Great caution and profound shame

by Oliver Gillie

The Chief Medical Officers and Cancer Research UK have given cautious advice on sunshine and vitamin D, but it is the wrong kind of caution and poor advice, writes Oliver Gillie

News that the Chief Medical Officer, Dame Sally Davies, is “profoundly ashamed” at the return of rickets is greatly encouraging. Rickets, the bone disease of children, is only one of dozens of diseases associated with, or known to be caused by, insufficient vitamin D in early life. At last it seems the risks of vitamin D deficiency are being taken seriously.

Dermatologists worldwide have persuaded a generation of people to stay out of the sun and cover up with suncream, desperately depriving them of vitamin D. While this has made millions for suncream sales, the consequence has been a rapid increase in multiple sclerosis, type 1diabetes and other autoimmune diseases which we are only now beginning to understand. [1]

Nivea has recently given Cancer Research UK £2.5 million, and this is not the first generous donation of millions that CRUK have taken from a suncream company. It comes in gratitude for the advice CRUK has given over many years to use suncream regularly and in ever larger amounts. A small dollop is not enough– suncream manufacturers say handfuls need to be put on 20 to 30 minutes before venturing outside.

Cancer charity frightened a generation

The advice may make sense on a Mediterranean holiday when English people stay on the beach midday while wiser people move into the shade. In England suncream may be needed on exceptionally hot sunny days around midday, especially for sports people obliged to stay in the sun. But CRUK have frightened a generation of British people with advice better suited to Australians.

Oliver Gillie

Oliver Gillie

Former medical correspondent for both the Sunday Times and The Independent Oliver Gillie is a scientist and writer who has won 17 awards for his work on national newspapers. He has also conducted an award-winning campaign to raise public and government awareness about the benefits of vitamin D.
Oliver Gillie

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  • Thanks for a well written article.

    I would like to point out that even Down Under in Australia we have to a large extent become Vitamin D deficient. In part I believe this is due to the insistence of covering up when out doors, wearing a sun hat and slopping on the sunscreen.

    Vitamin D screening is a part of regular pathology done down here.

    States do advise when the UV will be high and when protection is needed, but there is also a drive to get people to get at least some time in the sun – away from midday – 3 pm in summer months to build up natural D reserves.

    Hope this helps.

    • I also live in Australia now, moved here in 2009; and am regularly incensed by the Slip Slop Slap Seek and Slide ads, which still advocate covering up, shovelling on the sunscreen and basically staying out of the sun.
      Yes, Vit D awareness is higher among the medical professionals here, I have certainly benefited from that myself – but STILL the same message is given out – sun = bad. The ads for melanoma are shockingly bad too.

      I have not seen any drive to get people to spend time in the sun though – in fact, with small children, the emphasis seems to be on keeping them out of the sun and covered in sun screen at all times, especially in pre-school and primary – perhaps we are in different states? (I’m in NSW).

      • Dear Ann YES we are States Apart…you in NSW while I am in Tasmania, next stop South Pole :-) It is well recognised that down here the angle of the sun gets too low at certain times of the year, and so there are adverts and there is information about getting sufficient sunshine during certain times of the year.

        I do still however see, while passing the local kindergarten – every child (no matter the season) playing outside wears a sun hat. Same applies at the local primary school.

        Hope this helps…… BTW I love Sydney :-)

    • Unfortuately, the only time that the UVB rays that give us vitamin D are available are over the solar noon during the late spring to early autumn months, so going out in the mid to late afternoon will only give us UVA rays. A further note is that UVB rays do not penetrate glass. There are a number of apps and websites which will give you the daily UVB availability times for your area.

  • Excellent article. People used to mock me 10 years ago when I said that a certain amount of sun exposure was vital and that a lack caused far more than just rickets. The latest trend (which utterly incenses me) is the almost burka-style full cover up for young children, complete with legionnaire style hats and waterproof long-sleeve tops and bottoms. God forbid the sun’s rays should reach their body for more than a second. These same children are invariably more ‘sickly’ than average with repeated respiratory infections and skin problems.

  • Thanks for this – the sun cream obsession as you say has left people with lower risk of mostly non life threatening skin tumours but the resulting vitamin d deficiency causes a significant rise in the risk of solid tumours, see: – asyou say, in the UK, we only need suncream on holiday, when having prolonged exposure on very hot days or if very fair skinned – otherwise, we need all the sunlight we can get.

  • I have just reviewed all the blood work on just over 2,200 patients collected over almost two years. Over half the results were BELOW the “normal” range. Just on 9% were in the top half of the normal range. The remaining 40% were in the bottom half of the range and two results were above the range.

    I have not broken the results into seasons yet but there seems to be a trend to the lower results for samples in the colder months. This is not a statement of fact- just an impression!

    Am puzzled by the presence of good suntans and low Vitamin D levels but perhaps that is a bias of seeing people tanned from last summer showing up with low levels now (post winter).

    I discussed with Medicare about calling for routine Vitamin D level screening but they reiterated that apart from PAP smears, there is no consideration of routine screening for anything in Australia! So, the doctor must supply a diagnosis in order to attract a rebate from Medicare. Strange. I am thinking of putting “Australian” on the blood request form as a “diagnosis.”

  • I think you are right. You have to LOVE sunscreens. And fully shirted kids with hats. ARGGHHHHHHHHHHH!!!!

  • Melanin, the primary pigment that determines skin colour, and that in fair-skinned people gives rise to a tan, is the only sun-block a person should ever need. And unlike artificial sunblock it is not something that has been identified for harbouring known carcinogens.
    Melanin is synthesised from vitamin, and vitamin D is synthesised from cholesterol in the skin, this all arises just beneath the surface. It’s the action of photons of certain wavelengths (sunlight) acting upon the precursors that has them change and reform. To all intents and purposes this is photosynthesis, it turns us brown, although the more familiar use of the term describes the synthesis of chlorophyll in leaves, and it this case it renders them green.
    Fair skinned people who burn have not been conditioned to the sun by earlier more modest exposure. The ease with which a person tans requires some years, perhaps, of pre-conditioning. Its catch 22 in some ways, because you have to ‘bank’ repeated short exposure to the sun to get some measures of pre-conditioning that means you’ll tan with more ease, get the protective benefits of melanin, and without burning.
    On the web, there are some accounts of people who have made efforts to raise the levels of the hormone calciferol in body. Calciferol is the alternate name for vitamin D – which is technically a hormone. These people who have done this have reported they tan easier and burn less when they venture out in bright sunlight.
    In some ways, then, we can wonder if the capacity to suffer sunburn, is down to a lack of melanin, diminished capacity to produce melanin when needed (some lack of preconditioning), and perhaps linked to sub-optimal levels of vitamin D.
    Of course, as is often the case, the people funding research are not interested in a low-input solution, such as identifying and explaining the business of cause and effect properly, instead they want to offer a ‘treatment’ or precautionary preparation (sunblock) for sale.
    This weeks New Scientist (2945, p4) offers evidence of the same process aligning itself with Alzeimers. You’ll need to read carefully and have a bit of background knowledge to spot it.
    Science has lost its rigour in some quarters, and has become a tool of marketing. We need to kick-ass (metaphorically speaking), there is no need yet to compromise our pride or dignity.
    Great caution is called for, it is a shame we’ve been so long in realising.
    Thanks Ollie!

  • Does cholesterol level factor in to Vitamin D production?

    • Editorial

      It is perfectly possible – vitamin D is made in the skin from cholesterol (actually from a precursor of cholesterol called 7-dehydroxycholesterol) so driving down cholesterol with statins might make it harder to make vitamin D. I’ve asked several experts about this and my sense is that no one really knows. Someone who has done more research on this than anyone else is a UK GP called David Grimes who wrote a book called “vitamin D and cholesterol”. He points out that a lack of Vitamin D might push cholesterol levels up. His thinking is this: we know that cholesterol levels aren’t constant, they are quite a bit higher in the winter than the summer in northern countries like the UK. If the 7-dehydroxycholesterol isn’t exposed to sunlight it gets turned into regular cholesterol in the liver. Since we can’t get enough sunshine in winter to make vitamin D, production of cholesterol in the liver goes up. So supplementing with vitamin D in the winter might lower cholesterol levels. However just to make things more complicated it now seems very likely that raised cholesterol is not a factor in heart disease, just a sign that something else is increasing your risk – see the post that has just gone up “A guided tour around the statin Wonderland”.

  • ” .. .. However just to make things more complicated it now seems very likely that raised cholesterol is not a factor in heart disease, just a sign that something else is increasing your risk – see the post that has just gone up “A guided tour around the statin Wonderland”. .. .. ”

    Quite right. The first atherogenic biochemical found to induce atheromas in experiments upon animals was cholestane triol. For those who haven’t heard of cholestane triol, and let’s face it few people have, it is an oxidised derivative of cholesterol itself.

    Pure cholesterol readily oxidises in air to form each of three possible oxidised variations called oxycholesterols, and cholestane triol is one of the three. Cholestane triol takes its name because it results when three atoms of oxygen react with and attach to a molecule of pure cholesterol.

    The distinction between cholesterol and cholestane triol is that pure cholesterol is not at all atherogenic (ie it does not result in the growth of atheromas or fatty plaques that narrow arteries) whereas cholestane triol is the most potent of the oxycholesterols where capacity to potentate the process of atherogenesis (formation or atheromas) is concerned.

    Cholesterol does not give rise to atherosclerosis or arteriosclerosis but oxycholesterols may, and cholestane triol would seem to be the most potent of the oxycholesterols.

    The prospects that cholesterol may oxidised in the body to become cholestane triol, I think it a prospect, is greatly promoted by rising levels of homocysteine.

    One avenue by which levels of homocysteine rise is when an amino acid called methionine is present, but the necessary B vitamins for the management and metabolism of methionine are in short supply, which results in persistence of homocyteine molecules and rising counts of homocysteine.

    The second avenue is that homocsyteine levels appear to be responsive to rising levels of cortisol, and levels of cortisol may be influenced by several factors.

    When the effects of cholestane triol were first witnessed around 1913 the team involved (lead by Anichkov) had no knowledge of cholestane triol, with the term not appearing in the write-up, and so pure cholesterol ended up taking the wrap for the atherogenic capacity of cholestane triol. It’s an instance of what’s termed a confounding error in the trade. While Dr Ancel Keys had traits I cannot warm to, and committed a fraud no-one should forgive him for, he was mislead by this confounding error, and so despite my general loathing I do preserve some measure of sympathy for him.

    Homocysteine is the second biochemical with known atherogenic properties

    An axis with implied promise has been established. Cortisol bears upon homocysteine, Inadeqaute supply of certain B vitamins has consequences for the reduction of homoscyteine. Homeocysteine has implications for cholesterol, and cholesterol may be commuted to cholestane triol under the influence of homocyteine. Then cholestane triol has implications for the behaviour of cells in proximity to, or belonging to, the endothelial layer.

    In at least one of his books upon the topic Dr Kilmer McCully discussed homocyteine in relation to multiple risk factors for heart disease but did not venture far into the discussion of stress. Coming to recognise in the passing of time since that cortisol can bear upon homocysteine determines additional risk factors can be worked in with the notion of the cortisol – homcysteine – cholestane triol axis which no doubt has ties with the HPA axis. It’s an interesting cognitive development of the last decade that has not been given the airtime it deserves.

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