Ethically and Responsibly Bred, Health Tested Golden Retrievers for ALL
Est 2019 - Treasure Valley, Idaho
The Full Story
All About Golden Retrievers
Golden Retrievers have our hearts and we love their fascinating origin story, how the breed split occurred, and what the future of the breed looks like now, and the common health problems that plague the breed.
Origin Story
This story takes us back to 1859 Guisachan estate, owned by Sir Dudley Marjoribanks, or Lord Tweedmouth, in the Scottish Highlands.
Lord Tweedmouth came across a wavy coated yellow retriever owned by a local cobbler, in need of a versatile hunting dog, he purchased him. At this time many hunting dogs were black coated and black dogs were desired over lighter colored ones. But Sir Dudley bought Nous, thought to be a setter mix, who had two black coated parents himself. Sir Dudley eventually bred Nous to his Tweed Water Spaniel bitch ( a now extinct curly haired, liver colored breed with white chests, toes, and faces) named Belle, with the hopes of creating a hunting dog able to navigate the marshes in the area and hunt well despite the cold and unpredictable weather.
This litter of 1868 is considered the first "golden retriever" litter. The first goldens produced were called Cowslip, Crocus, Primrose and Ada( from a repeat breeding). These pups were gifted to family members and their offspring tracked and recorded by Sir Dudley.
Marjoribanks son, Edward, was given Crocus and the fact that he also owned a red setter named Sampson, may have had something to do with the dark red coat color we now refer to as "dark golden" appearing very early on in the breed.
Ada was gifted to Marjoribanks nephew, Henry, the Earl of Ilchester, whose line of golden retrievers at Melbury Hall in Dorset became well known.
From there, the youngest son of Sir Dudley, Archie, traveled to Texas with a female named Lady, thus introducing the breed to the states and starting the well known Culham line of golden retrievers.
Understanding the Breed Split- Field Vs. Show Lines in the United States
The Golden Retriever is often described as being a split breed, with two distinct looks favoring lines that have purposefully carried on those looks. This would be "field" and "bench" lines. The field goldens commonly seen in the United States are usually darker in color, leaner, more muscular and smaller in stature than their show bred counterparts who are often larger, lighter in color, with bulkier statures.
Although they are both "Golden Retrievers," it is important to understand how and why this breed split occurred.
Fern Hills Goldens has put it nicely:
"Before the 1970's there were no distinctions between working and conformation line Goldens. They were essentially the same dog! In the years since however, the breed has developed two distinct types. A male named Cumming's Gold Rush Charlie came along in 1970 and was like no golden before him, with a new and very distinct look, he became very influential in the show world. As a result, the conformation ring has increasingly belonged to heavy bone dogs with long-ish bodies that may appear rather low to the ground, and often with a somewhat downward slope along the top line. Coats on show dogs have become longer, straighter, and silkier and the more desired color is a paler cream shade of golden. As show ring success has become more difficult to achieve with the increase in goldens being shown, looks have become the most important attribute for many show line breeders. As a result of decreased attention to disposition and working talent, the prevalence of truly outstanding working dogs or dogs with both Field and Show championships, has declined in the conformation lines.
Around the same time, the field goldens, owing influence to a dog named AFC Holway Barty, diverged in the other direction. Forsaking looks as a principle target, field breeders worked to improve the hunting and retrieving abilities of their dogs. As a result intelligence, trainability, the "bold golden" disposition, high activity levels, and extreme athleticism are much more prevalent in these lines as these are the features most necessary for field and working success. While many of these dogs do have wonderful conformation *( after all they do need to hold up physically under demanding athletic competition), some of the features, such as pretty broad muzzled heads, full dentition, and a good scissor bite, correctly carried tails, dark brown eyes color and a full black nose leather, are not universally present. There are other differences in appearance as well- most of the field dogs are darker shades of red or "dark" golden, typically darker than show goldens. They are frequently smaller, lighter boned, longer in the leg, and have shorter curlier coats than the dogs that are currently successful in the show ring. White markings, highly discouraged in the show ring, are more common in the field lines as well."

The Breed Standard Set by the Golden Retriever Club of America
Below is the official breed standard set by the GRCA, which we are proud members of. It is our mission to produce dogs in accordance with the written breed standards set by our Breed Club in order to preserve the breed and their purpose as both a hunting dog ( all our dogs have natural hunting ability) and a well rounded, versatile, and temperamentally sound family pet.
As members of the breed club we adhere to the breeding code of ethics set by our parent club.
To learn more about the breed and the standard, check out The Golden Retriever Study Guide by the GRCA


In Short- we can only do our best to produce healthy dogs who will live long lives. We test for and screen for every possible thing we can- but many health issues are out of our control.
At Mountain Reign Retrievers we screen our dogs for
- Hip and Elbow Dysplasia
- Genetic Eye Conditions
- Genetic Heart Conditions
- Genetic Diseases through Embark ( there are thousands of them with genetic markers).
We cannot screen our dogs for:
- Illnesses they may contract from their environments
- Types of Cancers
- Infections or viruses
- Genetic Mutations that do NOT have biomarkers or available tests
A General Overview of Cancer
This is crazy long ( the full article is even longer) but it is SO worth reading!
Unfortunately, despite goldens being one of the most popular breeds in the world, they are among the breeds who are pre-disposed to many types of cancer.
The Following article, Understanding Cancer in Golden Retrievers, written by Rhonda Hovan in 2006 does an impeccable job of highlighting the issue of cancer in the breed and shedding some light on the subject, below we have pulled some paragraphs from the article that are worth a read. Click the button below to read the full article published by the Golden Retriever News Magazine.
"The Numbers:
Let’s get started with some data of how cancer affects our breed. Approximately 60% of all Goldens will die from cancer. By gender, it’s 57% of females and 66% of males. Human cancer is also skewed slightly toward males, so it’s not surprising that dogs are too. For comparison, the rate of cancer in Goldens is just slightly less than double the rate of cancer in all dogs, which is estimated to be about one in three (and which actually is about the same as in humans). But even though our cancer rate is nearly double the all-breed average, it’s important to keep in mind that the average lifespan of the breed is still within the same 10-11 year range as all breeds. Our two most common cancers are hemangiosarcoma, affecting about one in five Goldens; and lymphoma, affecting about one in eight Goldens. These two cancers represent about half of all the cancers in the breed." (1.)
"Cancer as a Genetic Disease:
One thing you will hear all scientists say about cancer is that it is a genetic disease. But to non-scientists – and particularly to breeders – the word “genetic” does not necessarily mean the same thing that it means to cancer researchers. When scientists use the word genetic, they mean that they always need to look at genes to understand what has gone wrong to cause a cancer to form, because it is errors in genes that allow cells to multiply without normal controls. But just because cancer is a genetic disease, does not mean that it is strictly an inherited disease. So how can it be genetic, and not be inherited? This is because genes are found in two kinds of cells, and one kind is inherited, and the other kind is not. The kinds of genes most breeders are used to considering are found in germ line cells, which are the sperm and the eggs. These are the cells that contain genes that are passed on to the next generation. (It may help in remembering “germ line” cells by thinking of “germinating seeds” that sprout to grow the next generation.) All other cells of the body are called somatic cells. They also contain genes, but the genes in somatic cells are not passed forward, and can have no effect on the next generation. Any mutations that might happen to somatic cells during the lifetime of the animal are confined to that one animal and cannot affect its offspring. So errors in genes lead to cancers, and those errors are called mutations. Every time a cell divides, it must make a copy of its genes for the new cell, and that copying process provides an opportunity for a mistake. Most of the time, the mistakes are either corrected, eliminated, or are harmless; but every now and then, a mistake that impairs the normal function of a gene will be maintained. Fortunately, very very few cancers are the result of a single mutation, and essentially all common cancers in Goldens require numerous genetic errors. This is called the “multiple hit” theory of cancer, and applies to humans as well as dogs. It is estimated that cancers require at least 5-6 meaningful mutations to gain a foothold, and probably more. These mutations can occur in germ line cells – the sperm and the egg – and they can occur in somatic cells. And it is most likely that the mutations leading to cancer come from a combination of germ line cells and somatic cells. Therefore, it is most accurate to say that cancer in Goldens is partially inherited, and partially not inherited. Neither inheritance by itself, nor environmental exposures by themselves, cause cancer in Goldens; but both contribute to cancer in Goldens. Inherited mutations can be the first steps toward cancer, giving a puppy the predisposition to develop cancer – but the next steps occur during the life of the dog, and are not influenced by heredity. This predisposition toward cancer certainly does not mean that cancer is inevitable, and many predisposed dogs will live long lives with no cancer. The basic steps necessary for a cancer to grow are defined in the IPP model – Initiation, Promotion, and Progression. In the Initiation phase, a cell is endowed with immortality or another growth or survival advantage, but is still held in check by its cellular environment. This step is particularly intriguing, because some very new research is pointing toward the strong possibility that this immortality can be an inherited component of cancer, and is part of the “cancer stem cell” theory. During the next step, Promotion, additional mutations allow the cell to out-compete neighboring cells, and a tumor mass is formed. Finally, Progression occurs when a third series of mutations leads to metastasis and clinical disease. Each of these steps is achieved through multiple mutations it must achieve the following capabilities:
• it must be able to tell itself to multiply
• it must be able to defy outside signals to stop multiplying
• it must be able to invade other tissues where it wouldn’t normally grow
• it must be able to replicate endlessly
• it must be able to commandeer its own blood supply
• it must be able to resist signals to commit suicide
Each one of these capabilities is abnormal for most cells, and one or more mutations must occur to endow the cell with each of these traits. Again, cancer is clearly not the result of a single event, exposure, or genetic cause; numerous things have to happen to result in a cancer. Because of the kinds of capabilities that a cell needs to become a cancer, it turns out that certain kinds of genes are most likely to be involved, and these kinds of genes are called tumor suppressor genes and oncogenes (or tumor promoter genes). When a tumor suppressor gene is deactivated, it may not be able to keep a cancer from growing; and when an oncogene is inappropriately activated, it may signal cells to keep growing when they should stop. In general, because they are usually recessively regulated, mutations in tumor suppressor genes are considered to be likely candidates implicated in an inherited risk of cancer. Hopefully Readers can begin to get the idea from this discussion that there will never be a single answer to the question of what causes cancer in our dogs, or what will prevent cancer. It’s all about what contributes to the risk of cancer, and what might improve the odds.(58-60).
"The greatest single cancer risk factor is life. And the more of it we or our dogs have, the higher the likelihood that a cancer will arise.... I mentioned above that any animal which has lived beyond its normal reproductive years is at increased risk for cancer, and let’s examine why this is. The basics of natural selection are well known: that animals having genes most suited for survival live to pass those good genes on to offspring; and animals with harmful genes aren’t as successful at reproducing, so those genes are diminished in the population. But natural selection can only operate in animals prior to the end of their reproductive years, and once the natural age of reproduction is past, Nature has no stake in what happens to the individual. That is, if an animal gets cancer at seven years old, but is no longer reproducing anyway, then its cancer genes cannot be weeded out via natural selection. Conversely, if an animal is especially resistant to cancer and is very long lived, but is no longer reproducing into old age, then natural selection has no way to favor those desirable genes....So very often, when a Golden is past its ancestral reproductive age, what separates one with cancer from a one without cancer are a few unlucky rolls of the dice – a few unlucky mutations. These random mutations result in what is known as sporadic cancer – that is, cancer that has no identifiable inherited cause. Most cancer in dogs, as most cancer in people, is considered to be sporadic cancer."
Cancer in Goldens:
"Now we’re going to get more specific about Goldens. First, data show that cancer rates in Goldens are elevated around the world. While other countries may have a slightly different proportion of certain cancers – for example, in the US our most common Golden cancer is hemangiosarcoma, but in the UK, the most common Golden cancer is lymphoma – the overall incidence of cancer in Goldens is high in all countries. It doesn’t seem to matter whether the line is US, Canadian, Australian, UK, Danish, etc – if it’s a Golden, its cancer risk is elevated. For the most part, national breeding lines today are separated by oceans; and we certainly don’t all provide the same environments for our dogs around the world...The leading theory to explain the breed-wide elevated incidence of cancer is that very early founder dogs in the breed carried genes that have concentrated over time, and which convey increased cancer risk to essentially all of today’s Goldens.
The next piece of the cancer genetics puzzle in Goldens is that our breed is also at increased risk for several immune-mediated diseases such as allergies and hypothyroidism. In fact, the number one reason for Goldens to be taken to the vet is various manifestations of allergy and atopy, which includes frequent hot spots, food allergies, goopy ears (that’s a medical term), orange toes, etc. And it turns out that these diseases are also found at higher than average rates in Goldens around the world. This is relevant to our discussion of cancer because the immune system plays an important role in destroying abnormal cells before they have a chance to cause a clinical cancer, and a compromised immune system often leads to cancer. Now if this is true, what it means to those who might be trying to assess cancer risk in pedigrees, is that the various manifestations of a compromised immune system would have to be considered to be a component of the inherited cancer risk profile of the breed...That starts to give us a clue that not only is our breed as a whole at increased risk for cancer and other immune-mediated disease, but in addition, certain lines within the breed may have risks associated with specific cancers or subtypes of cancer. More evidence for this line-specific risk profile comes from comparing UK data with US data. This shows us that while lymphoma is the most common cancer in UK Goldens, hemangiosarcoma is the most common cancer in US Goldens. In addition, UK Goldens appear to have more mast cell cancer than US Goldens. There is also some preliminary evidence that some US Golden lines may have an increased risk specifically of lymphoma or hemangiosarcoma."(68).
Can We Reduce Risk Thru Breeding Decisions?
With these theories of cancer genetics for the breed in mind, one of the questions breeders always ask is “Can we reduce cancer through breeding decisions?” Unfortunately, the quick and dirty answer to that question is “Probably not at this time." – the problem is that if pretty much all Goldens carry these defective genes – where do we go to get rid of them and bring in healthy genes? Still, the common logic is that if we keep breeding only dogs whose parents have been long-lived, and do that over and over, won’t we be contributing those long-lived genes to the puppies and at least make some progress? But here’s why that doesn’t seem to work with any consistency...In humans, the best data available indicate that genetics accounts for only about 1/3 of longevity, and the other 2/3’s is environment. There is no comparable data in dogs, but it is likely to be similar. Although this sounds counter-intuitive, longevity in parents does not seem to be predictive for longevity in offspring. Yes, there are pedigrees that will appear that way for a couple generations; but sometimes a chance roll of the dice will produce a “7” seven times in a row too. So while those things do happen, it does not mean those chance results have significance other than if enough rolls of the dice occur, someone gets lucky. Likewise, if enough examples are searched, a pedigree that appears especially long-lived can be found. Further, most pedigrees do not provide the complete sibling data that is necessary to accurately evaluate a family, and without this information about siblings, the full and accurate range of expression of the family genes is unknown. However, I really don’t want to discourage breeders from trying if that is in their heart, but the data would lead more toward the conclusion that we just don’t know enough yet of how to select dogs that may have true longevity in their genes.... But no such defined and detailed guidelines exist for breeders. What breeders tend to do is note that (for example), “two grandparents died from cancer, and two of the aunts or uncles died from cancer, and the father’s brother died from cancer” and conclude from that tally that the line is at risk. Unfortunately, in a breed with a 60% death rate from cancer, such information is just not helpful in predicting genetic risk. In fact, in pedigrees where enough information is known and available, this is normal for this breed.

So What Can be Done to Reduce Cancer Rates in the Breed?
Fortunately, A LOT can be done to further reduce your dog's chances of cancer. It's still important to note that life itself is a roll of the dice, sometimes we're struck with bad luck that doesn't have a rhyme or a reason. If environment is responsible for "turning on" the genes our dogs are born with, we're in luck. We can make many changes to our dog's environments that offer the best possible chance at a healthy life free of " cancer triggers."
Rhonda goes on to state, "Fortunately, we do have choices that may significantly improve our dogs’ cancer risk profile. Most important is to raise puppies to follow a very slow growth curve, and keep adults lean and fit. The data are incredibly strong on this point, and come from not only research in dogs, but also many other species, from humans to other primates to mice to worms. Although the exact mechanisms aren’t fully identified, it is thought that oxidation of food produces free-radicals, which cause DNA damage and inflammation, which are steps along the pathway to many diseases. Put in simple terms, we rust. And the more food we eat over a lifetime, the more we rust. Since cellular damage may take many years to fully manifest, and since cells are most susceptible to damage when they are most rapidly dividing (which is during growth), it is thought that overfeeding during the earliest ages of puppyhood has the greatest potential for causing harm, including increasing the risk of cancer"
There are also several dietary supplements that some research has suggested may possibly improve a dog’s cancer risk profile. Recommendations include serving fresh cruciferous vegetables such as cauliflower, broccoli, Brussels sprouts, and cabbage approximately three times per week. Other research supports the daily addition of the omega-3 and omega-6 fatty acids found in fish oil (also called DHA and EPA); and there is some support for adding 200 mcg selenium and 400 I.U. Vitamin E to the daily diet. Each of these acts as an anti-inflammatory and/or antioxidant, which counteract the inflammatory and oxidation effects of food discussed above. At the same time that we want to optimize the good things that go into our dogs, we also want to reduce their exposure to possible carcinogens. The following environmental exposures have been linked with an increased risk of cancer, and can act as carcinogens by damaging DNA and/or increasing the DNA mutation rate:
• Coal or kerosene heaters
• Fumes from paints and solvents
• Asbestos
• Second-hand smoke
• Radiation including 5G
• Phenoxy herbicides
• Pesticides, Herbicides, and Fungicides
Specifically, exposure to coal or kerosene heaters, fumes from paints and solvents, and asbestos seem to be correlated with increased risk of several canine cancers. At this time, second-hand smoke has only been linked with nasal cancers in dogs, but evidence is mounting that there may be other associations too."
Spay and Neuter May be More Impactful Than We realize
According to the study "Assisting Decision-Making on Age of Neutering for 35 Breeds of Dogs: Associated Joint Disorders, Cancers, and Urinary Incontinence,"
"In an attempt to address the absence of breed-specific information on joint disorders and cancers associated with neutering, we undertook a project focusing on various specific breeds using data collection and analyses with our extensive veterinary hospital database where the same diagnostic criteria could be applied to all breeds. We started with popular breeds well-represented in the database, initially with the Golden Retriever (11, 12), Labrador Retriever (12) and German Shepherd Dog (13). The joint disorders examined included cranial cruciate ligament tears or rupture (CCL), hip dysplasia (HD) and elbow dysplasia (ED). The cancers examined, which previous studies found could be affected by neutering, were lymphoma/lymphosarcoma (LSA), hemangiosarcoma (HSA), mast cell tumors (MCT), and osteosarcoma (OSA).
In the Labrador Retrievers, Golden Retrievers, and German Shepherd Dogs, there was an increase in the incidence of one or more of the joint disorders with neutering in the first year in males and females to 2–4 times >3–5% incidence in intact dogs. In female Golden Retrievers, neutering at any age was associated with an occurrence of one or more of the cancers followed to 2–4 times higher than the 5 percent incidence in intact females. But in male Golden Retrievers, and in male and female Labrador Retrievers and German Shepherd Dogs, there was no evident increase in cancers above that of the dogs left intact. Preliminary analyses from some small-dog breeds revealed no apparent increased risks of joint disorders with neutering. Thus, the research that had been undertaken revealed a wide range of breed-specific differences in disease vulnerability to neutering. The purpose of this study was to analyze, in a variety of additional breeds, the increased risks, if any, of the above specified joint disorders and cancers associated with neutering male and female dogs at various ages, so as to increase the information available to pet owners and veterinarians for consideration when making decisions regarding neutering specific dogs. We added 29 new breeds to the study, separating three varieties of Poodles, for a total of 32 breed groups (referred to as breeds); this made a total of 35 breeds with the Goldens, Labs and German Shepherds included. The goal was to use the same veterinary hospital database and diagnostic criteria for the diseases as was used with the published studies on the retrievers and German Shepherds so as to allow for direct comparisons among various breeds. The primary purpose was to offer readers some evidence-based information on breed-specific differences with vulnerability to neutering, including suggested guidelines for neutering ages to avoid increasing long-term health risks of neutering, if any. A secondary, unforeseen, purpose was to document breed-specific differences in the increases in some cancers associated with removal of gonadal hormones, as an area for possible research on genetic aspects of cancer occurrence."
For Golden Retrievers Specifically:
"The study population was 318 intact males, 365 neutered males, 190 intact females, and 374 spayed females for a total of 1,247 cases. In intact males and females, the level of occurrence of one or more joint disorders was 5 percent and 4 percent, respectively. Neutering males at <6 mo. and at 6–11 mo. was associated with risks of 25 percent and 11 percent, respectively (p <0.01). In females, spaying at <6 mo. and at 6–11 mo. was associated with risks of 18 percent and 11 percent (p <0.01, when combined). The occurrence of one or more of the cancers followed in intact males was a high 15 percent and for intact females 5 percent. Neutering males at <6 mo. and at 6–11 mo. was associated with increased risks of cancers to 19 and 16 percent, respectively (p <0.01). Spaying females at <6 mo. and at 6–11 mo., was associated with increases in cancers to 11 and 17 percent, respectively (p <0.05, when combined) and spaying at 1 year and at 2–8 years was associated with increased risks of 14 percent (p <0.01, when combined). The occurrence of MC in intact females was 1 percent and for those spayed at 2–8 years, 4 percent. For females left intact, 4 percent were reported with PYO. No cases of UI were reported in females spayed at any age. The suggested guideline for males, based on the increased risks of joint disorders and cancers, is delaying neutering until beyond a year of age. The suggested guideline for females, based on the increased occurrence of cancers at all spaying ages, is leaving the female intact or spaying at one year and remaining vigilant for the cancers."
