Pesticides in Food Linked to Causing T1 Diabetes | ||||
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SOURCE: Journal of Clinical Toxicology, Vol. 2(6): 2012 Does eating conventional grocery store food grown with chemical pesticides increase the risk for developing type-1 diabetes? This was one of several questions researchers wanted to answer at Mansoura University Children's Hospital in Egypt. The basic premise of the study was that if pesticide residues in food did increase diabetes - we would then see higher levels of these pesticides in children with type-1 diabetes.
Below are results from both groups of children. As can be seen by the higher numbers in diabetic children - eating foods grown using conventional pesticide agriculture would appear to play a significant role in the development of type-1 diabetes. In fact, children with type-1 diabetes were found to have a remarkable 10, 20 and even 50 times higher level of pesticides in their blood than children without diabetes. Each row shows the pesticide type and levels found in healthy and diabetic children. Measurements in nanograms per milliliter of blood (ng/ml).
In looking at the chart, we see the following: 1. Healthy non-diabetic children had no mesurable levels of the pesticide lindane (top row) - 2. Healthy children had no measurable levels of the pesticide DDT (second row) - 3. Healthy children had no measurable levels of the pesticide DDE (third row) - The same pattern was seen with the common organophosphate pesticides chlorpyrifos, profenofos and malathion. Chlorpyrifos levels were averaging .02 in the healthy children, The moderate to severely toxic pesticide profenofos was .03 in healthy children, The same pattern was also seen for the pesticide malathion. Healthy non-diabetic children had malathion levels of .03, but children with type-1 diabetes had malathion levels 18 times higher at .54. When using these numbers to determine increased risk from the pesticides, the researchers found that children with the higher levels of malathion had a 4 times greater risk of developing diabetes than children with low levels of malathion. What is very worrisome, when looking at the total body burden of pesticides in diabetic children compared to non-diabetic children, the total difference was immense - While healthy children had a total blood pesticide level of .08 (all pesticides together) - children with newly diagnosed diabetes had an average total level 29 times higher at 2.35. To put this into context, this means that children recently diagnosed with type-1 diabetes had 29 times more of these poisons traveling through their blood every minute and to all cells and organs in their body than children without diabetes. HOW FOOD PESTICIDES INCREASE DIABETES Along with this, many pesticides (including those found in this study) are listed as endocrine disrupting chemicals. This means they have the potential to increase glucose levels by contributing to insulin resistance. Interestingly, many children with type-1 diabetes are now being been found to have signs of insulin resistance - which is the hallmark of type-2 diabetes. So, instead of only type-1, diabetic children are now being called type 1.5 (a combination of both type-1 and type-2). THE SMOKING GUN: WHY SOME CHILDREN HAVE HIGHER PESTICIDES?
HOW THE BODY REGENERATES NEW BETA-CELLS IN THE PANCREAS When this new beta-cell growth process starts at the suggestion of the hormone exendin-4, the body is attempting to replace beta-cells that have been destroyed by autoimmunity. You could almost say there is an ongoing race between one team trying to destroy beta-cells and the another team trying to build beta-cells. Unfortunately for children with type-1 diabetes, the team destroying beta-calls is winning, although exendin-4 is trying its best to help the "building team" turn this around. In another study outlined below, researchers showed a dramatic drop in blood pesticide levels in children just 2 days after switching to organic food. Along with this - we have been involved in a study with a middle-school student here in North Carolina who has had type-1 diabetes for nearly 3 years who showed dramatic improvements in c-peptide and fasting glucose after intense avoidance of phthalates, bisphenol-A and switching to an organic food diet. After suspending the organic diet at the end of 6 weeks, his improvements were erased and insulin requirements increased dramatically. For more information on the Gordon Diabetes Reversal Project please go to gdrp.me THE NEXT STEP As evidence does suggest that pesticides may be increasing autoimmunity, it would also be informative to conduct a study to determine if switching to an organic diet could lead to lower autoantibody levels in siblings of children with diabetes, thereby reducing the risk of future type-1 diabetes. |
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Eating Organic Food Lowers Blood Pesticides in Children SOURCE: Environmental Health Perspectives, Vol. 114(2): 260-263, Feb 2006 In Children eating organic food (foods grown without pesticides) were found to have dramatically lower levels of pesticides when compared to eating conventional pesticide grown foods.
RESULTS: During phase 2, while eating organic foods, all children showed a dramatic drop in pesticide levels of chlorpyrifos and malathion (see chart above). Average levels of malathion metabolites while eating conventional food was approximately 1.2 micrograms per liter (of urine) but after switching to organic foods dropped to about less then 0.1 micrograms/liter. This represents a 12-fold decrease in body pesticide levels going from pesticide grown foods to organic foods. For the pesticide chlorpyrifos, (which has been linked to many health disorders affecting the brain and weakening the immune system), levels were approximately 6 micrograms/liter before eating organic and then dropped to 2 micrograms per liter while eating organic (a 3-fold reduction). Both malthion and chlorpyrifos are used extensively in agriculture with chlropyrifos also being used in home pest and termite control prior to 2002. In conclusion, the researchers stated,
Rollins School of Public Health, Emory University, Atlanta, Georgia, USA CHEM-TOX COMMENT: It is important that people realize that so-called safe levels of exposure are based upon studies done on "adults." Children have far lower levels of important liver enzymes that remove pesticides from the blood (i.e. paraoxanase) and this level can vary dramatically from one child to the next.. Therefore, chidren have pesticides remain in their blood for longer periods and at higher levels than adults. Also, critics of this study (such as those funded by agricultural interests) do not take into account that EPA guidelines on pesticide safety consider only at one pesticide at a time, however, children (and all of us) are exposed to many pesticides in food simulneously. This has been shown to result in far more harm than one pesticide alone, and can sometimes result in an exponential effect (1+1=100). Also, current EPA pesticide safety guidelines do not consider what is called subtle neurotoxicity (effects on learning/behavior) - subtle immune system effects (increased autoimmunity - lowering of white blood count - natural killer cell effects, etc.). The bottom line is that pesticides are designed specifically to kill - and our children are being exposed to small levels of these continuously in food. A follow-up study now needs to be done to determine if natural killer cells and autoimmunity are affected by these levels of pesticides. |
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Pesticides in Food - Diabetes Link SOURCE: Indian Pediatrics, Volume 48:74, 2011
A 12 year old male was brought to us with history of fatiguability, vomiting and loose stools for 6 hours. There was no history of fever, convulsion, and altered sensorium. The vitals were stable except some dehydration. Investigations revealed hemoglobin 10.8g/dL, TLC 16.6×103/mL, platelet 360×103/mL, blood sugar 299g/dL, blood urea 28g/dL, S creatinine 0.9g/dL, Na 139 mEq/L,K 3.3mEq/L, pH 7.38, PaCO2 32 mmHg, PaO2 96 mmHg, and Bicarbonate 19 mEq/L. Urine showed sugar 4+ and moderate ketone bodies. In view of dehydration, hyperglycemia, glycosuria, ketonuria, low bicarbonate levels, DKA treatment protocol was started with IV fluids and insulin infusion. The level of consiousness deteriorated by 12 hours and Glasgow Coma Scale was 12. He developed fasiculations and jerky movement of limbs. His respiration was 28/min and shallow, heart rate 64/min, BP 110/70 mm of Hg, oxygen saturation 96%. His pupils were 2mm in size and were reactive. CT scan head was normal. Due to fasiculations and shallow respiration, organophosphorus intoxication was suspected and plasma cholinesterase was done; it was 550 U/L (Normal=2710-11510 U/L). The diagnosis was revised to organophosphorus intoxication and child was managed with atropine and pralidoxime. He responded well and was discharged after 6 days. Retrospectively, boy gave history of ingestion of 4 tomatoes in the field without washing 6 hours prior to admission. The most common route of exposure to organophosphorus compounds is ingestion of agricultural products [1]. Probably our patient had poisoning from eating tomatoes contaminated with pesticide. Organophosphorus poisoning was not suspected at presentation, as the child presented to us with muscarinic symptoms like vomiting and diarrhea. Low levels of plasma choline-sterase support the diagnosis of OP poisoning [2]. Although plasma acetyl cholinesterase estimation was sufficient to support the diagnosis of organophosphorus poisoning in our case, we were unable to do estimation of RBCs ACE and urinary para-nitrophenol for technical reasons. Hyperglycemia is a known adverse effect of organophosphorus exposure and has been confirmed in animal studies [1,3-5]. The glucose metabolism is affected by several mechanisms, including oxidative stress, inhibition of paroxanase, stimulation of adrenal glands and release of catecholamines, and effect on metabolism of liver tryptophan [4]. In an earlier study glycosuria was observed in 69% of cases with OP poisoning. Organophasphorus intoxication can mimic DKA and its diagnosis may be delayed. Whenever there is discrepancy between clinical features and biochemical features in a suspected, DKA child, we should emphasize the need to look for an alternate diagnosis. References 1. Levy-Khademi F, Tenenbaum AN, Wexler ID, Amitai Y. Unintentional organophosphate intoxication in children. Pediatr Emerg Care. 2007;23:716-8. 2. El-Naggar Ael-R, Abdalla MS, El-Sebaey AS, Badawy SM. Clinical findings and cholinesterase levels in children of organophosphates and carbamates poisoning.Eur J Pediatr. 2009;168:951-6. 3. Akyildiz BN, Kondolot M, Kurtoðlu S, Akin L. Organophosphate intoxication presenting as diabetic ketoacidosis. Annals Trop Pediatr. 2009;29:155-9. 4. Rahimi R, Abdollahi M. A review on the mechanisms involved in hyperglycemia induced by organophosphorus pesticides.Pesticide Biochemistry Physiology. 2007; 88:115-21. 5. Shobha TR, Prakash O. Glycosuria in organophosphate and carbamate poisoning. J Assoc Physicians India. 2000;48:1197-9. JDepartment of Pediatrics |
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Comment from Stopspraying.org Why it can take years to see health problems
Also delaying the appearance of disease, many organs can sustain considerable damage before problems are noticed. For example, in type-1 diabetes, about 80% of the beta-cells in the pancreas must cease to function before diabetes symptoms appear. The human liver must sustain 70% damage before problems appear in routine blood tests. When this 70% threshold is reached, toxic chemicals stay in the body longer, thereby having more time to cause damage to other parts of the body - including the immune system. |
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