Our Stance on Vitamin D

We get asked all the time for guidance about raising vitamin D.

What has been taught in Magnesium Advocacy Group – discussing the Root Cause Protocol for many years is how the Vitamin D (aka ‘Hormone D’) tests that physicians often opt for, doesn’t give us a true view on what’s happening in our bodies.

Low Hormone D is giving us an indication that we are low in magnesium. Magnesium is needed for the conversion of the two types of Hormone D. Beyond that, low hormone D is flagging that the mineral movement in the body isn’t happening effectively. 

In RCP terms, the recycling system of the body is not at optimum, and we typically have symptoms of not feeling well, making energy effectively (etc) as a result.

 

Jim Stephenson Jr. taught us that the .25 vitamin D blood test is not an adequate marker:

  • What D3 you take in the body, the body decides what it becomes. This means that the body decides on what metabolite it will become and not necessarily the one they typically test (.25 vitamin D).
  • Vitamin D is usually stored in the liver, it is the same way a cod stored it in its liver. 
  • Humans have more than a dozen different forms (metabolites) of 25D and the typical vitamin D test works on two of them. 
  • In children, .25 vitamin D doesn’t always show up accurately, as kids have most their 25D in, epi-3 25D (another form of vitamin d that’s not generally tested). 
  • When .25 vitamin is low, 1.25 vitamin d is often high. The former does not usually get tested.

You can find Jim here on his Facebook group – Secosteroid Hormone D (at times this group is shifted to be “hidden” by admin, if the link isn’t working, please try again later)

Looking at a snapshot of one hormone or vitamin isn’t going to give us full context to what else is happening at the time.

Morley joined Matt Blackburn and Jim Stephenson Jr. for a discussion about hormone D and you can watch/listen to that here: 

Mitolife Radio – Matt Blackburn | Why You Shouldn’t Supplement Vitamin D with Jim Stephenson Jr and Morley Robbins – Episode 83 | August 7, 2020 – The Root Cause Protocol

Morley’s Message about Vitamin D
Our Stance on Vitamin D

The quotation below was provided by Morley as a list for practitioners he was addressing, to further gain context about vitamin/hormone D.

These are the top 5 reasons why hormone D is the biggest scam on planet Earth: 

Hormone D is the oldest hormone on the planet. It is also the most powerful hormone on planet Earth. It should not be ingested like “candy!” Here’s why:

  • “D”ecimates potassium status in the kidneys and thus the body.
    RENAL POTASSIUM-WASTING INDUCED BY VITAMIN D
    (Every client that I have that took synthetic, supplemental hormone D has uber low potassium on their HTMAs.)
  • “D”epletes the precious regulatory mineral, magnesium.
    https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3765911/
    (Please STUDY figure 1 to understand how important Mg is to hormone D metabolism. When “D” is low, it is really saying that Mg is low, as this key mineral is essential for its synthesis and motion)
  • “D”eepens iron storage in the tissue.
    https://www.ncbi.nlm.nih.gov/pubmed/10362817
    (Trust me, depleting renal tubular cells of ATP is not a good thing! And increasing iron-induced oxidative stress is no better! Also, know that one of the prerequisites to more iron is less potassium.)
  • “D”eception about taking low D to correct “inflammation!”
    https://www.ncbi.nlm.nih.gov/pubmed/25048990(Please spend some quality time on this stellar Study, “Low Vitamin-D does not cause Inflammation!” It is a proven clinical sign of inflammation. Taking more D does nothing to correct this metabolic issue that is caused by excess, unbound iron and lack of magnesium. (Weglicki & Phillips, 1992a, b, c, d)

Now we all know that hormone-D is — in fact — made naturally when cholesterol gets “kissed” by the sun that triggers the D metabolism in our body.

But as you’ll see from Fig 1 of Deng, 2013, not much happens without magnesium as Stephanie Seneff, PhD enlightens us, that sun-based D is water soluble, which is just how the body likes it!

In the United States, we are a nation that has the highest cholesterol levels on the planet, yet, we are also the nation with the lowest hormone-D Levels. Hmm.

When you understand that storage hormone D requires magnesium as explicitly shown above, then that Cu-nundrum  makes way more sense.

Also, if you are being swayed by the volumes of alleged research that low vitamin-D is connected to every condition known to man, you might want to understand and reflect on the fact that all that nonsensical research is based on correlation, and none is based on causation! (There is a big difference between those two research conditions.)

Key Question: “Do flies cause garbage?”

Finally, if you are swayed by the research from JM Lappe et al. at Tufts in 2007 that taking Vitamin-D will help prevent cancer, that same research team updated their research and reversed their findings in 2017 to declare that they were wrong!

Hormone D supplementation has no impact on cancer metabolism. I would strongly encourage you to read this excellent overview of how hormone D supplements are losing their luster: Vitamin D supplements aren’t living up to their hype (article now longer available without subscription)

That’s a lot of material to process. I’ve been working on understanding this destructive supplement for the better part of 10 years. There is no “one and done” article that will present a compelling set of facts against this “D”emonic supplement, although the Science News from Jan, 2019 study above comes close.

So, I do apologize for all the lengthy post, but wanted you and your colleagues who are lost in big Pharma rhetoric and research, to have the rest of the story. For all that I’ve shared above, Jim Stephenson Jr. has 10x more research to support these conclusions. All is not as it seems, nor as it is portrayed on the internet or your doctor’s office.

Hope you find this range of information helpful.


“A” votre
Morley M. Robbins

Key Hormone D Articles on RCP Website and Other References

Discussion around Sir Douglas Kell’s Research about Iron and Vitamin D

In this article, it has been outlined that there is a relationship between low levels of serum vitamin d calcidiol [25(OH)D3] and chronic infection and inflammation.  

“The studies listed in table 1 show associations, but not whether low vitamin D levels are a cause or an effect of inflammation..”

 

Kristan Kershaw has provided a summary of the article below:

The most prevalent problem behind “diseases” in modern health is inflammation.

  • These diseases have causes in common – stress induced iron dysregulation and its ability to awaken dormant, “non replicating” microbes. That is, iron dysregulation wakes up dormant microbes that may be present in the body and not otherwise causing a problem.
  • He presented evidence that low 25(OH) D3 levels are the result of inflammation not the cause. (This is the form that most Drs test for)
  • He also presented evidence that the 1,25(OH)2 form of D3 inhibits hepatic (liver) production of the 25(OH) form of D3…so that means if you supplement with D3, it can force the 1,25(OH)2 form up, and still have apparent low vitamin d.

The graphic shows the movement of vitamin d around the body and how it ties in with critical components in iron dysregulation.

Increased 1,25(OH)2 vitamin d puts pressure on iron related hepcidin and can lead to increased ferroportin…which leads to a drop in blood iron levels and increases in iron laden macrophages.

Macrophages are part of our immune system. If they become iron laden, then they can’t do their other jobs very effectively!

My take on this part of the content is that it’s saying increasing the wrong type of vitamin d (which is what we see from supplementation of synthetic vitamin d)… it’ll lead to changes in the liver which lead to iron loading in the body…

Kell, D.B., Pretorius, E. (2018). “No effects without causes: the Iron Dysregulation and Dormant Microbes hypothesis for chronic, inflammatory diseases”

 

Discussion on Magnesium Advocacy Group 

There is no clinical benefit to vitamin D over 21

There is no clinical benefit to Vitamin D over 21. (Those in Australia and some other countries should note our units are different, so it is more than 21 for us (52))

 

For an explanation, see:

Vitamin D Supplementation – Be Careful, Researchers Warn

“However, excessive vitamin D levels may be bad for you – any vitamin D levels above 21 nanograms per milliliter were found to be linked to an increase in CRP, which is associated with the hardening of blood vessels and a greater risk of developing cardiovascular problems. The team has also found a link between excess vitamin D and raised levels of homocysteine, which can increase the risk of cardiovascular diseases.”

 

Three other papers on no benefit over 21

Vitamin D in Breastmilk – Jim Stephenson Jr

This is the study that gets cited as support for fixing “lame” breastmilk. 

For context, think “human breast milk is the perfect human food”.  Women are told to take calcium during pregnancy so as to not deplete their own.  It’s not the same advice with hormone D. 

They say women are deficient in D so when they are pregnant they need to really load up on it so their breast milk won’t be deficient as well. Let me repeat that. The breast milk will be deficient according to the current Vitamin D push if a woman isn’t at least at the unscientific minimum currently proposed.  

In this study they had one group of women taking 400 iu, the current recommendation of the IOM New York Academy of Sciences, and another group taking 6,400 iu. The 6,400 was based upon calculations to maintain the unscientific level. 

What happened???  

Well the women’s 25D went up and stayed up in the women and breastfeeding children, in both groups. And what happened to the babies level after “helping out” our bodies making inferior breast milk? The ones with mothers taking 400 iu went from 13 to 43 in their 25D. The ones with mothers taking 6,400 went from 14 to 48 in their 25D.   

A difference of 5 in the end for SIXTEEN times the dose!  Looks like breast milk is the perfect food after all.  (The breast milk analysis itself left me scratching my head, FYI. Very old science used in that).

Maternal Versus Infant Vitamin D Supplementation During Lactation: A Randomized Controlled Trial 

Message about Vitamin D – Jim Stephenson Jr

It’s important to not lose sight of the fact that the body decides what to make and the body makes many molecules, not just D3.

There’s no way to take the other molecules the body makes. Think about that or feedback to prevent the over production of D.

I’m against taking pills of vitamin D. I want to make it perfectly clear why that’s not a sound practice.

This is chasing a number. 

The serum level of 25D, typically 30 or above to satisfy mainstream. If you don’t have that you will be advised to take D3. Notice, this is a different form of D. You will likely take a lot of it but you will never have it measured. There’s no test for that. (Don’t be silly by making sense). 

They will continue to measure 25D. What it may become and where they may by chance, find it (serum-it’s a fat soluble vitamin made for storage. Think of a hibernating bear).

I said may become. Here’s why:

  • It can stay D3 and hang in serum. Untested.
  • It can get stored in fat, as D3. Untested. 
  • It can become 20OHD, the sun protection analogue. Untested. 
  • It can become 24,25S/R. One is the bone healer. Untested. 
  • It can become 25D, stored in fat. Untested. 
  • It can become Epi-3 25D. D formed from another pathway, epimerization. There are at least 3. Hydroxylation and lactonization being two others. Hydroxylation is the one 25D is from. Some of these analogues can “cross over” into another pathway.

What is the take home message? The body decides what to make. Not the Vitamin D Council Psychiatrist Channel.

‘Diagram of a Scam’ – Jim Stephenson Jr

Diagram of a scam. The serum 25D level OBSESSION. (“Vitamin D”)

I can explain the high level focus. They took everyone’s 25D level. They broke them out and grouped them by disease/condition. Then they did something very unscientific and everyone fell for it. 

They said their D level was the cause of their disease/condition. How correlation got turned into causation. A huge no no in science. But remember, it’s been called a vitamin for generations. 

The thought of Rickets makes people tremble.  It was two genetic mutations OR a pure lack of sun. To be quite honest we may still not have discovered the molecule that fixes that. 

Think about it. It could be made by the sun and remain undiscovered. It may get transferred to food sources, as well. No one is looking. It could be one of the molecules I mention but remain an action not recognized or attributed to that molecule. Like 20OHD. The D molecule we make in the sun that protects us from the sun. Or 5,6 trans-vitamin D. I cannot stress enough that no one is looking. Where would that money come from??? The only reason anyone is studying D is to:

  1. Make a synthetic. There are thousands of synthetic analogues. Some as simple as D5
  2. Looking to piggyback their drug on the D delivery system. Serves about 33 tissue types. Great rail line.

You will notice the Coimbrio high dose isn’t a trial. Why not? It’s not like we don’t need them. It’s really a calcium avoidance diet with tons of D so you don’t rodenticide yourself. The lesions going away are the proof. And self reporting. The lesions wax and wane in the absence of D. It’s the placebo effect. It takes 7 days for D3 to become 25D. It can become 1,25D as needed after that. But folks are always telling me how great they feel when they take it. But way too soon. 

So the number that has become the target these days is way up there. Above any groupings of ANY ill people. It’s ludicrous. The folks are not converting any 25D to 1,25 D in something known as the immune response.

This study is a huge wake up call. The reason everyone missed it is because they didn’t use the same measurements. The study used nmol/liter, whereas most in the US are familiar with ng/ml.

“Vitamin D insufficiency (25-hydroxyvitamin D [25(OH)D] < 50 nmol/liter) is prevalent (1–3) and has been suggested to be involved in various diseases such as diabetes, cardiovascular disease, depression, immune system diseases, and certain cancers (4–8). The biomarker used for the determination of vitamin D status is 25(OH)D, rather than the biologically active hormone 1,25-dihydroxyvitamin D (9)”

But the results are shocking when you realize insufficiency level has the lowest mortality.

“All-cause mortality associated with serum 25(OH)D levels. The association between all-cause mortality and serum levels of 25(OH)D was reverse J-shaped (Fig. 1A). A serum 25(OH)D level of 50–60 nmol/liter was associated with the lowest mortality risk. The hazard ratios [95% confidence intervals (CI)] of all-cause mortality at very low (10 nmol/liter) and high (140 nmol/liter) serum levels of 25(OH)D were 2.13 (2.02–2.24) and 1.42 (1.31–1.53), respectively. In subjects at least 60 yr old, the mortality was, as in the total population, lowest at a serum 25(OH)D level of 50–60 nmol/liter. In this age group, the hazard ratios (95% CI) of all-cause mortality at low (10 nmol/liter) and high (140 nmol/liter) serum levels of 25(OH)D were 2.04 (1.94–2.17) and 1.44 (1.32–1.56), respectively.”

For perspective.

50 nmol/liter = 20 ng/ml

60 nmol/liter = 24 ng/ml

So lowest mortality is at the bottom end of insufficiency, one away from deficient. now think!!! The vitamin d council now wants to go for 80 ng/ml. Many are on some wellness protocols going for 100ng/ml. Insane!!

Again, for perspective:

140 nmol/liter = 56 ng/ml

That above is what “high” is in the numbers most people are familiar with. That’s a lot of folks these days.

Careful with the unit of measure. The middle one uses non US units.

Where Vitamin D gets Stored – Jim Stephenson Jr

“Vitamin D does not circulate for long in the bloodstream but, instead, is immediately taken up by adipose tissue for storage or liver for further metabolism. In humans, tissue storage of vitamin D can last for months or even years.”

In conclusion, from this cohort of asymptomatic adults, independent of traditional cardiovascular risk factors, we observed a statistically significant inverse relation between 25(OH)D at levels <21 ng/ml and CRP. 

We found that 25(OH)D at a level ≥21 ng/ml is associated with an increase in serum CRP. It is possible that the role of vitamin D supplementation to reduce inflammation is beneficial only among those with a lower serum 25(OH)D Current Understanding of the Molecular Actions of Vitamin D | Physiological Reviews

The roundtable participants expressed concern about the excessive focus on 25(OH)D concentrations, which do not indicate whether vitamin D is entering and leaving the tissues. 

For example, clinicians often prescribe vitamin D to bariatric patients before bypass surgery but as they lose weight, their 25(OH)D concentrations increase. As discussed earlier, we do not understand the dynamics of the relation between 25(OH)D and the mobilization of its stores, which could have relevance to excessive exposure in some physiologic conditions. (Vitamin D can become a weapon instead of a tool for balance if you get too much and the stores of this fat-soluble vitamin builds up and then spills into your blood in toxic doses.) Summary of roundtable discussion on vitamin D research needs

If I had a nickel for everyone I’ve pointed out folks take D3 and measure 25D I’d be RICH.

It matters but luckily for most they avoid physical harm.

Now think about number chasers taking high doses. Some struggle. Do you think Coimbria with his MS protocol knows this? Or Cannell at the VDC? 

This should cause everyone to pause, really.

With normal doses of D3 the body converts it to 25D fairly quickly. But those taking Supra-doses will store it as D3.

This is hugely important.

“CONCLUSIONS: At physiologic inputs, there is rapid conversion of precursor to product at low vitamin D(3) concentrations and a much slower rate of conversion at higher concentrations. These data suggest that, at typical vitamin D(3) inputs and serum concentrations, there is very little native cholecalciferol in the body, and 25(OH)D constitutes the bulk of vitamin D reserves. However, at supraphysiologic inputs, large quantities of vitamin D(3) are stored as the native compound, presumably in body fat, and are slowly released to be converted to 25(OH)D.“

With normal doses of D3, the body converts it to 25D fairly quickly.  But those taking super-doses will store it as D3.

This is hugely important.

“CONCLUSIONS: At physiologic inputs, there is rapid conversion of precursor to product at low vitamin D(3) concentrations and a much slower rate of conversion at higher concentrations. These data suggest that, at typical vitamin D(3) inputs and serum concentrations, there is very little native cholecalciferol in the body, and 25(OH)D constitutes the bulk of vitamin D reserves. However, at supraphysiologic inputs, large quantities of vitamin D(3) are stored as the native compound, presumably in body fat, and are slowly released to be converted to 25(OH)D.“

25-Hydroxylation of vitamin D3: relation to circulating vitamin D3 under various input conditions

Supplementing Vitamin D without Testing 1.25D – Jim Stephenson Jr

You wouldn’t want to supplement D with raising 1,25D as a goal. That getting higher isn’t a good thing because it IS the molecule of immune response. It’s being requested to encode the genes to create your chemical and biological warriors. It’s a genomic response molecule.

In fact I had to really think about it. I don’t know of anyone promoting increasing 1,25D. But it does increase in some folks. This is why it needs to be checked. 

Keep in mind this is the molecule the body monitors in the Calcium/pth/D axis. Drive it up and you increase calcium needs to the point you can get the body to induce osteoporosis.

Calcium has to come from somewhere to match the insane increases in D serum levels. (It’s D that sets the level, the ratio never changes. Calcium must match D. If you read the action of rodenticide this isEXACTLYwhat happens to people but they don’t die they just destroy their bones and maybe a kidney.)

In serum, vitamin D binding protein-vdbp, transports the two forms of D, 25D and 1,25D around the body. But, 25D has 1000 times higher affinity (attraction) to bind with this carrier protein than does 1,25D. Can you see how too much 25D could create an issue getting the 1,25D where it needs to be when it’s needed? We see this exact same thing with folic acid versus folate.

Testing is the key:

Testing is Key to Hormone-D! – The Root Cause Protocol

Vitamin D and Hypercalcemia – Jim Stephenson Jr

Pretty important message here:

“Hypercalcemia state continues for several months when D2 or D3 are responsible for the toxicity whereas the hypercalcemia would subside in a week when 1 alpha(OH) D3 or 1,25 (OH)2D3 are responsible for the toxicity.”

[Hypervitaminosis D] 

“Many older adults should avoid taking vitamin D and calcium supplements to prevent falls and fractures, and focus instead on exercises to improve balance and coordination, U.S. doctors recommend.

The conclusion issued Tuesday by the U.S. Preventive Services Task Force (USPSTF) on fall and fracture prevention comes amid growing debate in the medical community over the role of vitamin D, which may help some people at lower doses but is linked to an increased risk of fractures, falls, kidney stones and certain cancers at higher doses.”

Older adults may not need vitamin D to prevent falls, fractures 

Children and Adolescent Imprinting – Jim Stephenson Jr

Imprinting Part I

“Considering that in earlier experiments similar neonatal treatments influenced bone mineral mass and sexual behavior, the hormonal imprinting effect of vitamin D(3) and its harmful effect on the development of other members of the steroid receptor superfamily, seems to be unquestionable.”

Effect of vitamin D(3) treatment in the neonatal or adolescent age (hormonal imprinting) on the thymic glucocorticoid receptor of the adult male rat 

“For a long time, it was believed that the structural development of the central nervous system is finished at birth. However, recent investigations show that stem cells are present in the brain, which are able to build new structures (Mehler 2008). Any conception is accepted; the fact is that the central nervous system is hormonally imprintable (Csaba and Tekes 2005).”

“Vitamins A and D, months after the perinatal exposure, decreased or abolished males’ and females’ libido (Mirzahosseini et al. 1996; Csaba and Gaál 1997).”

“Single treatment with vitamin D3 or dexamethasone at puberty significantly influenced the glucocorticoid receptors’ binding capacity in the thymus (Csaba and Inczefi-Gonda 1999a).

Other molecules (benzpyrene, vitamins A and D) also can imprint the brain, is manifested in the change of biogenic amine levels of the brain and CSF (Tekes et al. 2007a, b, 2009a, b, c).”

“The physician does not treat untouched people, but (faulty) imprinted ones, and influence them further. In the early phase of development, the medical intervention also artificially imprints the receptors and not only molecules with DES strength, but by such molecules as perinatal vitamin A and D treatment (McGrath 2001), by surfactants as cortisol, by oxytocin and antihistamines.”

The biological basis and clinical significance of hormonal imprinting, an epigenetic process 

“In the offspring of untreated dams administered with vitamin D 24 hours before measurement, each cell type studied (lymphocyte, monocyte-granulocyte group, mast cell) had a one-third lower T3 content, which shows that vitamin D treatment can influence hormone content of immune cells. The experiments call attention to the transgenerational effect of perinatal treatment with lipid-soluble, intracellular receptor-bound vitamins.”

Transgenerational effect of neonatal vitamin A or D treatment (hormonal imprinting) on the hormone content of rat immune cells 

“As immune cells are differentiating during the whole life, faulty imprinting could develop any time, however, the most decisive is the perinatal imprinting. The faulty imprinting is inherited to the progenies in general and especially in the case of immune system. In our modern world the number and amount of artificial imprinters (e.g. endocrine disruptors and drugs) are enormously increasing. The effects of the faulty imprinters most dangerous to the immune system are shown in the paper. The present and future consequences of the flood of faulty imprintings are unpredictable however, it is discussed”

.http://www.ncbi.nlm.nih.gov/pubmed/24939679

Neonatal Imprinting – Jim Stephenson Jr

Imprinting Part II

“Vitamin D treatment was absolutely ineffective. The imprinting effects of vitamins A and D and their differences are discussed. The results call attention to the possible harmful effect of vitamin treatments during the perinatal critical period.”

Impact of neonatal imprinting with vitamin A or D on the hormone content of rat immune cells 

[Revaluation of the concept of developmental abnormality: the importance of faulty perinatal imprinting] 

[Hormonal imprinting–the unforeseeable future] 

“Biogenic amines (norepinephrine, dopamine, homovanillic acid, serotonin and 5-hyroxyindole acetic acid) were measured by HPLC method in adult F1 generation rats’ brain regions (brainstem, hypothalamus, hippocampus, striatum and frontal cortex), whose mothers (P generation) were treated with vitamin A or vitamin D neonatally (hormonal imprinting)The results call attention to the transgenerational effect of hormonal imprinting in the case of receptor level acting vitamins which are frequently used in the most imprinting-sensitive period (perinatally) of human life and suggests that caution is warranted.”

Transgenerational hormonal imprinting caused by vitamin A and vitamin D treatment of newborn rats. Alterations in the biogenic amine contents of the adult brain 

“1. Neonatal treatment of rats with vitamin D3 resulted in a change of sexual behavior in adulthood. 2. 2.5 mg vitamin D3 completely inhibited the ejaculation of males without any apparent influence on sexual desire. 250 mg vitamin D3 influenced both the desire and ejaculation. 3. Sexual activity of females was depressed by both doses. 4. The experiments demonstrate that vitamin D3, a steroid in structure, given in the critical period of hormonal imprinting may influence steroid hormone-receptor commanded events for life, in a way similar to the effects exhibited by synthetic steroid hormone analogues and benzpyrene in earlier studies.”

Changes in sexual behavior of adult male and female rats neonatally treated with vitamin D3 

“A fundamental problem is–considering the faulty imprinting effect – in the case of vitamin D, its name. Vitamin is a quite another category than hormone. In the mentality of laymen vitamin is a beneficial material, which is needed for health in contrast to hormones which are effective serious regulators, requesting the consideration of doctors. This opinion is supported by TV advertisements, which propagate vitamin D and multivitamins as well, as calcium preparations, containing also vitamin D which can be purchased without prescription. Doctors are knowing that vitamins can be harmful (dependent on type and dose), however, this opinion is weakened by the vitamin name. If vitamin D would be called hormone-D, or multihormone-D (a similar situation is in the case of vitamin A), and recognized as a hormone, advertisements would not be possible and less prescription would be given. At present, vitamin D is a harmless miracle-drug, recommended to almost all of the diseases for adults and infants, for prevention and treatment, and considering or disregarding its imprinting effect, this seems to be dangerous, because of its steroid hormone character.” 

https://austinpublishinggroup.com/nutrition-food-sciences/fulltext/ajnfs-v4-id1075.php

Effects on the Brain Imprinting – Jim Stephenson Jr

Imprinting Part III

“In light of the accumulating animal and in vitro evidence to date, it is likely that vitamin D plays a role in hippocampal development in vivo. However, the majority of animal studies to date have been carried on animals from several weeks old and upwards, and there are insufficient data on the effects of VD on newborn and adolescent animals.” 

Vitamin D and hippocampal development-the story so far 

“Vitamin D imprinting significantly elevated DA only in the brainstem and HVA levels in striatum and hypothalamus. Present and earlier brain-imprinting results (with brain-produced substances), show that the profound and life-long effect of neonatal hormonal imprinting on neurotransmitter production of the adult brain seems to be well established. As prophylactic treatment with these vitamins is frequent in the perinatal period, the imprinting effect of vitamin A and vitamin D must be taken into consideration.”

Influence of neonatal vitamin A or vitamin D treatment on the concentration of biogenic amines and their metabolites in the adult rat brain 

“Transgenerational hormonal imprinting caused by vitamin A and vitamin D treatment of newborn rats. Alterations in the biogenic amine contents of the adult brain.”

Transgenerational hormonal imprinting caused by vitamin A and vitamin D treatment of newborn rats. Alterations in the biogenic amine contents of the adult brain 

You can read more about imprinting and other vitamin D studies on Jim Stephenson Jr. Facebook page: Secosteroid Hormone D (at times this group is shifted to be “hidden” by admin, if the link isn’t working, please try again later)

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