A Deep Dive into The Unidentified Cause of Hot Flashes. Dr. Rick Cohen, M.D.

Hi all, 

Here's what medicine tells you about hot flashes:

"Changing hormone levels before, during and after menopause are the most common causes of hot flashes. It's not clear how hormonal changes cause hot flashes. But most research suggests that hot flashes happen when lower estrogen levels cause the body's heat manager, also called the hypothalamus, to respond to slight changes in body temperature."

This is at verbatim off the Mayo Clinic.

And here's also what medicine tells you about the risk factors for severe hot flashes:

Smoking, being obese (high BMI), gender specific surgeries, and race are factors that may raise the risk of having hot flashes

Risk factors for more severe and frequent hot flashes include smoking, being overweight or having obesity, a high-stress lifestyle including mental health conditions such as depression and anxiety, and socioeconomic factors like lower education and lower income

Thanks for hanging in there.  Now let me show you something that medicine sees but doesn't connect with all this:

Those are the exact same risk factors as:

• Type 2 diabetes
• Hypertension
• Cardiovascular disease
• Anxiety disorders
• Metabolic syndrome

And the smoking gun gets louder here:

Reporting any vasomotor symptoms was associated with 18% increased diabetes risk, which increased with severity (mild: HR=1.13; moderate: HR=1.29; severe: HR=1.48) and duration, independent of obesity.

Hot flashes were associated with higher HOMA index (insulin resistance) and higher glucose. Women who had hot flashes on six or more days over two weeks had 5.91% higher insulin resistance.

Hot flashes don't just correlate with metabolic disease. They predict it. Independent of obesity. Independent of estrogen levels.

Because they're the same disease.

Let me show you exactly what's happening.

Part 1: The Risk Factors Are Identical—Because the Mechanism Is Identical

What Predicts and Causes Severe Hot Flashes?

Anxiety, specifically the somatic symptom dimension, was strongly associated with hot flashes in the menopause transition in a 14-year follow-up interval, remaining strong after adjusting for age, menopausal stage, reproductive hormone levels, obesity, history of depression, education, race, perceived stress, alcohol use and smoking.

Disease states or conditions associated with respiratory or metabolic acidosis may be risk factors for hot flashes, including COPD, diabetic ketoacidosis, and factors that make breathing difficult such as in smokers, asthmatic persons, or obese persons.

Let me translate that:

The women who get severe, persistent hot flashes are the same women who have:

• Smoking history (autonomic stress)
• Obesity (metabolic dysregulation)
• Anxiety (sympathetic dominance)
• Low socioeconomic status (i.e. chronic stress)
• Respiratory issues (CO₂ sensitivity)
• Insulin resistance (autonomic-metabolic dysfunction)

These aren't separate risk factors. They're all manifestations of autonomic nervous system dysregulation.

And Here's the Kicker

Since longitudinal studies determined that anxiety is a strong risk factor for hot flashes, researchers hypothesized that an anxiogenic stimulus that signals air hunger (hypercapnic gas) would trigger hot flashes in symptomatic menopausal women. The studies demonstrate that this anxiogenic stimulus is capable of eliciting hot flashes in menopausal women.

They can TRIGGER hot flashes with CO₂ challenge—the exact same thing that triggers panic attacks in people with anxiety disorders.

Same autonomic dysfunction. Same failed CO₂ regulation. Same sympathetic overreaction.

Different symptom name. Same broken system.

Part 2: Hot Flashes Predict Cardiovascular Disease—Because They're Both Autonomic Dysregulation

If hot flashes were just "low estrogen," they wouldn't predict heart attacks.

But they do.

Women who have frequent hot flashes or hot flashes for many years faced a 50% to 77% increased risk of future cardiovascular disease events. Standard risk factors for cardiovascular disease could not account for this increase. The women's estrogen levels also could not explain their increased risk.

Read that again: Estrogen levels could not explain the increased cardiovascular risk.

So what does?

The Same Vascular Dysfunction

Research found that women who have hot flashes, especially younger women who have them early in the transition into menopause, have arteries that are less likely to relax appropriately during exercise or stress. Their arteries were stiffer than normal. Specifically, the researchers focused on flow-mediated dilation—the way an artery widens when blood flow increases. In the women who had hot flashes, flow-mediated dilation did not tend to work properly.

Women with hot flashes had reduced flow-mediated dilation and greater aortic calcification. Hot flashes may mark adverse underlying vascular changes among midlife women

Impaired endothelial function. Vascular stiffness. Reduced arterial compliance.

That's not a temperature problem. That's cardiovascular dysregulation.

And It's Mediated by the Autonomic Nervous System

In the Study of Women's Health Across the Nation (SWAN) Heart Study, women reporting hot flashes had greater evidence of subclinical cardiovascular disease compared to women not reporting hot flashes. Reductions in cardiac vagal control (as measured by high frequency heart rate variability) have been prospectively associated with cardiovascular morbidity and mortality.

Risk factors for hot flashes are also cardiovascular risk factors, including obesity and smoking. Another possible mechanism linking hot flashes to CVD is shared risk factors

They don't just share risk factors. They share the underlying mechanism:

Chronic sympathetic nervous system activation with impaired parasympathetic (vagal) recovery.

Part 3: The Real Mechanism—What Medicine Admits But Won't Address

Here's what actually happens during a hot flash:

Hot flashes are a rapid and exaggerated heat dissipation response, consisting of profuse sweating, peripheral vasodilation, and feelings of intense, internal heat. They are triggered by small elevations in core body temperature acting within a greatly reduced thermoneutral zone. This is due in part, but not entirely, to estrogen depletion at menopause. Elevated central sympathetic activation, mediated through α2-adrenergic receptors, is one factor responsible for narrowing of the thermoneutral zone

There was a four-fold increase in efferent skin sympathetic nerve activity before and during a hot flash

Translation:

1. The autonomic nervous system has narrowed the "safe" temperature range
2. Small temperature changes trigger massive sympathetic activation
3. This causes emergency cooling (vasodilation, sweating)
4. The system overreacts to a normal stimulus

Sound familiar?

• Hypertension: The system overreacts to normal pressure demands
• Diabetes: The system overreacts by maintaining high glucose
• Anxiety: The system overreacts to normal environmental stimuli
• Hot flashes: The system overreacts to normal body temperature

Same pattern. Different organ system. Same autonomic misclassification.

Part 4: Why Estrogen Withdrawal Triggers It (But Doesn't Cause It)

Hormonal changes alone do not explain the variability in hot flash frequency, severity, and bother reported by women during the menopause transition, nor the fact that hot flashes are not reported by all women undergoing either gradual or sudden estrogen withdrawal.

Four consistent patterns of vasomotor disturbances have rather been identified across different countries, making it unlikely that these patterns are solely explained by socioeconomic or cultural factors. The changing hormonal environment of menopause may unmask differences in the autonomic neurovascular control mechanisms that put an individual woman at risk

If hot flashes were just estrogen deficiency:

• Every woman with low estrogen would have them (they don't!)
• Hormone replacement would fix them 100% (it doesn't always)
• Severity would track estrogen levels precisely (it doesn't)
• They'd all follow the same pattern (they don't)

What actually determines who gets severe hot flashes?

Baseline autonomic regulation capacity.

What Estrogen Actually Does

Estrogens are known potent neuromodulators of numerous neuronal circuits throughout the central nervous system. Changing estrogen levels during menopause may impact multiple components involved in maintaining temperature homeostasis

Estrogen modulates:

• Thermoregulation
• Vascular tone
• Sleep architecture
• Stress response sensitivity
• Inflammatory signaling
• Autonomic nervous system reactivity

When it drops, the autonomic nervous system loses a major stabilizing input.

If your ANS is already:

• Stressed
• Fragile
• Compensating
• Operating with a narrow regulatory range

It can't recalibrate when estrogen withdraws.

So it defaults to sympathetic overdrive, vascular dysfunction, and thermoregulatory chaos.

Sympathetic nervous system activation has been identified as an important factor in the occurrence of hot flashes, and women with menopausal symptoms had a significantly higher low and high frequency ratio (indicator of sympathetic nerve activity) compared with those without menopausal symptoms

Part 5: The Metabolic Connection—Why Hot Flashes Predict Diabetes

This is where it gets undeniable.

Reporting any vasomotor symptoms was associated with 18% increased diabetes risk, which increased with severity (mild: HR=1.13; moderate: HR=1.29; severe: HR=1.48) and duration, independent of obesity.

Independent of obesity.

That means it's not just that heavier women have more hot flashes and also more diabetes.

The hot flashes themselves predict diabetes development.

Hot flashes were associated with higher HOMA index (insulin resistance) and higher glucose. Women who had hot flashes on six or more days over two weeks had 5.91% higher insulin resistance.

Hot flash severity was significantly associated with lower adiponectin levels and higher leptin levels, both markers of insulin resistance.

Why would temperature dysregulation predict glucose dysregulation?

Because they're both autonomic ANS issues!

The autonomic nervous system controls:

• Thermoregulation (via hypothalamus and sympathetic activation)
• Glucose metabolism (via sympathetic/parasympathetic balance)
• Vascular tone (via sympathetic vasoconstriction)
• Insulin sensitivity (via stress hormone release and metabolic signaling)

When autonomic regulation fails, ALL of these systems drift together.

Part 6: The Sleep Disruption Link—How Hot Flashes Worsen Everything

Nocturnal hot flashes are disruptive regardless of when they occur during the night. More hot flashes occur during the second half of the night when more REM sleep typically occurs and when such disruption has a greater chance of increasing the risk of heart disease. Disruptions to REM sleep can lead to an increased risk of developing heart disease

Here's the vicious cycle:

1. Autonomic dysregulation → hot flashes
2. Hot flashes → REM sleep disruption
3. REM disruption → worse autonomic recovery
4. Worse recovery → more sympathetic dominance
5. More sympathetic dominance → worse glucose control, worse vascular function, more hot flashes

It's a self-reinforcing loop.

And medicine treats it as: "menopause symptoms that should be tolerated."

Part 7: What Actually Helps (And Why Medicine Won't Say It)

Slow Breathing Works—Because It's Autonomic

Paced breathing (slow, deep, diaphragmatic breathing) reduces central sympathetic activity and facilitates the relaxation response. Participants reported hot flash reductions of 52% for paced breathing twice a day, 42% for paced breathing once a day

If hot flashes were purely hormonal, why would breathing change them?

Because slow breathing directly modulates autonomic balance—reducing sympathetic activation and widening the thermoneutral zone.

Stress Management Matters—Because It's Autonomic

There's evidence that stress itself can trigger hot flashes, and then you can get into a vicious circle of being stressed by your hot flashes and thus having more

Stress is an autonomic state. Hot flashes are an autonomic state.

They're not separate problems.

Why Some Women Adapt and Others Don't

Four consistent patterns of vasomotor disturbances have been identified across different countries. The changing hormonal environment of menopause may unmask differences in the autonomic neurovascular control mechanisms that put an individual woman at risk

Women with flexible, adaptive autonomic systems handle estrogen withdrawal fine.

Women with already-stressed, narrow-range autonomic systems—suffer.

Part 8: What Medicine Should Be Saying (But Isn't)

Is it time for the scientific and medical community to change the description of hot flashes and night sweats from "menopausal symptoms" to a term that describes the potential underlying pathophysiological phenomenon of autonomic neurovascular dysregulation?

Yes. It is.

Labeling hot flashes and night sweats as symptoms of menopause in some ways implies they are merely bothersome symptoms that should be tolerated or treated until they resolve rather than manifestations of one or several underlying pathophysiological processes

Here's what women deserve to know:

Hot flashes are not inevitable consequences of menopause.

They are a visible manifestation of autonomic nervous system dysregulation—the same dysregulation that causes:

• Insulin resistance and diabetes
• Hypertension
• Cardiovascular disease
• Anxiety
• Sleep disruption

If you have:

• Severe hot flashes
• Persistent hot flashes (years, not months)
• Hot flashes plus anxiety
• Hot flashes plus metabolic issues

You don't just have "menopause symptoms."

You have autonomic dysregulation that increases your risk for cardiovascular disease and diabetes.

And you can address it—not by just suppressing symptoms, but by restoring autonomic flexibility:

1. Slow breathing (6 breaths/min, 15 minutes twice daily—proven to reduce hot flashes 50%+)
2. Recovery-based exercise (not exhaustive training)
3. Sleep optimization (autonomic restoration time)
4. Stress recovery training (not just "stress management")
5. HRT can still help (removes trigger while you retrain regulation)

The Bottom Line

Medicine says:

• Hot flashes = menopause symptom
• Diabetes = metabolic disease
• Hypertension = cardiovascular disease
• Anxiety = mental health disorder

The research shows:

• Same risk factors (smoking, obesity, stress, low SES)
• Same mechanism (sympathetic dominance, impaired vagal recovery)
• Same predictive pattern (hot flashes predict diabetes and CVD)
• Same interventions work (slow breathing, autonomic training)

They're not separate diseases.

They're different manifestations of autonomic nervous system dysregulation.

Hot flashes just happen to be the most visible one—because you can't hide a thermoregulatory crisis the way you can hide rising glucose or creeping blood pressure.

The body isn't failing randomly in multiple systems.

One regulatory system is failing, and multiple organ systems are responding.

And until medicine stops treating hot flashes as "just menopause" and starts treating them as a warning sign of systemic autonomic dysfunction, women will keep being told to tolerate years of symptoms that predict heart attacks and diabetes.

The data is right there. The mechanism is clear. The interventions exist.

We're just calling it the wrong thing.