Obesogens and Weight gain PDF Print E-mail
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Written by Karel Nunnink   

Nearly two-thirds of Americans are now either overweight or obese and their health costs are 150% of those of normal weight, mostly due to the prevalence of type II diabetes, heart disease and other conditions.

16% of US children between the ages of 6 and 19 are now classified overweight or obese according to the US Centers for Disease Control and Prevention - a number that has tripled since 1980.

Where the US leads, other countries inevitably follow and in the UK, women have become broader, wider, taller and bigger than a generation or so ago. Since the 1950s, the average female waist has risen from 70 to 86 cm (27.5 to 34 inches) and the average bra size has grown from a 34B a decade ago to 36C today.

We are constantly told this is because we are lazy, make poor food choices and eat too much.

But here's a fact that might be hard to explain away.

In 2006 scientists at the Harvard School of Public Health reported that the prevalence of obesity in babies under 6 months had risen 73% in the previous 25 years!

Since these babies are only consuming formula or breast milk and all small babies are similarly inactive, the usual explanations for obesity do not apply.

The suggestion is that this observation is due to exposure in the womb and in early-life to hormone-mimicking environmental pollutants which have come to known as obesogens for their ability to:

  • Act on genes in the developing foetus and baby and convert precursor cells into fat cells which then remain with the individual for life
  • Promote the proliferation of fat cells
  • Alter the individual's metabolic rate so that the body hoards calories rather than burning them
  • Disrupt normal endocrine gland and hormone function and
  • Alter the processes of satiation so that affected individual is often hungry


Obesogens: The background

The lifelong effects of early life exposure to a variety of influences are only now just starting to be recognised under the newly developing speciality of foetal origins. We already know that exposure to hormone-like chemicals in the womb can cause serious illness decades later. For example, it is known that women whose mothers took the oestrogen-like drug DES during pregnancy to prevent miscarriage have a high risk of contracting cervical and vaginal cancer during their lifetime.

The link between the use of environmental chemicals such as pesticides and plasticisers and the current obesity epidemic was first mooted by Paula Baillie-Hamilton, a doctor at Stirling University in Scotland who published a paper on the subject in The Journal of Alternative and Complementary Medicine in 2002.

Subsequently, other researchers picked up Baillie-Hamilton's idea giving it exposure in more mainstream publications. One such researcher was Jerrold Heindel of the US National Institute of Environmental Health Services (NIEHS) who published a paper in a widely read toxicology journal in 2003.

In his paper he pointed out that when many of the chemicals Baillie-Hamilton discussed had been tested for toxicity, researchers had focussed on whether they caused weight loss, which is considered a toxic effect, but that researchers had overlooked the possibility of weight gain. Referring back to those studies, Heindel found that a number of the chemicals studied caused weight gain at the low doses that foetuses and newborns had been exposed to.

Heindel also referred to the work of scientists in Japan, who were finding in laboratory studies that low levels of certain compounds, such as bisphenol A (found in polycarbonate plastics) and some other industrial compounds, made cells destined to become fibroblasts (prefibroblasts) turn into fat cells. They also found that these compounds stimulated the proliferation of existing fat cells.

His colleague, Retha Newbold also of the NIEHS who had been studying the effects of oestrogens for 30 years now started to investigate the effect of low doses of hormone-mimicking compounds on newborn mice. Within six months, the mice were 20% heavier and had 36% more body fat than unexposed mice. And the study mice were measured carefully for activity and amounts consumed and there was no difference between the exposed and unexposed groups.

Bruce Blumberg of the University of California, Irvine had also read the 2002 Baillie-Hamilton paper and began to feed pregnant mice tributyltin, a disinfectant and fungicide used in marine paints and the production of plastics and other products, which has become a contaminant of seafood and drinking water. "The offspring were born with more fat already stored, more fat cells, and became 5 to 20% fatter by adulthood," Blumberg said.

Further genetic tests revealed the mechanism of action. The tributyltin was found to activate a cell receptor (PPAR gamma), which can switch the fate of the cell from becoming a fibroblast (fibrous cell) to becoming a fat cell. In fact, the diabetes drugs Actos and Avandia both activate this receptor for which reason one of their major side-effects is recognised to be obesity.

The term obesogen was originally coined by Felix Grün and was taken up by Bruce Blumberg for compounds which have the ability to alter a cell's fate. Later tests revealed phthalates [used to make soft vinyl plastics such as teats on babies' bottles and clingfilm (saran wrap)] and perfluoroalkyl compounds (used in stain repellents and non-stick cooking surfaces) are also obesogens.


Obesogens: The Research

  • Retha Newbold of NIEHS began feeding newborn rats genistein, an oestrogen-like compound found in soy, at doses like those in soy milk and soy formula. By 4 months, the rats fed genistein were heavier and fatter than the control mice, without eating significantly more.
  • In 2005 scientists in Spain reported that the more pesticides children were exposed to in the womb, the greater their risk of being overweight as toddlers.
  • A study by David Tenenbaum found an association between prenatal exposure to hexachlorobenzene (HCB) and being overweight or obese in childhood (October 2008, Acta Paediatrica). Although HCB is one of the Persistent Organic Pollutants now banned in Europe by the 2001 Stockholm Convention it had been widely used for the previous 7 decades to kill fungi on crop seeds and in some manufacturing processes. Its commercial use in the US was discontinued in 1965.
  • Prenatal exposure to HCB has also been linked to the age of puberty and menopause, asthma, fertility and to an increased likelihood of attention deficit hyperactivity disorder (ADHD).
  • In a prospective study conducted on the Spanish Mediterranean island of Minorca, umbilical cord levels of various pollutants were measured and the children monitored. Results showed a direct relationship between cord blood levels of HCB and weight at 6 years of age.
  • A Belgian study found that children exposed to higher levels of PCBs and DDE (the breakdown product of the pesticide DDT) in the womb were fatter than those exposed to lower levels.
  • Research published by Janet Osuch, an epidemiologist at Michigan State University followed up the daughters of previous research subjects whose toxin levels had been monitored in a previous study and whose average age was about 30. Her research showed no link between uterine PCB exposure and obesity, but did reveal a strong link between exposure to DDE in the womb and later obesity. She also found earlier puberty, more diabetes and other signs of endocrine disruption in the DDE exposed group (Occupational and Environmental Medicine, March 2009).


So far, so bad. But adipocytes are not just passive fat storage sites. Fat deposits also act as endocrine organs producing hormones such as leptin and oestrogen which further encourage fat deposition.



Oestrogen encourages fat to be deposited around the hips, thighs and bottom in the traditional pear shape. Although men traditionally store fat around their belly in an apple shape, some obese men do store fat around their avoirdupois and also may develop 'man boobs' or gynaecomastia as a result of excess oestrogen exposure.

Sperm counts too have dropped dramatically in recent decades and this may also be an effect of exposure to excess oestrogens and oestrogen-like chemicals in the environment.



The word leptin is derived from the Greek word leptos meaning thin and is a hormone which is primarily produced by body fat that plays an important role in controlling appetite and metabolism. It may be circulating leptin levels that ultimately defeat many a dieter!

It was first identified when obese and voracious laboratory mice were studied and found to carry genetic mutations for either the hormone leptin or its receptors. Further, when injected with leptin the body weight, amount of body fat and appetites of the formerly obese mice normalised.

The amount of leptin in circulation is directly proportional to the total amount of fat in the body. However, leptin can also be produced by the placenta, foetal membranes and uterus for which reason blood levels rise during pregnancy and it may be leptin that is responsible for morning sickness.

As fat deposits increase, so does leptin production and it is thought that individuals may become leptin resistant in the same way as some become insulin resistant in response to excessive amounts of circulating hormones. One study suggests that the consumption of high amounts of fructose may causes leptin resistance and elevated triglycerides in rats.


Are the obese to blame?

Although some obese people eat too much and of the wrong kinds of foods, they know who they are. Many however, genuinely eat no more than their slim friends and exercise no less, but are unable to lose weight.

However, exposure to obesogens in-utero can probably only held to be responsible for excess weight in those who have had lifelong weight problems and not for those who piled on the pounds in adulthood.

Also, this explanation probably only applies to those under the age of 50 who will have been exposed to these pollutants in the womb. Further, since almost everyone tests positive to these toxins, it is thought that timing, quantities and individual genetic susceptibilities must also play a role in determining later predispositions to obesity.

A 1990s study of identical twins discovered that genetics may account for 80% of your weight and body shape. In another study of 35 pairs of twins, where one twin was active and the other sedentary, the siblings who exercised had a lower BMI than their inactive twin but neither were overweight.

There is the role of activity to consider too and a Canadian study found that up to 40% of exercise habits are also acquired from the family and that 50% of a person's attitude towards activity comes from other environmental factors such as school and friends.

The mother's diet during pregnancy has also been implicated, with the widespread introduction of fructose over the last two decades coinciding with increases in weight gain during pregnancy and in birth weight.

Dr Robert Lustig, professor of paediatrics at the University of California at San Francisco has also identified hyperactivity of the beta cells of the pancreas in 20% of the obese population and which leads to excess insulin production and promotes fat deposition.

So regarding the body as a biological machine operating on the simple basis of calories consumed versus calories expended is starting to look not only simplistic, but downright wrong. Take heart though, according to Paula Baillie-Hamilton it IS possible to lose the weight and normalise your metabolism with sufficient detoxification.



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