal bands in the CSF of patients with MS (Rand KH, Houck H et al., Epstein-Barr virus nuclear antigen-1 (EBNA-1) associated oligoclonal bands in patients with multiple sclerosis. J Neurol Sci. 2000 Feb 1;173(1):32-9.) and CD8+ T cell responses to latent EBV proteins are higher in MS patients than in controls. (Sabine Cepok, Dun Zhou et al., Identification of Epstein-Barr virus proteins as putative targets of the immune response in multiple sclerosis. J Clin Invest. 2005 May 2; 115(5): 1352–1360)
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Endogenous retroviruses have been suggested as participants in the progression of MS. These ancient sequences of virus DNA are replicas of those inserted into the genome by an accident of infection during germ-cell formation.
Might HERVs play a role in the development of MS? It seems possible. Activation of the HERVs HERV-H/RGH, HERV-W and ERV-9 was described when specific cell types (mainly B cells) from MS patients were cultivated in vitro. Viral RNA from these HERVs has been detected by reverse-transcriptase PCR methods in sera/plasma and brain tissues from MS patients, although not exclusively from these patients [reviewed by Clausen J. Endogenous retroviruses and MS: using ERVs as disease markers. Int MS J. 2003 Apr;10(1):22-8.] Is their activation a cytokine-mediated epiphenomenon, or does it have a pathogenic input into the disease? The many-phased natural history of MS suggests the re-awakening of inherent viruses. Clausen comments: ‚preliminary evidence suggests that specific ERVs may act as auto-, super- or neoantigens with the potential to enhance inflammatory responses or induce autoimmune reactions.‘
Again, might these inner aliens return to a state of dormancy when the primary cause of cytokine disturbance is removed? It seems likely: we have been living with these beings, their genome trapped within ours, for untold time.
Hallo Andreas !
Bei heftigen Allergischen Reaktionen die üblichen Antihistaminika, zyrtec und Co.
Finde das aber keine gute Idee. Ansonsten Chromoglicinsäure für den Darm.
Vielleicht gleichzeitige Einnahme von Kohle oder Heilerde ?
Im übrigen pos. IGG reicht aus, seih froh das es überhaupt positiv war….
Bartonella
Explanation: Bartonella spp. bacterium
Symptoms: Fever, chills, headache and severe pain in the tibia, weight loss, sore throat, papular or angiomatous rash
Treatment: Erythromycin, plus a Fluoroquinolone or RifampinUnd hier aus der lyme disease solution
Bartonella/BLO
There are two antibiotics that have been found to be most useful for treating Bartonella/BLO. My choice of these two antibiotics depends on two issues: (1) the extent to which the central nervous system (CNS) is affected and (2) the presence of co-infections other than Bartonella/BLO.
Levofloxacin (Levaquin)
This antibiotic is generally considered to be the antibiotic of choice for the treatment of Bartonella/BLO. Levaquin is a member of the family of antibiotics known as fluoroquinolones, which also includes ciprofloxacin (Cipro). All the fluoroquinolones seem to have activity against Bartonella/BLO, but Levaquin seems to be the most effective. The dosage is 250-500 mg once a day. It is best to take Levaquin on an empty stomach (or with minimal food if you need to eat something due to gastrointestinal side effects). Also, it is important not to take minerals like calcium, zinc, iron, and magnesium within several hours of the dose of Levaquin, because these minerals will bind Levaquin and render it less effective. I advise that patients take levofloxacin early in the morning, or it can be taken late in the evening, but not at bedtime. Except for the tetracycline antibiotic group, the fluoroquinolones are not generally used in combination with other antibiotics. Usually the course of treatment for Bartonella/BLO is one to three months, but occasionally it may take much longer.
Precautions: Levaquin is usually very well tolerated. The major adverse reaction that may occur with use of this medication is tendonitis (inflammation of the tendons). This complication is not common, but when it occurs, the medication must be stopped for a few days to allow symptoms to resolve. It can then be restarted in a few days at a lower dose, but if the tendonitis recurs, the medication should be stopped. The mechanism for tendonitis is not clearly known, but magnesium deficiency may The play a role in some patients. For this reason, I recommend that Bartonella/BLO patients ideally take 600–1,000 mg of magnesium for two weeks before beginning Levaquin therapy. Once Levaquin is begun, the patient should continue the magnesium, being careful to take it three (or more) hours before or after the dose of Levaquin.
Rifampin
Rifampin is a very old antibiotic that for many years has been used for the treatment of chronic infections such as tuberculosis. It is very effective against Bartonella/BLO. In particular, it is very useful for the neurological and psychiatric manifestations of Bartonella/BLO—severe anxiety and mood swings, panic, seizure-like episodes, memory loss, “spaciness,” confusion, disorientation episodes, and many other symptoms. Expect a herx-like reaction during the first week or so; then significant progress often occurs during the second or third week on rifampin.
It is best used in combination with certain other antibiotics. Frequently, those combinations include rifampin with doxycycline or rifampin with clarithromycin. The combination of rifampin with doxycycline is especially helpful when a patient with Bartonella/BLO is also infected with either Ehrlichia or Lyme. The dosage of rifampin is 300 mg per day for the first week; increase to 600 mg once a day after the first week. It is advisable to use rifampin in the evening (not at bedtime) on an empty stomach, three hours or more after a meal. It may be used in the morning an hour before breakfast also.
Rifabutin is a medication in the same family as rifampin and is reportedly very effective against Bartonella also. Apparently, it can be combined effectively with azithromycin. I do not have enough experience with its use to recommend it at this time.
Precautions: Rifampin is usually very well tolerated. It will always turn a patient’s urine orange. It may cause headaches and sleepiness. Liver function and blood counts should be monitored at regular intervals while using rifampin. The greatest concern about rifampin is the potential for interactions with other medications. Rifampin speeds the metabolism of certain medications, resulting in an increased breakdown of the other medications. Clinically, this drug-interaction issue often becomes a problem when certain pain medications are being used, and often a patient will require higher doses of pain medications while on rifampin.
Das schreit nach Bart Symptomen.
Schon mal tavanic bekommen und besserung gehabt?
Oder Rifa und Atzi ?
Kribbelnde bis brennende Füße und Unterschenkel, vor allem abends und morgens, und Muskelzuckungen und Muskelzittern
Bartonellosis
Common symptoms of bartonellosis include:
___Fatigue (often with agitation, unlike Lyme disease, which is more exhaustion)
___Low grade fevers, especially morning and/or late afternoon, often associated with feelings of „coming down with the flu or a virus“
___Sweats, often morning or late afternoon (sometimes at night) – often described as „thick“ or „sticky“ in nature
___Headaches, especially frontal (often confused with sinus) or on top of head
___Eye symptoms including episodes of blurred vision, red eyes, dry eyes
___Ringing in the ears (tinnitusi) and sometimes hearing problems (decreased or even increased sensitivity – so-called hyperacusis)
___Sore throats (recurring)
___Swollen glands, especially neck and under arms
___Anxiety and worry attacks; others perceive as „very anxious“
___Episodes of confusion and disorientation that are usually transient (and very scary); often can be seizure-like in nature
___Poor sleep (especially difficulty falling asleep); poor sleep quality
___Joint pain and stiffness (often both Left and Right sides as opposed to Lyme which is often on one side only with pain and stiffness that changes locations)
___Muscle pains especially the calves; may be twitching and cramping also
___Foot pain, more in the morning involving the heels or soles of the feet (sometimes misdiagnosed as plantar fasciitis)
___Nerve irritation symptoms which can be described as burning, vibrating, numb, shooting, etc.
___Tremors and/or muscle twitching
___Heart palpitations and strange chest pains
___Episodes of breathlessness
___Strange rashes recurring on the body often, red stretch marks, and peculiar tender lumps and nodules along the sides of the legs or arms, spider veins
___Gastrointestinal symptoms, abdominal pain and acid reflux
___Shin bone pain and tenderness
Bartonella is a bacterium that causes illness, the most commonly known of which is a disease called „Cat Scratch Fever.“ Thousands of known cases of Bartonella occur in the U.S. each Year, with the vast majority of known cases due to bites from fleas that infest cats or infected dogs (may also occur directly from bites and scratches from infected dogs or cats). Bartonella can also be transmitted by ticks that transmit Lyme Disease. In fact, in a study published recently, deer ticks from New Jersey had a higher prevalence of Bartonella organisms than of Lyme organisms.
It is unclear whether the organism that we see transmitted along with Lyme disease is actually a Bartonella species (such as B. henselae or B. quintana) or is „Bartonella-Like Organism“ (BLO) that is yet to be fully identified. While BLO has features similar to organisms in the Bartonella family, it also has features slimiar to the Mycoplasma and the Francisella (causes tularemia) families.
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Das existierende Cap könnte entweder um plaquenil ergänzt werden (hat mir Stratton mal gemailt) oder man dosiert Doxy höher bzw.Mino.
Oder man kombiniert Chlarythromycin 2×500 mit Doxy. Gibt doch viele Spielvarianten.
VG
Das kann ich nicht beurteilen, aber warum ist die Erstmilch in den ersten 24 – 48 h nach der Geburt so wichtig für den Aufbau des Immunsystems – wenn eh nichts ankommen sollte….
Hab hier auch noch einen anderen Thread über Colostrum im Forum gepostet.
Hab über Colostrum schon viel positives gelesen…
z.B. wird dieses auf der enterovirus website empdohlen.
ImmunoPro – This product is reported to have antiviral properties in addition to immune modulating effects. It is a combination of denatured whey, lactoferrin, active peptides, transfer factors, and immunoglobulins, and is said to be a potent stimulant of glutathione. The product contains high levels of cysteine and other amino acids that are precursors to glutathione. The compound is also supposed to shift cytokines toward a th1 profile. http://www.allergyresearchgroup.com/proddesc/products/immunopro.htmSoweit ich weiß wäre Colostrum eine gute Massnahme.
Ich hab das von NOW 500 mg mit 25 IGG Anteil
How Colostrum Works.
THE IMMUNE RESPONSE
The immune response is a defence mechanism by which the body fights infection. It is divided into two functional systems, the innate immune system and the adaptive immune system. The innate system is the first line of defence by which the host combats infectious agents and pathogenic microbes. This is a non-specific response which proves effective against most infective agents. In case this primary response is not affective and the invading microbe is lead to proliferate the adaptive immune system comes into action. The adaptive immune system produces a specific response in the form of antibodies to the infective agent that normally proves effective in neutralising that agent. In the case of the innate system resistance (immunity) is not improved by repeated infection. The adaptive immune response involves memory and gives rise to resistance to repeated exposure to the same infective agent. Childhood diseases such as mumps, measles, and chickenpox produce life-long immunity following an infection.Most infectious agents enter the body proper via the epithelial surfaces of either the upper respiratory, digestive or genito-urinary tract. Once infectious agents have penetrated the body a variety of physical and chemical defence mechanisms come into play to help protect these tissues from most infections. This involves a specialised set of cells called leukocytes (white blood cells) and their products that have evolved to help combat infection and disease. Leukocytes fall into two broad categories of cell types: phagocytes and lymphocytes. Phagocytes form part of the innate immune system and provide non-specific immunity. Shark liver oil stimulates the production of these cells. Included in this category are neutrophils, basophils, eosinophils, monocytes, and macrophages. Lymphocytes form the adaptive immune system and provide specific immunity. Colostrum helps to stimulate the formation of these type of cells when they are needed. There are two types of lymphocytes B cells and T cells. The B cells are differentiated in the bone marrow and found mainly in the lymph nodes and spleen. They are the cells that make antibodies (immunoglobulins). The T cells are differentiated in the thymus and fulfil two major functions. They regulate the activity of the B cells and directly attack infectious agents.
Genau deswegen empfiehlt Stratton auch ACC lebenslang zu nehmen, alldieweil es die Sporen tötet und eine Reinfektion somit verhindert wird.
“ ist es nicht sehr wahrscheinlich, dass es sich dann auch nochmal bei einem chronifiziert -ich meine wenn man durch irgendwelche Defekte/Mängel dazu neigt!?? Ich habe doch keine Gewissheit, wenn ich Dich richtig verstehe, dass es nie wieder kommt, oder?? Man wird ja nicht immun gegen die CPN!“
auch noch ne gute anlaufstelle:
um das nochmal hervorzuheben : Ich frage mich immer ob mein darm das Zielorgan der Infektion (breiiger Stuhl) ist oder ob dieses nur Folgesymptomatik ist.
Ich glaube fast es ist toxinvermittelt, denn wenn ich durch hohe Vit C Dosen Durchfall provoziere geht es mir meistens dannach besser…Arzt anfordern lassen.
Habs probatorisch gemacht weil Nachweis wohl schwierig ist. Kenne kein Labor.
Hab mir das zeugs über apotheke ausm Ausland bestellt.
Geholfen hats mir nicht
Bei mir ist es ja auch überwiegend der Darm. Ist der schlecht geht es mir schlecht.
Und halt immer breiig ungeformt.
Aber ich hab mit so vielen Methoden versucht Darmprotozooen zu erlegen (Alinia, Rifaximin u.s.w.)
das ich eher denke das die Magen darmsymptomatik nur ein Folgephänomen ist.Wie z.B. von Babesien etc. Auch Malaria verursacht sekundär Durchfälle weil der körper die gifte loswerden will.
Auch Leute mit CPN können Durchfall haben ,als sekundaeres Phänomen.
Seit Ihr auch der Meinung das Durchfälle von Toxinen etc kommen können, ohne das der Darm das eigentliche targetorgan ist?
Hier also das Treatment:
FIRST LINE TREATMENT PROTOCOL FOR CO-EXISTING DIENTAMOEBA
FRAGILIS AND BLASTOCYSTIS HOMINIS INFECTION
Dientamoeba fragilis and Blastocystis hominis are parasites found in the human digestive tract and
many of those infected are asymptomatic carriers. They can, however, cause a range of
gastrointestinal symptoms including diarrhoea and/or constipation, bloating, flatulence, loss of
appetite, abdominal discomfort and pain. In chronic cases, symptoms can include weight loss, blood
in the stool, dizziness, nausea and vomiting, rectal itching, chronic fatigue and depression. D. fragilis
has also been implicated in some cases of colitis/ bowel inflammationi. Many people suffer symptoms
for years before diagnosis and are often misdiagnosed with irritable bowel syndrome (IBSi). It is
possible to treat this infection with a combination of drugs – after which, most patients report either a
complete resolution, or a great reduction, in symptoms.
Medication schedule:
The patient will take a combination of four medications for 10 days.
– Septrin DS (20 Tablets) 2 times a day
– Diloxinide Furoate 500 mg (30 Capsules) 3 times a day
– Secnidazole 400 mg (30 Capsules) 3 times a day
– Doxycycline 50 mg (20 Tablets) 2 times a day
Septrin
DS
DiloxinideFuroate
500mg
Secnidazole
400 mg
Doxycycline
50 mg
Breakfast 1 Tablet 1 Capsule 1 Capsule 1 Tablet
Lunch 0 1 Capsule 1 Capsule 0
Dinner 1 Tablet 1 Capsule 1 Capsule 1 Tablet
These medications should be taken at the same time every day with food.
These medications have been known to cause the following side effects:
– Nausea and vomiting – Dizziness
– Headaches – Itching
– Tiredness
The patient should avoid drinking alcohol for the duration of treatment.
To ensure successful treatment of D. fragilis, B. hominis it is important that the patient complete the
entire 10 day medication schedule.
Follow-up treatment:
Three or four weeks after finishing the treatment protocol the patient should repeat the stool test to
determine whether the parasites have been eradicated.
Note: The following protocol involves taking antibioticsi. If you take the Pill for contraceptive
purposes please be aware that taking antibiotics can reduce the efficacy of the Pill. Other
forms of contraceptive protection must be used——————————————————————————–
Integrative Approaches to Lyme Disease, Stealth Infectionsi, and Inflammation May 5-7, 2006
45
Dr. William Stuppy
“Neuroendocrine Manifestations of Gastrointestinal Infections”
In his experience, sending tests for parasites to labs in the US always came back negative. Assumption was that there were no parasites in the US. Testing with salivary SIgA provides useful information. Found parasites in 672 patients.
Organism
Prevalence
Cryptosporidium
243
E. Histolytica
213
H. Pylorii
212
Giardia Lamblia
163
C. Difficile
114
Blastocystis Hominis
41
Ascaris Lumbricoides
64
Taenia solium
32
Trichinella Spiralis
23
Adding up the numbers shows that several subjects had multiple infections. Assumption was that Cryptosporidium, C. Difficile, etc. were not going to be found.
95% of labs do not report blastocystis. There is also a debate on whether or not it is a commensal or pathenogen. Dr. Stuppy suggested to those that do not understand it is pathenogenic should consider drinking blastocystis and see how they feel.
Ascaris, Taenia, Trichinella not uncommon. When treated for Ascaris, salivary antibody goes away.
Follow adrenal function with saliva testing and autonomic nervous system with HRV (heart rate variability) – these manifestations are very common.
Adrenal Dysfunction – elevation of cortisol between 4am and 8am. DHEAi levels are low. Most are overweight and increased abdominal girth. Chronic infection with parasites will lead to weight gain. The parasites often cause adrenal dysfunction.
ANS Dysfunction – with parasites, often have sympathetic hyperactivity and parasympathetic hypoactivity especially at nighttime. HRV measures beat to beat variation in milliseconds. HRV represents the condition of the autonomic nervous system.
Other issues with parasites were diminished melatonini and irregularities of insulin activity related to cortisol. With salivary testing, melatonin is low. When parasites are eradicated, melatonin returns to normal.
Strongly suspect gastrointestinal infection in patient with adrenal dysfunction. Test and treat for adrenal dysfunction.——————————————————————————–
Despite what much of the current mainstream medical community claims, blastocystis hominis (or at least certain sub-strains) is clearly and unequivocally a pathogen.I’ve worked extensively in latin american countries and have come down, repeatedly, with amoebiasis and blastocystis hominis. The amoebas were relatively easy to beat. Not so blastocystis hominis.
Although I am not a doctor, I ascribe the failure of most treatments of blastocystis to a near complete lack of understanding of both its natural cycle and as well difficulty in its eradication. Doctor’s have an unfortunate tendancy of underprescribing for things they don’t understand, and third world have a tendancy to pass our antibiotics like candy. The result of this ignorance on both sides has created superbugs, and blastocystis is one them.
From my own extensive personal infection history I can tell you that the way to figure, better than doctors can, whether you are infected is to write down, exactly, when you are having the ‚worst‘ symptoms. I did this after doctors, including near-worthless tropical medicine disease ’specialists‘, told me there was ’nothing wrong because you have already completed treatment with metronidazol‘. Latin American doctors laugh at metronidazol (= Flagyl) because of widespread resistance of bugs to this. I have not yet met ONE American doctor who understands this. Further, doctors will typically treat you ONLY with metronidazol while being completely unaware of the fact that you have to KILL all the bugs through your intestinal track, something metronidazol does NOT do, or else they will come right back in a matter of weeks. You need a luminal antibiotic such as Kitnos (etofamide), Pharmeban (idioquino..something), and/or paromycin. If you don’t do these drugs in combination YOU WILL NOT GET CLEARED.
My personal bug cycle is strongly and clearly 5-6 days. The sicker you get, the fewer ‚good‘ days you have between the bad days. Realizing my bugs had a 5 days cycle I concluded I HAD TO kill at least two cycles, meaning you need to take AT LEAST 10 days of treatment. If you want to be even more agressive, 15 days is even better. I figured this out on my own, but have since run into one specialist in California who treats for 15 days as well.
To clear yourself of blasto, you might consider trying:
Kitnos (etofamide) 500 mg every 12 hours for 15 days
combined with
Albendazol 200 mg every 12 hours for 15 days
combined with
Rifaximin 200 mg every 8 hours for 15 daysI take these with Metamucil, about one tablespoon.
This rid me of ALL gas and bloating problems, it revived my appetite, and my energy level as well. It also cleared my stools of any signs of blastocystis hominis for many months of testing. My wife never cleared herself of these, and I got re-infected and am now treating myself again.
Also, if you have diahrrea research suggests you SHOULD take immodium with these drugs. The warnings against doing so are not borne out by research you can do yourself on the web. Controlled studies show that taking immodium actually speeds up the cure rate when taking antibiotics. It would seem that the idea of flushing your system of toxins is an old wives tale, and that probably taking immodium allows more residence times for the medicines in question, thus improving their efficacy.
Finally, for those who REALLY wish to whip this, I would strongly suggest duplicating the treatment I have listed above after a 10-15 day break.
DO NOT LISTEN TO DOCTORS WHO TELL YOU TO TAKE FLAGYL FOR FIVE DAYS AND THEN TELL YOU YOU MAY HAVE ‚IBS‘. They are bordering on, in my opinion, malpractice in doing so and will be helping to create in you more resistant bug strains.
The web site http://www.badbugs.org
is a GREAT place to learn how to take more control over your own health and not get ‚taken‘ by the medical community.
