North Seattle Natural Medicine

08/20/2026

Pregnenolone increases deep sleep. Its conversion to progesterone and allopregnanolone, along with the anti-cortisol and pro-GABA effects, support sleep onset and sleep depth while reducing wakings.

“Pregnenolone increased the amount of time spent in slow wave sleep... According to conventional visual scoring, pregnenolone improved the quality of sleep as documented by an increase in deep sleep, a higher sleep efficiency and a trend to decreased intermittent wakefulness.”

Ref: Neurosteroid pregnenolone induces sleep-EEG changes in man compatible with inverse agonistic GABAA-receptor modulation

“ Pregnenolone administration also increased serum progesterone over fourfold and DHEAS levels by approximately 16%...”

Ref: Proof-of-Concept Trial with the Neurosteroid Pregnenolone Targeting Cognitive and Negative Symptoms in Schizophrenia

“Progesterone had no effect on undisturbed sleep but restored normal sleep when sleep was disturbed (while currently available hypnotics tend to inhibit deep sleep), acting as a "physiologic" regulator rather than as a hypnotic drug...the present findings suggest that use of progesterone (300 mg) might provide novel therapeutic strategies for the treatment of sleep disturbances, in particular in the elderly.”

Ref: Progesterone prevents sleep disturbances and modulates GH, TSH, and melatonin secretion in postmenopausal women

Note: that’s 300 mg oral, not Progest-E formulation, which has higher bioavailability.

“In this single ascending dose study has clarified that 400 mg four times/day of progesterone is required to achieve maximum plasma ALLO concentrations of 50 ng/mL.”

Ref: Allopregnanolone Concentrations After Ascending Single Dose Administration of Progesterone to Healthy Volunteers

08/18/2026

08/13/2026

08/13/2026

https://www.facebook.com/share/p/1F1u2RhhLb/

Vitamin D really did slow telomere loss, and it did so in the kind of trial that should make you take the finding seriously.

In the VITAL Telomere study, 2,000 IU of vitamin D3 a day reduced the shortening of leukocyte telomeres over four years. The number the study actually produced was 140 base pairs. The number the internet produced was "3.5 to 4.7 years younger," and the distance between those two figures is the whole story.

VITAL was a large, double-blind, placebo-controlled trial in 25,871 US adults, built as a two-by-two factorial testing 2,000 IU of vitamin D3 and 1 gram of marine omega-3s against placebo over five years. The telomere arm followed 1,054 of those participants, measuring leukocyte telomere length at baseline, year 2, and year 4 across more than 2,500 samples. This matters because the telomere outcome was pre-specified, the primary endpoint the analysis was designed around, not a measure fished out after the fact. That alone puts it a tier above the post hoc aging-clock analyses that generate most "supplement reverses aging" headlines. Vitamin D moved the needle. Omega-3 did nothing to telomere length at either timepoint.

The size of the effect is worth noting. Vitamin D preserved about 140 base pairs of telomere over four years, and against a typical telomere of roughly 7,000 base pairs, that is on the order of 2 percent. The trend held in the same direction year over year, and the result cleared statistical significance, though the margin was thin enough that it should be read as a real but modest signal rather than a robust one. This is a genuine finding. It is also a small one.

Take the 140 base pairs vitamin D preserved, divide by an assumed rate of telomere loss somewhere around 30 to 40 base pairs per year, and you arrive at three to five years. The arithmetic is defensible, but it launders a narrow molecular measurement into a sweeping claim about lifespan. The authors themselves were restrained, concluding only that vitamin D "might have a role in counteracting telomere erosion or cell senescence."

Telomere length is a noisy stand-in for aging, and the strongest evidence of that is what happens when you check it against a different biomarker. In the DO-HEALTH trial, the same 2,000 IU of vitamin D did nothing to four DNA-methylation aging clocks. So the two most cited molecular yardsticks for biological age disagree about the same supplement at the same dose: telomeres say vitamin D helped, the methylation clocks say it did not. When your proxies contradict each other, the honest conclusion is that the proxies are imperfect, not that one of them has measured your remaining years.

A daily 2,000 IU of vitamin D produced a small, real reduction in telomere shortening in a rigorous trial, omega-3 did not, and telomere length is a marker of cellular aging whose link to how long or how well a person actually lives remains unsettled. That is a reason to keep vitamin D in the "plausibly worth it" column, especially at a dose this ordinary. It is not evidence that a supplement bought you four years.

What the study never did is follow anyone forward to see whether preserving those 140 base pairs changed a single hard outcome, which is the only test that would turn "younger telomeres" into "a longer life."

Zhu H, Manson JE, Lee IM, et al. Vitamin D3 and marine omega-3 fatty acids supplementation and leukocyte telomere length: 4-year findings from the VITAL randomized controlled trial. DOI 10.1016/j.ajcnut.2025.05.003. PMID 40409468.

08/07/2026

Seahawk wide receiver Cooper Kupp dined with his family at The Market Seafood Eatery in Edmonds recently. With him are employees Dominic Platt, left, and Augustine Chan. Photo courtesy Shubert Ho.

08/06/2026

Lipo (a) is not stuck! It can fall with diet, exercise and hormone use when needed! Lp(a) is “genetic,” so there’s nothing we can do about it, they say. 🙄 Or, actually, what "they" say is "you need a statin."

(Nevermind that statins can *increase* Lp(a) and insulin resistance which elevates clotting risk in women who are already carrying that risk).

Anyway, I see Lp(a) fall with transdermal estradiol in my own practice. I follow this biomarker over time, and I can tell you that it is modifiable. So when I hear it described as genetically determined and therefore untouchable, that does not match what I am actually observing in women.

And if the ivory tower is not following the biomarker closely enough to see the pattern, then perhaps the ivory tower is behind this community physician on this one. 💅🏾😏
But, for fun 😜, let’s pull some data.

Two randomized controlled trials showed that menopausal hormone therapy significantly lowered Lp(a) in postmenopausal women. In one study, transdermal estradiol reduced Lp(a) by approximately 12%, while oral estrogen reduced it by 22%. In another, cyclic transdermal therapy lowered Lp(a) by 16%, while continuous oral therapy lowered it by 31%.

Then a later meta-analysis pooled 24 randomized controlled trials and found that menopausal hormone therapy lowered Lp(a) by approximately 20% overall. So this is not one isolated finding. It is a reproducible physiologic response.

Lp(a) may be strongly influenced by genetics, but it is not biologically fixed. Genetic means that the baseline tendency is inherited, not that its immovable. And the expression of that tendency can still be shaped by the hormonal and metabolic environment. Menopause profoundly changes that environment.
So when Lp(a) rises during the menopausal transition, it is partially a response to the loss of estrogen signaling and the complete reorganization of lipid transport that occurs after ovarian hormone production declines.

And to be clear, restoring estradiol does not rewrite a woman’s genetics or erase predispositions but it does change the physiologic environment in which those genetics are being expressed.

How much of the cardiovascular risk that we casually attribute to “aging” is actually the downstream consequence of estrogen deficiency? 🧐 And how is adding a before *having a conversation* about appropriate?
We are living in the twilight zone in women's health.

08/02/2026

L-theanine not only sharpens attention but also influences the brain’s motivational circuitry. By subtly increasing GABA in the striatum, it lifts inhibition on dopamine neurons, allowing dopamine release to surge — in rodent studies, nearly 300% of baseline.

The result: reduced distraction, heightened motivation, and a system biased toward sustained engagement.

👉 Learn more about the mechanisms here: https://bit.ly/4rD4mgV