Endocrinologist have found out that endocrine disruptor found in man made common chemicals like DES, dioxin, PCBs, DDT , plasticizers and in many more chemical we use daily are responsible for this unusual phenomenon.
Endocrine disruptors gets locked in to your fatty tissues and they can not be excreted out of our bodies as they are insoluble in water and they get accumulated during our entire life time. Endocrine disrupting chemicals disturbs the endocrine glands that releases hormones into the bloodstream to control various organs of the body. The endocrine glands includes the pituitary, thyroid, adrenal, thymus, pancreas, ovaries, and testicles. Developing fetuses and infants are are more vulnerable to endocrine disruptors.
In 50s and 60s doctor prescribed a synthetic estrogen called diethylstilbestrol (DES) to pregnant women with the goal to prevent miscarriages which was later found to contain endocrine disruptors. Over five million women were effected by this drug. Miscarriages,spontaneous abortions, premature births ,birth defects of the the uterus,ovaries,immune system defects,undescended testicles, malformed sperm in boys,chronic depression and other psychiatric disorders were reported. Use of estrogen have caused breast cancer in some women. With not much of government control over this chemical manufacturer let us follow simple precaution to save our next generation:
Educate yourself,your family and friends about endocrine disruptors.
Use organic pesticides and fertilizers.
Do not give young children soft plastic teether or toys.
Buy organic food whenever possible.
Do not store fatty foods or water in plastic containers.
Use glass article were ever possible.
It is better to use natural estrogen replacement for men who require hormone replacement therapy. “
The present document is a short summary of the current knowledge of the effects of endocrine disrupters on child health. The main focus is on congenital disorders, cryptorchidism and hypospadias, which have an endocrine connection, on thyroid hormone-related problems, and on puberty. There is ample evidence of endocrine disruption in wildlife, and the mechanisms of action of endocrine disrupters have been elucidated in experimental animals, but there is limited knowledge of the association of human disorders with exposure to endocrine disrupters. Accumulating data suggest that many adult diseases have fetal origins, but the causes have remained unexplained. Improving fetal and child health will influence the whole life of an individual and improve the wellbeing of our society.
Focusing on exposures to environmental contaminants, this book provided the first comprehensive source of information in this field
Publisher: Cambridge University Press; 1 edition (March 15, 2010)
Many reproductive and developmental health problems are caused by exposure to chemicals that are widely dispersed in our environment. These problems include infertility, miscarriage, poor pregnancy outcomes, abnormal fetal development, early puberty, endometriosis, and diseases and cancers of reproductive organs. The compelling nature of the collective science has resulted in recognition of a new field of environmental reproductive health. Focusing on exposures to environmental contaminants, particularly during critical periods in development and their potential effects on all aspects of future reproductive life-course, this book provides the first comprehensive source of information bringing together the arguments that are spread out among various scientific disciplines in environmental health, clinical and public health fields. It provides a review of the science in key areas of the relationship between environmental contaminants and reproductive health outcomes, and recommendations on efforts toward prevention in clinical care and public policy.
Fredrick Vom Saal is a Professor of Biological Sciences, University of Missouri
You’ve said that the doses at which hormones affect the body are extremely low. Give me an example to make me understand that.
F Vom Saal: “The issue of the amount of hormone that actually causes effects is very difficult for scientists to talk to people about because we’re dealing with numbers that are outside of the frame of reference that anybody is going to be thinking about. We see changes, profound changes, in the course of development of essentially the whole body of experimental animals, and we’re working with mice and rats, and we see these changes at fifty femtograms of the hormone per milliliter of blood. That’s 0.05 trillionths of a gram of this hormone in a milliliter of blood.”
And what sort of effect does it have?
F Vom Saal: “We see changes in the functioning of the prostate. We see dramatic change in the sprouting of glands within the fetal prostate. We see changes in testicular sperm production. We see changes in the structure of the endocrine control region in the brain, which is accompanied by changes in sex behavior, aggression, the way these animals behave towards infants, their whole social interaction, the way they age, the time that they enter puberty, the age at which they cease reproduction. It changes their entire life history, and these changes are capable of occurring at very low levels of hormones. I remember when we first did this and I was a post doctoral fellow, and my advisor and I looked at the hormone levels and said, “My God, these levels are so staggeringly small and the consequences are so immense it’s amazing.” Even to biologists, it’s amazing.
But what you have is the entire field of toxicology thinking of a millionth of a gram of a hormone or a chemical as being this staggeringly tiny amount, and to most people if I said there’s only a millionth of a gram of it here you’d say, “How can it do anything?” A millionth of a gram of estradiol in blood is toxic. The natural hormone is actually operating at something like a hundred million times lower than that. So when you have a physiologist thinking of a millionth of a gram, you have that physiologist thinking this is a toxic high dose. When you are raised in the field of toxicology you are looking at that from the other perspective of “My gosh, that’s such a tiny dose, it couldn’t do anything.”
So now what we have are two different fields coming into this issue and looking at a dose as either staggeringly high or staggeringly low, and it’s not surprising that there is a clash occurring with regard to dose effects.”
How Girls Are Developing Earlier In An Age Of ‘New Puberty’
“ In the past, only 5% of U.S. girls were believed to be experiencing precocious puberty, defined as the onset of breast and hair development in girls age 7 or younger. Their research indicates the figure is now closer to 15%, with a 27% showing breast development by age 8. Similarly, public hair is now appearing in 19% of American girls by age 8.
Findings suggest an association between 2, 5-DCP, a potential EDC, and earlier age of menarche in the general U.S. population. Also phthalates may cause weight gain and so influence the timing of puberty…
At the turn of the 20th century, the average age for an American girl to get her period was 16 to 17. Today, it is less than 13, according to national data. The trend has been attributed to the epidemic of overweight children and a greater exposure to pollution – the n° 1 factor that is pushing girls into puberty early seems to be their body mass index.
Among the toxins causing this trend, the biggest offenders are plastic compounds, in particular phthalates, man-made chemicals found all over the place: in plastic food and beverage containers, carpeting, shampoos, insect repellents, vinyl flooring, shower curtains, plastic toys and in the steering wheels and dashboards of most cars. Our bodies cannot metabolize phthalates, which interfere with the endocrine system—the body’s system of glands and hormones—and harm fat cells. Indirectly, phthalates may cause weight gain and so influence the timing of puberty…
The observed age of menarche has fallen, which may have important adverse social and health consequences. Increased exposure to endocrine-disrupting compounds (EDCs) has been associated with adverse reproductive outcomes.
Our objective was to assess the relationship between EDC exposure and the age of menarche in adolescent girls.
We used data from female participants 12–16 years of age who had completed the reproductive health questionnaire and laboratory examination for the Centers for Disease Control and Prevention’s National Health and Nutrition Examination Survey (NHANES) for years 2003–2008 (2005–2008 for analyses of phthalates and parabens). Exposures were assessed based on creatinine-corrected natural log urine concentrations of selected environmental chemicals and metabolites found in at least 75% of samples in our study sample. We used Cox proportional hazards analysis in SAS 9.2 survey procedures to estimate associations after accounting for censored data among participants who had not reached menarche. We evaluated body mass index (BMI; kilograms per meter squared), family income-to-poverty ratio, race/ethnicity, mother’s smoking status during pregnancy, and birth weight as potential confounders.
The weighted mean age of menarche was 12.0 years of age. Among 440 girls with both reproductive health and laboratory data, after accounting for BMI and race/ethnicity, we found that 2, 5-dichlorophenol (2, 5-DCP) and summed environmental phenols (2, 5-DCP and 2, 4-DCP) were inversely associated with age of menarche [hazard ratios of 1.10; 95% confidence interval (CI): 1.01, 1.19 and 1.09; 95% CI: 1.01, 1.19, respectively]. Other exposures (total parabens, bisphenol A, triclosan, benzophenone-3, total phthalates, and 2, 4-DCP) were not significantly associated with age of menarche.
Our findings suggest an association between 2, 5-DCP, a potential EDC, and earlier age of menarche in the general U.S. population.
Sources and more information
Puberty Comes Earlier and Earlier for Girls, newsweek, January 26, 2015.
Phthalate exposure and pubertal development in a longitudinal study of US girls, NCBI PMID: 24781428, pub 2014 Apr 29.
Exposures to Endocrine-Disrupting Chemicals and Age of Menarche in Adolescent Girls in NHANES (2003–2008), Environ Health Perspect; DOI:10.1289/ehp.1104748 , 1 November 2012
Early puberty in girls has been linked to breast cancer. Data show that the worldwide incidence of precocious puberty has increased and the age of pubertal changes has decreased over the past two decades.
Many of the cases are attributed to excess weight gain but exposures to phthalates and endocrine disruptors chemicals have also been implicated as possible risk factors.
Endocrine Disruptors permanent effect on Obesity through at least three Generations
Girls between 9 and 12 years of age with higher-than-average levels of bisphenol-A (BPA) in their urine had double the risk of being obese than girls with lower levels of BPA, according to a Kaiser Permanente study published today … Read more, ScienceDaily, June 12, 2013.
Bisphenol-A (BPA) is a potential endocrine disruptor impacting metabolic processes and increasing the risk of obesity. To determine whether urine BPA level is associated with overweight/obesity in school-age children, we examined 1,326 students in grades 4–12 from three schools (one elementary, one middle, and one high school) in Shanghai. More than 98% of eligible students participated. Total urine BPA concentration was measured and anthropometric measures were taken by trained research staff. Information on risk factors for childhood obesity was collected for potential confounders. Age- and gender-specific weight greater than 90th percentile of the underlying population was the outcome measure. After adjustment for potential confounders, a higher urine BPA level (≥2 µg/L), at the level corresponding to the median urine BPA level in the U.S. population, was associated with more than two-fold increased risk of having weight >90th percentile among girls aged 9–12 (adjusted odds ratio (aOR) = 2.32, 95% confidence interval: 1.15–4.65). The association showed a dose-response relationship with increasing urine BPA level associated with further increased risk of overweight (p = 0.006 for trend test). Other anthropometric measures of obesity showed similar results. The same association was not observed among boys. This gender difference of BPA effect was consistent with findings from experimental studies and previous epidemiological studies. Our study suggests that BPA could be a potential new environmental obesogen. Widespread exposure to BPA in the human population may also be contributing to the worldwide obesity epidemic.