We are just starting the foundation for our Pug breeding program and our Boston Terrier breeding program is currently in a period of rebuilding (our original lines/dogs were born in 2001) and refinement. Our current focus is on our bloodlines, extensive health testing and keeping current with cutting edge research and genetic testing. Our focus continues to be on quality and not quantity. Once further along with our plans and breeding scheme, we will be showing again in the near future.
Our Pugs are of American and European bloodlines and our Boston Terriers are a blend of Canadian, American and European bloodlines. We have imported from reputable breeders in the United States and from many European countries. We do so, in order to promote genetic variability in our bloodlines. More specifically, to prevent homozygosity. Homozygosity is having two identical alleles of a particular gene/genes. While breeding related animals produces more consistent and predictable traits (as a result of homozygosity), loss in vitality and vigor is also the result (Beuchat, 2015). Breeding related animals also reduces fertility, produces smaller offspring, early death and a shorter lifespan (Beuchat, 2015). That is, the higher level of inbreeding, the greater the detrimental effects (Beuchat, 2015). All things considered and weighing the benefits and risks, we aim to breed puppies/dogs with inbreeding coefficients (ICs) as close to zero as possible. It is recommended that ICs are calculated over at least 8-10 generations (the more the better though!) and preferably 5% and under (Beuchat, 2015). Our ICs are calculated on TEN GENERATIONS and therefore reflect higher than they would otherwise (i.e. if calculated over 8 generations). In the past, we have always regarded 6.8% inbreeding coefficient top be an upper limit (again, trying to keep as low as possible), as suggested in the agricultural research available to us at that time. With advancements in genetics in the Veterinary field however, we now consider 5% over 8-10 generations to be an upper limit. In addition to taking into consideration our dogs' ICs when breeding, we also consider and compare these percentages to the Genetic Diversity/Heterozygosity percentage, as determined by DNA. Interestingly, one dog can have a low IC and higher homozygosity percentage and another dog can have a high relative IC and have a lower homozygosity percentage. Cool, right??!! A breeder must consider ALL!! The median heterozygosity percentage of purebred dogs is 34% (GENOSCOPER®). The higher the percentage, the greater the heterozygosity.
As per Our Story page, we breed for the "total dog", with an emphasis on health and temperament, while breeding to standard. Given the pitfalls of "breeding for show titles" (i.e. breeding dogs closely related to achieve consistency and predictability) and that breeds are created by inbreeding to begin with, our focus remains on health and temperament first and foremost. Yes, one must also breed to standard and we feel that showing is important in maintaining the integrity of the breed standard and the breed as a whole. However, this isn't our sole focus. Indeed, we enjoy showing and try to get to shows when our family life allows.
"The fewer generations used in calculating the inbreeding coefficient, the "better" (i.e. lower) it will appear to be. But this isn't an accurate assessment of the true degree of homozygosity in a dog, so it does not reflect the true level inbreeding depression and risk of genetic disease" (Beuchat, 2015).
The inbreeding coefficient is the estimated level of inbreeding/homozygosity of a particular mating/breeding. The inbreeding coefficient is the probability of inheriting the same allele from an ancestor on both sides of the pedigree and the fraction of all of the genes of a dog that are homozygous (Beuchat, 2015). A low inbreeding coefficient has a lower risk, but supposedly also lower benefits, as it relates to consistency in type. A high inbreeding coefficient would produce more consistency and prepotency in the puppies produced, but there would also be a significant loss of vigor and health (Beuchat, 2015). The detrimental effects of inbreeding start to become evident at 5%, with a significant loss of vitality and an increase in the expression of detrimental recessive mutations in puppies at 10% (Beuchat, 2015). An inbreeding coefficient of 10% is considered to be the "extinction vortex", in which smaller litters, higher mortality, and expression of genetic defects have a negative effect on the size of the population (Beuchat, 2015). Further, as the population gets smaller, the incidence of inbreeding goes up, culminating in a "negative feedback loop" that eventually drives a population to extinction (Beuchat, 2015).
Again, in terms of health, an inbreeding coefficient of 5% or less is most ideal, as above that, there are detrimental effects and risks. Thus, a breeder needs to weigh these against anticipated benefits gained (Beuchat, 2015). Inbreeding coefficients of 5-10% supposedly will have modest detrimental effects on the offspring, while levels above 10% will yield significant effects - not just on the quality of the offspring, but on the breed as a whole (Beuchat, 2015).
A breeder can use the inbreeding coefficient to reduce the risk of genetic disorders in their puppies, as it's an estimate of the predicted loss of vigor and general health expected as a repercussion of the expression of recessive mutations (Beuchat, 2015). However, the inbreeding coefficient is NOT a measure of health. Rather, it's a measure of RISK, and with or without DNA tests, it's the best way to ascertain the level of genetic risk one takes when breeding (Beuchat, 2015).
However, every dog has many mutations, and one has no way of knowing about them if the dog has only one copy and it's not expressed. Thus, if one breeds two dogs with some of the same mutations, one can expect that the puppies will be homozygous for 25% of them (Beuchat, 2015). Many of these mutations may only have very few effects and one may not recognize these as a "disease". It's the accumulation of these few effects that causes the loss of vigor and vitality in inbred animals (referred to as "inbreeding depression") (Beuchat, 2015). DNA tests tell you only about one particular gene, which is known as a risk for a particular disease (Beuchat, 2015).
To breed healthy animals, one needs to consider ALL of the potential risks, and there are many more recessive mutations than the ones we have DNA tests for (Beuchat, 2015). This is why now, we're now running (now that the tests are available) the largest DNA genetic health testing panel in the world (to date) on our dogs. In the past, we have always at least certified patellas, heart (by auscultation) and Juvenile Hereditary Cataracts and then Degenerative Myelopathy and Hyperuricosuria when the tests came out. We have also tested for the piebald gene in the past (and continue to do so) as well, as it's been hypothesized to be the cause of congenital deafness in related breeds such as Bulldogs, Bull Terriers, etc. Please note. there is no genetic marker for congenital deafness to date and indeed, there are many reasons for deafness genetics aside. However, we will continue to follow research and test for all possible causes. We have always remained informed of advancements in genetics and Veterinary research and now that the tests are available, we're currently running panels on our dogs to test for (and various mutations of):
Bleeding disorder due to P2RY12 defect, Canine Cyclic Neutropenia, Cyclic Hematopoiesis, Grey Collie Syndrome, (CN), Canine Leukocyte Adhesion Deficiency (CLAD), type III, Canine Scott Syndrome, (CSS), Factor IX Deficiency or Hemophilia B; mutation Gly379Glu, Factor IX Deficiency or Hemophilia B, Factor VII Deficiency, Factor VIII Deficiency or Hemophilia A, Factor VIII Deficiency or Hemophilia A, Factor VIII Deficiency or Hemophilia A, Factor VIII Deficiency or Hemophilia A, Factor VIII Deficiency or Hemophilia A; p.Cys548Tyr, Factor XI Deficiency, Glanzmann Thrombasthenia Type I, (GT), Glanzmann Thrombasthenia Type I, (GT), Hereditary Elliptocytosis, Hereditary Phosphofructokinase (PFK) Deficiency, Macrothrombocytopenia, May-Hegglin Anomaly (MHA), Prekallikrein Deficiency, Pyruvate Kinase Deficiency, Pyruvate Kinase Deficiency, Pyruvate Kinase Deficiency, Trapped Neutrophil Syndrome, (TNS), Von Willebrand's Disease (vWD) Type 1, Von Willebrand's Disease (vWD) Type 3
Canine Multifocal Retinopathy 1 (CMR1), Canine Multifocal Retinopathy 2 (CMR2), Canine Multifocal Retinopathy 3 (CMR3), Cone Degeneration (CD) or Achromatopsia, Cone-Rod Dystrophy 1 (crd1), Cone-Rod Dystrophy 2 (crd2), Cone-Rod Dystrophy (cord1-PRA / crd4), Cone-Rod Dystrophy, Congenital Eye Disease, Dominant Progressive Retinal Atrophy (DPRA), Generalized Progressive Retinal Atrophy, Golden Retriever Progressive Retinal Atrophy 1 (GR_PRA 1), Primary Hereditary Cataract (PHC), Primary Lens Luxation (PLL), Primary Open Angle Glaucoma (POAG), Primary lens luxation (PLL), Progressive Retinal Atrophy Type III (PRA type III), Progressive Retinal Atrophy (CNGA1-PRA), Progressive Retinal Atrophy (PAP1_PRA), Progressive Retinal Atrophy (PRA), Rod-Cone Dysplasia 1 (rcd1), Rod-Cone Dysplasia 1a (rdc1a), Rod-Cone Dysplasia 3 (rcd3), X-Linked Progressive Retinal Atrophy 2 (XLPRA2), OptiGen® Collie Eye Anomaly (CEA), OptiGen® Progressive Rod Cone Degeneration (prcd-PRA)
Dilated Cardiomyopathy (DCM), Long QT Syndrome
Autosomal Recessive Severe Combined Immunodeficiency (ARSCID), Complement 3 (C3) Deficiency, Myeloperoxidase Deficiency, Severe Combined Immunodeficiency, X-Linked Severe Combined Immunodeficiency (XSCID)
Cystinuria Type I-A, Cystinuria Type II-A, Fanconi Syndrome, Hyperuricosuria (HUU), Polycystic Kidney Disease in Bull Terriers (BTPKD), Primary Hyperoxaluria (PH), Protein Losing Nephropathy (PLN); NPHS1 gene variant, Renal Cystadenocarcinoma and Nodular Dermatofibrosis (RCND), X-Linked Hereditary Nephropathy (XLHN), Xanthinuria, Type 1a, Xanthinuria, Type 2a, Xanthinuria, Type 2b
Glycogen Storage Disease Type II or Pompe's Disease (GSD II), Glycogen Storage Disease Type IIIa (GSD IIIa), Glycogen Storage Disease Type Ia (GSD Ia), Hypocatalasia or Acatalasemia, Intestinal Cobalamin Malabsorption or Imerslund-Gräsbeck Syndrome (IGS), Mucopolysaccharidosis Type IIIA (MPS IIIA), Mucopolysaccharidosis Type VII (MPS VII), Pyruvate Dehydrogenase Phosphatase 1 (PDP1) Deficiency
Cavalier King Charles Spaniel Muscular Dystrophy (CKCS-MD), Centronuclear Myopathy (CNM), Duchenne or Dystrophin Muscular Dystrophy (DMD), Muscular Dystrophy, Ullrich-type, Myostatin deficiency (Double Muscling, "Bully"), Myotonia Congenita, Myotubular Myopathy, Nemaline Myopathy, X-Linked Myotubular Myopathy
Acral Mutilation Syndrome (AMS), Alaskan Husky Encephalopathy (AHE), Alexander Disease (AxD), Bandera's Neonatal Ataxia (BNAt), Benign Familial Juvenile Epilepsy or Remitting Focal Epilepsy, Cerebellar Cortical Degeneration (CCD), Cerebral Dysfunction, Dandy-Walker-Like Malformation (DWLM), Degenerative Myelopathy (DM), Early-Onset Progressive Polyneuropathy, Fetal Onset Neuroaxonal Dystrophy (FNAD), Hereditary Ataxia or Cerebellar Ataxia, Hyperekplexia or Startle Disease, Hypomyelination, Juvenile Myoclonic Epilepsy (JME), Juvenile encephalopathy, L-2-Hydroxyglutaric aciduria (L2HGA), L-2-Hydroxyglutaric aciduria (L2HGA), Lagotto Storage Disease (LSD), Neonatal Cerebellar Cortical Degeneration or Cerebellar Abiotrophy (NCCD), Neonatal Encephalopathy with Seizures (NEWS), Neuroaxonal Dystrophy (NAD), Neuronal Ceroid Lipofuscinosis 1 (NCL1), Neuronal Ceroid Lipofuscinosis 10 (NCL10), Neuronal Ceroid Lipofuscinosis 8 (NCL8), Neuronal Ceroid Lipofuscinosis (NCL7), Polyneuropathy with ocular abnormalities and neuronal vacuolation (POANV), Progressive Early-Onset Cerebellar Ataxia, Sensory Neuropathy, Spinal Dysraphism, Spinocerebellar Ataxia with Myokymia and/or Seizures (SCA), Spinocerebellar Ataxia/ Late-Onset Ataxia (SCA, LOA), Spongy degeneration with cerebellar ataxia (SDCA1), X-Linked Tremors
Congenital Myasthenic Syndrome (CMS), Episodic Falling Syndrome (EFS), Exercise-Induced Collapse (EIC), GM2 Gangliosidosis,
Paroxysmal Dyskinesia (PxD)
Chondrodysplasia, Cleft Palate, Cleft Lip and Palate with Syndactyly; ADAMTS20 gene, Cleft Palate; DLX6 gene, Craniomandibular Osteopathy (CMO), Hereditary Vitamin D-Resistant Rickets (HVDRR), Osteochondrodysplasia, Osteochondromatosis, Osteogenesis Imperfecta (OI), Skeletal Disease, Skeletal Dysplasia 2 (SD2), Spondylocostal Dysostosis, Van den Ende-Gupta Syndrome (VDEGS), Hip Laxity 1, Hip Laxity 2
Dystrophic Epidermolysis Bullosa, Dystrophic Epidermolysis Bullosa, Epidermolytic Hyperkeratosis, Focal Non-Epidermolytic Palmoplantar Keratoderma (FNEPPK), Hereditary Footpad Hyperkeratosis (HFH), Ichthyosis, Ichthyosis, Lamellar Ichthyosis (LI), Ligneous Membranitis, Musladin-Lueke syndrome (MLS), X-Linked Ectodermal Dysplasia (XHED)
Multi-Drug Resistance 1 (MDR1)
Acute Respiratory Distress Syndrome (ARDS), Amelogenesis Imperfecta (AI), Amelogenesis Imperfecta (AI), Congenital Keratoconjunctivitis Sicca and Ichthyosiform Dermatosis (CKCSID), Dental Hypomineralisation, Narcolepsy, Persistent Müllerian Duct Syndrome (PMDS), Primary Ciliary Dyskinesia (PCD)