Jillio -- we do not say that this study proves anything about ADHD. But what it proves is that synthetic petrochemical food dyes ARE NOT GOOD FOR KIDS. They DO have neurological toxicological effects. They DO affect attention and activity levels to some extent ... and that is an adverse effect ... at age 3 and at age 8. What about age 5? Are you going to suggest that magically it won't bother 5 year olds?
Consider the benefit-risk ratio. These food dyes and other synthetic additives added to food benefits ONLY the manufacturer, but has no benefit whatsoever to the consumer ... and in fact appears to cause damage. Even if that damage is not large, the benefit-risk ratio is not acceptable.
None of the dangerous (in my opinion) additives are necessary. There are safer colorings; there are safer preservatives; there are safer flavorings. The only benefit conferred by the synthetic additives is that they are CHEAPER. That is not good enough for me.
But okay, you don't like the McCann study. That is okay. Take a look at the series of Tanaka studies. He is a toxicologist and directly studied food dyes. In Japan. I am pasting them here but you can find the abstracts at
Research on Food Dye and Flavorings -- my conclusion is that they KNOW the colorings are not really safe, but they figure they are "not that bad." Ugh.
Effects of amaranth on F1 generation mice. Tanaka T. Toxicology letters 1992 May;60(3):315-24
" The color additive, amaranth, (Red No. 2) was given in the diet to provide dietary levels of 0 (control), 0.03, 0.09 and 0.27%, from 5 weeks of age in F0 generation mice to 9 weeks of age in F1 generation mice. . . There was no effect on the parameters of litters, litter size, pup weight and litter weight. The body weight of pups during the lactation period in the treatment groups increased less significantly, and the survival index at postnatal day (PND) 21 of the amaranth 0.27% group was reduced. Developmental parameters, direction of swimming on PND 4 in male pups and olfactory orientation in each sex were significantly reduced in the treatment groups. The dose levels of amaranth in this study influenced some reproductive, developmental and behavioral parameters in mice. "
Reproductive and neurobehavioral effects of amaranth administered to mice in drinking water. Tanaka T., Toxicology and industrial health. 1993 Nov-Dec;9(6):1027-35
" The color additive amaranth [Red #2] was given in the drinking water at levels of 0 (control), 0.025, 0.075, and 0.225% from 5 weeks of age in F0 generation until F1 generation mice were weaned,. . . Average body weight in both sexes of the F1 mice was significantly increased in the 0.025% group in both sexes. Survival index at postnatal day (PND) 21 was reduced in the 0.025% amaranth group. For the neurobehavioral parameters, surface righting at PND 4 in female offspring and olfactory orientation in both sexes were significantly affected by treatment. Several parameters of movement activity of male offspring at 3 weeks of age were affected in amaranth 0.075% group . . . "
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Reproductive and neurobehavioral effects of Sunset yellow FCF administered to mice in the diet. Tanaka T., Toxicol Ind Health 1996 Jan-Feb;12(1):69-79
Selected reproductive and neurobehavioral parameters were measured in mice given the color additive Sunset Yellow [FD&C Yellow #6] FCF in the diet. The additive was given at levels of 0 (control), 0.15, 0.30, and 0.60%, from five weeks of age in the F0 generation to nine weeks of age in the F1 generation. There were few adverse effects on litter size, weight, or sex ratio. Average body weight . . . was significantly increased . . . In the neurobehavioral parameters, swimming direction was significantly affected in a dose-related manner in male and female offspring . . . Also in the early lactation period, surface righting and negative geotaxis were significantly affected in male offspring in the middle-dose group, and swimming head angle was significantly affected in female offspring in a dose-related manner. The dose levels of Sunset Yellow FCF in this study did produce some adverse effects in reproductive and neurobehavioral parameters.
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Reproductive and neurobehavioural toxicity study of erythrosine administered to mice in the diet. Tanaka T. Food Chem Toxicol 2001 May;39(5):447-54
" Erythrosine was given in the diet to provide levels of 0 (control), 0.005, 0.015 and 0.045% from 5 weeks of age of the F(0) generation to 9 weeks of age of the F(1) generation in mice, and selected reproductive and neurobehavioural parameters were measured. . . .In movement activity of exploratory behaviour, several parameters were significantly changed in the high-dose group, and those effects were dose related in adult females in the F(0) and F(1) generations and in male offspring in the F(1) generation. . . . "
Reproductive and neurobehavioural toxicity study of tartrazine administered to mice in the diet. Tanaka T., Food Chem Toxicol. 2005 Aug 5 (epub ahead of print)
" Tartrazine was given in the diet . . . and selected reproductive and neurobehavioural parameters were measured. In movement activity of exploratory behaviour in the F(0) generation, number of vertical activity was significantly increased ...The average body weight . . .was significantly increased . . . In behavioural developmental parameters, surface righting . . . was significantly accelerated . . . Cliff avoidance at PND 7 was significantly accelerated . . . Negative geotaxis at PND 4 was significantly delayed . . . number of movement showed a significant tendency to be affected . . . Nevertheless, . . . the actual dietary intake of tartrazine is presumed to be much lower. It would therefore appear that the levels of actual dietary intake of tartrazine is unlikely to produce any adverse effects in humans. "
Please click on the link to the entire abstract and read it carefully. It is astonishing that in the face of these clear adverse effects on mice, he would conclude that it is not a problem for humans. And his basis for such a conclusion? Simply that we would theoretically eat less than the mice did.