Pesticides in Food Linked to Causing T1 Diabetes
See our latest project on environmental causes
of type-1 & 2 diabetes
 
 

Children with type-1 diabetes
have dramatically higher levels of food pesticides in blood

SOURCE: Journal of Clinical Toxicology, Vol. 2(6): 2012
View Journal Online

Does eating conventional grocery store food containing small levels of 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.

STUDY DESIGN: The study was started with 75 young children under age ten who were diagnosed with type-1 diabetes within the past 30 days. Blood samples were taken from the 75 children and also from 35 healthy control children who did not have diabetes. Blood samples in both groups were then tested for nine different pesticides. This included the pesticide lindane (used in head lice treatments and also in food crop agriculture), the agricultural pesticides malathion, chlorpyrifos and profenofos and also the pesticides DDT and DDE. While most people assume DDT is no longer used, this is actually incorrect as some countries in Africa and South America still use DDT in agriculture, and these foods are frequently imported into Europe and the United States, especially during the winter months. Another source of DDT in foods comes from a little publicized fact that the common pesticide dicofol (routinely used on citrus) contains DDT as an unintended by-product during manufacture.

EVIDENCE OF A LINK: By comparing the pesticide levels in children with and without diabetes, the doctors could easily see if a pattern exists. For example, if pesticide levels were the same in both groups, it suggests that pesticides do not increase the risk of diabetes. However, if pesticide levels are higher in children with diabetes, we begin painting a picture that eating conventional foods grown with chemical pesticides, may very well be a contributing to autoimmunity and increasing rates of type-1 diabetes.

Below are the results of the tests, and as can be seen, there is a very strong link suggesting that eating conventionally grown foods are a major risk factor for diabetes. All measurements are in levels of what is called nanograms per milliliter of blood (ng/ml). Each row shows the pesticide type and levels found in healthy and diabetic children.

Pesticide
Type
Healthy
Children
Diabetic
Children
Amount Higher
Lindane Not Detectable .54 >54x higher
DDT Not Detectable .20 >20x higher
DDE Not Detectable .37 >37x higher
Chlorpyrifos .02 .24 12x higher
Profenofos .03 .46 >15x higher
Malathion .03 .54 18x higher
TOTAL BURDEN .08 2.35 29x higher

In looking at the chart, we see the following:

1. Healthy non-diabetic children had no mesureable levels of the pesticide lindane (top row) -
but children with diabetes had a level of 0.54.

2. Healthy children had no measureable levels of the pesticide DDT (second row) -
but children with diabetes had levels of 0.20.

3. Healthy children had no measurable levels of the pesticide DDE (third row) -
but children with diabetes had levels of 0.37 .

The same pattern was seen with the common organophosphate pesticides chlorpyrifos, profenofos and malathion.

Chlorpyrifos levels were averaging .02 in the healthy children,
and .24 in children with diabetes.

The moderate to severely toxic pesticide profenofos was .03 in healthy children,
but 15x higher in diabetic children with levels of .46.

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 worrison, 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 average levels 29 times higher at 2.35. To put this into context, this means that newly diagnosed type-1 diabetic children had 29 times more of these poisons traveling through their blood every minute and to all cells and organs in the body than children without diabetes.

HOW FOOD PESTICIDES INCREASE DIABETES
In other parts of our report, we've provided detailed documentation that pesticides have the ability to damage the parts of the human body that protect us from autoimmunity. This includes the organ called the thymus, as well as our immune system's natural killer cells - which make up about 5% of our total white blood cells and (when working properly), can release substances that quickly calm any ongoing autoimmune attack.

Along with this, many pesticides (including those found in this study) are listed as endocrine disrupting chemicals. This means they have the potential to increas 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, these children have what is being called type 1.5 (a combination of both type-1 and type-2).

THE SMOKING GUN:
EVIDENCE FOR "CAUSE" AND "CAUSING" DIABETES
The fact that children with diabetes have much higher levels of food-based pesticides in their bodies than children without diabetes strongly suggests these chemicals play a role in causing the disease. This would be true for any chemical found at higher levels in people with diabetes, for example, people with diabetes also have higher blood levels of the chemicals phthalates and bisphenol-A, thereby, another smoking gun.

Since beta-cells in the pancreas have now been shown to regenerate continuously in children and adults, it must be considered that these high levels of food-based pesticides (and others) are not only a major contributor to type-1 diabetes, but also, are playing a role in worsening diabetes by accelerating beta-cell loss through increased autoimmunity and moving the child out of the "honeymoon" faster. In fact, with improvements now being seen in children who avoid pesticide based foods, it is reasonable to conclude that these same chemicals may very well may be preventing any possibility of reversing diabetes.

QUICKLY LOWER FOOD PESTICIDES IN CHIDREN
In a related study described below, researchers found that switching to organic food resulted in a dramatic drop in malathion levels in children. When results of both of these studies are viewed together, it provides strong support for the importance of switching to a 100% organic diet for children with diabetes and especially for children with newly diagnosed with type-1 diabetes (to improve chances of entering partial or full remission).

NEXT IMPORTANT STUDY NEEDS TO BE CONDUCTED
To carry this study to the next level, scientists should be encouraged to do a study to investigate if eating organic food increases the percentage of children reaching partial-remission (honeymoon) as well as the duration of the honeymoon period after T1 diagnosis.

Eating Organic Food Lowers Blood Pesticides in Children

SOURCE: Environmental Health Perspectives, 114(2): 260-263, Feb 2006
View Journal Online

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.

In this study, conducted in part by the Centers for Disease Control, scientists studied the effects of eating organic (non-pesticide) food among 23 elementary school children ages 3 to 11. Each child was tested daily for pesticide levels over 15 consecutive days. During the first 5 days (called phase 1) - children consumed their typical (pesticide) food diets. During phase 2 (days 6 to 10) - children ate only organic foods. In phase 3 (days 11 to 15), all children switched back to eating conventional foods grown with pesticides.

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,

We were able to demonstrate that an organic diet provides a dramatic and immediate protective effect against exposures to organophosphorus pesticides that are commonly used in agricultural production....The persistent existence of OP pesticide metabolites in urine during the conventional diet periods raises a concern of the possible chronic exposures to OP pesticides in children

Rollins School of Public Health, Emory University, Atlanta, Georgia, USA
University of Washington, Seattle, Washington, USA
Centers for Disease Control and Prevention, 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.

Pesticides in Food - Diabetes Link

SOURCE: Indian Pediatrics, Volume 48:74, 2011
View Journal Online

Below is the "Abstract" from the listed journal describing a patient who became ill after eating several non-washed tomatoe from a s:

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
JSS Medical College, JSS University
Mysore, Karnataka, India

Comment from Stopspraying.org

Why it can take years to see health problems
from eating pesticides in food

While pesticides are in nearly all non-organic foods you eat everyday, you may not personally notice the effects of the pesticides for decades. This is actually similar to why it takes decades of smoking to observe health problems as well. It is important to understand a few key points on how damage is not immediately 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.


BACK TO GORDON DIABETES HOME PAGE