Melatonin Linked to 90% Increase in Heart Failure (what to do next)

DeLauer explains glycine works through multiple mechanisms: it promotes a drop in body temperature, which is a natural sleep signal; it acts as a neurotransmitter/neuromodulator that lowers cortisol and calms the nervous system, preventing those 3 a.m. anxiety spikes; and it relaxes the bladder, reducing the urge to urinate. He highlights his own problem of waking to pee and not falling back asleep, which glycine solved. He references a dedicated video on his channel about glycine for nocturia. The 3-gram dose is well tolerated and not associated with next-day grogginess. It's a practical alternative for those wanting to avoid melatonin.

DeLauer positions magnesium as a simple way to quiet brain activity. By blocking NMDA receptors, it reduces excitatory neurotransmission and supports GABA activity, which is central to relaxation. The 400–500 mg range aligns with common supplement recommendations. He does not go into details about different magnesium types (e.g., glycinate vs. citrate), but the implication is a well-absorbed form that crosses the blood-brain barrier. This advice fits with a broader practice of using magnesium for insomnia and anxiety.

DeLauer acknowledges the evidence is limited, not because grounding doesn't work but because there's little financial incentive to study standing on grass. He cites salivary cortisol and inflammatory marker reductions in existing small studies. It's a free, low-risk practice that may support the parasympathetic shift before sleep. He emphasizes concrete (not asphalt) as a conductor. This advice is given as a complementary tool, not a primary intervention.

DeLauer points to studies showing elevated CO2 in closed bedrooms impairs sleep. Simply cracking a window can reduce CO2 build-up, which is a passive, cost-free intervention. It's a small behavioral change that doesn't require supplements.

This recommendation is brief. L-theanine is an amino acid found in green tea that increases alpha brain waves and GABA levels. The 200–400 mg dose is typical for sleep and anxiety support. DeLauer presents it as a quick stop-gap for stress without side effects.

DeLauer emphasizes that phosphatidylserine is not just a calming agent; it helps keep cortisol rhythms from becoming chaotic. He notes its role in protecting the phospholipid bilayer, providing antioxidant support from daily oxidative stress. The dose of 100–300 mg is specific, and it's positioned as a strategic use for particularly stressful days, not a nightly staple.

The study was presented at the American Heart Association Scientific Sessions in early November 2025 and is preliminary, lacking peer review. DeLauer emphasizes that the comparison was between two groups of insomniacs, which is better than comparing to healthy controls, but the critical flaw is that the 'melatonin group' was defined by having melatonin noted in their electronic health record. This likely selects for people with more severe, treatment-resistant insomnia—those who have complained enough to have it recorded and may have been prescribed clinical doses or adjunct sleep aids. The control group of insomniacs without melatonin in their chart could still be taking it over the counter without disclosure, further muddying the comparison. DeLauer calls this reverse causation: the severity of insomnia drives both the need for documented melatonin and the higher cardiovascular risk, not the melatonin itself. The study authors themselves note the correlation is unadjusted for such confounders and lacks mechanistic evidence.

He explains the unmeasured variables problem: people whose insomnia is severe enough to prompt a doctor to note melatonin in their chart are also more likely to have higher cortisol, sympathetic tone, inflammation, and to be self-medicating with alcohol or other drugs. The more severe the insomnia, the higher the cardiovascular risk, independent of melatonin. Moreover, because melatonin is over-the-counter, controls may be using it without reporting, biasing the result toward null or even underestimating the harm if it were real, but the crucial point is that the groups are not matched on insomnia severity. The study's matching only on 'having insomnia' is too crude. DeLauer also notes Dr. Domino, a neuroscychopharmacologist, argued on his channel that melatonin's antioxidant properties are beneficial, further casting doubt on a direct causal link.

He distinguishes between melatonin's role as a circadian tuner—signaling the body it's nighttime—and a sedative. Because its half-life is only 40–60 minutes, people may fall asleep quickly but then experience a cortisol spike or an arousal later, leading to middle-of-the-night waking. He believes some people respond well, others do not, and that his concern is about sleep architecture rather than any direct cardiovascular toxicity. This skepticism is separate from the study; he would not recommend melatonin based on its uneven effects.