The first one used pigs supposedly fed identical diets, only one being GM and the other non-GM feed, but in the comments:
You say in your paper “Mycotoxin analyses (Midwest Laboratories Inc, Omaha, Nebraska, US) showed 2.08 ppb total aflatoxins and 3.0 ppm total fumonisins in a pooled sample of the GM feed and no aflatoxins and 1.2 ppm total fumonisins in a pooled sample of the non-GM feed. No other mycotoxins were detected. These levels are well below the USA and EU limits for mycotoxins in pig feed. In addition, according to common industry practice, a mycotoxin binding agent (200 mesh bentonite clay) was added to the diets of young pigs (Table 1).”
Yet, aflatoxins are poisons caused by mold. This study fed GE corn contaminated with aflatoxins to the GE-fed hogs. The non-GE-fed hogs didn’t have aflatoxins in their feed. Also, the GE-fed hogs had over double the amount of fumonisins than the non-GE-fed hogs. Fumonisins are another toxin, caused by fungi.
So they were not fed identical diets.
Your second link was to an article later retracted:
http://www.sciencebasedmedicine.org/the-seralini-gmo-study-retraction-and-response-to-critics/
Your third link also has potential shortcomings:
http://gmopundit2.blogspot.com/2005/11/rats-fed-bad-diets-have-lots-of.html
Stanley Ewen and Arpad Pusztai report that, when fed to rats, GM potatoes containing the GNA lectin have proliferative and antiproliferative effects on the gut. They suggest that several of these effects are due to alterationsin the composition of the transgenic potatoes, rather than to the newly expressed gene product. However data on the composition of the different diets are not reported in the letter. Pusztai has released some of these details on the internet (
http://www.rri.sari.ac.uk/gmo/ajp.htm ). These details indicate that the content of starch, glucose polymers, lectin[GNA], and trypsin and chymotrypsininhibitors in GM potatoes differed from that of the parental line.
Unfortunately, these differences have notbeen examined further by analysis of anextended range of lines, for evidence on whether these differences are attributable to the genetic modification or to natural variations.
Another shortcoming of the study is that the diets were protein deficient; they contained only 6% protein by weight. There is convincing evidence that short-term protein stress and starvation impair the growth rate, development, hepatic metabolism, and immune function of rats. Ewen and Pusztai say that the significant differences between diet groups invariables such as mucosalthickness or crypt length are evidence of the biological effects of the GM foods.
Such a claim is easy to make but difficult to prove, because no consistent patterns of changes were observed in the study.
Ingestion of potatoes may be associated with several adaptive changes in the gut because of the low digestibility of raw or partly refined potato starch. In rats caecal hypertrophy is a common response to short-term feeding of various poorly digestible carbohydrates, such as raw potatostarch. A physiological response of this nature is probably of little toxicological significance. Dose -response studies would
have helped in the assessment of consistency of response.
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