Published on Feb 13, 2026
If you have type 2 diabetes or prediabetes, you have probably heard that you have an increased risk of having a heart attack or a stroke. It’s often assumed that this is only because of the chronically elevated blood sugar levels in these conditions, and that the only thing you’d need to do is ‘manage’ your blood sugar to bring your cardiovascular risk down to normal levels. That assumption is not correct. It’s not just your high blood sugar doing the damage. What has become clear is that the root causes commonly underlying glucose intolerance are at least as harmful as the chronically elevated blood sugar levels themselves.
So if you have type 2 diabetes or prediabetes, I will explain in this blog post WHY you have an increased risk of having a heart attack or a stroke, why it’s insufficient to just ‘manage’ your blood sugar levels, and what you should do instead to very meaningfully lower and potentially normalize that increased cardiovascular risk.
We will do this by discussing two fictitious individuals, Dave and Erin, who have impaired glucose tolerance and, as a result, elevated blood glucose levels, and both of whom are concerned about this raising their cardiovascular disease risk.
Dave is a 55-year-old African-American man with type 2 diabetes. His fasting glucose is typically around 140 mg/dL, and his most recent HbA1c is 7.4%, suggesting an average blood glucose of about 166 mg/dL. And that is even though he is already taking the anti-diabetes medication metformin. His fasting triglycerides are 180 mg/dL, his LDL-cholesterol is 145 mg/dL, and his HDL-cholesterol is 40 mg/dL. He also has elevated blood pressure, typically around 145 over 90 mg/dL. His doctor is quite concerned and tells him that his risk of having a heart attack or a stroke in the next 25 years is around 41%. He suggests adding more medications to control blood sugar levels better, and also to lower his LDL-cholesterol and blood pressure.
Erin is a 48-year-old Asian-American single mother of three children. She is very busy, often stressed, and doesn’t sleep well. She has recently been told that she has prediabetes, with fasting glucose often around 110 mg/dL and an HbA1c of around 6.0%. Her doctor isn’t too concerned about the prediabetes, and just recommends exercising more and trying to cut back on sweets and baked goods.
Now let’s take a look at WHY it is that Dave in particular has a very high risk of atherosclerotic cardiovascular diseases, or ASCVD, such as a heart attack or a stroke, and why even Erin should be aware that her prediabetes isn’t benign and also raises her risk.
Links between Prediabetes, Type 2 Diabetes and ASCVD
One obvious mechanism through which prediabetes and type 2 diabetes increase the risk of ASCVD is due to the elevated blood sugar levels. Having chronically high blood glucose levels is harmful to the endothelial cells lining our blood vessels, and glucose can also bind to various proteins and alter their function when blood glucose levels are chronically elevated. However, it’s important to be clear that in someone with prediabetes or type 2 diabetes, the elevated blood glucose levels are not the only issue. Instead, the fact that blood glucose concentrations are chronically elevated is ALWAYS a sign that something else in the body is not functioning optimally. And these other things that cause the blood sugar levels to be high are also often risk factors for ASCVD. Specifically, people who have type 2 diabetes or prediabetes are often insulin resistant, and that insulin resistance is a concern because, for one, it causes chronically high insulin levels, which is in and of itself a risk factor for ASCVD. One particular effect of hyperinsulinemia worth highlighting in this context is that when insulin levels are high, our kidneys have a hard time excreting sodium, and through this and other mechanisms, insulin resistance and hyperinsulinemia can cause hypertension. And so, it may not be a coincidence that Dave also has high blood pressure.
But there is more: if someone is insulin-resistant, we need to understand WHY they are insulin-resistant, because the factors that cause insulin resistance are often also risk factors for ASCVD.
Let’s take a concrete look at Dave. As we mentioned, Dave carries too much body fat. And he does not know this yet, because it has never been measured, but he specifically carries too much fat in the fat depots that surround his inner organs, deep inside his belly. We call this type of fat visceral fat or intra-abdominal fat. Everyone has a little bit of fat stored there, but if it’s too much, it can be a major cause of insulin resistance. When it’s expanded as it is in Dave, we often also find a low-level of chronic inflammation in this fat tissue, and that inflammation can directly induce insulin resistance. And because this fat tissue directly surrounds all of the inner organs, including the heart, such an expanded and inflamed visceral fat is also thought to increase the risk of atherosclerosis, particularly of the coronary arteries.
But Dave doesn’t just have excess visceral fat. He also has fat inside tissues that are not designed to store body fat at all. We call this type of fat ectopic fat, and it includes fat stored in muscle tissue and inside the inner organs, such as the liver and the pancreas. This type of fat is a real problem, because it is arguably the most important cause of insulin resistance (at least at this moment in time, where excess body fat is so common) and, by the way, intra-pancreatic fat is also a major cause of pancreatic beta-cell dysfunction, meaning that fat stored in the pancreas reduces the amount of insulin the pancreatic beta-cells can produce. So ectopic fat can be a cause of both insulin resistance, while also reducing the ability of the pancreas to secrete insulin.
But ectopic fat is bad for another reason. If we have a lot of fat in our liver, it tries to get rid of it by assembling lipoprotein particles called VLDL, which show up as elevated fasting triglycerides, like Dave’s at 180 mg/dL. And because VLDL particles are a precursor to LDL particles, this cascade also drives up the number of LDL particles, which probably contributes to Dave’s LDL-cholesterol also being pretty high. In short: excess liver fat causes an unfavorable shift in our fasting blood lipids.
But there is more: insulin resistance can be caused by many different things, not just excess visceral and ectopic fat. In Dave’s case, he also leads a very sedentary lifestyle: he sits a lot while commuting, in his office, while eating, and in his free time while watching TV. Not using your muscles enough in such a sedentary lifestyle is, in and of itself, a major cause of insulin resistance, as is having a low muscle mass. In a prior blog post, I summarized evidence showing that low muscle mass and a sedentary lifestyle are causes of insulin resistance. And all of that is relevant here because a lack of physical activity is also a major risk factor for ASCVD.
There are also a number of medical conditions that can cause insulin resistance, and Dave has one of these. Again, he doesn’t know this yet, but for years his wife has been telling him that he snores like crazy, and he often is tired during the day. He has obstructive sleep apnea, and sleep apnea can cause insulin resistance, and it is also a risk factor for ASCVD. In essence, not getting enough oxygen, and enough sleep, is bad for pretty much everything.
Dave also has a pretty poor diet, where he mostly eats energy-dense foods that are rich in carbs and fats, but low in micronutrients. Examples are his typical breakfast of white toast with butter and jam, or his lunches, which usually consist of a meal at a fast-food place. He also often snacks in the evening in front of the TV, having large bowls of chips or crackers and a few beers. Now, these types of meals are absolutely terrible for someone with diabetes, partly because they will trigger a huge acute increase in blood sugar and insulin after each meal, but also because they will make his condition worse over time. These types of meals have numerous characteristics that make overeating calories and weight gain more likely, and as we established, one issue with Dave is that he already carries too much body fat, so much so that his body doesn’t know where to put it and is forced to store it in tissues such as muscle and the liver that are not made for fat storage. Further, because his diet mostly provides a lot of empty calories, but not a lot of micronutrients, he is micronutrient-deficient. For example, his blood vitamin D level is very low, and his intake of several critical micronutrients, including magnesium, zinc, vitamin C, and several B vitamins, is far below the recommended levels. Now, again, all of this is a concern because several of these micronutrient deficiencies are risk factors for insulin resistance, and – even though our evidence in that area is incomplete – likely also not a good thing for cardiovascular health.
Taken together, what we can see is that with his type 2 diabetes, Dave is not just suffering from elevated blood glucose levels, but also insulin resistance and a whole host of issues that are both causes of that insulin resistance and that in and of themselves are also risk factors for ASCVD.
Erin is in better shape: while she is overweight, she only carries a little excess visceral fat. She doesn’t have a lot of ectopic fat, though, and we are also not seeing evidence of inflammation in her. Erin has other issues, however, that cause her to also be insulin resistant: she has thyroid disease, and sometimes she doesn’t have the cash needed to get her prescription filled for her thyroid hormone medication. She is also chronically sleep deprived, and very often feels stressed juggling her work, raising her kids, and all of the financial responsibilities. She is also way too sedentary and just doesn’t find time to exercise regularly. All of these are again issues that cause her to be insulin resistant, and many of these are also in and of themselves risk factors for ASCVD.
Next, we’ll take a look at the common medical approach to cases like these.
The Common Approach Is a Good First Step, But Insufficient
So if Dave sees his doctor, it is likely that the doctor will prescribe several different medications. His blood sugar control is not particularly good, and so he may be prescribed another medication to help lower his blood sugar concentrations. He may also be prescribed a statin to lower his LDL-cholesterol (or, what really matters, his apo B), and a blood pressure-lowering medication as well. And don’t get me wrong, none of this is a bad idea and certainly much better than doing nothing.
Dave would now be taking two medications for his blood sugar control, one statin to lower his lipids, and one blood pressure-lowering medication. We can expect that his LDL-cholesterol would drop by maybe 50 mg/dL, and his blood pressure would normalize. What would this do to his risk of having an ASCVD event?
A few studies have looked at this question. In a paper published in 2018 in the very prestigious New England Journal of Medicine, investigators assessed the risk of having a heart attack or a stroke in patients diagnosed with type 2 diabetes, and compared that to non-diabetic controls who had the same age and sex. The patients with type 2 diabetes were categorized based on how many ASCVD risk factors they had. These risk factors included a poor glycemic control, as measured by an HbA1c of 7.0% or higher, blood pressure of 140/80 or higher, LDL-cholesterol of 97 mg/dL or higher, presence of kidney disease, and smoking. The key finding was that in someone with type 2 diabetes who also has all five of these risk factors, their risk of having a heart attack would be 5.28-fold higher than in non-diabetic controls. In contrast, patients with type 2 diabetes who do not have any of these five risk factors have about the same risk of having a heart attack as non-diabetic controls. So based on this, one could argue that type 2 diabetes is not so bad and actually doesn’t raise our risk of having a heart attack or a stroke, as long as we control our blood sugar level, our lipids, our blood pressure, and make sure we don’t get kidney disease and don’t smoke. Now, this conclusion is incorrect. That is because the control group in this study was defined only as not having diabetes and having the same age and sex as the group of patients with diabetes. We don’t know their ASCVD risk, though, and many in this group will have high levels of LDL-cholesterol, high blood pressure, maybe prediabetes, and many will smoke or have kidney disease. And we know this because all of these conditions are common, and as a result, the risk of having a heart attack or a stroke in the normal population is already quite high. After all, cardiovascular diseases are still the number one cause of death in most countries.
In other words, these data suggest that someone with diabetes still has elevated ASCVD risk even if they control their blood sugar, their fasting lipids, their blood pressure, if they don’t smoke, and they don’t have kidney disease, if we compare their risk against that of truly healthy controls with no ASCVD risk factors.
That conclusion is supported by another study that showed that the risk of having an ASCVD event is still 21% higher in patients with type 2 diabetes than in controls, even if the diabetes patients have none of these risk factors. Again, though, we are comparing patients with type 2 diabetes without risk factors to a control group that has a lot of risk factors: 17% of the control patients in this study were smokers, 8% had kidney disease, 42% had high cholesterol, and 15% had high blood pressure.
The challenge in this research, it turns out, is finding a control group that is truly healthy and does not also have an elevated risk of ASCVD. But the conclusion is still that yes, patients with type 2 diabetes can substantially reduce their elevated ASCVD risk by controlling their blood sugar reasonably well and keeping their other traditional ASCVD risk factors, such as LDL-cholesterol, blood pressure, and smoking, under control. However, their risk still remains elevated compared to that of truly healthy people.
We can illustrate this as well using an ASCVD risk estimator. I like this one here that estimates the risk of a heart attack or stroke up to age 80. So Dave’s risk of having a heart attack or a stroke with his blood sugar somewhat suboptimally controlled, and with elevated fasting LDL-cholesterol, triglycerides, and blood pressure, was around 41%. If he adds another anti-diabetic medication to bring his HbA1c to below 7%, a statin to lower his LDL-cholesterol to below 100 mg/dL, and a blood pressure-lowering medication to bring his blood pressure into the normal range, his 25-year risk of having a heart attack or stroke would drop to around 11%.
That is a very meaningful reduction in his ASCVD risk. However, as we’ll see later in the blog post, Dave’s risk would be much lower still if he didn’t have diabetes. And so, one major downside of just managing the elevated blood sugar levels and controlling other ASCVD risk factors with medication is that Dave still has diabetes, and that we are NOT doing ANYTHING about the root causes underlying Dave’s glucose intolerance. As a result, we don’t even know that in his case, his insulin resistance is caused by excess visceral and ectopic fat, an extremely sedentary lifestyle, obstructive sleep apnea, and a deficiency in several critical micronutrients. So if the only thing he changed was to take more pills, all of the causes of his glucose intolerance would still be in play: if he continues following his poor diet, he will have substantial glucose and insulin responses after each meal. If he continues his sedentary lifestyle, that will reduce his muscle mass more and more over time, it will lower his cardiorepiratory fitness, and the combination of a poor diet low in micronutrients and low muscle mass will lead straight to osteoporosis as he ages. Because his fatty liver disease is not being treated, he will have a substantial risk of advanced liver diseases, such as fibrosis and eventually cirrhosis, and his eyes, his kidneys, and his nerves may be damaged. Because, in spite of two anti-diabetic medications, he still has diabetes, and all of the root causes underlying that diabetes are still there and affecting his long-term chronic disease risks.
For Erin, the situation is a bit more benign, and most often, a doctor would not do much about her prediabetes. If she had high cholesterol or blood pressure, she’d get a prescription to treat these, but the issue is the same as with Dave: there clearly are some things going on with her that are making her glucose intolerant. And quite often, such root causes are not addressed.
The big issue I see with the conventional approach is that it’s a huge missed opportunity.
Let me explain.
What to Do Instead: Identify the Root Causes
I am a huge fan of seeing a disease like type 2 diabetes and even prediabetes as a warning sign, as a trigger to ask the question: what is going on here? Why is my body no longer able to keep my blood sugar within the normal range?
So let’s ask these questions for Dave and Erin.
The very first thing Dave should do is assess his insulin sensitivity and beta-cell function. We can do that using the poster below, which you can download here. Dave uses his fasting glucose level, which is 140 mg/dL, or 7.8 mmol/L, and his fasting insulin, which is 10 uU/mL, and places a dot on the poster.
And this would give us an estimate of Dave’s insulin sensitivity and beta-cell function, i.e., how well his beta-cells are able to make enough insulin for his level of insulin sensitivity. Dave’s insulin sensitivity is about 25% of normal, and his beta-cell function is at about 50% of normal. So what this indicates is that Dave is pretty insulin resistant, and at his level of insulin resistance, his beta cells are NOT able to fully meet the increased demand for insulin. As a result, he may actually have fairly high insulin levels after meals rich in carbs, but not enough to keep his blood glucose in the normal range, and he is therefore glucose intolerant and has chronically elevated blood glucose concentrations. This is very important information because, as you will see, there are many ways we can improve insulin sensitivity, and even a few we can try to improve beta-cell function.
OK, the big takeaway here is that Dave is pretty insulin-resistant, and this should now trigger efforts to figure out WHY he is insulin-resistant. He could start his quest to identify the causes and contributors to insulin resistance through this blog post.
Dave knows that carrying too much body fat can be an issue, and he now wonders whether he may have excess visceral and ectopic fat. He completes an MRI scan, which shows that he has a lot of visceral fat, and his liver fat content is at 10%. So that suggests pretty strongly that one reason why Dave is so insulin-resistant is that he is carrying a lot of excess visceral fat, and because he has a fatty liver.
His chronic snoring and daytime fatigue are also major red flags that prompt him to request a sleep test, during which he learns that he has obstructive sleep apnea.
He also realizes that his diet quality is pretty poor. He eats a lot of refined carbs, which he now understands would cause his blood glucose AND insulin levels to go on a major rollercoaster after every meal. His diet is also not very satiating per calorie, so he needs to eat a lot of calories to feel comfortably full, and that is why he has been overeating for years and has gained so much weight. He also realizes that he eats a lot of empty-calorie foods and may be micronutrient-deficient as a result. Lastly, by taking a thorough look at his dietary habits, Dave realizes that one problem may relate not to WHAT he eats, but to WHEN he eats: he basically eats or drinks something as soon as he gets up in the morning at 7 AM all the way through late at night when he still snacks and has a beer right before going to bed.
Dave also becomes painfully aware of the fact that his very sedentary lifestyle is probably contributing to his insulin resistance and glucose intolerance. He hasn’t engaged in any kind of formal physical activity in years, and sits almost all day.
Taken together, Dave has a clear understanding now that his poor diet quality, sedentary lifestyle, his sleep apnea, and his excess visceral and ectopic fat are very likely the root causes of his insulin resistance and glucose intolerance.
How about Erin? Even though she ‘only’ has prediabetes, I recommend the same approach. That surprises some people, but already prediabetes is clearly a risk factor for several chronic diseases, and if we don’t address the root causes that have made us prediabetic, we have a very high likelihood of developing manifest type 2 diabetes. And I say: why wait? Address the root causes now, and normalize your blood sugar as soon as you can. Because even though it’s ‘only’ prediabetes, the normal regulation of blood glucose levels no longer works well, and all of the underlying problems, such as insulin resistance, as well as whatever is causing the insulin resistance, will also already be present. She realizes that her poorly controlled thyroid disease could be a factor, and that her lack of sleep, her stressful lifestyle, and her lack of physical activity could all be contributing factors. She vows to tackle these.
Addressing the Root Causes
So, how specifically do Dave and Erin need to change their diets and lifestyle to address these issues that are making them glucose intolerant?
Let’s start with Dave again.
Dave will change his diet to be centered around micronutrient-dense whole foods rich in protein and fiber and lower in refined carbohydrates. For example, he changes his breakfast from white toast with butter and jam to Greek yogurt with fruit or berries and a handful of nuts. For lunch and dinner, he focuses on protein, like meat, fish, eggs, or beans, lentils, or tofu, paired with a generous serving of fiber-rich whole plant foods, such as salad, leafy greens, cruciferous, or root vegetables. He also has mushrooms regularly now. If he also wants some more carbs, it’s fine to add some whole grains, but maybe later in the meal, as that’ll reduce the impact of the carbs on blood sugar if some fiber- and protein-rich foods have been eaten first. The latter strategy particularly makes sense for patients with poorly controlled type 2 diabetes, because eating meals with a high glycemic load without accompanying fiber and protein can lead to huge increases in glucose and potentially insulin. He also decides to avoid ultraprocessed and fast foods as well as sugar-sweetened beverages altogether, and to limit alcoholic beverages to one drink per week.
Why do I recommend such a dietary approach? For one, this diet would dramatically reduce how much Dave’s blood glucose and insulin levels rise in response to each meal, because it is low in high-glycemic index foods such as refined grains and added sugars, and because if carbs are eaten, they are eaten with or after a solid serving of a fiber-rich and a protein-rich food. So, acutely, this way of eating will help him lower both his blood glucose and his blood insulin levels throughout the day. That’s a big plus. Maybe more importantly, this diet would be extremely satiating per calorie, and this helps Dave feel full even though he is eating substantially fewer calories than before. This way of eating also eliminates or strongly limits all of the known triggers of overeating, such as hyperpalatable ultra-processed foods or liquid calories in the form of sugar-sweetened and alcoholic beverages. I am therefore fairly certain that if Dave switches from an average American diet rich in ultra-processed foods, fast foods, refined grains, and added sugars to this type of fiber- and protein-centered, micronutrient-dense whole-foods diet, he will spontaneously eat fewer calories without even trying and lose some weight. So with this diet, he has a good chance of lowering his body fat mass, specifically visceral and ectopic fat, and by eating a wide variety of micronutrient-dense foods, he also dramatically improves his chances of meeting his micronutrient needs.
If he is unable to lose enough weight with this approach, he could add on additional strategies. These include the use of meal-replacement shakes or shifting the dietary macronutrient into a more extreme low-carb or low-fat direction, based on his preference. This should still be done while applying the principles outlined above: focus each meal on fiber-rich and protein-rich foods first and foremost, as these are also consistently rich in micronutrients and highly satiating.
There is one micronutrient that even the best diet cannot provide enough of: vitamin D. Dave should have his blood level measured and supplement to get it to 30 ng/mL or higher.
Dave also wants to address WHEN he eats, and now adopts a mild form of time-restricted eating, or TRE, and eats only during a 10-hour window during the day, between 8 AM and 6 PM. Overnight, he fasts for 14 hours. Occasionally, he makes an exception when he goes out with his wife or when friends come over to play cards, but most of the time, he does not eat between 6 PM and 8 AM the next day. Research shows that TRE in general can help people reduce their calorie intake and lose weight, and this form of early TRE, where meals are only allowed in the earlier part of the day, also has additional benefits for glucose tolerance that are partly independent of whether or not they’ll lose weight.
Dave is also correct to suspect that his sedentary lifestyle and his low muscle mass could contribute to his insulin resistance and glucose intolerance. Exercise plays a huge role in blood sugar regulation. For one, muscles that are contracting can take up glucose from the blood in a manner that is independent of insulin, so this is a way for insulin-resistant and diabetic people to lower their blood glucose levels very effectively after a meal high in carbs. Even more important, exercising makes muscles more insulin sensitive, and that effect persists for a few days after each workout. Building more muscle mass is also very important, because the muscle tissue is the main tissue that takes up glucose from the blood after a meal, so having more muscle equals better blood sugar regulation, all other things being equal. Certain types of exercise, such as high-intensity interval training (HIIT), also are effective at helping reduce visceral and ectopic fat. And lastly, exercising while losing weight helps preserve muscle mass, so, in my opinion, exercise, particularly resistance training, should be a part of any weight-loss program. And while exercising by itself does not have a huge impact on weight loss, having a regular exercise routine can play a major role in helping maintain a lower body weight once we have lost weight. Dave decides to do resistance training twice a week in his garage, and high-intensity interval training, or HIIT, twice a week in his living room. He also bikes to work every day now, and takes a break after lunch to walk through a park.
Aside from that, it is very important for Dave to treat his obstructive sleep apnea. That likely means using a CPAP machine at night to reduce episodes of low oxygen intake.
Now, with these changes, I would be shocked if Dave’s blood glucose levels did not come down over time, and in my mind, he may very well be able to move his numbers into the prediabetes range within the first six months and achieve totally normal blood glucose regulation within a year. Now, let me be clear: not everyone can fully reverse their type 2 diabetes, but many people can, and I am certain that every patient would be much better off, including having much lower ASCVD risk, if they at least TRIED to identify and address the root causes underlying their diabetes.
So, what about the medications his doctor prescribed for him? Of course, even if Dave starts with his new diet and lifestyle, as I suggest here, he should follow the recommendations of his doctor, and take all of the medications that were prescribed to him. It is important to be clear that I don’t see medications and diet and lifestyle changes as mutually exclusive. What I suggest, however, is that in all cases where we have a disease, we try to identify and tackle the root cause or causes of that issue as well. And a lack of medications is never the root cause of a disease.
That said, it is also likely that he can reduce or even drop his anti-diabetes medications as his glucose tolerance improves. There is also a very good chance that he won’t need his blood pressure-lowering medication for a long time with the dietary and physical activity changes he is making, particularly if he improves his insulin sensitivity. Because he has diabetes and therewith a high risk of ASCVD, I think keeping lipids as low as possible makes sense, so if I were Dave, I would recommend continuing to take the statin even if he were able to put his type 2 diabetes into complete remission. That is because his arteries will have suffered from many years of insulin resistance and high glucose levels, and I would want to keep all other risk factors as low as possible.
At the same time, it is also possible that medications could help him if he does not achieve his goals by diet and lifestyle change alone. For example, if he is unable to reduce his body weight enough to eliminate all of the damaging excess visceral and ectopic fat, he may want to consider one of the new GLP-1 receptor agonist drugs. That is because the data are clear that carrying excess visceral and ectopic fat is highly damaging to our health, and getting rid of that comes with tremendous long-term benefits.
I would encourage anyone with type 2 diabetes to use this blueprint: determine your level of insulin sensitivity and beta-cell function, identify the root cause or causes of any insulin resistance or beta-cell dysfunction, and address them.
OK, now, why am I suggesting that these substantial changes to diet and lifestyle are preferable to just taking medications to control the blood sugar and all ASCVD risk factors?
Impact of Reversing Prediabetes or Type 2 Diabetes on ASCVD
So let’s assume that Dave is able to reverse his type 2 diabetes, and when I say reverse, I mean totally normalizing his glucose tolerance and his blood sugar levels, without any anti-diabetes medications. He achieved this by maintaining his new diet and physical activity regimen for 2 years and is quite happy with his new lifestyle, so he is confident he can maintain it indefinitely. And, by the way, I cannot emphasize this point enough: the point is NOT to ‘diet’ or go to the gym for a few weeks and then, after some first results, go back to your old ways. We will only benefit from a healthier diet and lifestyle while we are maintaining it, so I strongly recommend finding an approach that you can happily maintain over the long term. In my opinion, if that means making compromises or being less strict, then so be it: it is better make some changes that you can maintain forever than embark on one jojo-diet after another.
So Dave has lost 57 pounds over the past two years, and his insulin sensitivity has improved significantly. His fasting glucose concentration is now 90 mg/dL, or 5 mmol/L, and his fasting insulin is now 7 uU/mL. This suggests that his insulin sensitivity has substantially improved, from about 25% of normal to about 60% of normal. And because his body is now more insulin sensitive, it needs less insulin now than before. And now his pancreatic beta-cells CAN make about 100% of the insulin he needs to regulate his blood glucose levels and keep them in the normal range at all times, no matter what he eats. As a result of the improved diet and insulin sensitivity, his blood pressure has normalized, and he now averages 115/75. His triglycerides have totally normalized to about 60 mg/dL, and the fat content in his liver is now around 2%; that’s still not totally optimal (0% is optimal), but no longer a major concern. He no longer requires medication to control his blood sugar or his blood pressure, but he continues taking a low-dose statin. His LDL-cholesterol averages 95 mg/dL now.
How would that affect his risk of having an ASCVD event?
Well, let’s recall that when Dave first talked to his doctor about his ASCVD worries, his risk of having a heart attack or stroke by age 80 was 41%. If he just took all of the medications his doctor prescribed to better control his blood glucose, LDL-cholesterol, and blood pressure, that risk would be reduced to about 11%. A very meaningful reduction. However, if he actually identified all of the root causes of his insulin resistance and glucose tolerance, and made lasting diet and lifestyle changes to dramatically improve his insulin sensitivity and normalize his glucose tolerance, as described here, his risk would now be reduced to about 4%. From 41% to 4%. Let that sink in.
And that is even though he is now taking only one medication, the statin, as opposed to at least four. So medication-related side effects and costs are lower. Plus, not only has he lowered his risk of having a heart attack or a stroke, but also his risk of advanced liver diseases, his risk of chronic kidney disease, his risk of other diabetes complications, such as eye disease, neuropathy, and erectile dysfunction, all conditions that otherwise could substantially impair his quality of life. It’s also worth pointing out that he would have a much, much lower risk of certain types of cancer, such as those of the liver, oesophagus, colon, and pancreas. And because of his new exercise regime and much higher protein and micronutrient content of his diet, he will have a much lower risk of osteoporosis and also of sarcopenia, meaning very low muscle mass, as he gets older.
OK, how about Erin? Does it pay off for her as well to try to identify WHY she is glucose intolerant and insulin resistant, and address these root causes? Of course it does. First of all, doing this will dramatically reduce her risk of developing type 2 diabetes, with all of its nasty consequences. But even for ASCVD risk alone, a major new research finding was just published that I wanted to share with you. This was a secondary analysis of data from two clinical studies, one in the United States and the other in China. In both studies, patients with prediabetes participated in an intensive diet and lifestyle modification program. Now, not everyone randomized to that diet and lifestyle change program managed to reverse their prediabetes, but some people did. And those who reached normal glucose tolerance at any point were much less likely to die from cardiovascular disease or be hospitalized with heart failure over the next 20 to 30 years. The estimate, adjusted for other factors, suggested a reduction in risk by about 50%, even though some of these participants may have reverted to prediabetes or even have developed type 2 diabetes after the initial diet and lifestyle change program concluded. My best guess is that those who maintained normal glucose tolerance throughout the follow-up period may have had an even lower risk. These data are consistent with other studies and clearly show, first, that already prediabetes is strongly and consistently associated with increased ASCVD risk, and, second, that reversing prediabetes and achieving normal glucose tolerance is associated with tremendous benefits for ASCVD risk.
Summary & Conclusion
To summarize, both prediabetes and type 2 diabetes are clearly major risk factors for atherosclerotic cardiovascular disease, increasing the risk of having a heart attack or stroke. That increase in risk is partly due to chronically elevated blood glucose concentrations, partly due to insulin resistance that may underlie the glucose intolerance and the hyperinsulinemia that may result from it, and partly due to the root causes of that insulin resistance.
So to minimize the risk of an ASCVD event, such as a heart attack or a stroke, you want to work with your doctor to address all of the classic ASCVD risk factors you may be exposed to, such as elevated LDL-cholesterol, hypertension, and smoking, but for the biggest risk reduction, you will also need to take an honest look at how your diet and lifestyle are contributing to your glucose intolerance, and be willing to make changes to that diet and lifestyle to allow your glucose tolerance and insulin sensitivity to normalize. On this website, you will find many resources to support you in that quest. Here are the most important ones:
- The Nourished by Science Prevention Program, an online community where you work with me to address the root causes of the most common chronic diseases.
Or these resources, in this order:
- Blog post The Regulation of Blood Sugar
- Blog post Insulin Resistance: Top Causes & Contributing Factors
- Blog post Beta-Cell Dysfunction: The Overlooked Cause of Type 2 Diabetes, and How to Measure It
- A downloadable poster to assess your insulin sensitivity and beta-cell function
- Blog post How to Prevent or Reverse Insulin Resistance
- Blog post How to Lose Weight Without Counting Calories
Above all, though, I want you to take action. Create a physical folder, take notes while going through these blog posts, and take concrete action after each. Learn and implement it in your own life. And if you have friends or family members with prediabetes or type 2 diabetes, create a ‘club’ with them to support each other to get healthy. Meet to work out together, or just to go for a walk, and when you have social gatherings, work together to serve healthy foods that support your health goals rather than sabotage them.
Let me close by expressing my deepest thanks to the Patrons who support this website and the associated YouTube channel. Blog posts like this and the associated video would not be possible without their support, so if you value evidence-based, unbiased content free of affiliate marketing, sponsorships, or other financial conflicts, please consider becoming a Patron as well.
Thank you, and take care!
References
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2 Responses
Quick question, could the insulin resistance be genetically caused? (apart from the other factors you alluded in your first chart and comments)
Yes, there are a few genetic variants that can cause insulin resistance, but they are not common. One is lipodystrophy, an inability of the body to store fat in the subcutaneous fat depots. You could also count genetic predispositions to weight gain, I suppose.
On the other hand, our beta-cell function seems to be more strongly and more directly genetically regulated. There are very large differences between people how much insulin they can produce, and how susceptible they are to beta-cell dysfunction.
Cheers
Mario