Epigenetics and Height

The main components to epigenetics are DNA Methylation, Chromatin Folding,  telomere length, and histone acetylation.  Even if height was 100% genetic that gives us a great degree to manipulate genetics especially since genes can be upregulated and downregulated.  Here's a study that shows that paternal activity influences height growth:

Parental body size and early weight and height growth velocities in their offspring

"Whereas weight or height at a given age are the results of the cumulative growth experience, growth velocities allows the study of factors affecting growth at given ages.
235 parent-child trios belonging to 162 families [were] examined in 1999.
Weight and height growth velocities from birth to seven years were estimated from a modelling of individual growth curve and correlated with parent's body size in 1999.
Ponderal index and length at birth were significantly associated with maternal but not paternal BMI and height[babies spend time in the mothers womb but not the mans]. In the first six months, height growth velocity was significantly associated with maternal stature (at three months: 0.12+/-0.05 and 0.02+/-0.05 cm/month for a 10 cm difference in maternal and paternal height respectively) and weight growth velocity with paternal BMI (at three months: 5.7+/-2.8 and 1.9+/-2.3g/month for a difference of 1 kg/m(2) in paternal and maternal BMI respectively). Between two and five years, height growth velocity was more significantly associated with paternal height whereas weight growth velocity was more closely associated with maternal BMI.
Early childhood growth is characterised by alternate periods associated specifically with maternal or paternal BMI and height. This novel finding should trigger the search for specific genetic, epigenetic or environmentally shared factors from the mothers and fathers."

Maybe a parents height upregulates and downregulates genes that affect growth rate.  It's logical that the larger you are the faster you have to produce new bone and cartilage cells, maybe that rate is expressed in epigenetic mechanisms that can be passed down to the offspring.

"In a study published in 1954, weight at birth and in early infancy were more correlated with maternal than paternal stature, but this difference disappeared before adulthood"<-so it's likely an epigenetic change that influences genes that affect more growth velocity rather than final height so likely genes that affect the rate of cellular proliferation.

"The mother's height was more strongly associated with the offspring's height growth velocity in the first six months of life than father's height.  At one year, the height growth velocity was not associated with parental stature[maybe at this point the epigenetic mechanisms that affected stature growth are now adjusted for]. From two to five years, height growth was strongly associated with the father's height, whereas significant associations with the mother's height reappeared at four years and its effect remained much smaller than those with father's height"<-If height growth is affected by sex linked characteristics then it makes sense for fathers height to play a large impact on height growth.  If father is X(short)Y then he will carry those genes in height.  Whereas, Mother can be X(tall)X(short) and if short is recessive she will still be tall but still have potential to pass on X(short).  Mothers have the ability to carry sex-linked genes recessively and not show them in phenotype whereas males do not have that ability.

"over-expression of paternal alleles in the IGF2 gene in Beckwith–Wiedemann syndrome which results in a marked acceleration of bone growth in infancy and early childhood "<-an example given of epigenetics.  But children with Beckwith-Wiedemann syndrome usually grow to a height predicted by their parents height.  IGF-2 is strongly associated with growth velocity and IGF-2 expression decreases with age.

Secular trends in growth of African Pygmies and Bantu.

"The evolution in height of West Pygmies and Bantu farmers from 1911 to 2006 was evaluated using data from the literature as well as data gathered by our research team during an expedition to Cameroon in 2006.
During the last century, no secular trend in west Pygmies is apparent, as height changed from 151 cm to 155 cm in males and from 143 cm to 146 cm in females. A small though significant (p=0.026), increment (about 2 cm) was observed only in female subjects during the last ten years. By contrast, Bantu heights show a significant change from 1943 to 2006 for both males (from 159 cm to 172 cm; p=0.025) and females (from 148 cm to 160 cm; p=0.029).
Over the last century, the Bantu population exhibited a significant secular trend for height, whereas West Pygmies did not increase their linear growth. The lack of secular trend in Pygmies possibly suggests that their stature reflects adaptation to the forest lifestyle. We may hypothesize that not only environmental but epigenetic factors have also contributed to their growth potential."

"Most studies have concluded that the Pygmy growth pattern is normal up to the time of puberty and that their short stature is primarily due to insufficient growth acceleration at puberty."

"the BMI values of males and females in Bantu were significantly higher compared to those in Pygmies"<-Leptin which is produced by bodyfat stimulates longitudinal growth.

"it is quite possible that their short stature is epigenetically determined to facilitate adaptation to life in the dense tropical forest and endurance against starvation. Furthermore, their small body size could favour their life in the hot, humid climate of a tropical forest by minimizing the body’s heat production during exercise. With regard to possible pathophysiological mechanisms, it must be mentioned that [some have] reported normal GH secretion but low IGF-I levels. We also recently reported that reduced IGF-I and GHBP levels in Pygmies are associated with a marked decrease of the GHR gene expression which is not associated with variants in the sequence of the GHR gene. This supports the hypothesis of a genetically determined short stature in Pygmies"<-To test this take a kid born from Shaq and put him in the same forest that Pygmies grow up in and see how tall he grows. The excessive heat may downregulate pro-height growth genes or cause DNA damage and that may be the epigenetic cause for pygmy height.

Short stature may be more prone to epigenetic variations than tall stature.

Common variants show predicted polygenic effects on height in the tails of the distribution, except in extremely short individuals.

"Common genetic variants have been shown to explain a fraction of the inherited variation for many common diseases and quantitative traits, including height, a classic polygenic trait. The extent to which common variation determines the phenotype of highly heritable traits such as height is uncertain, as is the extent to which common variation is relevant to individuals with more extreme phenotypes. To address these questions, we studied 1,214 individuals from the top and bottom extremes of the height distribution (tallest and shortest ∼1.5%), drawn from ∼78,000 individuals from the HUNT and FINRISK cohorts. We found that common variants still influence height at the extremes of the distribution: common variants (49/141) were nominally associated with height in the expected direction more often than is expected by chance (p<5×10(-28)), and the odds ratios in the extreme samples were consistent with the effects estimated previously in population-based data. To examine more closely whether the common variants have the expected effects, we calculated a weighted allele score (WAS), which is a weighted prediction of height for each individual based on the previously estimated effect sizes of the common variants in the overall population. The average WAS is consistent with expectation in the tall individuals, but was not as extreme as expected in the shortest individuals (p<0.006), indicating that some of the short stature is explained by factors other than common genetic variation. The discrepancy was more pronounced (p<10(-6)) in the most extreme individuals (height<0.25 percentile). The results at the extreme short tails are consistent with a large number of models incorporating either rare genetic non-additive or rare non-genetic factors that decrease height. We conclude that common genetic variants are associated with height at the extremes as well as across the population, but that additional factors become more prominent at the shorter extreme. "

We'd hope to have found that there are some elements of tall stature that are not explained by genetic variation.  This leads to the suspicion that there was no existing environmental method that could epigenetically induce height growth.  However,  LSJL was not known at the time of the study and there are very few individuals who would go to extremes for height growth like hanging or the rack.  Several teenagers though weight train, run, and do sports so that rules out those methods at inducing epigenetic height growth.  Again though, if the stimulus required was very extreme than it's not likely to be significant statistically.

Here's a study that suggests epigenetic involvement in height growth specifically maternal exposure to Ultraviolet B:

Insights into the programming of bone development from the Avon Longitudinal Study of Parents and Children

"We examined associations between proxy measures of in utero nutrition and total body bone mineral content (BMC), bone area (BA), and bone mineral density (BMD) assessed at age 9.9 y in the Avon Longitudinal Study of Parents and Children (ALSPAC). There were positive relations between birth weight and BMC, BA, and BMD. These associations were explained by the co-association of birth weight with body size in later childhood. In height- and weight-adjusted analyses, an inverse association was observed between birth weight and BMD at age 9.9 y, which suggests that birth weight had a negative influence on bone mass after relations with bone and body size were taken into account. In analyses of associations between bone mass at age 9 y and background ultraviolet B exposure during the third trimester of pregnancy (a proxy measure for maternal vitamin D status), maternal ultraviolet B exposure was positively related to BMC, BA, and BMD. After adjustment for height, these associations were only partially attenuated, which suggests that maternal ultraviolet B exposure affected skeletal size and mass independently of longitudinal growth, possibly by the increase of periosteal expansion[so maternal ultraviolet B exposure increased longitudinal growth but it also increased skeletal mass independently of longitudinal growth as well]. There was a positive relation between maternal folate intake and BMD of the spine subregion independent of body size. Although a co-association with folate intake in childhood could explain this relation, the maternal methylenetetrahydrofolate reductase (MTHFR) genotype affected spine BMD independently of the child MTHFR genotype, which suggests that maternal folate status has an independent effect on bone development of offspring. Together, these results confirm that there is a relation between bone development in childhood and several proxy measures for nutritional status in utero."


Most of the light that gets through the atmosphere is UVA light.  UVB light is between 315 and 280 nm which is rare.  This lamp(Cole-Parmer 6-watt UV Lamp with 365nm and 302nm Wavelength Light Tubes, 115VAC), however, has a 302nm light tube.

"We also observed a positive association in ALSPAC between background ultraviolet B amounts and height at age 9 y, in keeping with the known season of birth effects on adult height."<-Although we don't know if maternal exposure to Ultravoilet B results in increased adult height.

"For example, an association was seen between maternal dietary intake of folate and BMD and aBMC at the spine subregion, which may point to a role of epigenetic changes in the programming of skeletal development because folate status was likely to influence the availability of methyl donors for methylation during gestation, which is a key mechanism in epigenetic gene silencing."<-So folate intake by the mother does likely affected by epigenetics as evidenced by the effects of BMD.  However, the lack of effect on height may indicate that methylation status has little effect on height.  Although, the effect on height is unclear as it is not directly mentioned whether Folate consumption impacts height at age 9 in the study(it's definitely mentioned that Ultraviolet B affects height however and it's speculated by the scientists that this effect is related to Vitamin D).

Magnesium is another compound that when taken by the mother influences the childs height.  The study mentions too that Magnesium and Folate maternal consumption has only a minor impact on skeletal development.

Impact of physical activity and doping on epigenetic gene regulation.

"The abuse of pharmaceuticals which improve athletic performance may alter the expression of specific genes involved in muscle and bone metabolism by epigenetic mechanisms, such as DNA methylation and histone modifications. Moreover, excessive and relentless training to increase the muscle mass, may also have an influence on the health of the athletes. This stress releases neurotransmitters and growth factors, and may affect the expression of endogenous genes by DNA methylation, too."

Couldn't get full study.

Epigenetic anomalies in childhood growth disorders.

"Fetal growth restriction is associated with morbidity among small for gestational age (SGA) neonates as well as in children and adults who were former SGA. Imprinted genes (whose expression is restricted to a single parental allele) have a critical role in controlling mammalian fetal growth. The human chromosome 11p15 encompasses two imprinted domains regulated by their own differentially methylated imprinted control region (ICR1 at the H19/IGF2 domain, and ICR2 at the KCNQ1/CDKN1C domain). Loss of imprinting at these two domains is implicated in two clinically opposite growth disorders. Indeed, our group has identified a loss of DNA methylation (LOM) at ICR1 in over 50% of patients with Russell-Silver syndrome (RSS) characterized by intrauterine and postnatal growth retardation with spared cranial growth, dysmorphic features, frequent body asymmetry and severe feeding difficulties. By contrast, gain of methylation at ICR1 is found in 10% of patients with Beckwith-Wiedemann syndrome (BWS), an overgrowth syndrome with an enhanced childhood tumor risk. We have now identified over 130 RSS patients with 11p15 LOM. This 11p15 epimutation is a frequent and specific cause of RSS as it has not been identified in non syndromic SGA patients. These new findings in the pathophysiology of RSS allow long-term follow-up studies to be performed based on molecular diagnosis. This will help to define appropriate clinical guidelines regarding growth, rapid bone age advance during puberty and feeding difficulties. Remarkably, we have also recently found that ∼10% of RSS patients and ∼25% of BWS patients showed multilocus LOM at imprinted regions other than ICR1 or ICR2 11p15, respectively."

Couldn't get this full study unfortunately.

Epigenetic regulation of osteogenic and chondrogenic differentiation of mesenchymal stem cells in culture.

TGFB1 and TGFB3 can promote chondrogenesis.


"In the cell laboratory, cartilage differentiation of MSCs can be performed in a pellet culture system. Approximately 2 × 105 cells (passages 2-3) must be condensed in to a pellet by centrifugation at 300 g for 4 minutes, followed by incubation in an atmosphere of 37˚C and 5% CO2 in a 0.5 ml chondrogenic medium. The chondrogenic medium should be composed of 10 ng/ml TGF-β3, 500 ng/ml BMP-6, 100 nM dexamethasone, 50 µg/ml ascorbic 2-phosphate, 50 µg/ml ITS and 1.25 mg/ml bovine serum albumin. Addition of Lithium Chloride and a small molecule refereed to as SB216763 can enhance glycoseaminoglycal deposition in the human marrow-derived MSC chondrogenic culture"


"DNA methylation levels of CpG-rich promoters of chondrocyte-specific genes were mostly maintained at low levels"


"Sox9 associates with CREB-binding protein (CBP)/p300 via its carboxyl termini activation domain and functions as an activator for cartilage tissue-specific gene expression during chondrocyte differentiation"

"p300 potentiated Sox9-dependent transcription through hyperacetylation of histones. P300/ CBP acts as a coactivator to cartilage homeoprotein- 1 (Cart1) through acetylation of the conserved lysine residue adjacent to the homeodomain"

"Histone deacetylation by HDAC1 has been reported to have a critical inhibitory role in cartilage noncollagenous matrix deposition during cartilage differentiation. Cartilage oligomeric matrix protein (COMP) is a noncollagenous matrix protein in cartilage. In a study using Sox-9-null mice, the COMP gene was inhibited by a transcription repressor,the negative regulatory element (NRE)-binding protein by recruiting HDAC1 to the COMP promoter.  Rat chondrosarcoma cells and BMP-2-treated C3H10T1/2 progenitor cells, it was observed that the leukemia/ lymphoma-related factor, a POZ domain-containing transcriptional repressor, interacted with HDAC1 and inhibited COMP gene expression and chondrogenesis"

"HDAC4 regulates chondrocyte hypertrophy and endochondral bone formation by inhibiting the activity of Runx2 which is a transcription factor necessary for chondrocyte hypertrophy.  HDAC4-null mice display premature ossification of developing bone; and conversely, over expression of HDAC4 in proliferating chondrocytes in vivo inhibits chondrocyte hypertrophy and differentiation"

"HDAC promotes collagen II expression by suppressing the transcription of Wnt-5a"