Pecanbread Update

Please avoid peanut butter, many SCD adults report problems with peanut butter. Peanuts are legumes,and legumes are advanced foods. You may add peanut butter when digestive problems have resolved but watch carefully that there are no changes after adding this food. Peanuts affect the thyroid.

PEANUT BUTTER SEEMS TO BE ONE OF THE MAJOR REASON FOR FAILURE WITH SCD.

Furthermore, most peanuts have aflatoxin, a certain toxic mold. A research paper found that the COMBINATION of the bacterial toxin, LPS, with aflatoxin creates liver damage. The article is at the bottom of this web page. People with IBD or autism have very high levels of the bacterial toxin, LPS, before they start SCD and the levels of LPS might not go down so quickly.

Please avoid peanuts during the early months of SCD!

http://www.ncbi.nlm.nih.gov/pubmed/10828277?dopt=Abstract

1: Toxicol Sci. 2000 Jun;55(2):444-52.

Bacterial lipopolysaccharide exposure augments aflatoxin B(1)-induced liver injury.

Barton CC, Hill DA, Yee SB, Barton EX, Ganey PE, Roth RA.

Department of Pharmacology and Toxicology, National Center for Food Safety and Toxicology and Institute for Environmental Toxicology, Michigan State University, East Lansing, Michigan 48824, USA.

Bacterial endotoxin (lipopolysaccharide; LPS) given to animals in large doses results in pronounced, midzonal liver injury. Exposure to smaller, non-injurious doses of LPS augments the toxicity of certain hepatotoxicants. This study was conducted to delineate the development of injury in a rat model of augmentation of aflatoxin B(1) (AFB(1)) hepatotoxicity by LPS. At large doses (i.e., > 1 mg/kg, ip), AFB(1) administration resulted in pronounced injury to the periportal regions of the liver. Male, Sprague-Dawley rats (250-350 g) were treated with 1 mg AFB(1)/kg, ip or its vehicle (0.5% DMSO/saline) and 4 h later with either E. coli LPS (7.4 x 106 EU/kg, iv) or its saline vehicle. Liver injury was assessed 6, 12, 24, 48, 72, or 96 h after AFB(1) administration. Hepatic parenchymal cell injury was evaluated as increased alanine aminotransferase (ALT) and aspartate aminotransferase (AST) activities in serum and from histologic examination of liver sections. Biliary tract alterations were evaluated as increased concentration of serum bile acids and activities of gamma-glutamyltransferase (GGT), alkaline phosphatase (ALP), and 5'-nucleotidase (5'-ND) in serum. At all times and for all markers, injury in rats treated with either AFB(1) or LPS alone was absent or modest. In the AFB(1)/LPS cotreated group, hepatic parenchymal cell injury was pronounced by 24 h and had returned to control values by 72 h. The injury began in the periportal region and spread midzonally with time. Furthermore, changes in serum markers indicative of biliary tract alterations were evident by 12 h and had returned to control values by 72 h. Thus, the nature of the hepatic lesions suggested that LPS potentiated the effects of AFB(1) on both parenchymal and bile duct epithelial cells.

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