F Rosa Rubicondior: Creationism in Crisis - How Our Need For Vitamin D Was A Bad Design That Went From Bad To Worse

Friday 2 February 2024

Creationism in Crisis - How Our Need For Vitamin D Was A Bad Design That Went From Bad To Worse

Fig 3. Permanent central maxillary incisors of CL 66.
Plane form hypoplasia is exhibited on the occlusal and labial surfaces.
Archaeological evidence of seasonal vitamin D deficiency discovered | University of Otago

The human need for vitamin D to ensure proper bone growth and development and various other health-related needs, is an example of how we were not intelligently designed but are the result utilitarian evolutionary compromises that balance benefit against detriment and that balance depends on the environment in which we evolved. It shows that we evolved in sunny climates where the sun comes directly through the atmosphere as it does in the tropics, rather than obliquely, as it does in the northern and southern parts of the globe.

We do not generally get enough vitamin D from our diet, so we need to manufacture it in our skin by the action of sunlight, in particular the ultraviolet B (UVB) spectrum. However, UVB sunlight is also harmful, so our skin needs to be protected from it with the pigment, melanin, which gives our skin its varying shades of brown or black. Generally, the darker the skin, the better protection it has from UVB but the less it can produce vitamin D.

This AI explanation outlines the problem:
Please explain the connection between Vitamin D, Skin Pigmentation and Rickets, especially in Industrial Northern England. The connection between Vitamin D, skin pigmentation, and rickets is rooted in the way the body produces Vitamin D through exposure to sunlight and how skin pigmentation affects this process. Rickets, a condition characterized by weakened and softened bones, is closely linked to Vitamin D deficiency.
  1. Vitamin D Production:
    • Vitamin D is essential for the body to absorb calcium and promote bone health.
    • The skin has the ability to produce Vitamin D when exposed to ultraviolet B (UVB) radiation from sunlight.
    • When UVB rays interact with the skin, a compound called 7-dehydrocholesterol is converted into Vitamin D3 (cholecalciferol).
  2. Skin Pigmentation:
    • Melanin, the pigment responsible for skin color, can act as a natural sunscreen by absorbing and dissipating UV radiation.
    • People with darker skin have higher melanin levels, which provide protection against excessive UVB radiation.
    • While this pigmentation is advantageous in regions with intense sunlight, it can hinder Vitamin D synthesis in areas with lower sunlight exposure.
  3. Geographical and Environmental Factors:
    • In regions with less sunlight, such as Industrial Northern England, there is a higher risk of Vitamin D deficiency, especially during the winter months when sunlight exposure is limited.
    • Darker-skinned individuals living in these regions may face challenges in producing sufficient Vitamin D due to their skin's natural sun protection.
  4. Rickets:
    • Vitamin D deficiency can lead to problems with calcium absorption, resulting in weakened and soft bones, a condition known as rickets.
    • Children are particularly susceptible to rickets, as their bones are still developing.
In Industrial Northern England, historical factors such as industrialization, urbanization, and the often-overcast climate have contributed to reduced sunlight exposure. Additionally, the prevalence of darker skin tones among the population can further increase the risk of Vitamin D deficiency. To address these issues, individuals in regions with limited sunlight exposure or with higher skin pigmentation may need to supplement their Vitamin D intake through diet, fortified foods, or supplements. Public health initiatives may also play a role in raising awareness and promoting measures to prevent Vitamin D deficiency and related conditions like rickets.

Why does skin need protecting from UVB?

Skin needs protection from UVB (Ultraviolet B) radiation because prolonged exposure to UVB rays can cause various harmful effects, including damage to the skin cells and an increased risk of skin cancer. Here are some reasons why protection from UVB is crucial:
  1. DNA Damage:
    • UVB radiation can directly damage the DNA in skin cells. This damage can lead to mutations and increase the risk of skin cancer over time.
  2. Sunburn:
    • UVB radiation is a major contributor to sunburn. Sunburn occurs when the skin is overexposed to UVB rays, leading to redness, inflammation, and pain.
  3. Premature Aging:
    • UVB exposure accelerates the aging process of the skin, leading to premature wrinkles, fine lines, and other signs of aging.
  4. Suppression of Immune System:
    • Prolonged exposure to UVB rays can suppress the immune system in the skin, making it more susceptible to infections and other skin conditions.
  5. Increased Risk of Skin Cancer:
    • UVB radiation is a known carcinogen, meaning it has the potential to cause cancer. Skin cancer, including melanoma, basal cell carcinoma, and squamous cell carcinoma, is strongly associated with UVB exposure.
  6. Eye Damage:
    • UVB rays can also cause damage to the eyes, leading to conditions such as cataracts and other eye-related problems.
  7. Photodermatitis:
    • Some individuals may experience an inflammatory skin reaction known as photodermatitis when exposed to UVB radiation. This can result in itchy, red, and swollen skin.
  8. Hyperpigmentation:
    • UVB exposure can contribute to the development of hyperpigmentation, including sunspots and uneven skin tone.
To protect the skin from the harmful effects of UVB radiation, it is essential to use sunscreen with a high SPF (Sun Protection Factor), wear protective clothing, seek shade during peak sunlight hours, and use sunglasses that block UV rays. These measures are particularly important in regions with high sun exposure and during activities that involve prolonged periods of time outdoors. Regular skin checks and dermatological screenings are also recommended to detect any potential signs of skin damage or cancer early on.

So, when the ancestors of present-day non-African people migrated out of Africa, they took this shoddy, Heath Robinson compromise with them into a climate and latitudes that the compromises hadn't evolved in, and now the detrimental factors became a much bigger problem as their dark skin now didn't manufacture enough vitamin D but the need for protection was much less, especially in winter, although UVB could still cause problems in Summer especially in the more southerly parts of their new range.

So, when they received a dose of DNA from their Neanderthal cousins, who had been evolving in Eurasia for some 500,000 years and had evolved paler skin, this quickly gave them the ability to manufacture vitamin D, but they still needed plenty of sunlight because so much of their skin was now covered up by the clothes needed to survive in the northern climate.

Then when Europe began to industrialise in the 18th and 19th century, starting in the Northern English towns, the balance was again tilted towards vitamin D deficiency as poor diet, cloudy climate, child labour and work in factories and mills meant children were growing up severely deficient in vitamin D - and all because of a shoddy, utilitarian evolutionary compromise in Africa in our early ancestors.

The effects of this problem are highlighted in a paper published a few days ago in PLOS ONE by a team of researchers from the University of Otago, New Zealand, Durham University and the University of Brighton, England, the University of Edinburgh, Scotland, and the University of Queensland, Australia. Their work is explained in a University of Otago news release:
Rickets ran rife in children following the Industrial Revolution, but University of Otago-led research has found factory work and polluted cities aren’t entirely to blame for the period’s vitamin D deficiencies …

Lead author Dr Annie Sohler-Snoddy, Research Fellow in Otago’s Department of Anatomy, says they uncovered some of the first clear evidence of seasonal vitamin D deficiency in an archaeological sample.

She says it has been known for many years that there was an increase in rickets, a childhood bone disease caused by vitamin D deficiency, in 18th and 19th Century Europe.

“It has been assumed that this was due to more people, including children, working long hours indoors, living in crowded housing and in smog-filled environments, all of which reduce the amount of sunlight that reaches a person’s skin, which is the main way humans make vitamin D.”

However, new bioarchaeological methods enabled the researchers to get a much clearer picture of how vitamin D deficiency affected the people living in industrial England, rather than looking at bone deformities alone.

Right permanent maxillary canine of a woman from Coach Lane, showing roughly annual episodes of interglobular dentin.
The study found markers associated with vitamin D deficiency in the interior part of 76 per cent of the teeth analysed. In many samples, these occurred regularly, in annual increments.

This shows clear evidence of seasonal vitamin D deficiency in the teeth of people living in the north of England. This is exciting because it highlights that latitude and seasonal lack of sunlight was a major factor in the amount of vitamin D these people could make in their skin – it’s more complicated than the factors associated with the industrial revolution like working indoors more.

We tend to think of archaeological human remains as belonging to a different world, but our biology hasn’t changed in the last 200 years. Teeth provide a really important source of information for archaeologists as they form in a very precise chronology and, importantly, their tissues do not change over the lifespan. This means that they lock in a record of a person’s development and this stays with them until they die, or the tooth is lost.

Understanding how vitamin D deficiency impacted past populations and why gives us an important deep-time perspective on the disease.

Dr Anne Marie E. Sohler-Snoddy, first author
Department of Anatomy
University of Otago,
Dunedin, Otago, New Zealand.
Poor vitamin D status is associated with several negative health outcomes including increased risk for infectious diseases, cardiovascular disease, and cancers.

Vitamin D deficiency has been an ongoing problem in society and Dr Sohler-Snoddy believes it is important to study what happened in the past in order to inform modern approaches to the ailment.

In their open access paper in PLOS ONE, the team give more technical details of their methodology and findings:


The post-medieval period in Europe saw a dramatic increase in metabolic bone disease related to vitamin D deficiency (VDD). Recent paleopathological work has utilized interglobular dentin (IGD) as a proxy for poor vitamin D status during development, while enamel peptide analysis allows the identification of chromosomal sex in non-adult remains. Here we explore the relationship between sex, the presence of IGD, and macroscopic markers of VDD in an industrial era assemblage from Northeast England.

Materials and methods

25 individuals (9 females, 9 males, 9 unknown sex) from the cemetery site at Coach Lane, North Shields (1711–1857) were selected for paleopathological analysis, histological assessment of IGD, and enamel peptide determination of chromosomal sex.


Ground tooth sections from 21 individuals were of suitable quality for detection of IGD, and enamel peptide analysis confirmed the chromosomal sex of ten individuals. Sixteen individuals (76.1%) exhibited ≥1 episode of IGD. Nine of these (42.8%) exhibited >1 episode and four (19%) exhibited ≥4 episodes in regular intervals. Male sex was significantly associated with the presence of IGD (p = 0.0351; 100% males vs. 54.5% females). Females were more likely to exhibit macroscopic evidence of VDD (45.5% females vs 30% males) but this was not statistically significant.

Discussion and conclusions

Periods of poor mineral metabolism during childhood appear much more prevalent at Coach Lane than macroscopic evidence suggests. Evidence of seasonal IGD episodes indicates that northern latitude played a major role in poor VD status in the Northeast of England. The significant association of IGD with male sex may be due to sex-related differences in dentinal mineralization or a higher risk of poor VD status in males aged <5 years. More work is needed to establish an evidence-based threshold for pathological levels of IGD before the presence of this feature can confidently be used as a biomarker for poor VD status.
Fig 1. Ground section of the right permanent mandibular first molar of CL 118.
Two bands of IGD are visible, the first occurring ~birth-6 months (teal dashed lines) and the second occurring between ~1 and 1.5 years (yellow dashed lines). Large image is 40x total magnification, inset box is 100x total magnification.

Fig 2. Ground section of the right permanent mandibular first molar of CL 66.
Ten episodes of IGD between crown and apex are visible. Whole tooth is 40x total magnification, inset boxes are 100x total magnification. Note that because this is a very lateral section, episodes 7–10 are partially obscured by the overlying cementum and Granular Layer of Tomes.
Fig 5. Right permanent maxillary canine of CL 129.
Four discrete episodes of IGD in approximately annual increments are apparent. Teal arrows indicate a Wilson band formed concurrently with the 2nd episode of IGD. Whole tooth and crown images are 40x total magnification (not to scale), inset box is 100x total magnification.

Citation: Snoddy AME, Shaw H, Newman S, Miszkiewicz JJ, Stewart NA, Jakob T, et al. (2024)
Vitamin D status in post-medieval Northern England: Insights from dental histology and enamel peptide analysis at Coach Lane, North Shields (AD 1711–1857). PLoS ONE 19(1): e0296203. https://doi.org/10.1371/journal.pone.0296203

Copyright: © 2024 The authors.
Published by PLoS. Open access.
Reprinted under a Creative Commons Attribution 4.0 International license (CC BY 4.0)
In their conclusion, the scientists said:
… IGD, indicative of periods of poor mineral metabolism, was widespread at Coach Lane with over 76% of individuals examined exhibiting one or more episodes. This is far higher than macroscopically recorded cases of rickets in this assemblage, which may suggest that the individuals with gross anatomical changes represent only a small proportion of a population suffering from poor vitamin D status during growth. Several individuals exhibited evidence of seasonal episodes, suggestive of an environmental deficit of vitamin D due to latitude. …
Obviously (to anyone who understand how evolution works and what good intelligent design is) none of those problems would have arisen as humans left Africa into the colder latitudes of the world where there is less sunlight and what there is comes obliquely through the atmosphere and varies significantly in strength on a seasonal basis, if humans had really been intelligently designed by an omnipotent omniscience designer.

It should not have been beyond the wit of such a god to devise a better way to get vitamin D into our bodies, if it couldn't avoid making our bone growth and development dependent on it in the first place and it should have anticipated that we would spread to other parts of the world where its clunky work-around for the problem it had designed, (if you listen to creationists) and designed a better solution.

But evolution has no foresight so can't plan for the future. It can only deal with the here and now and whatever solution is better than what preceded it will be retained and become fixed in the 'design' and the 'design' of all future generations.

And this is illustrated almost perfectly with the vitamin D/skin cancer evolutionary compromise and delicate balancing act, of which William Heath Robinson would have been proud, and for which any designer should be sacked.


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