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.