How Difficult to Absorb Carbohydrates Increase the Level of LPS in Animals

Experiments show that a high grain diet will result in a dramatic increase of LPS in the bodies of cows. Why are we looking at cows rather than mice, the usual animal model for human beings? The GI tracts of mice are good models for the GI tract of "neurotypical" humans without carbohydrate malabsorption because mice have a good capacity to digest grains and starches. Unfortunately, most children with ASD have carbohydrate malabsorption. People with carbohydrate malabsorption need a different animal model because their digestive system cannnot digest the grains and other starches.

Cows are animals that do have some difficulty with carbohydrate malabsorption; when cows are fed high grain diets, they get acidosis.[1] ASD children may also develop acidosis.[2] The connection between ASD and acidosis was discovered in 1985.[3] Although cows may not be a perfect animal model for the GI tract of people with carbohydrate malabsorption, the fact that cows get higher levels of LPS with a high grain diet does suggest there is a connection between unabsorbed carbohydrates and LPS levels.

View this article in PubMed
1: J Dairy Sci. 2007 Feb;90(2):856-66.
Ruminal lipopolysaccharide concentration and inflammatory response during grain-induced subacute ruminal acidosis in dairy cows.

* Gozho GN, * Krause DO, * Plaizier JC.

Department of Animal Science, University of Manitoba, Winnipeg, Manitoba, Canada R3T 2N2.

The effects of grain-induced subacute ruminal acidosis (SARA) in lactating dairy cows on free ruminal lipopolysaccharide (LPS) and indicators of inflammation were determined. Four mid lactation dairy cows were divided into 2 groups of 2 cows and used in a repeated switchover design. During each period, SARA was induced in 2 animals for 5 subsequent days by replacing 25% of their total mixed ration (dry matter basis) with a concentrate made of 50% wheat and 50% barley. The other 2 cows acted as controls and were fed a total mixed ration diet in which 44% of dry matter was concentrate. On average, inducing SARA did not affect milk composition, increased the duration of rumen pH below 5.6 from 187 to 309 min/d, and increased free ruminal LPS concentration from 24,547 endotoxin units (EU)/mL to 128,825 EU/mL. Averaged across treatments, milk fat yield and milk protein yield were 0.66 and 1.00 kg/d, respectively. Rumen pH and milk fat data suggest that control cows also experienced ruminal acidosis, albeit a milder form of this disease than SARA cows. Serum LPS concentration in both control and SARA cows was less than the detection limit of <0.01 EU/mL for the assay. Induction of SARA elevated serum amyloid A concentration from 286.8 to 498.8 mug/mL, but did not affect other markers of inflammation including haptoglobin, fibrinogen, serum copper, or white blood cells. These results suggest that grain-induced SARA in mid lactation dairy cows increases the lysis of gram-negative bacteria and activates an inflammatory response.

PMID: 17235162 [PubMed - indexed for MEDLINE]

* Gozho GN, * Krause DO, * Plaizier JC.

Department of Animal Science, University of Manitoba, Winnipeg, MB, Canada R3T 2N2.

Three rumen-fistulated Jersey steers were gradually adapted to a wheat-barley concentrate over a 4-wk period. Adaptation steps consisted of four 1-wk periods during which steers were fed diets with forage-to-concentrate (F:C) ratios of 100:0, 79:21, 59:41, and 39:61. The forage consisted of chopped hay (CH), and the concentrate consisted of pelleted concentrate containing 50% ground wheat and 50% ground barley. Steers were fed the all-forage diet ad libitum during wk 1. Feed offered in wk 2 to 4 was kept constant at the ad libitum intake during wk 1. On 2 d that were set 3 d apart during wk 5, subacute ruminal acidosis (SARA) was induced in the steers by feeding a diet with an F:C ratio of 24:76 by offering them 0.9 kg of CH at 0900 h followed by 2 meals of 3.0 kg each of wheat-barley pellets (WBP) at 1100 h and 1300 h and 0.9 kg of CH at 1700 h, to depress rumen pH for at least 3 h/d below 5.6. The average concentrate inclusion for the SARA induction diet was 76 +/- 10% DM. During stepwise adaptation, time with pH below 5.6 increased to an average of 121 min/d when the steers were consuming a diet containing 61% DM as WBP. Dietary inclusion of WBP at the rate of 76% DM induced SARA because the steers spent an average of 219 min/d with pH below 5.6. The free ruminal lipopolysaccharide (LPS) concentration increased from 6,310 endotoxin units (EU)/mL with the all-forage diet to 18,197 EU/mL with the 61% concentrate diet. The ruminal LPS concentration increased to 26,915 EU/mL when SARA was induced. Serum haptoglobin increased from 0.53 mg/mL when steers were on the all-forage diet to 1.90 mg/mL with the 61% concentrate diet and were not increased further by inducing SARA. The serum amyloid-A concentration was not affected by increasing dietary concentrate during stepwise adaptation to the concentrate, but increased from 71 to 163 microg/mL when SARA was induced. A gradual increase in dietary concentrate so that the F:C ratio decreased to 39:61 resulted in increased ruminal LPS concentrations. Subsequent induction of SARA further increased ruminal LPS and activated an inflammatory response.

* Goad DW, * Goad CL, * Nagaraja TG.

Department of Animal Sciences, Kansas State University, Manhattan 66506-1600, USA.

We used six ruminally cannulated steers in a two-period crossover design to study ruminal fermentative and microbial changes associated with induced subacute acidosis. Steers were adapted to either an 80% alfalfa hay (hay-adapted)- or corn grain (grain-adapted)-based concentrate diet. After feed was withheld for 24 h, steers were overfed with an all-grain diet at 3.5 x NEm daily for 3 d. Ruminal contents and jugular blood samples were collected before withholding feed and at 0 and 12 h daily for 3 d during the overfeeding period. Ruminal samples were analyzed for pH, lactate, VFA concentrations, and counts of total anaerobic, amylolytic, lactic acid-producing and -fermenting bacteria, and ciliated protozoa. Blood samples were analyzed to assess acid-base status. Ruminal pH declined to a range of 5.5 to 5.0 with increased VFA concentrations, but normal lactate concentrations (<5 mM) were indicative of subacute acidosis. Total viable and amylolytic bacterial counts were higher (P < .05) in grain-adapted than hay-adapted steers. Anaerobic lactobacilli counts increased over time (P < .01) in both groups and were generally higher in grain-adapted than hay-adapted steers. Lactate-utilizing bacteria were initially greater in grain-adapted than hay-adapted steers and increased over time in both groups following grain challenge. Total ciliates were initially higher (P < .05) in grain-adapted than hay-adapted steers and decreased after 48 h in both groups. Blood acid-base changes were minimal. Bacterial changes associated with subacute acidosis resemble those reported during adaptation to grain feeding, and the decline in ciliated protozoa may be the only microbial indicator of a potentially acidotic condition in the rumen.

PMID: 9464904 [PubMed - indexed for MEDLINE]

How SCD Eliminates the Harmful Gut Microorganisms

Why and how SCD eliminates the harmful gut bacteria:

Complex sugars and starches are the preferred food supply of gut pathogens. SCD eradicates these harmful bacteria by restricting the use of complex carbohydrates. They are much more difficult to digest than simple carbohydrates because they must be split into simple sugars before entering the blood stream. This is a problem for a compromised digestive system. Carbohydrates not absorbed into the blood stream become available food for harmful gut bacteria.

SCD excels because it excludes them and permits only monosaccharide carbohydrates, the type easy to digest because once absorbed, they vanish into the bloodstream before the bacteria can access them.

Two out of the following three research articles use The Hydrogen Breath test to measure amounts of anaerobic bacteria. ("anaerobic" is a technical word which means without air )

ABOUT THE HYDROGEN BREATH TEST
The hydrogen breath test utilizes the hydrogen measurement in the breath to diagnose several conditions that cause gastrointestinal symptoms.

Anaerobic bacteria are the only bacteria in the colon capable of producing hydrogen in humans. The gas develops as the result of exposure to unabsorbed food, particularly sugars and other carbohydrates like starch. Limited hydrogen is produced from the small amounts of unabsorbed food that normally reach the colon. Even larger amounts of hydrogen are present when there is a problem with food digestion and absorption in the small intestine. An environment is created that allows more unabsorbed food to reach the colon. Large amounts of hydrogen can also occur when colonic bacteria move back into the small intestine. ( "bacterial overgrowth" of the small bowel.) Once exposed to unabsorbed food, the bacteria are unable to completely traverse the small intestine to become fully digested and absorbed. Instead, some of the hydrogen produced is absorbed into the blood as it flows through the wall of the small intestine and colon and travels to the lungs. This hydrogen is released along with exhaled breath and can be measured.

The information above was taken from this website:
Click here to view the medicinenet website
Supporting Research from PubMed:

Scientific Article #1

An important scientific experiment shows that the sugars that are prohibited from the SCD diet feed the anaerobic bacteria in the gut.

When patients with GI problems consumed complex sugars, the hydrogen test showed increases bacterial counts. (There is one exception: fructose). Fructose is a simple sugar; yet that sugar which is not complex also produces an increase in bacterial levels. Today's fructose is made from corn starch and impurities remain and fructose that is used for experiments is now made from corn, so it acts like an SCD illegal sugar.

Websites about how fructose is manufactured from corn:
http://ific.org/nutrition/sugars/index.cfm?renderforprint=1

The following Israeli paper shows that the sugars that are not allowed by SCD lead to an increase in bacterial count. These sugars are not well absorbed and contribute to digestive problems:
View this article in PubMed
1: Isr Med Assoc J. 2000 Aug;2(8):583-7.

Carbohydrate malabsorption and the effect of dietary restriction on symptoms of irritable bowel syndrome and functional bowel complaints.

Goldstein R, Braverman D, Stankiewicz H.

Gastroenterology Institute, Shaare Zedek Medical Center, Jerusalem, Israel.

BACKGROUND: Carbohydrate malabsorption of lactose, fructose and sorbitol has already been described in normal volunteers and in patients with functional bowel complaints including irritable bowel syndrome. Elimination of the offending sugar(s) should result in clinical improvement. OBJECTIVE: To examine the importance of carbohydrate malabsorption in outpatients previously diagnosed as having functional bowel disorders, and to estimate the degree of clinical improvement following dietary restriction of the malabsorbed sugar(s). METHODS: A cohort of 239 patients defined as functional bowel complaints was divided into a group of 94 patients who met the Rome criteria for irritable bowel syndrome and a second group of 145 patients who did not fulfill these criteria and were defined as functional complaints. Lactose (18 g), fructose (25 g) and a mixture of fructose (25 g) plus sorbitol (5 g) solutions were administered at weekly intervals. End-expiratory hydrogen and methane breath samples were collected at 30 minute intervals for 4 hours. Incomplete absorption was defined as an increment in breath hydrogen of at least 20 ppm, or its equivalent in methane of at least 5 ppm. All patients received a diet without the offending sugar(s) for one month. RESULTS: Only 7% of patients with IBS and 8% of patients with FC absorbed all three sugars normally. The frequency of isolated lactose malabsorption was 16% and 12% respectively. The association of lactose and fructose-sorbitol malabsorption occurred in 61% of both patient groups. The frequency of sugar malabsorption among patients in both groups was 78% for lactose malabsorption (IBS 82%, FC 75%), 44% for fructose malabsorption and 73% for fructose-sorbitol malabsorption (IBS 70%, FC 75%). A marked improvement occurred in 56% of IBS and 60% of FC patients following dietary restriction. The number of symptoms decreased significantly in both groups (P < 0.01) and correlated with the improvement index (IBS P < 0.05, FC P < 0.025). CONCLUSIONS: Combined sugar malabsorption patterns are common in functional bowel disorders and may contribute to symptomatology in most patients. Dietary restriction of the offending sugar(s) should be implemented before the institution of drug therapy.

PMID: 10979349 [PubMed - indexed for MEDLINE]

Research paper #2 proves that bacterial fermentation is caused by unabsorbed starches. Half of the volunteers were fed starches together with acarbose, an inhibitor that would make them unable to absorb the starches. The volunteers who took acarbose were unable to digest their starches and showed signs of having increased bacterial counts in the colon.

View this article in PubMed
1: Gastroenterology. 1988 Dec;95(6):1549-55.

Effect of starch malabsorption on colonic function and metabolism in humans.

Scheppach W, Fabian C, Ahrens F, Spengler M, Kasper H.

Department of Medicine, Wuerzburg University, Federal Republic of Germany.

To study the impact of starch on colonic function and metabolism, 12 healthy volunteers consumed a controlled diet rich in starch for two 4-wk periods. In one of the study periods they received the glucosidase inhibitor acarbose (BAY g 5421) and placebo in the other. Stool wet weight increased by 68%, stool dry weight by 57%, fecal water content by 73%, and the mean transit time by 30% on acarbose. Breath hydrogen was significantly higher on acarbose, indicating stimulated carbohydrate fermentation in the colon. Fecal bacterial mass (+78%), total stool nitrogen (+53%), bacterial nitrogen (+200%), and stool fat (+56%) were higher in the acarbose than in the control period. The stimulation of fermentation in the human large intestine may be important in colonic and possibly other diseases.

Explanation of fermentation

http://en.wikipedia.org/wiki/Fermentation_%28food%29

Sorbitol is another carb that is not allowed on SCD. This research paper shows that consumption of Sorbitol produced an increase of bacterial counts on the hydrogen test.

View this article in PubMed
Website that explains that Anaerobic Bacteria are mostly pathogenic.
View the website

The home page of this website indicates that it is affiliated with the University of California at San Diego Medical School.
http://www.ratsteachmicro.com

[1] Cheng, K. J., T. A. McAllister, J. D. Popp, A. N. Hristov, Z. Mir, and H. T. Shin. 1998. A review of bloat in feedlot cattle. J. Anim. Sci. 76:299-308.[Abstract]
Moreno H, Borjas L, Arrieta A, Sáez L, Prassad A, Estévez J, Bonilla E. 1992. Clinical heterogeneity of the autistic syndrome: a study of 60 families. Invest Clin. 1992;33(1):13-31. Abstract
Coleman M, Blass JP. 1985. Autism and lactic acidosis. J Autism Dev Disord. 1985 Mar;15(1):1-8. Abstract
1: J Autism Dev Disord. 1985 Mar;15(1):1-8.Links Autism and lactic acidosis. Coleman M, Blass JP. View this article in PubMed
1: Invest Clin. 1992;33(1):13-31.Links [Clinical heterogeneity of the autistic syndrome: a study of 60 families] [Article in Spanish] Moreno H, Borjas L, Arrieta A, Sáez L, Prassad A, Estévez J, Bonilla E. Unidad de Genética Médica, Facultad de Medicina, Universidad del Zulia, Maracaibo, Venezuela. Sixty families ascertained through a single proband, has helped to better define infantile autism as a heterogeneous group of disorders. Forty four patients showed a characteristic facio- auricular dysplasia. Twenty four of these, showed increased pyruvate and lactate and laboratory findings of metabolic acidosis i.e., anion gap above 18 mEq/L or serum bicarbonate below 21 mEq/L but only nine of these probands demonstrated reduction of plasma bicarbonate below 18 mEq/lt. Plasma amino acids in 17 probands and matched controls showed increased taurine with the rest of amino acids significantly (p less than 0.05) below the control level. Glutamate and aspartate were also significantly elevated (p less than 0.05; Student t-test). Segregation analysis in thirty four of these families which linked through at least one ancestral family name, suggested autosomal recessive inheritance (p = 0.20). Three out of eight probands who received megadoses of pyridoxine (Vitamin B6), subjectively gained in language abilities, affectivity and response to behavior modification therapy. Five autistic patients proved to have clinically defined syndromes: two with the Martin-Bell syndrome, and three girls affected respectively with the Rett syndrome, phenylketonuria and dicarboxylic aciduria. PMID: 1391074 [PubMed - indexed for MEDLINE] View this article in PubMed
1: J Autism Dev Disord. 1985 Mar;15(1):1-8.Links Autism and lactic acidosis. Coleman M, Blass JP. Four patients are described who have two coexistent syndromes: the behavioral syndrome of autism and the biochemical syndrome of lactic acidosis. One of the four patients also had hyperuricemia and hyperuricosuria. These patients raise the possibility that one subgroup of the autism syndrome may be associated with inborn errors of carbohydrate metabolism. PMID: 3980425 [PubMed - indexed for MEDLINE]