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).

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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,