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The Quiet Signatures of Ancient Environments
Human populations are not biologically identical. Over the past 70,000 years, bands of Homo sapiens faced radically different climates, diets, altitudes, sunlight levels, and pathogens. Natural selection responded rapidly and repeatedly, producing a mosaic of genetic differences, some visible, most invisible, that helped our ancestors survive and that still powerfully influence health and physiology today.
According to wikipedia, "Race is a categorization of humans based on shared physical or social qualities into groups generally viewed as distinct ...."
I would add that social and cultural qualities are reflections of natural aspects of respective races.
Police rely on race as a basic descriptor when identifying suspects and detainees. In prisons, inmates voluntarily organize themselves by race, further illustrating the practical reality of racial categorization.
In the overwhelming majority of countries, race or ethnicity is recorded on birth certificates.
Current standard categories as of the 2024 OMB revision :
- White
- Black or African American
- American Indian or Alaska Native
- Asian Indian, Chinese, Filipino, Japanese, Korean, Vietnamese, Other Asian
- Native Hawaiian, Chamorro, Samoan, Other Pacific Islander
- Some other race
Below are some of the characteristics unique to the three primary races.
Unique to Sub-Saharan African (especially Bantu-speaking) ancestry
- Very high genetic diversity and the deepest-branching lineages on Earth (the root of the human family tree).
- Highest frequency of the ancestral (fast) twitch muscle fiber profile and ACTN3 “sprint” variants linked to West African-derived explosive athletic performance.
- Duplicated amylase gene copies (AMY1) in some groups adapted to high-starch agricultural diets.
- APOL1 renal-risk variants (G1/G2) that protect against trypanosome sleeping sickness but dramatically raise risk of hypertensive kidney disease in the modern environment.
- Stronger inflammatory immune response (higher baseline TLR and cytokine activity), likely selected by intense pathogen load.
- Derived EDAR variant (370A) causing thicker hair shafts, smaller breasts, more eccrine sweat glands, and distinctive shovel-shaped incisors, selected in northern Asia ~35,000 years ago.
- Extremely high frequency of the ALDH2*2 “alcohol flush” allele (30–50 %), the strongest genetic protection against alcoholism ever documented.
- ADH1B*47His “super-flusher” variant that further accelerates alcohol metabolism.
- Highest known copy number of salivary amylase genes (AMY1), reflecting 8,000+ years of rice-based agriculture.
- Strong selection on genes for dry earwax and reduced body-odor apocrine sweat glands (ABCC11).
- Highest global frequency of lactase persistence into adulthood (70–90 % in northern Europe).
- Multiple independent light-skin alleles (SLC24A5, SLC45A2, TYR) fixed or nearly fixed, producing the lightest skin tones on Earth.
- Highest rates of hereditary hemochromatosis (HFE C282Y), cystic fibrosis mutations, and multiple sclerosis risk alleles (HLA-DRB1*15:01).
- Derived alleles for blond hair, blue eyes, and freckling (MC1R, OCA2/HERC2).
Strong selection on height-increasing alleles; modern Northern Europeans (especially Dutch and Scandinavians) are the tallest populations in history.
Why it matters
Numerous health conditions exhibit well-documented race-related distinctives. African ancestry, for example, is associated with a significantly higher prevalence of hypertension. Ignoring this biological difference would lead healthcare providers to treat black patients identically to non-black patients, which is inappropriate.
The woke left is forced to explain away every biological disparity as the product of current social forces. One frequently cited example is the assertion that hypertension is far more common among black individuals because of stress induced by systemic racism.
Across
the globe, other signatures abound: compact Arctic bodies among the
Inuit, larger spleens in Bajau sea nomads, malaria-resistant
hemoglobinopathies around the Old-World tropics, and high-altitude
adaptations in Tibetans, Andeans, and Ethiopians.These same ancient
adaptations echo in today’s clinics. West African ancestry carries the
world’s highest prostate-cancer mortality and APOL1 kidney risk.
Northern European ancestry dominates cystic fibrosis and hemochromatosis
cases. East Asian ancestry shows the lowest rates of many cancers but
heightened esophageal cancer risk if alcohol is consumed despite
flushing. Native American and Pacific Islander populations suffer
extreme type 2 diabetes prevalence from “thrifty genes” meeting modern
diets.
None of these differences are socially constructed. They
not random. They are the direct, reproducible consequences of natural
selection acting on geographically separated populations under
dramatically different environmental pressures. They guide newborn
screening, drug dosing, cancer-risk models, and transplant matching
every single day.The story of humanity is not convergence toward one
ideal form, but controlled divergence into thousands of finely tuned
local solutions, each carrying gifts from a distant past and prices
still paid in the present.
(Supported
by Jablonski & Chaplin 2010; Tishkoff et al. 2007; Beall et al.
2010; Mathieson et al. 2015; Fumagalli et al. 2015; Ilardo et al. 2018;
Kamberov et al. 2013; Genovese et al. 2010; Yi et al. 2010; Perry et al.
2014; Marciniak & Perry 2017; and major reviews in Nature, Science,
NEJM, and Cell.)
The Quiet Signatures of Ancient Environments
A Brief Overview of Human Adaptation and Its Lasting Echoes
Human
populations are not biologically identical. Over the past 70,000 years,
as small bands of modern humans spread into every habitable corner of
the planet, local environments imposed powerful selection pressures. The
result is a mosaic of measurable genetic differences—some visible, most
invisible—that helped our ancestors survive and that still shape health
outcomes today.
Primary groupings
In
the intense sunlight near the equator, dark skin rich in eumelanin
evolved to shield against UV damage. Thousands of miles away, beneath
cloudy northern skies, lighter skin arose independently in Europe and
East Asia so scarce sunlight could still produce vitamin D. Pastoralists
in Northern Europe and a few African groups gained the rare ability to
digest milk into adulthood, while almost everyone else switches the
lactase gene off after weaning. At 4,000 meters on the Tibetan Plateau,
one set of genes keeps blood thin and oxygen delivery efficient; in the
Andes, a different set thickens the blood instead.
Cold selected
for compact, heat-conserving bodies among the Inuit; relentless heat
favored long, slim limbs among the Dinka and Maasai. Malaria carved deep
marks: sickle-cell, thalassemia, and G6PD deficiency swept through
tropical populations because one copy of the mutation protected against
the parasite—two copies, however, bring serious disease.
These
same ancient bargains appear in modern hospitals. Cystic fibrosis and
hereditary hemochromatosis are overwhelmingly affect people of Northern
European descent. Tay-Sachs remains largely confined to Ashkenazi Jewish
and a few other small founder populations. Type 2 diabetes strikes
Native Americans, Pacific Islanders, and South Asians with extraordinary
severity because their ancestors’ “thrifty genes” were optimized for
feast-and-famine cycles, not supermarket abundance turns that advantage
into vulnerability. Men of West African ancestry face the world’s
highest prostate-cancer mortality, while East Asians experience the
lowest.
None of these differences are arbitrary, and none are
trivial. They are the direct, predictable consequences of natural
selection acting on isolated populations under dramatically different
environmental stresses. They influence newborn screening panels, cancer
risk calculators, blood-pressure treatment guidelines, and genetic
counseling every single day.
The story of humanity is not one of
convergence toward a single template, but of divergence into thousands
of finely tuned solutions—each carrying both gifts from the past and
prices still paid in the present.
(Supported by landmark studies
including Jablonski & Chaplin 2010, Tishkoff et al. 2007, Beall et
al. 2010, Fumagalli et al. 2015, Ilardo et al. 2018, and numerous
clinical-genetic reviews in NEJM, Nature Genetics, and Science.)
The Quiet Signatures of Ancient Environments
A Brief Overview of Human Adaptation and Its Lasting Echoes
Again, human races are not biologically identical. It is virtually impossible for our races to be social constructs.
None of these differences can be attributed to social influences, further confirming that race is not a social construct.
Efforts to converge races into a single, global homogeneous race defies nature. It will inevitably erase the positive attributes that enhance all humanity, such as advances in science, healthcare in particular, and is not "progressive." Rather, it is dysgenics by design.
(Supported by landmark studies including Jablonski & Chaplin 2010, Tishkoff et al. 2007, Beall et al. 2010, Fumagalli et al. 2015, Ilardo et al. 2018, and numerous clinical-genetic reviews in NEJM, Nature Genetics, and Science.)
Below is a short list of racial distinctives.
Human Genetic Variation Shaped by Environment: Combined Reference List with Cited SourcesPart 1 – Physical and Physiological Adaptations
- Skin Pigmentation
Darker skin near equator; lighter skin in Europe and East Asia.
→ Jablonski & Chaplin (2010) – Human skin pigmentation as an adaptation to UV radiation
→ Norton et al. (2007) – Genetic evidence for the convergent evolution of light skin in Europeans and East Asians - Lactase Persistence
Multiple independent origins in Europe and Africa.
→ Tishkoff et al. (2007) – Convergent adaptation of human lactase persistence in Africa and Europe
→ Ingram et al. (2009) – Multiple rare variants as a cause of a common phenotype - High-Altitude Adaptation
Distinct mechanisms in Tibetans, Andeans, and Ethiopians.
→ Beall et al. (2010) – Natural selection on EPAS1 underlies high-altitude adaptation in Tibetans
→ Bigham et al. (2010) – Identifying signatures of natural selection in Tibetan and Andean populations
→ Scheinfeldt et al. (2012) – Genetic adaptation to high altitude in the Ethiopian highlands - Body Proportions (Bergmann’s & Allen’s Rules)
→ Roberts (1978) – Climate and Human Variability
→ Katzmarzyk & Leonard (1998) – Climatic influences on human body size and proportions - Sickle-Cell Trait & Thalassemias
Classic heterozygous advantage against malaria.
→ Allison (1954) – Protection afforded by sickle-cell trait against malarial infection
→ Modiano et al. (2001) – Haemoglobin C protects against clinical Plasmodium falciparum malaria - Arctic Cold & High-Fat Diet Adaptation
→ Fumagalli et al. (2015) – Greenlandic Inuit show genetic signatures of diet and climate adaptation
→ Cardona et al. (2014) – Genome-wide analysis of cold adaptation in indigenous Siberian populations - Diving Reflex & Spleen Size
→ Ilardo et al. (2018) – Physiological and genetic adaptations to diving in sea nomads
- Sickle-Cell Disease & Thalassemia Major
→ Piel et al. (2010) – Global distribution of the sickle cell gene - Cystic Fibrosis
→ Bobadilla et al. (2002) – Cystic fibrosis: a worldwide analysis of 1000 mutations - Tay-Sachs Disease
→ Myrianthopoulos & Aronson (1966) – Population dynamics of Tay-Sachs disease - Hereditary Hemochromatosis
→ Feder et al. (1996) – A novel MHC class I–like gene is mutated in patients with hereditary haemochromatosis - Salt-Sensitive Hypertension & Kidney Disease in African ancestry
→ Young et al. (2004) – The enigma of hypertensive ESRD: biological and societal determinants - Type 2 Diabetes in high-risk populations
→ Knowler et al. (1990) – Diabetes incidence in Pima Indians
→ Diamond (2003) – The double puzzle of diabetes - Prostate Cancer disparities
→ Rebbeck et al. (2013) – Global patterns of prostate cancer incidence and mortality - Adult Lactose Intolerance
→ Swallow (2003) – Genetics of lactase persistence and lactose intolerance - Alcohol Flush Reaction (ALDH2∗2)
→ Eng et al. (2007) – Genetic variation in aldehyde dehydrogenase 2 - G6PD Deficiency
→ Luzzatto et al. (2016) – Glucose-6-phosphate dehydrogenase deficiency - Keloid Formation, SLE, Multiple Sclerosis, Dupuytren’s Contracture
→ Reviews in Reich et al. (2021) – Ancestry and disease in the age of genomic medicine and Sirugo et al. (2019) – The missing diversity in human genetic studies
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