You Did Not Eat Your Way to Diabetes: The Real Causes
Don't fall for the toxic myth that you caused your diabetes by reckless overeating. While people with Type 2 diabetes often are seriously overweight, there is accumulating evidence that their overweight is a symptom, not the cause of the process that leads to Type 2 Diabetes.
Even so, it is likely that you've been told that you caused your diabetes by letting yourself get fat and that your response to this toxic myth is damaging your health.
Blaming you for your condition causes guilt and hopelessness. Even worse, the belief that people with diabetes have brought their disease on themselves inclines doctors to give people with diabetes abysmal care. They assume that since you did nothing to prevent your disease, you won't make the effort to control it. So they ignore your high blood sugars until they have lasted long enough to cause complications and then they prescribe the newest, most expensive, potentially dangerous but heavily marketed drugs, though the drug-maker's own Prescribing Information makes it clear that these drugs cannot lower your blood sugar to the levels that reverse or prevent complications.
The myth that diabetes is caused by overeating also hurts the one out of five people who are not overweight when they contract Type 2 Diabetes. Because doctors only think "Diabetes" when they see a patient who fits the stereotype--the grossly obese, inactive patient--they often neglect to check people of normal weight for blood sugar disorders even when they show up with classic symptoms of high blood sugar such as recurrent urinary tract infections or neuropathy.
Where Did This Toxic Myth Come From?
The way this myth originated is this: People with Type 2 Diabetes often are overweight. And many people who are overweight have a syndrome called "insulin resistance," where their cells do not respond properly to insulin, making them need larger than normal amounts of insulin to lower their blood sugar. So the conclusion was drawn, years ago, that insulin resistance was the cause of Type 2 Diabetes.
It made sense. Something was burning out the beta cells in these people, and it seemed logical that the something must be the stress of pumping out much higher than normal amounts of insulin, day after day. This idea was so compelling that it was widely believed by medical professionals, though few realized it had never been subjected to careful investigation by large-scale research.
That is why any time there is an article in the news about Type 2 Diabetes you are likely to read something that says, "While Type 1 diabetes (sometimes called Juvenile Diabetes) is a condition where the body does not produce insulin, Type 2 Diabetes is the opposite: a condition where the body produces far too much insulin because of insulin resistance caused by obesity."
Blaming the Victim
Your doctor is likely to tell you the same thing and assure you that if you would just lose all that excess weight your diabetes would go away. This is not true, as many of us who have diabetes have found when we have lost large amounts of weight and achieved healthy BMIs, but doctors continue to believe this.
This is why they often harbor judgmental thoughts about their patients with diabetes, believing that they caused their illness by overindulging themselves. Why waste their time on these greedy pigs when there are so many more deserving patients who need help with conditions that are merely strokes of bad luck
This same bias is common n the media. Articles on the "obesity epidemic" blame overeating for a huge increase in the number of people with diabetes, including children and teenagers whose condition is blamed on poor diets and laziness. In a society where the concepts "thin" and "healthy" have taken on the overtones of moral virtue, the only one of the seven deadly sins that still inspires horror and condemnation is gluttony.
Fat shaming is common, because people who were lucky enough to be born with normal metabolisms smugly believe that obesity is sure proof of moral weakness. So it is not surprising that the subtext of media coverage of obesity and diabetes is that if you get diabetes is is only the punishment you deserve for being such a glutton.
The belief that diabetes is caused by greedy overeating is easy to understand. It makes healthy, younger people who exercise and watch their diets feel superior and safe. There's only one problem with it: It isn't true.
Obesity Has Risen Dramatically While Diabetes Rates Have Not
The rate of obesity has grown alarmingly over the past decades, especially in certain regions of the U.S. The NIH reports that "From 1960-2 to 2005-6, the prevalence of obesity increased from 13.4 to 35.1 percent in U.S. adults age 20 to 74.7."
If obesity was causing diabetes, you'd expect to see a similar rise in the diabetes rate. But this has not happened. The CDC reports that "From 1980 through 2010, the crude prevalence of diagnosed diabetes increased ...from 2.5% to 6.9%."
However, if you look at the graph that accompanies this statement, you see that the rate of diabetes diagnoses rose only gradually through this period--to about 3.5% until it suddenly sped upward in the late 1990s. This sudden increase largely due to the fact that in 1998 the American Diabetes Association changed the criteria by which diabetes was to be diagnosed, lowering the fasting blood sugar level used to diagnose diabetes from 141 mg/dl to 126 mg/dl. (Details HERE)
Analyzing these statistics, it becomes clear that though roughly 65 million more Americans became fat over this period, only 13 million more Americans became diabetic. And to further confuse the matter, several factors other than the rise in obesity and the ADA's lowering of the diagnostic cutoff also came into play during this period which also raised the rate of diabetes diagnoses:
Diabetes becomes more common as people age as the pancreas like other organs, becomes less efficient. In 1950 only 12% of the U.S. population was over 65. By 2010 40% was, and of those 40%, 19% were over 75.
At the same time, the period during which the rate of diabetes rose was also the period in which doctors began to heavily prescribe statins, a class of drugs we now know raises the risk of developing diabetes. (Details HERE.)
Why Obesity Doesn't Cause Diabetes: The Genetic Basis of Diabetes
While people who have diabetes are often heavy, one out of five people diagnosed with diabetes are thin or normal weight. And though heavy people with diabetes are, indeed, likely to be insulin resistant, the majority of people who are overweight will never develop diabetes. In fact, they will not develop diabetes though they are likely to be just as insulin resistant as those who do--or even more so. The message that diabetes researchers in academic laboratories are coming up with about what really causes diabetes is quite different from what you read in the media. What they are finding is that to get Type 2 Diabetes you need to have some combination of damaged genes well known to scientists.
These genes are involved with the complex processes involved in regulating your blood sugar. These damaged genes are often inherited, but not always. The same kind of genetic damage turns out to be caused by a large number of pesticides, herbicides, plastics,and other environmental toxins which are found in alarming concentrations in the bodies of those exposed to them. These chemicals are found in the foods we eat, the water we drink, and even cosmetics and shampoos we apply to our skin. When these genes are damaged, they keep your body from being able to regulate your blood sugar. If you don't have these damaged genes, you can eat until you drop, pack on hundreds of pounds, and never develop diabetes.
That's the broad overview. Now let's take a deeper look at the scientific research that backs up this claim.
Twin Studies Back up a Genetic Cause for Diabetes
Studies of identical twins showed that twins have an 80% concordance for Type 2 Diabetes. In other words, if one twin has Type 2 Diabetes, the chance that the other will have it two are 4 out of 5. While you might assume that this might simply point to the fact that twins are raised in the same home by mothers who feed them the same unhealthy diets, studies of non-identical twins found NO such correlation. The chances that one non-identical twin might have Type 2 Diabetes if the other had it were much lower, though these non-identical twins, born at the same time and raised by the same caregivers were presumably also exposed to the same unhealthy diets.
This kind of finding begins to hint that there is more than just bad habits to blame for diabetes. A high concordance between identical twins which is not shared by non-identical twins is usually advanced as an argument for a genetic cause, though because one in five identical twins did not become diabetic, it is assumed that some additional factors beyond the inherited genome must come into play to cause the disease to appear. Often this factor is an exposure to an environmental toxin which knocks out some other, protective genetic factor.
The Genetic Basis of Type 2 Diabetes Mellitus: Impaired Insulin Secretion versus Impaired Insulin Sensitivity. John E. Gerich. Endocrine Reviews 19(4) 491-503, 1998.
The List of Genes Associated with Type 2 Keeps Growing
Here is a brief list of some of the abnormal genes that have been found to be associated with Type 2 Diabetes in people of European extraction:
TCF7L2, HNF4-a, PTPN, SHIP2, ENPP1, PPARG, FTO, KCNJ11, NOTCh3, WFS1, CDKAL1, IGF2BP2, SLC30A8, JAZF1, and HHEX.
People from non-European ethnic groups have been found to have entirely different sets of diabetic genes than do Western Europeans, like the UCP2 polymorphism found in Pima Indians and the three Calpain-10 gene polymorphisms that have been found to be associated with diabetes in Mexicans. The presence of a variation in yet another gene, SLC16A11, was recently found to be associated with a 25% higher risk of a Mexican developing Type 2 diabetes.
East Asian populations have some of the same diabetes genes as the ones described above, but a 2020 gene wide study identified yet another set of Type 2 diabetes genes found only in that population as well as variations that explain why diabetes is more prevalent in East Asians whose weight is closer to the normal range.
Cassandra N. Spracklen, et al. Identification of type 2 diabetes loci in 433,540 East Asian individuals. Nature, 2020; DOI: 10.1038/s41586-020-2263-3 https://www.nature.com/articles/s41586-020-2263-3
The More Diabetes Genes You Have The Worse Your Beta Cells Perform
A study published in the Journal Diabetologia in November 2008 studied how well the beta cells secreted insulin in 1,211 non-diabetic individuals. They then screened these people for abnormalities in seven genes that have been found associated with Type 2 Diabetes.
They found that with each abnormal gene found in a person's genome, there was an additive effect on that person's beta cell dysfunction with each additional gene causing poorer beta cell function.
The impact of these genetic flaws becomes clear when we learn that in these people who were believed to be normal, beta cell glucose sensitivity and insulin production at meal times was decreased by 39% in people who had abnormalities in five genes. That's almost half. And if your beta cells are only putting out half as much insulin as a normal person's it takes a lot less stress on those cells to push you into becoming diabetic.
Beta cell glucose sensitivity is decreased by 39% in non-diabetic individuals carrying multiple diabetes-risk alleles compared with those with no risk alleles L. Pascoe et al. Diabetologia, Volume 51, Number 11 / November, 2008.
Gene Tests Predict Diabetes Independent of Conventional "Risk Factors"
A study of 16,061 Swedish and 2770 Finnish subjects found that:
Variants in 11 genes (TCF7L2, PPARG, FTO, KCNJ11, NOTCh3, WFS1, CDKAL1, IGF2BP2, SLC30A8, JAZF1, and HHEX) were significantly associated with the risk of Type 2 Diabetes independently of clinical risk factors [i.e. family history, obesity etc.]; variants in 8 of these genes were associated with impaired beta-cell function.
Note that though the subjects here were being screened for Type 2 Diabetes, the defect found here was NOT insulin resistance, but rather deficient insulin secretion. This study also found that:
The discriminative power of genetic risk factors improved with an increasing duration of follow-up, whereas that of clinical risk factors decreased.
In short, the longer these people were studied, the more likely the people with these gene defects were to develop diabetes.
Clinical Risk Factors, DNA Variants, and the Development of Type 2 Diabetes Valeriya Lyssenko, M.D. et. al. New England Journal of Medicine, Volume 359:2220-2232, November 20, 2008,Number 21.
What A Common Diabetes Gene Does
A study published in July of 2009 sheds light on what exactly it is that an allele (gene variant) often found associated with diabetes does. The allele in question is one of TCF7L2 transcription factor gene. The study involved 81 normal healthy young Danish men whose genes were tested. They were then given a battery of tests to examine their glucose metabolisms. The researchers found that:
Carriers of the T allele were characterised by reduced 24 h insulin concentrations ... and reduced insulin secretion relative to glucose during a mixed meal test ... but not during an IVGTT [intravenous glucose tolerance test].
This is an interesting finding, because what damages our bodies is the blood sugar we experience after eating "a mixed meal" but so much research uses the artificial glucose tolerance (GTT) test to assess blood sugar health. This result suggests that the GTT may be missing important signs of early blood sugar dysfunction and that the mixed meal test may be a better diagnostic test than the GTT. I have long believed this to be true, since so many people experience reactive lows when they take the GTT which produces a seemingly "normal reading" though they routinely experience highs after eating meals. These highs are what damage our organs.
Young men with the TCF7L2 allele also responded with weak insulin secretion in response to the incretin hormone GLP-1 and "Despite elevated hepatic [liver] glucose production, carriers of the T allele had significantly reduced 24 h glucagon concentrations ... suggesting altered alpha cell function."
Here again we see evidence that long before obesity develops, people with this common diabetes gene variant show highly abnormal blood sugar behavior. Abnormal production of glucose by the liver may also contribute to obesity as metformin, a drug that that blocks the liver's production of glucose blocks weight gain and often causes weight loss.
The T allele of rs7903146 TCF7L2 is associated with impaired insulinotropic action of incretin hormones, reduced 24 h profiles of plasma insulin and glucagon, and increased hepatic glucose production in young healthy men. K. Pilgaard et al. Diabetologia, Issue Volume 52, Number 7 / July, 2009. DOI 10.1007/s00125-009-1307-x
Genes Linked to African Heritage are Linked to Poor Carbohydrate Metabolism
It has long been known that African-Americans have a much higher rate of diabetes and metabolic syndrome than the American population as a whole. This has been blamed on lifestyle, but a 2009 genetic study finds strong evidence that the problem is genetic.
The study reports,
Using genetic samples obtained from a cohort of subjects undergoing cardiac-related evaluation, a strict algorithm that filtered for genomic features at multiple levels identified 151 differentially-expressed genes between Americans of African ancestry and those of European ancestry. Many of the genes identified were associated with glucose and simple sugar metabolism, suggestive of a model whereby selective adaptation to the nutritional environment differs between populations of humans separated geographically over time.
In the full text discussion the authors state,
These results suggest that differences in glucose metabolism between Americans of African and European may reside at the transcriptional level. The down-regulation of these genes in the AA cohorts argues against these changes being a compensatory response to hyperglycemia and suggests instead a genetic adaptation to changes in the availability of dietary sugars that may no longer be appropriate to a Western Diet.
In conclusion the authors note that the vegetarian diet of the Seventh Day Adventists, often touted as proof of the usefulness of the "Diet Pyramid" doesn't provide the touted health benefits to people of African American Heritage. Obviously, when hundreds of carbohydrate metabolizing genes aren't working properly the diet needed is a low carbohydrate diet.
The study is available in full text here:
Stable Patterns of Gene Expression Regulating Carbohydrate Metabolism Determined by Geographic AncestryJonathan C. Schisler et. al. PLoS One 4(12): e8183. doi:10.1371/journal.pone.0008183
Gene that Disrupts Circadian Clock Associated with Type 2 Diabetes
It has been known for a while that people who suffer from sleep disturbances often suffer raised insulin resistance. In December of 2008, researchers identified a gene, "rs1387153, near MTNR1B (which encodes the melatonin receptor 2 (MT2)), as a modulator of fasting plasma glucose." They conclude,
Our data suggest a possible link between circadian rhythm regulation and glucose homeostasis through the melatonin signaling pathway.
Melatonin levels appear to control the body clock which, in turn, regulates the secretion of substances that modify blood pressure, hormone levels, insulin secretion and many other processes throughout the body.
A variant near MTNR1B is associated with increased fasting plasma glucose levels and type 2 diabetes risk. Nabila Bouatia-Naji et al. Nature Genetics Published online: 7 December 2008, doi:10.1038/ng.277
There's an excellent translation of what this study means, translated into layman's terms at Science Daily:
The Environmental Factors That Push Borderline Genes into Full-fledged Diabetes
We've seen so far that to get Type 2 Diabetes you seem to need to have some diabetes gene or genes, but that not everyone with these genes develops diabetes. There are what scientists call environmental factors that can push a borderline genetic case into full fledged diabetes. Let's look now at what the research has found about what some of these environmental factors might be.
Your Mother's Diet During Pregnancy May Have Caused Your Diabetes
Many "environmental factors" that scientists explore occur in the environment of the womb. Diabetes is no different, and the conditions you experienced when you were a fetus can have life-long impact on your blood sugar control.
Researchers following the children of mothers who had experienced a Dutch famine during World War II found that children of mothers who had experienced famine were far more likely to develop diabetes in later life than a control group from the same population whose mothers had been adequately fed.
Glucose tolerance in adults after prenatal exposure to famine. Ravelli AC et al.Lancet. 1998 Jan 17;351(9097):173-7.
A study of a Chinese population found a link between low birth weight and the development of both diabetes and impaired glucose regulation (i.e. prediabetes) that was independent of "sex, age, central obesity, smoking status, alcohol consumption, dyslipidemia, family history of diabetes, and occupational status." Low birth weight in this population may well be due to less than optimal maternal nutrition during pregnancy.
Evidence of a Relationship Between Infant Birth Weight and Later Diabetes and Impaired Glucose Regulation in a Chinese Population Xinhua Xiao et. al. Diabetes Care31:483-487, 2008.
This may not seem all that relevant to Americans whose mothers have not been exposed to famine conditions. But to conclude this is to forget how many American teens and young women suffer from eating disorders and how prevalent crash dieting is in the group of women most likely to get pregnant.
It is also true that until the 1980s obstetricians routinely warned pregnant women against gaining what is now understood to be a healthy amount of weight. When pregnant women started to gain weight, doctors often put them on highly restrictive diets which resulted in many case in the birth of underweight babies.
Your Mother's Gestational Diabetes May Have Caused Your Diabetes
Maternal starvation is not the only pre-birth factor associated with an increased risk of diabetes. Having a well-fed mother who suffered gestational diabetes also increases a child's risk both of obesity and of developing diabetes.
High Prevalence of Type 2 Diabetes and Pre-Diabetes in Adult Offspring of Women With Gestational Diabetes Mellitus or Type 1 Diabetes The role of intrauterine hyperglycemiaTine D. Clausen, MD et al. Diabetes Care 31:340-346, 2008
Pesticides and PCBs in Blood Stream Correlate with Incidence of Diabetes
A study conducted among members of New York State's Mohawk tribe found that the odds of being diagnosed with diabetes in this population was almost 4 times higher in members who had high concentrations of PCBs in their blood serum. It was even higher for those with high concentrations of pesticides in their blood.
Diabetes in Relation to Serum Levels of Polychlorinated Biphenyls and Chlorinated Pesticides in Adult Native Americans Neculai Codru, Maria J. Schymura,Serban Negoita,Robert Rej,and David O. Carpenter.Environ Health Perspect. 2007 October; 115(10): 1442-1447.Published online 2007 July 17. doi: 10.1289/ehp.10315.
It is very important to note that there is no reason to believe this phenomenon is limited to people of Native American heritage. Upstate NY has a well-known and very serious PCB problem--remember Love Canal? And the entire population of the U.S. has been overexposed to powerful pesticides for a generation.
More evidence that obesity may be caused by exposure to toxic pollutants which damage genes comes in a study published January of 2009. This study tracked the exposure of a group of pregnant Belgian woman to several common pollutants: hexachlorobenzene, dichlorodiphenyldichloroethylene (DDE) , dioxin-like compounds, and polychlorinated biphenyls (PCBs). It found a correlation between exposure to PCBs and DDE and obesity by age 3, especially in children of mothers who smoked.
Intrauterine Exposure to Environmental Pollutants and Body Mass Index during the First 3 Years of Life Stijn L. Verhulst et al., Environmental Health Perspectives. Volume 117, Number 1, January 2009
These studies, which garnered no press attention at all, probably have more to tell us about the reason for the so-called "diabetes epidemic" than any other published over the last decade.
Trace Amounts of Arsenic in Urine Correlate with Dramatic Rise in Diabetes
A study published in JAMA in August of 2008 found of 788 adults who had participated in the 2003-2004 National Health and Nutrition Examination Survey (NHANES) found those who had the most arsenic in their urine, were nearly four times more likely to have diabetes than those who had the least amount.
The study is reported here: Arsenic Exposure and Prevalence of Type 2 Diabetes in US Adults. Ana Navas-Acien et al. JAMA. 2008;300(7):814-822. The New York Times report about this study (no longer online) added this illuminating bit of information to the story:
Arsenic can get into drinking water naturally when minerals dissolve. It is also an industrial pollutant from coal burning and copper smelting. Utilities use filtration systems to get it out of drinking water. Seafood also contains nontoxic organic arsenic. The researchers adjusted their analysis for signs of seafood intake and found that people with Type 2 Diabetes had 26 percent higher inorganic arsenic levels than people without Type 2 Diabetes. How arsenic could contribute to diabetes is unknown, but prior studies have found impaired insulin secretion in pancreas cells treated with an arsenic compound.
Prescription Drugs, Especially SSRI Antidepressants Cause Obesity and Possibly Diabetes
Another important environmental factor is this: Type 2 Diabetes can be caused by some commonly prescribed drugs. Beta blockers and atypical antipsychotics like Zyprexa have been shown to cause diabetes in people who would not otherwise get it. This is discussed here.
There is some research that suggests that SSRI antidepressants may also promote diabetes. It is well known that antidepressants cause weight gain.
Spin doctors in the employ of the drug companies who sell these high-profit antidepressants have long tried to attribute the relationship between depression and obesity to depression, rather than the drugs used to treat the condition.
However, a new study published in June 2009 used data from the Canadian National Population Health Survey (NPHS), a longitudinal study of a representative cohort of household residents in Canada and tracked the incidence of obesity over ten years.
The study found that,
MDE [Major Depressive Episode] does not appear to increase the risk of obesity. ...Pharmacologic treatment with antidepressants may be associated with an increased risk of obesity. [emphasis mine].
The study concluded,
Unexpectedly, significant effects were seen for serotonin-reuptake-inhibiting antidepressants [Prozac,Celexa, Lovox, Paxil, Zoloft] and venlafaxine [Effexor], but neither for tricyclic antidepressants nor antipsychotic medications.
Scott B. Patten et al. Psychother Psychosom 2009;78:182-186
Here is an article posted by the Mayo Clinic that includes the statement "weight gain is a reported side effect of nearly all antidepressant medications currently available.
Here is a report about a paper presented at the 2006 ADA Conference that analyzed the Antidepressant-Diabetes connection in a major Diabetes prevention study:
Treatment for Cancer, Especially Radiation, Greatly Increases Diabetes Risk Independent of Obesity or Exercise Level
A study published in August 2009 analyzed data for 8599 survivors in the Childhood Cancer Survivor Study. It found that after adjusting for body mass and exercise levels, survivors of childhood cancer were 1.8 times more likely than the siblings to report that they had diabetes.
Even more significantly, those who had had full body radiation were 7.2 times more likely to have diabetes.
This raises the question of whether exposure to radiation in other contexts also causes Type 2 diabetes.
Diabetes Mellitus in Long-term Survivors of Childhood Cancer: Increased Risk Associated With Radiation Therapy: A Report for the Childhood Cancer Survivor Study.Lillian R. Meacham et al. Arch. Int. Med.Vol. 169 No. 15, Aug 10/24, 2009.
Common Organic Environmental Pollutants Greatly Increase Insulin Resistance, Straining Already Deficient Blood Sugar Control
Some environmental toxins cause diabetes by damaging genes or the pancreas. Others, while they don't cause diabetes in people who don't have diabetes genes, worsen blood sugar control in those people because they greatly increase insulin resistance. This greatly increases the amount of insulin it takes to stay in good control. Since people with diabetes genes already have a limited ability to secrete insulin, the demands of rising insulin resistance can not be met and the person's underlying, inborn problem with blood sugar control becomes obvious. The most common of these pollutants are discussed next.
BPA and Plasticizers from Packaging Are Strongly Linked to Obesity and Insulin Resistance
BPA, the plastic used to line most metal cans has long been suspected of causing obesity. Now we know why. A study published in 2008 reported that BPA suppresses a key hormone, adiponectin, which is responsible for regulating insulin sensitivity in the body and puts people at a substantially higher risk for metabolic syndrome.
The impact of BPA on children is dramatic. Analysis of 7 years of NHANES epidemiological data found that having a high urine level of BPA doubles a child's risk of being obese.
Bisphenol A and Chronic Disease Risk Factors in US Children. Eng, Donna et al.PediatricsPublished online August 19, 2013. doi: 10.1542/peds.2013-0106
You and your children are getting far more BPA from canned foods than what health authorities assumed they were getting. A research report published in 2011 reported that the level of BPA actually measured in people’s bodies after they consumed canned soup turned out to be extremely high. People who ate a serving of canned soup every day for five days had BPA levels of 20.8 micrograms per liter of urine, whereas people who instead ate fresh soup had levels of 1.1 micrograms per liter.
Canned Soup Consumption and Urinary Bisphenol A: A Randomized Crossover Trial Carwile, JL et al. JAMA. November 23/30, 2011, Vol 306, No. 20
Nevertheless, the FDA caved in to industry pressure in 2012 and refused to regulate BPA claiming that, as usual, more study was needed. (FDA: BPA)
BPA is not the only toxic chemical associated with plastics that may be promoting insulin resistance. Phthalates are compounds added to plastic to make it flexible. They rub off on our food and are found in our blood and urine. A study of 387 Hispanic and Black, New York City children who were between six and eight years old measured the phthalates in their urine and found that the more phthalates in their urine, the fatter the child was a year later.
Associations between phthalate metabolite urinary concentrations and body size measures in New York City children. Susan L. Teitelbaum et al.Environ Res. 2012 Jan;112:186-93.
This finding was echosed by another study: Urinary phthalates and increased insulin resistance in adolescents Trasande L, et al. Pediatrics 2013; DOI: 10.1542/peds.2012-4022.
And phthalates are everywhere. A study of 1,016 Swedes aged 70 years and older found that four phthalate metabolites were detected in the blood serum of almost all the participants. High levels of three of these were associated with the prevalence of diabetes. The researchers explain that one metabolite was mainly related to poor insulin secretion, whereas two others were related to insulin resistance. The researchers didn’t check to see whether this relationship held for prediabetes.
Circulating Levels of Phthalate Metabolites Are Associated With Prevalent Diabetes in the Elderly.Lind, MP et al. Diabetes. Published online before print April 12, 2012, doi: 10.2337/dc11-2396
Chances are very good that these same omnipresent phthalates are also causing insulin resistance and damaging insulin secretion in people whose ages fall between those of the two groups studied here.
Use of Herbicide Atrazine Maps to Obesity, Causes Insulin Resistance
A study published in April of 2009 mentions 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."
It found that when rats were given low doses of this pesticide in thier water, "Chronic administration of ATZ decreased basal metabolic rate, and increased body weight, intra-abdominal fat and insulin resistance without changing food intake or physical activity level." In short the animals got fat even without changing their food intake. When the animals were fed a high fat, high carb diet, the weight gain was even greater.
Insulin resistance was increased too, which if it happens in people, means that people who have genetically-caused borderline capacity to secrete insulin are more likely to become diabetic when they are exposed to this chemical via food or their drinking water.
Chronic Exposure to the Herbicide, Atrazine, Causes Mitochondrial Dysfunction and Insulin Resistance PLoS ONE Published 13 Apr 2009
2,4-D A Common Herbicide Blocks Secretion of GLP-1--A Blood Sugar Lowering Gastric Peptide
In 2007 scientists at New York's Mount Sinai Hospital discovered that the intestine has receptors for sugar identical to those found on the tongue and that these receptors regulate secretion of glucagon-like peptide-1 (GLP-1). GLP-1 is the peptide that is mimicked by the diabetes drug Byetta and which is kept elevated by Januvia and Onglyza. You can read about that finding in this Science Daily report:
In November 2009, these same scientists reported that a very common herbicide 2,4 D blocked this taste receptor, effectively turning off its ability to stimulate the production GLP-1. The fibrate drugs used to lower cholesterol were also found to block the receptor.
What was even more of concern was the discovery that the ability of these compounds to block this gut receptor "did not generalize across species to the rodent form of the receptor." The lead researcher was quoted as saying,
...most safety tests were done using animals, which have T1R3 receptors that are insensitive to these compounds,
This takes on additional meaning when you realize that most compounds released into the environment are tested only on animals, not humans. It may help explain why so many supposedly "safe" chemicals are damaging human glucose metabolisms.
The discussion of how diabetes genes cause obesity rather than obesity causing diabetes continues on this page: Obesity Doesn't Cause Diabetes -- Diabetes Causes Obesity