Our dog trainer has just sent us links to some info on the effects of neutering, and one of the links (A population study of neutering status as a risk fa... [Prostate. 2007] - PubMed - NCBI) states that neutering increases the likelihoods of ALL types of cancer.

I understood that neutering increases the chances of some types of cancer, including prostate cancer, but because it eliminates the likelihood of testicular cancer, it was difficult to come down on one side or the other in terms of cancer risk. The study above doesn't mention testicular cancer at all though. Is there a balanced study anywhere that isn't biased in one direction or the other?

In terms of testicular cancer, as this mainly effects old dogs, would it be most wise to leave young male dogs unneutered and then castrate them when they're older and have reached the target age for testicular cancer?

I don't plan on having Sherlock neutered, not just because of the health risks but also the behavioural ones (http://www.vizslacanada.ca/SNBehavio...taSnapShot.pdf) but I would like to know the facts and not feel as though I'm being swayed by biased reports.

Does anyone have any links to other studies that seem balanced?

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Where does it say that? It concluded that prostate cancer could be breed-related, while neutering may increase the risk of TCC. TCC is a recurring local tumour that isn't necessarily malignant yet. If caught early they can be removed without problem.

The study abstract hasn't mentioned the relevance of other associative factors, such as lifestyle, age, weight, genetic predisposition etc, so the full report would have to be read before making any real conclusions. Also, when stating the results, the authors haven't compared neutered vs breed, nor stated the significance values. Pretty lazy scientific publishing.

Please don't assume that neutering increases the risk of cancer; cancer is a multi-spectrum disease with many causative factors. It can't be simplified in such a way.

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It says "Neutered males had a significantly increased risk for each form of cancer". But yes, the abstract is pretty uninformative, which is why I'd be interested in seeing a more useful report! I just would have thought that there would be more helpful studies about but the things I can find on the internet seem to be biased one way or the other.

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My understanding of the subject is this:

Castrated dogs are up to four times more likely to suffer from cardiac hemangiosarcomas (almost always fatal), and up to twice as likely to suffer from osteoscarcomas (again, fast-spreading and almost always fatal) than unspayed/unneutered dogs. A castrated male dog is almost three times more susceptible to bladder cancer, a cancer which spreads quickly, is virtually undetectable until it has spread, and hence is almost always fatal.

However, whilst entire male dogs are at a small risk of prostate or testicular cancer, both are slow growing cancers that are easily detectable and hence rarely fatal, and can be removed with no further side effects by the very same op that is used for castration - so why do the op unnecessarily? Why not wait until there is actually a problem (and remember, there may never be a problem!) before you subject your dog to an invasive operation?

Many vets and rescue organisations push to have puppies neutered at an early age, but this causes far more problems than it solves. It may make the vets money, rescue centres may mistakenly think that they are helping to curb the canine population, but dogs and bitches will suffer if neutered too early. If you neuter before maturity - note, maturity, not puberty (ie 24 months in some large breeds) - the lack of sex hormones will lead to the formation of osteoclasts which delay the growth plates closing long after they would normally close. The delay in the closing of the growth plates causes extra growth, and the extra growth leads to long, malformed bones, cruciate ligament problems and dysplasic hip and elbow joints. In additon, because of the lack of hormones, dogs and bitches spayed before they reach maturity often stay in a "junior" time-warp - ie their behaviour never develops into adult behaviour, with all the training problems that can ensue from that.

As for references, try these. If you scrawl to the bottom of the second link, you will find links to the various scientific studies that have produced the figures quoted in my reply.

Stan Rawlinson explains the dangers of Spaying and Castration (Neutering) young Dogs

Stan Rawlinson Neutering (Spaying & Castration) Dogs and Suprelorin

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Bergies and borders - what more could anyone want? Siamese and maine coons, of course!

From the Rubaiyat of Omar Khayyam:
The Moving Finger writes, and, having writ,
Moves on, nor all thy Piety nor Wit
Shall lure it back to cancel half a Line,
Nor all thy Tears wash out a Word of it.
(But you can always edit your post, of course )

there are a number of indicators that neutering can increase the likelihood of cancers - certainly early neutering as well as temperament issues, incontinence for the girls and joint problems caused by additional growth if neutered before growth plates have closed (growth is restricted by hormones) the resulting changes to angles of joints can increase arthritis etc in older age.

I believe that if you wish to neuter then at least wait until the dog is physically (and mentally) mature to reduce health, behaviour and temperament issues caused by early neutering.

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Penny
Funfastquick Agility Dogs

Each form of cancer mentioned in the Methods section, not each form of potential cancer - that would be hundreds!

Agree it does take a LOT of reading to make an informed decision, which is why I'm still sitting on the fence regarding this. It just annoys me (absolutely not aimed at you!! ) when people wave their pro- or anti-neutering flags, citing the same tired and frankly poor studies to strengthen their arguement.

I'm just waiting for that one magic, independent, multi-author paper, that has carried out all procedures of the gold standard, headed by an eminent published professor and his/her department in collaboration with other international labs, looked at every aspect in the causative and associative spectrum, looked at the issue retrospectively and diagnostically, used randomised, double-blind subjects and controls, has statistically evaluated all the data in a useful way and not just for numbers' sake, and has presented the findings in a clear, concise report that conludes there is one single cause of cancer in dogs. Woohoo.

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There are many studies on neutering (as on all subjects) but, as in any area, the value of these studies depend on various factors including flaws extant in many outwith the difficulties faced by researchers such as ethical restraints etc.

Many studies are conducted on small sample sizes, with inadequate controls, interplay of factors confounding results and some are designed to confirm observations, not to test them. In addition there is evidence of both selection and reporting bias.

So as in any data mining, a deal of interpretation is required which is not always possible if you do not know all the facts in order for the data to be meaningful, also the words "absolute" and "relative" are often missing from the word "risk".......

You have some mistakes there.

Bladder cancer isn't "virtually undetectable until it has spread". Early stages can be signified by painless bleeding during urination. This is before metastasis.

Osteoclasts are part of bone. They don't appear due to lack of sex hormones as they aren't regulated by these hormones. They are a crucial part of bone growth and formation, along with osteoblasts and eventually osteocytes.


Oh dear, just quickly skimmed over the spiel on osteoclasts at the end of the first article - what is the man talking about??! To clarify, removing sex hormones does not have an effect on osteoclasts; furthermore, it is chondroblasts that are involved in growth plate closure. Chondroblast proliferation is affected by levels of oestrogen - high levels of oestrogen at the end of puberty lowers chondroblast activity, thereby causing endochondral ossification. This also accounts for the height difference between the sexes.

Neutering before this pubertal oestrogen surge slows down the rate of long bone fusion, therefore taller animals. In addition, taller animals are NOT predisposed to orthopaedic conditions, unless they are syndromic of another condition.

Very dissapointed that such fundamental and scaremongering errors are on Stan Rawlinson's website.

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On the contrary. Below are several unrelated, separate sites that clearly show what Stan Rawlinson says is correct, and that you clearly have no idea what you are talking about. A quick google by anyone will show many, many more supporting sites, but I think that these will be enough to get the point across.

Perhaps you should learn the full story before you attempt to contradict people with superior knowledge to yourself (not talking about me here, but Stan Rawlisnon, the scientists and their studies upon which he based his article, and the authors of the articles below). What is that saying? A little knowledge is a dangerous thing. You obvoiously have a little knowledge, but not enough, it would seem, to apply it correctly. I think you owe Stan Rawlinson, me, and any readers on here who may have been swayed by your dangerous lack of knowledge, an apology.

What Are Osteoclasts?

When the resorption process is initiated, the osteoclastic cell latches onto the bone to be resorbed, releases enzymes to deconstruct the tissue surface, and then breaks it down into calcium and phosphorus ions, which the cell eventually passes through the outer membrane and into the circulatory system. The process of resorption, from first osteoclastic contact to the release of ions into the blood, can take up to three weeks to complete. The resorption process is controlled by hormones in the bloodstream, which is why osteoporosis, a condition where the rate of bone loss exceeds the regrowth of bone tissue, is closely linked to hormonal changes.


Osteoclast - Wikipedia, the free encyclopedia
Osteoclasts are regulated by several hormones, including parathyroid hormone (PTH) from the parathyroid gland, calcitonin from the thyroid gland, and growth factor interleukin 6 (IL-6). This last hormone, IL-6, is one of the factors in the disease osteoporosis, which is an imbalance between bone resorption and bone formation. Osteoclast activity is also mediated by the interaction of two molecules produced by osteoblasts, namely osteoprotegerin and RANK ligand. Note that these molecules also regulate differentiation of the osteoclast.[7


Osteoclast definition - Medical Dictionary definitions of popular medical terms easily defined on MedTerms

In normal bone, bone formation and bone resorption are closely coupled processes involved in the normal remodeling of bone. In osteoporosis, the net rate of bone resorption exceeds the rate of bone formation, resulting in a decrease in bone mass without a defect in bone mineralization. In women, osteoclast activity is increased because of decreased estrogen after the menopause. (Men with prematurely decreased testosterone may also have increased osteoclast activity.) These changes result in further net loss of bone. The amount of bone available for mechanical support of the skeleton eventually falls below the fracture threshold and one may suffer a fracture with little or no trauma.


Bone

Many hormones affect bone growth and remodeling.

•Growth hormone (GH). As its name suggests, GH drives the growth of bones until the adult size is reached.
•Parathyroid hormone (PTH). It promotes the number and activity of osteoblasts.
•Estrogens. Until the end of puberty, estrogens are needed for maturation of the skeleton (in males as well as females — Link). In women, after the menopause, taking supplemental estrogen slows up the bone loss that so often leads to osteoporosis. The estrogen induces FasL in osteoclasts causing them to self-destruct by apoptosis and in this way slows up the destruction of bone.
•Calcitonin and thyroid stimulating hormone (TSH), both of which inhibit the activity of osteoclasts.
•Calcitriol (1,25[OH]2 vitamin D3. Needed for the deposition of calcium into bone.
•Osteoprotegerin is a protein secreted by osteoblasts and their precursors (thus a cytokine) that also inhibits the production and activity of osteoclasts. Clinical trials of a recombinant version (made in E. coli) are underway as a possible treatment for various bone-weakening disorders like osteoporosis and multiple myeloma.
•Leptin, which regulates the balance between osteoblast and osteoclast activity.
•Serotonin. Secreted by the duodenum, serotonin suppresses osteoblasts (at least in mice). This may account for the bone-weakening effect in humans of prolonged use of selective serotonin reuptake inhibitors (SSRIs).

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Bergies and borders - what more could anyone want? Siamese and maine coons, of course!

From the Rubaiyat of Omar Khayyam:
The Moving Finger writes, and, having writ,
Moves on, nor all thy Piety nor Wit
Shall lure it back to cancel half a Line,
Nor all thy Tears wash out a Word of it.
(But you can always edit your post, of course )

Actually, I am a scientist. Unless a first class honours degree from the Royal Veterinary College doesn't count. Please don't patronise me by quoting from Wikipedia.

None of the hormones that you mention that control osteoclasts are gonadal sex hormones. Yes, they are controlled by PTH etc, but they are released ELSEWHERE. Osteoclasts work in conjunction with osteoblasts in the formation of spongy bone of the weight-bearing long bones. It is chondroblasts that are involved in bone plate closure.

The only sex hormone you have there is oestrogen, which, as I have already mentioned, does have an effect on bone length.

Bowing out of this thread now as it appears that the ability to 'cut and paste' without ANY actual knowledge gives one the licence to be judge and jury, and a dangerous one at that. Apologise indeed *snorts*.

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