Type 2 Diabetes: What Is Actually Happening Inside Your Body?

Part 3 of the Thrive Beyond 50 10-Part Diabetes Series If you have followed this series from the beginning, we have already discussed two important pieces of the diabetes puzzle.…

Part 3 of the Thrive Beyond 50 10-Part Diabetes Series

If you have followed this series from the beginning, we have already discussed two important pieces of the diabetes puzzle.  In Part 1, we looked at prediabetes, a metabolic warning that often develops quietly and without obvious symptoms.  In Part 2, we went deeper and discussed insulin resistance, the underlying metabolic dysfunction that can begin years before blood sugar rises high enough for someone to be diagnosed with type 2 diabetes.  Now we arrive at the disease itself.

               Most people have at least a basic understanding of diabetes.  Blood sugar gets too high, your doctor checks your glucose or A1C, the numbers come back elevated, and suddenly the word “diabetes” appears in your medical record.  But that description barely scratches the surface.  Type 2 diabetes is not simply a disease of too much sugar in the blood.  Elevated blood glucose is what we can easily measure, but underneath that number is a much larger metabolic story involving insulin, skeletal muscle, the liver, body fat, the pancreas, and the body’s gradually declining ability to manage glucose.  To understand type 2 diabetes, we need to look at what is actually happening inside the body.

First, Let’s Talk About Glucose

               Glucose is not the enemy…that may sound strange in an article about diabetes, but glucose is an essential source of energy.  When we eat carbohydrates, many of them are eventually broken down into glucose, which enters the bloodstream and becomes available for the body to use.  Our brain requires a tremendous amount of energy, our muscles use glucose during activity, and our organs and tissues need energy every second of every day.  The problem is not that glucose exists; the problem occurs when the body can no longer regulate it effectively.

               After you eat a meal containing carbohydrates, blood glucose naturally rises.  In response, the pancreas releases insulin.  Insulin acts as a metabolic signal that helps regulate the movement and storage of glucose, particularly in tissues such as skeletal muscle and fat, while also signaling the liver to reduce its own glucose production.  In a metabolically healthy person, this system is remarkably efficient.  Blood glucose rises after eating, insulin responds, glucose is taken up or stored, and blood sugar gradually returns toward its normal range.

               With insulin resistance, however, this system begins to change.  The body is still producing insulin, and often it is producing quite a lot of it, but certain tissues are no longer responding to insulin as effectively as they once did.

When the Cells Stop Listening

               As we discussed in Part 2, insulin resistance occurs when tissues such as skeletal muscle, the liver, and adipose tissue become less responsive to insulin’s signals.  One way to think about this is to imagine insulin repeatedly knocking on the door and telling the cell that glucose is available.  Early in insulin resistance, the message is still being received, but the response has become weaker.  The pancreas compensates by producing more insulin, essentially making the signal louder.

               For a while, this strategy can work surprisingly well.  Blood glucose may remain within what appears to be a normal range because the pancreas is working overtime to keep it there.  This is one of the reasons metabolic dysfunction can exist long before someone is diagnosed with diabetes.  If we look only at glucose, everything may appear relatively normal while insulin levels have already increased substantially behind the scenes.

               Over time, maintaining that compensation can become increasingly difficult.  Insulin resistance may worsen, the pancreas must produce greater amounts of insulin to maintain glucose control, and eventually the system may no longer be able to keep up.  Blood glucose begins to remain elevated for longer periods, prediabetes may develop, and if the process continues, glucose eventually reaches the diagnostic range for type 2 diabetes.  This progression often develops gradually over many years rather than appearing suddenly.

The Pancreas Has Been Working Overtime

               The pancreas deserves much more attention in the diabetes conversation.  Within the pancreas are specialized cells called beta cells, which are responsible for producing insulin.  During the early stages of insulin resistance, these cells respond by increasing insulin production.  You might think of the pancreas as turning up the volume because other tissues are no longer hearing insulin’s message as clearly as they once did.

               Initially, this compensation can be remarkably effective, but the pancreas does not have unlimited capacity.  As insulin resistance persists, beta cells may become increasingly unable to meet the body’s insulin requirements, and in many people beta-cell function progressively declines.  This represents an important turning point in the development of type 2 diabetes.

               Type 2 diabetes therefore involves more than one metabolic problem – the body has become resistant to insulin, while at the same time insulin production eventually becomes insufficient to fully compensate for that resistance.  The result is persistent elevation of blood glucose.  This is a much more accurate picture of what is happening than simply saying that someone developed diabetes because they ate too much sugar.

Your Liver Is Part of the Story

               Most people associate diabetes almost entirely with the foods they eat, but some of the glucose circulating in your bloodstream did not come directly from your last meal – it came from your liver.  The liver acts as an energy warehouse, storing glucose in the form of glycogen and releasing glucose when the body needs it, particularly between meals and overnight.  The liver can also manufacture new glucose when necessary.  This is an essential survival mechanism because we would not want our blood glucose to collapse every time we went several hours without eating.

               Insulin normally helps regulate this process by signaling the liver to reduce glucose production when sufficient energy is already available.  When the liver becomes insulin resistant, however, it may not respond appropriately to that signal.  The liver can continue releasing glucose even when there is already plenty circulating in the bloodstream.

               This helps explain something that confuses many people with diabetes.  They may go to bed without eating anything for hours, wake up the following morning, check their glucose, and discover that it is elevated.  Understandably, they wonder how their blood sugar could have risen when they did not eat anything overnight.  The answer is that food is only one part of glucose regulation…the liver is participating in the process as well.

And Then There Is Muscle

               This part of the conversation becomes especially important for adults over 50.  Skeletal muscle is not simply tissue that allows us to lift weights, climb stairs, carry groceries, get out of a chair, or maintain our independence.  Muscle is also highly metabolically active tissue and one of the body’s major destinations for glucose.  After a meal, skeletal muscle can take up a substantial amount of circulating glucose, making healthy muscle tissue an important part of glucose regulation.

               When skeletal muscle becomes insulin resistant, glucose uptake in response to insulin becomes less efficient.  More glucose remains in circulation, placing additional demands on the pancreas to produce insulin.  But there is another fascinating side to this story – muscle contractions themselves can stimulate glucose uptake through mechanisms that are partly independent of insulin.  In practical terms, using your muscles helps your body manage glucose.

               This is one reason something as simple as walking after a meal can be helpful.  It is also one reason resistance training deserves a place in conversations about metabolic health rather than being viewed merely as something people do to build bigger muscles or improve their appearance.

               As we move beyond 50, preserving muscle becomes increasingly important.  Adults who are inactive can gradually lose muscle mass and strength with age.  If declining muscle is combined with increasing visceral fat, reduced physical activity, and worsening insulin sensitivity, we create an environment in which glucose regulation can become increasingly difficult.  Maintaining muscle, therefore, is not simply about remaining strong.  It may be one of the most valuable investments we can make in long-term metabolic health.  We will devote an entire article later in this series to muscle and insulin resistance because this relationship deserves much more attention.

Body Fat Is Not Just Storage

               Body fat is often discussed as though it were simply excess energy stored underneath the skin, but adipose tissue is biologically active.  It produces hormones and signaling molecules that can influence metabolism throughout the body.  Where fat is stored also matters – visceral fat, which is stored deeper within the abdomen around internal organs, is particularly associated with insulin resistance and increased cardiometabolic risk.

               Excess visceral fat commonly travels with other metabolic problems, including elevated triglycerides, low HDL cholesterol, fatty liver, higher blood pressure, and impaired glucose regulation.  This does not mean that every person carrying excess body weight will develop diabetes, nor does it mean that someone who appears thin is automatically metabolically healthy.  Metabolism is much more complicated than appearance or the number on a bathroom scale.

               Nevertheless, increasing abdominal fat, particularly when it appears alongside worsening blood pressure, abnormal blood lipids, fatty liver, or rising glucose, can provide an important clue that metabolic health is deteriorating.  We will explore the relationship between belly fat, fatty liver, and insulin resistance much more closely later in this series.

Type 2 Diabetes Is Not Simply “Eating Too Much Sugar”

               One of the biggest misconceptions surrounding type 2 diabetes is that it develops simply because someone ate too much sugar.  Certainly, a dietary pattern containing excessive added sugars, refined carbohydrates, sugary drinks, and ultra-processed foods can contribute to excess calorie intake, weight gain, and worsening metabolic health.  Liquid sugar can be particularly problematic because it allows us to consume a large amount of rapidly absorbed carbohydrate and calories without providing much satiety.

               But reducing the entire development of type 2 diabetes to sugar consumption is an enormous oversimplification – the following conditions matter:  

               -Genetics.

               -Body composition.

               -Physical.

               -Sleep.

               -Stress.

               -Age.

               -Diet quality.

               -Visceral fat.

               -Muscle mass.

Certain medications and medical conditions can also influence glucose regulation.  More importantly, these factors do not operate independently; they interact with one another over many years.

               Two people can eat similar diets and have very different metabolic responses because their genetics, muscle mass, physical activity, sleep patterns, body-fat distribution, medications, and overall metabolic health may be completely different.  Instead of searching for a single nutritional villain, we should ask a more useful question: What metabolic environment enabled insulin resistance and, eventually, diabetes to develop?

Why Type 2 Diabetes Often Appears After 50

               Age itself does not automatically cause type 2 diabetes, but several changes that commonly accompany aging can increase the risk.  We may become less physically active; we may gradually lose muscle mass; visceral fat may increase; sleep quality may deteriorate; hormonal changes can influence body composition; and decades of poor dietary habits may eventually catch up with us.  When these changes occur together, insulin sensitivity can worsen.

               The encouraging part of this story is that many of these factors are modifiable.  We cannot stop birthdays from arriving, and frankly, the alternative to getting older is not particularly appealing…but we can influence how we age.  We can build and preserve muscle, walk regularly, improve the quality of our diet, reduce excess visceral fat when necessary, prioritize sleep, avoid smoking, manage stress more effectively, and work with our healthcare providers to address blood pressure, cholesterol, glucose, and other health concerns.  When appropriate, medications can also play an important role in controlling blood glucose and reducing the risk of complications.

The Diagnosis Is Not the Beginning of the Disease

               This may be one of the most important concepts in this entire series.  The day someone is diagnosed with type 2 diabetes is usually not the day the metabolic dysfunction began; it is simply the day that dysfunction became significant enough to cross a diagnostic threshold.

               Insulin resistance may have been developing for years, while insulin levels may have gradually increased as the pancreas attempted to compensate.  Visceral fat may have been accumulating, the liver may have become increasingly insulin resistant, skeletal muscle may have become less responsive to insulin, and blood glucose may have slowly moved from normal to borderline to prediabetic before finally reaching the diabetic range.

               The diagnosis, therefore, is not necessarily the beginning of the story; it may simply be the moment when we finally recognize a metabolic story that has been unfolding quietly for a very long time.  This is exactly why understanding prediabetes and insulin resistance is so important.  If we can identify metabolic dysfunction earlier, we may have an opportunity to intervene before it progresses further.

Type 2 Diabetes Is Serious, but the Story Does Not End With the Diagnosis

               Type 2 diabetes should be taken seriously.  Chronically elevated blood glucose can eventually damage blood vessels, nerves, kidneys, eyes, and other tissues.  Diabetes also significantly increases the risk of cardiovascular disease.  We will discuss these complications later in this series because people deserve to understand what uncontrolled diabetes can do to the body.

               At the same time, I do not want the message of this article to be one of inevitability or hopelessness.  A diagnosis of type 2 diabetes does not mean that nothing can be done.  Nutrition and physical activity are important.  Losing excess body fat can be extremely powerful when it is contributing to insulin resistance.  Preserving and building muscle matters. Medications can be extremely valuable, and for some people, substantial and sustained lifestyle and weight changes can improve glucose regulation enough for type 2 diabetes to enter remission.

               The earlier metabolic dysfunction is addressed, the greater the opportunity may be to alter its trajectory.  That is why this conversation should begin long before someone’s glucose reaches the diabetic range.

Dr. Edwards’ Take

               One of the biggest mistakes we make when talking about diabetes is focusing exclusively on blood sugar.  Blood glucose is important…we absolutely need to measure it, monitor it, and manage it when it becomes elevated.  But I want you to think one level deeper and ask a different question: Why did the glucose become elevated in the first place?

               If insulin resistance, declining muscle mass, increasing visceral fat, physical inactivity, poor nutrition, inadequate sleep, or other modifiable factors are contributing to the problem, simply watching the glucose number does not tell us the entire story.  This is one of the reasons I believe metabolic health deserves attention well before someone receives a diagnosis of diabetes.  We should not wait until the check-engine light comes on before we begin taking care of the engine.

               If you have already been diagnosed with prediabetes or type 2 diabetes, however, do not view that diagnosis as a verdict – view it as information.  Information gives us something to work with; it tells us where we are today and gives us an opportunity to make decisions about where we want to go from here.

               For those of us over 50, this becomes especially important.  We are not simply trying to lower a laboratory number; we are trying to preserve muscle, maintain our independence, protect our cardiovascular system, support our brain and metabolic health, and remain physically capable of doing the things we want to do for as many years as possible.  Lowering blood glucose is important, but ultimately it is part of a much larger goal: maintaining health, function, resilience, and independence as we age.  That is the bigger picture, and it is what thriving beyond 50 is really about.

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