Science And GMOs Are Not The Bad Guys Here

[roseBudd]

25. You might want to listen to scientists on Seralini

We have known since the 60s that Sprague-Dawley rats develop tumors no matter what they are fed, and even more so when allowed to feed ad libitum. Two year old Sprague-Dawley rats with tumors is the nnorm, when allowed to feed ad libitum, as Seralini did. Unless Seralini is a stupid man, he is a fraud.

You know so much about science how it it that you are unaware that 10 rats are an inadequate control group given the above.

The Effects of Diet, Overfeeding and Moderate Dietary Restriction on Sprague-Dawley Rat Survival, Disease and Toxicology

http://jn.nutrition.org/content/127/5/851S.full

The most common neoplastic cause of death in Sprague-Dawley rats are pituitary tumors in both sexes. Because pituitary tumors are prolactin secreting, mammary gland tumors in females are the second most common cause of death in Sprague-Dawley rats (Keenan et al. 1992, 1994a, 1994b and 1995b). Ad libitum–fed Sprague-Dawley rats of both sexes have an early development of hyperplastic, large pituitaries, higher DNA labeling indices and a high incidence of focal pituitary cell hyperplasias and adenomas compared with moderate DR groups when examined at 1-y intervals (Keenan et al. 1994a). These lesions lead to fatal tumors in the second year of life.

Our laboratory was surprised by the wide interlaboratory variability in the Sprague-Dawley rats daily food consumption, body weights and 2-y survival (Keenan et al. 1994a). Subsequently, we studied the effects of AL food consumption (overfeeding) and moderate DR that was within the range of AL food intake in other laboratories (Keenan et al. 1994a). Feeding Sprague-Dawley rats diets varying in protein, fiber and energy content did not improve 2-y Sprague-Dawley rat survival above 50% if AL access to food was allowed.

It is now clear that AL overfeeding of otherwise nutritious food is one of the most insidious, underestimated and significant factors increasing degenerative disease and tumors and decreasing survival in both humans and laboratory animals. Uncontrolled AL overfeeding of excessive energy needs to be recognized as one of the most important determinate errors in the current rodent bioassays that can compromise the usefulness of these risk-assessment studies.

Over the past two decades, rodent bioassays have shown a steady increase in study-to-study variability, decreases in survival, and increases in the incidence, onset time and severity of degenerative diseases and tumors in most of the rodent species, strains and stocks currently used (Hart et al. 1995a and 1995b, Keenan et al. 1992, 1994a and 1995a, Lang 1991, Roe et al. 1995, Weindruch and Walford 1988). These adverse changes have been associated with increases in rodent weights, which seem to be influenced by selection for more rapid growth and greater fecundity but are also greatly influenced by excessive food intake (Masoro 1995, Yu 1995). The uncontrolled variable of allowing rodents to consume excessive energy and the complicating effects of this procedure on the design, results and interpretation of toxicology and carcinogenicity studies continues to be largely neglected by many regulators, toxicologists and pathologists (Hart et al. 1995a and 1995b).

Many toxicology laboratories have observed a steady but variable decline in survival in 2-y rodent carcinogenicity studies over the past 20 y that correlates with increased food consumption and adult body weight. This decline has been observed in the outbred Wistar and Sprague-Dawley rat stocks and in the formally long-lived inbred Fischer-344 rat strain (Hart et al. 1995, Haseman and Rao 1992, Keenan et al. 1992 and 1994a, Rao et al. 1990, Roe et al. 1995). This decreased survival has caused some to question the adequacy of studies that have less than 50% of the animals treated with the test substance for the full 2-y period because of high mortality. Potential statistical problems arise from evaluating treatment-related mortality in studies with low control survival (Keenan et al. 1994a, Keenan and Soper 1995). The simplest solution to the potential loss of statistical power is to increase 2-y survival to 50% or more, because the sensitivity of the bioassay to distinguish a true treatment effect from concurrent controls is greatly increased (Keenan and Soper 1995).

To improve poor rodent survival it is necessary to recognize that the cause of these early deaths is the early development of spontaneous tumors and severe degenerative disease, such as chronic nephropathy and cardiomyopathy, that are secondary to dietary (energy) overfeeding (Keenan and Soper 1995, Keenan et al. 1992, Roe et al. 1995). Although genetic, nutritional and environmental interactions are involved, laboratory rodent survival can be significantly improved by simple energy intake restriction or dietary restriction (DR). This procedure will improve survival and thus increase exposure time to a test compound and improve the statistical sensitivity of these bioassays to detect a true treatment effect during the test period."