Grow Taller with Galangal?

Galangal is a supplement available for purchase that may have height increase implications: Thai Fresh galangal - 14 oz.

Effect of galangin supplementation on oxidative damage and inflammatory changes in fructose-fed rat liver.

"The study examined the effects of galangin (GA) on oxidative stress, inflammatory cytokine levels and nuclear factor-kappa B (NF-κB) activation in fructose-fed rat liver. Adult male albino Wistar rats were divided into 4 groups. Groups 1 and 4 received the control diet containing starch as the source of carbohydrate while groups 2 and 3 were fed a diet containing fructose. Groups 3 and 4 additionally received GA (100μg/kg, p.o) from the 15th day. At the end of 60 days, the levels of plasma glucose, insulin and triglycerides, insulin sensitivity indices and oxidative stress markers in the liver were determined. Cytokines of interest were assayed by ELISA and RT-PCR and NF-κB p65 nuclear translocation by Western blot and RT-PCR. Compared to control diet-fed animals, fructose-fed animals developed hyperglycemia, hyperinsulinemia, hypertriglyceridemia and insulin resistance (IR) (all p<0.01). GA prevented the rise in plasma glucose, insulin and triglycerides and improved insulin sensitivity[note though that insulin resistance may actually increase height]. Tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) levels in plasma and the mRNA and protein levels of TNF-α and transforming growth factor-β1(TGF-β(1)) in liver were significantly higher in fructose-fed rats than control rats[TGF-Beta1 is good for height growth, IL-6 can inhibit IL-1 which is bad for growth but IL-6 can have negative effects of it's own but it's likely better to have IL-6 over IL-1, TNF-alpha stimulates the degradation of the extracellular matrix which isn't always a bad thing]. However, treatment with GA downregulated the expression of these cytokines. Translocation of NF-κB into the nucleus was also increased in fructose diet-fed animals, which was prevented by GA[Blocking the translocation of NF-kappaB into the nucleus blocks the inhibitory effect of IL-1 on chondrogenesis]. These results suggest that GA prevents oxidative damage and has a downregulatory effect on the inflammatory pathway in liver of fructose-fed rats."

So Galangal may increase height by inhibiting NF-kappaB's negative effect on chondrogenesis.  This would help in both developing individuals and individuals who want to restore chondrogenesis by a method such as LSJL.

"Dysregulated production of IL-6 and TNF-a have been found to inhibit hepatic insulin receptor activation and downstream insulin signaling in vivo"-hepatic means liver.  IRS-1 competes with the growth plate for insulin activity.  The less IRS-1 activity the more insulin that goes to the growth plate.  So IL-6 and TNF-alpha may actually increase height if they inhibit IRS-1 signaling in bone.  But they also reduce insulin signaling which may negate this beneficial effect.

"Under insulin resistant conditions, liver injury is associated with the upregulation of a fibrogenic cytokine called transforming growth factorb1 (TGF-b1) resulting in increased synthesis and accumulation of extracellular matrix proteins like collagen."<-This would actually be a good thing to occur in bone.

Both Fructose and Galangal have functions that are both height stimulating and height inhibiting but it's likely worth it go the route of Galangal as it reduces cell damage.  The non-fructose eating and galangin eating mice had the 10g increase in body weight(over control) and height increase may have been involved in that increase.  Fructose with no Galangin had a 25g increase in body weight over GA+control.  Although, how much of that is related to bone length?  I sent an email to ask.

CON+Ga versus CON had no change in TNF-alpha or IL-6.  The total collagen content was almost twice as much in the Fructose groups versus other groups.  The total collagen content was lowest in the CON+GA group.

What I'd expect is that both CON+GA and Fructose groups would have greater height than controls.  GA via inhibition of NF-kappaB translocation and Fructose via increased insulin resistance.  Both groups had greater weight increase than controls.  But I think the GA path is preferable in the long run due to less cell damage.  Eventually, the best way would be to find a way to increase insulin, TGF-Beta1 expression, and insulin resistance(in IRS-1 not the growth plate and stem cells) without more inflammatory cytokine activation.  You'd think that may be possible by combining Fructose and Galangal but they seem to cancel each other out with the effects of Galangal winning.

Here's a study on catch-up growth and inflammatory cytokines to see which method is better insulin resistance or preventing cell death:

The restricted potential for recovery of growth plate chondrogenesis and longitudinal bone growth following exposure to pro-inflammatory cytokines.

"Childhood chronic inflammatory disease can be associated with transient and permanent growth retardation. This study examined the potential for spontaneous growth recovery following pro-inflammatory cytokine exposure. Murine ATDC5 chondrogenic cells and postnatal metatarsals were exposed to interleukin (IL)-1beta, IL-6 and tumour necrosis factor-alpha (TNFalpha), and their growth and proliferative capacity were determined following recovery. TNFalpha and IL-1beta reduced chondrocyte proliferation and aggrecan and collagen types II and X expression at minimum concentrations of 10 ng/ml and 0.1 ng/ml respectively. TNFalpha but not IL-1beta exposure led to increased caspase-3 activity and altered cellular morphology, consistent with reduced viability[So TNF-alpha exposure may result in permanent reductions in height growth]. Cytokine exposure particularly inhibited proteoglycan synthesis. This effect was dose and duration dependent. Compared with the control, IL-1beta and TNFalpha led to a 71% and 45% reduction in metatarsal growth after 8 days of exposure respectively (P < 0.05). An additive effect of IL-1beta combined with TNFalpha was observed (110% decrease; P < 0.05). Metatarsals exposed to IL-1beta or TNFalpha individually for a 2-day period, and allowed to recover spontaneously in the absence of cytokines for a further 6 days, showed normal growth trajectories. In combination, growth was 59% lower (P < 0.01) compared with control metatarsals at the end of the recovery period. Exposure to the combination for 4 days followed by a 4-day recovery period resulted in 87% decrement compared with controls (P < 0.05). IL-6 did not alter any parameter studied. IL-1beta and TNFalpha exert diverse inhibitory effects on ATDC5 chondrocyte dynamics and metatarsal growth. The extent of recovery following cytokine exposure depends on the duration of exposure, and may be incomplete following longer periods of exposure."

<-So it may be worthwhile to keep those cytokines in check with anti-oxidants.  TNF-alpha seeming to be the most damaging and IL-6 being the most potentially beneficial(having no seemingly negative effects on growth and positive effects elucidated elsewhere).

"IL-1β reduced cell proliferation, as assessed by [3H]thymidine uptake, at every concentration studied. However, TNFα only reduced cell proliferation at the higher concentrations of 100 ng/ml and 10 ng/ml"<-so ideally you'd want complete knockout of IL-1Beta.

"TNFα and IL-1β had an additive effect and reduced metatarsal growth by 110% of control values. By 6 days the combination of TNFα and IL-1β had resulted in an actual reduction of absolute length."<-So elevated levels can permanently damage height if only for 6 days so you don't want a permanent 6 days of inflammation.

"the cell culture studies suggest a possible pro-proliferative effect of IL-6"

"cytokines may induce a state of IGF-I resistance by reducing IGF-I signal transduction in chondrocytes by inhibiting insulin receptor substrate-1 phosphorylation"

So you don't want inflammation at any period as it may reduce growth and trying to induce the expression of IL-6 over TNF-alpha and IL-1Beta may be a potential way to induce height growth.

The natural flavonoid galangin inhibits osteoclastic bone destruction and osteoclastogenesis by suppressing NF-κB in collagen-induced arthritis and bone marrow-derived macrophages.

"galangin inhibited osteoclastogenic factors and osteoclast formation in bone marrow-derived macrophages and osteoblast co-cultured cells, and increased osteoprotegerin (OPG) levels in osteoblasts. Galangin and NF-κB siRNA suppressed RANKL-induced phosphorylation of the c-jun N-terminal kinase (JNK) and p38 mitogen-activated protein kinase (MAPK), but not AKT and extracellular signal-regulated kinase 1/2 (ERK1/2). Also, the JNK inhibitor SP600125 and p38 inhibitor SB203580 reduced RANKL-induced expressions of phospho-c-Jun, c-fos and NFATc1 genes during osteoclast development. In addition, galangin suppressed RANKL-induced phosphorylation of NF-κB, phospho-IκBα, inflammatory cytokines and osteoclast formation in bone marrow-derived macrophages."<-it's unclear how any of this could affect height growth.

Galangin decreases cartilage destruction is osteoarthritic mice.