A new study finds that this one important biomarker raises the probability that you might have unstable plaque in your very important carotid as well as coronary arteries that can lead to major adverse cardiovascular events. Let's talk about the details. The title of this study is serum insulin levels are associated with vulnerable plaque components in the carotid artery. The Rotterdam study, Rotterdam, Netherlands.
This is a prospective cohort that has been followed. just much like the UK Biobank, much like NHANES here in the US. There's been a lot of interesting cardiovascular and metabolic health research that has emerged from this cohort. Okay, so in short, this study found that there was a strong statistical association with higher fasted insulin levels and higher concentrations per an MRI of vulnerable plaque called IHP. And this is an intra-hemorrhagic plaque.
And this plaque is more... are likely to be dislodged from the artery where it can cause either a stroke or a heart attack, which is problematic. Okay. So if you want to reduce the odds that you might die of a major adverse cardiovascular event or a major adverse cerebrovascular event, like a stroke, then you might want to keep watching because we're going to talk about specific ways to optimize the health of blood sugar as well as insulin.
But first talk about the study. I think it's important. There were 1,740 participants.
the median age was 72 years old. So these are individuals that are over the age of 65, higher risk of having a stroke or a heart attack. And so these investigators want to see, well, what common biomarkers would give insights with statistics after controlling for different variables? What biomarkers were linked with higher prevalences of this very vulnerable plaque that is actually quite dangerous? Because that's what we want to do.
We want to prevent death from heart disease and strokes along with cancer and Alzheimer's. They go on in the conclusion to say that serum insulin levels are associated with the presence of vulnerable components of carotid plaque. They measure the carotid artery, not the coronary artery. I don't think that means that this study interpretation can't be related to the coronary artery. Why would one suspect that, well, the carotid artery has all this vulnerable plaque, but other arteries don't?
They chose the carotid artery probably because it's easier to measure. Okay. And they say serum insulin levels are associated with the presence of vulnerable components of carotid plaque, specifically with intraplaque hemorrhage, the so-called IPH plaque. These findings suggest a complex role for serum insulin in the pathophysiology of carotid atherosclerosis and plaque vulnerability.
Okay, so we're going to continue and talk about this and focus on good old table one. We always want to look at the baseline characteristics of study participants and how they grouped people. into different cohorts based upon their insulin levels.
Now, what I love to see about these baseline characteristics of these individuals that, again, were stratified based upon their fasting insulin levels with a low or a medium or a high fasting insulin level, I wanted to see LDL cholesterol. I was really hoping to see LDL. Much to my chagrin, LDL isn't even in table one. Why would that be? This is the biomarker that is unequivocally linked with cardiovascular disease.
Shouldn't we see? LDL. It's not on there. We have HDL.
We have total cholesterol. We have fasting glucose. We have diabetes status. We have smoking status. We have gender.
We have statin use percentage, vitamin K antagonist percentage like warfarin. We have BMI. Why don't we have LDL? I thought for sure LDL would be in the supplementary materials. It's not.
This is really concerning to me. I'm tempted to email the author to ask them. Why we don't have LDL, because that would be actually quite interesting. Is there a correlation with LDL cholesterol levels and independent of insulin and the connection with this vulnerable plaque, the IPH plaque, the intrahemorrhagic plaque? Wouldn't that be fascinating?
Because again, the entire medical community is focused on lowering LDL. We don't hear much about lowering insulin now, do we? But it turns out that again, this that costs 11 bucks.
Every doctor should be measuring this. It turns out that high serum insulin levels are independently associated with greater odds of having higher prevalences of this plaque that's highly vulnerable to rupture and causing downstream problems, causing a heart attack or a stroke. Now, if we want to get more granular and talk about the enumeration of risk and talk about the odds ratio, there's a 32 to 46% greater odds of having high vulnerable plaque with high insulin.
meaning that not every single person that has high insulin has higher prevalences of this very vulnerable plaque, but between 32% and 46%, a greater risk of having this more vulnerable plaque, which we're going to get into the details more specifically. But first, friends, I want to thank you for being here. Thank you for enjoying this content. Let me know what you think of this study in this video breakdown in the comment section below. I also want to thank our good friends over at bondcharge.com for making this video possible and are offering a holiday sale during the months of November and December.
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The winter is a good time to get into sauna therapy and Bar and Charge has made this super easy. So I'll put links in the description below. I highly recommend you check that out. So let's get back to the study. Again, the investigators found that insulin levels increased the risk by about 32 to 46% that you might have a very vulnerable plaque that is prone to rupture and causing downstream negative effects such as a heart attack or a stroke.
The investigators say in this population-based study, subjects with subclinical carotid atherosclerosis, we observed that higher fasting serum insulin levels were associated with the presence of intraplaque hemorrhage within the carotid atherosclerotic plaque. Again, this is different from the coronary artery atherosclerotic plaque, but as we talked about with cardiac surgeon, Dr. Filavidya, plaque in the carotid arteries probably means plaque in the coronary arteries and vice versa. We see complications in the heart with coronary artery plaque because the arterial system is very small. And that's why over time, people might develop an infarct or a heart attack. That doesn't mean that the arteries that are Feeding blood and nutrients to the feet aren't also compromised.
In his words, the investigators say, we did not find an association between fasting glucose levels and any of the carotid plaque components. Until now, most of the evidence linking insulin and glucose to atherosclerosis, that's the formation of plaque buildup in your arteries, comes from studies in which atherosclerotic cardiovascular clinical endpoints, such as ischemic heart disease or ischemic stroke, were investigated. Hyperinsulinemia, was found to increase the risk of ischemic heart disease among 4,637 middle-aged men from the Quebec cardiovascular study.
This is another one of those studies like NHANES or Rotterdam, et cetera, UK Biobank. And the risk of acute coronary and cerebrovascular events in 1,521 men enrolled in the Kyopo ischemic heart disease risk factor study in Finland. Our results extend on these findings by showing. The preclinical changes in serum insulin levels relate to a more vulnerable composition of the carotid atherosclerotic plaque. More specifically, we demonstrated that high serum insulin levels, especially related to the presence of intraplaque hemorrhage, the plaque component, which is regarded as the most vulnerable.
They go on to say in contrast to high or low serum insulin levels, it may be speculated that physiological concentrations of insulin, median levels between 65 and 85 picomoles per liter. potentially behave protectively against atherosclerosis. I think that's important to recognize. We don't want to drop insulin to the floor in all cases. Insulin is a hormone, one of the only hormones that lowers blood glucose.
I mean, it's really unique, right? You have cortisol, you have adrenaline, you have growth hormone, you have noradrenaline, you have glucagon, you have all these hormones that actually raise glucose and so forth. But insulin is one of the only ones that lowers it.
And so I think that's interesting, but it goes to show that we do want some insulin around. I mean, insulin can increase growth. Insulin can increase muscle protein synthesis.
We just don't want supraphysiologic insulin levels all of the time. So I think that's important. Now, what I think is really important is what the investigators write right here. Observations in our study show that median levels of serum insulin were not associated with any vulnerable plaque component, but were associated with a lower presence of calcification, which may support the hypothesis that median levels of insulin have the protective effect. In the same line, a recent animal model study examined the role of insulin in atherosclerotic plaque reported the protective effect of insulin on atherosclerosis.
In this study, the insulin effect was tested on atherosclerosis in a mouse model, and insulin was found to decrease the plaque burden and increase plaque stability via nitric oxide synthase mechanisms. Furthermore, it was found that insulin reduced macrophage accumulation in plaque necrosis and increased collagen and smooth muscle cell accumulation. Surprisingly, we found no effects of serum glucose levels on carotid plaque composition.
In the context of glucose, our findings are in contrast with studies that link glucose levels below 7 millimoles per liter with an increased risk of vascular disease. However, a recent meta-analysis of 102 prospective studies that investigated the relationship between fasting glucose levels and risk of vascular disease concluded that glucose concentrations were nonlinear and modestly associated with risk of vascular diseases. among individuals without diabetes, meaning that glucose levels below and higher than seven millimoles per liter, which by the way is above 125 milligrams per deciliter, which is the cut point for pre-diabetes, were associated with increased risk for coronary heart disease and ischemic stroke.
So in conclusion, serum insulin levels are associated with the presence of vulnerable components of carotid plaques, specifically the intraplaque hemorrhage, suggesting that serum insulin may play a role in the vulnerability of carotid atherosclerotic plaque. Further studies are required to confirm our findings in a longitudinal design. What are your thoughts on this, my friends? Again, I'm going to email the author of this paper. I want to find the supplementary materials because they have, without question, LDL cholesterol.
And I would like to see that as it pertains to the presence of this vulnerable plaque known as the IHP plaque. What are your thoughts? Let me know in the comment section below.
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We'll catch you in a future one down the road.