Don't fall for the toxic myth that you caused your diabetes by reckless overeating

While people with diabetes often are seriously overweight, there is accumulating evidence that their overweight is yet another symptom, not the cause of the process that leads to type 2 diabetes.

But the chances are that you've been told that you caused your diabetes by letting yourself get fat.

This is a truly toxic myth. By blaming you for your condition it causes guilt and hopelessness. Even worse, the belief that people with diabetes have brought their disease on themselves inclines doctors to assume that since you did nothing to prevent your disease, you won't make the effort to control it--a belief that may lead to your getting extremely poor care.

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. Because people with type 2 diabetes are often overweight, and because many people who are overweight have a syndrome called "insulin resistance" in which their cells do not respond strongly to insulin and require larger amounts of insulin to process blood sugar, the conclusion was drawn years ago that insulin resistance is the cause of type 2 diabetes.

It made sense. Something was burning out the beta cells in these people, and it seemed clear that the something must be the stress of pumping out huge amounts of insulin, day after day. This has lead to the general assumption that it is insulin resistance that causes diabetes. 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, but where the cells, because of a condition called "insulin resistance" can no longer use that insulin."

It is very likely that if you ask why you have type 2 this is what your doctor will also tell you. If you ask for more information about "insulin resistance" you'll probably be told that what causes it is excess body fat.

So the conclusion is inescapable, your overeating caused you to put on excess fat. Your excess fat is what made you diabetic.

Blaming the Victim

This line of reasoning leads to subtle, often unexpressed, judge mental decisions on the part of your doctor, who is likely to believe that had you not been such a pig, you would not have given yourself this unnecessary disease. And because of this unspoken bias, unless you are able to "please" your doctor by losing a great deal of weight, very quickly, after diagnosis you may find your condition treated with a subtle but callous disregard because of the doctor's feeling that you have brought this condition down on yourself. This bias is similar to that held by doctors who face patients who smoke a pack a day and get lung cancer and still refuse to stop smoking.

You'll also see this bias frequently expressed in the media. Articles on the "obesity epidemic" blame overeating for a huge increase in the number of people with diabetes, including children and teenagers, who are pictured as greedily gorging on supersized fast foods while doing no exercise more strenuous than channel surfing. In a society where the concepts "thin" and "healthy" have taken on the overtones of moral virtue and where the only one of the seven deadly sins that still inspires horror and condemnation is gluttony, being fat is considered by many as sure proof of culpable moral weakness. So it is not surprising that the subtext of media coverage of obesity and diabetes is that diabetes is nothing less than the just punishment you deserve for being a glutton.

Except that it's not true.

Why Obesity Doesn't Necessarily Cause 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 likely to be insulin resistant, the majority of people who are overweight will never develop diabetes, though they are likely to be just as insulin resistant as those who do--or even more so.

In fact, 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 there are many different metabolic flaws that appear to develop into the syndrome that we call type 2 diabetes. Most of them appear to be genetic in origin. This means that unless you have damaged or abnormal genes, you can eat until you drop and never develop diabetes.

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 were much lower, though these 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 here. 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. (1)

Your Mother's Diet During Pregnancy May Have Caused Your Diabetes

Other metabolic defects that cause diabetes appear to occur when a baby is in the womb. 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. (2)

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. (3)

This finding was confirmed by another study published in 2008:

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

http://care.diabetesjournals.org/cgi/content/abstract/31/2/340

Insulin Resistance Develops in Thin Children of People with Type 2 Diabetes

Lab research has come up with some other intriguing findings that challenge the idea that obesity causes insulin resistance which causes diabetes.

One of these studies took two groups of thin subjects with normal blood sugar who were evenly matched for height and weight. The two groups differed only in that one group had close relatives who had developed type 2 diabetes, and hence, if there were a genetic component to the disorder, were more likely to have it. The other group had no relatives with type 2 diabetes. The researchers then and examined the subjects' glucose and insulin levels during a glucose tolerance test and calculated their insulin resistance. They found that the thin relatives of the people with Type 2 diabetes already had much more insulin resistance than did the thin people with no relatives with diabetes. (4)

Mitochondrial Dysfunction is Found in Lean Relatives of People with Type 2 Diabetes

Why this might be was made clear by a landmark 2004 study which looked at the cells of the "healthy, young, lean" but insulin-resistant relatives of people with type 2 diabetes and found that their mitochondria, the "power plant of the cells" that is the part of the cell that burns glucose, appeared to have a defect. While the mitochondria of people with no relatives with diabetes burned glucose well, the mitochondria of the people with an inherited genetic predisposition to diabetes were not able to burn off glucose as efficiently, but instead caused the glucose they could not burn and to be stored in the cells as fat.(5)

More Evidence that Abnormal Insulin Resistance Precedes Weight Gain and Probably Causes it

Thanks to Susan of alt.support.diabetes for posting about this study the day it was published. A study done at Yale University School of Medicine by Gerald I. Shulman and Kitt Falk Petersen, published in the prestigeous Proceedings of the National Academy of Science (PNAS) journal on July 16, 2007 reports on a study that compared energy usage by lean people who were insulin resistant and lean people who were insulin sensitive.

Using new imaging technologies, the researchers found that lean but insulin resistant subjects converted glucose from high carbohydrate meals into triglycerides--i.e. fat. Lean insulin-sensitive subjects, in contrast, stored the same gluocse in the form of muscle and liver glycogen.

The researchers conclude that "the insulin resistance, in these young, lean, insulin resistant individuals, was independent of abdominal obesity and circulating plasma adipocytokines, suggesting that these abnormalities develop later in the development of the metabolic syndrome."

In short, obesity looked to be a result, not a cause of the metabolic flaw that led these people to store high carb meals as fat rather than burn the glucose from these meals for energy.

The researchers suggested controlling insuliin resistance with exercise. It would also be a good idea for people who are insulin resistant, or have a family history of Type 2 diabetes to cut back on their carb intake, knowing that the glucose from the carbs they eat is more likely to turn into fat.

Beta Cells Fail to Reproduce in People with Diabetes

A study of pancreas autopsies that compared the pancreases of thin and fat people with diabetes with those of thin and fat normal people found that fat, insulin-resistant people who did not develop diabetes apparently were able to grow new beta-cells to produce the extra insulin they needed. In contrast, the beta cells of people who developed diabetes were unable to reproduce. This failure was independent of their weight.(6)

A Slow Developing form of Autoimmune Diabetes is "indistinguishable" from Type 2 Diabetes

A study published in Diabetes Care in April of 2007 finds that fully 4.5% of a sample of 4,250 people diagnosed as "Type 2" diabetics had GAD antibodies, which are the diagnostic sign of the form of autoimmune diabetes usually called "Type 1 diabetes."

As reported in Diabetes in Control, "The patients with autoimmune diabetes showed a clinical phenotype significantly different from that of type 2 diabetes, including higher fasting glucose and A1C and lower BMI and uric acid."

"In addition, compared with those with low GADA titers, patients with high GADA titers had more prominent traits of insulin deficiency, a profile of more severe autoimmunity, and a lower prevalence of metabolic syndrome."

However the article also says that "Dr. Buzzetti of La Sapienza University, Rome and colleagues note that slowly progressive autoimmune diabetes in adults is often indistinguishable from classic type 2 diabetes."

Autoimmune diabetes is caused when the body's own immune system confuses the beta cell with some kind of pathogen and attacks it. If the attack is robust, most of the beta cells die and the person ends up with Type 1 diabetes. However, the finding here suggests that people may get a "mild" autoimmune attack which kills off just enough of the beta cells to cause a form of diabetes easily confused with Type 2--especially if it happens to someone who is older then their teens (when Type 1 often strikes) or overweight (as a large proportion of the population now is.)

http://www.diabetesincontrol.com/results.php?storyarticle=4761

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.

This study, which garnered no press attention at all, probably has more to tell us about the reason for the so-called "diabetes epidemic" than any other published over the last decade.

Thanks to Prairie Mary for posting this in her blog!

Once Blood Sugars Rise They Impair a Muscle Gene that Regulates Insulin Sensitivity

Another piece of the puzzle falls into place thanks to a new research study published on Feb 8, 2008. As reported in Diabetes in Control:

"The research team identified a 'fat-burning' gene, the products of which are required to maintain the cells insulin sensitivity. They also discovered that this gene is reduced in muscle tissue from people with high blood sugar and type 2-diabetes. In the absence of the enzyme that is made by this gene, muscles have reduced insulin sensitivity, impaired fat burning ability, which leads to an increased risk of developing obesity.

"'The expression of this gene is reduced when blood sugar rises, but activity can be restored if blood sugar is controlled by pharmacological treatment or exercise", says Professor Juleen Zierath. "Our results underscore the importance of tight regulation of blood sugar for people with diabetes.'"

In short, once your blood sugar rises past a certain point, you become much more insulin resistant, which in turn pushes up your blood sugar more.

A New Model For How Diabetes Develops

These research findings open up a new way of understanding the relationship between obesity and diabetes.

Perhaps people with the genetic condition underlying type 2 diabetes inherit a defect in the beta cells that make those cells unable to reproduce normally to replace cells damaged by the normal wear and tear of life.

Perhaps, too, a defect in the way that their cells burn glucose inclines them to turn excess blood sugar into fat rather than burning it off as a person with normal mitochondria might do.

Put these two facts together and you suddenly get a fatal combination that is almost guaranteed to make a person fat.

Studies have shown that blood sugars only slightly over 100 mg/dl are high enough to render beta cells dysfunctional.(7) In a normal person who had the ability to grow new beta cells, any damaged beta cells would be replaced by new ones, which would keep the blood sugar at levels low enough to avoid further damage. But the beta cells of a person with a genetic heritage of diabetes are unable to reproduce So once blood sugars started to rise, more beta cells would succumb to the resulting glucose toxicity, and that would, in turn raise blood sugar higher.

As the concentration of glucose in their blood rose, these people would not be able to do what a normal person does with excess blood sugar--which is to burn it for energy. Instead their defective mitochondria will cause the excess glucose to be stored as fat. As this fat gets stored in the muscles it causes the insulin resistance so often observed in people with diabetes--long before the individual begins to gain visible weight. This insulin resistance puts a further strain on the remaining beta cells by making the person's cells less sensitive to insulin. Since the person with an inherited tendency to diabetes' pancreas can't grow the extra beta cells that a normal person could grow when their cells become insulin resistant this leads to ever escalating blood sugars which further damage the insulin-producing cells, and end up in the inevitable decline into diabetes.

Low Fat Diets Promote the Deterioration that Leads to Diabetes in People with the Genetic Predisposition

In the past two decades, when people who were headed towards diabetes begin to gain weight, they were advised to eat a low fat diet. Unfortunately, this low fat diet is also a high carbohydrate diet--one that exacerbates blood sugar problems by raising blood sugars dangerously high, destroying more insulin-producing beta-cells, and catalyzing the storage of more fat in the muscles of people with dysfunctional mitochondria. Though they may have stuck to diets to low fat for weeks or even months these people were tormented by relentless hunger and when they finally went off their ineffective diets, they got fatter. Unfortunately, when they reported these experiences to their doctors, they were almost universally accused of lying about their eating habits.

It has only been documented in medical research during the past two years that that many patients who have found it impossible to lose weight on the low fat high carbohydrate can lose weight--often dramatically--on a low carbohydrate diet while improving rather than harming their blood lipids. (8)

The low carb diet does two things. By limiting carbohydrate, it limits the concentration of blood glucose which often is enough to bring moderately elevated blood sugars down to normal or near normal levels. This means that there will be little excess glucose left to be converted to fat and stored.

It also gets around the mitochondrial defect in processing glucose by keeping blood sugars low so that the body switches into a mode where it burns ketones rather than glucose for muscle fuel.

Relentless Hunger Results from Roller Coaster Blood Sugars

There is one last reason why you may believe that obesity caused your diabetes, when, in fact, it was undiagnosed diabetes that caused your obesity.

Long before a person develops diabetes, they go through a phase where they have what doctors called "impaired glucose tolerance." This means that after they eat a meal containing carbohydrates, their blood sugar rockets up and may stay high for an hour or two before dropping back to a normal level.

What most people don't know is that when blood sugar moves swiftly up or down most people will experience intense hunger. The reasons for this are not completely clear. But what is certain is that this intense hunger caused by blood sugar swings can develop years before a person's blood sugar reaches the level where they'll be diagnosed as diabetic.

This relentless hunger, in fact, is often the very first diabetic symptom a person will experience, though most doctors do not recognize this hunger as a symptom. Instead, if you complain of experiencing intense hunger doctors may suggest you need an antidepressant or blame your weight gain, if you are female, on menopausal changes.

This relentless hunger caused by impaired glucose tolerance almost always leads to significant weight gain and an increase in insulin resistance. However, because it can take ten years between the time your blood sugar begins to rise steeply after meals and the time when your fasting blood sugar is abnormal enough for you to be diagnosed with diabetes, most people are, indeed, very fat at the time of diagnosis.

With better diagnosis of diabetes (discussed here) we would be able to catch early diabetes before people gained the enormous amounts of weight now believed to cause the syndrome. But at least now people with diabetic relatives who are at risk for developing diabetes can go a long way towards preventing the development of obesity by controlling their carbohydrate intake long before they begin to put on weight.

End Note: Prescription Drugs Also Cause both Obesity and Diabetes

There is one last, sinister, cause of diabetes that you may not be aware of, since the media never discusses it. 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 also cause diabetes. It is well known that antidepressants cause weight gain.

The drug companies earning huge profits on these drugs argue that the depression comes first--i.e. that people with Type 2 diabetes start out depressed before they take the drugs, but this is by no means clear. Unfortunately, no drug company is going to pay for research to prove that its blockbuster profit-earning drug harms people. So you are not likely to see a lot of research looking into this relationship. Instead, since it came out there has been some non-research based spin-control from the drug companies touting the idea that diabetics are a depressive bunch lucky to be able to take their wonderful drugs.

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."
Antidepressants and weight gain - Mayoclinic.com

Here is one study that found the Antidepressant-Diabetes connection: Medscape: Antidepressants linked to Type 2 Diabetes Risk."

Citations

1 John E. Gerich

The Genetic Basis of Type 2 Diabetes Mellitus: impaired Insulin Secretion versus Impaired Insulin Sensitivity. Endocrine Reviews 19(4) 491-503, 1998.

http://edrv.endojournals.org/cgi/content/full/19/4/491

2 Glucose metabolism in the Dutch famine birth cohort.

Glucose tolerance in adults after prenatal exposure to famine.Ravelli AC, van der Meulen JH, Michels RP, Osmond C, Barker DJ, Hales CN, Bleker OP.

3 Obesity and Type 2 Diabetes in the Pediatric Population: A Growing Concern.

http://www.medscape.com/viewarticle/413044

4 Straczkowski M, Kowalska I, Stepien A, Dzienis-Straczkowska S, Szelachowska M, Kinalska I, Krukowska A, Konicka M.

Insulin resistance in the first-degree relatives of persons with type 2 diabetes. Med Sci Monit. 2003 May;9(5):CR186-90.

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=12761455

5 Petersen KF, Dufour S, Befroy D, Garcia R, Shulman GI

Insulin resistance in children of type 2 parents who have abnormal mitochondria. New England J Med 2004 Feb 12; 350(7);639-41

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=14960743

Summarized at:

http://diabetes.about.com/cs/newswire/a/mitochondria204.htm
also

http://diabetes.diabetesjournals.org/cgi/content/full/55/Supplement_2/S9.
Molecular Mechanisms of Insulin Resistance in Humans and Their Potential Links With Mitochondrial Dysfunction.
Katsutaro Morino, Kitt Falk Petersen, and Gerald I. Shulman.
Diabetes 55:S9-S15, 2006

6 Alexandra E. Butler, Juliette Janson, Susan Bonner-Weir, Robert Ritzel, Robert A. Rizza, and Peter C. Butler

�-Cell Deficit and Increased �-Cell Apoptosis in Humans With Type 2 Diabetes. Diabetes 52:102-110, 2003

http://diabetes.diabetesjournals.org/cgi/content/full/52/1/102

7 Gastaldelli A, Ferrannini E, Miyazaki Y, Matsuda M, DeFronzo RA.

Beta-cell dysfunction and glucose intolerance: results from the San Antonio metabolism (SAM) study.
Diabetologia. 2004 Jan;47(1):31-9. Epub 2003 Dec 10.

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=14666364

8 Sharman MJ, Gomez AL, Kraemer WJ, Volek JS.

Very low-carbohydrate and low-fat diets affect fasting lipids and postprandial lipemia differently in overweight men.: J Nutr. 2004 Apr;134(4):880-5.

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=15051841

and

Volek JS, Sharman MJ, Gomez AL, Scheett TP, Kraemer WJ.

An isoenergetic very low carbohydrate diet improves serum HDL cholesterol and triacylglycerol concentrations, the total cholesterol to HDL cholesterol ratio and postprandial pipemic responses compared with a low fat diet in normal weight, normolipidemic women. J Nutr. 2003 Sep;133(9):2756-61.


http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=12949361