"We are faced with the seeming paradox of increased adiposity at both ends of the birth weight spectrum—higher BMI with higher birth weight and increased central obesity with lower birth weight" (Oken and Gillman, 2003). Thus prevention of childhood and adult obesity must start in utero.
Indeed, many synthetic chemicals are actually used to increase weight in animals.
This article provides fascinating examples of chemicals that have been tested for toxicity by standard tests that resulted in weight gain in the animals at lower doses than those that caused any obvious toxicity.
Chemicals having endocrine-disrupting activity rise to the top of the list as most act via receptors linked to activation of transcriptional activity.
In the adult, loss of circulating estrogen due to ovariectomy leads to increased body and adipose tissue weights. Estrogen receptor alpha knockout mice have a significantly increased body fat content, and estrogen decreases the activity of lipoprotein lipase
estrogenic endocrine-disrupting chemical bisphenol A at concentrations as low as 2 µg/ml, in the presence of insulin, stimulated differentiation of the 3T3L1 cells into adipocytes
he fact that an environmental chemical has the potential to stimulate growth of "preadipocytes" has enormous implications for the area of obesity and its control.
Differentiation could be inhibited and more potential fat cells could be formed, as seems to be the case with NP, or differentiation could be stimulated, as appears to be the case with BPA
Will these results extrapolate to the in vivo situation in rodents and other animal models?
Only time and more research will tell, but the door has been opened by the novel work being highlighted.
An article discussing how the area of research of obesity as a result of endocrine disrupting chemical exposure could be a beneficial area for intervention and prevention studies of obesity.
This was one of the first articles I found directly addressing how endocrine disrupting chemical exposure can lead to a predisposition to obesity
For Charlotte: EEDs do not have to be hormone based, they can just influence the natural functions of hormones. This site is recently developed to help people understand the effects of the BP Oil spill in the Gulf. I hope it is informative.
This was one of the first articles that I looked in depth at and pretty much read all of. It presents some of the original research done on the effects Bisphenol-A on reproductive development and mammary gland formamation and how in the process led to a noticeable pattern between exposure and weight gain. The study of obesogens is a new field that was in a way accidentally discovered. It has been hypothesized that estrogen causes embryonic cells to develop into fat cells through a process called adipogenesis by chemicals called organotins. New research to support this is addressed in this article.
This source is probably the biggest contribution to my paper. I accidentally shared it twice because I couldn't figure out how to edit the tags on this one since it didn't come from my library. I shared it before I figured out how to share the sources from my library to the group, I thought I had to do it separately.
Objectives: To investigate the effect of prenatal exposure to polychlorinated biphenyls (PCBs) and dichlorodiphenyl-dichloroethylene
(DDE) on weight, height and body mass index (BMI) in adult female offspring of the Michigan fisheater cohort examined between
1973 and 1991
Maternal height and BMI were significant predictors of the daughters’ height, weight and BMI.
The weight and BMI of adult offspring were statistically significantly associated with the extrapolated prenatal DDE levels of their mothers.
ncreasingly, however, prenatal exposure to toxicants is suspected of contributing to obesity.
Previous studies have shown that Michigan anglers and fisheaters have higher serum levels of PCBs and DDE than population
controls.
A total of 176 (82.6%) daughters
participated in at least one of two repeated investigations
Our results suggest that higher prenatal exposure to DDE, but not to PCBs, is statistically significantly associated with
increased weight and BMI in adult female offspring.
Liz, this article was already in my library and you might want to look at it. I feel as though the study isn't completely controlled since it deals with people who chose to participate in the study over the course of many years but there are some concepts that can be gathered that may be beneficial to you.
This is another epidemiological study similar to the study present by Suphada on sport fish consumption. There were many outside variables, leading to only a small sample size that could be used.
During embryonic development, steroid hormones like estrogen control gene-expression programs to coordinate cell differentiation, growth, organogenesis, and metabolism.
“The moment we published something on bisphenol A, the chemical industry went out and hired a number of corporate laboratories to replicate our research. What was stunning about what they did . . . was they hired people who had no idea how to do the work.”
“whole-animal toxicological studies,” which look at different endpoints than the more mechanistic studies do, Hughes says. “That doesn't let you look at changes in gene expression, changes in epigenetic control of gene expression.
“I can tell you simply by the size of the animal which is DES-exposed and which isn't.”
“We found out that brain is a target, bone is a target . . . and now the new target is adipocytes.”
When he removed all the soy-derived plant estrogens from the mother's diet, he was astonished to see endogenous estradiol levels in the fetus rise, and the offspring become “horrifically obese.
Adding the weak plant estrogens back in the diet suppressed the far more potent endogenous estradiol, he discovered, by inhibiting an enzyme required to make it.
Recent evidence suggests that a class of ubiquitous environmental pollutants called organotins can also stimulate adipogenesis and interfere with energy balance
This was one of the first articles that I looked in depth at and pretty much read all of. It presents some of the original research done on the effects Bisphenol-A on reproductive development and mammary gland formamation and how in the process led to a noticeable pattern between exposure and weight gain. The study of obesogens is a new field that was in a way accidentally discovered. It has been hypothesized that estrogen causes embryonic cells to develop into fat cells through a process called adipogenesis by chemicals called organotins. New research to support this is addressed in this article.
In addition to having highly permeable skin (which makes amphibians particularly vulnerable to chemical contaminants), amphibians also typically reproduce and pass through critical hormone-regulated developmental stages while in the aquatic environment
What about human skin and its permeability to these pesticides?
atrazine is of special concern because it is a ubiquitous, persistent contaminant of ground-water and surface water that is active at low, ecologically relevant concentrations
very sensitive technique used to measure concentrations of antigens (for example, hormone levels in the blood) without the need to use a bioassay.
With the exception of metalaxyl, no single compound affected mortality
mortality was 4% for animals exposed to single pesticides (range = 0–7.8%), with the highest mortality (7.8%)
Propiconizole significantly delayed time to initiate metamorphosis (FLE; F = 2.72, df = 10, p = 0.003) and time to complete metamorphosis (TR; F = 2.81, df = 10, p = 0.002) relative to controls (Figure 1).
Animals exposed to pesticide mixtures at 0.1 ppb had significantly longer larval periods: initiation of metamorphosis (days to FLE) was delayed
there was a significant effect on SVL at metamorphosis (F = 2.1, df = 10, p < 0.05; Figure 3). The smallest animals to metamorphose were those exposed to cyfluthrin, tebupirimphos, or atrazine
All the mixtures (0.1 ppb each pesticide) retarded growth
For the pesticide mixtures, 0.1 and 10 ppb atrazine + S-metolachlor resulted in a negative but nonsignificant relationship between TR and SVL, whereas 0.1 and 10 ppb Bicep II Magnum exposure resulted in maintenance of the positive relationship between TR and SVL, but the relationship was significant for the 0.1 ppb concentration only
Different combinations of pesticides will affect the organism differently.
Histologically, presumptive males maintained both a cortex and a medulla separated by connective tissue without clear formation of testicular lobules (e.g., undifferentiated), whereas females showed regression of the gonadal medulla and an ovarian vesicle but lacked significant numbers of developing oocytes in the cortical regions of the gonad
Seventy percent of the animals exposed to the nine-compound mixture were unable to sit upright. Exposure to the nine-compound pesticide mixture was associated with meningitis, otitis interna, and septicemia due to the gram-negative, water-borne bacteria Chryseobacterium (Flavobacterium) menigosepticum
Morbidity and mortality rates in animals treated with the nine-pesticide mixture were significant (G = 100.12, df = 4, p < 0.001) compared with those in controls or the other mixtures (all of which showed a 0% incidence) and reached 70% of the 59 animals that survived to complete metamorphosis in animals exposed to the pesticide mixture.
After noting that animals exposed to the nine-compound mixture contracted flavobacterial meningitis (see above “Flavobacterial response”), we examined the condition of the thymus as an estimate of immune function.
Although a sizable database examining the toxicological effects of pesticides on amphibians exists (Pauli 2004), most of these studies examine acute toxicity, morbidity, and mortality only
We demonstrated that a realistic pesticide mixture (based on a mixture applied to an actual field) at low ecologically relevant concentrations can have dramatic effects on amphibian development and growth, and ultimately (we predict) survivorship
one of these compounds (propiconizole) retards larval development and delays metamorphosis, and two others (tebupirimphos and cyfluthrin) retard larval growth. In addition to these new data, the present study confirms the retardation of amphibian development
Atrazine has a number of well-documented adverse effects on amphibian larvae. It is a potent endocrine disruptor that both chemically castrates and feminizes exposed male amphibian larvae and also retards larval development and growth
It also induces edema (Carr et al. 2003), erratic swimming (Carr et al. 2003), and irregular behavioral activity (Rohr and Palmer 2005) and is an immunosuppressant (Christin et al. 2003; Gendron et al. 2003; Kiesecker 2002) in amphibians.
As one of the world’s most commonly applied pesticides, it is the most common contaminant of groundwater and surface water
effects of atrazine on the gonads were not detectable because individuals from the present population do not complete sexual differentiation of the gonads before metamorphosis
retardation of growth and development was more severe when atrazine was combined with other pesticides (e.g., S-metolachlor), and the nine-pesticide mixture had the most severe impact.
amphibians (including leopard frogs) often breed in temporary water sources
Retardation of growth is also detrimental. Smaller size at metamorphosis limits food availability for newly metamorphosed frogs, which are gape-limited predators (Figure 12A). Further, smaller individuals are more susceptible to predators, which may also themselves be gape-limited predators
esticide mixtures retard growth and size at metamorphosis, exposed amphibians are less likely to find food and more likely to be preyed upon. Also, decreased size at metamorphosis combined with subsequent decreased postmetamorphic growth decreases the chances that amphibians will survive overwintering
alteration of the relationship between time to metamorphosis and size at metamorphosis is even more significant than either measured alone. In amphibians, the larval stage is a period of growth. A
pesticides that produce no effects alone may act as “enhancers” that worsen the effects of pesticides that act as “effectors” when the two groups of chemicals are combined.
characterize pesticide interactions as concentration additive or response additive
Pesticide-induced declines in populations as a result of decreased prey availability and increased susceptibility to predators (as a result of decreased size and the negation or reversal of the relationship between time to metamorphosis and size at metamorphosis) may be difficult to discern in the wild. Perhaps more important, emergent diseases caused by agents such as ranavirus
and chytrid
are considered major contributors to amphibian declines
the effects of atrazine on sex differentiation can negatively affect amphibian population
trazine has been shown to increase disease rates and parasite loads in amphibians by several pathogens
including the trematode associated with development of limb deformities
Although the use of DDT was banned a long time ago, it is still negatively affecting wild life. This page adds more detail to what we saw in the film, "The Estrogen Effect: Assault on the Male."
Under the metals section, there is a short description of heavy metals. These metals are known to damage organisms, and as shown in some of our mini-presentations, can act as EEDs. For example, erythropoietin's functions are inhibited by lead as an EED.
Report by an M.D. describing the ED effects of the dispersant used to "manage" the BP oil spill. Includes link to article on how PAH uptake by fish is increased when exposed to the dispersant (Corexit - give me a break on the name!).