Since drinking water contains Arsenic and Fluoride which can affect gene expression, it’s conceivable that drinking water could affect height growth.
Arsenic and fluoride co-exposure affects the expression of apoptotic and inflammatory genes and proteins in mononuclear cells from children.
“Humans may be exposed to arsenic (As) and fluoride (F) through water consumption. Herein, the expression of cIAP-1, XIAP, TNF-α, ENA-78[also known as CXCL5 which is downregulated by LSJL], survivin, CD25, and CD40 was evaluated by RT-PCR. Additionally, the surface expression of CD25, CD40, and CD40L on peripheral blood mononuclear cells were analyzed by flow cytometry, and TNF-α was measured by western blotting. This study examined 72 children 6-12 years old who were chronically exposed to As (154.2μg/L) and F (5.3mg/L) in drinking water and in food cooked with the same water. The urine concentrations of As (6.9 to122.4μg/L) were positively correlated with the urine concentrations of F (1.0 to 8.8mg/L). The CD25 gene expression levels and urine concentrations of As and F were negatively correlated, though the CD40 expression levels were negatively correlated only with the As concentration. Age and height influenced the expression of cIAP-1, whereas XIAP expression was correlated only with age. Additionally, there was a lower percentage of CD25- and CD40-positive cells in the group of 6- to 8-year-old children exposed to the highest concentrations of both As and F when compared to the 9- to 12-year-old group (CD25: 0.7±0.8 vs. 1.1±0.9. CD40: 16.0±7.0 vs. 21.8±5.8). PHA-stimulated lymphocytes did not show any changes in the induction of CD25, CD69, or CD95. In summary, high concentrations of As and F alter the expression patterns of CD25 and CD40 at both the genetic and protein levels. These changes could decrease immune responses in children exposed to As and F.”
“Studies of As-exposed populations have demonstrated unusual gene expression profiles for cell cycle control-related factors, transcription factors, and inflammatory molecules”
“Using microarrays, our group determined that the IL-6, IL-1β, TNF-α, TGF-β, CD40, IL-2RA, CD40L, CD25, ENA78, SURVIVIN, XIAP, and IAP-1 genes are differentially expressed in adults chronically exposed to high concentrations of As (22.5–148.9 μg/L) and F (2.3–5.4 mg/L) compared to the control group (As: 0.3–1.4 μg/L; F: 0.1–0.7 mg/L)”<-Not strong height altering genes except possibly TGF-Beta.
“cIAP-1 expression was positively correlated with age and height”<-Can clAP-1(also known as clasp1) affect height?
XIAP and TNFalpha were also associated with height but not above statistical significance but closer than the rest of the genes. p<0.15. TNFalpha definitely affects height but there is it is likely that there’s an optimal quantity of TNFalpha for height growth rather than it just being good or bad.
This study could link Clasp1 to height growth:
Association of TALS developmental disorder with defect in minor splicing component U4atac snRNA.
“The spliceosome, a ribonucleoprotein complex that includes proteins and small nuclear RNAs (snRNAs), catalyzes RNA splicing through intron excision and exon ligation to produce mature messenger RNAs, which, in turn serve as templates for protein translation. We identified four point mutations in the U4atac snRNA component of the minor spliceosome in patients with brain and bone malformations and unexplained postnatal death [microcephalic osteodysplastic primordial dwarfism type 1 (MOPD 1) or Taybi-Linder syndrome (TALS); Mendelian Inheritance in Man ID no. 210710]. Expression of a subgroup of genes, possibly linked to the disease phenotype, and minor intron splicing were affected in cell lines derived from TALS patients. Our findings demonstrate a crucial role of the minor spliceosome component U4atac snRNA in early human development and postnatal survival.”
” The TALS phenotype includes marked intrauterine and postnatal growth retardation; short, bowed long bones with severe delay in epiphyseal maturation”
“The U4atac snRNA is located within intron 2 of the CLASP1 gene, –682 base pairs (bp) to –556 bp upstream of exon 3. Because of this, TALS mutations could, in theory, alter CLASP1 splicing and/or expression. In silico splice site predictions, real time–quantitative polymerase chain reaction (RT-qPCR) analysis of CLASP1 mRNA levels, and an RT-PCR study of CLASP1 exon 3 splicing in TALS patients revealed no effects of TALS mutations on CLASP1 expression or splicing”
However, the study seems to show a lack of connection of CLASP1 to dwarfism.