Here's a little snippet from history, from this source:
Carefully defined purified diets with known amounts of nutrients, vitamins, and minerals have been recommended for use in animal studies of toxicity and carcinogenicity. The National Research Council Committee on Laboratory Animal Diet has emphasized the need to use such defined diets in order to make valid comparisons of studies in different laboratories (Newberne et al., 1978). For this reason, the American Institute of Nutrition (AIN) Committee on Standards for Nutritional Studies has recommended a purified diet composed of commercially refined proteins (casein), carbohydrates (sucrose, cornstarch), fat (corn oil), and fiber (cellulose) with added mineral and vitamin mixtures and supplemental choline and methionine (AIN-76A Purified diet) (Bieri et al., 1977; Bieri, 1980).
Since the introduction of this diet there have been reports of excessive bleeding (Roebuck et al., 1979; Medinsky et al., 1982), nephrocalcinosis (Nguyen and Woodard, 1980; Medinsky et al., 1982), and fatty liver (Medinsky et al., 1982; Hamm et al., 1982) in rats fed the AIN-76A diets. Excessive bleeding has been prevented by increasing the level of vitamin K added to the diet (Bieri, 1980). Problems with the development of fatty liver appear to be related to the high concentration of sucrose used in the diet (Hamm et al., 1982), and make the use of such a diet questionable in animal studies that require normal hepatic morphology and/or function. The current study was designed to determine more precisely the role of dietary sucrose concentration in the ddevelopment of hepatic triglyceride accumulation.
The AIN updated the diet in 1993, known as the AIN-93 diet. (“AIN-93” may be followed by “G” or “M” to designate growth or maintenance.) The AIN-93 diet, currently used, recommends corn starch, but includes some glucose and dextrinized corn starch (broken down to 4-unit carbohydrates) in order to aid in pelleting and to reduce the amount of time and heat needed for pelleting. Soybean oil replaced the corn oil in order to balance omega-3 and omega-6 fatty acids. Just in case they might be essential or beneficial, they added chromium, fluoride, boron, vanadium, arsenic, nickel, lithium, and tin. The official report gives the following reason:
Many of the ultratrace elements are found in plentiful quantities in the natural ingredients that make up cereal-based diets, but their concentrations in purified diets are often very low, and in chemically defined diets, they may be completely absent. Purified diets without added ultratrace elements suport growth and reproduction, but investigators have noted that animals exposed to stress, toxins, carcinogens or diet imbalances display more negative effects when fed purified diets than when fed cereal-based diets (Bounous 1987, Boyd 1972 and 1983, Evers 1982, Gans 1982, Hafez and Kratzer 1976, Longnecker 1981). This suggests that detrimental effects may occur with the omission of some substances found in the more natural, cereal-based diets; some of these substances may be the ultratrace elements.
The amount of vitamin K was increased by 50% (this was after a previous10-fold increase between the AIN-73 diet and the AIN-73A diet), and the form was changed from the toxic, synthetic vitamin K precursor menadione to the natural, plant-based form of vitamin K, phylloquinone. The ratio of calcium to phosphorus was also increased. This made the diet much less likely to cause kidney calcification in females:
Experiments showed that female rats fed the AIN-93G diet for 12 wk exhibited no increase in kidney calcium when compared with those fed a cereal-based diet. On the other hand, rats fed the AIN-76A diet had 23 times more calcium in their kidneys than rats fed the cereal-based diet. Calcium concentration in the kidneys of male rats was not affected by either diet.
The concentration of vitamin B12 was increased because the AIN-76A diet failed to minimize methylmalonic acid, a marker of B12 deficiency. The concentration of vitamin E was increased 50% because the amount of fat had been increased from 5% to 7% and because soybean oil contains more omega-3 than corn oil, and omega-3 fats are more vulnerable to oxidation than omega-6 fats. The amount of choline was increased from 0.08% to 0.1%.
Are all these changes sufficient? The increase in choline obviously isn't, since animals fed three times the recommended amount during pregnancy give birth to rats with a 30% increase in visuo-spatial and auditory memory, grow old without becoming senile, are less vulnerable to neurotoxins, are better able to multi-task, and have a lower rate of “interference memory,” which is what makes you forget where you parked your car when you get done grocery shopping. I describe this research in my article “Vitamins for Fetal Development: Conception to Birth.”
Another reason the choline level is clearly inadequate is because lab animals fed high-sucrose and high-fat diets develop fatty liver disease. But more on this in my next post. Should be up tonight or tomorrow.
Like the original report for the AIN93 diets stated, the content of purified diets containing what we believe to be essential depends on current knowledge, which is always subject to change:
It is unrealistic, however, to presume that a perfect diet can be formulated, one that can satisfy all circumstances. Moreover, the ingredients that supply the nutrients and the concentrations of individual nutrients themselves are based upon current knowledge in the field and may change with time. This may result in a need to change a standard diet formulation.
Before the advent of controlled experiments, purified lab rat diets, the refining and fortification of foods for human consumption, and the food pyramid, both rats and humans ate natural foods, and ate instinctively, “listening to their bodies.” When eating became science-based, humans and lab animals started developing degenerative disease as the norm rather than the exception. The primary culprit? Human arrogance. It primes us to believe that we almost know everything there is to know. If we just do a few more studies. It's the type of arrogance that leads us to perform epidemiological studies and then believe that the results “have been adjusted” as if we know what all, or most, of the confounding variables are.
Feel like a lab rat yet?