Low Muscle Mass – Tall & Obese Children

Low Muscle Mass – Tall & Obese Children
A Special Genre of Obesity
Ralt D., Med Hypotheses. 2007;68(4):750-5
The prevalence of over-weight and obesity has increased markedly in the last two decades and vast international resources have been directed toward researching these issues. Obesity would appear to be a problem that is easy to resolve: just eat less and move more. However, this very common condition has turned out to be extremely troublesome, and in some cases even insolvable. A perspective is presented here suggesting that some of the insoluble cases of obesity are the result of an inborn condition of a very low muscle mass.
The interplay between less muscle and more fat tissue is discussed from physiological and environmental perspectives with an emphasis on the early years of childhood. It is proposed that these interactions lead to bodily economic decisions sliding between thrift or prodigal strategies. The thrift strategy results not only in obesity and less physical activity but also in other maladies which the body is unable to manage.
 What leads to obesity (less muscle, more fat) in the medial population will result in morbid obesity when the children are short of muscle tissue from the start. Attempts to lessen the consequences of low muscle mass, which might be very difficult at adulthood, can be more fruitful if initiated at childhood. Early recognition of the ailment is thus crucial.   
Based on studies demonstrating a 'rivalry' between muscle build-up and height growth at childhood, it is postulated that among the both taller and more obese children the percentage of children with lower muscle mass will be significant. A survey of the height and BMI (Body Mass Index) of Israeli fifth graders supports this postulation.
A special, body/muscle-building gymnastics program for children is suggested as a potential early intervention to partially prevent this type of almost irreversible ill progress of obesity.
If being fit and thin is healthy, then why is obesity so predominant today [1-4]?  Moreover, why does the body surrender muscle tissue so easily [5]? A clue to the answers may lie in the high ‘price’ of muscle. Muscles are amongst the costliest tissues of the body to maintain
[6-8], so it is no wonder that under certain conditions muscle ‘deficiency’ could be of evolutionary benefit (conserving muscle energy may be advantageous, as the saved energy can actuate other functions, e.g. reproduction). This may explain why there is an astounding variation in the response to exercise. While the vast majority of subjects who exercise benefit in some way, there is a minority for whom quite strenuous exercise may have no effect on their fitness and well-being [9-11]. The value of conserving energy may explain why built-up muscles rapidly revert to their original size unless trained or used constantly [12, 13]. It may also suggest why, when walking, we naturally choose the pace that minimizes energy cost per distance, even when this strategy requires a greater relative aerobic effort [14]. The natural tendency to save energy, which results in obesity in our affluent society, is accompanied by other ailments which are not taken care of under the thrift strategy of the body. This may explain why obesity during childhood is linked to premature signs of cardiovascular disease [15], or why obese children are more likely to fracture their bones [16].
This article suggests an integrative novel perspective on obesity with special emphasis on a subgroup of obese population with a very low muscle mass. Such obesity might be very hard to resolve on adulthood and thus earliest characterization is crucial. Data of 1,003 Israeli fifth graders is analyzed and relations between obesity and their height indeed show that taller children (especially girls) are more likely to lack muscles and be obese. The approach presented here will hopefully contribute to the current perspective of biological issues integrating the core with the plasticity of metabolic networks [17].
Negotiations with muscles
Experiments with animals have shown that even the expression of a genetic predisposition to high physical performance strongly depends upon the environment experienced early in life. Fully fed lizards experienced a marked reversal of performance within only one month after birth [18]. The lizards take advantage of the excess food and save muscles activity. On the other hand, mice pups whose mothers had received 30% less energy during pregnancy were born underweight. These pups experience the normal increase in blood leptin a week earlier than usual, and when they receive a high-fat diet they gain weight faster than their counterparts born to normally-fed mothers [19]. These results indicate the ease with which fat is favored over muscle in the animal kingdom. The same trends of energy savings (less muscle, more fat) under deprivation were also observed in humans. Babies who were conceived during the Dutch famine of 1944–1945 showed higher rates of obesity at age 19 and age 50 than the rates of those conceived before or after that challenging period [20]. This suggests that babies who receive poor nutrition in the womb, ‘expect’ to face food shortages after birth as well, and their metabolism is programmed to be especially thrifty with the calories they receive. When such individuals eat the rich diets typical of today's developed countries, they quickly become overweight.
This obesity, which is part of natural developmental plasticity [21], will become inevitable and dramatically accentuated in the case of an inborn muscle deficiency, characterizing the Low Muscle Mass (LMM) special group. LMM definition is only generally referred to at this stage, before specific and of course more data on morbid obesity are evaluated. The relative decrease in muscle tissue is probably gradual in the population but there is a critical muscle mass below which irreversible obesity is expected.
Obesity in affluent Western societies is not necessarily obvious in less affluent environments [22]; it is related to food abundance. LMM physiology can also explain the obesity paradox where, under certain conditions fatter subjects are healthier [23, 24] or, why after age 70 obesity is not related to mortality [15, 25]. As mentioned above, saving muscle energy may benefit other functions like health or longevity. In spite of some of the potential benefits of LMM in non-affluent societies, in our plentiful society it is associated, like other types of obesity, with grave multiple health problems [26]. In addition, LMM might present an additional tough complication: it may not be resolved with physical activity like other obesity genres, as initially there is not enough muscle tissue with which to work out. LMM may result in morbid obesity where even surgical treatment [27], the more problematic solution, might not suffice. Prevention, important in all obesity types, is thus vital in the LMM group. As attempting to lessen the consequences of LMM is very difficult at adulthood, it becomes crucial to identify this malady at childhood, when prevention can be more effective.
It is important to emphasize that the majority of obese people have average muscle mass [28]. It is thus expected that the sub-group with low muscle mass will comprise only a small percentage of the population.    
Height and obesity
The high cost of the muscle mass can be observed in girls where ‘competition’ is created between muscle build-up and both spurts of height and menarcheal timing.
Female gymnasts experience adolescent growth spurts in height that occur approximately 1-2 years later than non-athletic adolescent girls and are slightly less intense [29-31]. Similar delayed height spurts were also demonstrated in male gymnasts [31]. Obesity itself is also correlated with earlier menarcheal age, while sexual maturation in female athletes is delayed [32, 33]. These data demonstrate the intervention of muscle in restraining obesity or withholding physical maturation. In light of these findings we can thus assume that girls with LMM will be taller and fatter compared to normal girls, and that they will also have early menarcheal timing. It might be that obese girls in the LMM group are more noticeable than boys, who initially have higher muscle mass.
A correlation between height and obesity has been established in children; moreover, the obesity trait was also correlated between their height in childhood and their adiposity in adulthood. A child with a height-for-age above the 95th percentile (P) was approximately two and a half times as likely to have a BMI (Body Mass Index = kg/m2) of 30 and approximately five times as likely to have a skinfold sum above the 90th P in adulthood [1].  
The correlation between obesity and height has been established in many countries. A French study showed that the increase in the prevalence of obesity is indeed accompanied by a global trend of accelerated growth [34] and a study in Chile has shown that obese preschool children were four centimeters taller than the normal weight controls [35]. Tracking body size from birth to late adolescence has shown that even in newborns, the tallest and heaviest baby girls had the strongest chance of becoming overweight at age 16 [36]. The interplay between growth and obesity represents a physiological adaptive trait. This trait enables the body to choose between investing energy in growth or saving energy for storage, a decision which naturally depends on the environmental conditions.  
Obesity hormones indeed do affect growth. It has been shown that tall and obese children exhibit variation in the ghrelin gene [37], and leptin was shown to stimulate growth even in the presence of caloric restriction [38].
The hypothesis presented here focuses on a subset of the obese population. Although BMI has complicated relationships with total fat mass, it does reflect adiposity in girls with high BMI [39]. In order to test whether the chance of becoming obese is higher above certain height, BMI data of 1,003 fifth-grade children from Tel Aviv, Israel were collected. As shown in Fig. 1, the girls' data exhibit correlation between BMI and height and above 1.54 m height there is a leap in the average BMI of the girls. This implies that taller girls have clearly an increased chance to become obese, suggesting a higher probability for initial lower muscle mass. The boys' data also exhibit correlation between height and BMI but as high BMI might not reflect only obesity in boys, interpretation of data is not simple and thus not discussed in this article.
What can be done?
The ease with which many individuals gain weight suggests that the energy homeostasis system in the body is inherently biased toward weight gain [40] and thrift strategy. Moreover, in many mammals, energy stores are held relatively constant [41]. These and other findings, like the many-fold regulatory materials [42, 43] excreted by fat cells, suggest that fat cells are not inert fat storage depots but rather active, manipulative cells in ‘dialogue’ with muscles and other tissues [44]. These fat tissue tactics may be a burden to any obesity solution, and are especially severe for those with Low Muscle Mass and hence less ‘muscle-negotiation’ capability. In the LMM group it is particularly important to avoid fat storage as early as possible, before it may become irreversible; thus early treatment of childhood obesity is mandated [45]. The difficulty in losing weight was stated by the U.S. Preventive Services Task Force, which found insufficient evidence for the effectiveness of behavioral counseling or other preventive interventions with overweight children [46].
A special effort should be directed toward defining the children that belong to this hazardous group. Besides tallness, obesity and early sexual maturity it may be interesting to look for additional parameters such as ghrelin levels [37] or a measure of diet-induced thermogenesis [47] that might discern the LMM group within the general obesity group.
All that is proposed to treat obesity [48] is also relevant to the LMM group, but as hypothesized it will fail more frequently than usual unless the muscle deficiency issue is addressed in early childhood. The recommendation of the American Academy of Pediatrics was that pre-adolescents and adolescents should avoid competitive weight lifting, power lifting, body building and maximal lifts until they reach physical and skeletal maturity [49]. It is suggested here that at least for the special group of LMM children, these recommendations should be reevaluated and body building should be allowed under close supervision.
A broader data pool (beyond the scope of this article) is needed to accurately define the LMM group, or the group in which the LMM phenotype will be more prevalent. However, data are available in many world centers and collaborative efforts can assist in defining the cutting point of height and weight for the prospects of LMM.
Not very many studies have directly tested the great benefits of exercise on children [50].
However, initial studies concerning strength training are starting to accumulate [51-53]. A recent study showed that obese children who participated in a weight-training group experienced a significant increase in muscle strength, while the control group had no such increase. In the same study, the fat mass of the children in the weight-training group did not change during the ten-week course of the study, while the children in the control group gained an average of more than 2.5 pounds of fat during the same period [54].
A body/muscle-building gymnastics program that is currently restricted to older youth is suggested for younger LMM children. As recommended by the ACSM, all youth strength training programs should be closely supervised by knowledgeable instructors who understand the uniqueness of children.
This novel approach can prevent or decrease weight gain early, thus avoiding the need to lose weight later, which is unquestionably a very difficult task to achieve.
1. Freedman DS, Khan LK, Mei Z, Dietz WH, Srinivasan SR, Berenson GS: Percentiles of childhood height-for-age are related not only to childhood adiposity but also to adult adiposity. Pediatrics 2002, 109:e23.
2. Marild S, Bondestam M, Bergstrom R, Ehnberg S, Hollsing A, Albertsson-Wikland K: Prevalence trends of obesity and overweight among 10-year-old children in western Sweden and relationship with parental body mass index. Acta Paediatr 2004, 93:1588-1595.
3. Will B, Zeeb H, Baune BT: Overweight and obesity at school entry among migrant and German children: a cross-sectional study. BMC Public Health 2005, 5:45.
4. Padez C, Fernandes T, Mourão I, Moreira P, Rosado V: Prevalence of overweight
and obesity in 7-9-year-old Portuguese children: trends in body mass index from 1970-2002. Am J Hum Biol 2004, 16:670-678.
5. Friedlander AL, Braun B, Pollack M, Macdonald JR, Fulco CS, Muza SR, Rock PB, Henderson GC, Horning MA, Brooks GA, Hoffman AR, Cymerman A: Three weeks of caloric restriction alters protein metabolism in normal weight, young men. Am J Physiol Endocrinol Metab 2005, 289:E446-455. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=15870104&query_hl=29
6. Henriksson J: The possible role of skeletal muscle in the adaptation to periods of energy deficiency. Eur J Clin Nutr 1990, 44:55-64.
7. Slentz CA, Duscha BD, Johnson JL, Ketchum K, Aiken LB, Samsa GP, Houmard JA, Bales CW, Kraus WE: Effects of the Amount of Exercise on Body Weight, Body Composition, and Measures of Central Obesity. Arch Intern Med 2004, 164:31-39.
8. Ralt D: Why do we eat? Med Hypotheses 1994, 42:5-10.
9. Eisenmann JC, Katzmarzyk PT, Perusse L, Tremblay A, Despres JP, Bouchard C: Aerobic fitness, body mass index, and CVD risk factors among adolescents: the Quebec family study. Int J Obes (Lond) 2005, 29:1077-1083. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=15917844&query_hl=6
10. Jakicic JM, Marcus BH, Gallagher KI, Napolitano M, Lang W: Effect of Exercise Duration and Intensity on Weight Loss in Overweight, Sedentary Women. JAMA 2003, 290:1323-1330.
11. Teran-Garcia M, Rankinen T, Koza RA, Rao DC, Bouchard C: Endurance training-induced changes in insulin sensitivity and gene expression. Am J Physiol Endocrinol Metab 2005, 288:E1168-1178.
12. Hattori K, Kondo M, Abe T, Tanaka S, Fukunaga T: Hierarchical differences in body composition of professional Sumo wrestlers. Ann Hum Biol 1999, 26:179-184.
13. Andersen LL, Tufekovic G, Zebis MK, Crameri RM, Verlaan G, Kjaer M, Suetta C, Magnusson P, Aagaard P: The effect of resistance training combined with timed ingestion of protein on muscle fiber size and muscle strength. Metabolism  2005, 54:151-156.
14. Browning RC, Kram R: Energetic cost and preferred speed of walking in obese vs. normal weight women. Obes Res 2005, 13:891-899.
15. von Haehling S, Doehner W, Anker SD: Obesity and the Heart: A Weighty Issue. J Am Coll Cardiol 2006, 47:2274-2276.
16. Taylor ED, Theim KR, Mirch MC, Ghorbani S, Tanofsky-Kraff M, Adler-Wailes DC, Brady S, Reynolds JC, Calis KA, Yanovski JA: Orthopedic Complications of Overweight in Children and Adolescents. Pediatrics 2006, 117:2167-2174.
17. Almaas E, Oltvai ZN, Barabasi AL: The activity reaction core and plasticity of metabolic networks. PLoS Comput Biol 2005, 1:e68.
18. Le Galliard JF, Clobert J, Ferriere R: Physical performance and Darwinian fitness in lizards. Nature 2004, 432:502-505.
19. Yura S, Itoh H, Sagawa N, Yamamoto H, Masuzaki H, Nakao K, Kawamura M, Takemura M, Kakui K, Ogawa Y, Fujii S: Role of premature leptin surge in obesity resulting from intrauterine undernutrition. Cell Metab 2005, 1:371-178. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=16054086&query_hl=15&itool=pubmed_docsum
20. Ravelli AC, van Der Meulen JH, Osmond C, Barker DJ, Bleker OP: Obesity at the age of 50 y in men and women exposed to famine prenatally. Am J Clin Nutr 1999, 70:811-816.

21. Barker DJ:  The developmental origins of well-being. Philos Trans R Soc Lond B Biol Sci 2004, 359:1359-1366.
22. Ravussin E, Valencia ME, Esparza J, Bennett PH, Schulz LO: Effects of a traditional lifestyle on obesity in Pima Indians. Diabetes Care 1994, 17:1067-1074.
23. Curtis JP, Selter JG, Wang Y, Rathore SS, Jovin IS, Jadbabaie F, Kosiborod M, Portnay EL, Sokol SI, Bader F, Krumholz HM: The obesity paradox: body mass index and outcomes in patients with heart failure. Arch Intern Med 2005, 165:55-61.
24. Sørensen TIA, Rissanen A, Korkeila M, Kaprio J: Intention to lose weight, weight changes, and 18-y mortality in overweight individuals without co-morbidities. PLoS Med 2005, 2:e200.
25. Blackberry I, Kouris-Blazos A, Wahlqvist ML, Steen B, Lukito W, Horie Y: Body mass index is not a significant predictor of survival amongst older people. Asia Pac J Clin Nutr 2004, Suppl 13:S137.
26. Thompson TJ: Calories Count – FDA Obesity Working Group Report and Related Information. FDA/Center for Food Safety & Applied Nutrition, March 12, 2004.
27. Crookes PF: Surgical treatment of morbid obesity. Annual Review of Medicine 2006, 57:243-264.
28. Lafortuna CL, Maffiuletti NA, Agosti F, Sartorio A: Gender variations of body composition, muscle strength and power output in morbid obesity. Int J Obes Relat Metab Disord 2005, 29:833-841.
29. Thomis M, Claessens A, Lefevre J, Philippaerts R, Beunen G, Malina R: Adolescent growth spurts in female gymnasts. J Pediatr 2005, 146:239-244.
30. Lindholm C, Hagenfeldt K, Ringertz BM: Pubertal development in elite juvenile gymnasts. Effects of physical training. Acta Obstet Gynecol Scand 1994, 73:269-273.
31. Markou KB, Mylonas P, Theodoropoulou A, Kontogiannis A, Leglise M, Vagenakis AG, Georgopoulos NA: The influence of intensive physical exercise on bone acquisition in adolescent elite female and male artistic gymnasts. J Clin Endocrinol Metab 2004, 89:4383-4387.
32. Garn SM, LaVelle M, Rosenberg KR, Hawthorne VM: Maturational timing as a factor in female fatness and obesity. Am J Clin Nutr 1986, 43:879-883.
33. Freedman DS, Khan LK, Serdula MK, Dietz WH, Srinivasan SR, Berenson GS: The relation of menarcheal age to obesity in childhood and adulthood: the Bogalusa heart study. BMC Pediatrics 2003, 3:3.
34. Heude B, Lafay L, Borys JM, Thibult N, Lommez A, Romon M, Ducimetiere P, Charles MA: Time trend in height, weight, and obesity prevalence in school children from Northern France, 1992-2000. Diabetes Metab 2003, 29:235-240.
35. Kain J, Albala C, Garcia F, Andrade M: Obesity in Chilean preschool children: anthropometric evolution and socioeconomic determinants. Rev Med Chil 1998, 126:271-278.
36. Pietilainen KH, Kaprio J, Rasanen M, Winter T, Rissanen A, Rose RJ: Tracking of body size from birth to late adolescence: contributions of birth length, birth weight, duration of gestation, parents' body size, and twinship. Am J Epidemiol 2001, 154:21-29.
37. Korbonits M, Gueorguiev M, O'Grady E, Lecoeur C, Swan DC, Mein CA, Weill J, Grossman AB, Froguel P: A variation in the ghrelin gene increases weight and decreases insulin secretion in tall, obese children. J Clin Endocrinol Metab 2002, 87:4005-4008.
38. Gat-Yablonski G, Ben-Ari T, Shtaif B, Potievsky O, Moran O, Eshet R, Maor G, Segev Y, Phillip M: Leptin reverses the inhibitory effect of caloric restriction on longitudinal growth. Endocrinology 2004, 145:343-350.

39. Demerath EW, Schubert CM, Maynard LM, Sun SS, Chumlea WC, Pickoff A, Czerwinski SA, Towne B, Siervogel RM: Do changes in body mass index percentile reflect changes in body composition in children? Data from the Fels Longitudinal Study. Pediatrics 2006, 117:e487-495.
40. Schwartz MW, Woods SC, Seeley RJ, Barsh GS, Baskin DG, Leibel RL: Is the Energy Homeostasis System Inherently Biased Toward Weight Gain? Diabetes 2003, 52:232-238.
41. Cowley MA, Pronchuk N, Fan W, Dinulescu DM, Colmers WF, Cone RD: Integration of NPY, AGRP, and Melanocortin Signals in the Hypothalamic Paraventricular Nucleus: Evidence of a Cellular Basis for the Adipostat. Neuron 1999, 24:155-163.
42. Nawrocki AR, Scherer PE: The delicate balance between fat and muscle: adipokines in metabolic disease and musculoskeletal inflammation. Curr Opin Pharmacol 2004, 4:281-289.
43. Seeley RJ, D'Alessio DA, Woods SC: Fat hormones pull their weight in the CNS. Nat Med 2004, 10:454-455.
44. Turtzo LC, Marx R, Lane MD: Cross-talk between sympathetic neurons and adipocytes in coculture. Proc Natl Acad Sci U S A 2001 98:12385-12390. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=11606782&query_hl=12&itool=pubmed_docsum
45. Nemet D, Barkan S, Epstein Y, Friedland O, Kowen G, Eliakim A: Short- and long-term beneficial effects of a combined dietary-behavioral-physical activity intervention for the treatment of childhood obesity. Pediatrics 2005, 115:e443-449.
46. US Preventive Services Task Force: Screening and Interventions for Overweight in Children and Adolescents: Recommendation Statement. Pediatrics 2005, 116:205-209.
47. Westerterp KR: Diet induced thermogenesis. Nutr Metab (Lond) 2004, 1:5.
48. Dietz WH, Robinson TN: Clinical practice. Overweight children and adolescents. N Engl J Med 2005, 352:2100-2109.
49. Committee on Sports Medicine and Fitness: Strength Training by Children and Adolescents. Pediatrics 2001, 107:1470-1472.
50. Watts K, Jones TW, Davis EA, Green D: Exercise training in obese children and adolescents: current concepts. Sports Med 2005, 35:375-392.
51. Benjamin HJ, Glow KM: Strength Training for Children and Adolescents. The physician and sportmedicine 2003, 31:9.
52. Faigenbaum AD: Strength training for children and adolescents. Clin Sports Med 2000, 19:593-619.
53. Weltman A, Janney C, Rians CB, Strand K, Berg B, Tippitt S, Wise J, Cahill BR, Katch FI: The effects of hydraulic resistance strength training in pre-pubertal males. Med Sci Sports Exerc 1986, 18:629-638.
54. Holian CM, King JT, Griffith JR, Adams KJ, Clasey JL: The Effects Of Resistance Training On Measures Of Body Composition And Strength In Children. American College of Sports Medicine 52nd Annual Meeting: 1-4 June, 2005; Nashville, Tenn.

Figure1.   BMI vs. height of 5th graders.


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