I am delighted to be able to present to you my academic
paper 'Chemical Toxins: A Hypothesis to Explain the
Global Obesity Epidemic' which was published on Thursday
25th of April 2002 in the Journal of Alternative and
My paper sets out the science underlying what I believe
to be causing the current global obesity epidemic. It
is for all those of you who are interested to delve
deeper into the scientific side of things.
For me it was a vital way of launching my ideas into
the academic world. As an academic, getting a paper
accepted for publication in a highly respected peer
reviewed journal was of immense importance. I now very
much hope that it will kick-start the scientific debate
into what is making us all fatter.
Please Click here to visit Journal of Alternative &
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Chemical Toxins: A Hypothesis to Explain the
Global Obesity Epidemic, Dr. Paula Baillie Hamilton,
Taken from THE JOURNAL OF ALTERNATIVE AND COMPLEMENTARY
Volume 8, Number 2, 2002, pp. 185-192
© Mary Ann Liebert, Inc.
The number of obese people worldwide has escalated recently,
revealing a complex picture of significant variations
among nations and different profiles among adults and
children, regions, and occupations. The commonly held
causes of obesity-overeating and inactivity-do not explain
the current obesity epidemic. There is evidence of a
general decrease in food consumption by humans and a
significant decline in their overall levels of physical
activity. There is also more evidence to indicate that
the body's natural weight-control mechanisms are not
functioning properly in obesity. Because the obesity
epidemic occurred relatively quickly, it has been suggested
that environmental causes instead of genetic factors
maybe largely responsible. What has, up to now, been
overlooked is that the earth's environment has changed
significantly during the last few decades because of
the exponential production and usage of synthetic organic
and inorganic chemicals. Many of these chemicals are
better known for causing weight loss at high levels
of exposure but much lower concentrations of these same
chemicals have powerful weight-promoting actions. This
property has already been widely exploited commercially
to produce growth hormones that fatten livestock and
pharmaceuticals that induce weight gain in grossly underweight
This paper presents a hypothesis that the current level
of human exposure to these chemicals may have damaged
many of the body's natural weight-control mechanisms.
Furthermore, it is posited here that these effects,
together with a wide range of additional, possibly synergistic,
factors may play a significant role in the worldwide
Excess body weight is a growing global health care concern
that affects adults and children in all socioeconomic
groups (Bundred et al., 2001; Flegal et al., 1998).
Although there are many theories about the causes of
today's obesity epidemic, to date, there is still much
uncertainty about obesity's etiology. Although many
non-lifestyle factors are known to influence weight,
such as genetic predisposition, carbohydrate craving,
and weight cycling, the main causes are thought to be
overeating and a lack of physical activity (Bray et
al., 1992; Prentice, 2001).
WHY THE OLD EXPLANATIONS ARE NOT VALID
Overeating Overeating has been suggested as an important
cause of modern obesity, particularly because highly
palatable convenience foods are Occupational and Environmental
Health Research Group at Stirling, Stirling University,
Stirling, Scotland. much more prevalent (Prentice and
Jebb, 1995). However, despite a general increase in
the intake of these foods, evidence suggests that, although
there is a perception among members of the general public
that people are consuming more calories in modern times,
overall levels of daily caloric consumption have declined
substantially thoughout the twentieth century. (Department
for Environment, Food and Rural Affairs, 2001).
Inactivity Because a fall in food intake obviously
would not account for an increase in the incidence of
obesity, it may be that that the modern sedentary lifestyle
is mainly responsible (Prentice and Jebb, 1995). However,
despite the advent of television, motorized transport,
and energysaving domestic appliances (which has resulted
in an overall reduction in manual labor) since the middle
of the twentieth century, hard evidence does not show
that levels of physical activity have plummeted sufficiently
to cause such a high incidence of obesity during this
time period (Morris, 1995; Rasvussin, 1995). Indeed,
a report by the British Sports Council (now known as
Sport England), London, England, on physical activity
noted the opposite phenomenon, stating that "participation
is increasing across all age bands and all social groupings"
(Sports Council, 1993).
Genetic predisposition Weight control is not simply
about energy intake and energy expenditure; these comprise
a superficial part of a very complex situation (Miller
and Mumford, 1966). Body weight is generally thought
to be homostatically regulated at a certain predetermined
level or "set point" by, largely genetically
determined, feedback- control mechanisms that enable
the body to maintain a stable weight for relatively
long periods of time (Harris, 1990). Because of the
genetic basis posited for these mechanisms, the "set
point" theory has not been widely used to explain
today's incidence of obesity, which has occurred over
a relatively short period of time. Thus, dramatic changes
in the gene pool that would have been sufficient to
cause the current problem can effectively be ruled out
(Prentice and Jebb, 1995).
However despite the stability of the human gene pool,
many largely genetically determined, underlying controlling
mechanisms that set body weight and metabolic efficiency
(e.g., hormones, neural pathways, various brain nuclei,
and many neurotransmitters), appear to be malfunctioning
frequently in patients who are obese (Baptista, 1999;
Harris, 1990; Wang et al., 2001). If genetic alterations
are not responsible for such changes in metabolic functioning,
perhaps there is another cause for them. Indeed, it
has been suggested that perhaps they have been caused
by some environmental factor or factors (Rasvussin,
ARE ENVIROMENTAL CHEMICALS RESPONSIBLE?
Toxic chemicals and their effects on weight Although
diet and behavioral changes have been considered to
be major causative factors, it is difficult to see how
they could produce many of these metabolic malfunctions.
However, the levels of certain substances- synthetic
organic/inorganic chemicals-in the environment have
coincided with the increasing incidence of obesity that
has been documented. These substances are known to damage
many of the mechanisms involved in weight control.
Since the creation, and subsequent introduction, of
synthetic organic/inorganic chemicals in the late nineteenth
century, the global community has been increasingly
exposed to an exponential rise in the production of
these substances (see Figure 1; Flegal et al., 1998;
United States Tariff Commission, [various documents]
1918-1994). In their daily lives, human beings are now
exposed to tens of thousands of these chemicals, in
the forms of pesticides, dyes, pigments, medicines,
flavorings, perfumes, plastics, resins, rubber-processing
chemicals, intermediate chemicals, plasticizers, solvents,
and surface-active agents (United States Tariff Commission,
[various documents] 1918-1994). Pesticide residues,
preservatives and addititives are ingested with foods
and contaminated water, inhaled from polluted indoor
and out- door air, and absorbed cutaneously via personal-
care products. As a result, the average person now has
many hundreds of industrial chemicals lodged in his
or her body, with many of these toxins being transferred
across the fetal -maternal blood barrier (Jacobson and
Jacobson, 1996). Many of these toxins are also appearing
in women's breast milk, thus, probably transferring
their effects to children who are breast fed (Alleva
et al., 1998; Bordet et al., 1993). One of the toxic
effects of these chemicals appears to be weight gain.
Unlike the well-known weight loss resulting from high
exposure to toxins, this weight gain tends to occur
at much lower levels of exposure, which fail to make
animals or humans obviously ill (Takahama et al., 1972).
However, as a result of a long-held idea in some cultures
that weight gain must be evidence of "good health,"
a significant amount of evidence showing these chemicals
to cause weight gain has been virtually ignored, explained
away, or even, on occasion, apologized for (Lamb et
al., 1987; Takahama et al., 1972). Although it has been
generally accepted, in recent years, that weight gain
can be evidence of chemotoxicity, much of the evidence
presented in earlier scientific papers was rarely mentioned
in their abstracts. Being that current computer-search
mechanisms depend on information contained in abstracts,
this may explain why the scale of this chemically caused
weight gain has effectively been "missed,"
by some researchers.
Numerous widely used synthetic and other industrial
chemicals produce weight gain. These chemicals-which
human beings are exposed to quite regularly-include:
- Pesticides, for example, organochlorines, such
as dichlorodiphenyltrichloroethane (DDT), endrin,
lindane, and hexachlorobenzene (Chadwick et al., 1988;
Deichmann et al., 1972; Deichmann et al., 1975; Dorgan
et al., 1999; Hovinga et al., 1993; Stellman et al.,
1997; Takahama et al., 1972; Villeneuve et al., 1977)
- Organophosphates (Breslin et al., 1996; Cranmer
et al., 1978; Nicolau, 1983; Trankina et al., 1985)
. Carbamates, including dithiocarbamates (Walker et
al., 1994; Yen et al., 1984)
- . Polychlorinated biphenyls (Clark, 1981; Dar et
al., 1992; Hovinga et al., 1993) .
- Polybrominated biphenyls, which are commonly used
as fire retardants (Gupta et al., 1983)
- . Plastics, such as phthalates and bisphenol A
(Ashby et al., 1999; Ema et al., 1990; Field et al.,
1993; Howdeshell et al., 1999; Lamb et al., 1987)
- Heavy metals, such as cadmium and lead (Antonio
et al., 1999; Hovinga et al., 1993) .
- Solvents (Chu et al., 1986; Gaworski et al., 1985;
Hardin et al., 1987; Moser et al., 1995; Wahlberg
and Boman, 1979).
The example of organochlorine pesticides:
Studies and biochemistry The organochlorine pesticides
illustrate how chemotoxicity can promote weight gain.
Because of previous extensive usage as pesticides, inherent
structural stability, persistence in body systems, and
ability to concentrate in animals that are higher up
on the food chain, many organochlorine pesticides are
currently present in human fat in relatively high levels
(Hovinga et al., 1993; Stellman et al., 1997). Much
of the observed organochlorine-induced weight gain appears
to come from increases in the overall proportion of
body fat. In one animal study, the pesticide dieldrin
more than doubled the total body-fat content of treated
mice (Deichmann et al., 1972). Another study showed
that a pesticide, commonly known as lindane, induced
obesity in animals (Chadwick et al., 1988). Indeed,
in yet another study, the overall weight-gain effect
of another pesticide, hexachlorobenzene, appeared to
be so powerful that a group of treated animals still
managed to gain significantly more weight despite the
fact that their food intake was cut by 50%than
untreated controls who were on full food rations (Villeneuve
et al., 1977). Organochlorines, and other types of synthetic
and industrial chemicals, appear to cause weight gain
by interfering with most of the different elements that
comprise the human weight control system. In particular,
these chemicals have been shown to: .
- Disrupt the major weight controlling hormones, such
as catecholamines, thyroid hormones, estrogens, testosterone,
corticosteroids, insulin, growth hormone, and leptin
(Yamagishi et al., 2001).
- Alter levels of, and sensitivity to, neurotransmitters
(in particular dopamine, noradrenaline, and serotonin)
- Interfere with many metabolic processes
- Cause widespread damage to body tissues (nerve and
muscle tissue in particular), often at levels that
human beings are currently exposed to.
This interference results in changes in appetite; food
efficiency; and fat, carbohydrate, and protein metabolism.
The desire, and ability, to exercise are also affected.
These changes have been thought to be responsible for
increases in body weight (Chadwick et al., 1988; Gupta
et al., 1983; Howdeshell et al., 1999; Moser et al.,
1995; Pearson & Dutson, 1991; Takahama et al., 1972;
Trankina et al., 1985; Yen et al., 1984).
Effects of toxic chemicals on the sympathetic nervous
To illustrate this, it is worthwhile to consider the
effects of many toxic chemicals on what is possibly
the key weight-controlling system (the sympathetic nervous
system (Bray, 1993). The sympathetic nervous system,
in conjunction withthe monoamine hormones it produces
(noradrenaline, dopamine, adrenaline), plays a key role
in controlling weight, body-fat levels, and nutrition
partitioning (Bray, 1993). The sympathetic nervous system
may do this by suppressing appetite, particularly the
appetite for fats (Leibowitz, 1992); by enabling the
body to mobilize fat stores for use (Hamann et al.,
1998; Paoletti et al., 1961); and by stimulating physical
activity levels powerfully (van Praag et al., 1990).
Thus, it is not surprising that abnormalities in the
sympathetic nervous system are very common in most forms
of obesity (Dulloo and Miller, 1986). Indeed, most of
the drugs commonly used to treat patients who are obese,
or who have eating disorders, primarily alter these
patients monoamine hormones levels. (Leibowitz,
1992). Unfortunately, many of the commonest synthetic
chemicals in the environment appear to target the sympathetic
nervous system. This can lower its effectiveness dramatically,
not only in the short term but also permanently (Goldman
et al., 1997; Knoth-Anderson and Abou-Donia, 1993; Seegal
et al., 1994). One study of pesticide factory workers,
revealed that those who were exposed to pesticides excreted
50% more catecholamines then control workers. Another
study showed that pesticide workers who were chronically
exposed to DDT, organophosphates, and carbamates had
plasma levels of adrenaline and noradrenaline that were
approximately 40% and 20% (respectively) lower than
nonexposed individuals (Embry et al., 1972; Richardson
et al., 1975).
The ability to manipulate the underlying systems that
control body weight has resulted in many synthetic chemicals
being used by the agricultural community to promote
animal fattening and growth. These substances, generally
known as growth promoters, include such synthetic chemicals
as antithyroid drugs, corticosteroids, anabolic steroids,
organophosphate pesticides, carbamates, antibacterials,
and ionophores (Pearson & Dutson, 1991; Trankina
et al., 1985; Yen et al., 1984). Although many of these
substances are now illegal for use as growth promoters,
they still are consumed in foods that human beings eat
because this practice has not been stopped effectively.
Similar chemicals also are retained in foods as pesticide
or chemical residues (Pearson & Dutson, 1991). Many
treated nonfood products also confer exposure to human
beings (Alleva et al., 1998).
Synthetic chemicals are heavily used in medicine to
treat certain illnesses because such chemicals can strongly
alter hormone systems, levels of neurotransmitters,
and other aspects of general body metabolism. Not surprisingly,
in altering these systems, synthetic chemicals can effectively
alter the weight set point. This has resulted in their
previous usage for promoting weight gain in patients
with anorexia (Morley, 1996). And more evidence that
synthetic chemicals promote weight gain in humans arises
from the extremely high number of synthetic pharmaceuticals
that make patients gain weight, an obviously unwanted
side-effect. Such pharmaceuticals include some medicines
commonly used in cardiology, oncology, psychiatry, and
immunology (Baptista, 1999; Chrysant et al, 1991; Simpson
et al, 2001; Varsano et al, 1993; Wiseman and Adkins,
SUMMARY OF THE HYPOTHESIS
Being that the levels of synthetic chemicals required
to cause weight gain are relatively low and that they
have been administered deliberately to livestock and
patients to produce this effect, it may well be that
nondeliberate exposure to low levels of contaminants
in food and the environment could have similar results.
This would not be too surprising because, despite being
generally many times less potent than natural hormones,
many environmental contaminants with endocrine-disrupting
properties are currently present in wildlife, in laboratory
animals, and in living human tissues at concentrations
that are thousands of times higher than the natural
hormones they are designed to mimic (Alleva et al.,
Evidence that this could be the case comes from several
studies of adults and children in free-living populations.
Researchers have reportedly found a positive association
between levels of certain toxic chemicals in the childrens
and adults body tissues and increased body weight in
these subjects (Dar et al., 1992; Hovinga et al., 1993;
Schildkraut et al., 1999; Stellman et al., 1997).
Therefore, it can be posited that the relatively recent
presence of synthetic chemicals in the environment may
be a significant causative factor in the current worldwide
obesity epidemic. These chemicals may be causing weight
gain via toxic effects on the bodys natural weightcontrol
mechanisms. The very speed of the marked increases in
the numbers of overweight people, as clearly shown in
Figure 1, indicates that changes in the environment
are more likely to be the source of the obesity epidemic
than genetic changes in human beings.
While a link between human exposure to evergreater
numbers and amounts of synthetic chemicals, which are
known to promote weight gain, has not yet been established,
the coincidence of the obesity epidemic with the appearance
of these chemicals in the environment indicates the
possibility of a causative relationship.
The idea that many toxic chemicals in foods and the
environment have, in effect, poisoned the bodys
natural weight-control mechanisms would help to explain
many of the functional differences found in the weight-control
systems of patients who are obese (Wang et al., 2001).
This concept would also explain the incongruity of continuing
weight gain in humans despite falling food intakes and
no excessive reductions in exercise. The concept also
may shed light on the marked failure of foodrestriction
diets to effect long-term weight loss. The extent to
which each individual is affected could also be significantly
related to a given individuals genetic ability
to deal with these toxins.
The high levels of chemotoxins shown to be present
in human fat and breast milk, the ease of transfer through
the fetal-maternal blood barrier and the increased sensitivity
of developing systems to these toxins may also help
to explain the increasingly early age at which this
problem is evident in infants and children and the increasing
extent to which individuals are now affected (Alleva
et al., 1998; Bundred et al., 2001; Flegal et al., 1998).
Research is now needed to investigate which of the
many chemicals in the environment are probably causing
the greatest damage to the human weight-control system.
A possible way to move forward would be to study the
effects of increasing industrialization, and subsequent
increases in chemical exposures, in the human population.
This could be done by studying subsets of the population,
for example, by comparing farmers who farm organically
to farmers who farm conventionally or people who work
with plastics and pharmaceuticals to people who work
I would like to thank Dr. Kim A. Jobst for helpful
advice and encouragement and the editors for invaluable
assistance in producing the final manuscript. This research
has been personally funded, with no conflicts of interest.
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