There are a few mechanisms at work that influence the vitamin D status for Europeans. Vitamin D is either eaten in the food, created with the help of sunlight or supplemented. Many appear to net have enough it:
Humans get vitamin D from exposure to sunlight, from their diet, and from dietary supplements. A diet high in oily fish prevents vitamin D deficiency. Solar ultraviolet B radiation (wavelength, 290 to 315 nm) penetrates the skin and converts 7-dehydrocholesterol to previtamin D3, which is rapidly converted to vitamin D3. Because any excess previtamin D3 or vitamin D3 is destroyed by sunlight, excessive exposure to sunlight does not cause vitamin D3 intoxication.
Few foods naturally contain or are fortified with vitamin D. The “D” represents D2 or D3. Vitamin D2 is manufactured through the ultraviolet irradiation of ergosterol from yeast, and vitamin D3 through the ultraviolet irradiation of 7-dehydrocholesterol from lanolin. Both are used in over-the-counter vitamin D supplements, but the form available by prescription in the United States is vitamin D2.
Vitamin D deficiency, MF Holick - New England Journal of Medicine, 2007 - Mass Medical Soc
Since you are primarily interested in D-sunlight:
Pigmentation of the skin: the amount of "black" people now living in Europe is rising. While that number is not significant for most cases often discussed, all of them (the more melanin the worse) have difficulty getting enough vitamin D from sunlight alone north of the 37th parallel.
From Harvard Women's Health Watch: Time for more vitamin D, 2008
Why the 35th, 37th or 40th parallel? Because the angle of the sun enables the atmosphere to filter out much of the UV rays needed to synthesise vitamin D. That angle is also varying during the day!
The reference Cancer Research UK. (2010). Vitamin D expert review already states clearly:
The amount of UVB in sunlight changes substantially with season, latitude and time of day. These factors greatly affect vitamin D production, which is greatest around two hours either side of solar noon, and during summer months.
Mad dogs and Englishmen go out in the midday sun? Many Europeans are around noon: in school, at work, in nursing homes -> indoors. Some cannot get out, others are not allowed to for different reasons.
Those that do get out at the right time, in summer, around noon, are now scared into wearing hats and sunscreens for "reasons" (skin cancer, photoaging etc). The sun's rays have to reach the skin and penetrate it. For the right amount of time and with the right amount of intensity. The equation UVB equals bad leads to inadequate sun exposure and that to inadequate vitamin D synthesis. We have to choose our poison here and are currently opting for weaker bones (excuse the exaggeration).
Some individuals in lower latitudes get enough sun for sure, and yet their vitamin D status is low:
"Low Vitamin D Status despite Abundant Sun Exposure" N. Binkley et al., The Journal of Clinical Endocrinology & Metabolism, Volume 92, Issue 6, 1 June 2007, Pages 2130–2135, https://doi.org/10.1210/jc.2006-2250
A probable explanation for the “low” 25(OH)D status of some individuals is found in their failure to obtain high circulating D3 concentrations. Possible explanations for this include inadequate cutaneous production of D3, enhanced cutaneous destruction of previtamin D3 or vitamin D3, down-regulation of cutaneous synthesis by sun-induced melanin production, or abnormalities of transport from the skin to the circulation.
From Wolfgang Herrmann and Rima Obeid (Eds): "Vitamins in the prevention of human diseases", 2011, Walter de Gruyter, Berlin/New York:
Cutaneously synthesized or orally ingested vitamin D is transported in the circulation bound to vitamin D binding protein (DBP). In the blood, only a small fraction is present as free, unbound vitamin D metabolites. The 25-hydroxylation of both vitamin D2 or vitamin D3, is the initial step in vitamin D activation. This takes place primarily in the liver. […] Nevertheless, extra-hepatic sources of 25-hydroxylation have been described in humans as well. They include macrophages, fibroblasts, keratinocytes and arterial endothelial cells (Gascon-Barre, 2005). (p. 365)
And there comes another factor into play: a trend to low animal derived nutrition or even veganism. You may eat a lot of liver and obtain all the vitamin D you need, and more, from that. Eating offal is on the decline and plant based nutrition is usually very low in vitamin D.
And low in cholesterol as well!
There are no reports of vitamin D intoxication in healthy adults after intensive sunlight exposure. Vitamin D in the skin reaches a plateau after only 15–30 min of UVB exposure. Then, vitamin D-inactive substances such as lumisterol and tachysterol are produced, which do not reach the systemic circulation. (p. 367)
That means that only a small amount is available:
Its precursor 7-dehydrocholesterol in the plasma membranes of both epidermal basal and suprabasal keratinocytes and dermal fibroblasts is converted to previtamin D3. Cutaneously synthesized vitamin D3 is released from the plasma membrane and enters the systemic circulation bound to vitamin D-binding protein (DBP) […] Factors influencing vitamin D levels Nutrient deficiencies are usually the result of dietary inadequacy, impaired absorption and use, increased requirement, or increased excretion. Vitamin D deficiency can occur when usual intake is lower than recommended levels over time, exposure to sunlight is limited, the kidneys cannot convert 25(OH)D to its active form, or absorption of vitamin D from the digestive tract is inadequate. Vitamin D-deficient diets are associated with milk allergy, lactose intolerance, ovo-vegetarianism, and veganism. Regarding the amount of vitamin D production in human skin, it depends on several variables including environmental factors such as geographic latitude, season, time of day, weather conditions (cloudiness), amount of air pollution and surface reflection which can all interfere with the amount of UVB radiation reaching the skin […] The skin is unique in being not only the source of vitamin D for the body but also in being capable of responding to the active metabolite of vitamin D, 1,25(OH)2D. Both 1,25(OH)2D and its receptor (VDR) play essential roles in the skin.
From: Vitamin D and the skin: Focus on a complex relationship: A review 2015.
While cholesterol is easily synthesised by humans, its presence in the blood is equally equated with bad! Low cholesterol and low synthesis of vitamin D are plain to see and taking drugs interfering with cholesterol metabolism – or eating cholesterol lowering food (more fibre please!) – might influence vitamin D synthesis. These relations are currently contested in heated debates with differing views.
If a citizen is obese, and those are said to increase in number and weight:
Andjela T. Drincic: "Volumetric Dilution, Rather Than Sequestration Best Explains the Low Vitamin D Status of Obesity" 2012 https://doi.org/10.1038/oby.2011.404
As one review summarised it:
Results
The definition of vitamin D insufficiency and deficiency, as well as assay methodology for 25-hydroxyvitamin D or 25(OH)D, vary between studies. However, serum 25(OH)D levels below 75 nmol/L are prevalent in every region studied whilst levels below 25 nmol/L are most common in regions such as South Asia and the Middle East. Older age, female sex, higher latitude, winter season, darker skin pigmentation, less sunlight exposure, dietary habits, and absence of vitamin D fortification are the main factors that are significantly associated with lower 25(OH)D levels.
A. Mithal et al.: "Global vitamin D status and determinants of hypovitaminosis D", Osteoporosis International, November 2009, Volume 20, Issue 11, pp 1807–1820.
Conclusion
Closer to the poles people need to have relatively: paler skin, more D in their food, adequate cholesterol levels, and more time in the sun at the right time with enough skin area exposed to meet the estimated demands for vitamin D. During winter it is almost impossible to meet the demand with UVB rays alone.
