Curculigo orchioides, a traditional Chinese medicinal plant, prevents bone loss in ovariectomized rats.
"Curculigo orchioides (CO) has a long history in the treatment of postmenopausal osteoporosis in traditional Chinese medicine. The present study was designed to investigate the protective effects of ethanol extracts of CO on ovariectomy-induced bone loss.
Sixty female (4.5-month-old) Sprague-Dawley rats were assigned to sham and OVX groups. The OVX rats were further divided into five subgroups treated respectively, with vehicle, nylestriol (1 mg/kg, i.g.) and CO extract (0.5, 1.0, and 2.0 g/kg, i.g.) for 12 weeks. Bone mineral density (BMD) and bone mineral content (BMC) were measured by peripheral quantitative computerized tomography (pQCT) densitometry. Serum phosphorus, calcium, ACTH, corticosterone, deoxypyridinoline crosslinks to creatinine ratio (DPD/Cr), alkaline phosphate (ALP), tartrate-resistant acid phosphatase (TRAP), osteoprotegerin (OPG), IL-6, and TNF-alpha were also determined.
Administration of CO extract prevented bone loss in the trabecular bone of the tibia in ovariectomized rats without affecting the weight of the body and the uterus, and increased serum phosphorus, calcium, and OPG levels, decreased serum DPD/Cr, TRAP, ACTH, and corticosterone levels, but did not alter serum TNF-alpha, IL-6, and ALP levels in ovariectomized rats.
CO ethanol extract has a definite protective effect on bone loss in ovariectomized rats by inhibiting bone resorption and increasing serum phosphorus and calcium levels, without affecting bone formation. Therefore, CO can be considered a potential antiosteoporosis herbal plant, although more studies are needed to clarify its real potential chemical constituents and their mechanism of action."
Osteoprotegerin is an inhibitor of osteoclasts. It inhibits corticosterone which is catabolic hormones(cortisol). It decreases ACTH which is bad as ACTH is involved with calcium signaling and may help increase height. TRAP is an anabolic compound but it is activated by osteoclasts which explains why it was reduced by an osteoclast inhibitor. A lower DPD/Cr ratio indicates less bone resporption.
Here's a study that suggests that Curculigo Orchioides can increase Alkaline Phosphatase activity(though in the previous study an increase in phosphorus activity would indicate an increase in removing phosphorus groups from molecules which Alkaline Phosphatase does).
Elevated Alkaline Phosphatase activity results in enlarged bone(like Paget's Disease but that involves an increase in bone absorption which Curculigo Orchioides inhibits)
Antiosteoporotic activity of phenolic compounds from Curculigo orchioides.
"Six phenolic compounds isolated from Curculigo orchioides, including 2,6-dimethoxy benzoic acid (1), curculigoside A (2), curculigoside B (3), curculigine A (4), curculigine D (5) and 3,3',5,5'-tetramethoxy-7,9':7',9-diepoxylignan-4,4'-di-O-beta-D-glucopyranoside (6), together with the ethanol extract of Curculigo orchioides were evaluated for their activity on osteoblasts in neonatal rat calvaria cultures and multinucleated osteoclasts derived from rat marrow cells so as to characterize the antiosteoporotic components of this plant and explore the relationship of chemical structure with antiosteoporotic activity. The proliferation of osteoblast was assayed by MTT methods. The activity of ALP (alkaline phosphatase) and TRAP (tartrate-resistant acid phosphatase) was measured by p-nitrophenyl sodium phosphate assay. The TRAP stain was used to identify osteoclast in morphology. The resorption pit area on the bone slices formed by osteoclast was measured by computer image processing. The ethanol extract exhibited stimulatory effect on both the osteoblast proliferation and the ALP activity. Six compounds all increased the osteoblast proliferation, and compounds (1), (2) and (4) also slightly increased the osteoblastic ALP activity. Compounds (1), (2), (3), (6) and the ethanol extract decreased area of bone resorption pit, osteoclastic formation and TRAP activity. These results indicated that phenolic compounds are antiosteoporotic chemical constituents from Curculigo orchioides, and their activities are related with chemical structures."
The reason why the first study didn't increase ALP activity could be due to the fact that it was performed on ovariectomized rats(rats who don't produce estrogen which is essential for building bone). An increase in Alkaline Phosphatase could result in height growth if the bone growth occurs on the longitudinal ends of the bone(the subchondral plate).
Curculigo Orchioides could increase height by inhibiting osteoclast activity and by increasing Alkaline Phosphatase levels. Though Osteoclasts are needed so we don't want to inhibit them too much.
And this study finds a link between elevated ACTH and growth:
Possible relationship between elevated plasma ACTH and tall stature in familial glucocorticoid deficiency.
"Familial glucocorticoid deficiency (FGD) is characterized clinically by severe glucocorticoid deficiency associated with failure of adrenal responsiveness to ACTH but not with mineralcorticoid deficiency. Excessive growth was described previously in some patients with FGD, many of whom were shown to have mutations in the ACTH receptor gene. The mechanisms responsible for their excessive growth are unknown. We analyzed the ACTH receptor gene in three patients with FGD and discussed the causes of excessive growth in FGD. No mutations were detected in the coding and promoter regions of the ACTH receptor gene of one female patient who had tall stature (+ 2.41S.D.) and advanced bone age (10 years 9 months) when she was 4 years 9 months old. Her plasma ACTH level had been elevated until then (124-2,684 pg/ml). Moreover, plasma estradiol was elevated for her age (21.3 pg/ml), and it decreased in response to the dexamethasone suppression test (from 25.4 to 6.9 pg/ml). Elevated plasma estradiol was apparently related to the increase in plasma ACTH and played a major role in excessive growth in this patient. On the other hand, the genetic analysis showed that the other two patients who were siblings were homozygous for the R137W mutation[So for FGD to cause tall stature you need normal ACTH receptors]. Clinically, they responded well to hydrocortisone replacement therapy with almost normal plasma ACTH levels. Although all patients with the R137W mutation reported previously were tall, our patients were of normal height. We speculate that the major causes of excessive growth in FGD are not only from ACTH receptor mutation, but also from the action of elevated plasma ACTH."
So maybe elevating plasma ACTH can make you taller? Although it's not clear whether this tall stature in childhood resulted in taller adult height.
High plasma ACTH levels correlates with high estradiol levels. Here's a study that explains why elevated ACTH levels may affect height:
ACTH enhances chondrogenesis in multipotential progenitor cells and matrix production in chondrocytes.
"The association of melanocortin peptide overproduction with enhanced linear growth prompted the current investigation of adrenocorticotropin hormone (ACTH) effects on multipotential chondroprogenitor populations and committed chondrocytes in culture. Two multipotential progenitor populations, rat bone marrow stromal cells (BMSC) and the clonal multipotential cell line RCJ3.1, and two committed chondrocyte populations, resting chondrocytes (RC) isolated from the rib of young rats and the chondrocyte restricted cell line RCJ3.1C5.18 (C5.18), were cultured in differentiation medium plus or minus ACTH. Alcian blue stain was used to quantitate proteoglycan matrix production in all populations treated with a range of ACTH concentrations. Changes in proliferation due to ACTH treatment of all cell types were measured using 3H-thymidine incorporation. Differences in matrix production of ACTH-treated and -untreated RC and C5.18 cells were determined using 3H-proline incorporation. Relative transcript expression of the chondrocyte matrix proteins collagen type II (COLL II) and aggrecan (AGR) in treated and untreated cells was analyzed by Northern blot. Collagen type X (COLL X), a marker of hypertrophic differentiation, was measured in committed chondrocytic populations. Western analysis was used to detect the melanocortin-3 receptor (MC3-R), which was a suspected mediator of the ACTH signal. Matrix deposition was dose-dependently increased by ACTH in all cell populations as measured by alcian blue stain. ACTH treatment increased proliferation in multipotential progenitor populations (BMSC and RCJ3.1) while proliferation was decreased in committed chondrocyte populations (RC and C5.18). Total protein and total cell-associated collagen production were significantly increased by ACTH treatment in committed populations. Relative COLL II and AGR transcript expressions were significantly increased in both the RC- and C5.18-committed population and very significantly increased in the progenitor populations. Additionally, collagen type X expression was detected earlier and in greater abundance in ACTH-treated committed chondrocyte populations. Finally, the melanocortin-3 receptor was detected in all examined cell types by Western blot. These data show that ACTH promotes the development of the chondrocyte phenotype from multipotential mesenchymal progenitor populations and increases matrix production and differentiation of committed chondrocytes."
"With melanocortin-4 receptor (MC4-R) deficiency, the most common form of monogenic obesity, this phenomenon of overgrowth is especially acute. MC4-R deficiency, like most forms of obesity, is associated with overeating "
"When FGD patients are treated with glucocorticoid, their ACTH levels are reduced and their growth patterns normalize somewhat"
"Doses of 10−9 to 10−7 M of ACTH are within the physiologic range of melanocortin peptide seen in FGD and with stress response in obesity"<-Thus we may want to get our levels of ACTH to these.
"the concentration of ACTH that elicited the strongest matrix response [was] (10−7 M)"
"the possibility that ACTH is involved in the recruitment of chondrocytes from the stem layer into the proliferative zone"<-So ACTH might be able to induce chondrogenic differentiation?
"the obligatory second messenger for ACTH is known to be cAMP"
"cAMP induces receptor-mediated Ca (2+) influx"