Do fats and sugars affect your height gain?

 Considering that there are several Vitamin D related genes that influence height but there are some instances where Vitamin D intake does not affect adult height.  Although, the levels of glucose consumed versus starch and fructose affect the pathways related to Vitamin D rather than just Vitamin D levels.  Therefore, it is likely that glucose versus starch and fructose consumption may affect adult height rather than just a temporary decrease in growth rate.

Eating high glucose foods versus high fructose and to a much less extent high starch foods will only affect people with open growth plates but could result in a little bit more adult height.

Ctrl-F (*NEW*) for the new content.

People are always looking for a quick fix.  Rather than hard, strenuous exercise to increase height people want to take some height increase pill.  In this blog entry, I'm going to look at if dietary factors can affect human height.

Now, I'm considering "normal" foods.  Anything that you put in your body could be considered part of your body.  The definition of diet as per this article is any chemical that could be found regularly in food(so no supplements, although they do have chondroitin and glucosamine in liquid form now but it still isn't what I would consider mainstream food).

High-fat, sucrose diet impairs geometrical and mechanical properties of cortical bone in mice.

"Exposure to diets high in fat and sucrose can induce hyperinsulinaemia, affect Ca and Mg metabolism, and alter bone mineralisation and mechanical properties."

One possible explanation for how diets high in fat and sucrose alter bone mechanical properties is that unesterified long-chain saturated fatty acids have a melting point above body temperature and, with sufficient calcium in the intestinal lumen, form insoluble calcium soaps.

So, sugar and fat competes with bone for calcium absorption. So, a very high diet with high fat and glucose levels could impair height gain.  Remember, that reduced sensitivity to insulin has been associated with possible height gain.

"The present study assessed morphological and mechanical changes in a murine model exposed to a high-fat/sucrose (HFS) diet, as well as corresponding molecular and endocrine markers of bone turnover. "

Bone turnover however doesn't necessarily have an affect on human height.  The old confusion between bone modeling and remodeling(neither of which can increase height) is an example of how things can be misconstrued.   Bone turnover can affect the rate at which microfractures heal however and microfractures in the cortical bone can be possibly used to help you grow taller.

"Both body mass and percentage body fat were greater in mice fed HFS diet. After adjusting for body mass, tibial structural and morphological properties were adversely affected in the HFS cohort. Cortical thickness, cross-sectional area, and load at maximum were all significantly lower in mice fed HFS diet. Receptor activator of nuclear factor kappabeta ligand (RANKL) mRNA was significantly upregulated in HFS mice, but osteoprotegerin/RANKL mRNA ratio remained unchanged between cohorts[So OPG increased to compensate for the increase in RANKL leading to a change in bone turnover] . Moreover, cyclo-oxygenase-2[also known as COX2] mRNA tended to be increased in HFS. Thus, ingestion of an HFS diet had a significant adverse effect on mouse bone morphology and mechanics, and these effects were likely due to elevated osteoclast activity associated with the inflammatory state of obesity, and not necessarily osteoclast recruitment/proliferation."

The investigators in this study theorized that obesity caused the change in cortical thickness not the high fat/fructose diet.  Any diet with a caloric surplus could have potentially caused the same effect.  A high caloric diet may be beneficial but a high fat diet may cause additional inflammatory factors that can be bad for height growth.

Study on the effect of T-2 toxin combined with low nutrition diet on rat epiphyseal plate growth and development.

"The purpose of this study was to observe early lesions of rat epiphyseal plates and metaphysis caused by T-2 toxin and T-2 toxin combined with a low nutrition diet to determine possible pathogenic factors of Kashin-Beck disease (KBD). Ninety Wistar rats were divided into three groups. Group A was fed with a normal diet as control; group B was fed with a normal diet and T-2 toxin; and group C was fed with a low nutrition diet and T-2 toxin."

T-2 toxin is a mold byproduct of a fungus.

"After two weeks, the epiphyseal plate showed necrosis of chondrocytes in groups B and C. After four weeks, more obvious chondrocyte necrosis appeared. The positive rate of Lamellar necrosis in group C was significantly higher than that in groups B and A (P < 0.01). Metaphyseal trabecular bone showed sparse disorder and disruption in group C. T-2 toxin combined with a low nutrition diet could lead to more serious chondrocyte necrosis in the epiphyseal plate and disturb metaphyseal trabecular bone formation."

So, the T-2 toxin has the potential to decrease height by destroying chondrocytes. Chondrocytes are the basis for height growth in the growth plates.  This shows you how detrimental toxins can be in terms of growing taller.

Dietary patterns in Canadian men and women ages 25 and older: relationship to demographics, body mass index, and bone mineral density.

"The objective of the study was to determine whether dietary patterns in men (ages 25-49, 50+) and women (pre-menopause, post-menopause) are related to femoral neck bone mineral density (BMD) independently of other lifestyle variables, and whether this relationship is mediated by body mass index."

The BMI is a perfect example of how people cling to something because it's the popular thing rather than because it's the correct thing.  The BMI is only useful for populations as the deviations average out.  Their is too much internal differences in bone size within individuals for a tool like the BMI to be useful.  Further, the BMI doesn't account for things like on average people's wingspans being larger than their height.

"We identified two underlying dietary patterns using factor analysis and then derived factor scores. The first factor (nutrient dense) was most strongly associated with intake of fruits, vegetables, and whole grains. The second factor (energy dense) was most strongly associated with intake of soft drinks, potato chips and French fries, certain meats (hamburger, hot dog, lunch meat, bacon, and sausage), and certain desserts (doughnuts, chocolate, ice cream). The energy dense factor was associated with higher body mass index independent of other demographic and lifestyle factors, and body mass index was a strong independent predictor of BMD. Surprisingly, we did not find a similar positive association between diet and BMD. In fact, when adjusted for body mass index, each standard deviation increase in the energy dense score was associated with a BMD decrease of 0.009 (95% CI: 0.002, 0.016) g/cm2 for men 50+ years old and 0.004 (95% CI: 0.000, 0.008) g/cm2 for postmenopausal women. In contrast, for men 25-49 years old, each standard deviation increase in the nutrient dense score, adjusted for body mass index, was associated with a BMD increase of 0.012 (95% CI: 0.002, 0.022) g/cm2."

BMD density was measured by dual x-ray absorptiometry so bone size could have been increased by increased diet.  Eating more was associated with increased BMD.  Now BMD may not be a causal way to increase height but it is a good measure of anabolism in the bone.  The reason that age had the affect of lowering BMD instead of racing BMD with energy dense score could possibly be that men over 50 had lower activity levels.

Regulation of Mesenchymal Stem Cell Chondrogenesis by Glucose through Protein Kinase C/Transforming Growth Factor Signaling.

"The extent of chondrogenesis of hMSCs previously cultured with different concentrations of glucose was evaluated. Transforming growth factor-beta (TGF-β) signaling molecules and protein kinase C (PKC) were analyzed to identify the role of these molecules in the regulation of glucose on chondrogenesis. In addition, hMSCs in high-glucose expansion culture were treated with the PKC inhibitor to modulate the activity of PKC and TGF-β signaling molecules.
High-glucose maintained hMSCs were less chondrogenic than low-glucose maintained cells upon receiving differentiation signals. High-glucose culture increased the phosphorylation of PKC and expression of type II TGF-β receptor (TGFβRII) in pre-differentiation hMSCs. However, low-glucose maintained hMSCs became more responsive to chondrogenic induction with increased PKC activation and TGFβRII expression than high-glucose maintained hMSCs during differentiation. Inhibiting the PKC activity of high-glucose maintained hMSCs during expansion culture upregulated the TGFβRII expression of chondrogenic cell pellets, and enhanced chondrogenesis."

"During chondrogenic induction, high-glucose medium enhances chondrogenesis of chick mesenchymal cells, in comparison with low-glucose medium"

"high-glucose expansion culture reduces the proliferation of hMSCs"

"TGF-β ligand binds to type II TGF-β receptor (TGFβRII) to form a heterodimeric complex with type I TGF-β receptor (TGFβRI), which phosphorylates downstream signaling molecule Smad2/3. Phosphorylated Smad2/3 forms a heteromeric complex with Smad4, acting as a transcriptional activator to regulate the activity of TGF-β-responsive genes, including Sox9 for chondrogenesis"

"Human MSCs transfected with the TGF-β1 or TGF-β2 gene have been shown to induce chondrogenesis with the production of cartilage-related collagen type II."

"Human bone marrow-derived MSCs were isolated from femoral heads of 3 patients between 25 to 50 years of age who underwent total hip arthroplasty"

"[The human MSCs] expressed CD73, CD90, and CD105, but not CD34 and CD45"

"HGMCs grew slower than LGMCs"

"at day 9, the levels of mRNA expression of cartilage-related markers Sox9 and aggrecan of HGMC pellets were significantly downregulated, and at day 22, the expression levels of aggrecan and collagen type II of HGMC pellets were also significantly decreased, compared to those of LGMC pellets."

During differentiation TGFBRI expression was barely detectable in either mesenchymal group and TGFBRII was downregulated in the High-Glucose group versus the Low-Glucose group.  Smad3-p and PKC-p were lower in HGMC pellets than LGMC.

Pre-differentiation PKC-p was actually higher in HGMC than LGMC.  Inhibition of PKC during pre-differentiation culture can increase PKC and TGFBRII levels during chondrogenesis.  At 14 days of chondrogenesis, pre-differentiation chondrocytes treated with PKC inhibitor had higher levels of Acan, Col2, and Col9.

"high-glucose chondrogenic culture is essential for maintaining matrix structural integrity"

Glucose: an energy currency and structural precursor in articular cartilage and bone with emerging roles as an extracellular signaling molecule and metabolic regulator.

"Glucose is vital for osteogenesis and chondrogenesis, and is used as a precursor for the synthesis of glycosaminoglycans, glycoproteins, and glycolipids. Glucose sensors are present in tissues and organs that carry out bulk glucose fluxes (i.e., intestine, kidney, and liver). The beta cells of the pancreatic islets of Langerhans respond to changes in blood glucose concentration by varying the rate of insulin synthesis and secretion. Neuronal cells in the hypothalamus are also capable of sensing extracellular glucose. Glucosensing neurons use glucose as a signaling molecule to alter their action potential frequency in response to variations in ambient glucose levels. Bone cells can influence (and be influenced by) systemic glucose metabolism. Cartilage and bone cells are sensitive to extracellular glucose and adjust their gene expression and metabolism in response to varying extracellular glucose concentrations."

"The transport of sugar across the plasma membrane of mammalian cells is mediated by members of the GLUT/SLC2A family of facilitative sugar transporters and the SGLT/SLC5A family of Na+-dependent sugar transporters"

"GLUT1, GLUT3, and GLUT4 are high-affinity transporters whereas GLUT2 is a low-affinity transporter; GLUT5 is primarily a fructose carrier " GLUT1 is expressed in articular cartilage and IVD cells.

"IVD is anatomically and functionally very similar to cartilage although in contrast to cartilage it develops from notocordal cells rather than mesenchymal cells"

"chondrocytes express multiple isoforms of the GLUT/SLC2A family"

"Chondrocytes are capable of adjusting to high and low glucose concentrations by changing the protein levels of GLUT1"

"OA chondrocytes exposed to high glucose were unable to down-regulate GLUT1. OA-derived chondrocytes accumulated more glucose and produced more ROS."

GLUT1 and GLUT4 are expressed in murine endochondral bone formation.

"high d(+)glucose may alter RANKL-induced osteoclast formation by inhibiting redox-sensitive NF-kappaB activity through an anti-oxidative mechanism."

"Mature osteoclasts rely on the citric acid cycle and mitochondrial respiration to generate high levels of ATP production for acid secretion and bone resorption."

" glucose metabolism is increased during osteoclast differentiation resulting in a metabolic shift toward accelerated glucose metabolism at an early stage of RANKL-stimulated osteoclast differentiation. Increased mitochondrial oxidative phosphorylation will then result in elevated ATP production and enhanced osteoclast differentiation."

"osteocalcin{up in LSJL} [is a] regulator of pancreatic insulin production and glucose metabolism"

"osteocalcin deficiency in knockout mice leads to decreased insulin and adiponectin secretion, insulin resistance, higher serum glucose levels, and increased adiposity"

Perinatal maternal dietary supplementation of ω3-fatty acids transiently affects bone marrow microenvironment, osteoblast and osteoclast formation, and bone mass in male offspring.

[Omega3-fatty acids]

"[Does] maternal supplementation with ω3-polyunsaturated fatty acids (n3FA) [improve] offspring bone growth and adult bone mas?. Female rats were fed a diet containing 0.1% (control, n = 10) or 1% (n3FA, n = 11) docosahexanoic acid (DHA) during pregnancy and lactation. Offspring were weaned onto a control rat chow diet. Tibial growth plate and metaphysis structure, osteoblast/osteoclast density and differentiation, and gene expression were assessed in offspring at 3 wk (weaning), 6 wk (adolescent), and 3 months (adult). Maternal n3FA supplementation elevated offspring plasma n3FA levels at 3 and 6 wk. Although total growth plate heights were unaffected at any age, the resting zone thickness was increased in both male and female offspring at 3 wk. In n3FA males, but not females, bone trabecular number and thickness were increased at 3 wk but not other ages. The wk 3 n3FA males also exhibited an increased bone volume, an increased osteoblast but decreased osteoclast density, and lower expression of osteoclastogenic cytokines receptor activator of nuclear factor-κB ligand, TNF-α, and IL-6. No effects were seen at 6 wk or 3 months in either sex. Thus, perinatal n3FA supplementation is associated with increased bone formation, decreased resorption, and a higher bone mass in males, but not in females, at weaning; these effects do not persist into adolescence and adulthood and are unlikely to produce lasting improvements in bone health."

"Despite n3FA supplementation being ceased at weaning, increased DHA and total n3FA levels persisted until 6 wk of age but had returned to control levels by 3 months of age."

"maternal n3FA supplementation did not alter body length or body weight of the offspring at the ends of critical growth periods (3 wk, 6 wk, and 3 months of age)."

"eicosapentaenoic acid (EPA) and DHA are never completely absent from breast milk, and the level is largely determined by the mother's diet"

"feeding postweaning male Fisher rats DHA substantially increased bone marrow cell number"<-more bone marrow cells means more possibilities for mesenchymal condensation and more ability to induce chondrogenesis.

Glucose reduction prevents replicative senescence and increases mitochondrial respiration in human mesenchymal stem cells.

"During in vitro expansion of MSCs, replicative senescence may occur and will compromise the quality of the expanded cells. Because calorie restriction has been shown to effectively extend the life span of various organisms, the purpose of this study is to investigate the effect of glucose reduction on MSCs and the coordinated changes in energy utilization. It was found that the frequency of cycling cells was significantly increased, while senescence markers such as β-galactosidase activities and p16(INK4a) expression level were markedly reduced in MSCs under low-glucose culture condition. MSCs [maintained chondrogenic differentiation potential] after low-glucose treatment. Interestingly, the ability of osteogenic lineage commitment was improved, while the ability of adipogenic lineage commitment was delayed in MSCs after glucose reduction. We observed decreased lactate production, increased electron transport chain complexes expression, and increased oxygen consumption in MSCs after glucose reduction treatment. Increased antioxidant defensive responses were evidenced by increased antioxidant enzymes expression and decreased superoxide production after glucose reduction. MSCs utilize energy more efficiently under restricted glucose treatment and exhibit greater self-renewal and antisenescence abilities, while their differentiation potentials remain unaffected."

"CR induces SIR2 family gene expression to regulate the downstream stress resistance reaction and to slow the aging processes"

"during cell proliferation an increase in lactate production will occur when there is excessive amount of glucose"

E and F are chondroinduction metrics to progressively higher concentrations of glucose(left to right).

(*NEW*)
 
Excessive fructose intake causes 1,25-(OH)2D3-dependent inhibition of intestinal and renal calcium transport in growing rats.

"chronic high fructose intakes by lactating rats prevented adaptive increases in rates of active intestinal Ca2+ transport and in levels of 1,25-(OH)2D3, the active form of vitamin D. Since sufficient Ca2+ absorption is essential for skeletal growth, our discovery may explain findings that excessive consumption of sweeteners compromises bone integrity in children. We tested the hypothesis that 1,25-(OH)2D3 mediates the inhibitory effect of excessive fructose intake on active Ca2+ transport. First, compared with those fed glucose or starch, growing rats fed fructose for 4 wk had a marked reduction in intestinal Ca2+ transport rate as well as in expression of intestinal and renal Ca2+ transporters that was tightly associated with decreases in circulating levels of 1,25-(OH)2D3, bone length, and total bone ash weight but not with serum PTH. Dietary fructose increased the expression of 24-hydroxylase (CYP24A1) and decreased that of 1α-hydroxylase (CYP27B1), suggesting that fructose might enhance the renal catabolism and impair the synthesis, respectively, of 1,25-(OH)2D3. Serum FGF23, which is secreted by osteocytes and inhibits CYP27B1 expression, was upregulated, suggesting a potential role of bone in mediating the fructose effects on 1,25-(OH)2D3 synthesis. Second, 1,25-(OH)2D3 treatment rescued the fructose effect and normalized intestinal and renal Ca2+ transporter expression. The mechanism underlying the deleterious effect of excessive fructose intake on intestinal and renal Ca2+ transporters is a reduction in serum levels of 1,25-(OH)2D3."

"1,25-(OH)2D3 is one of the key hormones controlling intestinal active Ca2+ transport, mainly by regulating TRPV6 and CaBP9k expression"

"Expression levels of TRPV5 and CaBP28k decreased in the fructose-fed compared to the glucose- and starch-fed rats"

The glucose fed group had the highest Vitamin D and PTH levels.

Glucose had the most bone length. 34.4mm for glucose versus 32.4mm for fructose.  Although we can't be sure if this decrease in growth rate translates into decreased adult height.

Glucose diet was slightly superior than starch diet as well.

Foods high in Glucose:
Vegetables, Fruits, Breads, Grains, Dairy, Meats

Foods high in fructose:
Mostly processed foods

Foods high in starch:
Potatoes, bread, rice, cereal,

The Grow Taller Diet

All this information in the brackets need to be updated but I moved this post up due to the last study listed which has interesting insights on maternal diet and height growth.

{I've seen a lot of "grow tall" websites that espouse the benefits of Alfalfa and Arginine and those supplements do have height increase purposes.  However, I'm going to talk about caloric consumption and how much you need for the methods endorsed for this blog like LSJL, LIPUS, PEMF, and Tensile Strain.

The main goal of any diet is to eat enough so that you can live.  Although caloric excess during puberty can cause height growth by causing insulin resistance(via IRS-1).  You also want a sufficient supply of essential vitamins and minerals(like Folic Acid to prevent DNA damage).  In terms of things like Calcium and other compounds the exact amount is controversial.  Elevated serum levels of Calcium for instance inhibits Parathyroid Hormone which is anabolic to bone.

The way that LSJL works is by generating hydrostatic pressure.  This requires additional calories in your diet to perform.  Tensile strain +microfractures also requires calories to heal the microcracks.

Here are a few tips on eating economically. Junk Food is cheap and gives us a lot of calories.  Now I don't know how much Junk Food does in terms of stimulating things that are bad for height growth like inflammatory cytokines but I can spend a dollar on junk food and get about 800 calories.  But there are other options to eat economically that have vitamins and minerals.  I like Pro-Max bars, normally they are about a dollar for 300 calories but can be cheaper than that if there's a clearance sale, you buy in bulk, or their are other deals.  I'm not sure if any of the other ingredients in a ProMax bar can cause damage to height growth, I'd have to investigate each individual ingredient and as for now that's beyond the scope of my knowledge at this point..  It's much cheaper to buy at your local bodybuilding store then off of Amazon.

On the one hand, low body fat percentage allows us to better see our bones and less fat to cushion them potentially causing more microfractures(if we can see our bones better we can more effectively gauge exercise effectiveness).  Malnourishment(specifically Vitamin D) may cause bone marrow to turn to fat being detrimental to LSJL.  Also body fat can cause inflammation which is very bad for height growth by causing cellular necrosis.  On the other hand, heavier weight puts more load on the bone(encouraging anabolism in the bone) and the increase in your body weight can be leveraged in certain exercises.

The problem with gaining weight is that overeating can make it very hard to exercise(not LSJL but if you do supplemental programs to enhance cell growth in general like cardio or weight training).  I find that gaining 10lbs of fat on the body results in a decrease in the amount of weight you can use more than 10lbs.  Fat is also less dense than muscle and bone and tends to hang farther away from the body than muscle would which makes it unwieldy to control.  However, fat is a great natural weight set if no other system of weights is available and you're willing to take everything that goes with having a high body fat percentage.

Overeating also causes inflammation which again is bad for growing taller but again there's evidence that insulin resistance can increase your height gain during puberty.  But it may be better just to inhibit IRS-1 if you're trying that method.  But like many things in height gain there's an equilibrium level for things like BMP-2, Estrogen, FGF, IRS-1, Calcium, etc. and it's hard to get things to a certain level without getting your serum levels tested.

So that's why for height growth I recommend eating around maintenance calories and plus or minus a little to gain or lose weight based on your goals.  In terms of specific compounds, if anyone knows of any compounds that cause DNA Damage in various foods please post them in the comments.  In general you want to avoid chemicals that cause DNA Damage and increase inflammation.}

Associations of food and nutrient intakes with serum IGF-I, IGF-II, IGFBP-3, TGF-b1, total SOD activity and sFas levels among middle-aged Japanese: the Japan Collaborative Cohort study.

"We therefore assessed sex-specific food and nutrient intakes according to serum IGF-I, IGF-II, IGFBP-3, TGF-b1, total SOD activity and sFas levels, under a cross-sectional study of 10,350 control subjects who answered the food frequency questionnaire in the first-wave nested case-control study within the Japan Collaborative Cohort Study. For both men and women, IGF-I levels were associated with higher intakes of milk, fruits, green tea, calcium and vitamin C. IGF-II levels were associated with higher intakes of milk, yogurt, fruits and miso soup, and lower intakes of rice, coffee and carbohydrate. IGFBP-3 levels were associated with higher intakes of milk, yogurt, fruits and vitamin C, and lower intakes of rice, energy, protein, carbohydrate, sodium and polyunsaturated fatty acids[IGFBP-3 inhibits the mitogenic effect of IGF-1 it is anti-anabolic]. TGF-b1 levels were associated with lower intakes of coffee intakes, and higher intakes of miso soup and sodium. Total SOD activity levels were associated with lower intakes of most nutrients other than energy, carbohydrate, iron, copper, manganese, retinol equivalents, vitamin A, B2, B12, niacin, folic acid, vitamin C and fish fat. sFas levels were associated with higher intakes of manganese and folic acids."

So drink more milk and green tea but don't drink coffee.  Of course this is all correlation.  Miso soup increases IGF-II with no increase in IGFBP-3.  Protein and sodium decreases IGFBP-3 without lowering IGF-1 or IGF-2.  Miso soup is available for sale: Miso-Cup Japanese Restaurant Style, 2.9-Ounce Pouch(Pack of 6)

Nutrition and Bone Growth in Pediatrics

"The most rapid growth during the lifetime takes place in utero, when a complete fetus of about 50 cm in length is produced from a single cell in just 9 months."

"GH and IGF-I concentrations are responsive to changing nutritional status and intake of amino acids and free fatty acids"

"Whereas fasting increased serum GH levels in humans, rabbits, sheep, cows and pigs, it reduced serum GH levels in mice and rats; nevertheless, in all animals examined, IGF-I levels were reduced."

"ghrelin, in its acylated form, releases GH by binding to its hypothalamic receptor, GHSRa 1." Mutations in Ghrelin can cause short stature.

"in several animal models, knock out of either ghrelin or its receptor genes was not associated with any attenuation of growth." Since Ghrelin increases hunger maybe these people just didn't eat enough?

"GHSR levels are stimulated by fasting, and high levels of IGF-I inhibit pituitary GHSR mRNA levels. By contrast, neither total nor octanoylated ghrelin increased during fasting in parallel to the massive increase in GH secretion." Ghrelin is produced by growth plate chondrocytes.

Leptin stimulates

"leptin stimulated femoral length and the midshaft cortical area independently of peripheral IGF-I. Furthermore, leptin administration to rat with intrauterine growth retardation significantly improved structural properties and elongation rate of bone"

"leptin can act as a metabolic signal connecting adipocyte tissues with the GH axis and that its stimulatory effect on growth under conditions of food restriction is not dependent on circulating IGF-I."

There has been one instance mentioned with a person with mutated leptin(that the leptin levels were lower was alluded too) that was tall.

"Insulin, a 51-amino acid beta-cell–specific hormone, is secreted from the pancreas in response to increased glucose levels and binds to its receptors on peripheral cells and tissues to enable the assimilation of glucose into cells"

"[Some] children [have] mutations in the gene encoding for glucokinase (GCK), which catalyzes the rate limiting step in glycolysis and serves as a pancreatic b-cell glucose sensor. Mutations in GCK result in altered glucose sensing and decreased insulin secretion. Children with a mutation in GCK are approximately 500 g smaller than unaffected siblings."

"In most cases, there is no correlation between glycemic control and skeletal growth, and many children with apparently marginal control appear to grow well."

"Children with marasmus (a form of malnutrition caused by long-lasting insufficient caloric intake) and kwashiorkor (a form of malnutrition caused mainly by insufficient protein consumption) had significantly lower body weight and height than healthy subjects, as well as reduced levels of serum leptin, insulin, and IGF-I."

"Weight gain was necessary for catch-up growth [in anorexia], but the weight had to be gained before the ability to grow was lost with age"

"We showed that in rats, 40% food restriction for 10 days induced dramatic changes in the expression of several genes. One of them was HIF1a, a key subunit of HIF, which serves as a master transcription factor
regulating the expression of several genes that code for proteins involved in angiogenesis, cell metabolism, proliferation, motility, adhesion, and survival"

"[HIF1alpha up-regulates] the expression of the cartilage transcription factor Sox9 and [regulates] the enzymes responsible for the hydroxylation of collagen prolines (P4HaI and P4HaII), and the enzyme lysyl oxidase, which is responsible for the formation of cross links between collagen molecules."

"mTOR is found in the form of two multiprotein complexes, mTOR Complex 1(TORC1) and mTOR Complex 2 (TORC2). TORC1 is sensitive to the cellular nutritional state, and it targets the phosphorylation of proteins that regulate protein translation, gene expression, and autophagy. TORC2, by contrast, does not respond to changes in nutritional conditions but has been implicated in cytoskeleton regulation"

"TORC1 is regulated by insulin and nutrients, including glucose and amino acids, particularly leucine, as well as a variety of cellular stresses. In some cell types, amino acids can activate mTOR alone; in others, they collaborate with growth factors, such as insulin. In the absence of amino acids, growth factors are helpless."

"Modulation of mTOR signaling was shown to stimulate chondrocyte differentiation. TOR, together with HIF1a, is also involved in the autophagy of the maturing chondrocytes of the EGP. Autophagy is induced under energy-restricted environmental conditions and inhibited by nutrient sufficiency. It plays a role in the control of several physiologic processes. Specifically, in response to nutrient deprivation, the cells degrade the cytosolic content by the formation of a double-walled vesicular structure that eventually fuses with lysosomes, so that energy can be generated from the cells’ own protein and lipid stores. Nutrient-stimulated activation of the TOR protein kinase leads to the phosphorylation and inactivation of components of the autophagy pathway."

"Vps34 (vacuolar protein sorting 34), a member of the PI3K family of lipid kinases, also participates in nutrient signaling to mTOR. It is inhibited by amino acid deprivation and up-regulated with mTOR signaling."

"maturing chondrocytes were found to exhibit an autophagic phase. Its regulation was dependent on the activities of mTOR and AMP kinase in response to the AMP/ATP ratio in the cells. When AMP kinase activity was blocked, autophagy could not be activated. Thus, nutrient insufficiency may increase the autophagic response in the growth plate chondrocytes, reducing the size of the cells and growth plate and leading to growth attenuation. When the restriction is short, this process may be reversible, but when it is prolonged, cell number may be reduced and growth stunted."

"SIRT1 was induced in vitro by nutrient deprivation and in vivo after long-term Calorie Restriction."

"The enzymatic activity of SIRT1 appears to be positively regulated by NAD1, which increases during CR and fasting. Mice overexpressing SIRT1 exhibited similar physiologic properties to mice on a CR regimen."

"SIRT1 may regulate cell proliferation, senescence, and apoptosis by regulating several transcription factors that govern metabolism and endocrine signaling, including PPAR-g, PGC-1a, FOXOs, and p53."

"six months of vitamin A, iron and zinc supplementation induces growth acceleration in short children born SGA with subnormal nutrients intake similar to growth hormone therapy"  Vitamin A may have some growth inhibitory mechanism but some studies have shown no growth inhibition.

"zinc supplementation led to a highly significant increase in height and weight, with a greater growth response in children with initially low Z-scores for weight or height, especially those known to be zinc deficient. By contrast, when zinc was administered to children with idiopathic short stature and normal serum zinc levels there was no effect on height."

"Zinc deficiency reduces IGF-I production and may also decrease cellular IGF-I responsiveness, and transient partial GH deficiency due to zinc deficiency was reported in children. Zinc supplementation was found to increase basal levels of IGF-I, IGFBP-3, alkaline phosphatase, and osteocalcin, without changing GH levels or increasing subjects’ sensitivity to exogenous GH. Others reported that Zinc supplementation led to a significant increase in growth rate and GH levels."


Maternal high-fat diet promotes body length increases and insulin insensitivity in second-generation mice.

"Nutrition during development is clearly linked to somatic growth.  Here we report the novel finding of a significant body length increase that persisted across at least two generations of offspring in response to maternal high-fat diet exposure. This phenotype is not attributable to altered intrauterine conditions or maternal feeding behavior because maternal and paternal lineages were able to transmit the effect, supporting a true epigenetic manner of inheritance. We also detected a heritable feature of reduced insulin sensitivity across two generations. Alterations in the GH secretagogue receptor (GHSR), the GHSR transcriptional repressor AF5q31, plasma IGF-I concentrations, and IGF-binding protein-3 (IGFBP3) suggest a contribution of the GH axis. These studies provide evidence that the heritability of body length and glucose homeostasis are modulated by maternal diet across multiple generations, providing a mechanism where length can increase rapidly in concert with caloric availability."

"First-generation E17 embryos exhibited increased body length after exposure to maternal high-fat diet (1HF, 45% fat) relative to those exposed to chow (1Ch, 12% fat)"<-about 2.5mm for adult males was observed.  So a maternal high fat diet can result in a permanent increase in height for her offspring.  That's about 3% in height.  For a 69 inch height male that's about a 2 inch increase in height.

The change is even more significant in the second generation.

"In our examination of first- and second-generation offspring leptin levels, we found that male and female offspring had reduced leptin"

"IGFBP-3 can enhance the biological efficacy of IGF-I when complexed"

"first- and second-generation females appeared to masculinize their IGF-I levels in response to maternal high-fat diet, suggesting that females may be recruiting a mechanism already present in males that contributes to the typically enhanced body length in males relative to females."

"mice hemizygous for AF5q31 have recently been shown to express increased levels of GHSR and display a similar phenotype of increased body length and reduced adiposity to mice in our study. Early developmental alterations in AF5q31 expression may provide a fundamental signal that results in increased GHSR expression leading to enhanced GH and IGF-I secretion during critical developmental windows, thus leading to augmented linear growth."

So you could be taller if your mom ate more fat.

Nutritional modulators of bone remodeling during aging.

"Bone morphogenetic proteins (BMPs) have been shown to stimulate bone formation {and chondrogenesis}. BMP-2 therefore represents one potential molecular target to identify new agents to simulate bone formation. Research is accumulating on the positive effects of dietary sources that stimulate the BMP2 promoter and their effects on bone formation. Flavonoids and statins occur naturally in food products and have been shown to promote bone formation."

"BMP-2 stimulates the differentiation of mesenchymal cells into osteoblasts and chondrocytes. BMP-2 binds to its receptor, a Ser/Thr kinase, which phosphorylates and activates the intracellular signaling molecules Smad 1 and Smad 5."

"Statins, drugs widely used for lowering serum cholesterol, have been found to enhance new bone formation"

"Flavonoids are a class of phytoestrogens, plant-derived chemicals, that when absorbed via the gut mimic the actions of estrogen and that have been found to increase BMP2 gene transcription"

"Genistein triggers transcriptional activation of the murine Bmp2 gene with estrogen receptor alpha (ERα), but not ERβ"

Consumption of green tea extract results in osteopenia in growing male mice.

"[We] determine the effects of green tea extract (GTE) on bone mass and architecture in rapidly growing lean [C57BL/6 wild type (WT)] and genetically obese, leptin-deficient (ob/ob) male mice {they don't produce leptin}. Five-week-old lean and ob/ob mice were assigned to diets containing GTE at 0, 1, or 2% for 6 wk. Compared with WT mice, ob/ob mice had shorter femora, lower femoral bone volume, and lower femoral bone mineral content, but higher cancellous bone volume in lumbar vertebrae (P < 001). Neither genotype nor treatment affected femoral bone mineral density, indicating normal mineralization. GTE consumption resulted in lower femur length, volume, mineral content, cortical volume, and cortical thickness, as well as lower cancellous bone volume/tissue volume and trabecular thickness in lumbar vertebrae. Leptin is not essential for the reduced gains in body weight and bone mass due to GTE in growing mice and suggest that consumption of large quantities of green tea may reduce the rate of bone accumulation during growth{but does it result in decreased adult height?}."

"green tea extract (GTE) decreases intestinal lipid absorption"

GTE had a much greater impact on decreasing femur length in the leptin non-producing mice than wild type.

Femur length between 0-1% GTE extracts were virtually identically however there was a slight noticeable decrease at 2% GTE in wild type.

"Green tea catechins enhanced chondrogenesis and suppressed osteogenesis in a rat model for ectopic bone formation"

"Because mice in the present study were fed a diet in which calcium exceeded requirements, it is unlikely that the reduced bone growth in mice fed GTE is attributable to caffeine."

Evaluation of body composition and cartilage biomarkers in large-breed dogs fed two foods designed for growth.

"Large-breed 2 month-old-puppies [were used].
Dogs were randomly assigned to receive 1 of 2 foods until 18 months of age. Dogs were evaluated at 2, 5, 12, and 18 months of age via dual energy x-ray absorptiometry (DEXA), CBC, serum biochemical profile, and concentrations or activities of taurine, vitamin E, fatty acids, glutathione peroxidase, C-propeptide of type II collagen (CPII), cartilage oligomeric matrix protein (COMP), carboxy-terminal cross-linked fragment of type II collagen (CTXII), bone specific alkaline phosphatase (BAP), osteocalcin, ghrelin, and growth hormone.
Blood components largely reflected the composition of the foods. Dogs fed the food with a higher concentration of protein, calcium, n-3 fatty acids, and antioxidants had a lower percentage of body fat and greater percentage of lean body mass at 5, 12, and 18 months of age, and higher CPII:CTXII ratio and lower COMP at 18 months of age. The BAP activity, osteocalcin concentration, and CTXII concentration declined with age, whereas COMP concentration and CPII concentration were similar at all time points for both foods.
The BAP activity, osteocalcin concentration, and CTXII concentration were greater during growth than at 18 months of age. The food that was proportionately higher in protein, calcium, n-3 fatty acids, and antioxidants increased lean body mass and may have positively affected cartilage turnover as maturity was attained."

Couldn't get this full study but what there is shows that diet matters.

Does dieting stunt growth?

In order, to truly understand the effect of diet on height growth, we have to understand the effects of caloric deficit and surplus on chondrocytes and osteoblasts(other cell types may affect height growth as well, not to mention endocrinological and nutritional effects).  We have to understand if caloric surplus and deficit alone have an effect on the cells that can increase height and not just an indirect effect via say a nutritional deficiency which can be alleviated by supplements.  And then there's the whole issue of growth rate versus final adult height.

Before we learned that Leptin and IGF-1 are downregulated during fasting and upregulated during catch-up growth.  Leptin and IGF-1 stimulate the PI3K pathways that stimulate cellular proliferation.  Levels of GHR and IGF-1R went down as well during fasting, however, the mRNA levels remained the same so they should be able to recover efficiently during catch up growth.  Other chondrocytes should operate similarly including articular chondrocytes(which can undergo endochondral ossification during osteoarthritis) and hydrostatic pressure induced chondrocytes. 


Leptin reverses the inhibitory effect of caloric restriction on longitudinal growth.

"Caloric imbalance, particularly in critical periods of growth and development, is often the underlying cause of growth abnormalities. Serum levels of leptin are elevated in obesity and are low in malnutrition and malabsorption. The aim of the present study was to determine whether leptin integrates energy levels and growth in vivo even in the presence of caloric restriction. In the first part of the study, mice were divided into three groups. Two groups were fed ad libitum[when hungry] and received leptin or vehicle only, and the third group was pair-fed with the group injected with leptin to dissociate leptin's effect on growth from its effect on food consumption. Mice given leptin had a significantly greater tibial length than untreated pair-fed animals and a similar tibial length as control mice fed ad libitum despite their lower weight. In addition, leptin significantly increased the overall size of the epiphyseal growth plate by 11%. On immunohistochemistry and in situ hybridization studies, leptin stimulated both the proliferation and differentiation of tibial growth plate chondrocytes without affecting the overall organization of the plate. There was also a marked increase in the expression and level of IGF-IR. In the second part of the study, two groups of mice were fed only 60% of their normal chow; one was injected with leptin, and the other was injected with vehicle alone. Caloric deprivation by itself reduced serum levels of IGF-I by 70% and the length of the tibia by 5%. Leptin treatment corrected the fasting-induced growth deficiency, but further reduced the level of serum IGF-I. These results indicate that leptin stimulates growth even in the presence of caloric restriction independently of peripheral IGF-I." 


Leptin is produced by adipocytes which is related to caloric surplus and restriction.  However, you could have a lot of body fat and be under caloric restriction for example. You can take Leptin as a supplement.  This supplement for example contains Leptin(not sure if there are better deals) and it also contains green tea (which inhibits PGE2 and COX2) which may have beneficial effects on height: Lepti-Trim Night Time Formula (16 oz). 

So, caloric restriction may have height lowering effects as a result of lowering Leptin and IGF-1 levels but caloric restriction may not independently have any height decreasing effects.  The amount of Leptin receptors change with age so altering the number of Leptin receptors may affect height growth.


Age-related variations of leptin receptor expression in the growth plate of spine and limb: gender- and region-specific changes.

"Leptin is a potent growth-stimulating factor of bone. The effects of leptin on bone growth differ significantly between axial and appendicular regions. Gender differences of leptin function have also been suggested in normal pubertal development. To explore the mechanisms underlying these effects, we investigated the spatial and temporal expressions of the active form of the leptin receptor (Ob-Rb) in the tibial and spinal growth plates of the female and male rats during postnatal development. The 1-, 4-, 7-, 12- and 16-week age stages are representative for early life, puberty and early adulthood after puberty, respectively. Quantitative real-time PCR was used for Ob-Rb mRNA examination and comparison. The spatial location of Ob-Rb was determined by immunohistochemical analysis. There were gender- and region-specific differences in Ob-Rb mRNA expression in the growth plate. Mainly cytoplasm staining of Ob-Rb immunoreactivity was observed in the spinal and tibial growth plate chondrocytes of both genders. Spatial differences of region- and gender-related Ob-Rb expression were not observed. Ob-Rb immunoreactivity was detected in the resting, proliferative and prehypertrophic chondrocytes in early life stage and during puberty. After puberty, staining was mainly located in the late proliferative and hypertrophic chondrocytes[So new chondrocytes no longer have leptin receptors?]. The results of Ob-Rb HSCORE analysis were similar to those obtained from quantitative real-time PCR. Our study indicated direct effects on the chondrocytes of the growth plate in different development stages. The region-specific expression patterns of Ob-Rb gene might be one possible reason for contrasting phenotypes in limb and spine. Different Ob-Rb expression patterns might partly contribute to age- and gender- related differences in trabecular bone mass."

Why would new chondrocytes lose leptin receptors over time?  Maybe it has to do with methylation status or telomere length?  Newer cells may be undermethylated.  Maybe the Ob-Rb status serves to regulate chondrocyte proliferative capacity.

"By affecting the proliferation, hypertrophy and calcification of chondrocytes through Ob-Rb, leptin has a direct effect on longitudinal growth. The balance among chondrocytes of different zone is crucial for bone metabolic regulation in the growth plate. The rate of the proliferative chondrocytes and accelerated or delayed differentiation could lead to abnormal longitudinal growth of bone. The regulation process is controlled by various growth factors/hormones via their receptors. In the present study, Ob-Rb immunostaining was mainly revealed in the cytoplasm of the chondrocytes in the tibial and spinal growth plates. Low staining in nuclei of chondrocytes was also detected. These results indicate the main target of leptin in the chondrocytes at different stages and layers of the growth plate."<-The number of Leptin receptors is important.  How do we increase the number of those receptors?


Determinants of height in adolescent girls with anorexia nervosa.

"Anorexia nervosa, a condition characterized by marked caloric restriction and low insulin like growth factor-1 levels, would be expected to cause short stature. However, this disorder is also associated with hypogonadotropic hypogonadism[basically a deficiency in sex hormones] and high growth hormone levels. Delays in growth-plate closure from associated hypogonadism may result in a longer period of time available for statural growth with protective effects on stature[growth plates don't close, senescence followed by ossification]. In addition, growth hormone may have direct effects on the growth plate independent of insulin-like growth factor 1 to increase statural growth.
To determine the impact of undernutrition, hypogonadism, and acquired growth hormone resistance on height in adolescents with anorexia nervosa (aged 12-18 years), we examined 208 girls: 110 with anorexia nervosa and 98 controls of comparable chronological age. Sixty-three girls with anorexia nervosa and 79 controls were followed prospectively over 1 year. Mean duration of illness was 11.6 +/- 13.2 months. In a subset, overnight growth hormone sampling was performed every 30 minutes for 12 hours, and fasting insulin-like growth factor 1 levels were obtained.
The difference between height and target height and between predicted adult height and target height did not differ between the groups, indicating preservation of height potential. The groups had comparable bone age, but bone age was lower than chronological age in girls with anorexia nervosa. Girls with anorexia nervosa had lower insulin-like growth factor 1 levels and higher nadir growth hormone levels than those of controls. Nadir growth hormone levels predicted height SD scores and predicted adult-height SD scores in controls but not in the girls with anorexia nervosa. In girls with anorexia nervosa, insulin-like growth factor 1 and duration of illness predicted height measures. Height SD scores of <0 were more likely after 32 months of illness and at insulin-like growth factor 1 levels of <134 ng/mL. Delayed baseline bone age predicted subsequent increases in height SD scores in immature girls with anorexia nervosa.
Our data suggest that preservation of height potential in this cohort of girls with anorexia nervosa may be a consequence of delayed bone age. Hypogonadism may negate the deleterious effects of undernutrition on stature by allowing for a longer duration of growth."

So, Height is conserved during Anorexia Nervosa.  Now some may point out that the AN girls produced less Estrogen, however Estrogen needs to be kept in a certain range for optimal height growth although low levels of estrogen are much less detrimental to height growth than high levels.  Girls are more likely to be above this Estrogen range than males.  Thus the Anorexia may have knocked them out of the high end of Estrogen.

However, it is more likely that growth is conserved during periods of under nutrition.

So, basically the benefits of caloric restriction and surplus are mainly affected by Leptin and IGF-1.  Leptin of which is available as a supplement.