Insulin, Hormones, and Midlife Metabolism

When we talk about metabolic health, insulin often gets a bad reputation. We hear phrases like “insulin resistance” and assume insulin itself is the problem.

Hormones play a central role in how the body regulates insulin and blood sugar. Yet this connection is often overlooked in traditional diabetes care — especially for women.

As women move through perimenopause and menopause, changes in hormone levels can significantly affect metabolism and insulin function. This is a major reason insulin resistance and type 2 diabetes become far more common in midlife.

Hormones That Influence Insulin Function

Several hormones play an important role in insulin regulation and blood sugar balance, including:

• Estrogen

• Progesterone

• Testosterone

• DHEA

• Pregnenolone

• Thyroid hormone

  
  

These hormones don’t work in isolation. They function as an interconnected system — and when one is off, insulin regulation often suffers.

Estrogen: A Key Metabolic Hormone

Estrogen has profound effects on metabolism and insulin sensitivity.

As estrogen levels decline:

• Fat redistributes toward the abdomen

• Basal metabolic rate decreases

• Insulin signaling becomes less efficient

  
  

This is a major reason diabetes risk rises after menopause. It’s not simply aging — it’s hormonal change.

Estrogen loss plays a significant role in:

• Weight gain that feels resistant to diet and exercise

• Worsening insulin resistance

• Changes in body composition and energy

  
  

This is why insulin resistance often shows up or accelerates during perimenopause and menopause.

Testosterone: Helpful or Harmful Depends on Balance

Testosterone affects insulin sensitivity in both men and women.

• Low testosterone in men is associated with an increased risk of diabetes, and testosterone therapy is considered an effective treatment for insulin resistance in appropriately selected men.

• Too much testosterone, particularly in women, can worsen insulin resistance.

  
  

Once again, balance matters. More is not better.

Thyroid, DHEA, and Pregnenolone

Other hormones also influence insulin regulation:

• Hypothyroidism slows metabolism and worsens insulin resistance

• Both excess and deficiency of DHEA can impair glucose regulation

• Pregnenolone plays a supportive role in metabolic and neurologic health

  
  

This is why I rarely look at insulin or blood sugar in isolation. Hormones matter.

Cortisol and Stress

Cortisol and insulin are closely linked.

• Chronically high cortisol impairs insulin signaling

• Low cortisol can also disrupt insulin function

• Ongoing stress makes insulin resistance harder to reverse

  
  

Sleep, stress management, and nervous system regulation are essential parts of metabolic health — not optional extras.

Why Insulin Regulation Matters (Beyond Blood Sugar)

Healthy insulin function supports:

• Brain health and memory

• Weight regulation

• Stable blood sugar

• Cardiovascular health

• Blood pressure control

• Bone health

• Reduced breast cancer risk

  
  

Insulin resistance and obesity are very commonly associated with the development of breast cancer, particularly after menopause.

This is about much more than avoiding diabetes — it’s about protecting long-term health and quality of life.

The Big Picture

Insulin resistance is never just about sugar.

It’s influenced by:

• Nutrition

• Movement

• Supplements

• Hormones

• Stress

• Sleep

• Muscle mass

• Midlife physiology

  
  

When addressed early, insulin resistance is very treatable — and often reversible.

The Takeaway

Insulin is not the villain.

It is a hormone of repair, and when it functions well, it protects nearly every system in the body.

This is why I pay attention to insulin long before diabetes develops — and why addressing hormones in midlife is such an important part of that work.

A gentle next step

If insulin resistance, weight changes, fatigue, or shifting labs have started to show up in midlife, this is something I help patients navigate every day.

Early attention makes all the difference.