Height is a complex trait that is influenced by both genetic and environmental factors. This article will examine whether height is primarily determined by genetics (nature) or by environmental conditions (nurture).
Quick Answer
Height is influenced by both inherited genetic factors and environmental conditions, especially nutrition, during childhood and adolescence. However, studies estimate that 60-80% of variation in height within a population is due to genetic factors. This indicates that genetics plays a stronger role than environment in determining height.
Human height is a classic polygenic trait, meaning that it is influenced by the interactions of multiple genes. However, environmental factors, especially nutrition, also play an important role in determining height during childhood and adolescence when growth is occurring.
The relative contribution of genes versus environment to height has been extensively studied by scientists. Research methods include twin studies, family studies, genome-wide association studies (GWAS), and investigating populations with very different heights. The evidence overwhelmingly shows that genetics is the primary determinant of height, although environmental factors can modify growth.
Evidence That Height is Primarily Genetic
There are several key lines of evidence demonstrating the strong genetic influence on height:
- Twin studies: Identical twins with nearly 100% of genes in common show much higher correlation in height compared to non-identical twins. This indicates a strong genetic component.
- Heritability estimates: Height is 60-80% heritable, meaning genetic differences account for 60-80% of height variation in a population.
- Extreme height populations: Groups with very short or tall average heights illustrate that genetics trumps environment.
- GWAS studies: Hundreds of genetic variants associated with height have been identified.
- Rare height disorders: Single gene mutations can cause growth disorders, showing that disrupting genetics affects height.
Twin Studies Demonstrate High Heritability
Twin studies compare the trait similarity between identical (monozygotic) twins that share 100% of genetic material and non-identical (dizygotic) twins that share only 50% on average. A much higher correlation for a trait in identical twins demonstrates high heritability.
Numerous twin studies on height from around the world have found a very high degree of correlation between the heights of identical twins. For example, a meta-analysis found the mean correlation was 0.92 for male identical twin pairs and 0.94 for female identical pairs across 25 twin studies. In contrast, non-identical twins had a correlation of only 0.46 for males and 0.63 for females. This indicates genetics strongly influences height.
Heritability Estimates Are 60-80% for Height
Heritability measures the proportion of variation in a trait within a population that can be attributed to genetic differences. Height is estimated to have a heritability between 60-80% based on family and twin studies. This indicates genetics plays a more important role than environment in driving height variability.
For example, a 2021 study analyzed the heights of over 280,000 full sibling pairs from the UK Biobank. They estimated height had a heritability of 69.4% in their cohort. Other large studies have reported heritability estimates between 60-80%. This shows the substantial effect of genetics on height compared to environmental factors.
Extreme Height Populations: Pygmies and Dinka
Populations with very short or tall average heights, such as Pygmies and Dinka people, provide “natural experiments” that illustrate the overriding influence of genetics on height. Even with different upbringings, genetics trumps environment in determining their extreme heights.
Pygmies from Africa have very short average heights, such as men from the Efe tribe averaging around 150 cm. This is due genetic adaptations over many generations. Transplanting Pygmy children outside their normal environment does not increase their height to population norms.
Similarly, the Dinka people of Sudan have very tall average heights, with men averaging around 182 cm. This is likely due to genetics rather than environment. When Dinka children were adopted overseas, their genetically taller heights persisted.
Hundreds of Genetic Loci Identified by GWAS
Recent genome-wide association studies (GWAS) have identified hundreds of genetic loci associated with height. The large number of variants shows that height is a highly polygenic trait influenced by many genes working in combination. This provides direct genetic evidence for the heritability of height.
One of the largest GWAS on height analyzed over 250,000 individuals and identified 183 height-associated genetic loci. Together, these loci explained about 10% of height heritability. Hundreds more genetic variants have since been found, confirming the highly polygenic nature of human height.
Rare Height Disorders: Single Gene Mutations
There are also hundreds of rare genetic syndromes caused by mutations in single genes that dramatically affect growth and result in short or tall stature. These disorders demonstrate that disrupting genetics directly impacts height development.
For example, Achondroplasia is a form of dwarfism caused by a FGFR3 gene mutation. Marfan syndrome causes tall stature and is caused by fibrillin-1 (FBN1) gene mutations. The identification of single gene disorders provides definitive evidence that genetics regulates human height.
Evidence That Environment Also Plays a Role
While genetics is the primary determinant of height, environmental factors, especially nutrition, can modify growth and final height. Evidence for environmental impacts on height include:
- Socioeconomic status: Poor childhood nutrition linked to low SES limits growth.
- Secular height trend: Average heights have increased alongside improving nutrition.
- Growth velocity: Growth rates respond to changes in diet and disease burden.
Socioeconomic Status and Nutrition
There are well-established associations between height and socioeconomic status (SES), which often relates to the availability of adequate nutrition. Poor childhood nutrition linked to poverty can restrict growth and limit final height achievement.
For example, a British study found that boys from unskilled labor backgrounds were 3.6 cm shorter on average than boys from professional backgrounds at age 7. This demonstrates environmental impacts on height through factors linked to SES.
Secular Changes in Height Over Time
Average heights within populations have substantially increased over the past century alongside improvements in nutrition and healthcare. This secular height trend reflects how aspects of environment influence growth.
For example, the average height of American men increased by around 6 cm between the 1900s and 2000s. Improved childhood nutrition and disease environment allowed more people to achieve their genetic height potential over time.
| Decade of Birth | Average Height of American Men (cm) |
|---|---|
| 1900s | 170.2 |
| 1950s | 177.0 |
| 2000s | 176.4 |
Growth Velocity Responds to Environment
Growth velocity, or the rate of growth, reflects how environmental factors influence height even when final height is constrained by genetics. For example, malnutrition, disease, and trauma can all slow or stop growth temporarily.
A classic example is stunted growth observed in children raised in emotionally or nutritionally deprived orphanages who experience “catch-up growth” when placed in loving family environments with better nutrition.
Relative Contribution of Genetic and Environmental Factors
Studies that simultaneously assess genetic and environmental influences on height provide the most direct insights into their relative contributions. These studies consistently find that genetics outpaces environment, especially for final attained height.
For example, a 2021 study analyzed both genetic variants and childhood SES factors in 120,000 individuals. Genetic factors accounted for 69% of height variation while childhood environment accounted for only 31%. However, environment explained 9% of adult height differences, showing it still has a measurable effect.
Overall, most studies estimate that genetics account for 60-80% of height variation while environment explains 20-40%. The environment substantially influences growth velocity but genetics ultimately determines final height.
How Genes Influence Height
Genes impact height through hormonal signaling involved in skeletal growth and development. Although over 700 genetic loci associated with height have been identified, many converge on a few key growth regulation pathways:
- Growth hormone / IGF1 signaling
- Cell division and proliferation
- Skeletal development
- Extracellular matrix production
Genetic variations in these pathways likely account for a significant portion of height heritability. However, there are still many unknown genes and molecular mechanisms involved in determining height.
Growth Hormone and IGF1 Signaling
Growth hormone (GH) and insulin-like growth factor 1 (IGF1) are key hormones that stimulate growth in childhood. Many genetic variants linked to height are in genes related to GH and IGF1 signaling, such as the GH receptor gene.
Mutations causing extreme short stature highlight this pathway. For example, Laron syndrome is caused by severe GH receptor mutations leading to highly deficient IGF1 production and short statue.
Cell Division and Proliferation
Height increase occurs through cell divisions in the growth plates of bones to produce more cartilage and bone tissue. Genetic variants associated with height are enriched in genes involved in mitosis, meiosis, and overall cell cycle regulation.
For example, mutations in ACAN, the aggrecan gene involved in growth plate expansion, cause short stature disorders. Variants in CCND3 regulating cell cycle also associate with height.
Skeletal Development
Numerous height-related genetic variants are in key developmental genes for connective tissue, cartilage, and bone. This includes variants in BMPs, FGFRs, extracellular matrix genes, and enzymes modifying skeletal proteins.
For example, FGFR3 mutations cause achondroplasia dwarfism. Mutations in COL2A1 and COL11A2 alter collagen fibrils in cartilage and bone leading to short stature.
Extracellular Matrix Production
The extracellular matrix (ECM) provides structural support for tissues. Genetic variants related to height are enriched in genes encoding ECM proteins and ECM-modifying enzymes.
For example, ADAMTS enzymes modify cartilage ECM proteins and ADAMTS10 variants associate with height. Variants in LTBP2, which binds matrix protein TGF-beta, also correlate with height differences.
How Environment Affects Height
While genetics sets boundaries, environmental influences like nutrition and disease can impact height by affecting growth velocity, especially during developmental periods.
Childhood Nutrition
Adequate nutrition is crucial for achieving genetic height potential. Malnutrition during critical growth periods limits production of bone, muscle, and other tissues.
Protein is essential for growth. Essential fatty acids are also needed for bone health. Deficiencies in minerals like calcium, phosphorus, magnesium, and zinc inhibit growth.
Micronutrient deficiencies in vitamin D, folate, and other vitamins can also impair growth. Overall nutrition optimizes growth velocity.
Disease Burden
Chronic diseases impair growth by directing nutrients to fight infection rather than support growth. Short-term illnesses also slow growth velocity.
For example, coeliac disease, kidney disease, and asthma are associated with reduced height. Certain medications used in illness may also inhibit growth.
Conversely, decreased infectious disease exposure as sanitation improves may contribute to increased heights over time.
Psychosocial Deprivation
Psychosocial deprivation, including emotional neglect, stress, and abuse, is linked to growth impairment. Stress hormones may divert energy away from growth.
Children raised in deprived orphanages often experience stunted growth that can be partially reversed if they are adopted into more nurturing families at young ages.
Critical Periods for Environmental Impacts on Height
The effects of environment on height are most significant during critical periods of rapid growth and development:
- Prenatal period
- Infancy
- Childhood before puberty
- Pubertal growth spurt
For example, infancy is critical for accumulation of muscle, bone, and fat that contribute to height. Puberty includes rapid bone growth under hormonal control that completes adult stature.
However, environment impacts height most severely if experienced consistently across multiple critical periods. Catch-up growth may occur if conditions improve between periods.
Balanced Contributions of Nature and Nurture
Overall, height is a classic example of a polygenic trait resulting from combined effects of both nature (genes) and nurture (environment).
Genes likely influence height primarily through hormonal signaling pathways that regulate bone growth and development. However, environmental factors like childhood nutrition strongly modulate growth velocities to determine final height.
While genetics outweigh environment overall, both remain important influences on human height. Optimum height results from genetic potential fulfilled through favorable childhood conditions.
Conclusion
In conclusion, human height is determined by a complex interaction between genetic factors and childhood environment. However, large twin studies, heritability estimates, and identification of height-related genes convincingly demonstrate that genetics plays the predominant role, accounting for 60-80% of height variation.
Environmental influences, especially nutrition, can modify growth rates during development. But they act primarily to help individuals achieve their innate genetic height potential programmed by DNA sequence variants. Overall, nature via genetics supersedes nurture in dictating height for most individuals.
