Dr Ritamarie
What do fatty liver, polycystic ovarian syndrome, skin tags, high blood pressure, and frozen shoulders have in common?
On the surface, they seem to be completely different health problems. One involves the liver, another involves the reproductive hormones, another affects the skin, and one involves a painful stiff shoulder, but in some people, these conditions may provide clues to an underlying metabolic disturbance.
Here’s what’s especially interesting. Their fasting blood sugar and A1C may still look perfectly normal or at least within the conventional normal ranges. We’ve been taught to look for insulin resistance only when glucose starts rising, but what if some of the earlier clues are showing up in places we aren’t even accustomed to looking?
Today, we’re going to explore seven surprising conditions and clinical findings associated with insulin resistance and how recognizing these connections can help us ask better questions, because sometimes the most important metabolic clue has nothing obvious to do with blood sugar.
We’ve talked in recent episodes about how the pancreas can compensate for reduced insulin sensitivity, how glucose can remain normal while other aspects of metabolic regulation are changing, but insulin is more than a glucose hormone.
It influences lipid metabolism, vascular signaling, reproductive hormones, and other pathways.
Let’s look at seven places where clues might appear.
Fatty liver is the first place we’re going to look. It’s a metabolic warning sign. We’re going to start with Metabolic Dysfunction-Associated Steatotic Liver Disease or MASLD.
Insulin normally helps suppress hepatic glucose production. Insulin resistance can disrupt glucose and lipid regulation in the liver. Excess fatty acid delivery from adipose tissue and increased hepatic lipid synthesis can contribute to, guess what? Liver fat accumulation.
A person can have significant liver fat despite normal fasting glucose, and in some cases, normal liver enzymes. When you see hepatic steatosis, are you evaluating the person’s broader cardiometabolic health rather than just monitoring ALT and AST? I remember having a person who joined our metabolic health program, because she wanted to get rid of her belly fat.
What turned out was that was the last thing to change, honestly. She got rid of her brain fog first, but she went in for her annual checkup and realized that her fatty liver had disappeared just by working on the insulin resistance and the glucose levels. It has to go beyond ALT and AST. The liver can be telling us something about metabolic health before blood sugar gets our attention.
Another one is PCOS, which has a new name now. It’s when metabolic signaling affects reproductive hormones.
Insulin resistance is common in PCOS, although not everyone with PCOS has the same metabolic abnormalities. And forgive me, I’ve been calling it PCOS for decades, and I can’t get used to the new acronym for it.
Hyperinsulinemia, elevated insulin, can amplify the ovarian androgen production and affect sex hormone binding globulin. Reproductive and metabolic signaling interact big time, so PCOS is not just an ovarian disorder, nor is it always caused by insulin resistance.
When someone presents to you with irregular cycles, acne, or androgen excess, are we considering their metabolic picture along with their reproductive hormones? Sometimes a reproductive hormone problem is also a metabolic signaling problem. We need to think about all the interconnections between these systems.
The international PCOS guideline identifies insulin resistance as an important feature while emphasizing that currently available insulin measures have limitations. Most doctors aren’t doing those measures, and sometimes the insulin can be off.
I like to look at the C peptide and also the insulin, so we get a sense of how much insulin this person is producing.
The next one is high blood pressure. Insulin and vascular signaling have huge amounts to do with hypertension. Insulin influences the vascular endothelial function. It stiffens the endothelial linings and promotes high blood pressure that way.
The other pathway that we look at is the nitric oxide production and vasodilation, and with excess insulin and insulin resistance, we see a decrease in nitric oxide production, which leads to vasoconstriction, which can contribute to high blood pressure.
When we see people with high blood pressure, we want to be looking at other underlying causes, and metabolic dysfunction is huge. It’s associated with altered vascular signaling, sympathetic activity, and sodium regulation. Although hypertension does have many different causes, insulin resistance is one possible contributor, which is not often looked at. That’s why we as functional clinical practitioners and nutritional endocrinology practitioners are looking at all the interconnections.
When blood pressure is increasing along with triglycerides or waist circumference, could those findings really represent a broader metabolic pattern? That’s often overlooked. I think insulin resistance and excess insulin are overlooked in so many different conditions.
When we have elevated blood pressure in somebody, we should be looking at all the signs of blood sugar regulation, looking at yes, their A1C and yes, their fasting glucose, but also their insulin and their HDL triglyceride ratio, their belly fat, and their symptoms.
Another thing that happens is skin changes, and these are things we can actually see. Acanthosis nigricans appears as thickened, velvety, often darker skin, commonly around the neck or body folds. It’s strongly associated with insulin resistance, although other causes do exist.
Skin tags are another thing. I know in some people you see little skin tags around their eyes or in their armpits or others, and some people are covered with them, That’s a sign of insulin resistance and metabolic dysfunction. Insulin and insulin-like growth factor signaling can contribute to these skin changes.
Are we paying attention to the physical findings, not just the laboratory findings? Oftentimes people are overlooked, because they show up, they do their annual physical, their fasting glucose is in the 90s, nobody bothers to test their A1C or their insulin, and they’re saying, “You don’t have a good glucose problem,” even though the person has belly fat and waist hip ratio altered, waist height ratio elevated, yet they’re not looking further.
All these other signs, they’re surprising, and I want you to keep these in your toolbox so that you can figure out what’s going on before they show up with metabolic syndrome or diabetes. Sometimes a clue to insulin signaling is visible, before we order the lab test.
I can usually tell somebody with insulin resistance from across the room. The acanthosis nigricans is a recognized metabolic clue, as is skin tags, as is the waist-hip ratio. We should be looking at these things.
Another one is sleep apnea. So many people have sleep apnea. So many people are on those CPAP machines, and obstructive sleep apnea is associated with insulin resistance and metabolic disease. Most people don’t look at that.
Intermittent hypoxia during sleep, sleep fragmentation, and sympathetic activation can contribute to impaired metabolic regulation. Metabolic dysfunction and adiposity also influence sleep apnea risk. Sleep apnea can occur in people without obesity.
Is a person with fatigue, snoring, unrefreshing sleep, and metabolic warning signs being evaluated for sleep disordered breathing? It’s really important that we look at this, because so many people are suffering from sleep disturbances. Sometimes the missing metabolic intervention isn’t another supplement, it’s recognizing a sleep disorder.
Another one that’s very surprising is frozen shoulder. It’s an unexpected musculoskeletal clue. Adhesive capsulitis or frozen shoulder is more common among people with diabetes. Chronic dysglycemia, dysregulation of the glucose, and advanced glycation can contribute to connective tissue changes.
Metabolic factors and inflammation can also be relevant. Importantly, the evidence connecting frozen shoulder directly to early insulin resistance with normal glucose is less established than its association with diabetes, but certainly something to look more closely at.
With someone with frozen shoulder, you need to look at are there underlying metabolic factors? A stiff shoulder, of course, isn’t a diagnosis of insulin resistance, but it may be just one more clue. There was a 2026 systematic review that found substantially greater odds of adhesive capsulitis, frozen shoulder, among people with diabetes.
Which is stronger evidence than the direct association with insulin resistance alone. This is something we need to look at if somebody’s complaining of chronic capsulitis, adhesive capsulitis, frozen shoulder, that’s not getting better with therapy.
I know when I’ve worked with people with frozen shoulder that was caused by an injury, we could help them to get that cleared up within weeks. Okay. If somebody has this ongoing for weeks or months or years even, then there might be an underlying metabolic disturbance that’s been overlooked.
The last one we’re going to look at today, although there’s many more, is periodontal disease. Disease involving the gums and the tissue in the mouth and around the teeth. Diabetes and periodontitis have a well-recognized bi directional relationship.
Systemic inflammation contributes to impaired insulin signaling and periodontal disease contributes to systemic inflammation. In fact, it’s been associated or found in relationship with cardiovascular stiffening, cardiovascular inflammation, and there’s specific markers like myeloperoxidase and LP-PLA2 that are associated with that, the gut, the bacteria in the mouth that affect the blood vessel lining.
The relationship between periodontal disease and early insulin resistance is an area that we need to be looking at.
I have a question for you. When you do an evaluation of somebody, are you asking and looking at oral health and evaluating the overall inflammatory metabolic burden? The mouth isn’t separate from the body, and oral inflammation deserves a place in the clinical picture.
We’ve looked at seven very different findings.
The liver, reproductive hormones, blood pressure, skin, sleep, musculoskeletal health, and the oral microbiome. I want to emphasize something that I think you should be aware of. These aren’t seven ways to diagnose insulin resistance. Every one of these has other possible causes, of course, but when we start seeing several of these findings in the same person, shouldn’t we ask whether they share an underlying metabolic contribution?
And I keep talking about the belly fat. Not everybody with insulin dysregulation has the belly fat. Some people are quite skinny. We need to develop the power of pattern recognition. We shouldn’t assume everything has one cause. I mean, that’s what we talk about all the time in functional medicine and in nutritional endocrinology. But, recognizing when an apparently unrelated collection of findings can be connected is super critical.
Here’s what I want you to remember.
Insulin resistance doesn’t always announce itself with high blood sugar. Sometimes the clues are showing up elsewhere, and understanding those connections can help us recognize when metabolic health deserves a closer look.
In one of our next episodes, we’re going to explore five major physiologic pathways that help explain why insulin resistance affects so many parts of the body, because understanding the mechanisms is what helps us move from recognizing patterns to understanding them.
If you’re a health practitioner and you want to get better at recognizing these patterns and connecting the dots, download our guide, Beyond Protocols, A Practitioner’s Guide to Root Cause Pattern Recognition. It’s totally free, and you’ll find the link in the show notes. It’s a great starting point for moving beyond protocols and one size fits all protocols.
I also recommend checking out the link in the show notes for our Metabolic Mastery program for practitioners to help you see all the connections and put all the pieces together.
This is what my mission of reinventing healthcare is all about. We need to learn to recognize underlying patterns, understand their physiology, and create personalized approaches to care.
If you found this episode valuable, follow the podcast and share it with another practitioner, and thanks for joining me on my quest to reinvent healthcare. And until next time, shine on.
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