Pesticides May Cause U.S.A. Insulin Resistance and Obesity Trends
Posted Mar 21 2012 2:29am
Modern Big Tobacco-Agra/Monsatan Crops
Crops are generally coated with pesticides for the last 30-50 years. Are they toxic? Pesticides are upregulated into the food chain via consumption (corn, soy) by feedlot livestock and poultry. Let's not forget tobacco (cigarettes, snuff, cigars, etc). 'Tobacco is a pesticide-intensive crop. With nearly 27 million pounds of pesticides (including insecticides, herbicides, fungicides, and suckercides) applied to the U.S.-grown crop from 1994 to 1998, it ranks SIXTH in terms of the amount of pesticides applied per acre. The tobacco industry regards pesticides as essential to tobacco production, stating that “the crop could not be produced economically without them”.'
Additionally pesticides are employed in municipalities (public schools, parks, government land) and personal home use (termites, ant control, weeds control, lawns, etc). Although pesticides do not taste, smell or look toxic, they are not benign and without metabolic dysregulation consequences.
New studies in PubMed are cropping (pun intended) up in number pointing directly to insulin resistance, obesogenic, neurologic and inflammatory damage secondary to this broad group of pervasive chemicals known as persistent organic pollutants (POPs). They are difficult to avoid as once in the soil, air or bodies of water, fish, birds and animals, they typically fail to degrade and significantly impact the environment.
The researcher Alavanja states 'Over 1 billion pounds of pesticides are used in the United State (US) each year and approximately 5.6 billion pounds are used worldwide (1). In many developing countries programs to control exposures are limited or non-existent. As a consequence; it has been estimated that as many as 25 million agricultural workers worldwide experience unintentional pesticide poisonings each year (4). In a large prospective study of pesticide users in the United States, the Agricultural Health Study, it was estimated that 16% of the cohort had at least one pesticide poisoning or an unusually high pesticide exposure episode in their lifetime (5).
Although attempts to reduce pesticide use through organic agricultural practices and the use of other technologies to control pests continue, exposure to pesticides occupationally, through home and garden use, through termite control or indirectly through spray drifts and through residues in household dust, and in food and water are common (6). The US Department of Agriculture has estimated that 50 million people in the United States obtain their drinking water from groundwater that is potentially contaminated by pesticides and other agricultural chemicals (7, 8). Children from 3-6 years old received most of their dermal and non-dietary oral doses from playing with toys and while playing on carpets which contributed the largest portion of their exposure (9-12).'
U.S.A. Obesity Trends With Pesticide Use
Pesticide use on crops grown in the South (tobacco) and Mid-West (corn, wheat, soy) trends well with U.S.A. obesity patterns [hat tip: LePine MD]. Above is the trend of obesity that starts mid-1980s then grows exponentially each few years. Maps are from Lim et al and BFRSS data.
Smart people in Korea (Lim et al) report that 'There is an apparent overlap between areas in the USA where the herbicide, atrazine (ATZ), is heavily used and obesity-prevalence maps of people with a BMI over 30. Given that herbicides act on photosystem II of the thylakoid membrane of chloroplasts, which have a functional structure similar to mitochondria, we investigated whether chronic exposure to low concentrations of ATZ might cause obesity or insulin resistance by damaging mitochondrial function.'
Pesticides Kill Pests, Including Our Bug-like Mitochondria
It's therefore not surprising to read about the toxic effects of pesticides on pests whose networked pathways overlap almost precisely with our own cells. Atrazine is a mitochondrial toxin, and our mitochondria are the sole energy generators and powerhouses whether the substrate is glycogen, glucose or fatty acids.
Mitochondrial Dysfunction Causes Fatness and Insulin Resistance (IR)
'A close association between mitochondrial dysfunction and insulin resistance is well established –. In in vitro studies, we found that artificial induction of mitochondrial dysfunction induced insulin resistance , .' This is discussed by Lim et al. He and his colleagues performed an experiment on rodents. They fed low levels of atrazine to rats then examined lab parameters for insulin resistance (IR). What happened? The higher the dose of atrazine, the higher the obesity and insulin resistance. Atrazine was associated with mitochondrial dysfunction, higher visceral (organ) fat deposition, higher blood glucoses and decreased energy metabolism.
Another group of researchers, Ruzzin et al, tested a similar hypothesis. They fed crude Atlantic salmon oil to rodents and examined IR parameters. They state 'POPs accumulate in the lipid fraction of fish, and fish consumption represents a source of POP exposure to humans ( Dougherty et al. 2000 ; Hites et al. 2004 ; Schafer and Kegley 2002 ). Therefore, certain European countries have dietary recommendations to limit the consumption of fatty fish per week ( Scientific Advisory Committee on Nutrition 2004 ).' They discovered similar insulin resistant results when they exposed fat cells in vitro to a POP mixture that mimicked the relative abundance of contaminants found in crude salmon oil. Insulin signalling was broken and impaired.