Sugar Does NOT Cause Insulin Resistance or Diabetes

Insulin resistance is one of the main components of metabolic syndrome, which increases heart disease risk, diabetes risk, and overall mortality (1).

Diabetes and prediabetes, which are considered to be a result of insulin resistance, have reached epidemic levels. 114 million U.S. adults have diabetes or prediabetes, accounting for a staggering 35% of the entire U.S. population! (2) And the numbers are only increasing.

The worst part is that the current recommendations for handling insulin resistance and diabetes only make them worse. These recommendations center around the mistaken belief that the consumption of carbohydrates, specifically sugar, is to blame for causing and worsening these conditions.

This is a huge problem, to say the least.

What are Insulin Resistance and Diabetes?

Insulin is one of the regulators of our blood sugar.

When we consume any form of carbohydrates, including sugars, our blood sugar increases. The increase in blood sugar triggers the release of insulin, which allows sugar to move from the blood into the cells where it can be used to produce energy.

The conventional view of insulin resistance is that the cells don’t respond as well to insulin (they “resist” insulin’s effects), so the sugar isn’t moved from the blood into the cells, causing blood sugar levels to remain slightly elevated. Diabetes (type 2) is considered to be the result of a more intense form of insulin resistance, where the cells respond even less to insulin and blood sugar levels remain very high.

From this view, the problem in insulin resistance and diabetes is that sugar can’t be transported into the cells where it’s needed. But, as you’ll read in a little bit, this isn’t at all the case. In fact, insulin resistance is only a symptom of the problem.

Why Would Sugar Cause Insulin Resistance and Diabetes?

Carbohydrates, specifically sugar, are typically blamed for insulin resistance and diabetes for 2 reasons:

1. Carbohydrates increase blood sugar, which increases the secretion of insulin. It’s assumed that as our bodies secrete and use more insulin, our cells become less sensitive to it.

This idea clearly reflects the mechanical, reductionist view of the human body that permeates conventional medicine. This view focuses heavily on symptoms, and therefore has a tendency to blame the symptoms for causing the disease or condition.

In the case of insulin resistance and diabetes, this has taken the form of blaming foods that raise blood sugar and increase insulin secretion. (The same has happened with heart disease and cholesterol, as I explained here)

But, just because blood sugar increases and insulin can’t properly function in these conditions doesn’t mean that insulin resistance and diabetes are caused by too much insulin or the raising of blood sugar.

Aside from this idea being born out of the mechanical and reductionistic views of the human body, there is little evidence, if any, supporting that cells become less sensitive to insulin as they’re exposed to more insulin or higher blood sugar levels.

However, there is substantial evidence against this idea, including that high carbohydrate and sugar intakes are not associated with insulin resistance and diabetes (3, 4, 5, 6, 7). And, that increasing carbohydrate consumption actually increases insulin sensitivity (the opposite of insulin resistance) (8, 9, 10, 11, 12).

When considering that our bodies complex, adaptive systems, this isn’t surprising. Instead, it’s the expected, logical adaption to increased carbohydrate intake.

2. Carbohydrates, specifically fructose, can stimulate inflammatory pathways that cause insulin resistance.

Fructose doesn’t raise the blood sugar and increase insulin like most carbohydrates, but it’s considered the culprit for insulin resistance due to its “inflammatory and fat-producing effects.”

However, as I explained here and here, sugar, and specifically fructose, doesn’t cause inflammation and fat-production in humans unless it’s consumed in extremely large quantities (like the equivalent of 40 cans of soda over 2 days) or it isn’t being efficiently used to produce energy (we’ll talk more about this in a little bit). And, the inflammation it causes is very different from the chronic inflammation that underlies chronic diseases.

One thing that I didn’t mention in those articles is that when those inflammatory and fat-producing pathways are stimulated, they also cause insulin resistance.

But, like the “inflammation,” this insulin resistance is only temporary and doesn’t have the same consequences as the insulin resistance in metabolic syndrome and diabetes.

Instead, this temporary insulin resistance is a protective mechanism that stops more fructose from entering a liver that already has more than enough fructose. But as the liver uses this fructose, the insulin resistance dissipates.

This temporary insulin resistance is similar to the insulin resistance seen in response to low-carb and ketogenic diets, which often dissipates once the body becomes accustomed to glucose metabolism, as talked about here.

It may sound like I’m saying that not all insulin resistance is the same. And, that’s kind of true, but it would be more accurate to say that insulin resistance is only one part of the picture. The important question is why is the insulin resistance there?

It All Comes Down to Energy

As I mentioned earlier, the conventional idea that insulin resistance occurs because our cells no longer respond as well to insulin, preventing them from getting enough sugar, is a fallacy. In fact, insulin resistance isn’t the problem at all, but we’ll get to that in a second.

The problem in diabetes isn’t that the cells can’t get enough sugar, it’s that they can’t use the sugar they have to produce energy (13, 14, 15, 16). Because sugar isn’t being used to produce energy, it builds up in the cells. This blocks more sugar from entering the cells, which prevents insulin from doing its job (15).

In this situation, even giving someone extra insulin doesn’t increase the amount of sugar that enters the cells or the amount of sugar used to produce energy (13, 14, 17).

Plus, because sugar can’t enter the cells it remains in the blood, which partially accounts for the high blood sugar seen in diabetes.

And, due to the cells’ inability to use sugar to produce energy, those with diabetes have elevated levels of glucagon and cortisol, which are typically elevated under conditions of low blood sugar (or more accurately, low energy supply), despite the high blood sugar seen in diabetes (18, 19, 20).

These stress hormones cause the liver to continue to release large amounts of sugar, which is largely responsible for the high blood sugar seen in diabetes (17).

In other words, insulin resistance isn’t really the problem in diabetes! The problem is an inability to use sugar to produce energy, which inhibits the function of insulin. The lack of energy also causes high levels of glucagon and cortisol, which cause the liver to release large amounts of sugar and results in high blood sugar.

Instead of being the underlying problem, insulin resistance is simply the way that our cells say “we don’t need any more fuel.”

It can happen under conditions of extreme fructose excess or a low-carb/ketogenic diet, as was mentioned earlier. But, it’s really only a symptom of a problem when energy production is inhibited (like in diabetes), in which case the real problem is the lack of energy!

With that in mind, carbohydrates, including sugar, are most definitely not the cause of insulin resistance and diabetes. And, avoiding carbohydrates simply avoids the problem rather than solving it.

If you want to learn more about what actually causes type 2 diabetes and insulin resistance, check out this video. And, make sure to sign up for the free mini-course below, where you’ll learn how you can correct energy production and usage in order to improve these conditions!

  • Kristy Alford
    Posted at 22:37h, 09 March Reply

    Great article! I wish we could do an experiment and get 100 people who have diabetes and get them to stop eating PUFAs for a year and see what happens. Might just be the proof we need!

    • Jay Feldman
      Posted at 11:19h, 10 March Reply

      Thanks Kristy! I wish we could too, it would be a great experiment!

  • D Sharp
    Posted at 15:45h, 26 March Reply

    Given the statement below and your comments I could conclude fructose and sucrose are equal as far as insulin issues are concerned. However, the hypertriglyceridemia caution with fructose use is something I’ve experienced personally. How do you view this? The reference is from the cited article in the Journal of Nutrition. This is for my information and learning, not being argumentative.

    Both fructose and sucrose are associated with lower glucose excursions after ingestion, and some recommendations have even advocated the use of fructose as a beneficial sweetener for individuals with type 2 diabetes. The most recent nutritional recommendations of the American Diabetes Association do not advocate or discourage the use of these sweeteners on the basis of available data. They do caution about the development of hypertriglyceridemia with high fructose diets. Epidemiologic studies have also failed to show a relationship between fructose or sucrose consumption and the development of type 2 diabetes.

    • Jay Feldman
      Posted at 17:14h, 26 March Reply

      Don’t worry, you’re not coming off as argumentative.
      If the liver is healthy, fructose shouldn’t cause hypertriglyceridemia. I explained in more detail why fructose doesn’t increase triglycerides (as long as the liver is healthy) in this article:
      If you found that consuming fructose increased your triglycerides, then PUFA, endotoxin, or nutrient deficiences would be the most likely culprits.

  • D Sharp
    Posted at 23:01h, 26 March Reply

    Thank you. And yes, it is helpful to read the article you cited. Most helpful, and one corresponding to my experience, is the statement that when there is too much fructose for the liver to handle, the fructose is converted to triglyderides. When I dropped from a 2:1 Carb to protein ratio to a 1.5:1 ratio my triglycerides dropped also. I’m please this happened, but I like to know the why behind the what. Your articles makes sense of it. I will also bear in mind the other causes cited in your reply.

    • Jay Feldman
      Posted at 10:50h, 27 March Reply

      You’re welcome, I’m glad the article was helpful. If a 2:1 carb to protein ratio caused an increase in triglycerides then your liver may not be functioning optimally. Ideally, your liver should be able to handle more fructose, so I would consider the other causes I mentioned which might be impairing your liver’s ability to use the fructose.

  • D Sharp
    Posted at 16:17h, 28 March Reply

    I’ve been thinking about your reply and how it relates to de novo lipogenesis not occurring until approx 500 grams carbs are ingested. To me it seems the taste for sugar is a good gauge for when enough is enough. In relation to increased triglycerides with carbs being no where near the amount to instigate DNL it may not be the carbs/liver that are faulty. Turnover of adipose tissue (which can be saturated or PUFA) also instigates high TG and does so at a higher percentage than DNL. TG from this type turnover can last for 6-9 months. I’m sort of talking out loud here, but if my taste for sugar is not satiated at a 1.5:1 carb/protein ratio then perhaps it is the fat turnover creating the high TG and not liver issues. I’ve been concentrating on the idea of it being an excess of carbs relative to what the liver could assimilate but never could really buy into it as I never came near the 500grams threshhold for DNL and often could have eaten more carbs than I was doing. For me, it is real clear when I’ve had enough sugar of any type. Taste for it completely turns off. It is also possible the niacinamide daily is doing its job in slowing down FFA’s release and without it the TG could be higher.. Your thoughts?

    • Jay Feldman
      Posted at 17:47h, 28 March Reply

      Keep in mind that in the study showing that DNL doesn’t occur until around 500 grams of carbs are ingested, the subjects were in a glycogen-depleted state. So DNL may occur with fewer than 500 grams of carbohydrates depending on the context.
      Could you elaborate on the idea of adipose tissue turnover increasing TG levels? Do you have a source? Triglyceride levels seem to be inversely related to adipose tissue turnover, although I haven’t looked into this extensively and may be missing something:
      I’ve also found that taste is a good gauge for determining what and how much to eat. But having a taste for more sugar can mean that your body wants it even though it can’t properly use it – this is pretty common. So I don’t think that’s evidence against liver issues.
      Niacinamide could definitely be reducing FFA and TG.
      Considering that the 500g threshold is probably not relevant to your situation and that the change in TG levels was noticed when carbohydrates were increased, I think impaired liver function is the most likely answer. But with such an incomplete picture it’s hard to say.

      • D Sharp
        Posted at 10:55h, 21 May Reply

        So sorry for delay in thanking you for your reply. I do appreciate your thoughts on this subject. The reference for TG turnover is: I was actually searching for an answer to my Mom’s increased TG to 400 with a decrease in calories and a 25lb weight loss fairly quickly. She is 84. It just did not make sense to me for TG’s to be that high with overall decreased calories. It gave thought to my own situation also.

        Again thank you for replying and giving me more to consider.

        • Jay Feldman
          Posted at 22:16h, 21 May Reply

          No problem. I think in that case it’s likely that the rapid weight loss accounts for the high triglycerides as opposed to DNL.

  • Lee
    Posted at 21:08h, 13 October Reply

    Who funded your research?

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