Catastrophe Theory Model for the Regulation of Human Growth

Author(s): Barry Bogin

Source: Human Biology, Vol. 52, No. 2 (May 1980), pp. 215-227
Published by: Wayne State University Press
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Catastrophe Theory Model for the Regulation of Human
Growth

By BarryBogin1

ABSTRACT

Over200mathematical formulae that

exist model someaspect ofhuman growthand
development. Whilemanyofthesequantitative functions describethegrowth
processwithgreat noneexplains
precision, howgrowth is regulated.
Buildingon
earlier
attemptstodevelop a conceptualmodelofgrowth thispaper
regulation,
presentsa qualitative
modelofgrowth basedon catastrophe theory.Thisis a
newbranch
relatively ofmathematicsthatinvestigates
thewaythings change.The
modeldescribes
catastrophe thenormal rangeofvariation and
forpreadolescent
adolescent
growth andsuggestsa novelexplanation
forthechange ingrowth rate
thattakesplaceduring Catastrophe
puberty. theoryis alsousedtomodelselect
ontogeneticchangesinneuroendocrinedevelopment thatarebelieved tobe re-
latedtothegrowth process.Areasofoverlapbetween thecatastrophe modelfor
growth and thecatastrophe modelforneuroendocrine ontogeny suggest how
growthmaybe regulated andhelpdefine testable
research questions.

Over 200 mathematicalformulaehave been proposed thatmodel some

aspect ofgrowthand development(Timeras,1972). Of these,about halfa
dozen are widelyused fortheanalysisofhumangrowth(Marubini,1978).
These functions(e.g. the Gompertz and logistic functions)describe
growthover timeverywell, but theydo notexplainwhygrowthoccursor
how it is regulated.Moreover,the parametersof these functions, while
mathematicallyprecise, are arbitraryand have little or no biological
meaning.In 1963,Tannerproposeda conceptualmodelfortheregulation
ofhumangrowth.Figure 1 representsitsbasic elements.A majorfeature
The
of this model is that growthis targetseekingand self-stabilizing.
curve labeled Time Tally 1 representsa hypotheticalmechanismthat
providesa "targetsize" forbody growth,and also, keeps trackofbiologi-
cal time during infancyand childhood. The curve labeled "Inhibitor"
representsthe concentrationin the body of a hypotheticalsubstance,
perhapsa by-productofcell divisionor proteinsynthesis,thatacts upon
the time tally to regulate growthrate. The amount of mismatch,M,
betweenthe two curvesdeterminesrate ofgrowthat each chronological
age. The model accountsforthe decelerationof growthvelocityduring
infancyand childhoodand explainsthe phenomenonofcatch-upgrowth

ofAnthropology,
department WayneStateUniversity,
Detroit, 48202.
Michigan

Human May1980
Biology, , Vol.52,No.2, pp.215-227.
StateUniversity
Wayne Press,1980

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216 Bogin
Barry

Fig. 1. Tanner's model

conceptual ofhuman
fortheregulation Seetext
growth. for
expla-
nation Tanner,
(After 1963).

followingserious illness or starvation(see Tanner, 1963 fordetails). To

accountforthe abruptchangesin growththatoccurat adolescence,Tan-
ner proposesthe existenceofa second timetally.The new tallyoperates
in the same manneras the old one but both the new tallyand its inhi-
bitorysubstanceare assumed to be distinct.Tanner suggeststhat the
switchto the new tallyoccurs when a minimumvelocityof growthor
minimummismatchon the old tally is achieved, point L. When the
switchoccursa new largermismatchis establishedand a rapidincreasein
growthrate resultsuntilthe mismatchis stabilizedonce more. Variation
in the timingofthe adolescentspurtbetweenindividualsis explainedby
changingthe pointat whichthe switchtakes place.
This model is as conceptuallystimulatingtodayas it was when pro-
posed by Tanner 16 yearsago. But, it has been politelyignoredby most
researchersin thefieldofhumangrowth.The reasonforthismaybe that
the model conflicts,in at least fourways, with the more widely used
descriptivegrowthfunctions.Tanner'smodel conflictswiththese in that
1) its parameters,althoughspeculative,are biologicallymeaningful, 2) it
is explanatoryand predictiveratherthanonlydescriptive,3) it is qualita-
tive ratherthanquantitative,and 4) it proposesa discontinuousrelation-
ship between the factorsthatregulategrowthbeforeand duringadoles-

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 Catastrophe ModelofGrowth
Theory 217

cence. The firsttwodifferences are desirablein anybiologicalmodel. But

the qualitativenature of the model and the discontinuouschanges it
proposesare at odds withtheconventionalmethodofbuildingmathemat-
ical modelsforbiologicalsystems.This methoduses differential calculus,
which assumes a quantitativeanalysisand a systemthat behaves in a
smoothcontinuousfashion.
Recentlya mathematicalmethodhas been developed wherebyqual-
itative and discontinuousphenomena can be formallydescribed and
analysed.The new methodis derivedfromtopologyand is called catas-
trophe theory(Thom, 1975). Althoughthe name implies disaster,the
purposeofthemethodis to analyseanyphenomenonin whichcontinuous
change in the controllingvariables resultsin discontinuouschange in
theireffect.Catastrophes,in the mathematicalsense, include the sound
produced by pressingon a stampedmetal "clicker,"the change which
comes fromthrowing a lightswitch,and thebreakingofa wave as it nears
the shoreline.In a physicalsense, these catastrophesrepresentthe sud-
den transitionfromone stableequilibriumto another.Figure2 illustrates
thistypeofsimplecatastropheas a suddenchangein the perceptionofan
opticalillusion,the Neckercube. The circleis eitherin the centerofone
face ofthe cube or in the cornerofanotherface.The transition is instan-
taneousand discontinuouswithno sense ofmotionfromone stablecon-
figurationto the otherperceived.The neurologicalbasis forthisillusionis
unknownbut thisexampleillustratesthatdiscontinuouschangeis partof

ofa simple
cube:anillustration
Fig. 2. TheNecker inperception.
catastrope

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218 Barry
Bogin

nature. This "either-or"type of catastropheis the most simple and is

formally called thefoldcatastrophe(Zeeman,.1977).There are, ofcourse,
more complexcatastrophes.But, Thom (1975) has proved thatforpro-
cesses controlledby no more than four factorsthere are just seven
elementarycatastrophes,each witha unique shape and set ofproperties.
One of these, the cusp catastrophe,has a shape and set of properties
similarto severalgrowthphenomena,and therefore it maybe worthwhile
to exploresome ofits features.
The cusp catastropheis illustratedin Figure3. It is a graphofa curved
suffacewitha pleat, called the behaviorsurface,above a planar surface
overwhichtwocontrolfactorsvary.Mathematically, thecusp catastrophe
is associatedwiththefunctionVa(x4)- ax - Vi(bx2),wherea and b are the
controlfactorsand x is the variable whose behavior is plotted on the
behaviorsurface.The topologicalfeaturesof the behaviorsurfacerepre-
sent "the graphof all pointswhere the firstderivitiveof thisfunctionis
equal to zero" (Zeeman, 1976 p. 78). The firstderivitiveof the cusp

Fig. 3. Thecuspcatastrophe
graphwithpathways anddiscontinuous
forcontinuous
change.

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 Catastrophe ModelofGrowth
Theory 219

function is X3- a - bx. Rigorousbut readablemathematical discussionsof

catastrophetheorymay be found in Woodcock and Davis (1978) and
Zeeman (1976, 1977). The glimpseat the mathematicalfoundationofthe
theorygiven here is meant to demonstratethat the graphic repre-
sentationsof the cusp catastrophepresentedin this paper are not arbi-
traryconfigurations or post-factoconstructions.
When plottingthe behavior surface,most combinationsof control
factorone and two resultin a unique solutionforsettingthe firstderiva-
tive equal to zero. These unique solutionsare pointsof stable equilib-
rium,or, the mostlikelymode ofbehaviorforthe particularcombination
ofcontrolfactors.The set ofthese pointsrepresentsthe areas thatdefine
the stable,non-pleated,partofthebehaviorsurface.But forsome combi-
nationsof controlfactorsthere are two solutions,two stable equilibria,
and twomodes oflikelybehavior.Thus, in the middleofthe graphthere
are two over-lappingsheets, connectedby a thirdsheet to make a con-
tinuouspleated surface.The thirdsheet representsunstable equilibria
and itssurfaceis generallyinaccessable.Variationin thecontrolfactorsin
the area ofthe pleat will shiftthe behavioralvariablebetweenthe upper
and lower stable surfaces.Even thoughthe changes in the controlvar-
iables are continuousand smooth,as reflectedin the smoothcontinuity of
the pleated surface,smallchanges in theirrelativelevels cause sudden,
discontinuouschange in behavior. The discontinuousjump between
stablesurfacesis a catastrophe.Both smoothand catastrophicchangecan
occur with the cusp catastrophemodel. Smoothtransitionbetween the
upper and lowersurfacecan occuras in the movementbetween pointsA
and B. Smoothtransitionsalong eithersurfaceare seen in the path be-
tween pointsA and or and D. Discontinuouschange occurswhen a
pathlikethatfrompoint to D is followed.MovementfromD back to
will also resultin a catastrophewhen the edge of the upper surfaceis
reached.
Ifwe now recallTanner'smodel,we mayconsiderthetwotimetallies
to representcurvedline segmentsof the lower and upper behaviorsur-
facesofthecusp model. In Figure 1 these lineswere notconnected.But,
ifwe considerthis graph,which is two dimensional,to be a "slice" cut
throughthe pleated area ofthe cusp model we can visualizehow a third
continuousline can join the othertwo (Figure 4). By expandingthis to
threedimensionswe achieve a fullvisualizationof the cusp catastrophe
model as applied to human growth(Figure 5).
The numberof factorscontrollinggrowthare numerous,but can be
roughlydivided between those thatcontrolamountof growthand those

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220 Barry
Bogin

Fig. 4. TheTannermodelconvertedintoa twodimensional withthe

cuspcatastrophe
ofa pleated
addition curve.

thatcontrolrateofmaturation.I have chosen these as controlfactorsfor

the catastrophemodel. The lowerand upper behaviorsurfacesrepresent
the preadolescentand adolescentgrowthpatterns.These patternsresult
fromthe complexinteractionbetween the species specificgeneticpro-
gram for growthpotential and environmentalfactorsthat influence
growthand maturation.The shape of the behaviorsurfacesof the cusp
catastrophemodel reflectthe shape of the velocitycurve for human
growthduring childhood and adolescence. The rate of preadolescent
growthconstantlydeclines untiladolescence, when there is a rapid in-
crease in growthrate, peak velocityis achieved, and then growthrate
declines. The line, or trajectory,labeled A in Figure 5 parallels this
sequence of changes. The rapid increasein growthrate (the adolescent
growthspurt)is labeled as the pubertycatastrophe.How the changesin
growthrateare regulatedis stillunknown.Tannerproposedthatcontrol
is maintainedby theconcentration ofa growthinhibitingsubstanceacting
directlyon a time tally,presumed to be located in the hypothalamus.
Goss (1978) suggeststhatoverallgrowthrate ofthe body is regulatedby
the geneticallyprogrammedpotentialforenlargementofcertainvisceral
organs. I believe the presentevidence favorsa centralnervoussystem
locationforthe controlmechanism,withgrowthregulationachievedby a

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 ModelofGrowth
Theory
Catastrophe 221

complexsystemof neuroendocrineactivity.A possible controlsystemis

discussedbelow.
Advantageousfeaturesof the cusp catastrophemodel fordescribing
the variabilityof growthrates may be seen by followingthe varietyof
growthtrajectoriespresentedin Figure 5. Startingat the convergenceof
the controlaxes, which representsan arbitrarystartingpoint in mid-
childhood,a child proceeds to growin size and mature.Maturationmay
and integration
be definedas the differentiation ofthe functionalunitsof
the body. Human growthis not possible withoutmaturationifthe indi-
vidual is to remainviable, thus, the smoothpath fromlower to upper
surfacescannotbe followed.An equally unviablepath is one thatresults
froman increasein maturation withouta concomitantincreasein amount
ofgrowth.In thiscase the individualremainsat the pre-adolescentsur-
face. This situationshould not be confusedwith precocious puberty,
whichresultsfroman abnormallyearlymovementto the adolescentsur-
face.(Whilepossiblya variationofthisgeneralmodel,precociouspuberty

model
Fig. 5. Cuspcatastrophe ofhuman
fortheregulation growth.

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222 Barry
Bogin

will not be discussed furtherhere). We are leftin the middle range of

possibletrajectoriesforfavorablegrowth.Ifa childfollowstrajectory A, in
whichrate ofmaturationrunstowardsthe fastend of the normalrange,
the child reaches the end of the lower surfacein an area where the
greatestdistance between lower and upper surfaceexists. The model
predictsgreaterintensitywhen the jump between surfacetakes place.
Trajectory representsthe slowlymaturingchild. The path ofdevelop-
ment moves under the pleat in an area where a relativelyless intense
jump is predicted.The model also predictsthat,afterthejump, child A
will reach maturity(adult size) beforechild B. The predictionsare in
agreementwiththe observedintensityofthe adolescentgrowthspurtin
earlyand late maturingchildrenand theirsubsequentgrowth.The catas-
trophemodelalsoexplains"unusual"casesofadolescentgrowth.The model
predictsthatwhen rate ofmaturationproceeds veryslowly,the puberty
catastrophewill occur near the point of minimaldistance between sur-
faces,and the intensityof thejump will be extremelysmall. The trajec-
torylabeled Q representsthe growthof PeruvianQuechua Indian chil-
dren livingat high altitude.Frisancho(1977, p. 120) reportsthatthese
children"have a late and poorlydefinedadolescentgrowthspurtand a
veryprolongedgrowthperiod."The reasonforthe extremelyslow rateof
maturationis not known but the model predicts both features of
Quechua growth.
Because ofits threedimensionality and topologicalfeatures,the cusp
catastrophemodelprovidesa qualitativelysatisfyingdescriptionofhuman
growth.The model also suggestssome unexpectedpossibilitiesabout the
underlyingfactorsthatactuallyregulategrowth.The catastrophemodel
illustratesan overlapbetweenthepreadolescentand adolescentbehavior
surfaces.This suggeststhatfactorsresponsibleforboth growthpatterns
are operatingsimultaneously forsome period of time. The smoothfold
curve connectingthe two surfacesimplies thatthe variablesregulating
the changebetweenpatternsact in a continuousfashioneven thoughthe
switchfromone patternto the other mustbe discontinuous.I believe
these implicationsof the catastrophemodel are consistentwith recent
advances in our understanding of adolescentdevelopment.Table 1 out-
lines the major neuroendocrinechanges in the hypothalamic-pituitary-
gonadal axis thatoccur duringdevelopment.This table is based on the
clinicaldata gatheredby Grumbachet al. (1974) and Grumbach(1978).
The events listedforma continuousseries of changes between periods,
but resultin severaldiscontinuities
in growthand development,e.g. the
adolescent growthspurtand menarche. Several growththeoristshave

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 Catastrophe ModelofGrowth
Theory 223

TABLE 1.
PostulatedOntogencyof NeuroendocrineActivityof the Hypothalamic-
Axisa'b
Pituitary-Gonadal

FetalPeriod
1. Maturation
ofnegative sexsteroid
feedback mechanismafter
150daysgestation.
2. LowlevelofLRFsecretion atterm.
InfancyandChildhoodPeriod
3. Negative
feedbackcontrol ofFSH andLH secretionbecomes sensitive
highly tosex
by2-4years
steroids ofage.
LatePreadolescentPeriod
4. Decreasing ofhypothalamus
sensitivity tosexsteroids.
5. Increased ofLRFindependent
secretion ofgonadalcontrol.
6. Increased
pituitary
responsivenesstoLRF.
7. Increased
responsivenessofgonads toFSH andLH.
8. Increased
responsivenessofgonads toFSH andLH.
ofgonadal
secretion
9. Increased hormones.
AdolescentPeriod
10. Continueddecreaseinsensitivity
ofnegative mechanisms
feedback tosexsteroids.
increase
11. Sleep-associated inepisodic ofLH andT.
secretion
12. Maturationofpositivefeedbackmechanism andmaintain
to exhibit an estrogen
LH surge.
induced
inmales;ovulation
13. Spermatogenesis infemales.
aModified
from 1978.
Grumbach,
bFSH,follicle hormone;
stimulating LRF,LH-releasing
hormone;
LH,luteinizing factor;
T, testosterone.

emphasized that not only the growthspurt,but the entire patternof

adolescentgrowthis completelydifferent fromthe patternbeforeadoles-
cence (Bertalanfiy,1960; Mellits and Cheek, 1968; Bock et al. 1973;
Frisch, 1974; Habicht, 1974; Largo al. 1978; Bogin, 1978). It is this
et
qualitativecharacteristicof human growththat makes it amenable to
catastrophemodeling.For "whenevera continuouslychangingforcehas
an abruptlychangingeffect,the process must be described by a catas-
trophe"(Zeeman, 1976,p. 80). Similarly,theontogenyofneuroendocrine
activityoutlinedin Table 1 is a candidateforcatastrophemodeling.Fig-
ure 6 presentsthe cusp catastrophemodel withchanges in neuroendo-
crinedevelopmentlabeled at pointsalonga pathwayofdevelopment.The
pointoforiginforthe controlaxes, althoughusuallyarbitrary, maycorre-
spond to a state of maturationthat occurs about 150 days afterfertiliza-
tion.Atthistimethefetalhypothalamus becomes sensitiveto thelevelsof
circulatingsex steroids.This sensitivitymaturesintoa negativefeedback

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224 Barry
Bogin

Fig. 6. Relation
ofneuroendocrine ofthehypothalamic-pituitary-gonadal
ontogeny axisto
ingrowth
changes rate.

systemregulatingthe secretionof luteinizinghormone-releasing factor

(LRF). Low LRF secretiondiminishesthe pituitarysecretionof follicle
stimulating hormone(FSH) and luteinizinghormone(LH), and thismain-
tainsgonadalhormonesecretionat low levels. LRF secretionis relatively
low at term,and the entire negativefeedbacksystembecomes highly
sensitiveand stableby two to fouryearsofage. This systemofneuroen-
docrineactivitymay,in part,regulatethe preadolescentgrowthpattern.
As this systemmatures,rate of growthrapidlydiminishes,reachinga
stable level between the ages of two to fouryears,or at about the same
timeas the negativefeedbacksystemstabilizes.During the late preado-
lescentperiod,twochangesoccur.The firstis thedecreasingsensitivity of
the hypothalamusto sex steroidlevels in circulation.The second is the
initiationof a new LRF secretionregulatingsystem.There is recent
evidence that this new system may be influenced by changing
hypothalamicsensitivityto, or productionof new, morphine-like brain

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 Catastrophe ModelofGrowth
Theory 225

peptides(Blanket al. 1979). In fact,the new systemcan begin operating

independentlyof gonadal functionand the negative feedback control
characteristicof the earlierpreadolescentperiod. An increase in LRF,
LH, and FSH (but not sex steroids)has been observed to occur in indi-
viduals with gonadal dysgenesisat about the same time as in normal
children(Boyaret al. , 1973;Grumbach,1978). Because thelatepreadoles-
centrisein gonadatrophic hormonesis independentofpre-existing gonadal
function,and since the gonadal steroidsand the morphine-likebrain
peptidesoriginatefromwidelydivergenttissuesin the body, it has been
suggestedthatthese neuroendocrinechanges providea biologicalindex
forthe initiationof puberty(Boyer et al. 1972, 1973, 1974; Grumbach,
1978; Blank et al. 1979). An interactionbetween the prepubertaland
pubertalsystemscontinuesforsome time,as indicatedby the overlapof
surfaceson the model. The influenceofthe pubertalsystemis markedby
the rapid increase of sex steroidlevels and the various developmental
changesin secondarysexual characteristics. The influenceof the prepu-
bertalsystemmaybe seen in the patternofgrowthwhichcontinuesto be
regulatedby preadolescentcontrolsuntila sudden discontinuousswitch
to theadolescentsystemtakesplace. The workofBoyeret al. (1972, 1974)
suggeststhatthe switchoccurs when the adolescent systemmaturesto
the point definedby the sleep-associatedincreasein LH and T (testos-
terone) secretion. At this point the negative feedback control of
hypothalamic LRF secretionvirtuallyterminatesand the influenceofthe
preadolescentsystemends. The growthtrajectory canntogo back to pick
up where the adolescent systembegan, as thiswould necessitatedemat-
uration,so the onlyalternativeis a jump between surfaces.The adoles-
centgrowthspurtmaybe one oftheobservableresultsofthiscatastrophic
change in neuroendocrinegrowthregulatingsystems.As the adolescent
systemcontinuesto mature,a positivefeedbackmechanismdevelopsfor
the capacityto exhibitan estrogen-inducedsurge of LH secretion.This
pulsaterelease ofLH resultsin spermatogenesis in malesand ovulationin
females.At thistime,bothphysiologicmaturationand growthin size are
nearlycomplete.

Discussion
The cusp catastropheparsimoniouslymodels many of the physical
changesthatoccurduringhumangrowth.It also providesa modelforthe
neuroendocrinechangesthatoccurduringdevelopment.The tendencyof
changesin growthand changesin neuroendocrinedevelopmentto coin-

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226 Bogin
Barry

cide suggeststhatthe two processes are related. This, I believe, is the

majoradvantageof the catastrophemodel. Unlike quantitativeformulae
which only describe growthcurves, the qualitativecatastrophemodel
describesthe shape ofthe growthprocessand providessome insightinto
the natureofboth growthand development.These insightsare specula-
tive, but they can be posed as testable researchquestions. Two such
questionsare:
1. Does the sleep-associatedepisodic secretionof LH and testos-
teronemarkthe"take-off" pointfortheadolescentgrowthspurt?
2. What is the relationshipbetween the sleep-associatedrelease of
LH and testosterone,and the sleep-associatedrelease ofgrowth
hormone(or somatomedin)to changes in growthrate at adoles-
cence?
Many more questionscould be posed. If any one of themleads to a
better understandingof adolescent developmentand the regulationof
growthrate, this speculativeand possible purelyimaginarymodel will
have served its purpose.

Acknowledgments
I wish to thankDrs. StephenA. Williamsand Lawrence J. Brenton,
and ProfessorsEdward I. Fry,RobertM. Malina and GabrielW. Lasker
forhelpfuldiscussionsand suggestionsthat substantiallyimprovedthis
paper. I also thankSandraL. Boginforassistancein thepreparationofthe
figures.
23 August1979.
Received:

Literature Cited
Bertalanffy, L. von 1960 Principlesandtheoryofgrowth. In: Fundamentalaspects
ofnormal andmalignant
growth.W. W. Nowinsky (ed.).Elsevier,Amsterdam,pp.
217-255.
Blank,M.S.,A.PaneraiandH. Griesan 1979 Opioid peptides modulateluteinizing
hormone secretion
duringsexualmaturation.
Science,203:1129-1131.
Bock,D., H. Wainer,A. Peterson,D. Thissen,J.MurrayandA. Roche 1973 A
forindividual
parameterization human growthcurves.Human Biol.45:63-80.
Bogin,B. A. 1978 Seasonalpatternintherateofgrowth inheight ofchildren in
living
Guatemala.Amer.J.Phys.Anthrop.49:205-210.
Boyar, R., J. Finkelstein,H. Roffwarg,S. Kapen,E. Weitzmanand L.
Hellman 1972 Synchronization ofaugmented hormone
luteinizing with
secretion
sleepduring N. Engl.J.Med.287(12):
puberty. 582-586.

This content downloaded from 185.44.78.129 on Sat, 21 Jun 2014 13:44:49 PM

All use subject to JSTOR Terms and Conditions
 Catastrophe ModelofGrowth
Theory 227

1973 Twenty-four hourluteinizing hormone andfollicle-stimulating hormone se-

cretory patternsingonadaldysgenesis. J.Clin.Endocrinol. Metab.37:521-524.
Boyar,R. M.,R.S. Rosenfeld,S. Kapen,J.W.Finkelstein, H. P. Roffwarg, E. D.
Weitzman andL. Hellman 1974 Simultaneous augmented secretion
ofluteiniz-
inghormone andtestosterone during sleep.J.Clin.Invest. 54:609-618.
Frisancho,A. R. 1977 Human growth anddevelopment among high-altitudepopula-
tions.In:Thebiology ofhigh-altitude peoples. P. Baker (ed.).Cambridge University
Press,Cambridge, pp.117-171.
Frisch,R. E. 1974 Critical weight at menarche, initiationoftheadolescent growth
spurtandcontrol ofpuberty. In:Control oftheonset ofpuberty. M.M.Grumbach, G.
D. Grace,andF. F. Mayer (eds.).Wiley, NewYork, pp.403-423.
Goss,R. 1978 Adaptive mechanisms ofgrowth control. In: Human growth. Volume 1:
Principles andprenatal growth. F. Falkner andJ.M. Tanner (eds.).Plenum, New
York,pp.1-22.
Grumbach, M. M. 1978 Thecentral nervous system andtheonsetofpuberty. In:
Humangrowth. Volume 2: Postnatal growth, F. Falkner andJ.M. Tanner (eds.).
Plenum, NewYork, pp.215-238.
Grumbach, M. M.,J.. Roth,S. L. KaplanandR. P. Kelch 1974 Hypothalamic-
pituitaryregulationofpuberty inman:evidence andconcepts derived from clinical
research.In:Control oftheonsetofpuberty. M. M. Grumbach, G. D. Grave andF.
E. Mayer (eds.).Wiley,NewYork, pp.115-166.
Habicht,J.-P., R. Marorell, C. Yarbrough,R. M. Malina and R. Klein
1974 Height andweight standards forpreschool children. Lancet, 1:611-615.
615.
Largo, R. H., T. H. Gasser, A. Prader, W. Stuetzle and P. J.
Huber 1978 Analysis of theadolescent growth spurtusingsmoothing spline
functions.Ann.Hum.Biol.5: 421-434.
Marubini, E. 1978 Thefitting oflongitudinalgrowth dataofman.In:Auxology: human
growth inhealthanddisorder. L. GeddaandP. Parisi (eds.).Academic Press, London,
pp.123-132.
Mellits,E. D. and D. B. Cheek 1968 Growth andbodywater. In: Human growth.
D. B. Cheek(ed.).Lee andFebiger, Philadelphia,pp.135-149.
Tanner,J.M. 1963 Theregulation ofhuman growth. ChildDevelopment, 34:817-847.
Thom,R. 1975 Structural stabilityandmorphogenesis. Translated byD. E. Fowler.
Benjamin, Reading.
Timeras,P. S. 1972 Developmental physiology andaging. Macmillan, NewYork.
Woodcock, A.and M. Davis 1978 Catastrophe theory. Dutton, NewYork.
Zeeman,E. C. 1976 Catastrophe theory. Sci.Amer. 234(April): 65-83.
1977 Catastrophe theory: selected papers 1972-1977. Benjamin, Reading.

This content downloaded from 185.44.78.129 on Sat, 21 Jun 2014 13:44:49 PM

All use subject to JSTOR Terms and Conditions