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What density-independent (abiotic) regulating factor was central to early human adaptation?
Ultraviolet (UV) radiation, which influences folate synthesis, vitamin D production, and skin pigmentation.
How did humans first adapt to high UV levels in tropical regions?
Through increased melanin production, leading to darker skin pigmentation that:
Protects folate synthesis.
Minimizes UV damage.
Provides a selective advantage where UV levels are high.
How did human dispersal to non-equatorial regions affect skin pigmentation?
Migration to higher latitudes exposed populations to lower UV levels.
With colder climates and more clothing (~150 kya), UV exposure decreased.
Selection favored reduced melanin to allow greater UV-B penetration for vitamin D synthesis.
Result: Lighter skin pigmentation evolved in low-UV environments.
What happens when dark-skinned populations migrate back to low latitudes?
Their descendants show re-darkening of skin colour — a reversal of phenotype due to the same adaptive process operating in the opposite selective environment.
How do humans respond to UV radiation in both genetic and plastic (short-term) ways?
Genetic adaptation: Variation in melanin and skin colour inherited over generations.
Acclimatization: Tanning, an individual’s short-term increase in melanin production in response to UV exposure.
What predictions arise from selection pressures related to UV and temperature?
Clinal patterns: Incremental phenotypic changes correlated with latitude and environment.
High-altitude populations: Shorter, thicker stature for thermoregulation.
Recent migrations: More exceptions to established skin colour–latitude relationships due to less time for adaptation.
Why are “racial groupings” not biologically valid?
Race is a social construct, not a biological category.
Skin colour has a biological basis, but “race” classifications are arbitrary and based on superficial traits.
Genetic data show no discrete boundaries between human populations.
What type of variation does skin colour represent?
A cline — a continuous, gradual variation in a trait (like height or skin colour) across geographic gradients without sharp boundaries.
What pigments influence skin colour?
Eumelanin: Brown–black pigment.
Pheomelanin: Reddish–yellow pigment.
The ratio and distribution of these determine overall skin tone.
What genes are involved in determining skin colour?
SLC24A5 and MFSD12: Lower expression → more eumelanin (darker skin).
OCA2 (under balancing selection) and HERC2 (regulates OCA2 expression).
Skin pigmentation is polygenic — determined by multiple interacting genes.
What is convergent evolution of body form?
When populations in similar environments evolve similar external body forms independently, despite having different genetic backgrounds (e.g., Indigenous Australians and Africans).
What does genetic variation tell us about human populations?
88% of genetic variation occurs within populations, not between continents.
Only 9.2% of variation is between continental groups.
External features don’t reflect total genetic diversity.
What are polymorphism and polytypism?
Polymorphism: Variation within a population.
Polytypism: Variation between populations.
Humans exhibit high polymorphism and low polytypism.
Why did the concept of “race” arise historically?
Due to sampling problems — small, isolated samples from distant regions gave the illusion of discrete racial groups when variation is actually continuous.
What does clinal variation in blood groups show?
Blood group frequencies (e.g., Type A) also vary gradually across geographic space, not discretely. Migration and founder effects explain apparent regional differences.
What is the difference between abiotic and biotic selection pressures?
Abiotic: Non-living environmental factors — temperature, light, humidity, natural disasters.
Biotic: Living factors — pathogens, predators, prey, and competition.
Give examples of recent biotic selection pressures on humans.
Zika virus and COVID-19 represent recent biotic pressures.
Unclear whether they produce significant genetic selection, unlike long-term pressures such as malaria.
Why is malaria considered a strong ongoing selective pressure?
Caused by Plasmodium parasites transmitted by Anopheles mosquitoes.
Every two minutes a child dies of malaria (WHO 2018).
It remains a major cause of mortality and drives genetic adaptations such as sickle cell and thalassemia.
What is sickle cell disease and why is it adaptive?
Caused by the S allele in the hemoglobin gene, producing sickled red blood cells.
Advantage: Heterozygotes (AS) are less susceptible to malaria.
Disadvantage: Homozygotes (SS) suffer from sickle-cell anemia (poor oxygen binding).
This demonstrates a trade-off — disease resistance vs. physiological cost.
What is heterozygote advantage?
When heterozygous individuals (AS) have higher fitness than either homozygote (AA or SS), maintaining both alleles in the population — a balanced polymorphism.
How do sickle cell allele frequencies correspond to malaria distribution?
The geographic distributions overlap closely, showing selection pressure (malaria) and adaptive response (sickle cell gene) operate together.
What are the relative fitness values for sickle cell genotypes?
Environment | AA | AS | SS |
|---|---|---|---|
No malaria | 1 | 1 | 0.14 |
Malaria present | 0.88 | 1 | 0.14 |
AS has the highest fitness in malaria regions.
What is thalassemia and how does it relate to malaria?
Involves four genes affecting hemoglobin structure.
Some variants (α-thalassemia) provide partial resistance to malaria.
Represents another case of convergent evolution — different genetic changes producing similar protective effects.
What are examples of cultural responses to malaria?
Behavioural: Sleeping under bed nets; avoiding mosquito breeding areas.
Environmental: Reducing standing water; improving drainage.
Chemical: Use of insecticides and repellents (e.g., DEET).
Example: Timor-Leste reduced malaria incidence from 220/1000 → 1/1000 in 10 years through combined interventions.
What is lactose and how is it digested?
Lactose: The sugar found in milk.
Broken down by the enzyme lactase into glucose + galactose for absorption.
What happens to most mammals after weaning?
Lactase production stops, leading to lactose intolerance.
Symptoms when consuming milk: bloating, gas, abdominal pain, and diarrhea.
What is lactose tolerance and when did it evolve?
Lactose tolerance (lactase persistence) evolved ~6.5 kya in some human populations.
Genetic mutation in LCT gene:
LCT*R (recessive wild type): Lactase stops after weaning.
LCT*P (dominant mutant): Lactase continues through adulthood.
Origin associated with pastoralist cultures and dairy consumption.
What cultural adaptations preceded genetic lactose tolerance?
Fermentation of milk (7–10 kya): Using bacteria like Lactobacillus to convert lactose to lactic acid → reduces lactose content.
Examples: Yoghurt, cheese, kefir, which provided energy benefits with fewer symptoms.
What does the global distribution of lactose tolerance show?
Highest frequencies in cattle-herding populations (Europe, East Africa, parts of the Middle East).
Low frequencies in non-pastoral societies (East Asia, Indigenous Australia).
Reflects combined effects of mutation, migration, culture, and selection.
What do the three major human-environment case studies illustrate?
UV radiation: Biological and acclimatization responses (melanin, tanning).
Malaria: Genetic and cultural adaptations (sickle cell, bed nets).
Lactose tolerance: Cultural innovation followed by genetic evolution.
Together, they show the interplay between biology, culture, and environment in human evolution.
What does modern genetic evidence reveal about global variation?
Patterns of genetic diversity reflect serial founder effects as humans migrated from Africa.
Most genetic variation remains within populations, not between continents.
Human genetic structure forms a continuum rather than distinct clusters.