Optimizing Metabolic Health for Women: A Troubleshooting Approach to Insulin Resistance

Lara Briden, ND

Insulin resistance goes far beyond blood sugar—affecting hormones, cardiovascular health, and long-term disease risk. An individualized, root-cause approach can restore metabolic flexibility and resilience in women.

Abstract

This article explores insulin resistance as a systemic condition often overlooked in women’s health. Using clinical clues, assessment tools, and a troubleshooting treatment model, it highlights strategies for improving metabolic flexibility and preventing long-term complications.

The Epidemic Hiding in Plain Sight

Insulin resistance is the epidemic hiding in plain sight. It is a primary driver of heart disease, dementia, and some cancers, yet most patients trying to prevent these conditions have either never heard of insulin resistance or mistakenly believe it is mainly about blood sugar. It is not.

Beyond the Blood Sugar Paradigm

Because glucose was the first metric medicine could easily measure, it became the lens through which metabolic health has traditionally been viewed. Starting in the early 20th century, clinicians defined diabetes and related conditions almost entirely by blood sugar levels, and that “glucose-centric” paradigm still dominates with an over-reliance on fasting glucose, HbA1c, and oral glucose tolerance tests.¹

It’s time to look beyond that paradigm, because by the time glucose rises in type 2 diabetes, insulin has often been elevated for decades.

Recognizing the Negative Impacts of Chronically Elevated Insulin 

Insulin resistance is a whole-body hormonal condition, and its main feature is hyperinsulinemia, or chronically elevated insulin. Because insulin influences almost every tissue, hyperinsulinemia has far-reaching effects on the brain, bones, liver, ovaries, uterus, and breasts. Over time, it can contribute to dementia,² osteoporotic fractures,³ fatty liver disease, polycystic ovary syndrome (PCOS), and even uterine and breast cancers.⁴

It also promotes cardiovascular disease. Notably, “metabolic syndrome,” with its high-risk features of increased waist circumference, high blood pressure, high triglycerides, and low HDL, was originally called “insulin resistance syndrome”⁵ because of the central role insulin plays in those abnormalities.

Chronically elevated insulin can also promote fat gain by impairing fuel partitioning and driving compensatory hunger.⁶ The resulting “metabolic inflexibility” or reduced ability to access fat stores for energy can leave patients feeling they must continuously eat carbohydrate-rich foods just to maintain energy. 

Case Example: Erica 

My patient Erica described insulin resistance this way: “I can’t diet or go too long between meals, or I feel really weak. And I feel totally wiped out by exercise.”

Despite her best efforts, she could not benefit from the same strategies that worked for others, and she blamed herself: “I should try harder. I should have more willpower.” In reality, Erica’s problem was not willpower but the underlying condition of insulin resistance, where her cells could not access the energy they needed.

Once we identified insulin resistance (based on high fasting triglycerides and ALT; see below), Erica shifted her focus away from “just losing weight” toward improving insulin sensitivity and metabolic flexibility. With that shift, she finally regained the energy and satiety required for sustainable weight loss and long-term health.

Clinical Clues and Assessment Tools

“A disease known is half cured.” ~ Thomas Fuller

The only definitive test for insulin resistance is the hyperinsulinemic euglycemic clamp, used in research but not practical clinically. The next most reliable test is the HOMA-IR index, a calculated ratio of fasting glucose to fasting insulin. A healthy HOMA-IR reading should be less than 1. Other methods that directly measure insulin, such as fasting insulin or an OGTT with insulin, can be helpful but are limited by the challenge of variability in insulin assays.

Fortunately, clinicians can build a strong clinical picture of insulin resistance from signs, symptoms, and routine pathology.

Clinical signs and symptoms include:

• Skin tags
• Acanthosis nigricans (skin darkening)
• Waist circumference >38 inches in men, >33 inches in women
• Hypertension
• Reactive hypoglycemia
• Constant hunger for carbohydrates, sometimes escalating to ultra-processed food addiction⁷

Laboratory findings suggesting insulin resistance include:

• Triglycerides >150 mg/dL (1.7 mmol/L)
• Uric acid >0.33 mmol/L
• C-reactive protein (CRP) >1 mg/L, in the absence of other causes, suggesting metabolic endotoxemia as a driver
• Serum ferritin >200 ng/mL. Iron overload increases cardiometabolic risk, especially in postmenopausal women⁸
• ALT >19 IU/L or ALT/AST ratio >1. High ALT is highly predictive of insulin resistance (especially in women) and is associated with MASLD (formerly NAFLD)⁹

Continuous glucose monitoring (CGM) may also provide new insights. A 2024 Stanford study found that CGM, used as a standardized at-home OGTT combined with machine learning, can identify distinct metabolic phenotypes.¹⁰ By analyzing the shape of glucose curves, researchers could distinguish between muscle insulin resistance, β-cell dysfunction, hepatic insulin resistance, and impaired incretin response. Standard glucose and HbA1c testing failed to detect these patterns, underscoring the need to move beyond the glucose-centric paradigm. Importantly, the Stanford work also points to an individualized approach, where treatment is guided by the specific driver of insulin resistance.

An Individualized, Troubleshooting Approach to Treatment

From a naturopathic perspective, we can extend this individualized approach further, identifying each patient’s metabolic obstacles, the mechanisms or conditions impairing their insulin sensitivity.

Examples of such obstacles include:

• Modern exposures: ultraprocessed food, alcohol, and environmental toxins
• Subclinical nutrient deficiencies (e.g., magnesium, choline, inositol)
• Gut dysfunction and food sensitivities
• Circadian misalignment
• Medications including androgenic progestins (e.g., levonorgestrel)
• Androgen excess in PCOS and menopause
• Hashimoto’s thyroid disease
• Premenstrual changes in dopamine, histamine, and estrogen

Each obstacle can be rated as high or medium priority, and easy or difficult to fix,¹¹ with patients encouraged to start with “easy wins.” Because all systems are connected, addressing one obstacle often improves others.

For example, treating small intestinal bacterial overgrowth (SIBO) can restore energy, normalize hunger, and reduce sugar cravings. Two of the ten patient stories in my book involve gut repair. Stopping an androgenic progestin (such as a contraceptive implant) can be another important metabolic strategy, since androgen excess promotes insulin resistance in women.¹² Other key approaches include building muscle, supporting the autonomic nervous system, and managing premenstrual mood changes.

A Plan for Erica 

For Erica, priority obstacles included exposure to ultraprocessed food, SIBO, and premenstrual mood symptoms triggering binge eating.

Her treatment plan consisted of:

• Building highly satiating protein-centered meals (especially breakfast) and removing junk food triggers to “shelter” from ultraprocessed food
• Treating SIBO with an 8-week course of berberine (500 mg twice daily with meals)
• Supporting satiety and reducing premenstrual cravings with magnesium glycinate (300 mg daily) and inositol (2 g twice daily)
• Further addressing premenstrual mood with oral micronized progesterone (100 mg nightly in the luteal phase)

Three-Month Follow-Up

Erica noticed benefits almost immediately. After introducing a protein-rich breakfast, she reported greater morning satiety and often no longer needed the mid-morning granola bar to make it through to lunch. Her premenstrual symptoms, including cravings, also improved markedly. From a baseline of three to four binge episodes each premenstrual cycle, she experienced none by the second month and only one in the third month before follow-up. Notably, the cycle without binges coincided with the final weeks of her berberine course.

She also lost 4 inches from her waist circumference, suggesting both improved insulin sensitivity and reduced visceral fat. At the six-month follow-up, the plan is to reassess her progress with repeat triglyceride and ALT testing to track metabolic changes objectively alongside her clinical improvements.

Conclusion 

Insulin resistance is much more than a blood sugar problem. It’s a systemic condition that can impact every aspect of health. By shifting focus from glucose to insulin, from static labs to dynamic patterns, and from generic prescriptions to individualized troubleshooting, we can help our patients reclaim metabolic flexibility and health.

References

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