riclapaz
Dagobah Resident
Laura said:Carl said:And Also Xylitol (In this case used against oral biofilms)
http://www.ncbi.nlm.nih.gov/pubmed/19178100
PURPOSE:
The aim of the present study was to examine whether xylitol, at different concentrations, inhibits the formation of an experimental model of oral biofilm.
MATERIALS AND METHODS:
Biofilms of six bacterial species (Streptococcus mutans, Streptococcus sobrinus, Lactobacillus rhamnosus, Actinomyces viscosus, Porphyromonas gingivalis and Fusobacterium nucleatum) were prepared on hydroxyapatite (HA) discs according to the Zürich Biofilm Model. Xylitol was tested at two concentrations, 1% and 3%. At the end of their designated incubation times, some HA discs were destined for confocal laser scanning microscopy (CLSM) and the others were harvested using a sterile surgical instrument. Aliquots of harvested biofilms were diluted and plated onto specific media. After a 48-h anaerobic incubation at 37 degrees C, the colony-forming units (CFUs) were counted.
RESULTS:
CLSM images showed that only a small amount of isolated bacteria was observed on the surface of HA discs. Culture of harvested biofilms showed an inhibition in the growth of different species included in the biofilms.
CONCLUSIONS:
Xylitol has a clear inhibitory effect on the formation of the experimental biofilms. This study shows that xylitol is not only efficient in inhibiting the acid production of cariogenic bacteria, but also in preventing the formation of a multispecies biofilm; it confirms the relevance of the use of this polyol for the prevention of oral diseases caused by dental plaque.
Well, that's pretty interesting. Perhaps the reason some of us have issues with xylitol is that the mycoplasmas/biofilms react against it. Maybe that's one clue to those who have such infections: they have a reaction to xylitol???
I wonder if the coconut oil could be another clue?
_http://www.easihealth.co.za/wordpress/wp-content/uploads/downloads/2011/02/trials/Monolaurin.pdf
author said:COCONUT OIL IN HEALTH AND DISEASE: ITS AND MONOLAURIN’S
POTENTIAL AS CURE FOR HIV/AIDS*
By
Dr. Conrado S. Dayrit**
HIV-AIDS Patients and the Coconut
According to Mary Enig(11), the AIDS organization, Keep Hope Alive, has documented several
HIV -AIDS patients whose viral load fell to as low as undetectable levels, when they took coconut
oil or ate coconut (half a coconut a day) or when they added coconut to their anti-HIV medication
(anti protease and/or antiretrovirals) that had previously not been effective. The amount of coconut
oil consumed (50 ml or 3 1/2 tablespoonfuls) or half of a coconut, would contain 20-25 grams of
lauric acid, which indicates that the oil is metabolized in the body to release lauric acid and/or
monolaurin.
The Monolaurin Trial on HIV-AIDS
The first clinical trial (pilot study) using Monolaurin for 6 months as monotherapy on 15 mv
patients was just completed (12). These 15 patients (Table 1) ages 21 to 38 years, 5 males and 10
females, were all regularly reporting to San Lazaro Hospital, the hospital for infectious disease of
the Department of Health. None of them could afford’ or ever received anti-HIV treatment. The
males averaged 58 k in weight (49 to 68 k) and the females, 54k (39 to 65 k). Seven showed
elevated liver enzymes (ALT and AST) and 12 had unexplained eosinophilia. Two patients had
high serum cholesterol and one had elevated triglyceride. No one had renal dysfunction. Their viral
load ranged from 1,960 to 1,190,000 except for one patient (#94-022B) whose load was too low to
3
count (below 400). This fact unfortunately was not determined before the random assignment of the
patients to the 3 treatment groups. The monolaurin used was 95% pure. It was given in capsules,
each containing 800 mg ML. The coconut oil was administered by tablespoonfuls.
The 3 treatment groups to which the 15 patients were randomly assigned were {Table II):
a) High Dose Monolaurin (HML): 7.2 grams (9 capsules) ML 3 time daily or about
22 grams daily
b) Low Dose Monolaurin (LML): 2.4 grams (3 capsules) ML 3 times daily or 7.2
grams daily.
c) Coconut oil (CNO): 15 ml 3 times daily or 45 ml daily. The ML content of this
dose is about the same as HML.
All patients were observed daily for any side effects. Baseline, 3-month and 6-month laboratory
examinations included: viral load (by PCR method), CD4 and CD8 counts (by-flow-cytometric
method), complete blood count, tests for liver function (ALT, AST), renal function (urea N and
creatinine), blood lipids (cholesterol, triglycerides, HDL) and body weight (k). Treatment benefit
was defmed as reduction in viral load and increase in CD4 count.
Tables II and III summarize the effects of the 3 treatment groups on the viral load, CD4 and
CD8 counts. On the 3rd month, 2 showed decreased viral count with HML, 2 with LML and 3 with
CNO for a total of 7 patients benefited. The other patients all had increased viral load. Patient #94-
022A continued to have undeterminable viral load and was excluded from the computation. On the
6th month, and end of the study. 8 of the 14 patients had decreased viral count, (2 of the 4 given
HML, 4 of the 5 given LML and 3 of the 5 given CNO). The decrease in viral count was, however,
significant only in 3 patients using the log Baseline-log 6th month ~ 0.5 criterion. Two of these
significant decreases were in the CNO group and one in the LML group.
The CD4. and CD8 counts (Table III) increased only in 5 patients and did not quite correlate
with the fall in viral load, decreasing even when the viral load fell and increasing when the viral
load rose. Patient #93006 had a steady viral load during the first 3 months but suffered a severe
secondary infection in the 5th and 6th month, which caused the HIV infection to worsen despite
fairly good CD4/CD8 response.
AIDS (CD4 less than 200) developed in 3 patients on the 3ni month of LML therapy (2 patients)
and CNO therapy (1 patient). The last mentioned patient (#86-001) died 2 weeks after the termination
of the study. The patient under LML, however, fared better; one (# 93028) recovered by the 6th
month. and the other (#95052) was showing improvement of both CD4 and CD8 counts at the end
of the study.
Eleven (11) subjects gained weight -from 1 k to 23 k -including the 2 who developed AIDS and
were recovering. The single AIDS fatality lost 6 k. The other 3 who failed to gain weight had
decreasing viral and rising CD4 counts.
4
About one-half of the subjects in this study complained of feeling of warmth and a greenish
hue to their urine (Table IV A), Both occurred at the beginning of the study and did not interfere
with its continuation. Another 3 subjects had flaring up of their acne.
There were 11 subjects with eosinophilia at the start and 7 subjects with some liver dysfunction
(Table 1). The treatment caused a rise of the eosinophilia in 7 of the II, and a rise in ALT/AST in 3
of the 7 (Table IVA).
The patients with normal liver and kidney functions showed no effect from the treatments.
At the beginning, 2 subjects had elevated cholesterol and another one had high serum triglyceride
(Table !VB). After 6 months, 4 patients had abnormal cholesterol and triglyceride, 3 had high
cholesterol only and 2 had high triglyceride only.
Conclusion from the Study
This initial trial confirmed the anecdotal reports that coconut oil does have an anti-viral effect
and can beneficially reduce the viral load of HIV patients.The positive anti-viral action was seen
not only with the monoglyceride of lauric acid but with coconut oil itself. This indicates that coconut
oil is metabolized to monoglyceride forms of C-8, C-IO, C- 12 to which it must owe its antipathogenic
activity.
More and longer therapies using monolaurin will have to be designed and done before the
defmitive role of such coco products can be determined. With such products, the outlook for more
efficacious and cheaper anti HIV therapy is improved.
Anti-pathogen Mechanism of Monotriglycerides of MCT
The fact dlat monolaurin’s activity is limited to lipid coated organisms (gram positive bacteria,
enveloped viruses) suggests strongly that the relatively short C-12, C-IO or C-8 [Icelandic scientists
have recently reported on the effectiveness of monocaprin (C-IO) against HIV virus] probably exert
their action on the lipid-layered coat or plasma membrane to destabilize it or even to cause its
rupture. If this mechanism proves correct, monolaurin (and monocaprin and monocapryliu) could
be bactericidal and could act synergistically with the present anti-HIV agents (the antiretrovirals
and protease inhibitors).
Reprise
With all the opprobrium cast against it, it bears repeating again and again that no evidence has
ever been presented to prove that coconut oil causes coronary heart disease in humans. All the
evidences presented have been in various species of animals who were given coconut oil alone
without the necessary dose of essential fats or PUFA that should be given, just like the essential
vitamins and minerals. On the contrary, the human epidemiologic evidence proves that coconut oil
is safe. Coconut eating peoples like the Polynesians (Table V) and Filipinos (Fig. I) have low
cholesterol, on the average, and very low incidence of heart disease.