Hip/Elbow Dysplasia

Hip and elbow dysplasia are categorized as developmental disorders caused by dysmorphic and lax joint formation. This malformation consequentially results in abnormal wearing of bone over time, inducing the secondary development of osteoarthritis (OA) or arthrosis, and degenerative joint disease. Unfortunately, the pathology of neither hip nor elbow dysplasia can be reversed and so, for an affected individual, the best outcome is management of the disease through pain medication or replacement surgery, with the latter having additional consequences of cost and an extensive recovery period. Hip dysplasia is not a congenital defect; it is not present at birth. Multiple studies have demonstrated that all normal puppies are born with "perfect" hips; that is, they are "normal" for a newborn with no signs of dysplasia. The structures of the hip joint are cartilage at birth and only become bone as the puppy grows. If a puppy is going to develop hip dysplasia, the process begins shortly after birth. Hip dysplasia tends to be more common in some breeds than others and in some lines than others, which indicates that there is a genetic component to the disorder. However, scientists have been looking for genes that are responsible for the development of hip dysplasia in dogs for decades without success. Although there is a genetic influence on hip dysplasia, the heritability of the trait is rather low. Many studies have shown that genetic variation accounts for only a modest fraction of the variation in hip scores, usually 15-40%. This means that some fraction of the variation in the quality of the hips is the result of non-genetic, or "environmental" influences. This is one reason why decades of strong selection has resulted in only modest reductions in hip dysplasia in some breeds. At the current rate of progress and selecting only by phenotype, it could take decades to achieve a meaningful reduction in the incidence of hip dysplasia. ​The top three environmental factors that have been found to play a significant role in the develop of dysplastic hips are: a) joint laxity, b) weight, and c) exercise.

 

Laxity- Puppies are born with perfect hips, and if the hips do not develop laxity the dog does not develop hip dysplasia (Riser 1985). Joint laxity occurs when the head of the femur does not fit snugly into the acetabulum. This could be the result of traumatic injury, overloading of the joint by weight, lack of muscle strength, or adductor forces. Joint laxity is the primary factor that predisposes a dog to the development of hip dysplasia.

 

Weight-If there is laxity in the hip joint, the amount of damage done to the femur and acetabulum will depend on the magnitude of the forces in the hip joint. The heavier the dog, the greater the forces will be and also therefore the higher the risk of hip dysplasia and osteoarthritis. Growing puppies need to eat enough to support growth but they should not be fat, because any extra weight can increase the risk of developing hip dysplasia. At four years old, less than 10% of dogs kept on a restricted diet (25% less than the control diet) were dysplastic, while at the same time more than 30% of the dogs in the control group were dysplastic. As an added advantage, dogs on restricted diets live longer, too. Unfortunately, many dogs (including show dogs!) are overweight, and obesity could well be the single most significant environmental factor affecting the development of hip dysplasia and osteoarthritis. But body weight is a factor that we can control!​ Although progress from genetic selection will take many generations, the incidence of hip/elbow dysplasia in dogs could be immediately and dramatically reduced simply by practicing better weight management.

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Exercise- Exercise strengthens the muscles of the legs and pelvis, and this will increase the stability of the hip joint. But all exercise is not created equal. Puppies raised on slippery surfaces or with access to stairs when they are less than 3 months old have a higher risk of hip dysplasia,while those who are allowed off-lead exercise on soft, uneven ground (such as in a park) have a lower risk. Dogs born in summer have a lower risk of hip dysplasia, presumably because they have more opportunity for exercise outdoors. On the other hand, dogs from 12-24 months old that regularly chase a ball or stick thrown by the owner have an higher risk of developing dysplastic hips. Controlling the type of exercise puppies are exposed to from a very young age is very important in decreasing the risk for hip/elbow dysplasia.

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At Maverick Ranch we have our dams and sires hips and elbows evaluated by the Orthopedic Foundation for Animals. Hip/Elbow Radiographs are taken and submitted to the OFA for reviewing. The OFA grades their hips in categories of Severe, Moderate, Mild, Borderline, Fair, Good, or Excellent. Preliminary OFA grades can be done before two years of age, but final OFA results must be done after two years of age. The OFA has approximately 165,000 golden retriever hip screenings recorded, and of that 19.8% were abnormal. The OFA has approximately 58,000 golden retriever elbow screenings recorded, and of that 11.6% were abnormal. The OFA has approximately 33,000 poodle hip screenings recorded, and of that 12% were abnormal. The OFA has approximately 6,000 poodle elbow screenings recorded, and of that 3.2% were abnormal. We also take great care to make sure our puppies are raised on grippy surfaces from day one, get proper nutrition and diet, and get puppy-appropriate exercise. Even taking all of these precautions, the possible risk of hip and elbow dysplasia cannot currently be eliminated.

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Degenerative Myelopathy (DM)

The dog equivalent of Amyotrophic Lateral Sclerosis, or Lou Gehrig’s disease, DM is a progressive degenerative disorder of the spinal cord. Because the nerves that control the hind limbs are the first to degenerate, the most common clinical signs are back muscle wasting and gait abnormalities. Affected dogs do not usually show signs of DM until they are at least eight years of age. The condition is not typically painful for the dog, but will progress until the dog is no longer able to walk. The gait of dogs affected with degenerative myelopathy can be difficult to distinguish from the gait of dogs with hip dysplasia, arthritis of other joints of the hind limbs, or intervertebral disc disease. Late in the progression of disease, dogs may lose fecal and urinary continence and the forelimbs may be affected. Affected dogs may fully lose the ability to walk 6 months to 2 years after the onset of symptoms. As dogs are seniors at the time of onset, the treatment for DM is aimed towards increasing their comfort through a combination of lifestyle changes, medication, and physical therapy.

Degenerative Myelopathy is a recessive inherrited gene, meaning a puppy must carry two copies (one from the dam and one from the sire) to be at risk for developing DM. The overall frequency of this disease is unreported in Goldendoodles. However, in one study of 533 Standard Poodles, 11.3% were carriers of the mutation. In that same study 32 miniature and toy poodles tested, 9.4% were carriers, and of 334 golden retrievers tested, 0.6% were carriers of the mutation. In addition, 3% of the Golden Retrievers and 0.9% of the Standard Poodles tested were at-risk/affected.

At Maverick Ranch our Goldendoodle breeding program dams and sires are genetically tested for this mutation. Our breeding program will NEVER produce puppies that are at risk for this mutation. Currently, our breeding program will only produce puppies that are clear or carrier/unaffected of this mutation.

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Ichthyosis (PNPLA1)

Ichthyosis (golden retriever type) is an inherited condition of the skin affecting dogs. The age of onset and severity of disease are highly variable, however most affected dogs present before one year of age with flaky skin and dull hair. Over time the skin develops a grayish color and appears thick and scaly, especially over the abdomen. The symptoms may progress to severe scaling all over the body, may improve with age, or may come and go over the dog’s lifetime. While the prognosis is generally good for affected dogs, they are at increased risk for skin infections.

Ichthyosis (golden retriever type) is inherited in an autosomal recessive manner in dogs meaning that they must receive two copies of the mutated gene (one from each parent) to develop the disease. The Mutation of the PNPLA1 gene associated with ichthyosis (golden retriever type) has been identified in the goldendoodle. Though the exact frequency in the overall goldendoodle population is unknown, approximately 44% out of 1600 golden retrievers tested from Australia, France, Switzerland, and the United States were carriers of the mutation and approximately 29% were affected.

At Maverick Ranch, we test our Goldendoodle breeding program for this mutation. Currently, our breeding program will only produce puppies that are clear of this mutation.

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Progressive Retinal Atrophy, Golden Retriever 1 (GR-PRA1)

Progressive Retinal Atrophy, golden retriever 1 (GR-PRA1) is a late-onset inherited eye disease affecting dogs. Affected dogs begin showing clinical symptoms related to retinal degeneration between 6 to 7 years of age on average, though age of onset can vary. Initial clinical signs of progressive retinal atrophy involve changes in reflectivity and appearance of a structure behind the retina called the tapetum that can be observed on a veterinary eye exam. Progression of the disease leads to thinning of the retinal blood vessels, signifying decreased blood flow to the retina. Affected dogs initially have vision loss in dim light (night blindness) and loss of peripheral vision, eventually progressing to complete blindness in most affected dogs.

GR-PRA1 is inherited in an autosomal recessive manner in dogs meaning that they must receive two copies of the mutated gene (one from each parent) to develop the disease. The goldendoodle is included as a breed susceptible to progressive retinal atrophy, golden retriever 1 because golden retrievers are known to develop this disease due to mutation of the SLC4A3 gene. The frequency of the causal mutation in the general goldendoodle population is unknown. However, in one study of 369 golden retrievers clinically free of disease tested from the UK, US, Sweden, and France, 10.5% were carriers of the mutation.

At Maverick Ranch, we test our breeding program for this mutation. Currently, our breeding program will only produce puppies that are clear of this mutation.

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Progressive Retinal Atrophy, Golden Retriever 2 (GR-PRA2)

Progressive Retinal Atrophy, golden retriever 2 (GR-PRA2) is a late-onset inherited eye disease affecting dogs. Affected dogs begin showing clinical symptoms related to retinal degeneration at around 4 to 5 years of age on average, though age of onset can vary. Initial clinical signs of progressive retinal atrophy involve changes in reflectivity and appearance of a structure behind the Retina called the Tapetum that can be observed on a veterinary eye exam. Progression of the disease leads to thinning of the retinal blood vessels, signifying decreased blood flow to the retina. Affected dogs initially have vision loss in dim light (night blindness) and loss of peripheral vision, progressing to complete blindness in most affected dogs.

GR-PRA2 is inherited in an Autosomal Recessive manner in dogs meaning that they must receive two copies of the mutated gene (one from each parent) to develop the disease. The goldendoodle is included as a breed susceptible to GR-PRA2 because golden retrievers are known to develop this disease due to mutation of the TTC8 gene. The frequency of the causal mutation in the general goldendoodle population is unknown. However, in one study of golden retrievers either free of clinical disease or of unknown PRA status tested from the UK, US, France, and Sweden, 3% were carriers of the mutation.

At Maverick Ranch, we test our breeding program for this mutation. Currently, our breeding program will only produce puppies that are clear of this mutation.

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Progressive Retinal Atrophy, Progressive Rod-Cone Degeneration (PRA-PRCD)

Progressive Retinal Atrophy, Progressive Rod-Cone Degeneration (PRA-prcd) is a late onset, inherited eye disease affecting Goldendoodles. PRA-prcd occurs as a result of degeneration of both rod and cone type photoreceptor cells of the retina, which are important for vision in dim and bright light, respectively. Evidence of retinal disease in affected dogs can first be seen on an electroretinogram around 1.5 years of age for most breeds, but most affected dogs will not show signs of vision loss until 3 to 5 years of age or later. The rod type cells are affected first and affected dogs will initially have vision deficits in dim light (night blindness) and loss of peripheral vision. Over time affected dogs continue to lose night vision and begin to show visual deficits in bright light. Other signs of progressive retinal atrophy involve changes in reflectivity and appearance of a structure behind the retina called the tapetum that can be observed on a veterinary eye exam. Although there is individual and breed variation in the age of onset and the rate of disease progression, the disease eventually progresses to complete blindness in most dogs. Other inherited disorders of the eye can appear similar to PRA-prcd. Genetic testing may help clarify if a dog is affected with PRA-prcd or another inherited condition of the eye.

PRA-prcd is inherited in an autosomal recessive manner in dogs meaning that they must receive two copies of the mutated gene (one from each parent) to develop the disease. Goldendoodle is included as a breed susceptible to progressive retinal atrophy, progressive rod-cone degeneration because of its close relatedness to the Golden Retriever and Poodle breeds, which are known to develop this disease due to mutation of the PRCD gene. The frequency of the causal mutation in the general Goldendoodle population is unknown.

At Maverick Ranch, we test our breeding program for this mutation. Currently, our breeding program will only produce puppies that are clear or carrier/unaffected of this mutation.

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Von Willebrands Disease Type I (VWDI)

Von Willebrand Disease I (VWDI) is an inherited bleeding disorder affecting Goldendoodles. Dogs affected with VWDI have less than half of the normal level of von Willebrand coagulation factor (vWf), which is an essential protein needed for normal blood clotting. There is variability in the amount of vWf such that not all dogs with two copies of the Mutation are equally affected. Dogs that have less than 35% of the normal amount of vWf generally have mild to moderate signs of a bleeding disorder. Affected dogs may bruise easily, have frequent nosebleeds, bleed from the mouth when juvenile teeth are lost, and experience prolonged bleeding after surgery or trauma. Less often, the bleeding may be severe enough to cause death. Due to the variable severity of the disorder, affected dogs may not be identified until a surgery is performed or trauma occurs at which time excessive bleeding is noted. Veterinarians performing surgery on known affected dogs should have ready access to blood banked for transfusions. Most dogs will have a normal lifespan with this condition despite increased blood clotting times.

Von Willebrands Disease is a recessive inherited gene, meaning a puppy must carry two copies (one from the dam and one from the sire) to be at-risk for developing the disease. Goldendoodle is included as a breed susceptible to von Willebrand disease I because of its close relatedness to the Standard Poodle breed, which is known to develop this disease due to mutation of the VWF gene. The frequency of the causal mutation in the general Goldendoodle population is unknown.

At Maverick Ranch, we test our breeding program for this mutation. Currently, our breeding program will only produce puppies that are clear of this mutation.

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Duchenne Muscular Dystrophy, X-linked (DMD)

Duchenne Muscular Dystrophy is an inherited disease affecting Golden Retrievers. Affected dogs are unable to produce adequate amounts of a protein important for muscle contraction and relaxation. Clinical signs of affected dogs include generalized muscle Atrophy, a stiff or shuffling gait, difficulty standing, exercise intolerance and over flexion of the ankle joint. Affected dogs have difficulties feeding and often drool. Affected dogs are often significantly smaller than littermates by 6 weeks of age. Cardiac muscle is also compromised in affected dogs, potentially resulting in clinical heart disease.Affected dogs may also suffer from aspiration pneumonia and cardiac disease. The prognosis is related to disease severity with some dogs dying soon after birth due to disease complications and others surviving for years with only mild symptoms. Genetic testing of the DMD gene in Golden Retrievers will reliably determine whether a dog is a genetic carrier of this form of Duchenne muscular dystrophy.

Duchenne muscular dystrophy is inherited in an X-Linked Recessive manner in dogs meaning that female dogs must receive two copies of the mutated gene (one from each parent) to develop the disease while male dogs only require one copy of the mutated gene from the mother in order to develop the disease. Therefore, male dogs more commonly present with symptoms of the disease. Each male pup that is born to a female dog known to be a carrier of Golden Retriever muscular dystrophy has a 50% chance of inheriting the disease.

At Maverick Ranch, we test our breeding program for this mutation. Our breeding program will only produce puppies that are clear of this mutation.

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GM2 Gangliosidosis (HEXB)

GM2 gangliosidosis (poodle type) is an inherited Lysosomal Storage Disorder affecting dogs. Affected dogs have insufficient activity of the enzyme hexosaminidase B, which is responsible for breaking down specific carbohydrates in the cells. As a result, there is an accumulation of a glycoprotein, GM2 ganglioside, in cells, especially cells of the brain and nervous system. Affected dogs typically present with symptoms of neurologic disease around 9 to 12 months of age. Symptoms include vision loss, difficulties walking, loss of balance, head tremors and vomiting. Once an affected dog begins to show signs of the disease, the disease progression is rapid and dogs usually die between the ages of 18 and 23 months.

GM2 gangliosidosis (poodle type) is inherited in an autosomal recessive manner in dogs meaning that they must receive two copies of the mutated gene (one from each parent) to develop the disease. The frequency of this mutation in Goldendoodles in unknown. The mutation of the HEXB gene associated with GM2 gangliosidosis (poodle type) has been identified in toy poodles. Though the exact frequency overall in the toy poodle population is unknown, 0.2% out of 496 toy poodles from a randomly selected population from Japan were carriers of the mutation. The frequency of the causal mutation is unknown for other varieties of poodles.

At Maverick Ranch, we test our breeding program for this mutation. Currently, our breeding program will only produce puppies that are clear of this mutation.

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Neonatal Encephalopathy with Seizures (ATF2)

Neonatal Encephalopathy with Seizures is an inherited neurologic disease known to affect dogs. Affected puppies are smaller than littermates at birth, have difficulty nursing after a few days of life, and often die by 1 week of age. By 3 weeks of age, surviving puppies present with neurologic symptoms including muscle weakness, tremors, inability to walk, wide-based stance and frequent falling. The disease quickly progresses to severe seizures that become non-responsive to treatment. Affected dogs typically die or are euthanized by 7 weeks of age.

Neonatal Encephalopathy with Seizures is inherited in an autosomal recessive manner in dogs meaning that they must receive two copies of the mutated gene (one from each parent) to develop the disease. The Goldendoodle is included as a breed susceptible to neonatal encephalopathy with seizures because the mutation of the ATF2 gene associated with this disease has been identified in Standard Poodles. The frequency of the causal mutation in Goldendoodles and Poodles is unknown.

At Maverick Ranch, we test our breeding program for this mutation. Currently, our breeding program will only produce puppies that are clear of this mutation.

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Neuronal Ceroid Lipofuscinosis (NCL)

Neuronal ceroid lipofuscinosis 5 (golden retriever type) is an inherited lysosomal storage disease affecting dogs. Affected dogs lack adequate activity of a specific enzyme necessary for normal cellular metabolism. As a result, there is an abnormal accumulation of waste compounds primarily in the cells of the nervous system, leading to a range of neurological symptoms. Affected dogs usually present around 13 months of age with progressive neurological disease beginning with loss of coordination, balance issues, or difficulty climbing stairs which may be more pronounced when excited. The disease progresses to include severe incoordination, anxiety, agitation, persistent circling or pacing, loss of response to learned commands or behaviors, snapping at air (called “fly-biting”), blindness, aggression, and seizures. Affected dogs typically die or are humanely euthanized by 3 years of age.

Neuronal ceroid lipofuscinosis 5 (golden retriever type) is inherited in an autosomal recessive manner in dogs meaning that they must receive two copies of the mutated gene (one from each parent) to develop the disease. The frequency of this mutation in the Golden Retriever and Goldendoodle is unknown.

At Maverick Ranch, we test our breeding program for this mutation. Currently, our breeding program will only produce puppies that are clear of this mutation.

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Osteochondrodysplasia (OCD)

Osteochondrodysplasia is an inherited musculoskeletal disease affecting dogs. Affected dogs typically present at about 3 weeks of age with stunted growth. Puppies often walk differently than unaffected littermates and stand with their feet turned out and hind legs splayed. Their legs are short and bent with enlarged joints and clubbed feet. They also have flatted rib cages and under bites, which can affect their ability to nurse and breathe. While affected dogs can survive for many years with supportive care, they will develop arthritis and will likely have breathing difficulty due to their deformed ribcages.

Osteochondrodysplasia is inherited in an autosomal recessive manner in dogs meaning that they must receive two copies of the mutated gene (one from each parent) to develop the disease. The mutation of the SLC13A1 gene associated with osteochondrodysplasia has been identified in Miniature Poodles, although its overall frequency in this breed and other varieties of Poodles is unknown.

At Maverick Ranch, we test our breeding program for this mutation. Currently, our breeding program will only produce puppies that are clear of this mutation.

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Osteogenesis Imperfecta (OI)

Osteogenesis imperfecta (OI) is an inherited collagen disorder affecting dogs. Affected dogs typically present between 3 to 4 weeks of age with pain, lameness and fractures. OI is caused by a defect is in the way collagen is made. Because collagen is an important component of bone, bones of affected dogs are thinner than normal, fracture easily and do not heal properly. Other features of the disorder include loose joints and brittle teeth. Affected puppies may die shortly after birth and be smaller than littermates. Because of the severity of the disease, pups with OI are usually euthanized by 3 months of age.

Osteogenesis imperfecta (golden retriever type) is inherited in an autosomal dominant manner in dogs meaning that they only need to inherit one copy of the mutated gene to develop the disease. The mutation in the COL1A1 gene associated with osteogenesis imperfecta (golden retriever type) has been identified in a golden retriever, although its overall frequency in this breed is unknown.

At Maverick Ranch, we test our breeding program for this mutation. Currently, our breeding program will only produce puppies that are clear of this mutation.

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Dystrophic Epidermolysis Bullosa (DEB)

Dystrophic epidermolysis bullosa (DEB) is a hereditary skin disease affecting dogs. Clinical signs of DEB are present at birth. Affected dogs have fragile skin that is easily damaged from rubbing or trauma resulting in blisters, ulcers and scarring of the skin. Areas that are most prone to blisters are the face, foot pads, genital areas and ears. In addition, affected dogs will develop blisters and ulcers inside the mouth and in the esophagus. Ulcerations of the skin and mucous membranes are painful and can become infected. Blistering of the skin tends to cease at around 8 months of age however, ulcers of the mouth and esophagus persist into adulthood. Dogs with DEB are often smaller than littermates, likely due to difficulties eating.

Dystrophic epidermolysis bullosa is inherited in an autosomal recessive manner in dogs meaning that they must receive two copies of the mutated gene (one from each parent) to develop the disease. The mutation of the COL7A1 gene associated with dystrophic epidermolysis bullosa has been identified in Golden Retrievers, although its overall frequency in this breed is unknown.

At Maverick Ranch, we test our breeding program for this mutation. Currently, our breeding program will only produce puppies that are clear of this mutation.

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Intervertebral Disc Disease (IVDD)

Type I Intervertebral Disc Disease (IVDD) is a back/spine issue that refers to a health condition affecting the discs that act as cushions between vertebrae. With Type I IVDD, affected dogs can have a disc event where it ruptures or herniates towards the spinal cord. This pressure on the spinal cord causes neurologic signs which can range from a wobbly gait to impairment of movement. IVDD is treated differently based on the severity of the disease. Mild cases often respond to medical management which includes cage rest and pain management, while severe cases are often treated with surgical intervention.

Research indicates that dogs with one or two copies of this variant have a similar risk of developing IVDD. However, there are some breeds (e.g. Beagles, Cocker Spaniels, and Corgis, among others) where this variant has been passed down to nearly all dogs of the breed and most do not show overt clinical signs of the disorder. Nearly 100% of the dogs in some short-legged breeds have two copies of this mutation (e.g. dachshund, corgis), making it virtually impossible to breed away from this mutation in these breeds. This suggests that there are other genetic and environmental factors (such as weight, mobility, and family history) that contribute to an individual dog’s risk of developing clinical IVDD. 

Although the inheritance risk of this mutation is not fully understood, it is important to recognize the risk. Nearly all short legged dogs carry this mutation because it is linked to the mutation that gives them their distinct build and appearance. The frequency of Intervertebral Disc Disease varies between breeds. The genetic IVDD risk factor is very common in miniature poodles because of the genetic components that gives them their small build, making IVDD more common in miniature doodle hybrids.

At Maverick Ranch, we are working hard to build a breeding program that is free of IVDD. We try to educate our puppy buyers about weight management and proper exercise to help reduce the environmental risks for this disease. All dogs should always have their weight managed and avoid excessive jumping and flights of stairs.  

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Obesity

One of the main health problems facing dogs today is obesity. Society has normalized fat dogs, and many pet owners don't know what the proper body score should look like. By using phrases like "thick","chonker", and "big-boned" we've altered the perception of a healthy dog. We can no longer see the extra weight for what it is, dangerous. It's very important to monitor your dog's calorie intake and adjust it accordingly. Dogs should NEVER be fed free choice. Most dogs love to eat, and given the chance will get very fat. Sadly, obesity can also lead to an increased risk of heart disease, diabetes, hip dysplasia, intervertebral disc disease, and joint damage, among other things. It is the responsibility of the dog owner to give their dog the proper amount of food, because their dog's health depends on it. 

At Maverick Ranch we try to educate our puppy families on proper nutrition and weight management. We give our puppy families information on our "Puppy Manual" page to help explain proper body score and how to tell what score your dog or puppy is. 

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Information on this page is sourced mostly from Paw Print Genetics, Embark Vet, and the OFA

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