Endocrine disrupters are chemicals in the environment that are similarin structure to natural sex hormones and interfere with their normal functions, usually by binding to the cell receptors and preventing the hormone from binding to the receptor.
When hormones bind to their receptors, this triggers their biological effects. Endocrine disrupters are found in plastics and foods.
Infertility is an emotive issue, and having children is a recognized "right," so any implication that environmental pollution affects reproduction has to be taken seriously.
When the causative agents might also be responsible for various cancers and other diseases, then the level of interest that the issue attracts is unsurprising hence the calls in the early 1990s for action in line with the "precautionary principle."1
In men hypospadias, cryptorchidism (undescended testicles), cancer of the prostate, testicular cancer, and semen quality and in women breast cancer, cystic ovaries, and endometriosis have all been suggested as indicators of adverse trends in reproductive health.2
The idea that these trends are real and are connected with environmental pollution is gaining credence internationally. The effect on human health of environmental chemicals that are mediated through the endocrine system endocrine disrupters has generated huge interest and investment.
Why Is This, and What Is the Evidence for the Assumed Association?
Changes in the sexual morphology of fish exposed to sewage effluent have led some scientists to conjecture that humans also live in a "sea of estrogens" and that the apparent increases in the incidence of certain reproductive conditions may be due to exposure to chemicals in the environment.
The so called Sharpe-Skakkebaek hypothesis offered a possible common cause and toxicological mechanism for abnormalities in men and boys that is, increased exposure to estrogen in utero may interfere with the multiplication of fetal Sertoli cells, resulting in hormonally mediated developmental effects and, after puberty, reduced quality of semen.3
It was postulated that synthetic chemicals in the environment are the prime source of the excessive estrogenic stimulation, with exposure through food and water being the primary route.
Further research has extended the concern to the role of antiandrogens and has led to the recognition that a range of systems and processes may be susceptible to hormonal modulation, including immune function, behavior, and learning and memory, as well as reproduction.
The term environmental estrogen has given way to the more encompassing term "environmental endocrine disrupter," defined as "an exogenous substance that causes adverse health effects in an intact organism, or its progeny, subsequent to changes in endocrine function."4
Endocrine disrupters are potentially present in food as natural "phytoestrogens" and chemical contaminants, and there is a divide in the perception of natural and synthetic substances.5
Hence the drive in some quarters to market "healthy" bread that is rich in soy flour and linseed at the same time that other people are warning against low levels of weak estrogenic synthetic chemicals as contaminants in food. Perhaps this reflects the common view of natural things as good and synthetic things as necessarily bad.
Two Questions Need To Be Addressed
- Do indicators of reproductive health
truly reveal a worsening situation?
- Can exposure to environmental chemical contaminants conceivably be the cause of any such temporal changes?
Baseline data on many of the implicated conditions are so poor that it is not possible to say for sure whether trends are occurring. There is also the issue of geographical variability in the measured indices, which can be related to genetic differences in the population or to climatic differences or changes in lifestyle, for example.
None the less, there is agreement that the incidence of testicular and prostate cancer is increasing and that semen quality is probably worsening in some regions of the world.
There is also some evidence for an increasing incidence of cryptorchidism and hypospadias; and in women endometriosis and polycystic ovaries may be more common.4-6
Perhaps the most controversial issues in research on endocrine disrupters are the possible disproportionate effects of low levels of exposure, as proposed by Vom Saal et al and recently accepted by the US national toxicology program.
At least for a limited number of chemicals7-9; the question of synergism in mixtures, which has become something of a no go area since the withdrawal of the much quoted paper by Arnold et al10; and the development of appropriate test methods.
Large amounts of resources have been invested in this last activity, through the work of the endocrine disrupter screening and testing advisory committee in the United States. Yet according to Ashby the developmental effects of endocrine disruptors that are seen in rodent studies cannot be extrapolated to humans.
This is not only because of the uncertainty of applying such results across species but also because of the absence of an agreed control database in rodents and the variability in test protocols and in the developmental effects in test animals.11
Among specific chemicals implicated as endocrine disrupters phthalates may be of particular importance because of their ubiquity.
Similarly bisphenol A has been shown in both in vitro and in vivo assays to have high potential for endocrine disruption and potential for exposure to humans for example, through its use in can linings.
These are issues of major interest, not least because of the possible exposure of infants to these chemicals at critical stages of development. Sharpe has argued that, until appropriate in vivo experiments are done, phthalates and similar chemicals will continue to cause concern for testicular development.12
British Medical Journal December 8, 2001;323:1317-1318
There is no question that one should avoid toxic chemicals like dioxin (a toxic byproduct of chlorine) as it is a potent mimic of estrogen that can cause very serious hormonal disruption.
The U.S. Environmental Protection Agency (EPA) has found dioxin to be 300,000 times more potent as a carcinogen than DDT. Dioxin is commonly found in plastics that are made with polyvinyl chloride (PVC). This is one of the reasons why you NEVER want to use a water bottle that is made from the cloudy plastic bottles (commonly used to store milk). One should always use the clear polyethylene bottles.
Bisphenol A, which is very common in canned foods is another potent endocrine disruptor and is one of the reasons you want to keep canned foods to an absolute minimum. You should NEVER regularly consume foods from cans.
Then we come to the issue of soy. Even the conservative US government has recognized that soy formula is a potent endocrine disruptor. There is absolutely no reason to ever give your child soy formula or soy milk. It is one of the worst foods you could possibly give your child and the long-term health complications can be quite significant.
Prostate and breast cancer, early puberty, endometriosis and infertility, irregular and painful menstrual periods are only a few of the things your children will have increased risk for if they are given soy formula or soy milk.
If you have already given your child these foods the best way to reverse the damage is to have them rigidly follow the eating plan. The nutrition from whole organic foods is the most potent corrective force for these disruptions in hormones.
If you still aren't convinced of the dangers of soy you might want to review the protest letter two FDA experts wrote earlier this year which points to studies that show a link between soy and health problems in certain animals.
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2. Harrison PTC, Holmes P, Humfrey CDN. Reproductive health in humans and wildlife: are adverse trends associated with environmental chemical exposure? Sci Total Environ 1997; 205: 97-106[Medline].
3. Sharpe RM, Skakkebæk NE. Are oestrogens involved in falling sperm counts and disorders of the male reproductive tract? Lancet 1993; 341: 1392-1395[Medline].
4. European Commission. European workshop on the impact of endocrine disrupters on human health and wildlife: report of the proceedings. Brussels: European Commission, 1997. (EUR 17549)
5. Holmes P, Phillips B. Human health effects of phytoestrogens. In: Hester RE, Harrison RM, eds. Issues in environmental science and technology. , Vol 12. Endocrine disrupting chemicals Cambridge, UK: Royal Society of Chemistry, 1999:109-134.
6. Joffe M. Are problems with male reproductive health caused by endocrine disruption? Occup Environ Med 2001; 58: 281-287[Full Text].
7. Vom Saal FS, Timms BG, Montano MM, Palanza P, Thayer KA, Nagel SC, et al. Prostate enlargement in mice due to fetal exposure to low doses of estradiol or diethylstilbestrol and opposite effects at high doses. Proc Natl Acad Sci USA 1997; 94: 2056-2061[Abstract/Full Text].
8. Welshons WV, Nagel SC, Thayer KA, Judy BM, vom Saal FS. Low-dose bioactivity of xenoestrogens in animals: fetal exposure to low doses of methoxychlor and other xenoestrogens increases adult prostate size in mice. Toxicol Ind Health 1999; 15: 12-25[Medline].
9. National Toxicology Program. Endocrine disruptors low-dose peer review. http://ntp-server.niehs.nih.gov/htdocs/liason/LowDoseWebPage.html (accessed 24 May 2001).
10. McLachlan JA. Synergistic effect of environmental estrogens: report withdrawn [retraction of Arnold SF, Klotz DM, Collins BM, Vonier PM, Guillette LJ Jr, McLachlan JA. In: Science 1996;272:1489-92]. Science 1997; 277: 462-463[Medline].
11. Ashby J. Testing for endocrine disruption post-EDSTAC: extrapolation of low dose rodent effects to humans. Toxicol Lett 2001; 120: 233-242[Medline].
12. Sharpe RM. Hormones and testis development and the possible adverse effects of environmental chemicals. Toxicol Lett 2001; 120: 221-232[Medline].
13. Holmes P, Harrison PTC. Environmental and dietary endocrine disruptors and women's health. J Brit Menopause Soc 2001; 7: 53-59.