We want doctors to listen, we crave guidance from the very souls who inject our children with poison and send them reeling in toxic blood baths. Why the bittersweet battle? In one word - MONEY! We want our children to benefit from our costly health insurance and rightfully so!! Who wouldn't want their health issues addressed by their doctors and covered by their insurance?!
Be careful what you wish for.
What happens when mainstream doctors finally DO acknowledge that our children are walking medical books rather than genetically neurological head cases? Are we really ready for that?
This is already in the process of happening, so we KNOW what will transpire the minute doctors realize they can cash in on "curing" autism symptoms. Notice I said curing symptoms? Mainstream medicine is a pharmaceutical conundrum, the proverbial symptom band-aid, if you will.
Take PANDAS for example. PANDAS stands for Pediatric Autoimmune Neuropsychiatric Disorder Associated with Streptococcus. Let's thank ADHD.com for this detailed description of the 5 diagnostic criteria for the diagnosis of PANDAS below.
What are the diagnostic criteria for PANDAS?
Pandas is diagnosed if there is an episodic history of the following symptoms associated with strep infections.
- Presence of Obsessive-compulsive disorder and/or a tic disorder, ADHD symptoms or oppositional behaviors
- Association with neurological abnormalities (motor hyperactivity, or adventitious movements, such as choreiform movements)
- Pediatric onset of symptoms (age 3 years to puberty)
Episodic course of symptom severity. (symptoms come and go)
- Association with group A Beta-hemolytic streptococcal infection (GABHS)
- GABHS evidenced by either a positive throat culture for strep or positive for streptococcus serology (ASOT or AntiDNAse-B)
- A history of Scarlet Fever or Rheumatic fever
It is quickly gaining popularity with mainstream doctors. And what is their treatment for it, you ask? Well, medication, of course....pharmaceuticals. One of the worst things you can do to a child with an autoimmune disorder such as autism is prescribe them antibiotics, it messes with their already dysfunctional immune system. It tears down the already lacking terrain of their gut and it messes with their ability to fight off ANYTHING, let alone the nasty strep infections. In fact, one of the reasons people have problems with oxalates, is because antibiotics kill the oxalobacter formigenes bacteria and there is no known way to replenish it, via probiotics.
And when parents become desperate, because antibiotics no longer work (the bacteria become resistant to antibiotics and they build a matrix of biofilm to protect themselves) they are instructed that the only next step for them is a treatment called IVIG where blood plasma with protective antibodies is provided via a blood transfusion. Sounds ideal, doesn't it....a quick fix?! One IVIG treatment requires upwards of 10,000 donors!! Knowing what I know about illnesses like Lyme Disease, you couldn't pay ME to have this done with my kids. I don't want someone else's undiagnosed illness. Think about how hard it is to detect Lyme Disease, and how common it's become!! Even, if I were assured and RE-assured that the blood was specifically tested for Lyme Disease (among other illnesses), that would not be enough for me to risk my already fragile kids lives with the possibility that even one of those 10,000 donors could have Lyme Disease. There are other ways...
How should PANDAS be treated? I'm no doctor, of course. All I can tell you is that our older son had all of the symptoms associated with PANDAS at one point, errrr ok many points...HAD is the key word there though. I'm not convinced that all of the children being diagnosed with PANDAS actually have it, because many bad bacteria can exhibit the same symptoms. In fact, although Grayson had Hemolytic Strep bacteria, his more dysbiotic bacteria was Clostridia. My guess is that none of these doctors are checking their patients for heavy metal toxicity (properly) and I am sure they aren't considering a GFCFSF diet or any other diet for that matter. Like Lyme, Clostridia, Klebsiella, yeast overgrowth (and so many other pathogenic illnesses), PANDAS responds well to all the same methods of recovery being used in biomedicine. Ironically, camel milk has been compared to doing IVIG, perhaps this is one of the other reasons we are seeing such results with our treatment choices. If you want to learn more about why camel milk works, this link will take you to an earlier blog entry on camel milk.
If I were to consider all aspects involved with PANDAS, this is how I would approach it (wait, this is how I DID approach it, although in a slightly different order).
- GFCFSF diet
- Avoid refined sugars, simple carbs, and food coloring
- Introduce camel milk
- Add a liver support like artichoke extract or Liver Life.
- Natural anti-microbials for yeast, bacteria, parasites and viruses
- Weed and seed - It's EXTREMELY important to replenish the good bacteria with very high numbers of probiotics when you are spending most of your day killing off the bad guys. I call this weeding and seeding...we give about 350-500 billion CFUs nightly, at least 3 hours away from any natural antimicrobial. We were careful to increase their probiotics slowly, because this can cause significant die too.
- IgG food sensitivity testing and removal of all IgG positive foods
- Rotation diet for foods that are approved in diet
- Clean up toxins in environment like play-doh, markers, lotions, shampoos, and toothpaste, to avoid the gluten and casein as well as cleaning products, their mattresses, plates, pajamas, etc.
- Organic Acid Test from Great Plains (addressing issues as per the results)
- If high oxalic acid comes up on OAT, immediately start the low oxalate diet, heck, I would even go as far as to recommend trying a low oxalate diet for any and ALL kids with chronic pathogenic issues
- Supplementation for possible deficiencies
- The biofilm protocol (without EDTA, very important!) for persistent bacterial and yeast infections
- Hair "toxic and essential elements" test via DirectLabs.com (it's called Hair Elements-DDI KIT) to assess toxicity levels (reviewed against Andy Cutler's book, Hair Test Interpretation)
- Andy Cutler chelation protocol - this is another great link for his protocol
- Possibly even do a stool test anywhere along the way for the sake of knowing exactly which gut bugs you are dealing with so you know how to tailor your antimicrobials
Be careful what you wish for.
UPDATE December 8th...This just in from MercuryExposure.org!
From a 1984 study by Rowland et al. Antibiotics and Milk play a role in the efficency of Hg Excretion. In this study rats were given high doses of oral antibiotics the half-life for excretion of mercury increased from 10 days to >100 days. If the rats were also on a milk diet the excretion half-life increased to over 300 days. These results are consistent with the theory that demethylation of methylmercury by intestinal microflora is a major factor determining the excretion rate of mercury.
Effects of Diet on Mercury Metabolism and Excretion in Mice Given Methylmercury: Role of Gut Flora
Mice fed either (1) a pelleted rodent diet, (2) evaporated milk, or (3) a synthetic diet (high protein, low fat) exhibited different rates of whole body mercury elimination and fecal mercury excretion after exposure (per os) to methylmercuric chloride. The percentage of the total mercury body burden present as mercuric mercury was highest (35.3%) in mice fed the synthetic diet (which had the highest rate of mercury elimination) and lowest (6.6%) in the animals having the lowest mercury elimination rate (milk-fed mice). Mice fed the syn-thetic diet had lower mercury concentrations and had a higher proportion of mercuric mer-cury in their tissues than the mice from the other dietary groups. Treatment of the mice with antibiotics throughout the experimental period to suppress the gut flora reduced fecal mer-cury excretion and the dietary differences in whole body retention of mercury. Tissue mercury concentrations and proportion of organic mercury in feces, cecal contents, liver, and kidneys were increased by antibiotic treatment of mice fed the pelleted or synthetic diets.
These results are consistent with the theory that demethylation of methylmercury by intestinal microflora is a major factor determining the excretion rate of mercury.
The marked diet-related differences in whole body retention of Hg after MeHg exposure confirm the re-sults of Landry et al. 3 In addition, the differences in whole body retention were reflected in the amount or concentration of Hg present in the carcass (the major site of deposition of Hg in the mice), brain, blood, liver, and kidneys. The effect of diet on Hg concentration in brain (a target organ for MeHg toxicity) suggests that diet may influence MeHg-induced neurotoxicity since the concentration of Hg in tissues, particularly the central nervous system, has been correlated with the inci-dence of neurotoxicity in rats and mice.· 19 20
The three diets used in this study have many differences which make it difficult to differentiate the effects of specific dietary components1 although it would appear that dietary fiber is not an important factor governing the rate of Hg excretion since both the milk and GIBCO diets contained little indigestible residues.
Although differences in concentrations of Se were found in the three diets, it is unlikely that these were responsible for the differences in Hg elimination rates since the RMH3000 diet contained by far the highest Se concentration, yet mice fed this diet had an intermediate rate of Hg elimination. These results agree with those of Stil-lings el al., 21 who found that though dietary Se reduced the toxicity of MeHg, it did not appear to influence Hg elimination in feces or urine.
Over short time periods (up to 5 hrl co-administration of MeHgCI and low-molecular-weight thiol compounds has been shown to decrease blood Hg concentration and increase Hg accumulation by various organs by comparison to MeHgCI given alone. 22-24
Thus, differences in thiol concentrations in the diets and tissues may be responsible for diet-related changes in HHg tissue concentrations. However, in the present study, the thiol concentrations of the three diets were similar, and although some differences were detected in concentration of nonprotein-bound thiols in liver, they could not be correlated with Hg excretion rates or tissue Hg levels since mice fed milk or GIBCO diets had almost identical hepatic thiol concentrations. The con-centration of sulfhydryl compounds in the small intes-tine was highest in those mice fed milk probably due to an increase in glutathione from bile, because the ma-jority of the sulfhydryl groups were not protein-bound. However, it seems unlikely that differences in intestinal thiol concentration significantly affect Hg excretion rate since the sulfhydryl concentrations were greatly in excess of the Hg concentration to which the mice were exposed. It is noteworthy that the administration of MeHgCI increased (by 1-2 JLmoles/g tissue) the concentration of nonprotein-bound thiols in the livers of mice in all dietary groups, presumably affecting an increased synthesis of glutathione in bile.
It is possible that diet may also affect the whole body elimination of Hg via an effect on excretion of Hg in bile, since age-related changes in Hg elimination, can be as-cribed, at least in part, to changes in biliary excretion. 25
The differences in the amount of mercuric Hg in the whole body (Table 2), in the various tissues (Tables 3 and 4), and in cecal and colon contents (Fig. 4) in the animals fed the different diets suggest that diet-induced differences in Hg elimination are related to the extent of MeHg demethylation by the animals. The mice with the highest rates of Hg elimination, namely those fed GIBCO diet, had the highest proportion of their Hg body burden as mercuric Hg.
The previously demonstrated ability of the intestinal microilora to demethylate MeHg6 and its capacity to alter its metabolic activity in response to dietary modifi-cation 13•16 suggest that diet-induced changes in demeth-ylating activity of the gut flora are responsible for the differences in Hg elimination seen. Tlw results of the present study lend support to this theory.
It is clear that in all dietary groups a large proportion of total Hg in the gut was present in the mercuric form, especially in the cecum and colon. In particular, the GIBCO-fed animals reatained very high levels of Hg in the cecum and colon. Furthermore, the major route of excretion of Hg was the feces with only small amounts emerging in the urine, and in the GIBCO-fed mice the increased Hg elimination occurred via the feces rather than the urine. This indicates that MeHg demethylation occurs at sites where the product, mercuric Hg, does not re-enter the general circulation since parenterally administered HgCI2 is excreted mainly in the urine (Landry et al., unpublished observation, 1982).
Treatment of the mice with antibiotics to sterilize the gut contents virtually eliminated the diet-related dif-ferences in whole body Hg retention, in Hg excretion in feces and urine, and in the amount of mercuric Hg in whole body, gut contents, and tissues (especially in liver and kidney). These results are consistent with the theory that demethylation by the gut flora is a major determinant of the rate of Hg excretion after MeHg ex-posure. The almost complete retention of the dose of MeHg (apparent elimination of half-times> 100 days) in the animals without a gut flora and the increase in MeHg concentration in blood and liver is also consis-tent with the theory since it would be expected that the greater proportion of MeHg relative to total Hg in the gut of antibiotic-treated animals would result in greater absorption of the administered mercury dose.
Landry et al. (unpublished observation), using mice give MeHgCI intramuscularly, have reproduced the dietary-related differences in Hg elimination seen in orally dosed animals, but the three diets had little effect on Hg retention after parenteral administration of HgCI,. It would appear, therefore, that if MeHg is demethylated, diet is unlikely to exert any differential effects on Hg ... retention, suggesting that the differential effects of diet oc-cur on demethylation or on excretion of MeHg in bile.
In the mice given antibiotics, some residual formation November/December 1984 [Vol. 39, (No.6)] of mercuric Hg was apparent (Table 2) suggesting that sites of demethylation other than the gut flora exist. One possible site is the liver, although enzymatic demethyla-tion of MeHg by this organ has been little studied. It is also possible that the slow release of inorganic Hg from MeHg in the presence of thiol compounds17 contributes to inorganic Hg formation in vivo. \1\€ have confirmed (unpublished observations, 1981) that this can occur in the presence of thiol concentrations found in bile and in the liver (approximately 5 ~-tmole/mll.
In conclusion, the results of this study confirm previous reports 10 that the gut flora is the major site of de-methylation of MeHg in the mouse and strongly suggest that dietary effects on Hg elimination rates are mediated by changes in demethylating activity of the flora. The result of a high demethylation rate would be the formation in the gut lumen of mercuric Hg which, being poorly absorbed, interrupts the enterohepatic recycling of MeHg. 4
Large variations have been reported in rates of elimi-nation of Hg in human populations exposed to MeHg.18 It is conceivable that this variation may be related to the wide variation in composition of gut flora among individuals.29 Furthermore, if the major differences in gut flora that have been observed in populations in different geographic areas 10 are reflected in their MeHg demethylation rates, it is possible that there are inter-individual as well as inter-regional differences in suscep-tibility to MeHg poisoning.
Effects of Diet on Mercury Metabolism and Excretion in Mice Given Methylmercury: Role of Gut Flora
I. R. ROWLAND, Ph.D. The British Industrial Biological Research Association Woodmansterne Road Carshalton, Surrvey, United Kingdom R. D. ROBINSON, M.S. R. A. DOHERTY, M.D. Department of Pediatrics Environmental Health Sciences Center University of Rochester Rochester, New York 14642
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