Dissertation

J a m e s W M a r s t e r s o n 1 0 2 5 4 0 2 9 P a g e | 1
Fingerprint patterns and their predictive
value in diagnosing individuals at risk of
developing atopy.
Author
James W Marsterson
Project Advisor
Andrew J Evenden BSc PhD FHEA
Abstract
Background: Atopic disease is a common and major health problem.
Dermatoglyphics have been known to have predictive values for certain diseases of
the atopic triad.
Objective: To see if there is a relationship between fingerprint patterns (loops,
whorls and arches) and an individual’s atopic status.
Method: Created questionnaire and produced atopic and control groups from the
data. The chi square test was used to analyze the data. 201 participants took part.
Results: No statistic or scientific results found between atopic and control groups.
Conclusion: There is no significant difference in the number and type of fingerprint
patterns (loops, whorls and arches) in patients with atopy compared to patients
without atopy.
Key Message
Dermatoglyphics is a simple, in evasive predictive tool for diagnosing certain
diseases of a genetic origin.
 Atopy is known to have a genetic origin, as well as an environmental one.
 No Significant results found between atopic and control groups.
Capsule Summary
Results provided showed no significant difference between atopic and control

groups in relation with fingerprint patterns (whorls, loops and arches).
Key Words
Dermatoglyphics, Atopy, Atopic triad, Asthma, Atopic Dermatitis, hay fever
Abbreviations
IgE = Immunoglobulin E, TH1 = T- helper cell1, TH12 = T-helper cell 12, TH2 = T-
helper cell 2, INFN-y = interferon gamma.

Introduction1
Dermatoglyphics is a form of science used to study patterns of skin ridges (dermal2
ridges) found on fingers, palms, toes and soles of humans (1). It is used in particular3
as an identification tool e.g. for criminal records. Nonetheless, dermatoglyphics has4
sparked serious interest in the fields of medicine and genetics as a form of5
inexpensive, in evasive and simple means of diagnosing patients with diseases.6
In addition, due to the discovery of other previously unknown aspects of7
dermatoglyphics, the subject is developing in all sorts of fields of science8
(anthropology, genetics, medicine and biology) (2). The area of dermatoglyphics has9
increased dramatically since Harold Cummins first described the epidermal ridges10
found on the fingers, palms, toes and soles as dermatoglyphics (3). Further work in11
this area, performed by Cummins and Midlo, has been made in interpreting the12
associations between a number of medical disorders and dermatoglyphics (4).13
For example, in medical conditions such as Turner’s syndrome (5) and Downs14
syndrome (6), studies have suggested that individuals with down syndrome have15
abnormal creases on their palms known as simian creases (6); whereas, individual’s16
with Turner’s syndrome tend to have a higher amount of ulnar loops on their palm17
prints (5). More recently, a study has found a link between the number of whorls and18
patients suffering from a myocardial infarction; with these patients having a higher19
number of whorls on their fingerprints (7).20
Evidence of diseases associated with dermatoglyphics21
Other conditions associated with the predictive value of dermatoglyphics include22
breast cancer (8), schizophrenia (9) and even psoria sis (10).23

Fingerprint formation24
Dermatoglyphics involves the configuration of epidermal ridges that are found on the25
volar surfaces, which are situated on an individual’s toes, palms, soles and fingers26
(11). The traits of dermatoglyphics have their origins developed from the third month27
after fertilization has occurred (12). These traits are unique for each individual28
(including identical twins) and they do not alter after birth (12) (13). It has been claimed29
that dermatoglyphics are an individual’s timeline of events that occur in30
embryological development (12).31
The first visible results of fingerprint pattern formation can be seen between 3-832
weeks of development; a process known as grastulation occurs, where certain cells33
move towards the centre of the sphere; which results in the formation of the primary34
tissue distinctions between the mesoderm, endoderm and ectoderm (14). The35
ectoderm will go on to form the epidermis, which includes the friction ridge skin36
pattern; essential for the development of dermatoglyphic finger patterns (14).37
Between weeks 7-8 of gestation the volar pads (swellings of mesenchyme) begin to38
develop on the fingertips and palms (15). From week 11 the volar pads begin to39
regress, where they are overtaken by the faster growth of the surrounding tissue,40
such as the epidermal ridges, which appear between 10-11 weeks of gestation (12)41
and by week 16 the volar pads have fully merged with the contours of the fingers,42
palms and soles of feet (15). By week 12 the distal finger pads have become fully43
developed (16).44
The events that establish the pattern of an individual’s dermatoglyphics has been45
shown to be genetically determined (17). Nonetheless, dermatoglyphics are still46
affected by the foetuses intrauterine environment as well as their genetic makeup. It47

has been proposed that fingerprint patterns are a result of the buckling instability in48
the basal cell layer of the fetal epidermis; with the stress being induced by the49
resistance of furrows and creases to the differential growth of the basal layer and the50
regression of the volar pads during ridge formation (see figure 1) (18). Environmental51
stresses within the foetuses intrauterine environment help to produce an individual’s52
unique fingerprint (19); some of these environmental stresses include growth stress53
(46), neurotrophic factors (46), volar topography (41), ridge bundles (42) and skeletal54
factors (43) . Many authors have explained the role of different factors in the55
development of fingerprint patterns: growth stress and different growth factors (20),56
the water-logged state of the epidermis cells and thickness of the fetal epidermis (41),57
prenatal maternal environment or prenatal testosterone levels (21).58
Atopy59
An atopic individual is an individual, who has a genetically determined tendency, to60
respond to foreign allergens (harmless antigens) with a mounted immunoglobulin E61
antibody response (IgE) (23). An individual, who is deemed atopic, will have a genetic62
predisposition towards allergic reactions; this could manifest into a triad of diseases63
known as the atopic triad and consists of: allergic asthma, atopic dermatitis and64
allergic rhinitis (24). Recent research has suggested that atopy is a result of genetic65
and environmental factors combined (19) (22) (25) (26). In particular, the genetic basis of66
atopy is affected by a complex interaction of interacting genes or common genetic67
variants (26). Sensitization of allergens occurs within the intrauterine environment of68
the fetus, where environmental factors and genetic factors can influence the69
development of atopy (27). An example of this is a recent study that found that a70
variant of the chromosome 11q13 was associated with individuals with atopic71
dermatitis (28).72

Further studies have shown an association between filaggrin (FLG) gene and73
allergic diseases (29) (30) (31). Furthermore, it has been suggested that maternal history74
of atopic diseases can be a factor; with a study concluding that the maternal history75
of atopic dermatitis was associated with an increased risk of the baby developing76
atopic dermatitis within his/hers first six months of life (32) (48).77
Placental IgE is produced in the mother, which is used to aide the developing foetus78
as its immune system is developing (33). IgE levels have been first observed in the79
foetus at around week 11 (34) by week 20 IgE antibodies can be detected within the80
foetuses blood (33). Studies have found that there are low levels of IgE within cord81
blood; its mere presence suggests that the foetus can produce IgE, as it does not82
cross the placental barrier (35). However, IgE levels can be transferred from the83
mother and enter the foetus (36); thus elevating the levels of IgE within the fetal cords84
blood.85
Atopy and immune system development86
The formation of fingerprints reaches its critical development stage between 9-1787
weeks after gestation (15). At this stage the immune system is also developing (37).88
Intensity of atopy may be related to an individual’s ability to recognise and respond89
to Th1-inducing signals from their extrauterine environment; this has recently been90
suggested by the linking of intensity of atopy with polymorphism in the CD14 gene91
(38). Further studies have suggested that interferon gamma (IFN-y) is associated with92
individuals with atopic diseases. In infants (one year of age) with cow’s milk-93
mediated disease, there was found to be a down-regulation of off IFN-y by beta-94
lactoglobulin-stimulated CBMC (45). With more recent research, finding that TH1795
cells was an enhancer of the development of atopic dermatitis in individuals and that96
IFN-y producing T-cells were associated with chronic lesions of atopic dermatitis (46).97

Atopic individuals also have a higher rate of apoptosis amongst Th1 cells this leads98
to an imbalance in Th2 cells due to apoptosis of allergen-activated IFN-y-producing99
cells (47).100
An individual’s dermatoglyphics remain constant and as such are a lifelong marker of101
the events that occur in gestation. There is no current research that links102
dermatoglyphics with individuals with atopy; with the core literature focusing on103
bronchial asthma and atopic dermatitis (39) (40). With this in mind, an individual’s104
dermatoglyphic characteristics (whorls, loops and arches) were tested along with the105
atopic status of an individual to see if there was a relationship between these two106
variables. The main objectives was to see if a predictive value of dermatoglyphics107
could be found within atopic individuals; in the hope of using it as a predictive tool in108
the medical world.109
110
111
112

Method113
Subject and Study design114
115
Questionnaire116
A questionnaire (figure 2) was produced to separate the control groups (people117
without atopy) against the selective population (people with atopy triad). This118
questionnaire also included sub-categories such as family history of allergy and119
other allergies (that were not part of the atopic triad).120
Data Collection121
Ethical approval was given by the Human ethics committee based at the University122
of Plymouth’s campus on the 29th November 2013. Data was collected on campus.123
Each individual was interviewed and their fingerprints were taken (see figure 3), with124
their consent; these fingerprints and interview answers were then used in the125
statistical analysis. The collection of the participant’s confidential information126
required an explanation of information about the purpose of the research. Further,127
explanation about the right to have data withdrawn was also given.128
Population Selection129
One hundred and twenty nine students and eighteen individuals in full time work130
were used the other fifty three were unidentifiable. Data was collected in a group131
between four people, 201 pieces of data was collected. The age of the participants132
varied from 18 and above; with the greater majority of participants being in their 20s.133
The minimum age was 18 as any participants that were lower would be classed as a134
minor and this would have had an effect on the ethical approval.135
136

Diagnosis of Atopy137
Atopy was diagnosed with the help of the atopic triad: eczema, hayfever and asthma.138
Individuals, whom had all three of these allergic diseases, were put into the atopic139
group. Control groups were healthy individuals without any allergic diseases, any140
known family history of allergic diseases and no known past allergies.141
Result Analysis142
143
Selective Population Analysis144
Frequencies of fingerprint patterns were counted on each hand (left and right) and145
added to give the frequency of both hands for the control and atopic groups.146
Percentages were then calculated to work out the incidence of the type of pattern on147
each hand separately and both hands.148
The acquired categorical data was analysed via the chi square test. The test was149
performed to see if there was a significant difference between characteristics of150
fingerprint patterns (whorls, loops and arches) and an individual’s atopic status.151
Chi Square Test152
A chi squared test was used to show an association between fingerprint patterns and153
atopy. The chi square test was carried out on atopic individuals and the control154
group; results were acquired for the left hand, right hand and both hands. The data155
analysis was performed in Microsoft Excel 2010 and Minitab 16.156
157
158
159
160

Results161
Fingerprint patterns162
163
The traits of dermatolgyphics were analysed by collecting the frequency of each164
pattern (whorl, loop and arch) per print. The results were then totalled for the control165
and atopic groups; where a percentage was calculated to formulate the incidence of166
each type of pattern (see table I). A chi square test was then performed to observe167
any significant difference between the atopic and control groups.168
Whorls169
From this table, it is apparent that the atopic group had a higher incidence of whorls170
on the right hand (32.5%) compared to the control group (17.07%). Furthermore, the171
left hand had a higher incidence (20%) compared to the control group (12%). With172
both hands having a higher percentage for the atopic group (26.25%) than the173
control group (14.52%). However, a chi square test was performed to find any174
significant difference between these two variables (p-value= 0.791). No significance175
was found.176
Loops177
From the table, it can be seen that the control group have a higher incidence of loops178
with the left hand (77.6%), the right hand (69.11%) and both hands combined179
(73.39%); whereas the atopic group’s left hand, right hand and both hands have180
lower incidence values. The frequencies of each pattern were also different with the181
control group having the highest amount of frequencies in the left, right and both182
hands categories.183
184

Arches185
From the table, it can be seen that the control group has the highest incidence of186
arches. With the left hand having a 10.4% incidence value, the right hand having a187
13.82% incidence value and both hands combined having a 12.10% value. However,188
the atopic group only had incidence values of 5% (left hand), 12.5% (right hand) and189
8.75% (both hands). The frequency values were also higher in the control group190
compared to the atopic group.191
Chi Square192
Chi square results were produced from table one. The p-value of these results for193
the left hand of participants was 0.303, the right hand was 0.111 and the results for194
both hands were 0.050 in respect to fingerprint patterns (whorls, loops and arches).195
196
197
198
199
200
201
202
203
204
205
206
207

Discussion208
The diseases eczema, asthma and hayfever make up the atopic triad. They are the209
most common diseases found in developed societies (39) (40). The relationship210
between these diseases and dermatoglyphics has been studied separately. With the211
core literature mostly focusing on bronchial asthma (39) and atopic dermatitis (40), in212
association with fingerprint patterns. However, the relationship between213
dermatoglyphics and atopic individuals has never been studied.214
The hypothesis tested was there is a relationship between the number and type of215
fingerprint patterns (loops, whorls and arches) and the atopic status of an individual.216
The dermatoglyphic fingerprint patterns were categorised into whorls, loops and217
arches. Their frequencies and percentages were calculated to allow an analysis to218
identify any significant differences in the dermatoglyphic pattern between atopic and219
control subjects.220
A chi square of the two groups (atopic and control) was performed and produced a221
result of 0.303 on the left hand, 0.111 on the right hand and 0.050 on both hands.222
These results are greater than the 0.005 value (critical value); therefore the223
hypothesis has to be rejected and the null hypothesis has to be accepted. However,224
there is no current literature to compare these results to.225
Nonetheless, whilst there is no literature that compares atopic subjects against non-226
atopic subjects in relation to fingerprint patterns; other research has found an227
increase in the incidence of whorls in the atopic individuals in diseases such as228
bronchial asthma (39) and atopic dermatitis (40). In relation to this study, no significant229
difference was found between the atopic and control groups (p-value= 0.791) in230

accordance with the incidence of whorls on each hand separately and both hands231
together.232
Limitations233
One of the key limitations of the study was that out of 201 participants there were234
only eight individuals that were deemed atopic. This has a huge effect on the validity235
of the results as the number of participants is not large enough to draw a reliable236
conclusion. However, this could be due to the categorisation of atopic individuals; as237
the categorisation of atopic participants did not include people whom had symptoms238
of the atopic march.239
A further limitation was that there was not an equal number of data for each240
category. For example, in table I it can be seen that there only eight atopic241
individuals compared to 25 individuals in the control group.242
Problems relating to the collection of data were also evident. With many of the prints243
acquired being unreadable due to the poor printer quality of the fingerprints. A better244
quality of print would have led to more samples for the atopic and control groups;245
further increasing the number of fingerprints used for analysis. For example, in data246
number 230 the fingerprints were unreadable.247
The questionnaire is also limited as no anthropological differences were included in248
the questionnaire. For example, it has been found that race can have an effect on249
dermatoglyphic traits (49), where differences were found in the frequencies of palmer250
patterns in negroids (individuals found in Sub-Saharan Africa), mongoloids251
(individuals found in Asia) and Europoids (Caucasians).252

Overall, the results of this study do not provide any further insight into the predictive253
value of dermatoglyphics and their use in diagnosing populations at risk of254
developing atopy. No recommendations for further study are provided as the results255
of this study showed no significant difference between the fingerprint patterns256
(whorls, loops and arches) and the atopic status of the participant.257
258
259
260
261
262
263
264
265
266
267
268
269

Acknowledgements270
I would like to thank all participants that took part in this study. I would also like to271
thank my project advisor Andrew Evenden and my group members Lillie Wilkinson,272
Michaela Jakes and David Knowles for their contribution to the study.273
274
275
276
277
278
279
280

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49.I. Schwidetzky. Race differences in the sex dimorphism of dermatoglyphic traits.431
Journal of Human Evolution.1979;8(8):773-776432
433
434
435
436
437

Tables438
Fingerprint patterns of atopic and control groups (Table I)439
440
Finger
print
patter
n
Atopic (n=8/201) Control (n=25/201)
Left
hand
Percenta
ge (%)
Right
hand
Percenta
ge (%)
Both
hands
Percenta
ge (%)
Left
hand
Percenta
ge (%)
Right
hand
Percenta
ge (%)
Both
hands
Percenta
ge (%)
Whorl 8 20 13 32.5 21 26.25 15 12 21 17.07 36 14.52
loop 30 75 22 55 52 65 97 77.6 85 69.11 182 73.39
arch 2 5 5 12.5 7 8.75 13 10.4 17 13.82 30 12.10
Table I: n = number of participants441
The results table shows the frequency of whorls, loops and arches on the right hand,442
left hand and both hands of Atopic and control groups. It also shows the incident443
percentage of each category. The chi square test was used to observe a significant444
difference between the control and atopic groups.445
446
447
448
449
450
451
452
453
454
455
456
457
458
459

Figure Legends460
Figure 1461
Illustration of the formation of grooves that form a fingerprint (44). From the top left:462
the image shows the epidermis and the dermis. Right: Basal layer rapidly grows.463
Bottom right: Generation of compressive loads. Left: Mechanical loads cause the464
formation of wrinkles that make up the print.465
Figure2466
Questionnaire produced for diagnosis of atopic and control individuals. Provided by467
Andrew Evenden.468
Figure 3469
An example of one of the palm prints taken in the data collection procedure (data470
number 48, left hand).471

Figures472
Figure 1- image showing formation of fingerprints(44)473
474
Figure 2- questionnaire475
See attached page 24476
Figure 3- Image of palm print477
478
479
480
481
482
483
484
485
486
487

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