Late castration to improve conformation

[cornbrodolly]

Our colt foals were always castrated whilst on their dams,say at 7 or 8 months old - they never seemed to suffer at all- no weight loss,no traumas, as mum was there for comfort . We bred warmbloods ,or warmblood crosses.
I think on welfare grounds alone ,early castration is the best. We began this on the advice of a vet, and never regretted it. Saw herds of colts of differing ages in germany - the younger ones were kicked and bitten to ribbons. I cant think our early gelded boys had less muscle or grew more or less. Who wants too much muscle on a youngster anyway?

 

[Illusion100]

Yes, but the problem of differung genetics and variable physiology also exists with people or lab animals involved in drug trials. Even in the unusual situation of creating identical genetics and environment there will be some biological variation. That's why we use statistics.

Suppose researchers recorded the age of horses at growth plate closure in a good number of individuals. These ages will be spread out due to a combination of genetic and environmental factors. If they then divided the horses into two groups - entire and ungelded - and found that there was a significant difference in time of growth plate closure, wouldn't you consider that quite compelling evidence for testosterone (whose levels we know are markedly different in the two groups) being involved in the process?

It would be much better if levels of testosterone were also measured - and that's not impossible.

Correlation isn't causation, of course. But such a result would be very suggestive, no? Further experiments could be done to manipulate hormone levels or block their effects or whatever other interventions endocrinologists and biochemists have at their disposal. The fact that this would be done in different individuals is no more of a barrier to discovery than it would be in a trial in which a drug is given (or not) to different people.

In my opinion, this is a long way from saying it's impossible to prove that testosterone levels affects growth plate closure, the statement that puzzled me initially.

Example experiment

"The long-term effect of anabolic steroid was investigated in 3 experiments. In experiment I, 500 mg of 19-norandrostenololylaurate was given to 5 colts and a dose of 100 mg to another 5 colts every 3rd week. Six colts served as untreated controls. The animals were 12-16 months old at the start, and 24 months at the end of treatment. In experiment II, a dose of 1 mg/kg was given every 3rd week to 4 colts and 0.3 mg/kg every week to another 4 colts. Six colts served as controls. The colts were treated from 7 months to 12 months of age. In experiment III, 1 mg/kg of steroid was given every 3rd week to 3 foals between 3 and 8 months of age. Three foals were used as controls. Libido and hCG-induced serum testosterone concentrations were studied after the cessation of treatments, up to 3 or 4 years of age. Closure of the right distal radial growth plate was determined between 21 and 36 months of age. Treated colts had lower testosterone levels 4.5 months after cessation of treatment in experiment I (p < 0.001) and experiment II (p < 0.05) when compared with the corresponding control groups. Two years after treatments in experiment I, hCG-induced testosterone levels were higher in treated colts than in untreated controls, but the difference was not statistically significant."

 

[fburton]

Illusion100, I'm not not sure what point you're making with the quote above. Could you please explain?

 

[Illusion100]

Illusion100, I'm not not sure what point you're making with the quote above. Could you please explain?

You previously questioned why can't statistics quantify the effects of testosterone on growth plate closure using and examining various factors. I provided an example experiment demonstrating the findings weren't statistically significant.

 

[fburton]

Ah, okay. I guess the whole abstract should be quoted then, including the bit that reports an effect of the anabolic steroid treatment on the closure of growth plates:

"The treatments had no effect on libido. The anabolic steroid treatment did not cause premature closure of epiphyseal growth plates in any of the experiments, but closure appeared to be delayed. It was concluded that anabolic steroids have long term effects on reproduction. Their influence on serum testosterone can last for years after cessation of treatment, and they can delay the closure of growth plates which can cause increased susceptibility to cartilage injury during exercise."

This isn't the experiment/survey that I suggested earlier, but does provide evidence that hormones (including testosterone) are implicated in growth plate development.

 

[Illusion100]

Ah, okay. I guess the whole abstract should be quoted then, including the bit that reports an effect of the anabolic steroid treatment on the closure of growth plates:

"The treatments had no effect on libido. The anabolic steroid treatment did not cause premature closure of epiphyseal growth plates in any of the experiments, but closure appeared to be delayed. It was concluded that anabolic steroids have long term effects on reproduction. Their influence on serum testosterone can last for years after cessation of treatment, and they can delay the closure of growth plates which can cause increased susceptibility to cartilage injury during exercise."

This isn't the experiment/survey that I suggested earlier, but does provide evidence that hormones (including testosterone) are implicated in growth plate development.

Do you actually understand the abstract?

 

[ester]

Just because results aren't stat significant doesn't mean they are irrelevant or incorrect, with such a small sample it would be pretty impossible for them to be stat significant!

 

[fburton]

Do you actually understand the abstract?

Yes, I think so. I will assume that you do too. So could you please explain how this abstract/experiment shows that it is impossible to prove that testosterone levels affects growth plate closure (your original statement), because quoting any example where the findings weren't statistically significant does not rule out the possibility of showing an effect, especially if the study was underpowered?

Also, you will know that the abstract you quoted (only partially!) doesn't address the question of an effect of testosterone level (e.g. after gelding) on growth plate closure directly, because it was exogenous anabolic steroid that was tested.

Finally, the researchers did report a delay in growth plate closure with steroid treatment. I haven't been able to get hold of the full Acta Vet Scand paper, so can't comment on the statistics. Nevertheless, the presence or absence of a significant effect on time of growth plate closure in this study in no way invalidates the principle of testing for an effect of gelding, or other manipulation of testosterone levels, using larger numbers of horses or with a different statistical or experimental design. There is nothing inherently impossible about such a result, as far as I can see, contrary to what you claimed. If I am wrong on that point (which is entirely possible) I would be grateful to be enlightened as to why.

If you had said that studies have failed to show that castration has any effect on growth plate closure, that would have been perfectly reasonable, and people could look at the published results to fill the details if they wanted. However, you said it was "impossible to prove", implying that there is no way to show any effect (or lack of effect) in principle. That was the assertion I was and am questioning, and that you haven't yet explained.

I hope that spelling things out in such a long-winded way makes my position clear, if it wasn't before.

ETA: Thank you, Ester, for saying part of what I wanted to say so succinctly!

 

[Illusion100]

Yes, I think so. I will assume that you do too. So could you please explain how this abstract/experiment shows that it is impossible to prove that testosterone levels affects growth plate closure (your original statement), because quoting any example where the findings weren't statistically significant does not rule out the possibility of showing an effect, especially if the study was underpowered?

Also, you will know that the abstract you quoted (only partially!) doesn't address the question of an effect of testosterone level (e.g. after gelding) on growth plate closure directly, because it was exogenous anabolic steroid that was tested.

Finally, the researchers did report a delay in growth plate closure with steroid treatment. I haven't been able to get hold of the full Acta Vet Scand paper, so can't comment on the statistics. Nevertheless, the presence or absence of a significant effect on time of growth plate closure in this study in no way invalidates the principle of testing for an effect of gelding, or other manipulation of testosterone levels, using larger numbers of horses or with a different statistical or experimental design. There is nothing inherently impossible about such a result, as far as I can see, contrary to what you claimed. If I am wrong on that point (which is entirely possible) I would be grateful to be enlightened as to why.

If you had said that studies have failed to show that castration has any effect on growth plate closure, that would have been perfectly reasonable, and people could look at the published results to fill the details if they wanted. However, you said it was "impossible to prove", implying that there is no way to show any effect (or lack of effect) in principle. That was the assertion I was and am questioning, and that you haven't yet explained.

I hope that spelling things out in such a long-winded way makes my position clear, if it wasn't before.

ETA: Thank you, Ester, for saying part of what I wanted to say so succinctly!

Yes, failure and impossible have different meanings, perhaps I could have used fail/failure instead of impossible, however impossible is simply my view in relation to this subject. Failure can imply that the vast amount of scientific research has been botched, whereas impossible can imply that no conclusive evidence has found regardless of repeated experimentation. I still believe it is impossible to determine. Choice of wording doesn't change the fact that no conclusive evidence exists though.

I'm sure I've expressed that sex hormones may have an effect on growth plate closure, however no evidence can confirm this. Please note that my use of impossible was not in relation to providing the abstract. I did not supply an opinion when providing the example experiment of monitoring a synthetic controllable factor using various groups and the significance statistically, which you previously wished to know existed.

 

[Dry Rot]

As the OP, I haven't read all the replies but thank you all anyway. My choice is probably led more by necessity than science!

The two 2yo colts were not gelded last year because frosts intervened -- but we thought it would be interesting to run them on anyway, because we could. The vet was due a couple of days ago but was rained off. (Don't you just love Scotland?). We've decided to leave the weaned foal as I'd much prefer to geld in the open field and at the moment trying to lead him anywhere is going to be be a wrestling match!

But I still think my Arnold Schwarzenegger example applies. Would his shape have been any different if he'd been castrated at 12 and would it change if he was now? I think the answer is pretty obvious, isn't it? Are horses likely to be any different?

 

[fburton]

Yes, failure and impossible have different meanings, perhaps I could have used fail/failure instead of impossible, however impossible is simply my view in relation to this subject. Failure can imply that the vast amount of scientific research has been botched, whereas impossible can imply that no conclusive evidence has found regardless of repeated experimentation. I still believe it is impossible to determine. Choice of wording doesn't change the fact that no conclusive evidence exists though.

I'm sure I've expressed that sex hormones may have an effect on growth plate closure, however no evidence can confirm this. Please note that my use of impossible was not in relation to providing the abstract. I did not supply an opinion when providing the example experiment of monitoring a synthetic controllable factor using various groups and the significance statistically, which you previously wished to know existed.

I confess to finding this point of view rather baffling. Might your opinion be modified if you saw evidence for testosterone delaying growth plate closure in another mammalian species? Are you willing to admit that any lack of evidence in horses could simply be due to the fact that the experiment hasn't been performed yet? If someone has done the experiment, and showed no effect of testosterone on growth plate closure, I would expect the evidence to be quite easy to find. Instead, however, one finds statements like the following which seem to suggest there is a widespread recognition of an effect among vets (even if they are generalizing from what is known about other species, such as man):

http://www.netvet.co.uk/equine/neutering/castrating-a-stallion.htm

"Myths... Stallions are taller than geldings

Commonly, horses that have been gelded at an early stage of their life have a delayed closing time of the growth plates in their legs. The hormone responsible for the closing of the growth plates is testosterone and this it is this hormone which is prevented from being produced following castration. As a result geldings are usually taller than stallions and not the other way around."

 

[fburton]

There is a paper in JAVMA titled Gonadectomy in immature dogs: effects on skeletal, physical, and behavioral development.

According to the abstract:

"In a 15-month study, the effects of prepubertal gonadectomy on skeletal growth, weight gain, food intake, body fat, secondary sex characteristics, and behavioral development were investigated in 32 mixed-breed dogs. Male and female pups from 5 litters were randomly allotted to 3 groups: group I, neuter at 7 weeks (n = 14); group II, neuter at 7 months (n = 8); and group III, sexually intact dogs (n = 10). Growth plate closure was delayed (group I vs group III; P less than 0.000001; group II vs group III, P less than 0.000001) in all neutered dogs, as compared with sexually intact dogs. Growth plate closure was delayed longer (group I vs group II, P less than 0.000045) in dogs neutered at 7 weeks old, compared with dogs neutered at 7 months old. The rate of growth was unaffected by gonadectomy, but the extended growth period resulted in greater final radial/ulnar length in all male dogs and bitches neutered at 7 weeks."

The full reference can be found here: http://www.ncbi.nlm.nih.gov/pubmed/2045340

If an effect can be seen in dogs, I'm not sure why this it wouldn't also be possible in principle to look for (and maybe find) a comparable effect in horses, genetic variation notwithstanding.

 

[bakewell]

There is a paper in JAVMA titled Gonadectomy in immature dogs: effects on skeletal, physical, and behavioral development.

According to the abstract:

"In a 15-month study, the effects of prepubertal gonadectomy on skeletal growth, weight gain, food intake, body fat, secondary sex characteristics, and behavioral development were investigated in 32 mixed-breed dogs. Male and female pups from 5 litters were randomly allotted to 3 groups: group I, neuter at 7 weeks (n = 14); group II, neuter at 7 months (n = 8); and group III, sexually intact dogs (n = 10). Growth plate closure was delayed (group I vs group III; P less than 0.000001; group II vs group III, P less than 0.000001) in all neutered dogs, as compared with sexually intact dogs. Growth plate closure was delayed longer (group I vs group II, P less than 0.000045) in dogs neutered at 7 weeks old, compared with dogs neutered at 7 months old. The rate of growth was unaffected by gonadectomy, but the extended growth period resulted in greater final radial/ulnar length in all male dogs and bitches neutered at 7 weeks."

The full reference can be found here: http://www.ncbi.nlm.nih.gov/pubmed/2045340

If an effect can be seen in dogs, I'm not sure why this it wouldn't also be possible in principle to look for (and maybe find) a comparable effect in horses, genetic variation notwithstanding.

I often wonder if there is a link between hip dysplasia/ other joint issues in dogs and neutering. Not in a condemnatory fashion, just curious. Does seem much more common now.

 

[Illusion100]

With relation to the dog experiment, again the results IMO aren't statistically significant.

A very important factor is that whether or not sex hormones influence the closure of growth plates, is the significance of the growth rate while the growth plates are open. Delayed closure does not necessarily equate increased growth.

It is considered that the lower levels of testosterone and higher presence of androgens in human females causes earlier growth plate closure, hence women reaching skeletal maturity faster than males. However in non-human mammals the argument is that reduction of testosterone delays growth plate closure and therefore increases height.

Two examples;

My unneutered male dog is notably taller than any other male dog of his breed I've met, regardless of whether they are entire or not.

I know of a Stallion that when bred with mares of equal or very similar height produces offspring notably smaller than himself and all of the male offspring, afaik, have been gelded.

The bottom line is that the effects of castration and effects on skeletal growth has long been debated and investigated without conclusive evidence either way.

My personal opinion is that castration does not significantly alter skeletal maturity as no evidence to date can prove this without question or doubt.

 

[Palindrome]

Also do male equines have a longer growth period than female generally as do humans or is this totally hormone dependent? Human males seem to continue to develop height post puberty.

Not wishing to cause a yes/ no argument here, more a point for consideration and discussion. Unlikely to be any one answer!

Yes, I do remember reading an article about skeletal maturity in horses that said gelding took a bit longer than mares.

http://www.equinestudies.org/ranger_2008/ranger_piece_2008_pdf1.pdf
page 8:
"The taller your horse and the longer its neck, the later the last fusions will occur. And for a
male – is this a surprise? – you add six months. So, for example, a 17-hand Thoroughbred, Saddlebred or
Warmblood gelding may not be fully mature until his 8th year"

 

[bakewell]

y'know I've just thought of something, I don't know what it proves, if anything, may be totally irrelevant but... antlers, and horns are notably deformed or more feminine on castrated or hormonally impaired animals. (see Devil's antlers). Could this show the influence of testosterone on formation of bone type structures?

 

[Illusion100]

I often wonder if there is a link between hip dysplasia/ other joint issues in dogs and neutering. Not in a condemnatory fashion, just curious. Does seem much more common now.

Rapid growth rate due to high protein commercial foods does have a significant effect on skeletal deformities. Also the quality of the food, particularly the protein and exercise levels have effect. Plus there is the inbreeding!

 

[fburton]

With relation to the dog experiment, again the results IMO aren't statistically significant.

Hang on a minute... The paper reports highly significant differences in time of growth plate closure, as indicated by the very small P values, but you're saying you don't think they are significant?

A very important factor is that whether or not sex hormones influence the closure of growth plates, is the significance of the growth rate while the growth plates are open. Delayed closure does not necessarily equate increased growth.

Okay, but they do say "The rate of growth was unaffected by gonadectomy...". Why would that say that if it wasn't true? Do you have reason to disbelieve their reporting of their results?

(Next time I'm in the vet school library, I will read the whole paper to see in detail what the authors say.)

It is considered that the lower levels of testosterone and higher presence of androgens in human females causes earlier growth plate closure, hence women reaching skeletal maturity faster than males. However in non-human mammals the argument is that reduction of testosterone delays growth plate closure and therefore increases height.

I'm not sure that comparisons between the sexes are helpful here because sexual dimorphism is a feature of many species, and in humans there are well recognized differences in 'conformation' between men and women.

Two examples;

My unneutered male dog is notably taller than any other male dog of his breed I've met, regardless of whether they are entire or not.

A single counter-example doesn't prove anything, unfortunately. There may well be overlap between neutered and unneutered groups, with some neutered animals being smaller than unneutered ones, but the difference between the groups may still be statistically significant in favour of neutering increasing limb length.

I know of a Stallion that when bred with mares of equal or very similar height produces offspring notably smaller than himself and all of the male offspring, afaik, have been gelded.

Again that isn't proof of anything, although it does support the idea of a genetic factor determining adult height. The factor in this case may not even reside in the expression of hormones. However, if hormones were involved, it would have been interesting to see if gelding made any difference in this group (if it was large enough to be amenable to statistical test).

The bottom line is that the effects of castration and effects on skeletal growth has long been debated and investigated without conclusive evidence either way.

You may believe that, but is there any support in the scientific literature for that view? What I have found so far is pretty much a consensus that neutering leads to an increase in limb length via delay of growth plate closure. Maybe I am just looking in the wrong places?

 

[Illusion100]

Hang on a minute... The paper reports highly significant differences in time of growth plate closure, as indicated by the very small P values, but you're saying you don't think they are significant?


Okay, but they do say "The rate of growth was unaffected by gonadectomy...". Why would that say that if it wasn't true? Do you have reason to disbelieve their reporting of their results?

(Next time I'm in the vet school library, I will read the whole paper to see in detail what the authors say.)


I'm not sure that comparisons between the sexes are helpful here because sexual dimorphism is a feature of many species, and in humans there are well recognized differences in 'conformation' between men and women.


A single counter-example doesn't prove anything, unfortunately. There may well be overlap between neutered and unneutered groups, with some neutered animals being smaller than unneutered ones, but the difference between the groups may still be statistically significant in favour of neutering increasing limb length.


Again that isn't proof of anything, although it does support the idea of a genetic factor determining adult height. The factor in this case may not even reside in the expression of hormones. However, if hormones were involved, it would have been interesting to see if gelding made any difference in this group (if it was large enough to be amenable to statistical test).


You may believe that, but is there any support in the scientific literature for that view? What I have found so far is pretty much a consensus that neutering leads to an increase in limb length via delay of growth plate closure. Maybe I am just looking in the wrong places?

The abstract doesn't provide the competing hypotheses, so P value can't be deemed significant without that info, again imo.

''The rate of growth was unaffected by gonadectomy, but the extended growth period resulted in greater final radial/ulnar length in all male dogs and bitches neutered at 7 weeks." So what exactly is this saying without a P value?

My comparson between sexes is relevant as the abstract you provided uses both sexes as subjects.

My personal examples highlight that experimental evidence is not significant enough to provide definitive proof that castration will have a sterotypical effect based on apparent consensus.

But really.....you and I are as obviously stubborn in our beliefs as each other! I appreciate your examples and opinion regardless that we aren't going to see eye to eye on this subject.

 

[ester]

You don't have to put your P values in an abstract- you are trying to fit it all in to 200-250 words here! If you say they are significant, a significant P value is inferred and am sure will appear in the discussion.....

 

[fburton]

The abstract doesn't provide the competing hypotheses, so P value can't be deemed significant without that info, again imo.

TBH, I don't think opinion can negate the statistics! The only 'competing' hypothesis needed in any statistical test for there being a difference e.g. in the mean values of two sets of data is the one that says the opposite - in this case, that there is no difference. We aim to reject this 'null hypothesis'. Whether it is more correct simply to reject the null hypothesis, or to compare the null hypothesis with alternate hypothesis that says the mean values are greater, less, or just different, is a rather esoteric argument, and not at all the same as having another hypothesis that competes in terms of explanation or mechanism - which is what I think you mean.

I could have drawn two samples of numbers at random from larger populations, hand them to a statistician and ask if the averages of each set are different. I wouldn't need to supply any further information in the way of different hypotheses for him or her to derive something meaningful from the numbers, and provide me with an answer to my question. (The test could fail because the samples were too small, or the populations weren't approximately normally distributed or the variances were different - so one would use a non-parametric test instead - but if a P value was obtained that was a small as the ones in the abstract, it would be exceedingly unlikely that the difference seen could have arisen by chance alone.)

Of course the authors could have falsified their data (for what reason, heaven knows!) and there were no significant effects on time of growth plate closure, or neutering actually accelerated it - but one really shouldn't make a habit of ruling out findings completely and finally just because they contradict one's personally held opinion.

''The rate of growth was unaffected by gonadectomy, but the extended growth period resulted in greater final radial/ulnar length in all male dogs and bitches neutered at 7 weeks." So what exactly is this saying without a P value?

As Ester pointed out, not quoting a P value for everything stated in an abstract isn't usually taken as meaning the statement without a P value is false! I promise I will check what the paper says when I get a chance.

Even if rate of growth had been affected by gonadectomy, it is still the case that they reported a significant effect of neutering (and therefore one might reasonably assume testosterone levels) on growth plate closure time - the original bone (no pun intended) of contention.

But really.....you and I are as obviously stubborn in our beliefs as each other! I appreciate your examples and opinion regardless that we aren't going to see eye to eye on this subject.

Fair enough. I still hold up a smidgen of hope that you will come to really understand my point of view - and even if you don't, other readers may get something out of our exchange.

 

[Illusion100]

I do understand your point of view! I appreciate it even though we don't agree.

However you previously asked why the effects of testosterone/castration couldn't be determined via statistics, I provided an equine based abstract (without opinion) that wasn't significant. You provided a canine abstract that you believe is.

Abstracts are an overview and when the full experiment is read, then an opinion can be formed. Personally, I am a critical even if I want the experiment to confirm my belief, I'm awkward!

For every experiment to confirm castration etc effects growth there is another that doesn't. I hope you can understand my POV as well!

Anyway, while this has been interesting I hope we can move on and start to hog and debate many other threads , my opinion remains the same on this subject, as does yours!

P.s. I wonder why 2 of my ferrets, both purchased at the same age, from the same litter, same sex, same environment, same food, exercise regime, castrated on same day are so different in size...... Yes, sorry, had to put in another real life example!

 

[lazybee]

So to cut a long story short, it makes no difference. At the end of the day (hate saying that) when either an early or late castrated horse has matured they will both end up the same. If a late castration made any difference at all, I'm sure the French veterinary association for example wouldn't lop them off as soon as they've dropped. The risk of behavioural problems sometimes associated with a late castrated, is just one of the advantages of early chop.