Tuesday, September 4, 2012

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.


  1. I'm not surprised by this finding. Women who eat a low carb, high fat diet tend to have very well developed kids, not only tall but with powerful brain power as well. Fats really are the key to body AND brain health, but unfortunately they're so misunderstood.

    This is off topic to this particular post, but I'm wondering how your growth journey is going? Have you thought of switching from jointing load to LIPUS? I imagine LIPUS being much more gentle and less time consuming. Plus, it's easier to stimulate the spine with LIPUS than with joint loading.

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

    ya haha.. but i don't see how that is significant or the main point,
    should of, could of, would of..

    relates to the past

  3. Tyler I've been doing LSJL for 8 months in a row but I still haven't seen any results yet. Any suggestions on what I might be doing wrong or what might help boost growth?

  4. Have you noticed any changes in your bone shape? Any bony bumps on your bone? <-this could be a sign of ectopic chondrogenesis which means that LSJL is effective at forming bone beneath the periosteum.

    Also, take time off every 1 to 2 weeks. Or alternate between arms and legs. I do 4 days arms, 4 days legs.

    Also, try loading for 3 minutes.

    1. My joints have gotten a lot thicker but no length increase as of yet. I'll keep at it though. Last month I did 2 minutes of loading per joint but now I'm up to 3 minutes. Thanks for the reply.

  5. I know that in Bulletproof Executive Asprey has stated a lot that certain kinds of fat is very good for you. He seems to really enjoy getting a lot of fat. He puts like a quarter of a stick of butter into his morning coffee.

    Yeah, fat is key to have big healthy children. There is a reason why men prefer women who are slightly bigger than slightly skinnier.