AKG for height augmentation?

According to Wikipedia AKG contains 2-oxyglutaric acid: Olympian Labs - A-Akg, 90 g powder.  2-oxyglutaric acid is a synonym for α-ketoglutarate.

The effect of dietary administration of 2-oxoglutaric acid on the cartilage and bone of growing rats.

"2-Oxoglutaric acid (2-Ox), a precursor to hydroxyproline, [proline, glutamate, arginine and asparagine], exerts protective effects on bone development during different stages of organism development. [What's] the influence of dietary 2-Ox supplementation on the growth plate, articular cartilage and bone of growing rats? A total of twelve male Sprague-Dawley rats were used in the study. Half of the rats received 2-oxoglutarate at a dose of 0·75 g/kg body weight per d in their drinking-water.  Rats receiving 2-Ox had an increased body mass and absolute liver weight. Femoral length and bone mineral density, overall thickness of growth plate and the thickness of femoral articular cartilage{so 2-oxoglutaric acid could also cause a miniscule increase in height in adults} were also increased. Dietary supplementation with 2-Ox to growing rats exerts its effects mainly on cartilage tissue, having only a slight influence on bone."

"2-Ox, together with Fe2+, have been proposed to be active participants in the conversion of proline to hydroxyproline, the main amino acid of bone collagen. Moreover, 2-Ox acts as a cofactor for Fe2+ absorption from the intestine"<-Iron decreases FGF23, which affects height.

" resting and calcification zones of the femoral growth plate and calcification zone of the tibial growth plate were significantly thicker in the [supplement] group"

A stands for supplement group, C stands for control.  Above is femoral growth plate.

Above is tibial growth plate.

Above is the increase in articular cartilage thickness and the difference is pretty big(28%).  Unfortunately, articular cartilage thickness only makes a small difference in height.  Perhaps if it affects the intervertebral discs as well.

"2-Ox is a N scavenger and a source and precursor of glutamine, synthesised in human skeletal muscles, which improves and stimulates protein synthesis and inhibits protein degradation in skeletal muscles"<-Thus another connection between muscle and height growth.

" The question that arises is whether 2-Ox is the cause of the cartilage thickening, in particular the articular cartilage, or whether the bone loading (by a heavier body mass) is the key factor stimulating better nutrient utilisation facilitated by 2-Ox abundance?"<-So the heavier bone mass is a confounding variable.  Would anything that makes heavier bones stimulate GP's and AC's in the same way?  It should be noted that LSJL makes bones heavier too but other effects unrelated to bone weight have been established due to LSJL such as fluid flow and an increase in pressure within the bone.

"Within the femur articular cartilage, the most loaded point of the knee joint, thickening was the predominant reaction to additional 2-Ox."

"Unlike articular cartilage, growth plate cartilage is a tissue which is sensitive to load and overload and may slow down the growth, which is mostly related to the hypertrophy zone of this particular tissue. And yet we observed an increase in growth plate thickness, in the present study, in the rats treated with 2-Ox. "

The question is also would byproducts of 2-Ox like arginine have similar effects and thus there would be no need for both.  Since AKG is so promising in bodybuilding perhaps there are answers.

But so far, based on the results in this study it seems possible that AKG supplementation may increase height by miniscule amounts via articular cartilage thickness it may also help people grow taller via their growth plates.

The long‐term effect of α‐ketoglutarate, given early in postnatal life, on both growth and various bone parameters in pigs

"The long-term effect of α-ketoglutarate (AKG) given for 21–24 days post-partum, on the skeleton of commercial pigs, was investigated. In experiment A, 12 pigs were given AKG [0.1 g/kg of body weight (b.w.) per day per os], while 12 controls were administered vehicle. At day 169, the left and right femur, humerus and sixth ribs were analysed for mechanical and geometrical properties and quantitative computed tomography. In experiment B, 32 piglets were divided equally into an AKG group (0.3 g/kg of b.w. per day) or a control group. Blood, taken at days 24 and 53 was analysed for plasma 17 β-oestradiol. The main bone effect of AKG was to increase bone length in the sixth rib (7.3%, p < 0.01), ultimate strength (23%, p < 0.05), Young´s modulus (52%, p < 0.001) and maximum elastic strength (31%, p = 0.056) compared with controls. In both experiments, AKG preferentially increased the growth of female piglets, whilst for male piglets AKG had the opposite effect. In addition, AKG elevated plasma 17 β-oestradiol levels compared to those of controls at the end of the period of treatment (20%, p = 0.002). It is concluded that AKG has long-term effects on rib properties when given early in postnatal life whilst it elevates plasma 17 β-oestradiol levels only so long as it is being administered."

So AKG may increase height in an estrogen mediated way.  Meaning it may not increase height in all circumstances.  Couldn't get the full study.

Locally Delivered Metabolite Derivative Promotes Bone Regeneration in Aged Mice

"Repair of large bone defects is still a major challenge, especially for the aged population. One alternative to address this issue is using the biomaterial-mediated bone morphogenetic protein 2 (BMP2) delivery technique, although high-dose BMP2 can cause serious concerns. α-Ketoglutarate (AKG) is a key intermediate in the tricarboxylic acid cycle and emerging as an intriguing antiaging molecule to extend the life/health span in different organisms. While one recent study indicates that the dietary AKG could significantly reduce bone loss and improve bone anabolism in aged mice, the therapeutic potential of AKG for bone regeneration has not been studied so far. Moreover, the poor cell permeability, large dose requirement, and long-term systemic administration of AKG hinder its applications in clinics and cellular mechanism studies. Dimethyl α-ketoglutarate (DMAKG) is a cell-permeable derivative of AKG with promising potential, although its role in osteogenesis is still elusive. Therefore, we aim to study the potential roles of DMAKG for bone regeneration using both in vitro cell culture and in vivo aged mouse models. Compared to AKG, our data indicated that DMAKG could more effectively improve osteoblastic differentiation. In addition, DMAKG significantly reduced adipogenic differentiation and improved osteogenic differentiation of a mouse multipotential mesenchymal stem cell line. Importantly, our result indicated that DMAKG significantly promoted BMP2-induced osteoblastic differentiation and mineralization in vitro. Moreover, DMAKG could not only significantly mitigate lipopolysaccharide (LPS)-stimulated inflammation in macrophages but also largely rescue LPS-inhibited osteoblastic differentiation. Consistently, our in vivo study demonstrated that gelatin scaffold-mediated local release of DMAKG significantly promoted BMP2-induced bone regeneration in aged mice, which is compromised by chronic inflammation and high adipogenesis. Overall, we, for the first time, report that locally delivered metabolite derivative, DMAKG, could improve BMP2-induced bone regeneration in aged mice. Our study suggests DMAKG has a promising therapeutic potential for bone regeneration through modulating local inflammation and stem cell differentiation."

Couldn't get this full study.

The Protective Role of Alpha-Ketoglutaric Acid on the Growth and Bone Development of Experimentally Induced Perinatal Growth-Retarded Piglets

"The effect of alpha-ketoglutaric acid (AKG) supplementation to experimentally-induced, perinatal growth-retarded piglets was examined. Sows were treated with a synthetic glucocorticoid (Gc) during the last 25 days of pregnancy, and after the birth, piglets were randomly divided into three groups depending on the treatment. The Gc/Gc + AKG and Gc/AKG groups born by Gc-treated sows after the birth were treated with Gc or Gc + AKG for 35 days. Significantly lower serum growth hormone, IGF-I, osteocalcin, leptin, and cortisol concentrations were observed in the Gc/Gc + AKG group, while the bone alkaline phosphatase activity was significantly higher. Serum insulin concentration was higher in the control group. Serum alanine, lysine, histidine, and tryptophan concentrations were higher in the Gc/Gc + AKG and Gc/AKG groups. The perinatal action of Gc significantly affects histomorphometry of articular cartilage and trabecular bone and bone mechanics. The results clearly showed that dietary AKG had positive effects with regards to the profile of free amino acids. Taking into account the function of AKG as an energy donor and stimulator of collagen synthesis, it can be concluded that the anabolic role of AKG may be the main mechanism responsible for its protective effect against the GC-induced perinatal intensified catabolic state."

"Many studies have shown that glutamine and its derivatives, such as glutamate, can counteract growth inhibition resulting from a negative nitrogen balance in the body as a result of stress, malnutrition, and a poorly balanced diet. Glutamine is a conditionally essential amino acid found mainly in skeletal muscle cells and accounts for more than half of the total pool of free amino acids in the body; it is the main amino acid in the cerebrospinal fluid. In the case of glutamine deficiency, glutamine can be produced from other amino acids, causing quantitative and qualitative losses in the pool of amino acids necessary primarily for muscles. Alpha-ketoglutaric acid (AKG; 2-oxoketoglutaric acid, 2-Ox), the precursor of glutamine, is a key intermediate in many metabolic pathways, including the Krebs cycle "

Item	Control	Gc/Gc + AKG	Gc/AKG	p-Value
Reserve zone, μm	382 ± 46 b	287 ± 34 a	374 ± 45 b	<0.001
Proliferative zone, μm	133 ± 27 a	243 ± 40 b	141 ± 45 a	<0.001
Hypertrophy zone, μm	108 ± 26	105 ± 22	96 ± 16	0.382
Calcification zone, μm	163 ± 42 b	115 ± 18 a	131 ± 29 a,b	0.002

"AKG is a precursor of glutamine and glutamate. Glutamine is synthesized in living organisms from glutamic acid and does not need to be present in food. It constitutes over 60% of all muscle-building amino acids, which are its largest reservoir. Under unfavorable conditions (stress, illness, exercise), the need for glutamine (an important energy source for many cells) increases rapidly, which thus reduces its supply. The body produces small amounts of this amino acid, but under conditions where there is a large deficit, glutamine is obtained from other sources, such as skeletal muscles as a result of catabolic reactions. The administration of AKG prevents this glutamine loss from muscles"<-so AKG should have only beneficial effects.