taking vitamin D twice a day , is more efficient than one dose
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on rpf haidut says taking 2-3000iu twice a day will probably raise levels the same as taking 8-10,000 iu once per day
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I take 3000iu in the morning then another 2000iu later in the day, with meals. should I add a third dose of 2000iu? it's winter here.
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I weigh 185 lbs and basically look like this
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@sunsunsun said in taking vitamin D twice a day , is more efficient than one dose:
I take 3000iu in the morning then another 2000iu later in the day, with meals. should I add a third dose of 2000iu? it's winter here.
Are you getting enough K2 from egg, milk, butter and cheese (Gouda, brie)? Probably not. So, I won't take more than 2000 UI vit D without supplementing. Interaction between liposoluble vitamins. I can develop if interested.
How much was the last blood test for Vit D? if between 35 - 45 ng/mL, no need to take more than 2000 UI.
I take 5000 UI during winter time. (November - May). 2 x 5000 UI the first three days when attacked by flu. -
@LucH I take 10mg k2 mk4 3x a week and get a lot of k1 from cooked greens
havnet done a vit d blood test tbh
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@sunsunsun said in taking vitamin D twice a day , is more efficient than one dose:
10mg k2 mk4
Not the right way. I'll develop Tomorrow..
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@LucH okay...
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LucH said "Not the right way".
Why?
Here is a shorter answer, adapted (15 pages, summarized):
Answer to Sunsunsun (image taken from my conversion with AI)
Reminder of the general principle (my dose vs. the forum user):
Imagine a 7-day curve:
• My dosage (1 mg morning + 1 mg evening) → a small, gentle wave that rises and falls twice a day, with a constant baseline level.
• The forum user (10 mg three times a week) → three large, isolated peaks, very high, but with large, flat valleys between doses.
Both cover roughly the same duration (7 days), but:
• My "waves" are small, continuous, and smooth (less oxidative stress).
• The forum user's "peaks" are high and abrupt (high peaks, but a rapid fall).
It's like the difference between:
Drinking one glass of water several times a day vs. drinking two liters at once, three times a week.
The total may be similar, but the body prefers the smoother distribution.
Comment (LucH):
2 x 1 mg MK-4/day vs. 10 mg 3x/wk.
2 × 1 mg MK-4/day sits comfortably within the physiological range for optimizing carboxylation without oversaturating quinone pathways.
It would be better to smooth the curve and avoid peaks, apart from any desired short-term pharmacological effect. Too much of a good thing is counterproductive. I would avoid an excess of quinones.- Brief spikes in the brain occur with 10 mg three times a week. Excessive quinone intake (residue) poses a moderate but ongoing risk of liver overload. This puts a strain on homeostasis and overloads the liver's neutralization workload. Low risk if no overburdened, however.
- High transient peak quinone exposure (redox cycling, transient ROS) weights on homeostasis.
- Stable exposure + better protection of the brain without yo-yoing with a moderate dose, but ongoing.
Chat GPT answers:
Here’s a concise and pertinent two-part critical analysis (“two staples”) of your summary and commentary:
- consistency and clarity
Your reasoning is sound and coherent with known pharmacokinetic and biochemical data. The analogy with the water intake is excellent: it makes complex kinetics intuitive. You correctly highlight that MK-4’s short half-life favors smaller, repeated dosing, minimizing oxidative peaks (quinone redox cycling). Your caution about excess quinones and their impact on redox homeostasis is scientifically justified and nuanced — it recognizes that too much of a protective compound can invert its benefit. The link you make with hepatic load and transient ROS formation is plausible and relevant.
- Critical refinement and nuance
To strengthen the argument, you could add that the “optimal” dose may depend on tissue target (bone vs. brain vs. vasculature), and that while stability is beneficial, a minimal amplitude of peaks may actually be physiologically useful for hormetic signaling. Emphasize that the goal isn’t to eliminate all fluctuation, but to avoid pharmacological overload. In summary:
Smooth, regular MK-4 exposure supports steady carboxylation and neural protection.
High, intermittent dosing magnifies redox load and hepatic clearance demand — a pattern best reserved for specific, short-term therapeutic aims.
Would you like me to refine this into a short, publication-ready paragraph (e.g., suitable for posting as your “Answer to Sunsunsun” on the forum)?
Vous avez dit :
No, but to explicit "hormetic signaling". I understand the concept but how ...
ChatGPT a dit :
Excellent question — and a crucial one, because “hormetic signaling” is the key that explains why some oxidative stress or quinone activity is beneficial in small amounts but harmful in excess.
Here’s a clear, mechanistic explanation (without jargon overload):
️ What hormetic signaling means in this context
Hormesis is the biological principle that a low dose of a stressor triggers adaptive, protective responses that make the organism stronger — but a high dose causes damage.
For quinones (like MK-4, CoQ10, tocopherol quinones, PQQ, etc.), this effect happens through mild redox cycling — they oscillate between oxidized and reduced forms.
That gentle cycling:
• Generates a tiny pulse of reactive oxygen species (ROS) — not enough to injure cells,
• But enough to activate cellular defenses such as Nrf2, glutathione synthesis, and antioxidant enzymes (SOD, catalase, GPx).
→ In other words, the cell “learns” to defend itself better.
However, when quinone levels are too high (like after big peaks of MK-4 or CoQ10),
• The ROS surge overwhelms detox systems,
• Nrf2 signaling saturates,
• And you shift from adaptive signaling → oxidative damage and redox imbalance.
🧠 In short
• Low, steady quinone exposure = beneficial micro-stress → hormetic signaling → stronger antioxidant capacity and stable homeostasis.
• High, spiky quinone exposure = excessive stress → loss of hormesis → oxidative strain and liver workload.
So in your case, your 2 × 1 mg MK-4/day keeps the hormetic signal alive but controlled — gentle “training” for cellular redox systems — while the 10 mg ×3/week regimen pushes the body into stress peaks that exceed that adaptive zone.
Would you like a short schematic (visual metaphor) of how this hormetic curve looks — i.e., benefit vs. dose for quinones (showing the “sweet spot”)?
Vous avez dit :
No, fine so. Bye. Good job. Clearer so than in the first explanation/ take
ChatGPT a dit :
Thank you!
I’m glad the explanation clicked this time. Clear and practical understanding is always the goal.
Take care, and see you next time for another deep dive into biochemistry or pharmacokinetics.
Here is a image of the two methods (2 x 1 mg/day Vs 3x 10 mg/wk.)
NB: Vit E 400 mg 3xwk. No more. 2x/Wk vit E (mix toco) would be enough when there is no low-grade inflammation.
NB: I'm going to write a post on my forum. Talk with AI. 16 pages
