Recently The New York Times reported the following:
Where Do Autoimmune Diseases Come From? (1/2)
Our genes evolved to fight ancient threats, but in the
modern world, some of those changes may be turning against us.
The NYT - By David Quammen (David Quammen is a science
journalist and author of 19 books. This piece is part of “Disease States,” his
new series on evolution and disease.)
Published Oct. 20, 2026, Updated Oct. 22, 2026
Evolution doesn’t have purposes, only results. Darwinian
natural selection doesn’t shape creatures to be “better” or “higher” in some
objective, transcendent sense — it shapes creatures to succeed in the here and
now. And what works in one environment or period of time may prove harmful in
another. Some scientists say this fact of evolution might help explain the
origins of human autoimmune diseases.
They are a bit mysterious, autoimmune diseases, but far from rare. They include multiple sclerosis, rheumatoid arthritis, Type 1 diabetes, lupus, Crohn’s disease, psoriasis and possibly more than 100 others. Some of them cause misery, some discomfort and inconvenience and some can be fatal. What these conditions share is that, for reasons still unclear, a person’s immune cells begin attacking the body’s own tissues and organs instead of just defending against invaders like viruses and bacteria.
Autoimmune diseases are believed to affect about 15 million
people in the United States and between 5 and 10 percent of the population of
industrialized countries, as well as a smaller percentage in developing
countries. And the numbers are rising, probably because of environmental
factors, including diet and pollutants, which play a role in setting off these
illnesses. But genetic factors likely play a role, too, and that’s where
research in recent years has revealed an intriguing pattern.
Autoimmune diseases may arise partly from the action of
genes and gene combinations that were valuable at earlier stages of human
history but are now disadvantageous. More specifically, scientists have found
evidence of natural selection for certain gene variants during the Bronze Age,
which began about 5,000 years ago and spanned two millenniums. Those same
variants may increase the risk of autoimmune disease in people who carry them
today. The term for such opposing effects is “antagonistic pleiotropy,” and a
simple way of explaining it is that sometimes a gene helps, and other times it
harms.
Why would some gene variants perform a valuable service for
ancient humans but be a disservice now? One answer, supported by recent studies
that draw on genetic sequencing of ancient human DNA and comparisons of those
sequences with modern genomes, involves infectious disease.
During those earlier millenniums, humans transitioned from
being hunter-gatherers in small, mobile bands to two other ways of living: as
farmers and as pastoralists. Farmers were sedentary. Pastoralists turned wild
animals into cattle, sheep and goats, and traveled across wide areas so their
livestock could graze. Farming brought people into close contact with plants.
Pastoralism brought people into close contact with the viruses, bacteria and
other infectious agents that wild (and then domesticated) animals carry.
Many of those pathogens crossed into the pastoralists,
creating what are now called zoonotic diseases — animal infections that spill
over to humans. Survival against such disease threats involved luck and genes.
Natural selection culled out the unlucky, leaving populations of survivors who
carried lucky gene variants that offered resistance against the
infections.
But those protective gene variants of the Bronze Age, it now
seems, may have a negative effect in our modern era of good sanitation systems,
antibiotics, antiseptics and other infection control measures. By increasing
the sensitivity of the immune system to an extreme level, they have become risk
factors for autoimmune diseases. That’s the antagonistic pleiotropy hypothesis
anyway.
And scientists have found evidence to support it.
Researchers at the University of Oxford and their collaborators elsewhere
reported a strong correlation between certain gene variants that spread rapidly
among European populations around 5,000 years ago and those linked to an
elevated chance of having multiple sclerosis today. The variants became more
common as migrant pastoralists from the Eurasian steppe began arriving in
Europe. Most of those gene variants delivered some protection against certain
viral and bacterial infections, or against parasites, helping humans to adapt
not just to the pastoral lifestyle, but to increases in population density,
which intensified the transmission and circulation of infectious diseases.
(to be continued)
自體免疫疾病從何而來？ （1/2）
我們的基因演化是為了對抗古老的威脅，但在現代社會，其中一些變化可能對我們不利
進化沒有目的，只有結果。達爾文的自然選擇 並非塑造生物體使其在某種客觀、超越日常經驗的意義上“更好”或“更高”，而是塑造生物體使其在當下取得成功。在一個特定環境或時期有效，在另一種環境或時期可能有害。一些科學家認為，演化的事實或許有助於解釋人類自體免疫疾病的起源。
自體免疫疾病有些神秘，但絕非罕見。這些疾病包括多發性硬化症、類風濕性關節炎、第1型糖尿病、紅斑性狼瘡、克隆氏症、乾癬，以及其他可能超過100種的疾病。有些疾病會造成痛苦，有些會造成不適和不便，有些則可能致命。這些疾病的共同點在於，由於一些尚未明確的原因，人體的免疫細胞開始攻擊自身的組織和器官，而不是像正常情況下那樣抵抗病毒和細菌等入侵者。
美國相信約有1,500萬人患有自體免疫疾病，已開發國家的盛行率在5%到10%之間，發展中國家的盛行率則更低。而且，患病人數還在上升，這可能是由於環境因素，包括飲食和污染物，在誘發這些疾病方面發揮了作用。但遺傳因素也可能發揮了作用，而近年來，研究揭示了一種有趣的模式。
自體免疫疾病的出現可能部分源自於某些基因及其組合的作用，這些基因在人類歷史早期階段具有重要價值，但如今卻有害。更具體地說，科學家發現了青銅時代（始於約5,000年前，持續兩千年）某些基因變異受到自然選擇的證據。如今，攜帶這些變異的人群罹患自體免疫疾病的風險可能會增加。這種相反的作用被稱為“拮抗性多效性”(antagonistic pleiotropy)，簡單來說就是一個基因有時有益，有時卻有害。
為什麼有些基因變異對古代人類有益，但如今卻有害呢？近期一些研究利用古代人類DNA的基因定序，並將這些序列與現代基因組進行比較，得出的答案之一與傳染病有關。
在早期的幾千年裡，人類從小型遊牧部落的狩獵採集生活方式過渡到另外兩種生活方式：農業和畜牧。農業是定居的。牧民將野生動物馴化成牛、羊和山羊，並遷移到廣闊的地區放牧。農業使人們與植物密切接觸。而畜牧業則使人們與野生（後來是家養）動物攜帶的病毒、細菌和其他病原體密切接觸。
許多病原體透過畜牧業傳播到牧民身上，形成瞭如今被稱為人畜共患病的疾病 - 動物受到感染後傳染給人類的疾病。抵禦此類疾病威脅的生存取決於運氣和基因。自然選擇 淘汰了不幸者，留下了攜帶幸運基因變異的倖存者，這些基因變異能夠抵抗感染。
但現在看來，這些青銅時代的保護性基因變異，在我們這個擁有良好衛生系統、抗生素、消毒劑和其他感染控制措施的現代社會，可能產生了負面影響。它們將免疫系統的敏感性提高到極致，從而成為自體免疫疾病的危險因子。這就是拮抗性多效性假設。
科學家已經找到了支持這項假設的證據。牛津大學的研究人員及其合作者報告稱，大約5,000年前在歐洲人群中迅速傳播的某些基因變異，與如今多發性硬化症高發生風險相關的基因變異之間存在很強的相關性。隨著來自歐亞草原的牧民遷移到歐洲，這些基因變異變得越來越普遍。大多數基因變異能夠提供一定的保護，抵抗某些病毒、細菌感染或寄生蟲，幫助人類不僅適應了遊牧生活方式，也適應了人口密度增加帶來的傳染病傳播和加劇擴散。
Note:
1. Antagonistic
pleiotropy (拮抗性多效性) is a theory in evolutionary biology that holds that certain genes
confer beneficial effects early in an organism's life, enhancing survival or
fertility, while also causing detrimental effects later in life. It provides an
explanation for why some genes are not eliminated by natural selection even
though they are associated with catastrophic health outcomes, especially in
older age. (Wikipedia)
2.
Darwinian natural selection (自然選擇) theories that evolution doesn’t have
purposes, it doesn’t shape creatures to be “better” or “higher” in some
objective, transcendent sense — it only shapes creatures to succeed in the here
and now.
