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Extreme Morphologies Compromise Canine Health and Welfare and Require Evidence-Based Breeding Reform

Submitted:

30 September 2026

Posted:

02 October 2026

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Abstract
In recent years, morphology-driven welfare issues in the domestic dog have moved from the periphery to the center of public and professional attention, driven by breed-specific legislation and bans, dedicated sessions at major welfare conferences, and sustained scrutiny on social media. While these concerns are supported by a growing body of evidence linking extreme traits to chronic disease and compromised welfare, most research has asked only whether one breed or trait extreme differs from another. These approaches leave a critical question unanswered: which range of a given morphological trait is actually healthiest? Advice to “breed away from extremes” therefore lacks an evidence-based target. This review surveys common canine morphological phenotypes including body size, skull shape (brachycephaly), chondrodysplasia and chondrodystrophy, thoracic depth, tail and vertebral conformation, skin folds, and coat-color and hairlessness. For each, we summarize the associated disorders, the underlying biological mechanisms where known, and the welfare consequences. Examining these phenotypes in aggregate rather than trait by trait reveals insights that single-trait studies cannot. Shared mechanisms (e.g., accelerated growth, soft tissue/skeleton mismatch, melanocyte loss) drive multiple disorders simultaneously, and trade-offs across body systems become apparent. We argue that meaningful progress — the kind these legislative, professional, and public efforts are ultimately seeking — requires reframing canine welfare research toward optimization, namely, identifying the phenotypic range that minimizes total morbidity. Such targets are prerequisite to evidence-based breeding goals, revised breed standards, and informed public decision-making. This manuscript is signed by over 30 canine biology and welfare experts who support its content.
Keywords: 
dogs
;  
animal welfare
;  
canine welfare
;  
canine health
;  
animal breeding
Subject: 
Biology and Life Sciences  -   Animal Science, Veterinary Science and Zoology

Introduction

Domestic dogs exhibit exceptional morphological diversity, reflecting a long history of artificial selection that culminated in the development of the modern closed-breed system during the Victorian era [1] (Figure 1). Concerns about the health impacts of extreme morphologies have prompted increasing professional scrutiny, stricter legal regulation of dog breeding in some jurisdictions, and calls for breed standards to remove language that promotes extreme conformation [1]. Health problems related to extreme morphologies are not limited to a few breeds. They are pervasive and endemic, and may be the norm rather than the exception. A number of breed standards permit or prioritize harmful morphologies (Table 1), and the 10 most common breeds in the United States are all marked by two or more such conditions (Figure 2). However, despite ample evidence linking unusual phenotypes with poor health, which range of phenotypes is healthiest remains unanswered. Advice to breed away from the most extreme traits lacks clarity – what is the healthy range to aim for?
This review provides an evidence-based overview of common canine phenotypes, detailing their associated disorders, underlying biological mechanisms where understood, resulting welfare implications, and areas where more research is needed to describe the ideal phenotypic range. Our survey is deliberately broad, because the scale and structure of the problem emerge only in aggregate. We selected morphological extremes present in common breeds and performed a literature search for each morphology, as well as a search for health issues in affected breeds (to catch articles that did not include the name of the morphology in the article title.) We argue that (a) morphology-linked harm is pervasive and convergent rather than confined to single breeds or traits, (b) surveying this harm across traits exposes trade-offs and shared mechanisms invisible to single-trait studies, and (c) progress requires a shift away from comparative questions (whether large dogs differ from small) toward optimization questions which range of values of a trait is healthiest. We intend for this review to inspire future research focused on traits rather than on breeds, a compilation of evidence-based breeding goals, and a foundation for public awareness.

Size

Canine body size is extremely variable, ranging from the Chihuahua (weighing under 6 pounds per the AKC, or as little as 1-3 kg per FCI breed standard) to the Mastiff (weighing up to 230 pounds per the AKC). The largest single genetic contributor to this variation is an IGF-1 polymorphism, with differences in circulating IGF-1 hormone levels influencing body size via differential growth rates [2,3]. Large- and small-breed dogs also differ substantially in growth rate and circulating IGF-I concentrations [4].Canine allometric scaling differs from other similarly sized mammals, with pathologies potentially resulting from size-related differences in organ ratios [5].

Size and Lifespan

Lifespan is strongly and inversely correlated with body size; small dogs live longer than larger dogs [6], with a mean predicted difference of 4.5 years between the smallest and largest breeds [7]. This relationship is linear: a 1 kg increase in body mass is associated with approximately 26 days’ decrease in expected lifespan [7]. Notably, giant breed dogs can reach senescence (the point where mortality risk begins to increase) before achieving their full adult growth [8]. Larger dogs face a higher mortality hazard at every time point once maturity is reached [6,8]. Larger dogs also typically require increased lifetime veterinary care [9].
The mechanism for this difference is likely the negative correlation between lifespan in mammals and postnatal growth rates [6]. Large dogs grow faster and longer to reach their size, with early growth increasing by 0.22 kg/week per 10 kg of adult size [6]. This difference is primarily driven by circulating levels of IGF-1; reduced IGF-1 signaling is associated with increased longevity across species [10]. Whether an inflection point exists in the size-lifespan relationship (how big is too big?) remains undetermined and could guide breeding for longevity.

Size and Cancer

Cancer risk is multifactorial, influenced by many environmental factors including diet and spay/neuter status. Consistent with this review’s focus on morphological phenotypes, we address only the component of risk attributable to body size [6,7,11]. The relationship is approximately linear for toy to medium-sized dogs but flattens for the largest breeds, potentially because their reduced lifespans prevent them from reaching the age of high cancer risk [11,12]. Osteosarcoma provides a particularly clear morphology-linked example: risk rises sharply with body mass and with long-limbed conformation [13].
Osteosarcoma risk rises with body mass and long-limbed conformation [13]. Associated loci include GRB10 [14] and growth-related genes IGF1 and FGF9 [15]. Large and giant breeds show increased risk based on standard weight and height, while dogs at or above their breed’s mean bodyweight have 1.65 times the risk of lighter dogs [13,16]. These findings indicate that body mass contributes beyond skeletal length or breed identity, although the optimal size target remains undefined [13].

Size and Orthopedics

Orthopedic disorders are common and significantly predispose dogs to secondary osteoarthritis, a painful condition of old age that reduces quality of life [17]. Bone and orthopedic disease history increases with body size. In a recent cohort of 131,140 dogs, higher adult body weight was associated with greater risk of an osteoarthritis diagnosis; gonadectomy and younger age at gonadectomy were additional risk factors [13,17]. However, small dogs are more susceptible to specific disorders like patellar luxation, with dogs under 10 kg having 2.8 times greater odds of diagnosis compared to dogs in the 10–19.9 kg range [18].
Canine hip dysplasia (CHD), a developmental malformation of the hip joint, leads to lameness in young dogs and osteoarthritis in older dogs [19]. A 2024 Labrador Retriever genome-wide association study identified separate loci for hip dysplasia and body weight [19]. Elbow dysplasia (ED), an umbrella term for multiple disorders, also commonly affects large dogs [20]. A 2024 study of 17,861 radiographs from 13 breeds found 11.4% sample-wide prevalence, with the highest rates in Rottweilers, Bernese Mountain Dogs, Cane Corsos, and Dogue de Bordeaux [20]. Cranial cruciate ligament (CCL) disease is one of the most common orthopedic injuries in dogs [21]. Large dogs are diagnosed at younger ages and higher frequencies [21]. Further studies should separate the influence of frame size from body condition across disorders.

Size and Heart Disease

Cardiac disease patterns vary with body size. Myxomatous mitral valve disease predominates in small and medium dogs, although recent work confirms clinically important disease in large breeds in the study population [22]. Conversely, dilated cardiomyopathy remains a concern in large dogs [23]. The size range minimizing total cardiac morbidity remains unclear.

Size and Dental Disease

A 2021 primary-care study found that risk of periodontal disease (PD) increases as adult body weight decreases, with diagnoses occurring most frequently in small-to-medium sized dogs [24]. These breeds are also predisposed to retained deciduous teeth and dental overcrowding due to a mismatch between tooth and skull size, which can exacerbate disease severity [24].

Size and Energy Regulation

Body mass extremes present different energetic challenges. Very small dogs have an elevated risk of hypoglycemia due to their low body mass index and must allocate more metabolism to thermoregulation; conversely, large dogs have a reduced surface area-to-volume ratio, making heat dissipation difficult [25]. In a recent VetCompass study of dogs with heat-related illness, bodyweight was associated with the risk of severe disease, emphasizing the growing welfare consequences of rising global temperatures [25].

Size and Labor Difficulties

Bitches at both size extremes are at increased risk for dystocia [26]. The risk for small breeds, with toy breeds particularly affected. One hypothesized mechanism is decreased litter size, which yields larger individual puppies that mismatch the maternal birth canal [26]. Recent data further show that Caesarean delivery is more frequent at both litter-size extremes and varies substantially among breeds [27].

Size and Behavior

Behavioral differences are correlated with body size. Smaller breeds exhibit increased risk of fearful and/or aggressive behavior and decreased ability to follow human pointing gestures, while trainability is positively associated with size [28,29]. These differences could stem from anatomical factors, such as reduced neocortex (linked to trainability and flexibility) and enlarged subcortical regions (linked to fear and aggression) in smaller breeds [29], or from owner management, as owners of smaller dogs may be less likely to train or socialize them.

Skull Shape

Canine skull shape ranges from long and narrow (dolichocephalic) to average (mesocephalic) to the shortened muzzle and wide head characteristic of brachycephalic dogs (Figure 3). Recent population-level analyses illustrate the cumulative health burden associated with the latter extreme. A recent UK life-table analysis estimated the breed’s life expectancy at birth at 4.53 years in the study population [30]. Furthermore, in a 2021 VetCompass study, French Bulldogs had increased odds of 20 of 43 common disorders compared with other dogs, including approximately 31-fold greater odds of BOAS [31].

Skull Shape - Brachycephalic Obstructive Airway Syndrome (BOAS)

BOAS is the syndrome most associated with brachycephaly. It results from artificial selection that has reduced the muzzle bones without proportionally reducing surrounding soft tissues [32]. This size mismatch creates severe upper airway obstruction, leading to secondary pathologies due to chronically increased negative airway pressure [32,33]. Consequences include dyspnea, heat and exercise intolerance, sleep apnea, gastrointestinal signs (e.g., reflux, regurgitation), collapse, and death [32,33].
The congenital soft tissue changes typically begin with stenotic nares (narrowed nostrils), followed by a thickened soft palate and a potentially thickened tongue, all of which impede air passage [32,33,34]. The trachea may be narrowed, and the nasal turbinates (bony structures designed for thermoregulation) may protrude into the airway [32,33].
BOAS is often progressive due to chronic resistance to airflow. Secondary changes include further thickening of soft tissues [34] and degradation of laryngeal tissue, which can lead to life-threatening laryngeal collapse [32,33]. The persistent negative airway pressure also affects the gastrointestinal tract, commonly causing reflux, regurgitation, vomiting, and temporary herniation of the stomach [32]. A recent primary-care study found the highest alimentary-disease incidence in French Bulldogs [35]. Furthermore, impaired airflow severely affects thermoregulation; impeded panting puts brachycephalic dogs at high risk for hyperthermia, even at rest in mild conditions [36]. Recent Finnish testing found moderate-to-severe BOAS in 20–30% of English Bulldogs, French Bulldogs, and Pugs, with moderate-to-high heritability; combined assessment of exercise tolerance, respiratory signs, and nostril stenosis was recommended for breeding [37].

Skull Shape and Brain & Nervous System Abnormalities

The compressed skull shape associated with brachycephaly predisposes dogs to disorders of cerebrospinal fluid (CSF) flow, including Chiari-type malformation (CM), and syringomyelia (SM) [38,39]. CM is characterized by crowding of the brain and cervical spinal cord and is often indicated by behavioral signs of pain [38,40]. SM, closely associated with CM, is defined by the presence of a fluid-filled cavity (syrinx) within the spinal cord [38,39,40]. Symptomatic dogs commonly present with pain, reduced activity, phantom scratching, and weakness [39]. In Chihuahuas, persistent fontanelles (open cranial sutures) are associated with SM [39].
SM is a significant welfare issue. It is often progressive and frequently requires chronic analgesia, often leading to euthanasia due to quality of life concerns [39,41]. CM and SM are strongly associated with a shortened, domed skull shape and a tight angle between the nasal and frontal bone [39]. CM prevalence is nearly fixed in some breeds (e.g., 91–100% in Cavalier King Charles Spaniels [CKCS]), and SM prevalence is also high (e.g., 70–74% in CKCS). Breeding efforts to reduce SM have yielded minimal success, likely due to the high heritability of symptomatic SM [41], and strong selection for the desirable domed head shape.The CKCS shows a trend toward a more domed skull and sharper stop [42], despite the breed standard that the skull should not be domed (Table 1). MRI-based selection has produced modest improvement. Among 2,125 Dutch and Danish CKCS MRI scans, SM prevalence declined from 38% in dogs born during 2010–2014 to 27% in those born during 2015–2019; offspring of two affected parents had approximately three times the odds of SM as offspring of unaffected parents [43]. These findings support MRI screening at three years or older and exclusion of affected dogs from breeding.

Skull Shape and Eye Disease

Brachycephalic ocular syndrome arises from interacting conformational abnormalities, including shallow orbits, excessive eyelid aperture, incomplete blinking, nasal-fold trichiasis, and reduced corneal sensitivity. Together these expose and chronically injure the ocular surface, causing pain, ulceration, visual impairment, proptosis, and sometimes loss of the globe [44]. Brachycephalic dogs have 11.18 times the risk of corneal ulcerative disease compared with mesocephalic dogs [45]; nasal folds increase risk fivefold, and a craniofacial ratio below 0.5 increases it twentyfold [46]. Selective breeding toward more moderate ocular conformation could reduce these disorders [44,46].

Skull Shape and Ear Infections

Ear infections (otitis externa and media) are highly prevalent in brachycephalic breeds. The brachycephalic skull shape narrows the external ear canal, impairing drainage and predisposing the dog to infection [47]. Middle ear effusion is often seen even in asymptomatic brachycephalic dogs, further suggesting an underlying drainage problem [47]. A 2022 CT study found severe narrowing of the proximal external ear canal in French Bulldogs and Pugs, although the degree of narrowing was not significantly associated with otitis externa [48]. Middle-ear effusion was also common, occurring in 44% of dogs in that study [48]. A separate 2022 series identified incidental middle-ear effusion in 32% of brachycephalic dogs undergoing evaluation for BOAS, with particularly high prevalence in French Bulldogs [49]. Together, these findings show that brachycephaly is associated with substantial otic anatomical and inflammatory abnormalities, although the pathway from canal narrowing to clinically apparent infection requires further study.

Skull Shape and Developmental Abnormalities of the Skull

Beyond dystocia, a 2024 review found that congenital malformations affect nearly 7% of canine newborns, with brachycephalic dogs particularly predisposed to cleft lip and palate (CL/CP), hydrocephalus, and anasarca [50]. CL/CP results from incomplete tissue fusion during embryonic development and has multifactorial causes, including genetic and environmental influences [50]. These conditions carry substantial mortality and may require intensive management, monitoring, or surgical correction [50,51]. In a 2022 study of 768 neonates, cleft palate was the most frequent malformation, and brachycephalic breeds had approximately three times the odds of producing malformed puppies [51]. Prognosis depends on the location and severity of the defect.

Skull Shape and Labor Difficulties

Dystocia can similarly result from mismatch between fetal head size and the maternal pelvic opening [52]. Large-headed breeds, including English Bulldogs, Boston Terriers, and French Bulldogs, are overrepresented in dystocia cases [26,27,52]. Among 35,121 Danish Kennel Club litters, 37.6% to 40.1% of brachycephalic litters were delivered by Caesarean section, compared with 12.7% to 15.5% overall [53]. In some breeds, C-section prevalence exceeds 80%, and elective procedures are common [52]. Rates are so high that some insurers exclude coverage. Although Caesarean delivery can reduce immediate mortality in high-risk pregnancies, repeated reliance on it may perpetuate morphologies incompatible with unassisted birth.

Dwarfism: Hondrodysplasia

Canine dwarfism is often caused by an fgf4 retrogene insertion on chromosome 18, which results in chondrodysplasia due to a disorder of the growth plate cartilage cells [54,55]. While the limb shortening itself may be benign, this mutation is closely associated with forelimb curvature, or angular limb deformity (ALD) [54,56], which increases the risk of ulnar valgus and complex ALD [54]. The retarded growth of the ulna can cause a compensatory bowing of the radius and carpal valgus [54]. A 2023 clinical study further showed that breed-typical angular limb deformities, including carpal valgus, limb rotation, elbow incongruity, and radial-head subluxation, are associated with functional abnormalities, discomfort, and lameness [56]. These deformities cause greater joint space and significantly increase the risk of elbow joint disease and lameness at an unusually young age [56]. The connection between chondrodysplasia and severe bowing is not fully elucidated, but bowed legs are explicitly called for in the conformation standards of several breeds, including the Skye Terrier, Dachshund, and Cardigan Welsh Corgi, and in addenda to the Basset Hound standard [56] (Table 1).

Dwarfism: Chondrodystrophy

An fgf4 retrogene on chromosome 12 causes chondrodystrophy [57]. Although this mutation contributes less to leg length reduction than chondrodysplasia, it acts additively with the chr 18 insertion and is frequent in many short-legged breeds [57]. The primary welfare concern with this dominant gain-of-function mutation is a significantly increased risk of intervertebral disc herniation (IVDH) [57,58].
In chondrodystrophic dogs, disc degeneration begins early and progresses rapidly.. Almost 100% of the discs in affected dogs degenerate, and herniation can be observed in dogs as young as two years old [59,60]. IVDH is a major welfare issue, often presenting with acute pain so severe that the dog “screams” [61]. The majority of affected dogs are non-ambulatory at diagnosis, and up to 60% require spinal surgery [61]. Even successful treatment does not prevent a high risk of new herniations elsewhere [62]. Recurrence can remain common even after successful surgery; in one recent French Bulldog cohort, 51% experienced recurrent clinical signs [63]. These consequences substantially impact quality of life, and some animals are euthanized after diagnosis or failed treatment. IVDH is highest in Dachshunds (14–33%) but also elevated in Beagles (6%) and Cocker Spaniels (5–6%) [58,61,64]. The allele is highly prevalent in these breeds, making selective breeding away from this serious welfare issue particularly challenging.
Recent work has begun to translate this genetic association into practical breeding strategies. MRI evaluation of young, clinically asymptomatic Dachshunds found degeneration in nearly all examined discs, but also considerable variation among dogs; radiographic disc-calcification scores correlated with both MRI-assessed degeneration and FGF4L2 genotype, supporting the combined use of radiographic and genetic screening [59]. A larger 2025 study of 407 Dachshunds further found that host heterozygous dogs had radiographic calcification scores associated with substantially lower symptomatic-disease risk, leading the authors to propose breeding toward one copy of the deleterious allele as a pragmatic short-term goal [65].

Chest Depth

Historical morphometric work identified thoracic depth relative to width as a strong risk factor for gastric dilatation and volvulus (GDV) [66,67], a life-threatening condition; recent reviews continue to identify deep chest conformation as a central predisposition [68]. GDV is most common in large dogs (6% incidence) [69]. A deep chest results in a large abdominal cavity that allows a full stomach to stretch the hepatogastric ligament, enabling the stomach to twist and cut off blood flow. Risk is higher in dogs with deeper chests; the odds ratio for GDV can be 8.45 from the deepest to the shallowest thorax [67]. Commonly affected breeds include German Shepherd Dogs and Great Danes [68]. GDV is extremely serious, with high mortality rates [68]. Selective breeding away from this phenotype would be effective, but breed standards German Shepherd and Great Dane explicitly mandate a deep chest (Table 1).

Facial Skin Folds in Brachycephalic Dogs

Excessive facial skin in brachycephalic dogs creates deep skin folds that predispose the dog to intertrigo, a painful skin infection caused by the close proximity of skin surfaces, which traps moisture and bacteria. A 2022 VetCompass study of 905,553 dogs quantified the strong relationship between folded-skin conformation and dermatitis; bulldogs showed 49 times the risk of developing intertrigo compared to crossbred dogs, French Bulldogs 26 times, and Pugs 16 times the risk [70]. This condition causes chronic itching, pain, and behavioral changes, often requiring surgery to reduce the folding [70].

Skin Folds Around the Eyes: Entropion and Ectropion

Loose skin around the eyes can cause two distinct but related welfare issues:
  • Entropion: The eyelid margin rolls inward, causing fur to rub on the cornea. This irritation leads to conjunctivitis, dry eye, corneal ulceration, and potential blindness, often requiring surgical correction. Entropion is the most common disorder reported in Shar-peis, affecting 18% of the breed [71].
  • Ectropion: The lower eyelid everts away from the globe, compromising eye protection and lubrication. This causes chronic inflammation and ocular disease, potentially requiring surgery. Loose skin and a “prominent haw” (third eyelid exposure) are explicitly required in the Basset Hound breed standard (Table 1), and recent population-level data confirm that Basset Hounds are among the breeds with the highest ectropion prevalence [72].

Shar Pei Skin Folds

The deep, thick skin folds of the Shar Pei are linked to genetic mutations associated with chronic inflammation and Shar Pei fever, a breed-specific disease characterized by periodic fever bouts [73]. A 2023 study of 1,913 Shar-Pei found that these folds also predispose the dog to entropion, intertrigo, and ear infections [71]. Despite these severe welfare concerns, the breed standard specifically requires “profuse wrinkles on the forehead continuing into side wrinkles framing the face” [71] (Table 1).

Tail Curl: Neurological Disorders

Tightly curled tails are strongly associated with high incidence of congenital vertebral malformations (CVMs) [74,75]. The “screw tail” phenotype in English and French Bulldogs, characterized by an extremely short, curled tail, is linked to the DISHEVELLED 2 (DVL2) mutation [75,76,77]. A separate, unidentified mutation causes the tightly curled, but normal-length, tail in Pugs [75].
CVM prevalence is extremely high in true screw-tailed breeds, ranging from 50% to 80% in neurologically normal French and English Bulldogs, and may approach 100% in Pugs [75].Recent whole-spine screening has strengthened the connection between the externally visible tail and internal vertebral disease. Among 265 French Bulldogs, English Bulldogs, and Pugs, severe tail malformation was significantly associated with congenital vertebral-body malformations, while particular malformation types and greater kyphosis were associated with neurologic deficits [78]. Although CVMs were historically considered benign, they are associated with spinal curvature (kyphosis) [74]. Severe kyphosis (over 35 degrees) is linked to significant neurologic deficits, resulting in non-ambulatory dogs requiring complex, often unsuccessful spinal surgery. Milder kyphosis contributes to spinal instability, which increases the risk of intervertebral disc herniation (IVDH) and discospondylitis (spinal infection) [79]. French Bulldogs are highly affected, suffering IVDH a mean of two years earlier than Dachshunds [79]. This vulnerability is compounded by the breed’s high prevalence of both CVMs (from the screw tail) and the chromosome 12 FGF4 chondrodystrophy allele (91% prevalence) [79]. Similarly, a 2024 study found substantially elevated discospondylitis prevalence in English and French Bulldogs, with affected discs frequently located adjacent to malformed vertebrae [80]. Selective breeding away from the screw-tail phenotype has therefore been recommended to improve welfare [78].

Skin Folds Around the Tail

The deep skin folds surrounding short, curled screw tails frequently trap moisture and become sites of chronic infection. In a 2022 primary-care study, the tail was a commonly affected site in English Bulldogs with skin-fold dermatitis [70]. When medical treatment fails, resolution often requires partial or complete surgical removal of the tail.

Tail Length and Communication

Dogs rely on tail position and movement to communicate emotional states and intentions to both humans and other dogs. Dogs with artificially short or rigidly curled tails may therefore face greater difficulties in social communication, warranting further welfare research.

Coat: Ridge

The Rhodesian Ridgeback is defined by a dorsal ridge, a line of hair growing in the opposite direction. This phenotype is caused by a copy-number mutation involving three fibroblast growth factor genes [81]. An increasing copy number of this duplication is directly linked to an increased risk of dermoid sinus (DS), a developmental disorder in which a sinus tract runs from the skin along the spine, potentially reaching the dura mater [81]. Recent population data indicate, however, that the relationship is more complex than a simple one-locus model. Among 12,700 German Rhodesian Ridgeback puppies, although estimated heritability was high, segregation did not fit a simple Mendelian model and genetic correlation with ridgelessness was weak [82]. DS creates a pathway for infection into the central nervous system. Surgical excision is the treatment, but is not always curative. DS occurs in about 5% of Rhodesian Ridgebacks [83]. Because the mutation is closely associated with both the desired ridge phenotype and DS risk, breeders face a challenge: using heterozygous dogs (which have a ridge and decreased DS risk) requires breeding with ridgeless dogs, a practice met with resistance in the breeding community [83]. These findings suggest that selection against dermoid sinus may be possible without necessarily eliminating the ridge, but better identification of the additional genetic contributors is needed.

Coat: Hairlessness

Hairlessness in breeds like the Chinese Crested is caused by a mutation in FOXI3 and results in canine ectodermal dysplasia (CED) [84]. CED is characterized by dysplastic hair follicles and numerous comedones (acne). Critically, it is also associated with a variable number of missing, malpositioned, undersized, or malformed teeth (Figure 4) [85].

Coat Color and Pattern

  • Recent genetic work has shown that canine coat colors and patterns arise through complex interactions among multiple loci and that only some pigmentation variants have demonstrated health consequences [86]. Extensive White Markings and Deafness: Extensive white markings, due to melanocyte suppression, are associated with congenital deafness in over 90 dog breeds [86]. In Dalmatians, a 2022 genome-wide meta-analysis identified a significant deafness-risk haplotype near MITF, strengthening evidence for a pigmentation-related genetic contribution while indicating that the underlying risk architecture is more complex than a single visible coat characteristic [87]. A mutation in the MITF gene is linked to white markings, blue eyes, and deafness, resulting from a lack of cochlear melanocytes [88]. In Dalmatians, where deafness is prevalent, black patches on the ears correlate with reduced risk [88]. Yet, the AKC Dalmatian breed standard disqualifies dogs with patches (Table 1).
  • Dalmatian Spots and Uric Acid: The gene controlling Dalmatian spotting is closely linked to a mutation in SLC2A9, which disrupts uric acid transport, leading to hyperuricosuria and a high risk of urinary stones [89]. An outcross to the Pointer introduced the wild-type allele, which reduces this health risk. Additionally, recent work identified a duplication within USH2A that contributes to the spotted phenotype through interaction with an incompletely characterized modifier locus [90]. However, some breeders resist using these outcrossed dogs because their spots are sometimes perceived as “frosted.”
  • Merle: The merle pattern is caused by a variable-length SINE insertion in the SILV gene [91]. Recent work in Dachshunds identified cryptic, visually hidden, and mosaic merle variants, including a phenotypically nonmerle dog that produced a double-merle puppy with anophthalmia [92]. Homozygous merle dogs (often mostly white) are at severe risk of deafness (unilateral or bilateral), blindness, microphthalmia, and sterility; heterozygous merles are also at risk, though it is reduced compared to homozygotes [88]. Despite these risks, the pattern is increasingly introduced into new breeds, such as the Poodle and French Bulldog [86].
  • Dilution (CDA): Variants in the MLPH gene cause coat color dilution (e.g., black to “blue”, brown to “isabella” or “fawn”) [93]. One variant (d1) is clearly associated with color dilution alopecia (CDA) [94], a dysfunction of the hair follicle characterized by progressive hair loss, itching, and infection [95]. While association varies by breed (e.g., low in Weimaraners) [94], the prevalence can be high (e.g., up to 60% in dilute Dobermans) [95]. Despite the risk, dilution variants are gaining popularity and being introduced into breeds like Labrador Retrievers and French Bulldogs, suggesting the need for evidence-based review of breeding policies.

Discussion and Conclusions

This review summarizes the clear, extensive evidence that artificial selection for extreme morphological traits has profound negative impacts on the health and welfare of purebred dogs [96]. The exaggerated morphologies common in modern breeds are a direct product of aesthetic selective breeding [1]. Current breeding practices often perpetuate or exacerbate harmful traits, driven in part by consumer demand for “exotic” or extreme phenotypes, which is now introducing these morphologies into new breeds (e.g., merle French Bulldogs) or pushing existing ones to greater extremes (e.g., excessive wrinkling). The French Bulldog, one of the most popular breeds globally, is a prime example, exhibiting multiple extreme traits that converge into a syndrome of adverse health outcomes: severe respiratory obstruction, gastrointestinal distress, dystocia, painful skin infections, and vertebral disc disease [31,70,79]. This convergence is not apparent from single-trait studies. Only a broad view reveals that unrelated traits often share underlying mechanisms. For example, accelerated growth and IGF-1 signaling link the size-related risks of reduced lifespan, cancer, and orthopedic disease, while a mismatch between soft tissue and skeleton links airway obstruction, dental crowding, and cerebrospinal fluid disorders. The popularity of breeds with harm-inducing extreme morphologies not only increases the prevalence of these phenotypes but also normalizes the associated suffering. These negative physical impacts, such as chronic pain, are also linked to secondary behavioral issues, including increased aggression and decreased trainability [97,98].
Existing literature has established that extremes are harmful, giving us a guide for what to breed away from. However, research currently rarely identifies the targets that we should breed toward. For many continuous traits the risks at the two extremes run in opposite directions. Small dogs are predisposed to dental disease, patellar luxation, and mitral valve disease, whereas large dogs are predisposed to osteosarcoma, cardiomyopathy, gastric dilatation-volvulus, and reduced lifespan. This pattern suggests that the healthiest values for such traits are likely to be intermediate rather than maximal or minimal, but their location cannot be read off studies that only compare groups at the extremes. Identifying them requires refocusing from individual breeds and traits to ask which values minimize harm across the full range of outcomes. An empirical starting point for where these healthier values may lie could be offered by free-ranging village dogs, who are shaped by natural selection rather than artificially-selected aesthetic preference, and tend to converge on a medium size and moderate conformation. For example, studies investigating size or head shape could use median phenotypic values from a village dog population as a baseline.
The evidence therefore calls not only for breeding differently but for researching differently. Recent initiatives show that the field is moving from documenting harm toward implementing reform. Current proposals include removing wording from breed standards that promotes extreme conformation, reopening closed registries, selecting against disease-predisposing phenotypes and genotypes, and supporting controlled crossbreeding where necessary [1]. The 2025 report from the Fifth International Dog Health Workshop documents broad international agreement that canine organizations should eliminate extreme conformations while protecting genetic diversity and improving education of breeders, judges, veterinarians, and puppy purchasers [99]. Welfare epidemiology should be designed to locate optima, asking which body size, craniofacial ratio, or chest depth minimizes total morbidity across outcomes. This logic separates morphological traits into two classes. Continuous conformation traits, such as size and skull proportion, should be bred toward an evidence-based optimal range, whereas discrete deleterious alleles, such as those causing merle homozygosity, ectodermal dysplasia, and screw-tail malformation, have no safe form and should be eliminated. Building guidelines on such targets will require the scientific and veterinary communities to define, from objective physiological and health data, where morphology crosses into a welfare issue. Initiatives like the Brachycephalic Working Group, and recent revisions to breed standards in the United Kingdom, show that change is achievable. Ultimately, success depends on providing clear guidelines about optimal phenotypic ranges, and using those to educate the public about the consequences of their purchasing decisions, so that canine welfare is prioritized over arbitrary aesthetic standards.

Acknowledgments

The Canine Morphology and Welfare Working Group includes the following members: Mia Cobb, PhD (Chaser Innovation Research Fellow, Animal Welfare Science Centre, The University of Melbourne, Australia), Craig Daniell (Chief Executive Officer, British Columbia Society for the Prevention of Cruelty to Animals), Nicholas H. Dodman, BVMS, DACVA, DACVB (Professor Emeritus, Cummings School of Veterinary Medicine, Tufts University), Hille Fieten, DVM, PhD (Diplomate ECVIM-CA Internal Medicine, MSc Genetic Epidemiology, Expertise Centre of Veterinary Genetics, Faculty of Veterinary Medicine, Utrecht University), Simon Gadbois, PhD (Wildlife Ethology and Canine Olfaction Lab, Dalhousie University), Temple Grandin, PhD (Distinguished Professor, Department of Animal Science, Colorado State University), Alexandra Horowitz, PhD (Associate Professor of Professional Practice, Psychology, Barnard College), Katherine Houpt VMD, PhD, DACVB (Emeritus Professor of Veterinary Behavior, Cornell University College of Veterinary Medicine), Ana G. Jiménez, PhD (Vice-Chair of the Canine Science Society, Associate Professor in Biology, Colgate University), Juliane Kaminski, PhD (Associate Professor, Director Dog Cognition Centre, Centre for Comparative and Evolutionary Psychology, University of Portsmouth), Susan Penelope Knowler, BSc, PGDE, PhD (Visiting Researcher, School of Veterinary Medicine, University of Surrey), Anna Kukekova, PhD (Associate Professor, Department of Animal Sciences, University of Illinois Urbana-Champaign), Monique Megens, DVM (Chair, International Collaborative on Extreme Conformations In Dogs (ICECDogs)), Ádám Miklósi, PhD (Department of Ethology, Eötvös Loránd University, Budapest, Hungary), Daniel S. Mills BVSc, PhD, CBiol, FRSB, FHEA, CCAB, Dip ECAWBM(BM), FRCVS (RCVS and EBVS European Veterinary Specialist in Behavioural Medicine), Emma Milne, BVSc, FRCVS (Founder of Vets Against Brachycephalism), Siobhan Mullan, DVM, PhD (UCD, Chair of the Brachycephalic sub-group of the Advisory Council on Companion Animal Welfare, Ireland), Dan O’Neill, MVB, BSc (hons), GPCert (SAP), GPCert (FelP), GPCert (Derm), GPCert (B&PS), PGCertVetEd, FHEA, MSc (VetEpi), PhD, FRCVS (Professor in Companion Animal Epidemiology, Royal Veterinary College, London), Alexandra Protopopova, PhD, CAAB (Associate Professor, Animal Welfare Program, Faculty of Land and Food Systems, The University of British Columbia), Rodrigo Gutierrez Quintana, MVZ, MVM, DipECVN, MRCVS (Professor of Comparative Neurology, School of Biodiversity, One Health and Veterinary Medicine, University of Glasgow), Clare Rusbridge, MBE BVMS PhD DECVN FRCVS (Professor in Veterinary Neurology, RCVS and European Specialist in Veterinary Neurology), Rick F. Sanchez DVM, DipECVO, CertVetEd / FHEA, Diplomate of the European College of Veterinary Ophthalmology (Specialistische Dierenkliniek Utrecht (SDU-AniCUra)), Lionel Sebbag, DVM, PhD, DACVO (Veterinary Ophthalmologist, Expert in Brachycephalic Ocular Syndrome), James Serpell, PhD (Emeritus Professor of Animal Welfare, School of Veterinary Medicine, Dept of Clinical Sciences & Advanced Medicine, University of Pennsylvania), Rosemary Strasser, PhD (Director of the Neuroscience & Behavior Graduate Program, University of Nebraska Omaha), Silvan R. Urfer, Dr. Med. Vet. (Dog Aging Project, Seattle), Carolyn Walsh, PhD (Associate Professor, Canine Research Unit, Psychology Department, Memorial University of Newfoundland), C. D. L. Wynne, PhD (Professor, Department of Psychology, Arizona State University), Isain Zapata, PhD (Associate Professor, Department of Biomedical Sciences, Rocky Vista University).

Funding

National Science Foundation grant CAREER 2238071.

Author Contributions

Conceptualization: JPH, SAB, EEH. Visualization: JPH, EEH. Supervision: EEH. Writing—original draft: JPH, SAB, EEH. Writing—review & editing: JPH, SAB, EEH, Canine Conformation and Welfare Working Group.

Conflicts of Interest

Authors declare that they have no competing interests.

Data Availability Statement

No data is associated with this review.

AI disclosure

Artificial intelligence (Claude Opus 4.8; Anthropic) was used to improve readability and to renumber references after shortening the reference list to comply with journal requirements. Microsoft Copilot (Microsoft) was used to facilitate creation of some of the morphology icons in Figure 2. The authors confirm that they take responsibility for the integrity of all content.

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Figure 1. George Du Maurier, “Dog Fashions for 1889.” Punch, 25 Jan. 1889. This 19th-century cartoon illustrates the long history of artificial selection for exaggerated canine morphological traits driven by fashion and breed ideals rather than health. The present review surveys common canine morphological phenotypes — including body size, brachycephaly, chondrodysplasia and chondrodystrophy, thoracic depth, tail and vertebral conformation, skin folds, and coat-color/hairlessness traits — summarizing the disorders, mechanisms, and welfare consequences associated with each, with the goal of identifying the phenotypic range that minimizes total morbidity across body systems.
Figure 1. George Du Maurier, “Dog Fashions for 1889.” Punch, 25 Jan. 1889. This 19th-century cartoon illustrates the long history of artificial selection for exaggerated canine morphological traits driven by fashion and breed ideals rather than health. The present review surveys common canine morphological phenotypes — including body size, brachycephaly, chondrodysplasia and chondrodystrophy, thoracic depth, tail and vertebral conformation, skin folds, and coat-color/hairlessness traits — summarizing the disorders, mechanisms, and welfare consequences associated with each, with the goal of identifying the phenotypic range that minimizes total morbidity across body systems.
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Figure 2. Consequences of morphologies selected for in the ten most popular breeds registered with the American Kennel Club in 2025. (1-10): Ten most popular breeds. (a-l): Morphologies associated with deleterious health conditions.
Figure 2. Consequences of morphologies selected for in the ten most popular breeds registered with the American Kennel Club in 2025. (1-10): Ten most popular breeds. (a-l): Morphologies associated with deleterious health conditions.
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Figure 4. 3D renderings of skulls from (a) coated and (b) hairless dog [85]. Note the significant lack of teeth in the hairless dog.
Figure 4. 3D renderings of skulls from (a) coated and (b) hairless dog [85]. Note the significant lack of teeth in the hairless dog.
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Figure 3. Computer tomography of mesocephalic skull (A,C,E) and brachycephalic skull (B,D,F). Tongue is highlighted with green. (Aqua represents the oropharynx, blue the nasopharynx, and pink the palatal tissues.) Note the difference in tongue thickness between the two skull types and its potential to block the airway (marked with red lines in A, B) [34]. BOAS comprises a complex set of changes and an individual dog may be diagnosed with one or more of them. Breed differences have been recognized, and appear to support the theory that reduced airway space further towards the nostrils (rostral) affects function more than reduced space further down the airway (caudal) [100]. Reproduced from Oshita et al. (2022), Animals, 12(13), 1636, https://doi.org/10.3390/ani12131636, licensed under CC BY 3.0.
Figure 3. Computer tomography of mesocephalic skull (A,C,E) and brachycephalic skull (B,D,F). Tongue is highlighted with green. (Aqua represents the oropharynx, blue the nasopharynx, and pink the palatal tissues.) Note the difference in tongue thickness between the two skull types and its potential to block the airway (marked with red lines in A, B) [34]. BOAS comprises a complex set of changes and an individual dog may be diagnosed with one or more of them. Breed differences have been recognized, and appear to support the theory that reduced airway space further towards the nostrils (rostral) affects function more than reduced space further down the airway (caudal) [100]. Reproduced from Oshita et al. (2022), Animals, 12(13), 1636, https://doi.org/10.3390/ani12131636, licensed under CC BY 3.0.
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Table 1. Abridged list of morphological traits named in American Kennel Club breed standards and their principal associated health impacts. The present review examines the relationship between canine morphological phenotypes selected for by breed standards and their associated health and welfare consequences, arguing for a shift toward identifying the phenotypic range that minimizes total morbidity rather than simply comparing one breed or trait extreme against another. For continuous traits (size, chest depth), impacts reflect the extreme end favored by the standard; for discrete alleles (merle, dilution, screw tail), impacts follow from the causal variant. Merle-associated blindness occurs chiefly in homozygotes. Additional breeds and traits, direct quotations from the published breed standards, and source URLs are provided in Supplementary Table S1. ALD = angular limb deformity. BOAS = brachycephalic obstructive airway syndrome. CDA = color dilution alopecia. CED = canine ectodermal dysplasia. CM = Chiari-like malformation. CVM = congenital vertebral malformation. GDV = gastric dilatation–volvulus. IVDH = intervertebral disc herniation. OSA = osteosarcoma. SM = syringomyelia.
Table 1. Abridged list of morphological traits named in American Kennel Club breed standards and their principal associated health impacts. The present review examines the relationship between canine morphological phenotypes selected for by breed standards and their associated health and welfare consequences, arguing for a shift toward identifying the phenotypic range that minimizes total morbidity rather than simply comparing one breed or trait extreme against another. For continuous traits (size, chest depth), impacts reflect the extreme end favored by the standard; for discrete alleles (merle, dilution, screw tail), impacts follow from the causal variant. Merle-associated blindness occurs chiefly in homozygotes. Additional breeds and traits, direct quotations from the published breed standards, and source URLs are provided in Supplementary Table S1. ALD = angular limb deformity. BOAS = brachycephalic obstructive airway syndrome. CDA = color dilution alopecia. CED = canine ectodermal dysplasia. CM = Chiari-like malformation. CVM = congenital vertebral malformation. GDV = gastric dilatation–volvulus. IVDH = intervertebral disc herniation. OSA = osteosarcoma. SM = syringomyelia.
Breed Trait in standard Health impact
Australian Shepherd Merle Deafness; blindness
Basset Hound Chondrodysplasia ALD; elbow disease; IVDH
Basset Hound Ectropion / haw Ocular irritation
Basset Hound Pendulous ears Otitis externa
Beagle Chondrodystrophy IVDH
Boston Terrier Brachycephaly BOAS; eye disease; dystocia
Boston Terrier Prominent eyes Corneal ulcer; proptosis
Brussels Griffon Domed skull CM; SM
Cardigan Welsh Corgi Chondrodysplasia ALD; elbow disease; IVDH
Cavalier King Charles Spaniel Brachycephaly BOAS; eye disease
Cavalier King Charles Spaniel Domed skull CM; SM
Chihuahua Domed skull SM; open fontanelle
Chinese Crested Hairlessness CED; missing teeth
Cocker Spaniel Chondrodystrophy IVDH
Dachshund Chondrodysplasia ALD; elbow disease; IVDH
Dalmatian White spotting Congenital deafness
(note: patches are protective)
Doberman Pinscher Dilute color CDA
English Bulldog Brachycephaly BOAS; otitis; dystocia
English Bulldog Skin folds Skin-fold dermatitis
English Bulldog Screw tail CVM; kyphosis
French Bulldog Brachycephaly BOAS; eye disease; dystocia
French Bulldog Screw tail CVM; IVDH; kyphosis
French Bulldog Skin folds Skin-fold dermatitis
German Shepherd Dog Deep chest GDV
Golden Retriever Large size Hip dysplasia; OSA
Great Dane Deep chest GDV
Great Dane Giant size Short lifespan; OSA
Irish Wolfhound Giant size Short lifespan; OSA
Labrador Retriever Large size Hip dysplasia; OSA
Mastiff Giant size Short lifespan; OSA
Pug Brachycephaly BOAS; otitis; eye disease
Pug Curled tail CVM
Pug Skin folds Skin-fold dermatitis
Rhodesian Ridgeback Dorsal ridge Dermoid sinus
Rottweiler Large size Hip dysplasia; OSA
Shar-Pei Skin folds Dermatitis; Shar-Pei fever
Shar-Pei Entropion Corneal ulcer; blindness
Skye Terrier Chondrodysplasia ALD; elbow disease; IVDH
Skye Terrier Long, low body IVDH; back pain
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