Most people with insomnia don’t know they have it.
Not because the signs aren’t there — but because the signs have become so familiar they no longer register as signs. The TV stays on until midnight. The phone comes to bed. Sleep gets pushed later and later until late becomes the schedule. Waking at 3am feels like a personality trait. Lying in bed with a mind that won’t stop feels like the price of a busy life.
The body adapts. The routine adjusts. And somewhere along the way, a sleep problem becomes a lifestyle.
This is how insomnia survives — not dramatically, but quietly, hiding inside habits that feel normal because they are common. Common and normal are not the same thing. And the distance between them, compounded over years, is where chronic health problems are born.
The Sleep Epidemic Nobody Is Talking About Honestly
Insomnia is not a fringe condition. It is one of the most prevalent health problems in the modern world — and one of the least honestly addressed.
The numbers are significant. Roughly one in three adults report symptoms of insomnia. About one in ten meet the clinical criteria for insomnia disorder — difficulty sleeping at least three nights a week for three months or more. The consequences extend well beyond fatigue: insomnia is associated with a 53% increase in cardiovascular mortality, a 48% increase in heart attack risk, and elevated rates of type 2 diabetes, cognitive decline, mood disorders, and dementia. These are not soft associations. Genetic studies suggest the relationship is likely causal.
This is a public health problem. It is being managed, in large part, as a personal inconvenience.
Part of what makes insomnia so persistent is the modern environment it lives in. We have built a world that is structurally hostile to sleep — artificial light that suppresses melatonin, 24-hour access to screens and social networks, work schedules that ignore biology, and a culture that treats sleep deprivation as a productivity trade-off rather than a health crisis. The distractions available at midnight now are not just keeping people awake. For many, they have become the coping mechanism for a sleep system that was already struggling.
As we explored in You Were Built Around the Sun, the circadian rhythm — the body’s 24-hour biological clock — governs far more than when you feel tired. It coordinates hormone release, metabolism, immune function, cardiovascular activity, and cellular repair across every organ system. When that rhythm is disrupted night after night, chronic insomnia causes consequences that are systemic and cumulative — not just fatigue, but organ-level disruption that compounds over time.
And there is a consequence most people have never heard of: the brain has its own waste clearance system — the glymphatic system — that operates primarily during deep sleep. It flushes out the metabolic byproducts that accumulate during waking hours, including the proteins associated with Alzheimer’s disease and other neurodegenerative conditions. When sleep is disrupted chronically, that clearance system runs at a fraction of its capacity. The brain is not just tired. It is not being cleaned.
Understanding chronic insomnia causes begins here: this is not just a bad night. It is a circadian system under sustained pressure — and a body that is not getting the recovery it was designed to depend on.
What Standard Care Gets Right — and Where It Stops
When someone finally does seek help for insomnia, the pathway is more predictable than it should be.
A sleep study may identify disordered breathing and lead to a CPAP prescription — a meaningful intervention for obstructive sleep apnea, but one that addresses airway mechanics, not the underlying drivers of sleeplessness. And as we explored in The Bridge That Collapses, many people don’t have just one sleep problem. Roughly 30–50% of people with sleep apnea also have clinically significant insomnia, and 30–40% of people with chronic insomnia meet criteria for sleep apnea. These conditions feed each other — the fragmented sleep from apnea worsens insomnia, and the hyperarousal from insomnia worsens apnea. Treating one without evaluating the other leaves half the problem unaddressed.
A primary care visit is more likely to produce a prescription: sedatives, sleep aids, anxiety medications, or referrals to pain management if chronic pain is part of the picture. In recent years, CBD and medical cannabis have joined the list of commonly reached-for solutions.
Here is what deserves more attention: the most effective treatment for chronic insomnia is not a pill. It is cognitive behavioral therapy for insomnia — CBT-I. Every major medical guideline — from the American College of Physicians to the American Academy of Sleep Medicine to the VA/DoD — recommends CBT-I as the first-line treatment, ahead of any medication. And the evidence backs it up: CBT-I produces better long-term outcomes than sleeping pills, with a 41% long-term remission rate compared to 28% for medication, and without the side effects or dependency risk.
CBT-I works by changing the behaviors and thought patterns that perpetuate insomnia — things like stimulus control, sleep restriction, cognitive restructuring, and relaxation techniques including abdominal breathing and progressive muscle relaxation.
This is important because it aligns with something we believe deeply: the most powerful interventions for sleep are behavioral and physiological, not pharmaceutical. Breath control, consistent routines, and retraining the nervous system’s relationship with rest are the foundations of what we teach — and they overlap significantly with what CBT-I delivers.
Where CBT-I stops, however, is where our work continues. CBT-I addresses the behavioral and cognitive patterns that perpetuate insomnia effectively. But it does not investigate the physiological drivers that created the conditions for insomnia in the first place — the organ-level dysfunctions, the inflammatory inputs, the structural and neurological factors that keep the body in a state of alert when it should be in recovery. Those require a different kind of evaluation. And they are where the deeper answers often live.
Chronic Insomnia Causes Are Not All the Same
This is the clinical reality that most insomnia conversations skip entirely: the experience of not sleeping well can arise from several distinct physiological dysfunctions, each with its own mechanism and its own pattern of symptoms.
Treating all of them the same way — with a sedative, a sleep hygiene checklist, or a CPAP — is like treating all chest pain the same way regardless of whether the cause is muscular, cardiac, or gastrointestinal. The symptom is the same. The cause is not.
The Liver and Circadian Hormone Processing
The liver plays a role in the sleep-wake cycle that standard care almost never addresses.
The liver is the primary site where melatonin — the hormone of darkness — is metabolized and cleared from the bloodstream. In people with significant liver disease, this clearance is impaired: melatonin levels remain elevated during the day, and the nighttime peak is delayed. The result is a person who feels drowsy in the afternoon and alert at night — a pattern many people chalk up to being a “night owl” when it may reflect impaired liver function disrupting the circadian hormone cycle. Sleep disturbances affect 50–80% of patients with liver cirrhosis, making it one of the strongest organ-sleep associations in medicine.
The cortisol rhythm is driven primarily by the brain’s HPA axis, which reduces its output in the evening to allow sleep onset. But the liver participates in this system too — it metabolizes cortisol, and when liver function is compromised, the downstream hormonal environment shifts in ways that interfere with the body’s ability to transition into sleep.
Traditional Chinese medicine identified liver disharmony as a primary pattern associated with difficulty falling asleep long before Western medicine had tools to measure hormone clearance. Both traditions recognize that when the body’s metabolic processing system is under stress, sleep onset suffers. Chronic stress, poor diet, alcohol, and metabolic burden all compromise liver function — and all are extremely common.
The Heart-Kidney Connection and Dream-Disturbed Sleep
Another pattern — dream-disturbed sleep, night sweats, and a sense of the mind never fully quieting — points to a different physiological dynamic.
Traditional Chinese medicine describes this as a disconnect between the heart and kidney systems — heart-kidney yin deficiency. In their framework, the heart governs the mind and circulation while the kidney system governs the body’s deep reserves, fluid balance, and cooling mechanisms. When these systems fall out of coordination, the result is shallow, dream-heavy sleep that leaves the person feeling unrestored regardless of how many hours they spent in bed.
Western medicine describes a parallel phenomenon through a different lens: the hyperarousal model. Research shows that people with chronic insomnia have measurably elevated cortisol — running about 30% higher than in good sleepers, with the greatest elevations occurring in the evening and first half of the night, precisely when cortisol should be at its lowest. Their sympathetic nervous system remains overactive during sleep. Their brains show elevated metabolic activity even during rest.
Different traditions, different language, same observation: something is preventing the body from settling into the deep, quiet state that restorative sleep requires.
Kidney Function and the Inability to Stay Asleep
Difficulty staying asleep — waking in the middle of the night and being unable to return to sleep — is strongly associated with kidney dysfunction. Sleep disorders affect 30–79% of people with chronic kidney disease, compared to about 10% of the general population, and the relationship worsens as kidney function declines.
The mechanisms are straightforward: the kidneys regulate the filtration and balance of electrolytes, fluids, and metabolic waste products. When that regulation is impaired, the internal environment becomes less stable overnight — and sustained sleep requires a stable internal environment. Traditional Chinese medicine has long associated kidney deficiency patterns with sleep maintenance insomnia and early morning waking — again, a different framework arriving at a clinically consistent observation.
Neurological Overactivation and the Brain That Won’t Quiet
The brain has two major signaling systems working in opposition: excitatory signals that keep it active and inhibitory signals that quiet it down. Sleep requires the inhibitory system to gain the upper hand.
In people with chronic insomnia, that balance is off. Research using advanced brain imaging has found that GABA levels — the brain’s primary inhibitory neurotransmitter — are nearly 30% lower in people with primary insomnia compared to good sleepers. The brain’s braking system is running low.
This is not anxiety in the conventional psychological sense, though the two often coexist. It is neurochemical — the brain’s firing pattern is stuck in a mode incompatible with sleep onset. The person’s experience is a mind that races, that cannot stop processing, that generates thoughts and worries the moment the lights go out. It feels psychological. Its roots are physiological.
The Stress Response That Won’t Turn Off
A fifth pattern involves the body’s HPA axis running chronically hot. Stress hormones remain elevated not just during the day but through the night, keeping the nervous system in a low-grade state of alert incompatible with deep, restorative sleep.
This pattern often presents as insomnia with a strong restlessness character — the person who cannot lie still, whose body feels wired, who may have a racing heart or feel physically keyed up beyond mental worry. The elevated stress hormones drive cardiovascular changes too — higher nighttime blood pressure, reduced blood pressure dipping, and increased strain on the heart and blood vessels. Over time, chronic insomnia causes measurable cardiovascular damage — elevated nighttime blood pressure, reduced heart rate recovery, and sustained arterial strain.
As we explored in The Bridge That Collapses, the structural and breathing patterns that keep the body locked in a stress state are often part of what prevents the system from resetting.
The Gut Connection
There is one more upstream driver worth naming here. Emerging research has found that people with insomnia have measurably different gut bacteria than good sleepers — reduced microbial diversity and altered bacterial ratios that correlate with inflammatory markers and metabolic disturbances. The gut and the brain communicate directly through the vagus nerve, and gut microbiome disruption has been shown to alter the expression of the clock genes that govern circadian rhythm.
Diet quality, gut health, and metabolic inflammation are upstream drivers of the hormonal and neurological disruptions that make sleep difficult. This is a thread that runs through our nutrition programming — and one worth exploring in depth with a practitioner who evaluates the whole system.
What a Different Approach Looks Like
Understanding chronic insomnia causes changes the clinical question from “what will help you sleep tonight?” to “which of these systems is driving your insomnia — and what does that system need to function correctly?”
That is a harder question to answer. It requires a more complete evaluation. It takes longer to address. And the interventions it leads to — liver support, nervous system regulation, kidney function optimization, circadian rhythm restoration, structural and neurological assessment, breath control — are not as simple as writing a prescription.But they address the cause. And addressing the cause is the only path to resolution rather than management.
CBT-I gets the behavioral foundation right — and we encourage it. But behavior change alone cannot repair a liver struggling to clear hormones, calm a nervous system structurally locked in a stress response, or restore the breathing mechanics that drive the body’s deepest recovery processes.
The work we do starts where CBT-I leaves off: with the physiology. Breath control — diaphragmatic retraining, nasal breathing restoration, and the autonomic regulation that comes with it — is the clinical lever that connects behavioral change to the body’s deeper systems. Natural clinical approaches — herbal and nutritional support for liver function, kidney health, and neurological balance — have a legitimate evidence base and a long clinical tradition. They do not receive institutional promotion because they do not fit the prescription model. That is a structural reality of healthcare, not a reflection of their clinical validity.
The question every person with insomnia deserves to be asked — and rarely is — is not just how bad their sleep is. It is why their sleep is the way it is. What would it take to change that, rather than simply manage it?
A Clinical Note from Dr. Bajaj
In 25 years of clinical practice, insomnia is one of the conditions I see most consistently misunderstood — by patients and by the healthcare system alike. People come in having normalized years of poor sleep. They’ve built their lives around it. They’ve tried the medications, the supplements, the devices. Some of them help. None of them have asked why.
What I find, almost universally, is that the underlying physiology has never been fully evaluated. The liver’s role in hormone processing. The nervous system’s inability to downregulate. The structural and breathing patterns that keep the body locked in alert when it should be in recovery. These are not exotic findings. They are common — and they are almost never addressed.
The sleep epidemic is real. It will not be resolved by better sedatives. It will be resolved when we start asking better questions about what the body actually needs in order to sleep — and building care around the answers.
The Larger Point
Insomnia is common. It is not normal — and the distinction matters enormously for long-term health. The path out begins with identifying the chronic insomnia causes driving your specific pattern — and then the sustained work of restoring them through behavioral retraining, physiological correction, and the breath control that connects them. That work is available. It simply requires practitioners who are willing to look beyond the symptom to the cause — and patients who are willing to ask for more than a prescription.
If you have been managing around poor sleep — with routines, medications, supplements, or simply acceptance — the conversation worth having is not about what to take tonight. It is about what your body needs to sleep on its own.
Ready to understand what’s actually driving your insomnia?
Well Rooted Health in Westfield, NJ and Well Rooted Chiropractic in New York City approach sleep as a whole-body clinical question. Schedule a consultation and let’s look at the full picture.
References
1. Morin CM, Buysse DJ. Management of Insomnia. New England Journal of Medicine. 2024.
2. Fernandez-Mendoza J. Insomnia Phenotypes, Cardiovascular Risk and Their Link to Brain Health. Circulation Research. 2025.
3. Fernandez-Mendoza J. Mechanisms Linking Insomnia and Cardiometabolic Disease Risk. Arteriosclerosis, Thrombosis, and Vascular Biology. 2026.
4. Ali E, Shaikh A, Yasmin F, et al. Incidence of Adverse Cardiovascular Events in Patients With Insomnia: A Systematic Review and Meta-Analysis. PLoS One. 2023.
5. Chen Y, et al. Associations of Sleep Duration and Insomnia With Cardiometabolic Disease Onset, Multimorbidity, and Mortality. Sleep Medicine. 2026.
6. Pengo MF, et al. Insomnia and Cardiovascular Disease: Untangling a Complex Relationship. Journal of Sleep Research. 2026.
7. Edinger JD, et al. Behavioral and Psychological Treatments for Chronic Insomnia Disorder in Adults: An AASM Clinical Practice Guideline. Journal of Clinical Sleep Medicine. 2021.
8. Qaseem A, et al. Management of Chronic Insomnia Disorder in Adults: A Clinical Practice Guideline From the American College of Physicians. Annals of Internal Medicine. 2016.
9. Mysliwiec V, et al. The Management of Chronic Insomnia Disorder and Obstructive Sleep Apnea: VA/DoD Clinical Practice Guidelines. Annals of Internal Medicine. 2020.
10. Furukawa Y, et al. Components and Delivery Formats of CBT for Chronic Insomnia: A Systematic Review and Network Meta-Analysis. JAMA Psychiatry. 2024.
11. Furukawa Y, et al. Initial Treatment Choices for Long-Term Remission of Chronic Insomnia. Psychiatry and Clinical Neurosciences. 2024.
12. Matheson EM, Brown BD, DeCastro AO. Treatment of Chronic Insomnia in Adults. American Family Physician. 2024.
13. Sweetman A, et al. Bi-Directional Relationships Between Co-Morbid Insomnia and Sleep Apnea (COMISA). Sleep Medicine Reviews. 2021.
14. Hoc TV, Lee HC. Clinical and Polysomnographic Characteristics of Asian Patients With COMISA. Scientific Reports. 2025.
15. Ragnoli B, et al. Comorbid Insomnia and Obstructive Sleep Apnea: Current Concepts. International Journal of Environmental Research and Public Health. 2021.
16. Marjot T, Ray DW, Williams FR, Tomlinson JW, Armstrong MJ. Sleep and Liver Disease: A Bidirectional Relationship. Lancet Gastroenterology & Hepatology. 2021.
17. Montagnese S, et al. Sleep-Wake Abnormalities in Patients With Cirrhosis. Hepatology. 2014.
18. Montagnese S, et al. On the Origin and the Consequences of Circadian Abnormalities in Patients With Cirrhosis. American Journal of Gastroenterology. 2010.
19. Dressle RJ, et al. HPA Axis Activity in Patients With Chronic Insomnia: A Systematic Review and Meta-Analysis. Sleep Medicine Reviews. 2022.
20. Vargas I, et al. Altered Ultradian Cortisol Rhythmicity as a Potential Neurobiologic Substrate for Chronic Insomnia. Sleep Medicine Reviews. 2018.
21. Vgontzas AN, et al. Chronic Insomnia Is Associated With Nyctohemeral Activation of the HPA Axis. Journal of Clinical Endocrinology & Metabolism. 2001.
22. Winkelman JW, et al. Reduced Brain GABA in Primary Insomnia. Sleep. 2008.
23. Dai M, et al. Thalamic GABA+ Levels Are Negatively Associated With Neuropsychiatric Symptoms in Insomnia. Frontiers in Human Neuroscience. 2025.
24. Park S, et al. Shorter Sleep Duration Is Associated With Lower GABA Levels in the Anterior Cingulate Cortex. Sleep Medicine. 2020.
25. Lyons OD. Sleep Disorders in Chronic Kidney Disease. Nature Reviews Nephrology. 2024.
26. Gopal A, et al. Sleep Disorders in CKD: A Review. American Journal of Kidney Diseases. 2025.
27. Vendeville N, et al. Sleep-Related Disorders in Patients With CKD and Kidney Transplant Recipients. Clinical Journal of the American Society of Nephrology. 2025.
28. Gottesman RF, et al. Impact of Sleep Disorders and Disturbed Sleep on Brain Health: AHA Scientific Statement. Stroke. 2024.
29. Santerre M, et al. AQP4-mediated Glymphatic Clearance: Sleep, Neurodegeneration, and the Translational Gap. Neuroscience & Biobehavioral Reviews. 2026.
30. Chen S, et al. The Association Between Gut Microbiota and Insomnia: A Systematic Review and Meta-Analysis. Sleep Medicine Reviews. 2026.
31. Zhao D, et al. Circadian Rhythms and Gut Microbiota Dysbiosis: Emerging Gut-Brain Axis Pathways in Insomnia. Brain, Behavior, and Immunity. 2025.
32. Bruyneel M, Sersté T. Sleep Disturbances in Patients With Liver Cirrhosis. Nature and Science of Sleep. 2018;10:369–375.
33. Wei Laboratories. Insomnia Protocol. Wei Laboratories, Inc.