Excerpt for Prescribing Sunshine: Why vitamin D should be flying off shelves by , available in its entirety at Smashwords




Prescribing Sunshine: Why vitamin D should be flying off shelves

Smashwords Edition


First digital edition, August 2012

Copyright M. Aziz 2012

email: mo79uk@gmail.com


Cover photo provided by Sam Mugraby under an extended license. Copyright Photos8.com.


All quotations in this title have been used under the understanding of fair dealing or fair use under UK and US Copyright Law.


Smashwords Edition, License Notes

This ebook is licensed for your personal enjoyment only. This ebook may not be re-sold or given away to other people. If you would like to share this book with another person, please purchase an additional copy for each recipient. If you’re reading this book and did not purchase it, or it was not purchased for your use only, then please return to Smashwords.com and purchase your own copy. Thank you for respecting the hard work of this author.

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Table of Contents

Title page

Copyright & License

Disclaimer

Quote

Introduction: D & I

1. Awakening

2. Skeletal Effects

3. Brain Development & Maintenance

Interview: Oliver Gillie

4. Vegetable, Mineral & Animal

5. Human D-volution

6. Cholesterol & Heart Disease

Interview: Dr. David Grimes

7. HIV/AIDS

Interview: Joan Shenton

8. Approaching Repletion

9. Influenza & Autoimmunity

10. Popping Cancer

Interview: Prof. Bruce Hollis

11. A Brighter Future

Bonus: New Dawn Fades – Does vitamin D deficiency help fuel the blues?

References

Index

Further information

Acknowledgements

Disclaimer

The author will not be held liable for any adverse outcomes that may result from acting upon information in this book. Precedence must always be given to the advice of qualified health professionals.


Audience outside of the United Kingdom: Please note that this book has been written in British English.

***


“It is man's consolation that the future is to be a sunrise instead of a sunset.” – Victor Hugo

***

Introduction: D & I

My younger brother cannot talk. He has severe learning difficulties. He is autistic.


Born on a February in the early 1980s, he was lucky to have survived as a premature arrival thanks to one available incubator. Though low in weight with a large head covered in translucent skin, the care provided helped him become a seemingly healthy newborn.


It wasn't until after the age he was supposed to speak that concern grew about his development. I was a late talker, but my brother did not utter anything significant beyond mama or baba at the same age. A hospital investigation soon confirmed my parents' worst nightmare. Adding to the blow was his diagnosis of knock knees, a condition where both legs turn inward and touch at the caps. This made walking problematic and uncomfortable.

For his autism he was offered speech therapy which yielded no progress. His knock knees persisted, leading to the diagnosis of rickets, a childhood bone softening disorder. It wasn't until his early teens that he was able to have corrective surgery, leaving him with two large scars down the sides of his legs; but this finally allowed him to enjoy walking and running. Prior to this, he was advised soya milk over cow's as doctors believed his rickets may have been caused by an allergy...


As the years passed my brother's behaviour deteriorated. He turned from a boy that engaged in some play with me as a child to one that became self-absorbed and less co-operative. His days at a popular special school were a negative experience too, and he ended up residing entirely at home under the care of our mother.


A few years after he was born she herself began to complain of bodily pains which she attributed to the intense care she had to offer. Unfortunately, it wasn't as simple as that, it was osteoporosis. Her bones were said to be paper-thin. At the time, and even now, it was unheard of for a woman in her mid-thirties to contract this disease. Resultantly, despite drug intervention which helped to prevent fractures, she developed curvature of the spine that chopped down some height. Regardless of her painful condition and the development of further complications such as arthritis and iron-deficiency anaemia she continued caring for my brother.


It became clear that the cause of his rickets and her osteoporosis was likely one and the same. Though the link had never been clearly defined I was regardless kept an eye on due to being an at risk candidate.

While I have remained free of bone problems my brother hadn't seen the back of them. Shortly after his operation his legs returned to a slight knock-kneed position. At the time this was believed to be out of habit from his previous state. As it did not impact his ability to walk and he appeared to be in no pain no more was thought of it.

A decade later, however, my brother was unable to get up off the floor. Once leveraged into standing position he could walk, but sitting back on the floor would test my strength in getting him up again. Getting him seen to at A&E didn't help as the doctors focused on treating the thigh rash he developed in reaction to a muscle rub I believed would help him. They believed what resembled herpes was his underlying problem.

The fortunate misfortune was that weeks after he was seen he had two seizures. The result of that was for him to be given long-term what he was prescribed briefly after his legs operation. My brother's diagnosis was the adult form of rickets: osteomalacia. I recognised the given vitamin D and calcium as it formed part of our mother's repeat prescription.


This was the moment a light bulb appeared over my head, albeit dimly. Why was my brother not offered a permanent vitamin D and calcium regimen straight after his legs operation? Since our mother already took both in combined tablets it would have been a no-brainer to consider offering it to him too. The preoperative advice about soya over cow's milk is also unforgivable due to calcium alongside vitamin D being implicated in bone maintenance since the early 1920s.

Why did I not raise this issue back in the 1980s? I was just a child myself then and there was little or nothing available to the public to distinguish the sunshine vitamin.


The development of bone diseases in my brother and mother but not myself seemed strange. More so considering that there is no evident history further up in my maternal or even paternal family trees. My maternal aunt, however, did develop severe arthritis, and one thing that links both sisters together is leaving their childhood home of Pakistan for the markedly less sunny England...

Not wanting to take any risks after my brother's diagnosis a doctor advised me to have a vitamin D test myself. It turned out that I too was severely deficient and likely had been for some time. The reason why I may have avoided bone problems could be due to simply treading a fine line or genetic blessings from my father who only suffers general back pain. Whatever the reason, I decided to pop common over-the-counter pills as suggested.


The light bulb above my head flickered a little brightly after a general GP check-up – just months after my vitamin D deficiency diagnosis – revealed I had mildly high cholesterol levels. This did not result in a printout for cholesterol-lowering medication but if my levels remained that way it would've been considered.

While luck may have preserved my bones, my cholesterol reading was unsettling, because the one strong illness link in my maternal family history is indeed heart disease. It had taken my grandfather at a relatively young age, and my mother had developed heart failure just years before my brother's seizures. My father's genes could not provide a safety mat here as he, a long-term sufferer of high blood pressure and cholesterol, went on to develop diabetes in his late sixties. Interestingly though, my paternal family history of health is better than my maternal one; possibly because my poor, dark-skinned father, and those before him, played outside on the abundantly sunny streets of Multan, whereas my comparatively pale mother was often sheltered within a haveli (mansion) in Lahore.

Being inquisitive and living in an era where information literally is at the fingertips, I pondered if the only two things wrong in my blood tests were connected in some way. I was surprised to be proved correct, but I thought I must be misinterpreting. At that point I had very little interest in healthcare and knew how easy it could be to link one thing to another by cherry picking.

A part of me, however, could not let it go, so I spilled my thoughts on the link between cholesterol and vitamin D in a personal blog site entry in hope that someone would read the post and tell me why I was wrong. Then I could drop the subject and be happy.

I proved unsuccessful.

Not long after I published the piece the Vitamin D Council of America linked it on their news page, resulting in an extraordinary number of hits, elevating the post's ranking in the top search engines for associated keywords. Of the tens of thousands of hits to date not one person has disputed what I theorised. Or should I say what I thought I theorised.

Just a year prior to my post Dr. David Grimes of the Royal Manchester Infirmary created a small ripple in the medical world by questioning if cholesterol-lowering drugs called statins work by mimicking vitamin D. In my opinion this ripple should've been an earthquake, but perhaps the powerful aftershock has yet to arrive.

Enthused by the fact that I shared an opinion with at least one medical professional my blog entry grew in size as I added new findings and shared some familial experiences. I received many comments, one of which was from Dr. Grimes himself who gave the messy piece a thumbs up. As my knowledge grew so did my dissatisfaction with the status quo.


While it is true that doctors were instrumental in diagnosing and treating members of my family, I came to realise that not only were their epiphanies late in the case of my brother, they were also backed up by inadequate treatment guidelines. They have no consensus. Despite attending the same hospital, my brother and mother had different information on what a sufficient level is and how to achieve it.


By fortune my brother's endocrinologist was one of the rare breed of doctors who was more than happy to be flexible on treatment. I explained to him my understanding of vitamin D and presented a short abstract of a study, to which he did not find the need to explain the error of my audacity. Had I presented something outlandish I would have gladly not forced the idea upon the provision of an explanation.


Convinced by everything I learnt I became tired of trying to prove myself wrong. I needed to do something with my fully lit light bulb. This book is that something.

I wrote what you're reading not just for a few people. This problem affects us all. Vitamin D deficiency is a major pandemic and addressing this health concern could result in a radical overhaul of healthcare worldwide. You may find this a bold claim, but if you're willing to read the rest of this book I am sure you will be won over. I can tell you right now that vitamin D is not even a vitamin. It would be more accurate to call it hormone-like. It ranks as highly as food, water and the air we breathe.

To say vitamin D deficiency is connected to almost all ills is very audacious. But the truth of the matter is that your body is riddled with vitamin D receptors. You can think of these as solar panels waiting to relay energy to your body parts. The body, however, is very clever and can perform a number of tricks to compensate for deficiency – but only for so long; in the same way auxiliary power in a machine is not meant as a permanent replacement for main power.

Note too that the vitamin D you find in some shops and pharmacies is not the same as what you are able to make through sunlight exposure on the skin. You would also be shocked at the disparity between what's recommended and what nature could give you.

Just as I have observed some pattern of illness in my family it is likely you have too in your own. You may have attributed this to the lifestyles you lead or just bad luck. I believe, however, that what links you and your family's health problems could be the same thing that links me to mine. Why one vitamin D deficient person gets different illnesses to another is largely in the genes.


Of course though, I am not a doctor, so why should you choose this book over one by a white coat? This title, like any of theirs, lets the medical literature do most of the talking, but I add colour by relaying important personal experiences. I show and tell. You will need to trust me. I have adopted a semi-professional voice throughout here but only in order to appear polished, not to impersonate a scientist.

There are parts where I present theories by others and myself, but the distinction is made clear. These are important to stimulate debate and to fill in areas where future studies will eventually have the final say.

I'm not shy about appearing as a search engine pundit and I believe I have the gall to say that I know more about vitamin D than many overworked but otherwise knowledgeable and caring healthcare practitioners, who aren't relayed the latest data on the subject. I care because this matters to me. You too will think as I do because this book isn't built on health supplement company press releases but actual scientific papers and review articles. You can look up abstracts and full texts for verification in the references section. Single references per a claim are mostly offered so as not to swell up the book.

I must disclose that due to the immense cost required to read all the papers referenced, a number of sources were selected on the basis of their free summary text (abstract) alone. I defend this practice in that I often cite abstracts with clear, unambiguous statements that should not prove contrary to the full texts. Where feasible, I reference open access articles that are entirely free to the public, thus for that and other reasons it has not always been possible to cite primary sources over secondary ones. I leave it up to the reader to thoroughly investigate claims of deep interest; in fact I actively encourage that as you shouldn't just take my word. Could I be wrong somewhere? Yes. Any perception of cherry picking facts would be allowable too as I do not hide my bias towards vitamin D; after all, this book is about selling the subject. However, there has been no intentional dishonesty on my part. My approach may put me under crosshairs and be a disservice to other proponents of vitamin D, but hopefully it is of consolation that I at least care to admit it. If anything, this should help to keep you on your guard. I would like to add that I am not affiliated to any vitamin-related company.


This book doesn't completely blow its own trumpet, though. It acknowledges orthodox arguments on the dangers of the sun and even an opinion that vitamin D is bad for you. If this small portion of the book makes more sense, so be it. But I would hedge that it's because you didn't read from cover to cover, which I strongly recommend.

A handful of interviews conducted in the latter half of 2010 with individuals well-qualified to comment on specific sub-topics feature after relevant chapters to add weight or extra illumination to statements in this book. Responses have been edited for clarity and their inclusion does not necessarily imply mutual endorsement.


If you're thirsty for further commentary upon finishing the book I suggest following my blog at prescsun.com. News on vitamin D is appearing almost daily so some parts of the book may be behind the times if you're reading this long after its publication.


The ironic thing, then, is that the future of medicine may not be exclusively linked to vaccines and powerful drugs, but to something that has been with us all along.

***

1. Awakening

From even before the day you're born you need vitamin D.


Pre-eclampsia is a common condition that occurs in pregnant women. It is characterised by various symptoms, the most obvious of which is high blood pressure alongside large amounts of protein in the urine. Left untreated it can cause organ damage and progress to eclampsia – a dangerous but rare condition where seizures develop; foetal development is also compromised.


Research has indicated that vitamin D deficiency can lead to pre-eclampsia.1 Other theories have been suggested but I believe none are more important.

The reason why pre-eclampsia is a common pregnancy complication in light of this finding is because very few women are vitamin D sufficient. Once a woman becomes pregnant her body not only has to deal with the physical and emotional stress of the situation, her already low vitamin D levels may dip further as the body drives reserves towards an as yet sun-deprived new life. Humans do not thrive with inadequate amounts of vitamin D, so nature will oppose old life when a compromise has to be made. Any infection a vitamin D deficient pregnant woman acquires at this point would certainly be more harmful than usual to her and her child.

Mainstream treatment for pre-eclampsia and eclampsia is magnesium sulphate (a large dose intravenously) to prevent seizures. Magnesium is found in leafy green vegetables, meat and dairy, so it is not necessarily lacking in many diets. However, to aid oral magnesium absorption vitamin D is required.2 Selenium deficiency has also been implicated in the conditions3 but it is unlikely to be a more common factor in the developed world where it is not scarce in foods.

First time mothers and those who suffer from illnesses such as heart disease or diabetes are the most likely to suffer from pre-eclampsia. The reason in first timers is due to bodily rejection of the father's genes in a foetus. A mother's body can perceive a threat from what is not genetically hers and mount an attack, but a tolerance can build up for any subsequent pregnancies from the same father due to the adaptive immune system – the part which learns how to deal with foreign material – being eventually able to deal with it in a more considered manner. Innate immunity can be seen as the frontline army not prepared to differentiate between approaching friends or foes unless briefed; all must be attacked.

Vitamin D, fortunately, optimises innate immunity4 which can invoke a ceasefire on certain material straight away. This should theoretically allow people with donated organs to not require immunosuppressive drugs to stave off rejection.

Women who suffer from heart disease, diabetes and other diseases are already immunologically compromised making them more likely to suffer recurrences of pre-eclampsia regardless of adaptation to their partner's genes. If high blood pressure persists after delivery the term pre-eclampsia no longer applies. In many cases the problem resolves by itself, but traditional motherly roles which keep a woman indoors as much as she was during pregnancy will naturally decrease her chances of making vitamin D. Therefore, her blood pressure could remain high because of this.5 Associated problems such as persistent weight gain could also be linked.


Even if a vitamin D deficient child is born without complication it is not yet out of the woods. If the mother breastfeeds her child, her milk will naturally be lacking in vitamin D unless she deals with her deficiency.6 Should she opt to provide bottled milk, it may not be fortified with the vitamin depending on what country she is in. Even so, the fortification provided is bound to be inadequate compared to the form and level found in a sufficient mother's milk. But it would be better than nothing. The reason why a baby relies on a mother's store of vitamin D even after birth is perhaps part of a safety mechanism; a newborn is not ready to go out into the open, fend for itself and obtain sunlight.

Things get worse. Even if the child secured enough vitamin D as a baby, once he or she is weaned off their daily source a replacement is harder to find. On top of that, unlike any other animal on Earth, they are clothed and sent to nursery, then school. Incidental sun exposure, therefore, only occurs when travelling to and from these environments – if they are not taken there by transport – or playing outside.


As touched on in the introduction, humans have the ability to create vitamin D when their bare skin receives adequate amounts of UVB radiation, unhindered by pollution or suncream, and when their shadow is shorter than them.7 If you walk into a darkened room, place your hand against a wall and shine a mobile light on it; – it could be a torch or lit phone screen – you'll notice that the further the light is from the hand, the shorter its shadow. The shorter your body's shadow is outside, the higher the sun is in the sky which is optimal for making vitamin D. If your shadow is too long, the sun is low and in no way over you.

But things aren't easy for the very old who, like autumnal leaves, are destined to fall than prosper. The reason for this is that less cholesterol is sent to elderly skin for conversion into vitamin D. It's nature's cruel but logical way of delivering us to death. However, this does not mean we cannot cheat nature by orally supplementing with vitamin D. Those interested in immortality or at minimum a smoother old age may find this a sort of elixir of life, or at least a component of it. It has been noted that longer telomeres on our chromosomes – think of them as similar to caps on a pen which prevent ink from drying – are associated with longer, healthier living. At least in women, high levels of vitamin D are associated with these not shortening.8


The problem with existing vitamin D guidelines is that they are based on a deficient population worldwide. At a top hospital in London, England a normal range for vitamin D – more specifically 25OHD and not 1,25D, as the latter is not indicative of reserves for the whole body – is roughly 20-120 nmol/L (nanomoles per millilitre). Some countries measure this in nanograms per millilitre (ng/mL). To convert nmol/L to ng/mL you need to divide by 2.5; multiply by that to convert in the opposite direction. Our range in other countries then is 8-48 ng/mL.

A conjecture on how this range was produced would be that researchers identified the minimum level needed to be free of rickets or osteomalacia, then sought out persons with the highest levels who perhaps do not supplement and are in good health. It is unlikely that they would have examined the level at which toxicity starts as it would be unethical to do, plus it is not an easy thing to achieve and observe. Those who measured around 120 nmol/L to help create the maximum reference are bound to be young fair-skinned people who thoroughly enjoyed a long sunny holiday or working climate, or perhaps use a tanning bed. Since vitamin D is still currently mostly associated with bone health, for a doctor to be satisfied you only need to reach the 'acceptable' minimum.

To confuse matters, in England there seems to be no definitive reference range. At another popular London hospital I learned the minimum starts from 50 nmol/L (20 ng/mL) while 70 nmol/L (28 ng/mL) is declared most desirable. In that same hospital two different consultants offered contrasting doses, measured in IUs (international units), to my mother and brother. While there is indeed no universal dose it was striking that my brother was and is taking more than her; a difference of 3400 IU. I take more than her too. His osteomalacia has disappeared while she is still osteoporotic, if less than before. That is not to say a higher dose would cure her or repair the damage done. I must confess, however, that I have not seen my mother's vitamin D levels. I cannot intervene for someone who can communicate for themselves and appears satisfied with their treatment.

It is not weak to obey mainstream guidelines, if anything it shows trust and respect for our care providers. The vast majority of their expertise is not to be ignored. But when you're simply not convinced by an orthodox view you will gravitate towards the radical. This applies to anything in life. The latest vitamin D guidelines will become mainstream in time though, once they go through all the proper channels. When that is, however, is unknown. The onus is on an individual to treat themselves now or when it may be too late.


When I had my level tested for the first time at the former stated hospital in mid-2006, I measured a mere 10 nmol/L (4 ng/mL). According to recent American guidelines by one laboratory this is severely deficient,9 and it is unlikely that in 2006 they classed my level as acceptable either. However, my otherwise respected specialist went by our book and suggested an over-the-counter supplement for my 'slight' deficiency. This translated as a recommendation to take the commonly found vitamin D2 at 400 IU. What perplexed me was, had my brother's endocrinologist seen me at his hospital, I would have been offered a much higher prescription-only dose, regardless of being apparently asymptomatic. At the time I did not question the dosage and took a daily gelcap.

The following year I reached 21 nmol/L (8.4 ng/mL). This satisfied my doctor, of course, because I was now 'in range', yet I was still lower than my brother who would not have been allowed to stay at that level. This seemed bizarre. I wondered if I was overreacting and thought maybe vitamin D doesn't matter as much to me as it does to my mother and brother. However, my maternal family history of illness burdened me.


I eventually learned, thanks to the Vitamin D Council through their website [vitamindcouncil.org], that a suggested median dose for beginning repletion is 5000 IU of natural vitamin D3. The target to aim for was 125-200 nmol/L (50-80 ng/mL) which was at odds with both hospitals...

The form of vitamin D didn't bother me but seeing four figures instead of three for the dose made me choke. Though my brother takes large amounts, I had not been advised to do that. A study convinced me, however, that vitamin D was safe to experiment with.10 I therefore decided to give it a go and if I didn't experience any side effects I would continue with it for a year and then get tested. Ordinarily, you should check your level every three to six months, but as an asymptomatic scrounger on the NHS (National Health Service) I allowed myself to be lax. Furthermore, to get a 25OHD test through my GP than a hospital requires a visit to a separate clinic. In-surgery blood drawing would have motivated me more.

The first hurdle, then, was obtaining a high dose of vitamin D. The best I could find in the physical world was 1000 IU at a popular local supplement shop, but the bottle didn't state if it was D2 or D3. Fortunately, from specialist outlets, D3 is very cheap and easy to find at higher doses. The main selling point for D3 over D2 is that it's natural to all animals and it's the form we make on sun exposure. Most importantly it doesn't deflate the wallet.

Taking the capsules with low fat yoghurt to aid absorption turned out to be a non-event. I did not experience anything really positive or negative to my awareness. After a month I was satisfied that I could take this for a little while and not keel over.


Eleven months later my level reached 79 nmol/L (31.6 ng/mL), which in America would be sufficient – but not optimal. I did not tell my specialist I had upped my dose, but as I was not directly told to take 400 IU anyway I wasn't technically being disobedient with my foreign over-the-counter purchase. My level did surprise me as I wondered if I would ramp up to 125-150 nmol/L (50-60 ng/mL) and hopefully not much higher. 5000 IU may have been a perfectly acceptable dose for the goal had I not been so deficient to begin with.

The following year I had my blood drawn again after twelve months on 10,000 IU via one 50,000 IU capsule every five days. I reached 141 nmol/L (56.4 ng/mL) which is seen as optimal by the aforementioned American guidelines. However, the hospital reference did not change so I was advised to lower my dose by half. This was an unknowing recommendation of 3000 IU more than they would have allowed.


It was just months after starting the 10,000 IU when I began noticing significant positive changes that I could feel or see in general blood tests. These will be revealed in the coming chapters. Such effects were almost certainly due to reaching a truly ideal level, comparative to those few who get significant amounts of sun exposure as nature intended.

What this proved to me was that while at 79 nmol/L I was no longer deficient, being sufficient was only a marginally better status. To become optimal was to reap the full effects. You can compare being sufficient to eating a starter course at a restaurant: it will sate some of your hunger but you are still hungry. If you want to be truly satisfied nothing less than the main course will do.

***

2. Skeletal Effects

Ask someone at random what vitamin D is good for and you'll see their brain whir for a second before usually correctly guessing that it helps keeps bones strong. Television advertisements for dairy products fortified with the vitamin explain how calcium products alone are inferior, but vitamin D's effect on bone is just the tip of the iceberg. Nonetheless, our skeletons are the foundation of our bodies.


The unearthing of vitamin D began as a search for the treatment and prevention of bone-softening conditions in children and adults, respectively called rickets – due to bones being seen as rickety – and osteomalacia. These conditions will have been around ever since man decided to wear clothing outside of winter and swapped hunting spears for work under a ceiling.

In 1919 Sir Edward Mellanby found that confined puppies kept away from any source of ultraviolet light developed rickets. Feeding them cod liver oil cured them, leading him to believe that rickets was a dietary concern.11 Later, Elmer McCollum isolated the magic part of cod liver oil which came to be named vitamin D as it was the next available alphabet letter. The reason it was tagged a vitamin is simple: vitamins are nutrients we consume in order to thrive and this beneficial substance was found in a fat, therefore there could be no dispute.

Harry Goldblatt and Katharine Soames expanded understanding by discovering that sunlight or UV light produced something virtually identical in the skin.12 An investigation by Alfred Hess and Mildred Weinstock added weight to this by finding that UV-exposed skin fed to lab rats protected them from rickets. The icing on the cake came when Adolf Windaus outlined the structural differences between the plant and animal forms, resulting in the names vitamin D2 and D3.13 In technical terms they are respectively called ergocalciferol and cholecalciferol. Both words are portmanteaus, highlighting that they are calciferol (vitamin D) derived by other means (ergo), in this case plants, or from animal cholesterol. There is also a D4 and D5 which are analogues of natural vitamin D. Analogues are synthetic copies used as pharmaceutical drugs. The reasons for their development are explained in the chapter Approaching Repletion.

It became clear that vitamin D, due to its structure and the fact that it did not have to be ingested, was not actually a vitamin at all but a type of steroid. However, because it had been discovered during a nutritional revolution, to discard it from the fashion would be to lose kudos. Another reason is that moving from the name vitamin D to calciferol would be to lose a more attractive label. Because we correctly think that a balanced diet can provide all the nutrients we need, so do we wrongly believe that the amount of vitamin D we can find in some foods is all that's required.

What about a vitamin D1? Its name suggests that it arose just prior or at least alongside vitamin D2. D1 is D2 with lumisterol, an additional substance that appears on the natural creation of ergocalciferol. To my knowledge D1 has never been used for treatment, perhaps because there is no therapeutic value in retaining lumisterol.


Parathyroid hormone (PTH) and vitamin D play off each other like people on a see-saw. As one goes up the other falls, though you would prefer it if PTH remained closer to the ground.

Parathyroid glands which are found in your neck, and not to be confused with the thyroid glands which they reside behind, produce PTH. These glands are responsible for controlling the amount of blood calcium through this hormone. You need some calcium in the blood in order to live, so if your level falls too low you will die. If it's too high you could also become ill and die. A high level could indicate a tumour in one of the glands causing excessive PTH production, but in most cases PTH elevates when you do not have enough vitamin D. The reason why we have parathyroid glands is simply for backup. As poor summers provide less opportunity for vitamin D production, rather than dying of hypocalcaemia, – the opposite of hypercalcaemia, which is high blood calcium – PTH takes out a 'loan'. But like all loans you're in trouble if you don't pay them back.

The tricks that PTH performs are to steal calcium from the bones to put into the blood, which can be detrimental to the skeleton if persistent, and to increase the amount of activated vitamin D – as opposed to the inactive form we can only create or consume for later activation – in the kidneys, which hurriedly absorbs any calcium we ingest. The kidneys also reduce reabsorption of phosphate from our calcium-leached bones to prevent kidney damage.

As supermarket product advertising will tell you, you need vitamin D to effectively absorb calcium just as you need cement to secure bricks on a building. Taking high amounts of calcium on its own can reduce PTH but this is akin to dropping tons of bricks from the sky and hoping enough fall in a fashion to form a vague, ramshackle structure. When you take an adequate amount of vitamin D for your body or expose yourself to ample sunlight, you actually need less calcium because it is now being effectively utilised. Unfortunately, mainstream guidance dictates taking more calcium than vitamin D, equating to more bricks than cement and leaving no room for functions beyond calcium maintenance. Why are we dosed in this way? Theoretical vitamin D toxicity. This is also talked about in Approaching Repletion.


It may surprise you to know that there is a link between the bone-thinning disease osteoporosis and heart disease.14 Corroborating this finding is that cholesterol-lowering drugs said to help prevent heart disease have a positive effect on bones.15 Indeed, one study supported by the maker of the world's best-selling drug of recent times, the statin called atorvastatin, – publicly known as Lipitor16 – shows that that statin increases vitamin D levels.17 It is also interesting to note that Lipitor contains calcium. I examine this in depth in the chapter Cholesterol & Heart Disease, but in brief what's implied is that it is not high cholesterol which leads to heart disease but the material released from bones that flows into arteries and looks similar to cholesterol. Inflammation is another reason.


Because my brother suffered from bone-softening twice and my mother has osteoporosis, I have been offered precautionary bone mineral density (BMD) scans since my mid-twenties every three to five years. To date I have had two scans. They are quick, painless, and in most cases only the hip and spine need to be scanned. The higher your BMD the less likely your bones are to break.

On my first scan I was relieved to hear that my bone density was fine, this tallied with the fact that I'd never suffered bone pain. At the time I had not been taking any form of vitamin D and was very likely deficient. By the time of my second scan I had been taking 10,000 IU in D3 form which raised me to an optimal level – notably, the only side effect I noticed in the year prior on 5000 IU was frequent non-painful joint clicking which stopped after about six months. I had guessed that my bone density would increase as my PTH had dropped from 4.1 pmol/L (picomoles per litre; hospital reference range: 1.6-6.9) during a vitamin D level of 21 nmol/L (8.4 ng/mL) to 3.7 pmol/L when I had reached a sufficient 76 nmol/L (31.6 ng/mL). It undoubtedly dropped further at 141 nmol/L (56.4 ng/mL) but it was not measured at this point which was when my scan was; in the following two years of increased vitamin D levels, though, my PTH descended to 2.3 then 2.2 pmol/L. The graph below shows a clear downward slope.


Graph 2.1.


My spinal BMD indeed had risen from 1.076 to 1.156, a 7.4% increase. Additionally, T-scores were provided which compare density to that of a healthy thirty-year-old. In total I rose from -0.6 to 1.0, which are both healthy scores. This was interesting as I was months from turning thirty, the age where you are said to reach the most density you ever will. Z-scores are also used to compare your density to someone your exact age and size, but for me, perhaps due to varying hospital policy, these were not provided. These are also not used to diagnose osteoporosis in older individuals.

In my hip my BMD decreased very slightly from 0.946 to 0.932, yet my T-score rose from -0.6 to -0.7 because of an individual increase in the middle part of my hip (intertrochanteric area). Nevertheless, this was in total counted as a 1.4% decrease, which when viewed on a graph isn't significant. So overall I achieved a 6% improvement in bone density, showing that there was room for improvement since the first scan even though my original readings were normal. If you suffer from common bone and muscle pain or fibromyalgia it is worth seeing what vitamin D could do for you, considering that such sufferers are frequently deficient.18


The strange thing, however, was that if my hospital's calcium reference range of 2.15-2.55 mmol/L (millimoles per litre) is correct, my blood calcium was slightly high before vitamin D optimality as well as after. I had measured 2.59 mmol/L in the year before my second bone density scan, then 2.7 mmol/L at the time of it. Neither of these alarmed my doctors because they didn't coincide with other risk factors for hypercalcaemia and the fact that I was asymptomatic. Also, according to one study, hypercalcaemia is defined as a level persistently above 2.7 mmol/L,19 so as far as I know 2.7 is the highest acceptable level, in line with an optimal vitamin D level. Hypercalcaemia could be indicative of excessive calcium release from the bones but that couldn't apply to me with my bone density increase.

The year after the scan though, my unintentionally still optimal vitamin D level of 147 nmol/L (58.8 ng/mL) was accompanied by a better blood calcium level of 2.47 mmol/L. I must add that I took 90 mcg of vitamin K2 MK-7 daily for a season prior to that blood test. I am uncertain if my level would've normalised without it but this is a vitamin that I want to keep as part of my regimen, and it is one that I would advise further personal research on; it has been noted for aiding in bone and heart health. In the following year when I reached a ceiling vitamin D level of 186 nmol/L (74.4 ng/mL) by taking 5000 IU daily for nine months and then 12,500 IU for three months, my calcium rose to an allowable 2.52 mmol/L; I had not been taking K2.

A calcium level that falls way at the lower end of the reference range could indicate that the parathyroid glands are making a perilous compromise between satisfying the blood level and bone destruction.


There is no doubt that calcium – and also magnesium,20 which is overlooked – is an essential component to health. However, it is puzzling that humans are the only animals to consume milk beyond infancy and often that produced by another animal, disregarding cats who do not need it too. Fruit, veg, beans and nuts contain calcium but these are seen as containing inadequate amounts, so we rely on milk and dairy products, not only for their good taste, but to maintain the levels we need. Some also take calcium as a supplement.

But compared to other animals our ratio of calcium to vitamin D seems disproportionate. To recall the brick and cement analogy, why would you need more bricks than your amount of cement could cover? If you lack cement you hope that the weight of extra bricks will compensate.

One study that introduced worry about the use of calcium and/or vitamin D outlined that intake may be associated with brain injury.21 The problem with this study was that it was not stated if vitamin D3 – the form natural to humans and other animals – was used. It will have been unlikely due to vitamin D2 being the common prescription. More importantly, the doses used were “approximately equal to the [recommended daily amount] for calcium (mean = 1280 mg) and... lower than current recommendations for vitamin D (mean = 341 IU).” What was not distinguished was whether that amount of calcium – which slightly exceeds common daily intake via food – coupled with an amount of vitamin D that is markedly less than what a naked body could produce daily through UVB attributed to the development of brain lesions. Simply put, they should have tested if high amounts of calcium alone would cause this problem and whether a higher amount of vitamin D3 could be protective. A conjecture on why these brain lesions happened in the elderly is the fact that having less capacity to produce vitamin D in the skin22 means that they will likely be more deficient than the rest of the population.

The only dairy I consume is a pot of yoghurt or two per day, with total calcium intake from all sources consisting of little more than 500 mg daily. Sometimes I'll treat myself to ice cream, pizza or cheese sandwiches but I don't believe I ever exceed 1000 mg. If you feel your calcium is lacking then a tablet might be wise.


Another calcium product we use is toothpaste which is combined with fluoride to combat and prevent tooth decay. While I do not dispute that regular brushing has helped protect our teeth and gums, there could be a more natural and effective adjuvant than fluoride. I don't need to spell out what that is.

In many developed countries fluoride is also added to drinking water, no doubt as extra protection for people who may be lax in oral hygiene, but there is controversy about its use.23 Fluoride binds calcium to teeth in a world where vitamin D deficiency is rampant. Given that vitamin D is available in cream form for topical use in skin conditions it would be easy to have it added to toothpaste. Even better than that, you could simply make sure your vitamin D level is optimised, chew calcium-containing foods and brush only with a substance that cleans your teeth and freshens breath.

Sugar has been implicated in causing tooth decay, be it from manufactured or natural foods, as well as acidic food and drink in general. But we do not know if this happens less or not at all in a vitamin D-optimised population. In my teens I used to drink a can of cola every single day; worse was that I had a habit of swilling it around in my mouth before swallowing. Resultantly, on top of likely being severely deficient even then, and despite practising good oral hygiene, I developed some dental erosion. One front tooth lost half its enamel, exposing some dentine. Fortunately, this and no other tooth became sensitive due to halting my fizzy drink intake in time. When I do drink I no longer swill, even with an optimal level of vitamin D. I've kept my dentist happy. It is also wise to remember that carbonated water is not natural. Sugar is fine in controlled amounts, but you need to make sure that your teeth can deal with it in one way or another.


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