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One GAPS advocate insists the GAPS introduction diet is better than SCD's intro. A careful comparison between the beginning stages of both diets reveals that the early phase of Pecanbread is more appropriate for children with autism than that of GAPS for scientific and practical reasons.

1 The Pecanbread protocol for the early phase of SCD is better suited for children with ASD because children with autism are notorious for being picky eaters.:

The GAPS intro diet is comprised of soups, fermented fish and other foods that are not appetizing to children with ASD The SCD intro diet is more appealing.

Here is how one mother views the difference:
"The children can have some "normal" stuff like burger patties and homemade jell-o, rather than just soup soup soup all the time. Aside from a few complaints about the lack of bread, my family adjusted very easily to the SCD, even the brief intro diet... but I know the GAPS intro and early stages would have been a huge adjustment."

Many with ASD have sensory issues which include an extreme dislike of soup. ( Even kids starting on SCD refuse to eat some of the foods on our intro diet).

Hunger strikes tax a child's body and may contribute to parents into giving up the new diet under pressure. Having the fruits and fruit juices allowed on SCD prevents hunger.

The Pecanbread/SCD website, encourages the use of soup during the intro diet too and those who tolerate soups are encouraged to have them. Parents whose children refuse soup need to be patient and wait until soup is accepted and enjoyed. Picky eating habits are usually lost several months after starting SCD, making clearing the way for lots of soups once poor habits are eliminated. Pecanbread protocols enable a head start on GAPS because SCD foods are more appealing.

The SCD intro phase offers a starch and sugar free diet that reduces pathogenic gut bacteria much sooner. This is crucial since scientific studies show that bacterial toxins injure the brains of children with ASD.

2. Reasons why the Pecanbread "Stages" ( the protocols for the early phase of SCD ) are best for children with ASD

Few children with ASD are on any medications for GI disorders. Many children with ASD are best to start SCD using only very easy to digest foods.

The GAPS intro avoids some but not all difficult to digest foods. Its beginning stages contain more difficult to digest foods than SCD's intro diet and beginning stages, thus providing more food for bacteria. GAPS kids face the challenge of having more bacteria to eliminate than children on SCD. SCD protocol is more focused on eliminating bacteria while the GAPS deals more with eliminating yeast.

It is not evident that GAPS eliminates yeast quickly. On the contrary, GAPS kids still struggle with yeast many months after starting the diet.

An example exists in the testimonial chapter of GAPS Guide. Chapter 16 is titled "More Stories" and follows the progress of three families who implemented GAPS. Chapter 16 of GAPS Guide contains only one testimonial by a parent who used the GAPS intro. According the testimonial, yeast issues still exist. The boy cannot eat fruit nor squash. His yeast flares whenever he eats squash.

It is preferable to reduce bacteria rather than both yeast and bacteria at the same time

SCD advocates argue that undergoing die off from yeast and bacteria simultaneously may be too stressful for ASD children.

How the Pecanbread protocol helps the yeast problem by eliminating the pathogenic bacteria

Research shows that bacteria have the capacity to trigger immunosuppression, thus hindering the body's defense against candida. Bacteria also can suppress the immune system. Some children with autism are likely to have an overgrowth of yeast because of their weakened immune systems. Being infected with these bacteria can cause immune system suppression. Eliminating bad bacteria helps strengthen the immune system so that it can fight the candida.
Scientific articles that demonstrate how pathogenic bacteria hurt the immune system

There are additional advantages for reducing the bacteria rather than the Candida

Most children with autism have both a yeast and bacterial overgrowth and have been found to have abnormal levels of gram negative bacteria, a kind of bacteria that contains LPS.

These are the reasons it is more important to eliminate bacteria first and how this results in improving the yeast problem.

1 The bacterial toxin, LPS, makes the candida more toxic.

Laboratory research, reveals that the bacterial toxin, LPS, makes candida more toxic. More mice died when they got injections with LPS three hours after being infected with candida albicans.[1] This means that children with autism will be harmed by candida if they have high levels of LPS resulting from the overgrowth of gram negative bacteria.

2 Bacteria are more harmful than yeast:

Many experts define autism as an autoimmune disease because the abberant immune reaction of autistic children is so harmful to their condition. Both yeast and bacteria are destructive to children with autism since they provoke an extreme immune response with the immune reaction from candida being less potent than the immune reaction from LPS, a very common bacterial toxin. The immune reaction from candida is predominantly anti-inflammatory as compared to the pro-inflammatory response from LPS. In other words, LPS, the bacterial toxin produces more inflammation and a stronger immune response.[2]

3 Candidiasis can be more easily cured in people who are not immunocompromised.

Children with autism are immunocompromised because of their autoimmune disorder. Many research articles state that LPS plays a key role in the development of autoimmune syndrome. The influence of LPS is so powerful that it can even overcome genetics. Mice who are genetically resistant to autoimmunity may develop autoimmune diseases if they are given a high dose of LPS.
Click here to view proof.

4 The bacteria actually protect the yeast from anti fungals.

Numerous candida and bacteria species live together in biofilms in nature and in the human body. In fact, the majority of bacteria and yeast grow in matrix-enclosed biofilms. The candida are surrounded by layers of bacteria which form a shield from anti fungals. Within the biofilm, the bacteria protect candida from the anti fungals.[3]

Bacteria free mice show resistance to systemic candidiasis.

Germ free mice have no bacteria. When these mice were injected with candida, they manifested resistance to extensive mucocutaneous and systemic candidiasis. This also happened to mice that were athymic (a kind of mice who have an immunity problem because they lack functional T-cells). This experiment shows that even in the absence of functional T-cells and a viable bacterial flora, bacteria free mice can overcome systemic candidiasis.[4]

References

[1] LPS Increases the Number of Viable Candida Albicans

View this article in PubMed

1: J Infect Dis. 1995 Jun;171(6):1539-44.
Mortality of Candida albicans-infected mice is facilitated by superinfection of Escherichia coli or administration of its lipopolysaccharide.

* Akagawa G, * Abe S, * Yamaguchi H.

Department of Microbiology and Immunology, Teikyo University School of Medicine, Tokyo, Japan.

Pathogenesis of complex infection with Candida albicans and gram-negative bacteria was studied by determining the influence of infection with Escherichia coli or injection of E. coli lipopolysaccharide (LPS) on mortality of C. albicans-infected mice. Mice were infected intravenously with lethal doses of C. albicans, then treated intravenously at various times with viable E. coli or E. coli LPS, which individually were not lethal. Treatments 3 h after C. albicans infection clearly facilitated the death of the mice. Corresponding to this facilitated death, production of tumor necrosis factor (TNF) in sera was augmented 2 h after LPS injection into the infected mice. Similar increased production of TNF was also observed in mice treated with a nonlethal combination of heat-killed C. albicans and LPS. The number of viable C. albicans in kidneys of the infected mice was increased by LPS treatment, which was assumed to be the main cause of the greater mortality rate.

PMID: 7769289 [PubMed - indexed for MEDLINE]



[2] Click here to view this article on NLM Gateway A service of the U.S. National Institutes of Health

Mannans are Major Immunostimulators of Candida albicans Characterized by an Anti-Inflammatory Cytokine Pattern.

ZIMMERMANN M, WENDEL A, HARTUNG T; Interscience Conference on Antimicrobial Agents and Chemotherapy.
Abstr Intersci Conf Antimicrob Agents Chemother Intersci Conf Antimicrob Agents Chemother. 1999 Sep 26-29; 39: 554 (abstract no. 696).

Univ. of Konstanz, Konstanz, GERMANY.

BACKGROUND: Candida infection is characterized by subacute inflammatory responses and often inefficient host defense. Mannoproteins (mannans) from Candida have been shown to activate human leukocytes.METHODS: Candida blastospores and their mannans prepared according to Kocourek and Ballou induced cytokine release in human whole blood. The pattern of mediators released was compared to bacterial endotoxins (LPS) from Salmonella abortus equi, E. coli, Klebsiella pneumoniae and Salmonella enteriditis.RESULTS: Candida spores even after heat inactivation as well as their mannan at microg levels induced similar amounts of IL-1beta in whole blood incubations. The kinetic of cytokine release induced by mannan compared to LPS was delayed by 4 h. The mannan was negative in the limulus assay for endotoxins and not inhibited by the LPS binding component polymyxin B. Mannan inducible but not LPS inducible cytokine release was inhibited by alpha -D-methyl-mannopyranosid or beta -mannosidase. Compared to the Candida mannan 10[3] to 10[6] times less LPS was required to induce similar amounts of IL-1beta. When equipotent concentrations of all stimuli with regard to IL-1beta stimulation were employed, the mannan induced twice as much TNFalpha , 5 to 10 times more IL-6 and 10 to 100 times more of the anti-inflammatory factors IL-10, prostaglandin E[2] and G-CSF. In contrast, the mannan failed to induce any IFNg . Inhibition of IL-10 by antibodies or prostaglandin E[2] formation by indomethacin significantly increased IL-1beta and TNFalpha formation 2- to 3-fold.CONCLUSIONS: Mannan appears to be a major immunostimulatory component from Candida albicans acting via the mannose receptor. Compared to LPS, mannan was less potent and induced predominantly anti-inflammatory factors which contribute to the poor induction of pro-inflammatory cytokines.


[3] How bacteria protect Candida

Click here to view this article on PubMed

1: J Med Microbiol. 2002 Apr;51(4):344-9.

Mixed species biofilms of Candida albicans and Staphylococcus epidermidis. Adam B, Baillie GS, Douglas LJ.

Division of Infection and Immunity, Institute of Biomedical and Life Sciences, University of Glasgow, UK.

A simple catheter disk model system was used to study the development in vitro of mixed species biofilms of Candida albicans and Staphylococcus epidermidis, two organisms commonly found in catheter-associated infections. Two strains of S. epidermidis were used: a slime-producing wild type (strain RP62A) and a slime-negative mutant (strain M7). In mixed fungal-bacterial biofilms, both staphylococcal strains showed extensive interactions with C. albicans. The susceptibility of 48-h biofilms to fluconazole, vancomycin and mixtures of the drugs was determined colorimetrically. The results indicated that the extracellular polymer produced by S. epidermidis RP62A could inhibit fluconazole penetration in mixed fungal-bacterial biofilms. Conversely, the presence of C. albicans in a biofilm appeared to protect the slime-negative staphylococcus against vancomycin. Overall, the findings suggest that fungal cells can modulate the action of antibiotics, and that bacteria can affect antifungal activity in mixed fungal-bacterial biofilms.

PMID: 11926741 [PubMed - indexed for MEDLINE]


[4]Bacteria free mice can overcome systemic candidiasis.

Click here to view this article on PubMed

1: Appl Environ Microbiol. 1984 Apr;47(4):647-52.

Colonization of congenitally athymic, gnotobiotic mice by Candida albicans. Balish E, Balish MJ, Salkowski CA, Lee KW, Bartizal KF.

Colony counts, scanning electron microscopy, and light microscopy were used to assess the capacity of Candida albicans to colonize (naturally) and infect the alimentary tract of adult and neonatal (athymic [nu/nu] or heterozygous [+/nu] littermates) germfree BALB/c mice. When exposed to yeast-phase C. albicans, the alimentary tract of adult germfree mice (nu/nu or +/nu) is quickly (within 24 to 48 h) colonized with yeast cells. Neither morbidity nor mortality was evident in any mice that were colonized with a pure culture of C. albicans for 6 months. Yeast cells of C. albicans predominated on mucosal surfaces in the oral cavities and vaginas of adult athymic and heterozygous mice. In both genotypes, C. albicans hyphae were observed in keratinized tissue on the dorsal posterior tongue surface and in the cardial-atrium section of the stomach. Conversely, neonatal athymic or heterozygous mice, born to germfree or C. albicans-colonized mothers, do not become heavily colonized or infected with C. albicans until 11 to 15 days after birth. Although yeast cells adhered to some mucosal surfaces in vivo, neither widespread mucocutaneous candidiasis, i.e., invasion of mucosal surfaces with C. albicans hyphae, nor overwhelming systemic candidiasis was evident in neonatal (nu/nu or +/nu) mice. Thus, even in the absence of functional T-cells and a viable bacterial flora, athymic and heterozygous littermate mice (adult or neonatal BALB/c) that are colonized with a pure culture of C. albicans manifest resistance to extensive mucocutaneous and systemic candidiasis.

PMID: 6372689 [PubMed - indexed for MEDLINE]