I am not going to go into detail in this blog post as to why the steroid hormone Vitamin D is essential to human health. In fact, I’ve talked about it before here & here. Besides, there’s plenty of other information available on the web. The purpose of this post is to present the findings of an 18-month study I have conducted into how serum vitamin D varies without supplementation.
It is a little-known fact that serum vitamin D comes in two forms, 25-OH and 1,25-OH, with 1,25 being the hormonally active portion. Yet only the 25-OH portion is routinely measured. Deficiencies are largely determined based on this reading alone but, as we shall see, this can be misleading.
The half-lives of the 2 vitamin D metabolites also vary considerably. That of the 25 portion can be measured in weeks whereas that of the 1,25 portion in days or even hours. The relative amounts of 25 and 1,25 circulating in your system also differ by a factor of a 1000 [nano vs. pico; see table of results, below]. These 2 facts are critical in understanding whether or not you have or are approaching a vitamin D deficiency.
Humans get their vitamin D from 3 main sources; the Sun, food and supplementation. Under current thinking, using the 25-OH model, there is no western diet that can deliver the required amount of vitamin D for optimum health by itself. Plenty of sunshine and supplementation are usually considered essential in order to maintain adequate levels of Vitamin D throughout the year. Indeed, most western government guidelines advise supplementing year-round, regardless of sun exposure.
Ever since going LIHF I have been supplementing vitamin D and the amount increased steadily over time. I started out at around 30-50 ug/ day but this rose to well over 100-150 ug/ day by spring 2018. Sometimes, if I felt the flu coming on, I would even increase this to well over 200 ug/ day. It was then that I discovered the link between 25 and 1,25 vitamin D.
Serum 25-OH vitamin D [derived from the liver & fat storage] is the precursor to 1,25-OH vitamin D [produced in the kidneys]. In other words, you can’t make 1,25 without 25, see graphic below. This means that all “incoming” vitamin D entering the body, be it from food, sun or supplements, is first stored as 25-OH and this is then broken down into 1,25-OH, the active form that the body can actually use. So why are we measuring 25-OH at all? This is a good question and one I can’t answer. One reason might be the general availability of the 25 test compared to 1,25, or it might just be down to plain old ignorance.
As stated above, up until the spring of 2018 I was supplementing vitamin D on a daily basis. It was during the previous winter that I found out about the vitamin D metabolites and decided then that I would stop supplementing and start tracking 1,25 vitamin D in order to understand exactly what was going on. To that end I have been supplement-free ever since. In other words, my only source of vitamin D since then has been from the sun, whatever little is to be found in my LIHF diet and a small weekly dose [10 mins] of sunbed in the winter, discussed at the end.
The results are presented in the table below, with the first set of bloods taken in March 2019 and a second batch taken in November 2019. With these two sets I hope to have captured a) minimum vitamin D levels at the end of the winter [empty tank] and b) maximum levels at the end of autumn going into the next winter [full tank]. All the usual blood tests that I take whenever I do any blood tests are also provided for reference, including lipids and blood sugars.
Quoted reference ranges from my blood testing service for vitamin D 25-OH are >75 nmol/L and 42-211 pmol/L for 1,25. I have become very skeptical of standard reference ranges in general since they all depend on the context in which they are measured. For example, it is now an established fact that total cholesterol rises on a low inflammation diet, witness my published results throughout this blog plus those of my Ultimate Fitness clients, in most cases exceeding standard guidelines. But it is also the case that triglycerides and HDL improve. Vitamin C is another example where the essential dose varies according to the diet, thanks to a process known as glucose ascorbate antagonism. With the exception of blood sugar, which operates in a tight and well-documented range, so-called ‘normal’ ranges are open to question unless and until we get a much better definition of what ‘normal’ actually is. Context is king and my findings show that there is good reason to question a) current reference values for 25-OH and b) why we are measuring it at all when there is a clear contradiction between it and the 1,25 reading, see below.
So what is the best way of interpreting these results? Well, the first stand-outs are the actual values themselves and how they have varied over time. It is interesting that both 25 and 1,25 values were higher at the end of winter than they were at the end of the autumn! After a summer of extensive sun exposure, instinct would tell us to expect the opposite. Perhaps I was too late with the autumn readings, having already depleted reserves? Further, in the latest set of readings, 25 is approaching critically low reference levels, being considerably lower than previous readings obtained during supplementation. On the other hand, both the 1,25 readings sit nicely towards the high end of the very broad reference range. As far as the other results are concerned there’s really not that much to say; with the exception of CRP which has fallen considerably and is nice to see, everything seems to be fairly consistent, including HOMA-IR.
One thing I noticed when I was on a high-dose supplementation regime was that my dental tooth plaque increased dramatically, so much so that I was visiting the hygienist once every 3 months to get it cleaned. I didn’t put two and two together until I stopped supplementation altogether, when my plaque cleared up almost completely. Remember, vitamin D is a vital co-factor in calcium transportation and this made me think that maybe my arteries were also getting bunged-up with plaque?!? The effect seemed to be all the greater when I was on my meat & water diet but, as I say, all seems to be back to normal now that I’ve stopped supplementing. The other more subjective thing I’ve noticed is a slight lethargy and drop in training performance as autumn gets into full swing. This was definitely not the case when supplementing.
So what’s the best way of interpreting these results and how should I proceed from now on?
As stated above, there’s a contradiction between the two results; one says I’m close to deficient levels whilst the other and, arguably the most important one, says I’m doing just fine! Which one do we believe? Since the hormonally active version, 1,25, is really what matters here, this is where I’ll be focusing all my attention from now on.
I’m in no rush to get back to supplementation, both because of the plaque/ calcium issues and the fact that 1,25-OH sits nicely at the higher end of that very broad range. Also, I am beginning to seriously question supplementation of any kind, especially in pill or capsule form. From an evolutionary point-of-view it seems like a complete anathema. It just doesn’t seem right to me. However, living as I do at 60N, I am concerned that the already low “header tank” of 25-OH that is the supply for 1,25-OH manufacture might get so low by the end of winter as to start affecting the latter, and that this too will start to get too low. So if supplementation is off the table that only leaves diet and the Sun. With diet, I intend to keep my vitamin D sources as high as possible, and so I will continue to eat plenty of fish and eggs throughout the winter but I’m pretty sure even that won’t be sufficient by itself. The only remaining option is the sunbed. I used the sunbed off and on throughout last winter, max once/ week for no more than 15 minutes. It felt really good to get some “sunshine” in the middle of winter, albeit artificial in nature. For some reason, the artificiality of the sunbed sits better with me than that of the supplement pill or capsule; it just seems much closer to the real thing, if that makes any sense at all. The threat of skin cancer doesn’t bother me either, a) because my dose is so low and b) because it is sun-burn events that correlate to melanoma rather than the exposure itself, and I never expose myself enough to get burned. To that end, I will also be maintaining this routine throughout the winter.
By way of a follow-up to this study, I will be taking another set of bloods at the end of this winter/ start of spring 2020.
- A Narrative Role of Vitamin D and Its Receptor: With Current Evidence on the Gastric Tissues https://www.mdpi.com/1422-0067/20/15/3832/htm
- Why We Get Sick – Nesse & Williams, p.71, “Radiation” & sunburn events.
- The China Study – Appendix C: The Vitamin D Network.
- Biochemistry, 4th Edition – Mathews, Van Holde, Appling, Anthony-Cahill, “Steroid Metabolism”
- Vitamin C and Disease: Insights from the Evolutionary Perspective – https://www.paleomedicina.com/en/vitamin_c_and_disease_insights_from_the_evolutionary_perspective
6 thoughts on “To supplement or not – studying the link between 25-OH & 1,25-OH Vitamin D”
I am if you have any experience with the Sperti Vit D-3 UVB light.
You or any of your references had tried, enjoyed, tested, failed…etc.
Check out my latest post on Vit D
were you supplementing vitamin K2 as well? ..this is thought to get the calcium to the right place, the bones.
No I wasn’t
Hi Nick, Is Vitamin D3 another name for 25-OH or 1,25-OH?
It’s the precursor to both, see here: