Supplementing More Than 10,000 IU Of Vitamin D A Day Based On The Work Of Jeff Bowles

[tankasnowgod]

I got interested in supplementing higher doses of vitamin D recently based on the threads discussing the Coimbra Protocol, which uses Vitamin D at doses of 40,000 to 300,000 IU a day to treat Auto Immune diseases. That protocol reminded me of seeing a book by Jeff Bowles who experimented with doses of fairly high daily doses of Vitamin D himself, ranging from 25,000 to 100,000 IU over the course of a year. One key thing to note in his protocol- he balanced every 10,000 IU of D with K2 (he was using Life Extension Super K) which had (at the time) 1,000 mcg of MK-4 and 100 mcg of MK-7 (now, Super K has 200 mcg of MK-7), and also recommended Magnesium.

Over a 10-12 month period, he noted some major improvements-

Cracking joints and hips resolved
Toenail fungus was cured, and nails became normal
Rough skin on feet became smooth
Ganglion Cysts Shrunk
A Bone Spur in his elbow dissapeared
He lost about 20 pounds without and conscious effort to lose weight

The reviews on his book, mostly positive, are in the hundreds now. He also maintains a blog where he talks about high vitamin D intake, among other "health hacks"- Jeff T Bowles

I was interested in the idea of higher D (I had seen a lot of benefits from supplementing D already), and gave it a try, but didn't really commit to it, and got disinterested after a few weeks.

Anyway, I have been supplementing less D over time (I don't think I supplemented ANY the past two summers). I have been supplementing K2 and Magnesium for years now, so thought I might up Vitamin D from the 5,000 IU five days a week I was taking to 25,000 IU a day. It's only been a week, but I have noticed a significant increase in energy, mood, and focus. I'm very curious about the effects on weight loss and skin, and plan to keep this level up for at least 6 months, maybe even upping it.

As far as safety and toxicity levels, I think the K2 and Magnesium will do a great job managing those, and I do plan to test serum levels.

Peat has mentioned that the body can make 10,000- 15,000 IU of Vitamin D from half an hour exposure to sunlight, so supplementing at those levels shouldn't be an issue. I think the Vitamin D council stated that 25,000 IU a day could be made from sun exposure in a day.

Beyond that, the following study draws the conclusion that Vitamin D can be supplemented at levels of 60,000 IU for months or years with no signs of toxicity- https://www.sciencedirect.com/science/article/abs/pii/S0960076016303569

Here, Ray Peat suggests that Vitamin D is parallel to Thryoid-


And interestingly, in this clip, Peat suggests that Vitamin D issues exist when too little calcium (and magnesium) is in the diet-


Peat on Vitamin D Deficiency-


So, I plan on updating my progress on this level of D. Also of note, I am doing Inclined Bed Therapy, and a lot of the testimonials overlap with some of the testimonials I have heard on higher dose D Supplementation. It would be really exciting if I get positive results compounded because of this.

 

[baccheion]

I'm doing this now and have been since Jan 2018. I haven't noticed any effects, but will continue (for the 9 months remaining) as I've also not noticed any negative effects.

I take 60,000 IU D3, 15 mg vitamin K2 MK-4, 400 mg chelated/TRAACS magnesium, and 1 Life Extension Two-per-day capsule.

300 IU/kg D3 may be the minimum if trying megadose vitamin D, with 500-1,000 IU/kg being even better.

10 IU D3 : 2 mcg+ MK-4..

 

[Tarmander]

Nice Summary and resources. I had no idea about Jeff Bowels...Bowles

 

[tankasnowgod]

I'm doing this now and have been since Jan 2018. I haven't noticed any effects, but will continue (for the 9 months remaining) as I've also not noticed any negative effects.

I take 60,000 IU D3, 15 mg vitamin K2 MK-4, 400 mg chelated/TRAACS magnesium, and 1 Life Extension Two-per-day capsule.

300 IU/kg D3 may be the minimum if trying megadose vitamin D, with 500-1,000 IU/kg being even better.

10 IU D3 : 2 mcg+ MK-4..

Cool. What are you basing the bolded part on? Is that from Bowles work, or something else? It would make sense to me that weight loss might occur when fat stores are saturated with D.

Part of the reason I want to experiment with topical D is that the areas where I have the worst skin and most fat also get the least sun exposure. I think topical application would help those areas quicker, especially since the body primarily get's vitamin D through the skin, at least until recent times.

 

[Blossom]

I read the vitamin D book by Jeff T. Bowles this summer. He has a very convincing writing style to be sure! I also read his book on melatonin (and a couple others) and I got the impression he is trying to increase longevity in exactly the opposite way of Peat by slowing down the metabolism. That doesn't necessarily have anything to do with vitamin D though.
I found his book on melatonin interesting because he claims in very high doses (75- 100 mg + IIRC) it can reverse Alzheimer's and menopause. I find it extremely hard to believe melatonin can do all of that but it would be nice for a lot of people if it were true. Sorry to veer slightly off topic @tankasnowgod.
Best wishes on your high dose vitamin D experiment!

 

[baccheion]

Cool. What are you basing the bolded part on? Is that from Bowles work, or something else? It would make sense to me that weight loss might occur when fat stores are saturated with D.

Part of the reason I want to experiment with topical D is that the areas where I have the worst skin and most fat also get the least sun exposure. I think topical application would help those areas quicker, especially since the body primarily get's vitamin D through the skin, at least until recent times.

300 IU/kg, a common dose for those with autism, tends to put vitamin D serum near the top of the range (100 ng/mL). Bowles mentioned that the goal is to get serum over 90 ng/mL. Other sites say being above 80 ng/mL is sufficient. It could also be the case that megadose magic happens between 90 and 150 ng/mL.

You can look into MSM lotion, as it includes many of the popular/common ingredients and MSM as a carrier results in deeper penetration.

I read the vitamin D book by Jeff T. Bowles this summer. He has a very convincing writing style to be sure! I also read his book on melatonin (and a couple others) and I got the impression he is trying to increase longevity in exactly the opposite way of Peat by slowing down the metabolism. That doesn't necessarily have anything to do with vitamin D though.
I found his book on melatonin interesting because he claims in very high doses (75- 100 mg + IIRC) it can reverse Alzheimer's and menopause. I find it extremely hard to believe melatonin can do all of that but it would be nice for a lot of people if it were true. Sorry to veer slightly off topic @tankasnowgod.
Best wishes on your high dose vitamin D experiment!

3 mg melatonin is associated with delayed/reversed menopause.

How to Stop Aging: Melatonin and the Pineal Gland

Why women must take melatonin

Is your fatigue and weight gain due to low levels of this hormone

 

[tankasnowgod]

I read the vitamin D book by Jeff T. Bowles this summer. He has a very convincing writing style to be sure! I also read his book on melatonin (and a couple others) and I got the impression he is trying to increase longevity in exactly the opposite way of Peat by slowing down the metabolism. That doesn't necessarily have anything to do with vitamin D though.
I found his book on melatonin interesting because he claims in very high doses (75- 100 mg + IIRC) it can reverse Alzheimer's and menopause. I find it extremely hard to believe melatonin can do all of that but it would be nice for a lot of people if it were true. Sorry to veer slightly off topic @tankasnowgod.
Best wishes on your high dose vitamin D experiment!

Thanks! I have not read or looked into his Melatonin book, and yes, that one seems opposed to Peat's ideas. However, some of his ideas certainly fall in line with Peat's. Check out this blog article- The 6 Changes in Lifetime Hormone Levels that Cause Aging – And How to Easily Reverse Them! | Jeff T Bowles

Aside from Melatonin, targeting higher levels of Pregnenolone, Progesterone, and DHEA is absolutely in line with Peat.

 

[tankasnowgod]

300 IU/kg, a common dose for those with autism, tends to put vitamin D serum near the top of the range (100 ng/mL). Bowles mentioned that the goal is to get serum over 90 ng/mL. Other sites say being above 80 ng/mL is sufficient. It could also be the case that megadose magic happens between 90 and 150 ng/mL.

I remember my serum D level being right around that 100 ng/ml in my best paleo days. I was thinking that was probably a nice target to see if any "magic" happens. I think the Coimbra protocol targets 150 ng/ml. Although the results are impressive, the lack of K2 and focus on lowering dietary calcium seem problematic, and if those two were addressed, that protocol would likely work better, or at least not have as many side effects.

 

[baccheion]

I remember my serum D level being right around that 100 ng/ml in my best paleo days. I was thinking that was probably a nice target to see if any "magic" happens. I think the Coimbra protocol targets 150 ng/ml. Although the results are impressive, the lack of K2 and focus on lowering dietary calcium seem problematic, and if those two were addressed, that protocol would likely work better, or at least not have as many side effects.

Were you taking vitamin D? How much? Was it 100 ng/mL or 100 nmol/L (equivalent to 40 ng/mL)? If I remember correctly, Coimbra protocol focuses on sufficiently lowering PTH.

 

[tankasnowgod]

Were you taking vitamin D? How much? Was it 100 ng/mL or 100 nmol/L (equivalent to 40 ng/mL)? If I remember correctly, Coimbra protocol focuses on sufficiently lowering PTH.

Yes, I was taking D, and it was ng/ml.

 

[ecstatichamster]

I think @Travis has pointed out that vitamin D actually lowers metabolism

 

[ecstatichamster]

Ah here is a cite.

https://www.physiology.org/doi/abs/10.1152/ajpendo.90763.2008

Recent studies have established that vitamin D plays multiple biological roles beyond calcium metabolism; however, whether vitamin D is involved in energy metabolism is unknown. To address this question, we characterized the metabolic phenotypes of vitamin D receptor (VDR)-null mutant mice. Under a normocalcemic condition, VDR-null mice displayed less body fat mass and lower plasma triglyceride and cholesterol levels compared with wild-type (WT) mice; when placed on a high-fat diet, VDR-null mice showed a slower growth rate and accumulated less fat mass globally than WT mice, even though their food intake and intestinal lipid transport capacity were the same as WT mice. Consistent with the lower adipose mass, plasma leptin levels were lower and white adipocytes were histologically smaller in VDR-null mice than WT mice. The rate of fatty acid β-oxidation in the white adipose tissue was higher, and the expression of uncoupling protein (UCP) 1, UCP2 and UCP3 was markedly upregulated in VDR-null mice, suggesting a higher energy expenditure in the mutant mice. Experiments using primary brown fat culture confirmed that 1,25-dihydroxyvitamin D3 directly suppressed the expression of the UCPs. Consistently, the energy expenditure, oxygen consumption, and CO2 production in VDR-null mice were markedly higher than in WT mice. These data indicate that vitamin D is involved in energy metabolism and adipocyte biology in vivo in part through regulation of β-oxidation and UCP expression.

 

[baccheion]

I think @Travis has pointed out that vitamin D actually lowers metabolism

How?

 

[Hugh Johnson]

interesting

 

[Amazoniac]

Vitamin D issues exist when there's too little calcium (and magnesium) is in the diet

It's unfortunate, I would like to read more posts from you in the future but you're implying here that you'll be ingesting a normal amount of calcium wih doses of vitamin D that start to enter the pharmacological territory.

Optimal Vitamin D Status: A Critical Analysis on the Basis of Evidence-Based Medicine | The Journal of Clinical Endocrinology & Metabolism | Oxford Academic

It was posted elsewhere how 10000 IU/d elevated some people's blood levels of 25(OH)D to 80-something ng/ml.

By the time magnesium has a chance to act, calcium has already turned you into a statue, an inverted marble centaur.
Coimbra also acknowledged that K2 in his protocol was optional because it's ineffective for the range that they're working with (he probably used mostly MK-7, though).

gave it a try, but didn't really commit to it, and got disinterested after a few weeks

It can be that there's a rap battle already going on between shoulder angel and devil.

 

[paymanz]

you need to test your blood level regularly with those dosages. at least once a month.

 

[RobertJM]

I noticed significant improvements just by increasing calcium.

I get unpleasant effects from d3 (mood being worst of all), and sitting in sunlight doesn’t feel particularly great either. I listen to my body in that respect. If it was crying out for d3 I’d surely see benefits. No ideas what my levels are, though.

I stick to supplementing sufficient calcium and minimal amounts of k2/d3 for hopefully being enough to put calcium where it should go in my body. And then I do magnesium at the end of each day.

 

[Blossom]

300 IU/kg, a common dose for those with autism, tends to put vitamin D serum near the top of the range (100 ng/mL). Bowles mentioned that the goal is to get serum over 90 ng/mL. Other sites say being above 80 ng/mL is sufficient. It could also be the case that megadose magic happens between 90 and 150 ng/mL.

You can look into MSM lotion, as it includes many of the popular/common ingredients and MSM as a carrier results in deeper penetration.



3 mg melatonin is associated with delayed/reversed menopause.

How to Stop Aging: Melatonin and the Pineal Gland

Why women must take melatonin

Is your fatigue and weight gain due to low levels of this hormone

3 mg seems more reasonable. Thanks for the links.

 

[Blossom]

After reading Bowles material on vitamin D, melatonin and longevity I asked Travis if he would share his thoughts on the subject. Here's his reply. Travis wrote:

"I think it can if used properly, yet too much would oppose the metabolic rate ≈ anti-aging scheme. Pro-melatonin ideas are often quite logical, at least superficially, and there are certainly no shortages of positive publications on melatonin. However, much of this seemingly-positive data on melatonin is counterintuitive: Most published melatonin science had been done using rats, a nocturnal species, and making extrapolations between them and humans in regards to pineal hormones must be make with caution if they should be made at all. Nocturnal species most active at night must respond to pineal hormones in a manner quite different to those diurnally active—at least in many ways.

Melatonin always appears to increase under darkness regardless of the species' circadian activity status. Yet some nocturnal species are very low excretors of melatonin, notably the owl and certain strains of rodents; some have a blunted response due to RORα receptor polymorphisms. Confusing the issue further is the fact that only some rodent species are low-excretors; some popular lab strains of mice had been bred according to the circadian cycle determined by the on/off switch of an artificial lamp. Upon each breeding cycle, the rodents had progressively assumed the the circadian whims of their keepers—litter through litter, little by little.

I am getting the impression the fully-nocturnal wild rats must produce melatonin membrane receptors either of lower activity or differential distribution. Cats appear to regulate their sleep–wake cycle more in response to oleamide than anything, ostensibly produced by eating antelopes and zebras. [Oleamide synthesis is a function of serum oleic acid × plasma ammonia concentration.]

Drawing assumptions based on epidemiological research can be confounded by vitamin D, a powerful hormone that also changes with latitude. Dr. John Cannell over-hypes vitamin D and cites many latitude-specific changes as evidence for its effect. Although melatonin certainly appears more powerful than vitamin D in general, even human latitudinal and interseasonal comparisons are still inter-confounded by each one. There are two hormones having concentrations that vary under UV light, and retinoids cis–trans isomerize under it's influence.

Most nearly everybody completely ignores methoxy-tryptophol, the 'other pineal hormone.' Long though as melatonin's little cousin, this long-ignored pineal hormone shouldn't be. Although it fails to activate melatonin membrane receptors, and thus cannot produce acute somnolence, it is equipotent on melatonin's hormonal nuclear receptors (i.e. RORα, RORβ, RORγ).

Melatonin is often said to 'stimulate the immune system,' yet in humans it puts neutrophils to sleep. The most extreme interspecial contradictions are noted between immunological studies of humans and rats: Since these two species are cumulatively responsible for most melatonin research on immunity, a marathon of superficial title & abstract-reading can quickly lead to the Cannell-type fallacy. The effect of melatonin on human immune cells is significant in in nanomolar concentrations, regulating both genetic expression through RORs and inhibiting defense enzymes directly. I feel the lower immunity observed during winter andversus latitude can more realistically be explained through 'more melatonin' than Cannell claim of 'lower vitamin D.'

Yet melatonin can be framed as 'anti-inflammatory' for this reason, and something can be said about that. I think some people could certainly benefit from a little melatonin at night, yet this greatly depends on the circumstance. Day/night cycles naturally modulate small-molecule redox immunity with repair, with imbalances enhancing infection risk in one direction and cancer risk in the other. I don't think that taking either vitamin D or melatonin is a particularly good idea, in general, although it is certain to help many people in some circumstances. [Even entire populations could perhaps 'benefit on average' depending on diet, stress, and latitude.] Although all B-vitamins are enzyme cofactors and thus tend always towards increased metabolic efficiency: pineal hormones, retinoids, and calciferols are circadian hormones that ought to be properly cycled. There lipid-solubility only potentiates their already high potency, and although some vitamins are safe in gram-sized doses these can be dangerous in the microgram range.

[*] Melatonin is amphiphilic, yet 5-methoxytryptophol is quite oil-soluble.
Melatonin does relax the brain facilitating cleansing: The interstices of the grey matter will relax at night—ostensibly effected by Na⁺/K⁺ redistribution—thereby allowing for the ingress of cerebrospinal fluid. This one melatonin effect certainly seems an important one, yet the amount of oral melatonin needed to achieve this—nighttime CSF concentration?—could probably be accomplished only by first inducing a nonphysiological plasma level. Melatonin works on immune cells in picomolar concentrations, and unnatural increases of that magnitude could have unanticipated effects—especially after considering the majority of immune & toxicity data had been obtained using melatonin-resistant nocturnals. Much safer for increasing brain melatonin at night may simply be the use of tinted eyeglasses in the evening, those excluding the blue spectral region:

Melatonin is far more potent than steroid hormones per molecule, with pharmacologists noting dissociation constants between 20 and 400 pM for the higher-affinity melatonin-1 receptor (MT₁). After converting into more intuitive mass units—equivalent to 86 to 172 pg/mL—this compares quite favorably with the human diurnal range:

Melatonin is sold in microgram-sized doses, yet those sold milligram-sized are more common. Not only would milligram-sized daily doses saturate all peripheral MT₁ receptors, these concentrations would be high enough to saturate them 27/7. Even when determining melatonin concentrations on the day after the last dose—after taking either 2.5 or 10 mg/d for months previous—the concentrations are an order of magnitude over the placebo group, in the nanogram per deciliter range:

'The melatonin groups had elevated daytime plasma melatonin levels relative to the placebo group by Holm-adjusted Mann-Whitney test. Residual daytime melatonin levels in the melatonin 10 mg group were highest (67.7 ± 281 ng/dL), followed by ML 2.5 mg (28.7 ± 67 ng/dL), and PLA (2.7 ± 4 ng/dL). Two subjects in the melatonin 10 group had midday melatonin levels greater than 600 ng/dL, and 1 subject in the melatonin 2.5 group had a level greater than 400 ng/dL. All subjects in the placebo group had melatonin levels that were normal midday values (<10 ng/dL).' ―Clifford

Since these levels are high enough to saturate both melatonin membrane receptors, MT₁ and MT₂, you could expect both cAMP and cGMP to be significantly reduced in all cells expressing both. Besides the two adenylate and guanylate cyclase-linked membrane receptors regulating the cell's metabolic rate, melatonin exerts genomic effects through three nuclear receptor transcription factors: RORα, RORβ, and RORγ. The expanded names of the class are 'retinoid orphan receptors,' being so-named before their endogenous ligand had been discovered. All immune cells express RORγt and bone cells, including osteoblasts and osteoclasts, express multiple forms including RORβ.

'To add to the confusion some authors have attempted to ascribe nomenclature to the receptors, such as ML-1 and ML-2. ML-1 has been used to encompass those receptors of high affinity (Kd = 20–400 pM) and selectivity for melatonin, whereas ML-2 refers to a [relatively] low affinity site...' ―Morgan

Retinoid orphan receptor β and γ are also clock genes. The expression of clock genes in the cell oscillates in a circadian manner, by definition, in cycles that can be entrained by only one of two things: Light, or melatonin. Since RORβ and RORγ are nuclear melatonin receptors, and also transcription factors, it would be natural to assume that they are responsible for melatonin-induced entrainment. The manner in which light does this is more esoteric: In some species, the photosensitive cryptochrome has been shown to quickly induce dNA transcription in response to light. Humans do have a cryptochrome homologue in the nucleus, yet the mainstream view is that it works only in the retinal. However! RORβ is also found in the pineal and suprachiasmic nucleus, notable on account of its expression being nearly exclusive to these two brain regions (and bone). Despite its rarity in fully-differentiated cells, retinoid orphan receptor β is expressed in all stem cells. This naturally leads to the thought that light and melatonin could direct the differentiation of stem cells

On account of the far-reaching implications surrounding clock gene desynchronization and bone turnover, long-term dosing in the milligram range might appear reckless. However, doses in microgram range could leave nuclear RORs largely unaffected: The two membrane receptors have quite substantial affinities for melatonin, with the former shown to prevent ACTH signalling in the adrenals. For RORs to become activated, it may be logical to then assume both high-affinity membrane receptors would initially need to become saturated, thereby allowing transmembrane permeation and nuclear activation. Nuclear receptor activation may require prior membrane saturation, which iscalculable.

Szymanska, Anna. "Diurnal profile of melatonin concentrations in patients with major depression: relationship to the clinical manifestation and antidepressant treatment." Neuroendocrinology Letters (2001)

Brainard, George. "Action spectrum for melatonin regulation in humans: evidence for a novel circadian photoreceptor." Journal of Neuroscience (2001)

Morgan, Peter. "Melatonin receptors: localization, molecular pharmacology and physiological significance."Neurochemistry international (1994)

Singer, Clifford. "A multicenter, placebo-controlled trial of melatonin for sleep disturbance in Alzheimer's disease." Sleep(2003)

Asher, Gad. "SIRT1 regulates circadian clock gene expression through PER2 deacetylation." Cell (2008)

Xie, Lulu. "Sleep drives metabolite clearance from the adult brain." Science (2013)"

I hope others find this information as helpful as I did!

 

[YourUniverse]

equipotent

What an awesome word