Published: March 18, 2026
“Eating Meat Is Linked With Diabetes Risk”. This was a headline in the New York Times in 2024. According to the article, every bite of red meat you eat could increase your risk of developing type 2 diabetes, be it unprocessed red meat, such as steak or pork chops, or processed red meat, such as bacon or sausage.
So if you enjoy an occasional steak or burger or some crispy bacon, that headline might make you wonder whether you are setting yourself up for a major chronic disease down the road.
But, …, is it true that eating red meat increases the risk of type 2 diabetes?
Let’s find out by doing what we do on this website: looking beyond the headline and instead at the entirety of the scientific evidence!
Where Does the Claim Come From? The Observational Evidence
Over the last 15 years, a number of observational studies have looked at the association between red meat intake and type 2 diabetes risk.
Observational studies are those where the researchers recruit large groups of participants, and ask them to complete one of these food frequency questionnaires to report on what they usually eat. And then the researchers follow the participants for many years to see who develops diabetes, who has a stroke, and who has cancer, and look for associations between what they ate and the development of these diseases.
For red meat and type 2 diabetes, we have data from 27 such observational studies. The most recent meta-analysis that summarizes all of their findings shows a clear and pretty consistent association, suggesting that eating more red meat increases the risk of developing type 2 diabetes. Specifically, each 100 g serving of unprocessed red meat per day, that’s about 3.3 ounces per day, is associated with a 27% higher risk, if we consider all of the available observational studies. Each 50 g serving of processed red meat per day, that’s about 1.7 ounces per day, is associated with a 44% higher risk of developing type 2 diabetes.
So many people would now think that if this association is seen pretty consistently in more than 20 different studies, then this must be true. And that’s why we have newspaper articles like the one in the New York Times.
I suggest we hold our horses though. Remember that these are observational studies that can detect associations only, so from these studies, we cannot know whether eating red meat actually causes type 2 diabetes.
Aside from the fact that observational studies show associations only, there are some specific concerns in this literature on red meat and diabetes. To understand these limitations, I suggest we take a thorough look at one of the individual studies. That’ll give you a much better sense of how these types of analyses are done, and what some of the key problems in observational studies can be.
To explain this, let’s take a look at the Women’s Health Study.
In that study, about 37,000 women completed a food frequency questionnaire at baseline to measure their normal diet, including their red meat intake, and then were followed for an average of 8.8 years to see who did and who did not develop type 2 diabetes.
The investigators then grouped participants into quintiles based on their unprocessed red meat intake. So the 20% that had the lowest red meat intake, they were all grouped together in quintile 1. Red meat intake was then higher in quintile 2, and so on, all the way to quintile 5, where the median intake was 1.42 servings per day.
In the next step, the researchers assessed how many women in each quintile developed type 2 diabetes. So that’s this number in the table above that shows the cases, and we can see quite clearly that this number goes up steadily from quintile to quintile, suggesting that the more red meat the women consumed, the more likely it was that they developed type 2 diabetes. This number of diabetes cases is then related to the person-years, that’s just the number of people in each quintile times the years of follow up. Because the more people are in a group, and the longer you observe them, the higher the likelihood that people will develop a disease.
In the next step, researchers transformed these numbers to make them easier to grasp. They simply set the risk in the first quintile to 1, so this is the reference group, and now we see that the risk in quintile 2 is 1.06, meaning 6% higher than in quintile 1, all the way up to 2.24 in the fifth quintile, that’s 124% higher risk than in quintile 1. Now, they had already done some statistical adjustments here by factoring in age and total energy intake, both of which are major risk factors for type 2 diabetes. And that makes sense, right? Because even if we think that red meat intake may increase the risk of type 2 diabetes, they don’t JUST develop it because of their red meat intake. Other factors certainly play major roles here.
And that means we need to adjust for several more of these other risk factors, such as physical activity or body mass index. Plus, and this is a key point, we need to adjust for other dietary and lifestyle factors because people who consume the most red meat eat quite differently from people who eat very little red meat. Take a look at the table below.
This compares people who eat the least red meat in quintile 1 with those who eat the most red meat in quintile 5. And what we can see is that those who eat the most red meat have an unhealthier lifestyle in almost every respect: they smoke more, they exercise less, they weigh more, they use fewer multivitamins, they eat way more calories, but less fiber meaning that a much smaller proportion of their food comes in the form of fiber-rich whole plant foods such as legumes, fruits and vegetables. Some of these differences are probably not relevant for type 2 diabetes risk, but some are probably very relevant, and what these differences generally show is that the overall diets and lifestyles of women who eat the most red meat is quite different from those of women who eat less meat.
Now, the concern here is what we call confounding. Confounding means confusion of effects. So we are interested in whether red meat consumption may increase the risk of type 2 diabetes. And we are finding an association, suggesting that, yes, it looks like red meat may increase diabetes risk. Now we have seen that people who eat the most red meat also have an unhealthy diet, they eat a lot more calories, and they exercise less. So what we are worried about is that the association we see between red meat intake and a higher diabetes risk isn’t really because eating red meat causes that increase in risk, but because red meat eaters have this unhealthy lifestyle, and that causes the increase in risk.
As expected, the researchers then statistically adjusted for all these factors, and we can see the relationship between unprocessed red meat consumption and type 2 diabetes risk in the table below, in the line labeled Multivariate Model 2. This is the fully adjusted statistical model that includes all of the main risk factors for diabetes and all of the potential confounders, such as diet and lifestyle factors. And what we see is that the relationship is now quite different, such that there is not much of an impact of red meat consumption on diabetes risk. Maybe an increased risk by 24% in the fifth quintile, but even that is way lower than our initial estimate of a 124% higher risk. So what we can clearly see is that most of that increased risk in women eating the most red meat is probably not because of the red meat, but because of other factors, including their unhealthy diet and sedentary lifestyle.
And I would add that even that adjustment is probably suboptimal. That is because some of these dietary variables that we want to adjust for cannot be measured well with these food frequency questionnaires. Total calorie intake, for example. We know people massively underreport their food intake when they complete these FFQs. On average, by around 25-30%. So that means that if someone actually eats 2,000 kcal per day, on their FFQ, they may report only eating 1,400 kcal per day. But it’s even worse, because the degree to which participants are underreporting is biased such that people who have obesity tend to underreport their calorie intake more. OK, and now, who has the greatest risk of developing type 2 diabetes? People with obesity, for sure.
So, you see the problem with these types of observational studies? It may sound great to have 27 studies with hundreds of thousands of participants, run by reputable researchers who no doubt are very well qualified, but if you look at the details behind the numbers, particularly in studies on red meat, you lose confidence that the observed associations are reflective of actual cause-effect-relationships.
So does this mean we should totally disregard data from these observational studies? No, because just as these studies may overestimate the role of red meat, there are other concerns that may lead to an underestimation. An important one is that in all of these studies, investigators adjusted for body mass index, or BMI. That is certainly correct, because a higher body fat mass, of which BMI is an imperfect indirect measure, is a major risk factor for type 2 diabetes. By all accounts a much, much bigger risk factor. For example, according to this observational study, people with a BMI of 35 kg/m2 or higher had a risk of developing type 2 diabetes that was 93-fold (!) higher than that of people with a BMI of 22 or lower. So, the portion of the risk that is explained by a higher BMI is much, much higher than that explained by eating red meat, or any other individual food for that matter, which means that removing the influence of BMI is a good idea. However, in many of these observational studies, those eating the most red meat also had higher energy intakes and higher BMIs. And that raises the possibility that eating more red meat may partly raise type 2 diabetes risk by causing people to eat more food and gain weight. And if that were the case, then BMI would be a mediator in the relationship between red meat consumption and the development of glucose intolerance and type 2 diabetes, and adjusting for BMI statistically would to some degree be an overadjustment, because we would be statistically removing part of the pathway through which red meat affects type 2 diabetes risk. Now, to be clear, I don’t consider it likely that consuming red meat per se causes overeating and weight gain, as numerous randomized controlled trials do not show such an effect in people consuming diets rich in red meat. However, it is a theoretical concern in an observational study, and there is no perfect way to address the role of BMI as both an important risk factor, a potential confounder, and a potential mediator. Another potential concern in observational studies is that red meat consumption may well be substantially underreported. During the time frame that most observational studies were initiated, there was a strong sentiment against animal fats rich in saturated fatty acids, i.e., they were generally considered unhealthy, and research participants are probably more likely to underreport their consumption of foods considered unhealthy than their consumption of fish or salad. Such underreporting could have limited our ability to detect associations between the consumption of such foods and disease outcomes.
So, given all the potential issues, my conclusion from these observational studies is that we now have a hypothesis. And that hypothesis is that red meat intake may modestly increase type 2 diabetes risk. I don’t have a lot of confidence that this is true due to the numerous limitations inherent in these studies, but that would for now be my best guess.
Now, I wouldn’t base any recommendations or public policy decisions on these rather weak data, but I think it’s an interesting hypothesis to study further because, if it’s true, it would be important to know, right?
OK, if we hypothesize that red meat is associated with an increased risk of type 2 diabetes because it somehow impairs glucose tolerance or insulin sensitivity, it would be a good idea to briefly consider the mechanisms by which this may occur.
Mechanisms Through Which Red Meat Could Affect Glucose Tolerance
When you first heard the claim that red meat causes diabetes, did that make sense to you? I’d argue that for most people, it doesn’t make a lot of sense at first because diabetes is an issue of dysfunctional carbohydrate metabolism, and red meat doesn’t have any carbs.
So the mechanism clearly cannot be that eating red meat acutely makes our blood sugar rise. However, what is possible is that regularly eating red meat somehow makes us insulin resistant or affects our ability to secrete insulin. And indeed, red meat has a few characteristics that have been shown in the past to induce insulin resistance.
For one, we often prepare red meat with high heat, such as grilling, broiling, or frying, and that can lead to the generation of advanced glycation end products. These are formed when sugars attach to proteins or other molecules, which occurs mostly at high temperatures. In the body, advanced glycation end products trigger inflammation, which is one of the most immediate and potent inducers of insulin resistance. And in fact, independent of red meat, we have some good evidence from clinical studies showing that insulin sensitivity is better on a diet low in advanced glycation products, so I do see this as a really plausible mechanism.
The second mechanism is that red meat is a rich source of branched-chain amino acids. These are three specific amino acids that are often enriched in the blood of people with obesity and type 2 diabetes, and in clinical studies, directly infusing a mixture of amino acids rich in branched-chain amino acids into the blood fairly strongly induces insulin resistance. At the same time, the role of branched-chain amino acids is complex and incompletely understood, and it is possible that diet-induced increases in blood branched-chain fatty acid concentrations do not negatively affect insulin sensitivity. Still, I’d say that this is quite a plausible potential mechanism.
The third mechanism is that the iron in red meat could reduce insulin sensitivity and even lead to beta-cell dysfunction, particularly if it triggers an increase in ferritin levels in the blood. I’d say this mechanism is most likely in people who consume a lot of red meat, and particularly in people with iron storage diseases, such as hemochromatosis. In populations that are prone to iron deficiency, such as menstruating women, this is probably not an issue.
A fourth potential mechanism is that red meat is a rich source of carnitine, which the gut microbiota can convert to a substance called TMA, and TMA can then be converted into TMAO by the liver. And according to some studies, TMAO can induce insulin resistance.
And lastly, red meat, particularly fatty red meat, contains a lot of saturated fatty acids, and at least in very high concentrations, long-chain saturated fatty acids have been shown to lower insulin sensitivity. This is not universally seen in studies of saturated fatty acid-rich diets, but is a likely mechanism on diets in which a high content of long-chain saturated fatty acids is combined with chronic caloric excess, as lipid metabolites called ceramides accumulate in liver and muscle in this scenario, which is a key driver of insulin resistance in these tissues.
Now, the science is not conclusive on all of these mechanisms, but I hope this illustrates that the idea that red meat consumption could trigger insulin resistance and contribute to the development of glucose intolerance and type 2 diabetes is not ridiculous.
What Do Randomized Controlled Trial Data Say?
Ideally, we’d have data from a trial in which participants were randomized to a diet rich in red meat vs. one without red meat and then followed for decades to see who develops type 2 diabetes. We don’t have such data, nor will we ever be able to conduct such a study. Imagine randomizing people to having steak every day for the next, say, 20 years, or to never have a steak or burger again. That’s not happening.
However, for diabetes, I argue that we don’t need such data with a hard disease endpoint, because we can directly measure the impact of foods such as red meat on glucose tolerance, insulin sensitivity, and beta-cell function. These are not just risk factors for type 2 diabetes, such as LDL-cholesterol for cardiovascular disease, but they directly measure the endpoints that characterize the disease itself. So let’s take a look at trials that have addressed the question of whether eating a diet rich in red meat causes insulin resistance, beta-cell dysfunction, and glucose intolerance compared to eating a diet low in red meat.
A trial conducted in Germany by Nowotny and colleagues randomized 59 patients with type 2 diabetes to a diet low in red meat or a diet rich in red meat, at 150 g or 6 ounces per day. Participants followed these diets for 8 weeks. If the observational data are correct that red meat actually increases type 2 diabetes risk, then eating this much red meat every day for 8 weeks should be worse for insulin sensitivity and glucose tolerance. So what did they find? Both groups lost the same amount of weight, and liver fat decreased to the same degree in both groups, which is because participants in both groups were encouraged to maintain a slight caloric deficit. Insulin sensitivity, as measured by the gold-standard hyperinsulinemic-euglycemic clamp, improved in both diet groups, and there was no difference in insulin sensitivity between the two diets. Liver insulin sensitivity also did not differ, and there was also no difference in beta-cell function. And as a result, there was no difference in glycemic control, as measured by HbA1c. So this study does not support our hypothesis that there is something about red meat that may cause insulin-resistance, beta-cell dysfunction, and glucose-intolerance. Otherwise, we would have expected insulin sensitivity to improve less on the diet rich in red meat.
OK, what about other RCTs? There are quite a few, and I didn’t want to discuss each in every detail, so I’ve summarized the key findings in the table below. In the first row, you’ll see the study by Nowotny we just discussed, which found no statistically significant difference in insulin sensitivity, beta-cell function, glucose tolerance, and glycemic control when comparing a diet rich in red meat and a diet without red meat. The abbreviation “n.s.” means no significant difference between the high red meat diet and the control group.
The next study, by Turner and colleagues, compared a diet rich in red meat with a diet rich in dairy as well as a diet low in both red meat and dairy. They again found no difference between diets rich vs. low in red meat, but they found higher insulin sensitivity on a diet rich in red meat compared to a diet rich in dairy. No difference in glucose tolerance or glycemic control, though.
The next study is the one by Maki, in which they compared a diet rich in red meat with a diet low in red meat and instead containing more carbs, in participants with prediabetes or metabolic syndrome. They found no difference in any measure related to blood sugar regulation.
Then we have a study by Guzman and colleagues, who compared a diet rich in red meat with a diet rich in poultry in participants with prediabetes, and they again found no significant difference between these two diets in insulin sensitivity, beta-cell function, glucose tolerance, or glycemic control.
We have a few more studies that were not specifically designed to test the impact of red meat on glucose homeostasis or insulin resistance. They were designed for another reason, but they did compare a diet rich in red meat with a control diet low in red meat, and they included measurements of fasting glucose and insulin levels. So these studies don’t have detailed data on glucose tolerance or beta-cell function or gold-standard measurements of insulin sensitivity, but they are still worth considering (see table for overview).
The first study is the one by Hill, who compared a diet rich in red meat with one rich in plant protein in people with the metabolic syndrome. They found no difference in fasting glucose and insulin concentrations. Crimarco and colleagues compared a diet rich in red meat with one using plant-based meat-replacement products from Beyond Meat in healthy omnivores, and they again found no statistically significant difference in fasting glucose and insulin concentrations. Hassanzadeh-Rostami compared a diet rich in red meat with one rich in legumes in participants with type 2 diabetes and again found no differential change in fasting glucose or insulin.
An important potential concern common in these types of secondary data analyses is that, because the study was not designed to assess the impact of red meat on insulin sensitivity, the trial may be underpowered (i.e., too few participants) to detect an effect. It is therefore noteworthy that all three of these studies were solidly null, meaning that there wasn’t even the slightest trend towards a difference in fasting glucose and fasting insulin between the red meat-rich and the control diets.
In other words, the entire evidence we have discussed so far does not support the hypothesis that unprocessed red meat somehow triggers insulin resistance or glucose intolerance. And no major expertise is required to come to that conclusion, because all of these studies are totally negative. The situation becomes a bit more complicated with the next three trials.
Navas-Carretero and colleagues compared a diet rich in red meat with one rich in fatty fish in healthy people, and this one now found lower insulin sensitivity when people were consuming the diet rich in red meat compared to when these same people – note this was a cross-over design study where every participant completed all diet phases – consumed a diet rich in fatty fish.
Azadbakht et al. compared a diet rich in red meat with one rich in either soy protein or whole soy nuts. And in that study as well, the investigators found higher insulin sensitivity on the soy diets compared to the red meat diet.
And lastly, Hodgson and colleagues compared a diet rich in lean red meat with a diet that, instead of the red meat, contained more carbs, in people with hypertension. They saw a trend towards slightly lower fasting glucose and insulin concentrations.
A possible limitation is that these studies were relatively short, typically 4-8 weeks. That may be too short to see all of the effects of red meat on glucose tolerance. For example, if eating more red meat made people gain weight over time, that could lead to an accumulation of fat in visceral and ectopic depots, and that is a major cause of both insulin resistance and beta-cell dysfunction. So this is the type of effect that could have been missed by these short- to medium-term trials. However, I see no good evidence that eating red meat, particularly the lean red meat that was used in most of the trials, increases ad libitum calorie intake and body weight. Unprocessed, lean red meat is very satiating per calorie, and a recent meta-analysis of 24 randomized controlled trials found no differential impact of diets rich vs. low in red meat on body weight. So I don’t think that weight gain on diets rich in red meat is a likely mechanism through which red meat affects diabetes risk. If we look at the other suspected mechanisms through which red meat may cause glucose intolerance we discussed earlier, all of these have been shown to exert their effect on insulin sensitivity in short-term studies of also 4-8 weeks duration, so there is no reason to think that an effect on insulin sensitivity could not have been detected in at least some of these RCTs.
Because some of you will ask, I’ll also mention that some of these studies were funded by Big Beef. I find these studies pretty solid, but it’s fair to say the funding source could have subtly affected the study design to make red meat look better. Definitely a good idea to be aware of this, because we do have good evidence that the funding source does affect the outcomes of studies.
So what do we make of all of this? As I always say, it’s important not to just consider one study, because each individual study has some limitations, but to instead consider all studies together. And if we do that, my conclusion is that eating unprocessed red meat, even a lot of it every day for several weeks or months at a time, does not per se seem to cause insulin resistance, beta-cell dysfunction, or glucose intolerance. Because otherwise we’d see a trend, a signal, in more of these studies of people following diets rich in red meat. What we see instead is that in most studies, no effect is apparent. However, the few trials that did find better insulin sensitivity on the control diet make it seem possible that some foods may be slightly better than red meat for insulin sensitivity and glucose tolerance, most notably fatty fish and soy foods. Now, these are just two studies, and they are pretty limited because they only included fasting glucose and insulin levels as secondary endpoints, and they didn’t include any sophisticated measures of glucose tolerance or insulin sensitivity, so in my mind, I’d frame their findings as a possibility rather than a clear fact.
Summary & Conclusions
Taken together, the observational literature shows an association between eating red meat and a higher risk of type 2 diabetes, giving rise to the HYOTHESIS that eating a diet rich in red meat may CAUSE glucose intolerance. That idea, however, is not supported by randomized controlled trials. In fact, in most studies, there is no difference in insulin sensitivity, beta-cell function, glucose tolerance, or glycemic control in people who eat a diet rich in unprocessed red meat and low in red meat. This includes all of the studies that were specifically designed to investigate this issue. At the same time, there is also no evidence to suggest that eating a lot of red meat improves glucose tolerance, unless eating more red meat helps you lose weight and fat mass, of course. And instead, the limited data suggest that some foods, such as fatty fish or soy may be slightly better for insulin sensitivity and glucose tolerance than red meat, but the evidence is limited, and the difference is small. So the best guidance from all of these studies would be to enjoy unprocessed red meat if you like it, ideally leaner cuts and cooked at lower temperatures, but if you prefer other whole protein foods, these are similarly good options and in the case of fatty fish or soy, potentially slightly better. In any case, I see no strong evidence to cut back on unprocessed red meat to lower your risk of type 2 diabetes.
How about processed red meat, though? The observational data suggest a stronger relationship between processed red meat and type 2 diabetes risk. Unfortunately, we don’t have any RCT data on processed meat, so we are left to speculate. My best guess is that a small amount of processed red meat occasionally is not likely a problem for glucose tolerance, but it can be a rich source of those advanced glycation end products, and because it’s usually pretty fatty and energy dense, it may promote weight gain if you eat a lot of processed red meat. So I would prioritize lean and unprocessed red meat, and treat processed red meat as an occasional indulgence, particularly if it’s fatty.
I hope this was helpful to clarify where the science stands in this area. If you learned something from this blog post, and appreciate the unbiased, evidence-based information we provide about nutrition and chronic disease prevention, please consider becoming a Patron of this website and the associated YouTube channel over on our Patreon page.
Until next time, stay healthy, and take care!
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