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Year : 2013  |  Volume : 13  |  Issue : 2  |  Page : 70-73

Physiological mechanisms underlying catch-up growth

1 Department of Physiology, Gian Sagar Medical College, Rajpura, India
2 Department of Physiology, Government Medical College, Patiala, Punjab, India
3 Department of Orthodontics, Surendra Dental College, Sri Ganganagar, Rajasthan, India
4 Department of Public Health Dentistry, Surendra Dental College, Sri Ganganagar, Rajasthan, India

Date of Web Publication20-Dec-2013

Correspondence Address:
Sharat Gupta
Hno# 849, SST Nagar, Rajpura Road, Patiala - 147 001, Punjab
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DOI: 10.4103/1319-6308.123372

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Linear growth is impaired by a variety of systemic illnesses. However, on remission, body growth usually normalizes or even accelerates beyond the normal rate for age, a phenomenon commonly known as catch-up growth. Until date, the exact mechanisms underlying this unique phenomenon are unclear. However, two possible mechanisms have been put forward to explain it. One theory postulates a central mechanism, which compares the target and actual body sizes and accordingly makes corrective adjustments in body growth. However, the second mechanism, which provides a newer explanation for this phenomenon, states that growth restricting illnesses reduce the proliferation of stem cells, thus conserving their proliferative potential temporarily. As soon as the crisis is over, the stem cell proliferation resumes at an accelerated rate. Further research into the exact mechanisms underlying catch-up growth may prove helpful in discovery of effective strategies for reversing the growth stunting in children with chronic diseases.

  Abstract in Arabic 

يعاقً النمو الخطي بمجموعة من الأمراض الجهازية ، ومع ذلك يعود نمو الجسم طبيعيا وحتى يتسارع بدرجة أكبر بالنسبة للعمر وهي ظاهرة تعرف بأنها " نمو تداركي " وحتى هذا التاريخ فإن الآليات الفيزيولوجية الحقيقية وراء هذه الظاهرة الفريدة هي غير واضحة،تم وضع آليتين مفترضتين لتفسير ذلك. النظرية الأولى تفترض آلية مركزية تقارن النمو المرجو مع النمو الفعلي وحسب ذلك تجري تعديلات تصحيحية على النمو البدني . بينما توفر النظرية الثانية تفسيراً أحدث لهذه الظاهرة ، وتقول أن الأمراض التي تعيق النمو تؤخر تكاثر الخلايا الجذعية وبذلك تحافظ على إمكانيات تكاثرها مؤقتاً . وفور انتهاء الأزمة يستأنف تكاثر الخلايا الجذعية بسرعة أكبر. لعل البحث عن الأسباب الدقيقة التي تستبطي النمو ألتداركي قد تكشف عن استراتيجيات فعالة تعكس تأخر النمو عند الأطفال المصابين بأمراض مزمنة .

Keywords: Catch-up growth, children, growth, growth plate, stunting, systemic illnesses

How to cite this article:
Gupta S, Mittal S, Mittal M, Gulati P. Physiological mechanisms underlying catch-up growth. Saudi J Sports Med 2013;13:70-3

How to cite this URL:
Gupta S, Mittal S, Mittal M, Gulati P. Physiological mechanisms underlying catch-up growth. Saudi J Sports Med [serial online] 2013 [cited 2021 Jun 25];13:70-3. Available from: https://www.sjosm.org/text.asp?2013/13/2/70/123372

  Introduction Top

Catch-up growth is defined as a height velocity above the statistical limits of normality for age and/or maturity, during a defined period of time, following a transient period of growth inhibition. [1] Optimal body growth is mainly dependent upon the health profile and nutritional status of an individual. Growth stunting has been commonly associated with undernourishment as well as with a gamut of systemic illnesses. [2]

It is believed that this down regulation of growth in illness is, in fact, just a temporary postponement. This belief originated from the observation that as and when the growth opposing illness is resolved, the body growth may not only just normalize, but may even exceed the normal rate for age, in some cases. [3],[4] Therefore, catch-up growth represents a remarkable auto corrective ability of the body, which tends to take a child right toward his/her original pre-retardation curve. [5]

The term "compensatory growth" has often been used synonymously with catch-up growth. However, Dr. Williams [6] has clearly differentiated between these two seemingly similar terms by stating that compensatory growth occurs after the "actual loss" of mass of any tissue (e.g., liver regeneration after partial hepatectomy or renal hypertrophy seen in the kidney of one side after removal of its counterpart on the opposite side). On the other hand, during catch-up growth, the body anticipates and compensates for "partial loss" of tissue. While compensatory growth was explained to be occurring under the influence of a simple feedback signal working on physiological mass/physical load, catch-up growth was said to be under the control of a much more complex mechanism.

The phenomenon of catch-up growth is not unique to humans, since it has also been observed in several other mammalian species. [7],[8],[9] In humans, it has been described following a wide variety of growth retarding conditions, including celiac disease, [10],[11] hypothyroidism, [12],[13] growth hormone deficiency [14] and intrauterine growth retardation. [15]

Despite the latest technological advancements in the field of medicine, the exact mechanisms that are responsible for this spectacular capacity of the body have not yet been fully identified. Therefore, we felt the urgent need to update the current knowledge of the fellow researchers so that further researches in this yet underexplored field can be conducted.

  Patterns of Catch-Up Growth Top

It has been suggested that catch-up growth may follow any of the three different patterns. [16],[17]

Type A catch-up growth

It is said to be occurring when, after cessation of growth restriction, there is early, marked growth acceleration, thereby reducing the growth deficit within a very short span of time. The child then grows along this improved percentile until adult height is achieved. Type A pattern has been widely accepted as an archetype of catch-up growth and is common during infancy and childhood.

Type B catch-up growth

In this, there is persistence of delayed growth even on removal of the condition causing growth cessation. However, growth continues for a prolonged period, so much so that ultimately the growth arrest is well-compensated in the long-term. This pattern is more common during adolescence, therefore it is impossible to distinguish it from pubertal growth spurt. In contrast to Type A pattern, in Type B pattern there is a negligible increase in height velocity as compared with mean velocity for chronological age.

Type C catch-up growth

It is a mixture of the above two patterns, i.e., there is an increase in height velocity as well as a delay and prolongation of growth.

Although there is a logical subdivision between the above three patterns, yet in practice, a clear cut demarcation may not be possible always. In general, catch-up growth tends to be incomplete, since the individual does not attain the same adult height that would have been achieved had there been no growth restriction in the first place. [18] The amount of the growth deficit that still remains depends upon the etiology, severity and duration of growth retardation as well as the age at which it occurred in that individual. [19]

  Mechanisms Contributing to Catch-up Growth Top

Currently, there are two mechanisms, which are widely believed to provide a probable explanation for this unusual phenomenon.

"Sizostat" or neuroendocrine hypothesis

This hypothetical model was described by Prof. Tanner, way back in 1963. [20] He proposed a mechanism that was able to compare the mismatch between an organism's actual body size and the target body size and could thus subsequently adjust the organism's growth rate to minimize the degree of this mismatch.

The "target body size" was supposedly based on the concentration of some substance within the nerve cells that should increase with age. The "actual body size" was proposed to be represented by a circulating inhibitory factor produced by the growing tissues. This inhibitory factor was thought to be present in a concentration, which reflected the size of the organism. This inhibitory factor must be acting as a kind of feedback signal that "satisfies" the receptors of central "sizostat" mechanism. The amount of "unsatisfied" receptors is thus directly proportional to the degree of mismatch sensed by the sizostat and this is thought to dictate the velocity of body growth. To put it in a simpler way, more the number of unsatisfied sizostat receptors, more is the mismatch and higher is the growth rate.

Some evidence was cited in favor of the central sizostat mechanism by Mosier. [21] It was observed that newborn mice, who were subjected to bilateral head irradiation, showed growth stunting. However, such animals were found to be capable of showing catch-up growth after fasting, but only to the smaller size of non-fasting irradiated rats. It was thus suggested that irradiation might have resulted in resetting of the set point for body size (i.e., the sizostat).

Although the neuroendocrine hypothesis appears to provide an attractive explanation to catch-up growth, yet there is not enough experimental evidence regarding the true existence of any of the components of this model, especially the presence of the growth inhibiting factor, as proposed by Dr. Tanner. Another major limitation in Tanner model is that there is no clear cut explanation as to whether the sizostat mechanism regulates both the body height and weight or only the latter.

In fact the recent discovery of the "ob" gene [22],[23] and its adipocyte specific protein leptin has paved way for the first physiological evidence that the sizostat mechanism might actually be controlling the body weight only. This has been explained on the basis of the following resemblances of weight regulatory mechanism with the components of the neuroendocrine model:

  1. A central structure comprising the satiety center in the hypothalamus, which corresponds to the central sizostat of Tanner
  2. A feedback signal "leptin" that is comparable with Tanner's inhibitory factor.

Since the evidence favoring the weight regulating central mechanism is strong, newer concept for regulation of catch-up growth in height has recently been proposed.

Growth plate hypothesis

In 1994, Baron et al.[24] put forward an alternative hypothesis that the mechanism governing catch-up growth resides in the growth plate itself and not within the central nervous system.

This notion was based on their experimental findings in 6-week-old rabbits. They observed that direct administration of dexamethasone into the tibial growth plate on one side, led to a diminished growth on that side as compared with the bone growth on the controlled healthy side. This down regulation of bone growth was seen not only to reverse and normalize, but in fact surpass the normal side upon stopping the dexamethasone infusion. Since the catch-up growth occurred only in the affected growth plate, thus it could not be explained by the Tanner model, since as per the latter mechanism all the growth plates should have been affected equally, which however, was not seen. Based on these findings, Baron et al. suggested the growth plate mechanism to explain catch-up growth.

The chondrocytes at the epiphyseal end of the proliferative column of growth plate serves as the stem cell. During normal senescence of the growth plate, there is a reduction in the proliferative rate of the chondrocytes with each successive stem cell cycle. Thus, the growth plate senescence is not a function of time per se but is in fact a function of the cumulative number of divisions, which the stem cell cells have undergone. Hence, as the total number of stem cell divisions increases, the rate of longitudinal bone growth declines. The growth inhibiting conditions reduce the proliferative rate of these chondrocytes, thus delaying their senescence. As soon as the offending condition is removed, there is seen rapid proliferation of these cells, thereby increasing the growth rate.

In fact, the growth plate hypothesis shows much semblance to the ideas put forward by Williams and Hughes, [25] who proposed that while catch-up growth appeared to be a whole body response, the various body parts seemed to respond in an individual manner within the same animal, suggesting that there was no single mechanism regulating catch-up growth.

  Conclusion Top

Catch-up growth is an intriguing event that has been long known, but poorly understood. Until date, not much data is available regarding the exact physiological mechanism of this unique phenomenon. The evidence in favor of Tanner's hypothesis appears to be weakening while the acceptability of the recently proposed growth plate hypothesis seems to be rising, since it provides a more plausible explanation. Further elucidation of the exact mechanism contributing to catch-up growth may lead to the development of novel therapeutic regimens that could prove useful in treatment of children with idiopathic growth anomalies, especially in cases where therapeutic response to growth hormone replacement therapy has been found unsatisfactory.

  Acknowledgments Top

The authors would like to thank Dr. Tanner and Dr. Mosier for their rich online repertoire on catch-up growth, which greatly facilitated the research for literature for this article.

  References Top

1.Jain V, Singhal A. Catch up growth in low birth weight infants: Striking a healthy balance. Rev Endocr Metab Disord 2012;13:141-7.  Back to cited text no. 1
2.Marshall WA. Evaluation of growth rate in height over periods of less than one year. Arch Dis Child 1971;46:414-20.  Back to cited text no. 2
3.Polychronakos C, Abu-Srair H, Guyda HJ. Transient growth deceleration in normal short children. A potential source of bias in growth studies. Eur J Pediatr 1988;147:582-3.  Back to cited text no. 3
4.Lampl M, Veldhuis JD, Johnson ML. Saltation and stasis: A model of human growth. Science 1992;258:801-3.  Back to cited text no. 4
5.Proos L, Gustafsson J. Is early puberty triggered by catch-up growth following undernutrition? Int J Environ Res Public Health 2012;9:1791-809.  Back to cited text no. 5
6.Williams JP. Catch-up growth. J Embryol Exp Morphol 1981;65 Suppl: 89-101.  Back to cited text no. 6
7.Williams JP, Tanner JM, Hughes PC. Catch-up growth in male rats after growth retardation during the suckling period. Pediatr Res 1974;8:149-56.  Back to cited text no. 7
8.Du Caju MV, Rooman RP. Isolation of several fractions from human serum, inhibiting rabbit cartilage metabolism in vitro. Acta Endocrinol (Copenh) 1990;122:277-82.  Back to cited text no. 8
9.Marin G, Malozowski SN, Barnes K, Southers J, Cristiano A, Cassorla F. Endocrine profile of catch-up growth in the cynomolgus monkey. Acta Endocrinol (Copenh) 1993;129:371-4.  Back to cited text no. 9
10.Cacciari E, Corazza GR, Salardi S, Pascucci MG, Tacconi M, Cicognani A, et al. What will be the adult height of coeliac patients? Eur J Pediatr 1991;150:407-9.  Back to cited text no. 10
11.Damen GM, Boersma B, Wit JM, Heymans HS. Catch-up growth in 60 children with celiac disease. J Pediatr Gastroenterol Nutr 1994;19:394-400.  Back to cited text no. 11
12.Grant DB. Growth in early treated congenital hypothyroidism. Arch Dis Child 1994;70:464-8.  Back to cited text no. 12
13.Pantsiouou S, Stanhope R, Uruena M, Preece MA, Grant DB. Growth prognosis and growth after menarche in primary hypothyroidism. Arch Dis Child 1991;66:838-40.  Back to cited text no. 13
14.Skuse D, Albanese A, Stanhope R, Gilmour J, Voss L. A new stress-related syndrome of growth failure and hyperphagia in children, associated with reversibility of growth-hormone insufficiency. Lancet 1996;348:353-8.  Back to cited text no. 14
15.Albertsson-Wikland K, Wennergren G, Wennergren M, Vilbergsson G, Rosberg S. Longitudinal follow-up of growth in children born small for gestational age. Acta Paediatr 1993;82:438-43.  Back to cited text no. 15
16.Tanner JM. Catch-up growth in man. Br Med Bull 1981;37:233-8.  Back to cited text no. 16
17.Largo RH. Catch-up growth during adolescence. Horm Res 1993;39 Suppl 3:41-8.  Back to cited text no. 17
18.Rivkees SA, Bode HH, Crawford JD. Long-term growth in juvenile acquired hypothyroidism: The failure to achieve normal adult stature. N Engl J Med 1988;318:599-602.  Back to cited text no. 18
19.Taal HR, Vd Heijden AJ, Steegers EA, Hofman A, Jaddoe VW. Small and large size for gestational age at birth, infant growth, and childhood overweight. Obesity (Silver Spring) 2013;21:1261-8.  Back to cited text no. 19
20.Tanner JM. Regulation of growth in size in mammals. Nature 1963;199:845-50.  Back to cited text no. 20
21.Mosier HD. Growth failure in the head-irradiated rat. Horm Res 1988;30:77-83.  Back to cited text no. 21
22.Considine RV, Sinha MK, Heiman ML, Kriauciunas A, Stephens TW, Nyce MR, et al. Serum immunoreactive-leptin concentrations in normal-weight and obese humans. N Engl J Med 1996;334:292-5.  Back to cited text no. 22
23.Hassink SG, Sheslow DV, de Lancey E, Opentanova I, Considine RV, Caro JF. Serum leptin in children with obesity: Relationship to gender and development. Pediatrics 1996;98:201-3.  Back to cited text no. 23
24.Baron J, Klein KO, Colli MJ, Yanovski JA, Novosad JA, Bacher JD, et al. Catch-up growth after glucocorticoid excess: A mechanism intrinsic to the growth plate. Endocrinology 1994;135:1367-71.  Back to cited text no. 24
25.Williams JP, Hughes PC. Catch-up growth in rats undernourished for different periods during the suckling period. Growth 1975;39:179-93.  Back to cited text no. 25


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