skin pigmentation - complex inheritance

polygentic / multi factorial traits

many highly visible (unlike RBCS).

Genetic inhertience and 'maximum potential' are influenced by limiting / facilitating environmental factors (ex diet). human biological variation adaptation to vaarious environmental contexts (such as global variation in RBC traits could be result of forces of selection)

complex inheritence (not mendelian)

skim pigmentation, body size, body form, body weight, head size and shape, face form, eye color. ex - stature and genetic potential (m/f difference - 5 to 10% larger)

genetic potential and the environment

change is also due to changes in access to good nutrition, health status, nature of childhood.

complex phenomenon -> genetic potential + environmental influences (during critical periods of growth)

skin pigmentation

1865 Broca used 36 colour tones to derive 'racial classification'. colour plates intended to represent faces. because it is easier to see, highly visible traits

reflectance spectrophotometer

quantitative measure of skin pigmentation genetic & environmental effects. Portable, lowkey cheap. shines light onto skin surface and looks at the light reflects back / is absorbed/. forehead and upper inner arm to be measured (less sun)

human skin and 5 pigment

pigment melanin important factor yielding diversity in darker - and lighter skin colours. Melanin is produced by "melanocytes" that is found in skin and eyes. there is also melanoid (yellow), cartoene (yellow,), oxyhemoglobin (red), reduced hemo (purple).

Melanin is flexible by responding to stressers like UVB radiation = melanocytes and increase production of melanin

what is tanning

a reaction to UV related cell damage. reddish tone is due to increased blood flow to the trauma. skin develops a brown colour as melanocytes are stimulated to increase melanin production.

Tan is a symptom of UV overdose and increased melanin = increased UV filtering to protect and prevent further UV damage.

also the outer layer of skin (strateum corneum) increases in thickness. heliotherapy -> this phenomenon of tanning comes from. to treat bone and joint tuberculosis -> potentially might be a vitamin D connection, therapeutic value was noteable that tanning was helpful. until risks of skin cancer started to rise

uneven pigmentation

'age spots'. melanocytes get worn out over time will cause some greater area of pigmentation

vitamin D hypothesis

the relationship between UV radiation and vitamin D synthesis in the human body. VItamin D synthesized in the epidermis exposed to UVB light (sunlight, fatty fish, fish oils, egg yolk alternatives).

Vitamin D facilitates the absorption of dietary calcium in the gut (calcium -> bone growth, immune health).

Hypothesis on ideas concerning relationship between skin pigmentation and vitamin D synthesis offered by murray and looms. UV penetration much higher in equator areas -> darker pigmentation protects skin and swear glands from UVB damage -> to ensure thermoregulation, protectign folate synthesis (UV skin penetration &photolysis), over production of vitamin D too -> too much calcium in kidneus

pigmentation and CANCER

with more effective melanin UYB filter, darker skin protetcts against excessive UV protection.

Risk varies -> high where UV light is intense (in and around equator) versus seasonal.

Uv damage -> malignant melanoma (deadly skin cancer). Develops in melanocytes -> can metastaize to other tissues / organs

Hypovitaminosis D

as hominins mirgrated out of africa & into new locales -> darker skin challenged to synthesize enough vitamin D in low UVB environments (6 times logner to make vit D).

Over time, selection for less melanin / lighter pigmentation (adaptation) - survival & reproduction

low vitamin D risks

rickets in children due to poor bone mineralization (cannot maintain calcium absorption - become soft bones). could be fatal / life span shortening. US 1930 -> noted problem among individuals with darker pigmentation

osteomalaca

adult form of rickets. occurs in adults if they cannot maintain bone mineralization. thin brittle, soft bones in legs and pelvis.

Eastmen -> vit D related deformities 2% women lighter 15% darker skin pigmetation.

life course perspective natural selection and Vitamin D

viability selection -> must survival to adulthood before it can reproduce (rickets, susceptibility to infections).

Survival selection -> longer survival in reproductive phase, more potential offspring (osteomalacia, infections, cancers, cardiovascular disease).

Fecundity selection -> relative reproductive success. Longevity selection -> survival beyond reproductive age, important for long offspring dependency on parents

Vitamin D and Fecundity Selection

pre zygotic -> Vitamin D deficient animal models = impaired folliculogenesis, low sperm count/motility.

Conception -> IVF studies (immune response/intolerance to fetus) – vit D status sig associated with rates.

VItamin D and longevity selection

Vitamin D status during post-reproductive years and Infections, Cancers, Autoimmune diseases, Cardiovascular Disease, Osteoporosis and fractures

Hypovitaminosis D (too little vit. D) can be caused by cultural factors

latitude -> clothing, Industrial revolution & the 'working day', smog, sunscreen. MAY BE reduced by reduced by cultural/ dietary factors ( vitamin D added to commercial milk supplies & maragine )

risk Insufficiency & Deficiency problem

1. northern latitudes, winter season, non - dairy & vegetarian/vegan, infants exclusively beastfed -> limited daytime outdoor time.

2. Any of the above exacerbated among individuals with darker skin pigmentation