New book in Dutch

Eet vet word slank

Eet vet word slank gepubliceerd januari 2013

In dit boek lees je o.a.: * heel veel informatie ter bevordering van je gezondheid; * hoe je door de juiste vetten te eten en te drinken kan afvallen; * hoe de overheid en de voedingsindustrie ons, uit financieel belang, verkeerd voorlichten; * dat je van bewerkte vetten ziek kan worden.

Trick and Treat:
How 'healthy eating' is making us ill
Trick and Treat cover

"A great book that shatters so many of the nutritional fantasies and fads of the last twenty years. Read it and prolong your life."
Clarissa Dickson Wright

Natural Health & Weight Loss cover

"NH&WL may be the best non-technical book on diet ever written"
Joel Kauffman, PhD, Professor Emeritus, University of the Sciences, Philadelphia, PA

Soy Online Service

ADM GRAS Application Letter of Opposition

from Daniel M. Sheenan

The first page of this document is available here.

(continued)..... consumption in human infants (cf., Van Wyk et al., 1959; Hydovitz, 1960; Shepard et al., 1960; Pinchera et al., 1965; Chorazy et al., 1995) and adults (McCarrison, 1933; Ishizaki, et al., 1991). Recently, we have identified genistein and daidzein as the goitrogenic isoflavonoid components of soy and defined the mechanisms for inhibition of thyroid peroxidase (TPO)-catalyzed thyroid hormone synthesis in vitro (Divi et al., 1997; Divi et al., 1996). The observed suicide inactivation of TPO by isoflavones, through covalent binding to TPO, raises the possibility of neoantigen formation and because anti-TPO is the principal autoantibody present in autoimmune thyroid disease, this hypothetical mechanism is consistent with the reports of Fort et al. (1986, 1990) of a doubling of risk for autoimmune thyroiditis in children who had received soy formulas as infants compared to infants receiving other forms of milk.

The thyroid findings in infants receiving soy formula are a result of serum levels of isoflavones that are about five times higher than in women receiving soy supplements who show menstrual cycle disturbances, including an increased estradiol level in the follicular phase (Setchell, et al, 1997). Assuming a dose-dependent risk, it is unreasonable to assert that the infant findings are irrelevant to adults who may consume smaller amounts of isoflavones. Additionally, while there is an unambiguous biological effect on menstrual cycle length (Cassidy, et al, 1994), it is unclear whether the soy effects are beneficial or adverse. Furthermore, we need to be concerned about transplacental passage of isoflavones as the DES case has shown us that estrogens can pass the placenta. No such studies have been conducted in humans or primates. As all estrogens which have been studied carefully in human populations are two-edged swords in humans (REF), with both beneficial and adverse effects resulting from the administration of the same estrogen, it is likely that the same characteristic is shared by the isoflavones. The animal data is also consistent with adverse effects in humans.

Finally, initial data from a robust (7,000 men) long-term (30+ years) prospective epidemiological study in Hawaii showed that Alzheimer disease prevalence in the Hawaii men was similar to European-ancestry Americans and to Japanese (White, et al, 1996a). In contrast, vascular dementia prevalence is similar in Hawaii and Japan and both are higher than in European-ancestry Americans. This suggests that common ancestry or environmental factors in Japan and Hawaii are responsible for the higher prevalence of vascular dementia in these locations. Subsequently, this same group showed a significant dose-dependent risk (up to 2.4 fold) for development of vascular dementia and brain atrophy from consumption of tofu, a soy product rich in isoflavones (White, et al, 1 996b). This finding is consistent with the environmental causation suggested from the earlier analysis, and provides evidence that soy (tofu) phytoestrogens causes vascular dementia. Given that estrogens are important for maintenance of brain function in women; that the male brain contains aromatase, the enzyme that converts testosterone to estradiol; and ‘hat isoflavones inhibit this enzymatic activity (Irvine, 1998), there is a mechanistic basis for the human findings. Given the great difficulty in discerning the relationship between exposures and long latency adverse effects in the human population (Sheehan, 1998), and the potential mechanistic explanation for the epidemiological findings, this is an important study. It is one of the more robust, well-designed prospective epidemiological studies generally available.

We rarely have such power in human studies, as well as a potential mechanism, and thus the results should be interpreted in this context.

Does the Asian experience provide us with reassurance that isoflavones are safe? A review of several examples lead to the conclusion "Given the parallels with herbal medicines with respect to attitudes, monitoring’ deficiencies, and the general difficulty of detecting toxicities with long latencies, I am unconvinced that the long history of apparent safe use of soy products can provide confidence that they are indeed without risk" (Sheehan, 1998)

Taken together, the findings presented here are self-consistent and demonstrate that genistein and other isoflavones have adverse effects in a variety of species, including humans. Animal studies are the front line in evaluating toxicity, as they predict, with good accuracy, adverse effects in humans. For the isoflavones, we additionally have evidence of two types of adverse effects in humans, despite the very few studies that have addressed this subject. While isoflavones may have beneficial effects at some ages or circumstances, this cannot be assumed to be true at all ages. Isoflavones are like other estrogens in that they are two-edged swords, conferring both benefits and risk (REF). As the benefits are not under consideration, the addition of isoflavones to foods needs to considered just as would the addition of any estrogen to foods, which is a bad idea.

Finally, NCTR is currently conducting a long-term multigeneration study of genistein administered in feed to rats. The dose range-finding studies were just completed. As preliminary data, which is still confidential, may be relevant to your decision, I suggest you contact Dr. Barry Delclos at the address on the letterhead, call him at 870-543-7372, or email him at <>.



I have removed the COMMENT facility, with regret, as I seem to be the only person who cannot leave a comment!