Sunlight Deficiency

Sunlight deficiency could increase blood cholesterol by allowing squalene metabolism to progress to cholesterol synthesis rather than to vitamin D synthesis as would occur with greater amounts of sunlight exposure, and the increased concentration of blood cholesterol during the winter months, confirmed in this study, may well be due to reduced sunlight exposure.

In very simple terms, these authors are suggesting that given the common precursor between cholesterol and vitamin D [squalene], when there is insufficient sun exposure occurring to drive the reaction down the vitamin D production pathway, then it heads down the cholesterol production pathway instead, increasing total blood cholesterol levels. Now the lipid hypothesis of coronary heart disease [CHD] would suggest that these high cholesterol levels are causative in the development of heart disease, hence cholesterol-lowering is a target of both dietary and pharmaceutical treatments. But, according to the hypothesis of the authors here, high cholesterol levels are simply a marker for a lack of sunlight exposure, and it is this lack of sunlight exposure (and the link to vitamin D status), which is behind the development and progression of coronary heart disease.

The structural similarities of cholesterol and vitamin D and their common precursor led us to wonder whether a high level of blood cholesterol within a population might be a manifestation of sunlight deficiency. Interesting…

They point to a few lines of evidence to support their take on things. Firstly, that deaths from coronary heart disease are more common with increasing distance of residence from the equator. Also, the death rate from coronary heart disease decreases with increasing altitude of residence…

These observations suggest that differential rates of sunlight exposure might be the common factor which determines susceptibility to coronary heart disease, the high levels of sunlight exposure at low latitudes and high altitudes being protective and the relative deficiency at high latitudes being responsible for a high incidence.

They also point to the lack of efficacy of interventions which have directly targeted cholesterol as evidence that cholesterol itself is merely a marker rather than a cause of CHD…

However the risk [of high cholesterol] to individuals without coronary heart disease is very small, and in such ‘normal’ people lowering blood cholesterol by drugs is of much less benefit…

Dietary manipulation aimed at reducing blood cholesterol has not shown any benefit…

The authors also make a reference to the much vaunted Mediterranean diet and its supposed cardioprotective effects, suggesting how it may not be the diet of the region that is cardioprotective, but rather the climate in which the olives and grapes grow in that is…

It is well-known that death rates from coronary heart disease are much lower in the Mediterranean countries of southern Europe than in the Atlantic fringes of north-west Europe, and it usually assumed that this is due to different dietary patterns reflecting local agriculture. Hence we in north-west England are advised to drink red wine and to add garlic and olive oil to our diets and at the same time to stop eating ‘fish and chips’. But whereas migration has an effect on mortality risk, the individual adopting the risk of the place to which he has migrated, people who migrate tend to take their dietary patterns with them.

Furthermore, the dietary manipulation that has been part of prevention trials of coronary heart disease has been very disappointing, and overviews of the many dietary primary prevention trials have shown that there is no overall benefit. These observations suggest that agricultural production and local diet might not be the explanation of susceptibility to coronary heart disease in a given country, and we suggest that local agriculture is a reflection of local climate, sun exposure in particular, and that this is directly cardioprotective.

The authors here delve into an alternative potential cause of CHD and the mechanism for why sun exposure may be cardioprotective, with their alternative underpinned by our old foe – inflammation…

More recently sunlight deficiency has been thought to precipitate clinical tuberculosis in Indo-Asian immigrants into this country [UK]. That vegetarian Hindus are more at risk than Muslims suggests that the latter obtain some vitamin D from meat and fish, and it is suggested that vitamin D deficiency suppresses immunity.

There is a distinct possibility that coronary heart disease has a microbial cause and at present the low-grade respiratory pathogen Chlamydia pneumoniae is the chief contender. We suggest that sunlight deficiency increases the opportunism of such an organism in the same way as with tuberculosis.

In much the same way that tuberculosis develops in those with low vitamin D status and therefore diminished immunocompetence, the authors are suggesting that coronary heart disease could have a microbial trigger, which is able to gain traction in a vitamin D deficient individual. The geographical feature of sunlight might be protective by enhancing immunity.

The paradigm for coronary heart disease in recent years has been along the lines that it is mainly self-induced through cigarette smoking and dietary misbehaviour, together with some family tendency or ill-defined genetic problem. The paradigm has been that coronary heart disease is ‘multifactorial’ and in some people effectively caused by one factor and in other people, by something else. We wish to challenge the traditional paradigm…

We propose that coronary heart disease is a specific disease with a specific cause which is probably a microbe and perhaps Chlamydia pneumoniae. We suggest that the rate of progress of the disease process can be modified by accelerating and inhibiting factors. We suggest that high blood cholesterol and cigarette smoking are accelerating factors of coronary heart disease but are not initiating factors. We propose that Vitamin D, or possibly one of its photometabolites, is an inhibiting factor, slowing down the rate of progress of disease. Other inhibiting factors are anti-oxidants such as Vitamin C and selenium, and it is clear that free oxygen radicals can increase the rate of progression of the disease.

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