Category Archives: Causes of Diabetes

Soft Drinks Raise Risk of T2 Diabetes and LADA

I enjoy an aspartame-flavored Fresca now and then

I enjoy an aspartame-flavored Fresca now and then

LADA is latent autoimmune diabetes in adults.

This new study is out of Sweden. The potential disease-inducing soft drink dose was 400 ml or 13.5 fl oz per day. In the U.S., a typical soda can is 10 fl oz or 355 ml. Surprisingly, artificially-sweetened soft drinks were just as guilty as regular beverages.

From MNT:

“The study included 2,874 Swedish adults, of whom 1,136 had type 2 diabetes, 357 had LADA, and 1,137 were healthy controls.

The team analyzed the self-reported dietary data of each adult, looking specifically at the number of soft drinks consumed up to 1 year before a diabetes diagnosis. Participants’ insulin resistance levels, beta cell function, and autoimmune response were also measured.

The researchers found that adults who reported drinking at least two 200-milliliter servings of soft drinks a day – whether they contained sugar or artificial sweetener – were twice as likely to develop LADA and 2.4 times more likely to develop type 2 diabetes, compared with those who consumed fewer than two soft drinks daily.

What is more, adults who consumed five 200-milliliter servings of soft drinks daily were found to be at 3.5 times greater risk of LADA and 10.5 times greater risk of type 2 diabetes, regardless of whether the drinks were sugary or artificially sweetened.”

Source: Diabetes risk doubles with more than two soft drinks daily – Medical News Today

Professor Tim Noakes: A Nutrition Heretic and His Low-Carb Epiphany

Paleo-compliant low-carb meal. I almost used this for my Paleobetic Diet book cover.

Paleo-compliant low-carb meal. I almost used this for my Paleobetic Diet book cover.

“I argue that the very reason we are facing an uncontrollable global diabetes/obesity pandemic at the moment, is because we have promoted dietary guidelines that are based solely on “evidence” from associational studies without acknowledging that RCTs [randomized controlled trials] have either not supported those conclusions or might have actively disproved them.

The solution in my mind is that we need to give dietary advice to persons with diabetes, T2DM [type 2 diabetes] especially, based on our understanding of the underlying patho-physiology of the condition, not on false information provided by associational epidemiological studies that are unable to prove causation.  I suggest that we know a number of features of the abnormal biology of T2DM with absolutely certainty.”

—Tim Noakes


Do Statin Drugs Cause Diabetes?

Roni Rabin at the New York Times suggests an answer:

“The Food and Drug Administration updated its advisory about statins in 2012 to include warnings about the slightly increased risk of higher blood sugars and Type 2 diabetes, based in part on two large analyses of earlier studies that controlled for diabetes risk factors like being overweight or being older. One found a 9 percent increase in the risk of diabetes among statin users, and the other a 12 percent increase, with a greater risk for those on intensive rather than moderate doses of the drugs.

The 2012 F.D.A. advisory also warns of other side effects of statins, such as muscle injury, rare cases of liver damage and reports of memory loss and confusion.”

Source: Can Statins Cause Diabetes? – The New York Times

Do Potatoes Make You Fat or Diabetic?

Researchers in Denmark say “no.” French fries, maybe.

“The identified studies do not provide convincing evidence to suggest an association between intake of potatoes and risks of obesity, T2D, or CVD. French fries may be associated with increased risks of obesity and T2D although confounding may be present. In this systematic review, only observational studies were identified. These findings underline the need for long-term randomized controlled trials.”

Source: Potatoes and risk of obesity, type 2 diabetes, and cardiovascular disease in apparently healthy adults: a systematic review of clinical intervention and observational studies

Almost Half of California Adults Have Prediabetes

The actual figure is 46%, according to researchers at UCLA. The LA Times has the story.

“Our genes and our environment are kind of on a collision course,” said Dr. Francine Kaufman, the former head of the American Diabetes Assn., who was not involved with the research. “It’s not stopping.”

The problem with prediabetes is that it often evolves into full-blown diabetes. It’s also associated with increased risk for cardiovascular disease such as heart attack and stroke. The Times article says “up to 70% of those with prediabetes develop diabetes in their lifetime.” I’d never heard that vague number before; I say vague because “up to 70%” could be anything between zero and 70. It’s more accurate to note that one in four people with prediabetes develops type 2 diabetes over the course of three to five years.

She has the genes of a cave woman

She has the genes of a cave woman

Prediabetes is defined as:

  1. fasting blood sugar between 100 and 125 mg/dl (5.56–6.94 mmol/l), or
  2. blood sugar level 140–199 mg/dl (7.78–11.06 mmol/l) two hours after drinking 75 grams of glucose

How To Prevent Progression of Prediabetes Into Diabetes

  • If you’re overweight or obese, lose excess fat weight. How much should you lose? Aim for at least 5% of body weight and see if that cures your prediabetes. For instance, if you weigh 200 lb (91 kg), lose 10 lb (4.5 kg).
  • If you’re sedentary, start exercising regularly.
  • Cut back on your consumption of sugar-sweetened beverages, other sugar sources, and other refined carbohydrates like wheat flour.

Steve Parker, M.D.

Paleobetic Diet-FrontCover_300dpi_RGB_5.5x8.5


Does Pollution Cause Type 2 Diabetes?

See text for mention of pancreatic alpha and beta cells

See text for mention of pancreatic alpha and beta cells

A panel of university-based scientists convened by The Endocrine Society recently reviewed the available literature on health effects of endocrine-disrupting chemicals (aka EDCs). The executive summary is available free online. Some excerpts:

The full Scientific Statement represents a comprehensive review of the literature on seven topics for which there is strong mechanistic, experimental, animal, and epidemiological evidence for endocrine disruption, namely: obesity and diabetes, female reproduction, male reproduction, hormone-sensitive cancers in females, prostate cancer, thyroid, and neurodevelopment and neuroendocrine systems. EDCs such as bisphenol A, phthalates, pesticides, persistent organic pollutants such as polychlorinated biphenyls, polybrominated diethyl ethers, and dioxins were emphasized because these chemicals had the greatest depth and breadth of available information.

*  *  *

Both cellular and animal models demonstrate a role for EDCs in the etiology of obesity and T2D [type 2 diabetes]. For obesity, animal studies show that EDC-induced weight gain depends on the timing of exposure and the age of the animals. Exposures during the perinatal period [the weeks before and after birth] trigger obesity later in life. New results covering a whole range of EDC doses have underscored the importance of nonmonotonic dose-response relationships; some doses induced weight increase, whereas others did not. Furthermore, EDCs elicit obesity by acting directly on white adipose tissue, al- though brain, liver, and even the endocrine pancreas may be direct targets as well.

Regarding T2D, animal studies indicate that some EDCs directly target 􏰁beta and alpha cells in the pancreas, adipocytes, and liver cells and provoke insulin resistance together with hyperinsulinemia. These changes can also be associated with altered levels of adiponectin and leptin— often in the absence of weight gain. This diabetogenic action is also a risk factor for cardiovascular diseases, and hyperinsulinemia can drive diet-induced obesity. Epide- miological studies in humans also point to an association between EDC exposures and obesity and/or T2D; however, because many epidemiological studies are cross-sectional, with diet as an important confounding factor in humans, it is not yet possible to infer causality.


Bix at Fanatic Cook blog says foods of animal origin are the major source of harmful persistent organic pollutants, some of which act as ECDs.

Keep your eyes and ears open for new research reports on this critically important topic.

Steve Parker, M.D.

Book front cover

Book front cover

Antibiotics May Cause Type 2 Diabetes

Denmark researchers found an association between antibiotic usage and later development of type 2 diabetes. Just because there’s a linkage between antibiotics and type 2 diabetes doesn’t mean there is a direct causal relationship.

One possible way that antibiotics could cause diabetes, however, would be through alteration of gut germs (aka microbiome). An antibiotic may do a great job curing your urinary tract infection, while at the same time eliminating millions of certain gut bacteria and allowing other species to have a population explosion. One of the most fascinating fields of medicine now is trying to figure out if and how the billions of bacteria in our intestines might influence health and disease. F’rinstance, gut bacteria may influence whether we are fat or slim.

I bet if you graphed antibiotic use and incidence of type 2 diabetes over the last 50 years, they would trend together pretty well. Any volunteers to do that?

Steve Parker, M.D.

Could Fructose Cause Diabetes?

Lumps of Diabetes

Cubes of Diabetes?

A Pharm.D (Dr of Pharmacology) and a pair of MD’s surveyed much of the available scientific literature—both animal and human studies—and concluded that fructose is a major culprit in the rise of type 2 diabetes and prediabetes. Fructose does its damage by increasing insulin resistance. ScienceDaily has the details.

Be aware that their conclusion is certainly not universally accepted. I read “Pathogenesis of type 2 diabetes mellitus” at a few months ago and saw no mention of fructose. Under dietary factors, they mainly talked about obesity and how that increases insulin resistance, leading to elevated blood sugars, while the reverse happens with weight loss. I haven’t looked at all the research so I have no definite opinion yet on the fructose-diabetes theory; I’m skeptical.

Fructose is a type of simple sugar. Common dietary sources of fructose are fruits, table sugar (aka sucrose, a 50:50 combination of glucose and fructose molecules), and high-fructose corn syrup (which is usually 42 or 55% fructose).

Damaging effects, if any, of fructose in these fruits may be mitigated by the fiber

Damaging effects, if any, of fructose in these fruits may be mitigated by the fiber

A few quotes from ScienceDaily:

“At current levels, added-sugar consumption, and added-fructose consumption in particular, are fueling a worsening epidemic of type 2 diabetes,” said lead author James J. DiNicolantonio, PharmD, a cardiovascular research scientist at Saint Luke’s Mid America Heart Institute, Kansas City, MO. “Approximately 40% of U.S. adults already have some degree of insulin resistance with projections that nearly the same percentage will eventually develop frank diabetes.”

*   *   *

While fructose is found naturally in some whole foods like fruits and vegetables, consuming these foods poses no problem for human health. Indeed, consuming fruits and vegetables is likely protective against diabetes and broader cardiometabolic dysfunction, explained DiNicolantonio and colleagues. The authors propose that dietary guidelines should be modified to encourage individuals to replace processed foods, laden with added sugars and fructose, with whole foods like fruits and vegetables. “Most existing guidelines fall short of this mark at the potential cost of worsening rates of diabetes and related cardiovascular and other consequences,” they wrote.

If you’re eating a typical Western or American diet, you’ll reduce your fructose consumption by adopting the Paleobetic DietMediterranean diet, or Low-Carb Mediterranean Diet.


Steve Parker, M.D.

The Glucagon-Centric Theory of Diabetes Pathology

Perhaps we’ve been wrong about diabetes all along: the problem isn’t so much with insulin as with glucagon.

At least one diabetes researcher would say that’s the case. Roger Unger, M.D., is a professor at the University of Texas Southwestern Medical Center. That’s one of the best medical schools in the U.S., by the way.

Glucagon is a hormone secreted by the alpha cells of the pancreas; it raises blood sugar. (There are also glucagon-secreting alpha cells in the lining of the stomach, and I believe also in the duodenum.) In the pancreas, the insulin-producing beta cells are adjacent to the glucagon-secreting alpha cells. Released insulin directly suppresses glucagon. So if your blood sugar’s too high, as in diabetes, may be you’ve got too much glucagon action rather than too little insulin action.


Don’t ask me what delta cells do

Dr. Unger says that insulin regulates glucagon. If your sugar’s too high, your insulin isn’t adequately keeping a lid on glucagon. Without glucagon, your blood sugar wouldn’t be high. All known forms of diabetes mellitus have been found to have high glucagon levels (if not in peripheral blood, then in veins draining glucagon-secreting organs).

This is pretty well proven in mice. And maybe hamsters. I don’t know if we have all the pertinent evidence in humans, because it’s harder to do the testing.

Here’s Dr. Unger’s glucagon-centric theory of the pathway to insulin-resistant type 2 diabetes: First we over-eat too many calories, leading to insulin over-secretion, leading to increased fat production (lipogenesis) and storage in pancreatic islet cells as triglycerides, in turn leading to increased ceramide (toxic) in those islet cells, leading to pancreas beta cell death (apoptosis) and insulin resistance in the alpha cell (so glucagon is over-produced), all culminating in type 2 diabetes.

For a diagram of this, click forward minute 40 and 10 seconds in the video below.

If this is all true, so what? It could lead to some new and more effective treatments for diabetes. Dr. Unger says that in type 2 diabetes, we need to suppress glucagon. Potential ways to do that include a chemical called somatostatin, glucagon receptor antibodies, and leptin (the latter mentioned in a 2012 article, I think). The glucagon-centric theory of diabetes also explains why type 1 diabetics rarely have totally normal blood sugars no matter how hard they try: we’re ignoring the glucagon side of the equation. I don’t yet understand his argument, but he also says that giving higher doses of insulin to T2 diabetics may well be harmful. I’m guessing the insulin leads to increased accumulation of lipids (and the associated toxic ceramide) in cells.

Not making sense? Try this YouTube video:

Steve Parker, M.D.

PS: Dr. Unger Says: “Without insulin, you can’t get fat.”

Apoptosis: the second p is apparently silent.

h/t George Henderson

If You Have Diabetes, You Need to Know About Glucagon

I couldn't find a pertinent picture

I couldn’t find a pertinent picture

Everybody knows that insulin is the key hormone gone haywire in diabetes, right? Did you know it’s not the only one out of whack? Roger Unger and Alan Cherrington in The Journal of Clinical Investigation point out that another hormone—glucagon—is also very important in regulation of blood sugar in both types of diabetes.

Insulin has a variety of actions the ultimately keep blood sugar levels from rising dangerously high. Glucagon, on the other hand, keeps blood sugar from dropping too low. For instance, when you stop eating food, as in an overnight or longer fast, glucagon stimulates glucose (sugar) production by your liver so you don’t go into a hypoglycemic coma and die. It does the same when you exercise, as your muscles soak up glucose from your blood stream.

Glucagon works so well to raise blood sugar that we inject it into diabetics who are hypoglycemic but comatose or otherwise unable to swallow carbohydrates.

Glucagon also has effects on fatty acid metabolism, ketone production, and liver protein metabolism, but this post is already complicated enough.

So where does glucagon come from? The islets of Langherhans, for one. You already know the healthy pancreas has beta cells that produce insulin. The pancreas has other cells—alpha or α cells—that produce glucagon. Furthermore, the stomach and duodenum (the first part of the small intestine) also have glucagon-producing alpha cells. The insulin and glucagon work together to keep blood sugar in an fairly narrow range. Insulin lowers blood sugar, glucagon raises it. It’s sort of like aiming for a hot bath by running a mix of cold and very hot water.

Update: I just licensed this from

Update: I just licensed this from

Ungar and Cherrington say that one reason it’s so hard to tightly control blood sugars in type 1 diabetes is because we don’t address the high levels of glucagon. The bath water’s not right because we’re fiddling with just one of the faucets. Maybe we’ll call this the Goldilocks Theory of Diabetes.

When you eat carbohydrates, your blood sugar starts to rise. Beta cells in the healthy pancreas start secreting insulin to keep a lid on the blood sugar rise. This is not the time you want uncontrolled release of glucagon from the alpha cells, which would work to raise blood sugars further. Within the pancreas, beta and alpha cells are in close proximity. Insulin from the beta cells directly affects the nearby alpha cells to suppress glucagon release. This localized hormone effect is referred to as “paracrine guidance” in the quote below, and it takes very little insulin to suppress glucagon.

From the Ungar and Cherrington article:

Here, we review evidence that the insulinocentric view of metabolic homeostasis is incomplete and that glucagon is indeed a key regulator of normal fuel metabolism, albeit under insulin’s paracrine guidance and control. Most importantly, we emphasize that, whenever paracrine control by insulin is lacking, as in T1DM, the resulting unbridled hyperglucagonemia is the proximal cause of the deadly consequences of uncontrolled diabetes and the glycemic volatility of even “well-controlled” patients.

*  *  *

All in all, it would seem that conventional monotherapy with insulin is incomplete because it can provide paracrine suppression of glucagon secretion only by seriously overdosing the extrapancreatic tissues.

So What?

Elucidation of diabetes’ disease mechanisms (pathophysiology) can lead to new drugs or other therapies that improve the lives of diabetics. A potential drug candidate is leptin, known to suppress glucagon hyper secretion in rodents with type 1 diabetes.


Steve Parker, M.D.

PS: Amylin is yet another hormone involved in blood sugar regulation, but I’ll save that for another day. If you can’t wait, read about it here in my review of pramlintide, a drug for type 1 diabetes.