Twin Studies indicate the likelihood of environmental factors influencing height growth

Even if height is 100% genetic, genes are still manipulable through DNA Methylation status, telomere length, chromatin folding, and histone acetylation. Things like mechanical stimulation, hydrostatic pressure, and shear strain like that induced by Lateral Synovial Joint Loading are capable of upregulating and downregulating genes.  So too are chemicals capable of upregulating and downregulating genes.  Leptin for instance stimulates the PI3K pathway.

Twin studies can provide us insight on environmental factors that can effect height.  Even if height is determined solely by genetics, environmental factors can manipulate epigentic factors and genetic regulation.  If height is found to be 20% environmental in twin studies where twins engage in normal activities that means that supranormal activities like LSJL may affect height much more.  And remember bone is a substance and that means it shares the properties of all substances like being capable of being stretched.

An assessment of the individual and collective effects of variants on height using twins and a developmentally informative study design.

"In a sample of 3,187 twins and 3,294 of their parents, we sought to investigate association of both individual variants and a genotype-based heightscore involving 176 of the 180 common genetic variants with adult height identified recently by the GIANT consortium. First, longitudinal observations on height spanning pre-adolescence through adulthood in the twin sample allowed us to investigate the separate effects of the previously identified SNPs on pre-pubertal height and pubertal growth spurt. We show that the effect of SNPs identified by the GIANT consortium is primarily on prepubertal height[so genes mainly influence height prepuberty?  intersting]. Only one SNP, rs7759938 in LIN28B, approached a significant association with pubertal growth. Second, we show how using the twin data to control statistically for environmental variance can provide insight into the ultimate magnitude of SNP effects and consequently the genetic architecture of a phenotype. Specifically, we computed a genetic score by weighting SNPs according to their effects as assessed via meta-analysis. This weighted score accounted for 9.2% of the phenotypic variance in height, but 14.3% of the corresponding genetic variance."

"Twin and adoption studies suggest that height is highly heritable (∼80%)"<-20% however is a very large amount of unheritable variance.

Interestingly, according to table 1 there's a .25 cm increase in height males between age 20 and 29(however there are so many other possibilities for this increase rather than a .25cm growth in adult males between 20 and 29, note for instance how females show an average height reduction between 25 and 29).

"Shared environmental effects accounted for 9% (0%, 27%) and 11% (0%, 31%) of the variance in the intercept and slope, respectively"<-environment accounts for around 10% of height in normal cases and in extraordinary cases that could be much more like with extreme loading or by LSJL.

Heritability of adult body height: a comparative study of twin cohorts in eight countries.

"A major component of variation in body height is due to genetic differences, but environmental factors have a substantial contributory effect. In this study we aimed to analyse whether the genetic architecture of body height varies between affluent western societies. We analysed twin data from eight countries comprising 30,111 complete twin pairs by using the univariate genetic model of the Mx statistical package. Body height and zygosity were self-reported in seven populations[this could be a problem as people with higher self esteem could report their height as higher] and measured directly in one population[we still have this data though]. We found that there was substantial variation in mean body height between countries; body height was least in Italy (177 cm in men and 163 cm in women) and greatest in the Netherlands (184 cm and 171 cm, respectively). In men there was no corresponding variation in heritability of body height, heritability estimates ranging from 0.87 to 0.93 in populations under an additive genes/unique environment (AE) model. Among women the heritability estimates were generally lower than among men with greater variation between countries, ranging from 0.68 to 0.84 when an additive genes/shared environment/unique environment (ACE) model was used. In four populations where an AE model fit equally well or better, heritability ranged from 0.89 to 0.93. This difference between the sexes was mainly due to the effect of the shared environmental component of variance, which appears to be more important among women than among men in our study populations. Our results indicate that, in general, there are only minor differences in the genetic architecture of height between affluent Caucasian populations, especially among men."

"Twin correlations for MZ male pairs were uniformly high in all countries, ranging from 0.87 to 0.94 in male
and from 0.84 to 0.94 in female MZ pairs"<-Still however a significant part that is not correlated between twins.

"Heritability of body height is lower among women than among men and there is also greater geographic variation in the heritability estimates among women"<-The study also found little effect of sex-linked characteristics on height so it may be an estrogen production factor.  High levels of estrogen can cause apoptosis of growth plate chondrocytes and estrogen may be influenced by environmental factors.

This study found that genetic factors account for 90% when self-reporting bias is removed.  10% is still a large place for enivornmental factors however and gives the possibility for even more environmental influence when you have extraordinary stimulation like LSJL.

Bias, precision and heritability of self-reported and clinically measured height in Australian twins.

"Here we report a detailed quantitative genetic analysis of stature. We characterise the degree of measurement error by utilising a large sample of Australian twin pairs (857 MZ, 815 DZ) with both clinical and self-reported measures of height. Self-report height measurements are shown to be more variable than clinical measures. This has led to lowered estimates of heritability in many previous studies of stature. In our twin sample the heritability estimate for clinical height exceeded 90%. Repeated measures analysis shows that 2-3 times as many self-report measures are required to recover heritability estimates similar to those obtained from clinical measures. Bivariate genetic repeated measures analysis of self-report and clinical height measures showed an additive genetic correlation >0.98[well still 2% is environmental]. We show that the accuracy of self-report height is upwardly biased in older individuals and in individuals of short stature. By comparing clinical and self-report measures we also showed that there was a genetic component to females systematically reporting their height incorrectly; this phenomenon appeared to not be present in males. The results from the measurement error analysis were subsequently used to assess the effects of error on the power to detect linkage in a genome scan. Moderate reduction in error (through the use of accurate clinical or multiple self-report measures) increased the effective sample size by 22%; elimination of measurement error led to increases in effective sample size of 41%."

"This corresponds to a decline in height of 4.5 cm over a 40 year period"<-So posture correction and stimulating cartilage growth in the discs of the spine can restore height of at least 2 inches.

This study however found a higher percentage of environmental factors affected height.  It used self reported height but it measured the accuracy of self-reported height against height measurements.

Genetic and environmental influences on growth from late childhood to adulthood: a longitudinal study of two Finnish twin cohorts.

"Two cohorts of monozygotic and dizygotic (same sex and opposite sex) Finnish twin pairs were studied longitudinally using self-reported height at 11-12, 14, and 17 years and adult age (FinnTwin12) and at 16, 17, and 18 years and adult age (FinnTwin16). Univariate and multivariate variance component models for twin data were used.
From childhood to adulthood, genetic differences explained 72-81% of the variation of height in boys and 65-86% in girls. Environmentalfactors common to co-twins explained 5-23% of the variation of height, with the residual variation explained by environmental factors unique to each twin individual. Common environmental factors affecting height were highly correlated between the analyzed ages (0.72-0.99 and 0.91-1.00 for boys and girls, respectively). Genetic (0.58-0.99 and 0.70-0.99, respectively) and unique environmental factors (0.32-0.78 and 0.54-0.82, respectively)[this is what we're looking more for as unique environmental factors we can alter] affecting height at different ages were more weakly, but still substantially, correlated.
The genetic contribution to height is strong during adolescence. The high genetic correlations detected across the ages encourage further efforts to identify genes affecting growth. Common and unique environmental factors affecting height during adolescence are also important"

"Reliability of self-reported height, analyzed in sub-samples of both twin cohorts after completion of the last wave of questionnaires, was found highly correlated with measured height in FinnTwin12 (r = 0.99, N = 797) and FinnTwin16 (r = 0.99, N = 566) "

"Nutrition is universally the most important environmental factor affecting growth. For example, milk [likely due to lactoferrin and IGF-1] consumption has been found to be positively associated with height in children and adults"

"growth before puberty is the main determinant of adult stature"<-Thus why some believe you should delay puberty to grow taller.

Here's one study that shows that the environmental factor muscle loading may affect foot length.

Association between foot growth and musculoskeletal loading in children with Prader-Willi syndrome before and during growth hormone treatment.

"In 37 children with PWS, foot length (FL) before and after 6 years of growth hormone therapy (GHT) was retrospectively evaluated with parental and sibling's FL, height, and factors reflecting musculoskeletal loading, such as weight for height (WfH), lean body mass (LBM; dual energy X-ray absorptiometry, deuterium labeled water), physical activity (accellerometry), and walk age. Because of the typically biphasic evolution of body mass and the late walk age in PWS, 2 age groups were separated (group 1, >2.5 years; group 2, < or =2.5 years).
Children with PWS normalized height, but not FL after 6 years of GHT. Parental FL correlation with PWS's FL was lower than with sibling's FL. In group 1, FL positively correlated with WfH, LBM, and physical activity[after 2.5 years of age foot length correlated with physical activity, body weight, and muscle mass]. In group 2, FL negatively correlated with age at onset of independent ambulation. Foot catch-up growth with GHT was slower in group 2 compared with group 1.
In PWS, FL is positively associated with musculoskeletal loading. Small feet in children with PWS before and during long-term GHT may be more than just another dysmorphic feature, but may possibly reflect decreased musculoskeletal loading influencing foot growth and genetic and endocrine factors[decreased musculoskeletal loading may affect foot growth in all individuals and not just children with PWS]."

"In patients with GH deficiency or GH insensitivity syndrome, the size of hands and feet is reduced in proportion to the patient's body height, feet being relatively longer than hands, with both normalizing on GH therapy (GHT)"<-height is composed larger of long bone length whereas feet length is mainly determined by short and irregular bone size.  This may indicate that GH plays a larger role on short bone growth than long bone growth.

"GHT normalizing height and hand length, but not foot length (FL)"<-that feet would be influenced by different factors than hands is very interesting.

" In hemiplegic children, the inactive leg is shorter than the active one"

"Factors other than GH and the genetic background may have an impact on foot growth."

"the later the onset of musculoskeletal loading, the shorter the FL"<-this means that you may only need to pass a threshold of musculoskeletal loading to maximize foot length and that as long as you are passed that threshold your foot length growth is maximized.  The lack of catch-up growth is not good news for the possibility of environmental musculoskeletal stimulation being a significant way to increase foot length(as long as you are above threshold).

"in the older group of children only, there was a significantly positive correlation between FL and WfH, indicating that body mass may be a stimulus for foot growth"<-this data however is very positive for environmental musculoskeletal stimulation stimulating foot length with body weight correlating positively with foot length.

"in addition to height, parental FL variables of musculoskeletal loading were significant predictors of FL measures."<-So even in parents who did not have PWS, musculoskeletal loading was correlated with foot length[weight and exercise]

So environmental factors accounted for around at most 20% of height and less than 2% of height in some studies.  Musculoskeletal loading is one such environmental factor that was found to affect foot length.  Another corollary environmental factor to that is nutrition which affects body weight which is positively correlated to foot length(referred to as weight for height in the study).  Is it possible that foot length could be influenced by factors other than bone length?  There's arch size which may decrease with increasing loads(thus increasing foot length).  Fat mass and lean body mass can contribute to foot size(however, those things can contribute to hand size as well).

Less people load their hands than walk(less people provide mechanical stimulation to hands than feet).  Thus, if mechanical stimulation stimulates foot growth thus foot length should increase greater than hand length in normal individuals(as not as many people do push-ups as walk).  Thus, meaning PWS individuals are less far behind in hand length than foot length.  This too means that studying hand size with exercise would be an interesting study.  One twin does push-ups whereas another lives life normally.