If it hadn’t been for the Big Macs that Joannie ate pretty much three times a week, she wouldn’t have gotten fat.  If she hadn’t been exposed while in her mother’s womb to chemicals x, y and z, Joannie wouldn’t have had the propensity to get fat.  And if Joannie’s mom had eaten more sensibly, both waistlines would be slimmer.

Fat people most likely are programmed to become fat before taking their first sip of milk.

Today’s news is, that pesticides are among the chemicals responsible for this reprogramming.

Two of three U.S. adults are now classified as overweight.  Type II diabetes has increased in like measure over the same decades, and so has heart disease.  This is not a coincidence.  These illnesses share common characteristics: they are triggered while in the womb by exposure to the same kinds of chemicals and the outcomes show up in adulthood.  Scientists now call this pattern “the fetal origins of adult diseases”.

The most likely culprits are chemicals now grouped together under the rubric “endocrine disrupters.” It’s been known for about two decades, though disputed by the manufacturers, that these chemicals alter the normal signaling pathways of hormones.  Think of Bisphenol A (BPA), right now the nation’s most celebrated endocrine disruptor.

Pesticides, though not specifically thought of as endocrine disruptors nor regulated as such, can similarly knock normal development off track.  Research has just found that a family of pesticides among the most widely used in the world is connected to these three adult illnesses.  This is the family of organophosphates, concocted from petroleum with an addition of phosphoric acid.

When lab rats are exposed to these pesticides through the mother’s diet, at a time in their development equivalent to a human baby’s second trimester in the womb, their metabolism changes in two ways: their cholesterol and triglycerides rise.  These abnormal and lasting changes resemble the major factors that predict and lead, later in life, to obesity, diabetes and cardiovascular heart disease (specifically, atherosclerosis, a condition in which fatty material collects along the arteries and hardens artery walls).

These changes in metabolism happen at low levels, within the levels we are uniformly exposed to, which the Environmental Protection Agency declares as “safe” but are evidently not.  The changes are the strongest when the mother rats are fed a high-fat diet.  Human babies may even be underweight at birth (and there’s an epidemic of underweight babies in the U.S.), but quickly become overweight

Humans run into these pesticides in our food and water.  Of course, children continue to be exposed once they are born and are in fact exposed more than adults because they eat and drink more in relation to their body weight and have a higher ratio of skin.

The other groups of people exposed most to organophosphates and other pesticides are the same groups with the highest rates of obesity – people who live in run-down inner-city neighborhoods, the poor, and farmworkers.  Again, not a coincidence but a connection, a trigger.

Dr. Ted Slotkin of Duke University, the researcher responsible for these discoveries, found another compelling clue: exposure caused harm to the rodent’s brain, as well as its metabolism.  Once the exposed lab animal was born and started to eat at will, its consumption of a high-fat diet reduced the adverse symptoms in its brain functioning.  As Dr. Slotkin muses, “If you’ve got neurofunctional deficits, and they can be offset by continually eating Big Macs, then you will naturally (but unconsciously) select that kind of food because it will make you feel better.”  Unfortunately, increased fat will further harm the animal’s, or human’s, metabolism.

What this means for you:

Particularly while trying to conceive, during pregnancy, while nursing, and for your children, avoid pesticides; eat organic foods.

For information about endocrine disruptors, read the new booklet published by the nonprofit Learning and Developmental Disabilities Initiative.

Author: Alice Shabecoff for CSN – Chemical Sensitivity Network, November 5, 2009

Alice Shabecoff is the co-author with her husband Philip of Poisoned Profits: The Toxic Assault on our Children, published by Random House last year.  See their website, www.poisonedprofits.com

Related article from Alice Shabecoff:

• Our planet, our children – How are your children doing?

Among dietary factors, learning and behavior are influenced not only by nutrients, but also by exposure to toxic food contaminants such as mercury that can disrupt metabolic processes and alter neuronal plasticity. 

Neurons lacking in plasticity are a factor in neurodevelopmental disorders such as autism and mental retardation. Essential nutrients help maintain normal neuronal plasticity. Nutritional deficiencies, including deficiencies in the long chain polyunsaturated fatty acids eicosapentaenoic acid and docosahexaenoic acid, the amino acid methionine, and the trace minerals zinc and selenium, have been shown to influence neuronal function and produce defects in neuronal plasticity, as well as impact behavior in children with attention deficit hyperactivity disorder. 

Nutritional deficiencies and mercury exposure have been shown to alter neuronal function and increase oxidative stress among children with autism. These dietary factors may be directly related to the development of behavior disorders and learning disabilities. 

Mercury, either individually or in concert with other factors, may be harmful if ingested in above average amounts or by sensitive individuals. High fructose corn syrup has been shown to contain trace amounts of mercury as a result of some manufacturing processes, and its consumption can also lead to zinc loss. Consumption of certain artificial food color additives has also been shown to lead to zinc deficiency. Dietary zinc is essential for maintaining the metabolic processes required for mercury elimination.

Since high fructose corn syrup and artificial food color additives are common ingredients in many foodstuffs, their consumption should be considered in those individuals with nutritional deficits such as zinc deficiency or who are allergic or sensitive to the effects of mercury or unable to effectively metabolize and eliminate it from the body. 

Reference:

Dufault R, Schnoll R, Lukiw WJ, Leblanc B, Cornett C, Patrick L, Wallinga D, Gilbert SG, Crider R., Mercury exposure, nutritional deficiencies and metabolic disruptions may affect learning in children, Behav. Brain Funct. 2009 Oct 27;5(1):44.

Gluten-free diet a must for children with celiac disease 

Celiac disease (CD) is an inherited intestinal disorder characterized by life-long intolerance to the ingestion of gluten, a protein found in wheat, rye, and barley. Although CD can be diagnosed at any age, it commonly occurs during early childhood (between 9 and 24 months). Reduced bone mineral density is often found in individuals with CD. A new article in the journal Nutrition Reviews examines the literature on the topic and reveals that a gluten-free diet can affect children’s recovery. 

Metabolic bone disease remains a significant and common complication of CD. Reduced bone mineral density can lead to the inability to develop optimal bone mass in children and the loss of bone in adults, both of which increase the risk of osteoporosis. There also exists an additional risk of fracture in people with CD. 

However, evidence suggests that a gluten-free diet (GFD) promotes a rapid increase in bone mineral density that leads to complete recovery of bone mineralization in children. A GFD improves, although rarely normalizes, bone mineral density in adults. Children may attain normal peak bone mass if the diagnosis is made and treatment is given before puberty, thereby preventing osteoporosis in later life. 

Also, nutritional supplements consisting of calcium and vitamin D seem to increase the bone mineral density of children and adolescents with CD. 

“Our findings reinforce the importance of a strict gluten-free diet, which remains the only scientific proven treatment for celiac disease to date,” the authors conclude. “Early diagnosis and therapy are critical in preventing celiac disease complications, like reduced bone mineral density.” 

Reference: Wiley-Blackwell, Gluten-free diet reduces bone problems in children with celiac disease, October 8, 2009

Increased prevalence of the autism spectrum disorders (ASD) and the failure to find genetic explanations has pushed the hunt for environmental causes. These disorders are defined clinically but lack objective characterization.

 To meet this need, we measured neurobehavioral and pulmonary functions in eight ASD boys aged 8 to 19 years diagnosed clinically and compared them to 145 unaffected children from a community with no known chemical exposures. As 6 of 35 consecutive mold/ mycotoxin (mold)-exposed children aged 5 to 13 years had ASD, we compared them to the 29 non-ASD mold-exposed children, and to the eight ASD boys. Comparisons were adjusted for age, height, weight, and grade attained in school. 

The eight ASD boys averaged 6.8 abnormalities compared to 1.0 in community control boys. The six mold-exposed ASD children averaged 12.2 abnormalities. The most frequent abnormality in both groups was balance, followed by visual field quadrants, and then prolonged blink reflex latency. 

Neuropsychological abnormalities were more frequent in mold-exposed than in terbutaline-exposed children and included digit symbol substitution, peg placement, fingertip number writing errors, and picture completion. Profile of mood status scores averaged 26.8 in terbutaline-exposed, 52 in mold exposed, and 26 in unexposed. The mean frequencies of 35 symptoms were 4.7 in terbutaline, 5.4 in mold/ mycotoxins exposed and 1.7 in community controls. 

Reference:   Kilburn KH, Thrasher JD, Immers NB., Do terbutaline- and mold-associated impairments of the brain and lung relate to autism?, Toxicol Ind Health. 2009 Sep 30.

The study described was initiated by the Israel Ministry of Health as an effort to respond to and deal with public concern about possible health disorders related to odorous emissions (composed of a great many of organic and inorganic chemicals) from the regional industrial park (IP) in the Negev, southern Israel. Previous ecological studies found that adverse health effects in the Negev Bedouin population were associated with residential proximity to the IP. The objective of the current study was to investigate a hypothesis concerning the link between the IP proximity and life prevalence (LP) of upper respiratory tract chronic diseases (URTCD) and asthma in children aged 0-14 years living in rural Negev, Israel, in small agricultural communities.  

The cross-sectional study was conducted in 7 localities simultaneously during 2002. The following indirect exposure indicators were used: (1) distance (less than 20 km/ more than 20 km) from the IP (‘distance’); (2) presence (yes/no) of the dominant wind direction being from the IP toward a child’s locality (‘wind direction’); and (3) the child’s mother having made odour complaints (yes/no) related to the IP (‘odour complaints’). A 20 km cut-off point was used for ‘distance’ dichotomization as derived from the maximum range of ‘odour complaints’. This gave 3 proximal and 4 distant localities, and division of these by the ‘wind direction’ gave one versus two localities. The study population consisted of 550 children born in the localities. Medical diagnoses were collected from local clinic records. The following were included in the interviewer-administered questionnaire for a child’s parents: (1) demography (the child’s birth date, gender, mother being married or not, parental origin and education, number of siblings); (2) the child’s birth history (pregnancy and delivery) and breast-feeding duration; (3) the child’s parental respiratory health; and (4) environmental factors (parental smoking and occupational hazardous exposure, domestic use of pesticides, domestic animals, outdoor odour related to the IP emissions). For statistical analysis, Pearson’s chi(2), t-tests and multivariate logistic regressions were used, as well as adjusted odds ratios (OR) within a 95% confidence interval.  

The multivariate analysis showed that increased LP of URTCD in children of proximal localities was statistically significant when associated with odour complaints (OR = 3.76 [1.16, 12.23]). In proximal localities, LP of URTCD was higher (at borderline level statistical insignificance p = 0.06) than in distant localities (OR = 2.31 [0.96, 5.55]). The following factors were found to be related to the excess of the LP of URTCD: (1) father’s lower education (by distance: OR = 2.62 [1.23, 5.57]; by wind direction: OR = 4.07 [1.65, 10.03]); (2) in-vitro fertilization (by distance: OR = 3.03 [1.17, 7.87]; by wind direction: OR = 4.34 [1.48, 12.72]). In proximal localities, the increase in asthma LP was associated with: (1) wind direction (OR = 1.95 [1.01, 3.76]); (2) a child’s male gender (OR = 2.95 [1.48, 5.87]); and (3) a child’s mother’s having had an acute infectious disease during pregnancy (OR = 4.84 [1.33, 17.63]).  

An increased LP of chronic respiratory morbidity among children living in small agricultural localities in the Negev was found to be associated with indirect measurements of exposure (distance, wind direction and odour complaints) to IP emissions. These results, in conjunction with previously reported findings in the Negev Bedouin population, indicate a need for environmental protection measures, and monitoring of air pollution and the health of the rural population. 

Reference: Karakis I, Kordysh E, Lahav T, Bolotin A, Glazer Y, Vardi H, Belmaker I, Sarov B., Life prevalence of upper respiratory tract diseases and asthma among children residing in rural area near a regional industrial park: cross-sectional study, School of Public Health, University of Haifa, Haifa, Israel. Rural Remote Health. 2009 Jul-Sep;9(3):1092