If you read Blood Sugar Control for Women: The Basics and the Menopause Shift, you already understand what blood glucose is, how it gets into the bloodstream, and what happens in the body when it spikes repeatedly. You also know that for women in perimenopause and postmenopause, blood sugar regulation becomes more challenging and insulin resistance becomes a daily reality, even when you haven’t changed anything about the way you eat or move.

This post picks up where that one left off. Here, we are going to look at what happens when blood sugar dysregulation is not addressed over time, including the full progression from insulin resistance to prediabetes to type 2 diabetes, and what the research says about whether that progression is reversible.

This is not a post about fear. It is a post for empowerment. Because when we understand how the changes in our bodies are unfolding, we can make conscious choices about how to support and nourish ourselves during this life transition, before our options become more limited.

When Blood Sugar Dysregulation Begins

Blood sugar dysregulation does not happen overnight. For some women, it develops gradually over months or years, driven by patterns in diet and lifestyle that repeatedly stress the body’s glucose management system. For others, it emerges from chronic physical or emotional stress, which raises cortisol and directly disrupts blood glucose regulation. And for many women in perimenopause and postmenopause, it arrives through hormonal shifts that change the metabolic terrain entirely, regardless of how well they have been eating or how active they have been.

All three pathways lead to the same place: a progressive loss of insulin efficiency that, if unaddressed, follows a clear and documented progression.

Understanding that it can begin from multiple root causes and that some or all of them can be present in this sometimes-overwhelming phase called midlife is why this conversation needs to be had. The earlier dysregulation is identified, the more opportunity there is to intervene and bring blood sugar back into normal range.

To understand how that progression happens, let’s look at what is happening at the cellular level for each stage of blood sugar regulation.

Stage 1: Healthy Blood Sugar Regulation

As you learned in Part 1, insulin is the hormone that signals cells to absorb glucose from the bloodstream. Think of it as a key that unlocks the cell door. Under normal circumstances, the key fits, the door opens, glucose enters the cell, and blood sugar returns to a healthy range within a few hours.

But when blood glucose spikes frequently or when the cell’s ability to respond is impaired, insulin is released at high levels again and again. This is the beginning of insulin resistance.

Stage 2: Insulin Resistance

Insulin resistance is the state in which the body’s cells have become less responsive to insulin’s signal. The cells are, in a sense, protecting themselves from repeated glucose surges that they don’t need. The consequence is that glucose remains in the bloodstream longer than is ideal.

The body’s first response to this is to produce more insulin. The pancreas works harder, essentially trying to force the cell open with a stronger signal. For a while, this works: blood glucose levels stay within a normal range because the elevated insulin is still moving glucose into cells, just less efficiently.

This is why insulin resistance often goes undetected. A standard fasting blood glucose test will likely look normal, because the pancreas is compensating. But fasting insulin levels, if measured, would already be elevated.

Insulin resistance is also associated with changes in how the body stores fat. As insulin rises, fat cells are increasingly directed to store rather than release energy. Visceral fat, the type that accumulates around the organs rather than beneath the skin, tends to increase. And visceral fat, in turn, worsens insulin resistance further, creating a self-perpetuating cycle, if nothing changes.

Stage 3: Prediabetes

If the pattern of glucose spikes and insulin surges continues without change, the cells become progressively less responsive, and the pancreas can no longer compensate fully. Glucose begins to accumulate in the bloodstream at higher levels, and this is when basic blood tests start to reflect the problem.

At this stage, a person may receive a diagnosis of prediabetes, which is defined by fasting blood glucose or hemoglobin A1c (HbA1c) levels that are elevated but not yet high enough to meet the clinical threshold for type 2 diabetes. The standard ranges for prediabetes diagnosis in the U.S. are:

• A1c: 5.7% – 6.4%
• Fasting blood glucose: 100 – 125 mg/dL (5.6 – 6.9 mmol/L)

Although it might feel like it, prediabetes is not a minor finding. It means the metabolic system is under strain, and the cellular damage associated with elevated blood glucose is already underway, even if a formal diabetes diagnosis has not been made and it doesn’t feel like anything has changed.

It is worth noting that prediabetes, like insulin resistance before it, often has no obvious symptoms. Some people may have darkened skin on the back or sides of their neck or in the armpit. Fatigue, difficulty losing weight, and increased hunger can all be present, but they are easy to attribute to other causes, especially in perimenopause and menopause, when hormonal shifts produce many of the same effects. This is why routine bloodwork and understanding what you are looking at when you see your results are so important.

Stage 4: Type 2 Diabetes

Type 2 diabetes mellitus (T2DM) is diagnosed when fasting blood glucose or HbA1c levels cross a clinical threshold that indicates the body is no longer able to regulate blood sugar effectively on its own. These levels are:

• A1c > 6.5%
• Fasting blood glucose: 126 mg/dL and above (7.0 mmol/L and above)

By this point, the pancreatic beta cells (the cells responsible for producing insulin) have been under stress for a significant period of time. The cells throughout the body remain resistant to insulin, blood glucose stays persistently elevated, and the cascade of damage described in Part 1, including vascular damage, inflammation, AGE accumulation, and oxidized lipids, continues to compound.

Type 2 diabetes is typically managed initially with lifestyle changes and oral medications that help improve insulin sensitivity or reduce glucose production in the liver. At this stage, the condition is serious but still often responsive to meaningful intervention.

Stage 5: Insulin-Dependent Type 2 Diabetes

If blood glucose remains poorly controlled over time, the pancreatic beta cells eventually begin to fail. After years of producing higher and higher amounts of insulin to compensate for cellular resistance, the body can no longer produce enough insulin on its own to move glucose into cells, regardless of lifestyle changes or oral medications.

At this stage, external insulin injections become necessary to achieve adequate blood glucose control. This is sometimes referred to as insulin-dependent type 2 diabetes, and it represents the most advanced stage of the progression.

It is important to understand that reaching this stage is not a personal failure. It is the result of a long physiological process, often compounded by factors outside of a person’s control, including genetics, hormonal shifts, chronic stress, and a food environment that makes blood sugar management genuinely difficult.

No matter where a person is on the continuum of blood sugar regulation, what the body needs is nourishing support to achieve healthy blood sugar levels and prevent the downstream consequences that can occur when it isn’t.

Why a Diabetes Diagnosis Often Comes Late

One of the most important things to understand about this progression is that the clinical diagnosis at each stage is based almost entirely on blood glucose levels, not insulin levels. But as described above, insulin is already elevated and the metabolic system is already straining well before blood glucose rises to a diagnosable threshold.

This means that by the time a person is told they have prediabetes or type 2 diabetes, they have typically been living with insulin resistance for a while, potentially even a decade or more. The diagnosis reflects how well blood glucose is being managed today, not when the underlying dysfunction began.

Unfortunately, conventional medicine tends to only look at fasting blood glucose and HbA1c. And this means that for women who want to be proactive about their metabolic health, especially in midlife when the hormonal environment is shifting, they may have to advocate for a more complete view of their blood sugar regulation.

Is Prediabetes or Insulin Resistance Reversible?

The research on this is clear and encouraging: yes, insulin resistance and prediabetes are often reversible, and even type 2 diabetes can go into remission in many cases.

The earlier in the progression a person intervenes, the greater the likelihood of full reversal. Studies consistently show that changes in nutrition, physical activity, sleep, and stress management can meaningfully improve insulin sensitivity and reduce blood glucose, sometimes to the point where a prediabetes or diabetes diagnosis no longer applies.

That said, reversal is not the same as cure. The underlying tendency toward insulin resistance does not disappear, and the conditions that support it, including a hormonal environment in flux, can reassert themselves if the supporting habits fall away. This is not a reason for discouragement. It is a reason for understanding the why behind the recommendations, so that the approach can be sustained and adjusted over time rather than followed until the outcome is achieved and then abandoned.

What those specific interventions look like, which dietary patterns the evidence supports most strongly, how to prioritize when life is full and time is short, is the kind of individualized guidance needed, but cannot fit into a single blog post. It requires a full understanding of your labs, your history, your hormonal picture, and your life. That said, the next post in this series will give an overview of how to achieve better blood sugar regulation, regardless of where you are on the continuum.

Insulin Resistance in the Menopause Transition

For women in perimenopause and postmenopause, this progression happens even when nothing else in our lives does. As covered in Part 1, declining estrogen directly affects insulin sensitivity, fat distribution, cortisol levels, and sleep quality. Each of those changes, on its own, nudges the body toward greater blood sugar variability. Together, they create a metabolic environment that is meaningfully different from what most women experienced in their 30s.

This means that the progression from insulin resistance to prediabetes can accelerate during the perimenopausal years, even in women who have eaten well and stayed active their whole lives. It also means that the standard tools for managing blood sugar may need to be recalibrated for this life stage.

Women are also disproportionately affected by the downstream consequences of poor blood sugar control, including cardiovascular disease, cognitive decline, and certain cancers. The good news is that these are not inevitable outcomes. But they are why knowing where you are on the blood sugar regulation continuum is crucial to your long-term wellness and wholeness.

A Note on Type 1 Diabetes

Everything described in this post refers to the development of type 2 diabetes, which is driven by insulin resistance. Type 1 diabetes is a different condition entirely. It is an autoimmune disease in which the immune system attacks and destroys the insulin-producing beta cells in the pancreas. The result is that the body cannot produce meaningful amounts of insulin at all, not because cells have stopped responding to it, but because the signal was never sent.

People with type 1 diabetes require external insulin from the time of diagnosis. The progression described above does not apply to them. However, the downstream consequences of chronically elevated blood glucose, including vascular damage, inflammation, and AGE accumulation, are equally relevant for anyone whose blood sugar is not well controlled, regardless of the cause.

Frequently Asked Questions

What is insulin resistance?

Insulin resistance is a state in which the body’s cells are less responsive to insulin’s signal. Insulin is the hormone that acts as a key, unlocking cell “doors” so glucose can enter and be used for energy. When cells stop responding efficiently to that signal, glucose remains in the bloodstream longer than it should, and the pancreas compensates by producing more insulin. Blood glucose can appear normal for years while this compensation is happening, which is why insulin resistance often goes undetected until it has been present for a long time.

What causes cells to be resistant to insulin?

There is no single cause. Insulin resistance can develop through one or more pathways. Repeated exposure to high levels of insulin over time, driven by frequent blood glucose spikes, is one well-established route: cells gradually dial back their response to insulin to protect themselves from too much glucose. Chronic physical or emotional stress raises cortisol, which directly disrupts blood glucose regulation and can push cells toward resistance as well. And for many women in midlife, the hormonal shifts of perimenopause and postmenopause reduce insulin sensitivity regardless of diet or lifestyle changes. Visceral fat, which tends to increase as estrogen declines, adds another layer: it produces inflammatory compounds that interfere with insulin signaling and worsen insulin resistance further. Understanding which of these pathways is most relevant for you is part of why personalized guidance matters more than general advice.

Can menopause cause diabetes?

Menopause does not directly cause diabetes, but the hormonal shifts of perimenopause and postmenopause increase the risk. Estrogen plays an active role in insulin sensitivity, and as it declines, cells become less responsive to insulin’s signal. Fat redistribution shifts toward the abdomen, which worsens insulin resistance further. Cortisol tends to rise, and sleep disruption adds additional metabolic stress. Together, these changes can accelerate a progression that might have unfolded much more slowly at a different time of life. Women who had no blood sugar concerns in their 30s can find fasting glucose creeping (or jumping) upward in their 40s and 50s.

What are the symptoms of insulin resistance in menopause?

Like so many chronic conditions, there are no symptoms that are directly attributable to and consistently experienced with insulin resistance. Many symptoms of insulin resistance overlap with common perimenopausal symptoms, which is one reason it goes undetected so often in midlife women. Symptoms can include difficulty losing weight despite no significant changes in diet or activity, increased hunger or cravings (particularly for carbohydrates), and fat accumulating around the abdomen. Brain fog and fatigue are also associated with insulin resistance. All of these are easy to attribute to menopause alone. If several of these feel familiar, it is worth asking your healthcare provider to look at the full picture, not just fasting glucose.

How long before prediabetes turns into diabetes?

There is no single timeline. Research suggests that 12.5% of people with prediabetes progress to type 2 diabetes within 10 years, while 36.1% revert back to healthy blood glucose levels with appropriate interventions. What determines the trajectory is a combination of factors including genetics, the degree of insulin resistance already present, hormonal environment, stress load, sleep quality, and lifestyle patterns. For women in perimenopause and postmenopause, the hormonal shifts of this life stage can accelerate the progression, which is why knowledge about where you are on the blood sugar regulation continuum is important. The earlier the intervention, the more opportunity there is to change the outcome.

Conclusion

The progression from insulin resistance to prediabetes to type 2 diabetes is not an overnight event, although it can feel that way. Sometimes it is a slow, gradual process, measurable at each stage, and interruptible at each stage as well. The fact that it often goes undetected for years is not because it is invisible, but because the standard tools for detection are not regularly utilized by conventional healthcare systems.

For women going through the menopausal transition, the progression can occur much faster. The hormonal shifts of perimenopause and postmenopause make blood sugar regulation more challenging, and the downstream consequences of poor control, including cardiovascular disease, cognitive decline, and hormonal disruption, more likely.

Fortunately, there are always changes we can make to our diet and lifestyle that will improve our blood sugar regulation, regardless of where we are on the continuum. But the first step is having a clear picture of what is happening and why, so that you can make informed decisions about the support you want.

If you want to receive updates when the next blogs about blood sugar regulation are posted. join my newsletter here. (I’ll also send you my free guide 3 Daily Tweaks to Reset Your Energy and Reclaim Wellness.)

Photo by Thirdman from Pexels.

Sources:

Arnett DK, Blumenthal RS, Albert MA, et al. 2019 ACC/AHA Guideline on the Primary Prevention of Cardiovascular Disease: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines. Circulation. 2019;140(11). https://doi.org/10.1161/CIR.0000000000000678

Borer KT. Why We Eat Too Much, Have an Easier Time Gaining Than Losing Weight, and Expend Too Little Energy: Suggestions for Counteracting or Mitigating These Problems. Nutrients. 2021;13(11):3812. doi:10.3390/nu13113812

Ciarambino T, Crispino P, Guarisco G, Giordano M. Gender Differences in Insulin Resistance: New Knowledge and Perspectives. Curr Issues Mol Biol. 2023;45(10):7845-7861. Published 2023 Sep 27. doi:10.3390/cimb45100496

Davoodian N, Lotfaliany M, Huxley R ,et al. Prediabetes transitions to normoglycaemia or type 2 diabetes and associated risk factors in the Obesity, Diabetes and Cardiovascular Disease Collaboration: an individual-level pooled analysis of 19 prospective cohort studies. The Lancet Global Health. 2025;13(9): e1533-e1542. https://www.thelancet.com/journals/langlo/article/PIIS2214-109X(25)00237-2/fulltext

De Paoli M, Zakharia A, Werstuck GH. The Role of Estrogen in Insulin Resistance: A Review of Clinical and Preclinical Data. Am J Pathology. 2021;191(9):1490-1498. https://doi.org/10.1016/j.ajpath.2021.05.011

Engin S, Akkan T, Dağdeviren M, Şengezer T, Altay M. Are disease-related symptoms important to predicting developing diabetes from prediabetes? Turk J Med Sci. 2022;52(4):1093-1102. doi:10.55730/1300-0144.5412

Genazzani A, Petrillo T, Semprini E, et al. Metabolic Syndrome, Insulin Resistance and Menopause: The Changes in Body Structure and the Therapeutic Approach. GREM Gynecological and Reproductive Endocrinology & Metabolism. 2024;4(2):086-091 doi:10.53260/grem.234026

Janssen JAMJL. Overnutrition, Hyperinsulinemia and Ectopic Fat: It Is Time for A Paradigm Shift in the Management of Type 2 Diabetes. Int J Molecular Sci. 2024; 25(10):5488. https://doi.org/10.3390/ijms25105488

Jiang K, Luan H, Pu X, Wang M, Yin J, Gong R. Association Between Visceral Adiposity Index and Insulin Resistance: A Cross-Sectional Study Based on US Adults. Front Endocrinol. 2022;13:921067. doi:10.3389/fendo.2022.921067

Lean ME, Leslie WS, Barnes AC, et al. Primary care-led weight management for remission of type 2 diabetes (DiRECT): an open-label, cluster-randomised trial. Lancet. 2018;391(10120):541-551. doi:10.1016/S0140-6736(17)33102-1

Shao Y, Li L, Zhong H, Wang X, Hua Y, Zhou X. Anticipated correlation between lean body mass to visceral fat mass ratio and insulin resistance: NHANES 2011-2018. Front Endocrinol. 2023;14:1232896. doi:10.3389/fendo.2023.1232896

U.S. National Library of Medicine. Prediabetes: MedlinePlus Health Topics. Accessed May 2026. https://medlineplus.gov/prediabetes.html