Insomnia affects somewhere between 30% and 40% of the general population. Another 10% to 15% experience chronic insomnia disorder lasting months or years. But recent research published in Circulation Research in August 2025 reveals that not all insomnia carries the same health risks.

The difference comes down to a single measurement—how long you actually sleep during the night when measured objectively with polysomnography, not how long you think you slept. That distinction separates two fundamentally different conditions with dramatically different implications for cardiovascular health.

Dr. Julio Fernandez-Mendoza from Penn State analyzed decades of research showing that insomnia with objective short sleep duration—less than six hours measured on sleep studies predicts incident hypertension, type 2 diabetes, heart failure, stroke, cognitive impairment, Alzheimer’s disease, and all-cause mortality. The other phenotype, insomnia with normal sleep duration, doesn’t carry the same cardiovascular risks despite causing significant distress.

The difference isn’t subtle. Penn State researchers found that chronic insomnia with objective short sleep duration increased the odds of hypertension nearly fourfold compared to people without sleep problems. When they looked at incident cardiovascular and cerebrovascular disease over time, only the short sleep phenotype predicted future events.

Two Phenotypes, Two Different Problems

The model proposed by Vgontzas and colleagues divides insomnia into distinct biological phenotypes based on what’s happening in your brain and body during attempted sleep.

Insomnia with normal sleep duration involves cognitive-emotional arousal. People with this phenotype experience racing thoughts, sleep anxiety, and hypervigilance. They feel like they’re awake much of the night. When you measure their actual sleep objectively, they’re getting close to normal amounts—maybe six to seven hours. The problem is predominantly psychological, though the subjective experience of sleeplessness causes real suffering and impairment.

Insomnia with objective short sleep duration operates differently. People with this phenotype show activation of both limbs of the stress system—the hypothalamic-pituitary-adrenal axis and the sympathetic nervous system. Their bodies remain physiologically hyperaroused throughout the night. They’re not just worried about sleep. Their nervous systems can’t downregulate into restorative states.

Research on heart rate variability demonstrates the difference. Insomnia patients with objectively short sleep showed reduced high-frequency heart rate variability—indicating dampened parasympathetic activation—and an elevated low-frequency-to-high-frequency ratio, reflecting sympathovagal imbalance. Their cardiovascular systems remained stressed even during sleep.

The keyword: objective. When researchers used self-reported sleep duration rather than polysomnographic measurements, the associations disappeared. What you think you slept doesn’t predict cardiovascular disease. What actually happens in your brain and body during the night does.

Why Short Sleep Duration Damages Cardiovascular Health

Multiple mechanisms link insufficient sleep with cardiovascular disease. During normal non-REM sleep, heart rate, cardiac output, and systemic blood pressure decrease, a phenomenon called nocturnal dipping. This adaptive process reduces cardiovascular workload and protects blood vessels by mitigating endothelial stress and promoting arterial compliance.

People with insomnia and objective short sleep duration don’t show normal nocturnal dipping. Their blood pressure remains elevated throughout the night. Their sympathetic nervous system stays active. Over the years, chronic activation has damaged the cardiovascular system through several pathways.

Chronic sleep deprivation disrupts homeostatic processes. The hypothalamic-pituitary-adrenal axis becomes hyperactive, flooding the body with cortisol. Sympathetic nervous system activity increases, raising basal blood pressure and contributing to arterial stiffness. Systemic inflammation rises. All of these changes increase the risk of hypertension and cardiovascular morbidity.

A 2011 systematic review found that short sleep duration was associated with a 45% increased risk of coronary heart disease. More recent meta-analyses confirmed that various insomnia symptoms—nonrestful sleep, difficulty initiating sleep, difficulty maintaining sleep—each independently increased cardiovascular disease risk by 13% to 22%.

Life expectancy data makes the stakes clear. Individuals with optimal sleep patterns at age 30 lived 4.7 years longer for men and 2.4 years longer for women compared to those with poor-quality sleep.

The Problem with Current Treatments

Cognitive-behavioral therapy for insomnia remains the first-line guideline-recommended treatment. It works well for some people, particularly those with normal sleep duration who mainly need help with anxiety about sleep and counterproductive sleep behaviors.

But Fernandez-Mendoza’s review notes a crucial point: randomized clinical trials haven’t demonstrated that CBT-I reduces cardiovascular disease risk. The treatment appears to help only with sleep complaints and subjective sleep quality. Whether it addresses the physiological hyperarousal driving the short sleep phenotype remains uncertain.

Some studies suggest people with the short sleep phenotype don’t respond well to CBT-I. The cognitive and behavioral interventions help manage the psychological aspects, but don’t necessarily normalize the underlying nervous system dysregulation that prevents sustained sleep.

Medications force sleep through sedation but don’t teach the brain anything. Stop the medication, and the underlying problem usually comes roaring back. Neither approach addresses why the brain generates excessive arousal in the first place or how to train it to behave differently.

Training the Brain to Regulate Itself More Efficiently

At Sleep Recovery, we don’t approach insomnia as a disorder requiring treatment. We see it as a brain that hasn’t learned to downregulate efficiently. Excessive cortical arousal, the inability to sustain deep sleep stages, and fragmented sleep architecture—these reflect the electrical patterns the brain generates. Those patterns can be trained.

Alpha-theta neurofeedback isn’t about treating insomnia directly. It’s about teaching the brain to access states it currently can’t reach on its own. The training provides real-time feedback on brainwave activity, reinforcing more efficient patterns through operant conditioning.

During sessions, sensors monitor EEG activity—audio feedback changes based on the frequency bands your brain produces. When you generate more alpha (8-12 Hz) and theta (4-7 Hz) frequencies associated with relaxed wakefulness and deep meditative states, the tones become pleasant and coherent.

Your brain learns through repeated exposure. Not through intellectual understanding or conscious effort. Through direct experience of different states paired with immediate reinforcement. Like learning to balance on a bicycle—you can’t think your way through it, you have to feel it enough times that your nervous system figures out how to maintain stability.

Over 30-minute sessions every other day, spread across weeks and months, the training produces measurable changes. Excessive beta activity during attempted sleep decreases. Alpha capacity increases. Theta rhythms strengthen. The brain develops greater flexibility—better able to shift between arousal states as circumstances require.

The goal isn’t to force sleep. The goal is efficient nervous system function. A brain that can activate when necessary and deactivate completely when it’s time to rest. That operates without chronic hypervigilance. That doesn’t waste energy maintaining unnecessary arousal.

Why Efficiency Matters More Than Sleep Duration

Someone with insomnia and objective short sleep duration isn’t just sleeping less. Their brains are working harder throughout the night, repeatedly pushing EEG arousal that serves no purpose. That inefficiency shows up across multiple systems.

Cardiovascular: Elevated nighttime blood pressure, reduced heart rate variability, persistent sympathetic activation. The heart and blood vessels never get the recovery period that normal nocturnal dipping provides.

Endocrine: Dysregulated cortisol patterns, with levels remaining elevated when they should drop. The hypothalamic-pituitary-adrenal axis is stuck in a state of stress.

Immune: Chronic activation impairs regular immune surveillance and regulation. We’ve already seen how anxiety and insomnia reduce natural killer cell counts.

Metabolic: Disrupted glucose metabolism, insulin resistance, and altered appetite regulation. The short sleep phenotype shows a significantly higher risk for type 2 diabetes.

All of these downstream effects trace back to the same source: a nervous system that can’t downregulate. Train the brain to operate more efficiently, and the benefits cascade through every system that depends on proper sleep architecture.

The Distinction Between Treatment and Training

Medical treatments target symptoms. The Sleep Recovery program addresses the nervous system’s capacity to regulate itself. The distinction matters.

If you have insomnia with an objectively short sleep duration, your cardiovascular disease risk is elevated. That risk comes from the physiological hyperarousal—the inability of your nervous system to enter restorative states. Treating the subjective complaint of sleeplessness doesn’t necessarily address the biological severity.

Training the brain to generate healthier EEG patterns during attempted sleep could reduce that biological severity. Better alpha-theta generation, reduced high-frequency beta, and more sustained slow-wave sleep. Those changes would reflect a nervous system learning to operate with less wasted energy.

If the brain learns to generate healthier sleep patterns, the downstream cardiovascular effects should improve. Heart rate variability should normalize. Nocturnal blood pressure dipping should return. Sympathetic-parasympathetic balance should shift toward parasympathetic dominance during rest.

None of that requires medication or direct intervention on sleep itself. It requires teaching the electrical patterns underlying efficient nervous system function. Sleep improves as the brain learns to function better.

Implications for Prevention

The Fernandez-Mendoza review emphasizes that insomnia, particularly when associated with objectively short sleep duration, should be included in cardiovascular disease prevention and management. The data support that conclusion. Nearly fourfold increased risk of hypertension. Significantly elevated risk for heart failure, stroke, and mortality.

But prevention requires intervening on the underlying physiology, not just managing symptoms. If someone has insomnia with short sleep duration measured objectively, their cardiovascular risk is elevated now. Waiting years to see if CBT-I helps or medications work misses the opportunity to address the biological severity before the disease develops.

Brainwave entrainment provides one approach. Not the only approach—exercise, stress management, and proper nutrition all matter. But the direct training of brain electrical patterns offers something that other interventions don’t: teaching the nervous system itself to function more efficiently.

Cardiovascular research makes clear that objective sleep duration matters more than subjective sleep experience. What your brain does during attempted sleep predicts your health outcomes. Training that brain to operate differently could reduce the risk that those objective measurements currently predict.

Your sleep tonight reflects how efficiently your brain can downregulate. If it can’t, that inefficiency is already damaging your cardiovascular system. It may be time to teach it something better.

For more info on this training modality, call: 800-927-2339