Can You Build a Healthy Heart on Broken Sleep?
Sleep loss doesn’t just make you tired — it may biologically accelerate heart disease. Here’s the hidden brain-to-heart pathway, plus tools to build resilience when sleep isn’t perfect.
If you struggle with sleep, you’re in good company. Or at least, you’re in my company.
Nearly half of adults in the United States sleep fewer than the recommended seven to eight hours per night.
Many of us—myself included—deal with outright insomnia.
Sometimes my brain just won’t turn off.
I’m exhausted, but the gears keep whirring. And while naturally “gifted” sleepers might find it hard to imagine, shifting states of consciousness is not a passive event.
Falling asleep is an active, complex biological process.
So first, if you struggle with sleep, you are absolutely not alone. But you probably already knew that.
Because sleep can be such a stubborn problem, many of us quietly accept it as our health Achilles’ heel.
I tell myself: My diet is locked in. So is my exercise routine. I eat well. It’s just… my sleep isn’t great.
The Study I Didn’t Want to Read
With that transparent preamble out of the way, I want to tell you about a study I genuinely did not want to read.
I didn’t want to read it for the exact reason I just described. If I can’t fix a problem, why would I want more evidence of how it’s hurting me?
I understand that instinct. But let’s be brave and look at the data! Maybe we’ll find solutions—or at least fresh motivation to prioritize and optimize sleep to the best of our abilities.
The paper was published in Nature, one of the world’s leading basic science journals.
The researchers set out to identify a causal mechanism linking poor sleep to atherosclerosis—the buildup of plaque in arteries that leads to heart attacks and strokes.
We already know poor sleep is associated with worse cardiovascular health. The lingering question is: Why?
Is it simply that sleep-deprived people are more likely to eat donuts at 2 a.m.? That may contribute—but it’s not the whole story.
To establish cause and effect, the researchers turned to animal models.
They took animals prone to heart disease and subjected them to “sleep fragmentation”—repeatedly disrupting their sleep. Importantly, this intervention did not change body weight, cholesterol levels, or even glucose tolerance.
Something worse happened…
Sleep Fragmentation Accelerates Atherosclerosis
The sleep-fragmented animals developed progressively larger atherosclerotic plaques compared to well-rested healthy control animals.
By 12 weeks—and even more so by week 16 (shown)—there was significantly more plaque buildup in their arteries (green arrows).
In other words, just four months of disrupted sleep accelerated cardiovascular disease. True, the effects would take longer in humans. However, as we will see, the mechanism underpinning this effect is highly conserved across vertebrae.
Digging deeper, the researchers found more immune cells invading the arteries of these sleep-fragmented animals.
Below are three different types of immune cells: Ly-6C monocytes, neutrophils, and macrophages, all of which play a role in atherosclerosis.
The specific function of each is not as important as the general pattern: sleep disruption (green bars) increases levels of these inflammatory immune cells in arteries.
Brief Summary
So, here’s the summary so far:
In humans, poor sleep is linked to worse cardiovascular health.
In animals, sleep disruption directly accelerates plaque buildup.
It does so alongside increased immune cell infiltration into the arteries.
But how?
Hypocretin: From Brain to Bone to Heart
The researchers focused on a hormone you may not have heard of: hypocretin, also known as orexin.
Hypocretin is produced in the brain, circulates in the blood, and regulates wakefulness, arousal, appetite, and mood. It’s something of a Swiss Army knife hormone.
Crucially, sleep fragmentation suppresses the release of hypocretin into the bloodstream.
Why does that matter?
Because hypocretin doesn’t just act in the brain.
It also signals in the bone marrow—the site of “hematopoiesis,” where new blood cells, including immune cells, are generated. Yes, many of your immune cells are born in your bone marrow.
What the researchers discovered is this: when sleep fragmentation suppresses hypocretin, it alters bone marrow signaling.
The result?
Increased production of inflammatory immune cells. These cells then migrate into the arteries, promoting inflammation and accelerating plaque progression, evidence for which we saw above.
In short, poor sleep doesn’t just correlate with heart disease. It can biologically drive it—through a brain-to-bone-marrow pathway that amplifies vascular inflammation.
But understanding the inner workings of our bodies shouldn’t spark shallow fear; rather it should ignite a drive to innovate, find solutions, and take meaningful action. That’s what you’re in for next…
In the rest of this letter, for StayCurious Metabolism Premium members, we’re going to pivot to something more upbeat: Action & Protocols!
I’ll walk through several evidence-based ways to at least partially offset the harmful effects of sleep loss. We’ll cover:
Vitamin D: A hypocretin connection?
Creatine: A cognitive “rescue” for those bad nights
Omega-3s: An essential nutrient for heart and brain
Throughout, I’ll include specific target levels and/or dosing to aim for and the exact supplements I use personally. So, take a power nap if you can (probably not)… And let’s keep moving!
