Is Excessive Fructose Consumption the Cause of Type 2 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 just read “Pathogenesis of type 2 diabetes mellitus” at 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 moving to the Mediterranean diet, the Advanced Mediterranean Diet, Low-Carb Mediterranean Diet, or the Paleobetic Diet.


Steve Parker, M.D.


Filed under Causes of Diabetes, Sugar

5 responses to “Is Excessive Fructose Consumption the Cause of Type 2 Diabetes?

  1. It may be the damage caused by fructose consumption is not via the URIC acid pathway but via lactate.
    Introduction to the molecular basis of cancer metabolism and the Warburg effect
    “When tumors increase in size, blood vessels supplying nutrients and oxygen relative to the size of the tumor is often not enough to sustain the development of the tumor.
    As a result of the Warburg effect, reduced oxygen supplied to the tumor acts as a compromise, ultimately leading to hypoxia.
    When four molecules of ATP lactate are yielded as a result of aerobic glycolysis in cancer cells, lactate is secreted into the tumor microenvironment .
    The consequence of the release of lactate leads to the development in growth and proliferation of cancer cells, also increasing the likelihood of metastasis.”
    When we look at the lactate response following fructose/glucose consumption we see from
    Fructose metabolism in humans – what isotopic tracer studies tell us “Approximately a quarter of ingested fructose can be converted into lactate within a few of hours. ”

    If we then look at the graphs showing lactate in blood following fructose/glucose meal from
    “Metabolic fate of fructose ingested with and without glucose in a mixed meal”
    we see the potential for damaging changes in acid levels within the normal tight margins.
    See Science Daily article
    “Small change in blood acidity could prove detrimental to kidney disease patients”
    The potentially damaging consequences of higher lactate levels do not appear to have been considered by Rippe although he states
    “dietary fructose (up to 25% of daily energy and 3 g/day-kg in these studies) can metabolically be converted into lactate and further result in blood lactate concentration increases.”

  2. If you give up on science, you can’t knock low-fat, USDA guidelines or anything. We explained at the interaction between fructose and glucose. Fructophobia is a way of dodging low-carb. And there is no “whole food” receptor and no “processed” receptor.

    Support your local biochemist.

    • Jim Jozwiak

      Well, fatty liver disease is a “receptor” of fructose, and it has a biochem connection to T2D, wouldn’t you say?

      • I am not sure what you are saying. I don’t think that we know what causes NAFLD. It would be surprising if carbohydrate were not involved given the role of insulin and glycerol-P in TAG synthesis and the effect of low carb diets on NAFLD. But you don’t know whether glucose is the key player or if fructose is the key player. or if the interaction is most important — what our paper described is how they interact. And of course they have a strong connection to T2DM. My concern is that emphasizing fructose specifically will allow us to maintain low-fat ideas and not face the benefit of low-carb. We have not done the important experiments distinguishing between effects of fructose and glucose. My criticism is that the demonization of fructose has way outstripped the data and is just like demonization of saturated fatty acids which is still with us. The most important consequence is that we will never find out how bad fructose is…or if it is bad at all…or if it is preferable to glucose…or anything…”A Pharm.D (Dr of Pharmacology) and a pair of MD’s surveyed much of the available scientific literature—both animal and human studies—” if it was what Dr. Fine and I surveyed, it could not reasonably come to the conclusion “that fructose is a major culprit in the rise of type 2 diabetes and pre diabetes.” By analogy, we can tell that animals have gotten into our lunch but you need to be sure before you go out and shoot the horses. Ok, not great but all I can think of now.

  3. Jim Jozwiak

    I am not a believer in Dr. McDougall’s approach, which doesn’t work for me–however, it was
    obvious to me that a diet of mostly starch increases insulin sensitivity and whole-body
    glucose disposal while fructose doesn’t do that. And it doesn’t matter if the fructose is from
    whole fruits or sugar–the sugar is more efficient, but the nasty effects are the same.