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more on phytoestrogen dispute

  i didn't mean to send my earlier post (in response to a request) giving
  references and expanding on the section of this paper dealing with early
  discoveries of e.d. before i posted this.  oh well.  the other interesting
  section, the 2nd half, and the heart of this paper, is an update on a post
  i sent a few weeks ago regarding the evidence on phytoestrogens.
             By Tony Tweedale
  MISSOULA, Montana, July 23, 1997 (ENS) - A surprising range of the body
  functions of living creatures, such as development, cellular growth and
  differentiation, are under the control of hormones. These substances are
  produced by organs known as glands and are carried by bodily fluids to
  other organs or tissues, where they each have a specific effect.
  For example, cancer, intimately associated with development, is a common
  occurrence in bodily systems like the breast and the prostrate which are
  controlled by hormones.
  Metabolism, immune protection, brain and sexual development - all are
  dependent on minute concentrations of hormones and their accompanying
  activating receptor molecules. These are substances in concentrations
  equivalent to one drop of vermouth in many thousands of rail tankers of
  A wide range of industrially produced chemicals also bind to these receptor
  molecules and become biologically active. They are known as endocrine
  (hormone) disruptors.
  The Environmental Protection Agency (EPA) has been gathering evidence for
  six years about the handful of dioxins and PCB endocrine disruptors that
  bind to the aryl hydrocarbon (Ah) hormone receptor in living organisms. The
  EPA is studying only the variety of effects that depends on this binding to
  Very tiny concentrations of hormones are normally required to elicit
  effects. These are typically in the low parts per trillion, just a few
  thousand hormone-receptor pairs in a developing embryo. For example, in
  male humans, testosterone is produced by a genetic command to change our
  (always female) developing sex organs to male ones in the third month after
  In mice, a single dose of the most potent Ah-binding dioxin of just 64
  parts per billion in the mother's food at the critical time of sexual
  differentiation can disrupt this process. This dioxin dose would cause
  severe malformation in the sex organs of her male offspring. In fact, this
  effect may occur at a lower dose, but this has not yet been tested.
  The EPA has said the majority of us already carry almost enough of these
  compounds in us to cause disregulation of the immune system and impairment
  of reproductive function in a variety of similar species. Millions more
  people have levels actually higher than that needed to cause immune
  disregulation. Some of us also carry as much as has been observed to cause
  various cancers in lab animals, while the rest of us are uncomfortably
  close. (For a review of this evidence, see DeVito et al., in the
  publication Environmental Health Perspectives (NIEHS) September 1995.
  The unavoidable implication of this evidence is that our exposure to these
  industrial chemicals should stop. But instead, some endocrine disruptors
  are being pumped into our living environment in massively larger quantities
  than dioxins, which are byproducts of incineration of plastics and other
  industrial processes. Some endocrine disruptors are being emitted in larger
  quantities even than the mass produced PCB compounds, such as the monomer
  to the plastic polycarbonate (bis-phenol-A) and the detergents and
  plasticizers known as the alkyl phenols.
  A large number of known or potential endocrine disruptors are chlorinated
  compounds, which often resist environmental degradation and build up in the
  food chain. In addition to dioxins, furans and PCBs, these include many
  chlorinated pesticides.
  For 60 to 70 years, since approximately the 1930s, when the structure of
  the sex hormone estrogen was detailed, people have been studying industrial
  chemicals for their ability to elicit hormonal-type effects. But only in
  the 1990s has anything like a systematic approach to studying, much less
  managing, this problem even begun.
  The effects of estrogen on improper sexual development, and the
  estrogen-like effects of alkyl phenols used as detergents were studied in
  the 1930s.
  In the 1940s, it was suggested in the scientific literature that industrial
  chemicals could be hormonally active. At that time the effects of
  testosterone on fish sex were investigated.
  In the 1950s, hormonal effects of the drug diethylstilbestrol (DES) were
  studied intensively and secretly, and DDT's estrogen-like effect on
  roosters was observed. So was the unusual sexual behavior of populations of
  wild birds.
  Estrogen's ability to cause cancer was observed at least by the early
  1960s, and DDT's estrogen-like effect on sex organs was seen in 1968 and
  The first conference on hormonal toxicity to be hosted by the National
  Institute for Environmental Health Sciences occurred in May 1980. The aryl
  hydrocarbon (Ah) hormone receptor was discovered in the 1980s, along with
  its ability to bind some PCBs, dioxins and furans. These are molecules of a
  somewhat similar shape to DDT and DES. By this time, over a dozen widely
  used pesticides were known to exhibit hormone-like effects.
  Very few, if any, of these industrial compounds have complete toxicological
  profiles. Several banned synthetic petro-synthetics, including the
  organochlorines the PCBs and the pesticide DDT, which were banned for other
  unanticipated effects, have been shown to be hormone disruptors.
  Industry and government rely on an absurd system for the management of risk
  from chemicals. With over 80,000 chemicals in commerce, it is still a
  largely after-the-fact and chemical-by-chemical and industry controlled and
  funded approach to risk management.
  This risk management system is largely limited to studies of just two
  health effects - cancer and acute effects. Neurological, reproductive,
  immune, endocrine and other health "end points" are largely ignored. Also
  avoided is study of the effects of mixtures of chemicals or cumulative
  exposures to chemicals.
  Rarely are the effects of these chemicals on minority populations such as
  fish-eaters, the pregnant, infants and children studied. Infants and
  children not only expose themselves to chemicals more thoroughly than
  adults through their behavior; they also eat, breathe and drink more per
  pound of body weight than adults. Crucially, all their bodily systems are
  developing and are very active genetically and so are incredibly vulnerable
  to endocrine disruption.
  It is legitimately hard to prove an actual cause and effect link between
  exposure to a chemical and a resulting health effect, given the complexity
  of real world exposure situations. Evidence from well-controlled lab animal
  experiments is required. Human results from the poorly controlled real
  world are needed - for example, repeated observations of declining sperm
  counts and ovary-like undescended testicles in recent decades. And, it is
  desirable to show a plausible mechanism by which such observations can come
  In the case of endocrine disruptor chemicals, a study of one plausible
  mechanism has shown mildly radioactive carbon containing molecules (for
  tracking) of the most potent Ah-binding dioxin attaching to the Ah receptor
  with the help of a third protein, entering a cell, interacting with yet
  other proteins, and finally binding to DNA on segments of the chromosone
  that code for some of the very effects this dioxin has been observed to
  cause. For a discussion of this mechanism read Janet Raloff's article, "The
  Gender Benders" in Science News, January 8, 1994.
  One more question must be dealt with before these compounds can
  unequivocally be called the deadly threat to life the evidence seems to
  show them to be. We have evolved as a species in an environment of
  hormones, mostly in our food chain. Many of these hormones are produced by
  plants and are known as phytoestrogens. One hypothesis says that if we are
  adapted to exposure to these natural hormones, industrial hormones may not
  affect our health, or at least not much.
  It is argued, mostly by people with enormous financial conflicts of interest:
  1) that we take in much, much more in natural hormones than we do
  industrial endocrine disruptors;
  2) that these natural hormones have been shown to have effects in humans; and
  3) that industrial endocrine disruptors are much weaker binders than our
  own hormones to the receptors necessary for biological activity.
  For a thorough and informative, if biased, factsheet by Jonathan Tolman of
  the Competitive Enterprise Institute visit the website
  The reason we carry body burdens of many industrial chemicals, including
  endocrine disruptors, is that those are the ones that are relatively inert,
  that resist degradation. As many industrial compounds are fat soluble, not
  water soluble, they end up attached to soil, sediment and in edible fats,
  meaning they become more concentrated as they move up a food chain. Humans
  eat at the top of many food chains, taking in higher concentrations of
  these compounds than do creatures lower down the chain.
  Data seems to be lacking on the relative resistance to breakdown of
  industrial endocrine disruptors versus phytoestrogens, but two things are
  known with certainty.
  One is that natural estrogens have been observed to be metabolized
  many,many times more rapidly than industrial endocrine disruptors. This
  counters the argument that industrial endocrine disruptors are inefficient
  at binding the
  activating receptor molecules. So does the second indisputable fact. The
  blood serum binding proteins (BBP) that assure temporary deactivation of
  our potent natural hormones for transportation are ineffective against
  industrial endocrine disruptors. This probably vastly increases the chances
  that an industrial endocrine disruptor will activate by finding a receptor
  These two important facts (inability to metabolize and inactivation by BBP)
  speak only to industrial endocrine disruptors versus our natural hormones,
  not to phytoestrogens, the plant hormones. Flocks of sheep eating plants
  especially rich in phytoestrogens lose the ability to reproduce.
  Phytoestrogens also appear to have a protective effect against breast
  cancer. These facts may be evidence that phytoestrogens are as biologically
  active as industrial chemical endocrine disruptors.
  In that case, arguing that industrial endocrine disruptors can have no
  effect, since we are healthy in spite of historically taking in many times
  more phytoestrogens, is inconsistent with arguments from the same parties
  that we are healthy despite phytoestrogens having effects on us!
  In fact, that phytoestrogens may be biologically active is a cause for
  concern about industrial endocrine disruptors, not for reassurance. If
  phytoestrogens are biologically active, it is even more plausible that
  similar exogenous compounds, such as the industrial endocrine disruptors,
  may also be active.
  Finally, it seems reasonable to assume that phytoestrogens may be more
  susceptible to metabolism than industrial endocrine disruptors. The same
  logic also applies in the environment, before phytoestrogens enter the
  body. Living creatures are only exposed to phytoestrogens via one route -
  the food chain. But beings are exposed to industrial endocrine disruptors
  by inhalation and adsorption as well. The degree of exposure to
  phytoestrogens has not increased rapidly if at all, but exposure to
  industrial endocrine disruptors has increased exponentially since the start
  of the Industrial Revolution.
  All of this may help to explain why humans and animals are now experiencing
  mutations, cancers, and immune system problems to an unprecendented degree.
  {Tony Tweedale is a toxics activist who works with MT-CHEER, Montana
  Coalition for Health, Environmental and Economic Rights. He holds a Master
  of Science degree in Environmental Studies from the University of Montana.
  He makes his home in Missoula, Montana.}
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  tony tweedale