Grow taller with ACTH(Magnesium)

Magnesium may help increase ACTH levels: Nature Made High Potency Magnesium 400 mg - 150 Liquid Softgels

Systemic and local ACTH produced during inflammatory states promotes osteochondrogenic mesenchymal cell differentiation contributing to the pathologic progression of calcified atherosclerosis.

"There are many well-known roles for the proopiomelanocortin (POMC) derived peptides and their receptors, the melanocortin receptors (MC-R). The focus here is on the evolving role of the melanocortin system in inflammation. Chronic inflammatory states such as those occurring in diabetes and obesity are associated with both a hyperactive hypothalamic-pituitary-adrenal (HPA) axis as well as increased incidence of atherosclerosis. An inflammation-induced hyperactive HPA axis along with increased leukocyte infiltration can lead to significant exposure to melanocortin peptides, particularly ACTH, in an inflamed vasculature. Mesenchymal progenitor cells are present throughout the vasculature, express receptors for the melanocortin peptides, and respond to ACTH with increased osteochondrogenic differentiation. Coupled to the increased exposure to ACTH during HPA hyperactivity is increased glucocorticoid (GC) exposure. GCs also promote chondrogenic differentiation of mesenchymal progenitors and increase their expression of MC-R as well as their expression of POMC and its cleavage products. It is hypothesized that during inflammatory states systemically produced ACTH and glucocorticoid as well as ACTH produced locally by macrophage and other immune cells, can influence and potentiate mesenchymal progenitor cell differentiation along the osteochondrogenic lineages."

"glucagon administration or the ingestion of a high carbohydrate meal will elicit an exaggerated HPA response, with both elevated ACTH and cortisol"

"POMC is the precursor peptide to ACTH and the melanocortin family of endocrine peptides. POMC is traditionally known as an endocrine prohormone secreted and processed by corticotropes of the anterior pituitary in response to hypothalamic corticotrophin releasing hormone (CRH). POMC is processed by prohormone convertases (PCs) into the melanocortin peptides. Cleavage via PC1/3 produces adrenocorticotropic hormone (ACTH) and β-lipotropic hormone (β-LPH), whereas PC2 is required for the generation of α-melanocyte-stimulating hormone (α-MSH), β-MSH, γ-MSH and the endorphins"

"Ligand binding to the MC-R results in the activation of second messenger pathways such as accumulation of adenylyl cyclase and the mobilization of intracellular calcium ([Ca2+]i)"

" the expression MC2-R, MC3-R and MC5-R [is present] in rat bone marrow derived mesenchymal progenitors"

"Factors that increase the differentiation of both chondrocytes and osteoblasts from progenitors also increase [Ca2+]i"

"calcium ionophore induced elevations in [Ca2+]i can promote chondrogenesis though a calcineurin/nuclear factor of activated T-cells (NFAT) axis"

Examination of the efficacy of acute L-alanyl-L-glutamine ingestion during hydration stress in endurance exercise.,  shows a possible but not a clear influence of glutamine on ACTH levels.

Effects of exhaustion and calcium supplementation on adrenocorticotropic hormone and cortisol levels in athletes., states that calcium supplementation does not affect ACTH but that strenuous excercise does and that may have trickle down effects to your bone marrow.

Magnesium can also increase ACTH according to Adrenocorticotropic hormone and cortisol levels in athletes and sedentary subjects at rest and exhaustion: effects of magnesium supplementation.  In sedentary individuals Magnesium increased ACTH levels by about 13%.  The dosage was 10mg per bodyweight per day.

Fish oil may inhibit ACTH levels according to Effects of fish oil on the neuro-endocrine responses to an endotoxin challenge in healthy volunteers.

2-DG may help improve ACTH levels but that supplement is not available: Dietary supplementation with 2-deoxy-D-glucose improves cardiovascular and neuroendocrine stress adaptation in rats.

Most amino acids may increase ACTH levels:

Acute amino acids supplementation enhances pituitary responsiveness in athletes.

"In a double blinded counterbalanced experimental protocol, 10 moderately trained male athletes performed the pituitary stimulation test 60 min after a single oral administration of a placebo (P1-AS) or an amino acid mixture solution (AS) (L-arginine hydrochloride 100 mg x kg(-1) + L-ornithine hydrochloride 80 mg x kg(-1) + L-branched chain amino acids 140 mg x kg(-1): 50% L-leucine, 25% L-isoleucine, 25% L-valine) on two different occasions. Plasma ACTH, LH, FSH, GH, and cortisol were evaluated before (-60, -30, 0 min) and after (+15, +30, +45, +60, +90 min) the stimulation test.

The ACTH, LH and FSH response to CRH + GnRH was significantly higher in AS group both as absolute values and area under curve (AUC) values than in P1-AS group. Pre-test and post-test cortisol AUC levels were significantly higher in P1-AS group although a higher percent increase in post-test cortisol was found in AS group. The total GH-AUC was higher in AS group and, as expected, the absolute GH concentrations at different time points were not influenced by CRH + GnRH administration.

The amino acid mixture used enhanced the ACTH, LH, and FSH response to CRH + GnRH."

I know bodybuilders for years have advocated high carbohydrate meals post workout so the effectiveness of that can be used as data for possible effectiveness of ACTH manipulation for increasing LSJL effectiveness(since ATCH enhances chondrogenic differentiation).  And, maybe some bodybuilders can provide ACTH increase techniques.  ACTH might do nothing in normal growth plates but it may enhance differentiation response to stimulus like by LSJL.

LSJL downregulates NR4A1 which is an inhibitor of ACTH under hypoxic conditions(source: String 9.0).  LSJL downregulates SSTR4 which binds to ACTH.  LSJL upregulates NPY2R which reacts to ACTH.

ACTH promotes chondrogenic nodule formation and induces transient elevations in intracellular calcium in rat bone marrow cell cultures via MC2-R signaling.

"Adrenocorticotropic hormone (ACTH) is among several melanocortin peptide hormones that are derived from proopiomelanocortin (POMC).  In the presence of dexamethasone, ACTH dose-dependently increases chondrogenic nodule formation in bone marrow stromal cells (BMSC) from the Wistar Kyoto (WKY) rat. The nodules consist in condensed cells highly expressing alkaline phosphatase, Sox9 and type II collagen transcripts and a proteoglycan-rich matrix. These cells express three melanocortin receptors (MC-R), namely MC2-R, MC3-R and MC5-R and the melanocortin 2-receptor accessory protein (MRAP). Neither α-MSH, a strong agonist of MC5-R, nor γ(2)-MSH, a strong agonist of MC3-R, duplicates ACTH effects in rat BMSC. In addition, calcium flux has been examined as a mechanism for ACTH action at the MC2-R. Consistent with MC2-R and MRAP expression patterns in the BMSC cultures, ACTH-induced transient increases in intracellular calcium are increased with dexamethasone treatment. Neither α-MSH nor γ(2)-MSH affects calcium flux. Dexamethasone increases MC2-R and MRAP expression and POMC peptide expression and cleavage increasing the production of the lipolytic β-lipotropic hormone product. The effects of ACTH in rat BMSC enriched for mesenchymal progenitors are consistent with an MC2-R signaling mechanism, with dexamethasone being capable of regulating components of the melanocortin system in these cells."

"All five MCRs are expressed by mesenchymal progenitors"

"Dexamethasone increases the expression of proopiomelanocortin (POMC), prohormone convertase 1/3 (PC1/3) and the POMC cleavage product, β-lipotropic hormone (LPH), in rat BMSC cultures enriched for mesenchymal progenitors."

"calcium-ionophore-induced elevations in [Ca2+]i can promote chondrogenesis though a calcineurin/nuclear factor of activated T-cells axis"

"ACTH initiates a MC2-R-mediated pathway that induces transient increases in [Ca2+]i and elevates basal [Ca2+]i in these cells."

Magnesium enhances adherence and cartilage formation of synovial mesenchymal stem cells through integrins.

"Magnesium increased adhesion of human synovial MSCs to collagen, and this effect was inhibited by neutralizing antibodies for integrin α3 and β1. Magnesium also promoted synthesis of cartilage matrix during in vitro chondrogenesis of synovial MSCs, which was diminished by neutralizing antibodies for integrin β1 but not for integrin α3. Ex vivo analyses demonstrated that magnesium enhanced adherence of human synovial MSCs to osteochondral defects. In vivo studies in rabbits showed that magnesium promoted adherence at 1 day and cartilage formation of synovial MSCs at 2 weeks."

"human synovial cells had characteristics similar to those of MSCs."

"Pellets cultured in 5 mM magnesium produced more sGAG than pellets cultured in 0.8 mM magnesium"

"magnesium increased cartilage matrix synthesis through integrin β1 during in vitro chondrogenesis of synovial MSCs"

Unphysiologically high magnesium concentrations support chondrocyte proliferation and redifferentiation.

"The effect of unphysiologically high extracellular magnesium concentrations on chondrocytes, induced by the supplementation of magnesium sulfate, was studied using a 3-phase tissue engineering model. The experiments showed that chondrocyte proliferation and redifferentiation, on the gene and protein expression level, are enhanced. A negative influence was found during chondrogenesis where an inhibition of extracellular matrix formation was observed. In addition, a direct impact on chondrocyte metabolism, elevated magnesium concentrations also affected growth factor effectiveness by consecutive influences during chondrogenesis. All observations were dosage dependent."

Magnesium concentrations up to 10Mm accelerated proliferation while doses from 10-20 Mm reduced proliferation.

"with increasing magnesium concentrations the production of collagen type II increased. The
highest expression levels were obtained using only growth factors, and high (10–20mM) magnesium concentrations during redifferentiation in combination with a growth factor supported chondrogenesis. The expression of collagen type I was directly correlated to the expression of collagen type II"

TRPM6 and TRPM7 may mediate the pro-chondrogenic effects of magnesium.

Alterations in growth plate and articular cartilage morphology are associated with reduced SOX9 localization in the magnesium-deficient rat.

"We have evaluated growth plate and articular cartilage in rats following a 6 month dietary Mg restriction. Histomorphometry demonstrated significantly decreased distal femur articular cartilage chondrocyte density and decreased tibial growth plate width in experimental animals compared to controls. Growth plates of Mg-restricted animals showed reduced chondrocyte column formation. Extracellular matrix of both articular cartilage and growth plates in experimental animals contained reduced amounts of proteoglycans. Immunolocalization of Sox9 was decreased in both articular and growth plate cartilage in experimental animals compared to controls, suggesting that reduced Mg intake causes cartilage changes that may be secondary to reduced levels of the SOX9 transcription factor."

Magnesium levels were 1/3rd less in experimental versus control.