Vet check question, during a vet visit should the vet pull a 3 month pups legs back to check hips - Page 4

[Hundmutter] 30.5.2016 - 16:05

● "Bubba, Malcolm Willis ... I have no recollection that he recanted anything !"
Actually, he admitted that he'd made a mistake by printing that
http://www.pedigreedatabase.com/german_shepherd_dog/dog.html?id=191-vello-zu-den-siebenfaulen
(greatgrandsire of my obedience bitch, Jena   http://lesp90.wix.com/lorelei-gsd-kennels   ) was KKl.1.
His argument as to why the allele for bi-colour and the allele for self-black could NOT BOTH be in the Agouti Pattern locus was impeccable. Unfortunately he stuck his neck out and guessed that bi-colour was IN and recessive self-black was OUT. But whether he bothered to correct it after DNA revealed the truth I don't know. When I last had an e-mail from him he was assembling his 3rd GSD book - but he died before finishing  it. He also made an error in the Colour locus and, I think, the Extension locus.


[bubbabooboo] 30.5.2016 - 17:05

● "I took an animal breeding genetics class in 1976 ...  This was during the time that Mendelian genetics was thought to be all there was. I asked some probing questions and the professors told me that science knew "everything" about genetic inheritance and there was no room for discussion."
Maybe in YOUR area - there are some VERY dogmatic Yanks! But I doubt that the whole world believed that in 1976.

● "In the 40 years hence the old science of Mendelian genetics has been replaced and amended with more complex non-Mendelian and epigenetic science."

Hence?

Replaced? NEVER!
Certainly what can now be analysed is more complex than was possible before the current VERY fast computer chips were available. But before breeders can START to understand post-Mendelian genetics they MUST have a very full understanding of the modes that Gregor Mendel worked out without even a pocket calculator. HE knew that his modes didn't cover EVERYTHING when he ran into a mechanism that involved alleles of TWO genes - I forget which plant it was.
As the term "Epigenetics" was coined by Waddington in 1942, deriving it from the 333± years old "epigenesis", you can be sure that Dr Willis knew about it, even if your lecturers didn't.

[Your] 30.5.2016 - 18:05
message is not worth arguing against - it demonstrates that your grasp of
#1: The way polygenic recessives operate and contribute to one another's damage probably doesn't extend to being able to see how mating an
A^ a^,  B^ b^,  C^ c^,  D^ d^,  E^ e^  pooch to an
A^ a^,  B^ b^,  C^ c^,  D^ d^,  E^ e^  pooch (inventing codes for genes in which the the dominants contribute to perfect hips, the recessives contribute to dysplastic hips) - both pooches having PERFECT hips under any xray scheme - can produce a range from pups with perfect hips to pups with the worst-possible hips, without any environmental influences being needed. The randomisation that occurs twice - one during the production of the gametes, the other during the process of fertilisation - provides enough variety to explain the variations. Of course, overweight, poor nutrition or over-feeding will HASTEN the moment at which the joint's development becomes too damaged for the sufferer to compensate for by such as shifting its weight onto the fore-hand and moving VERY smoothly.

But whether those ENVIRONMENTAL factors will produce dysplasia in individuals without ANY pairs of the undesirable recessives remains to be tested - we can't test it until all the genes & alleles involved are DNA-identified..
#2: You aren't aware of "susceptibility" and "threshholds". As a type2 diabetic with a type2 diabetic sister and a type2 diabetic father whose mother was a type2 diabetic but HER mother was far from diabetic (I don't know enough about that greatgrandfather)  I recognise that, so far as SOME OF "the change in diseases and health problems reflects this change" is concerned, but I dispute the "not a genetic causation" part. Using type2 diabetes as the tool to help you see WHY:
In my greatgrandparents' time sugar was scarce in most of the world, and so few people consumed enough sugar (fructose, glucose, lactose, maltose, sucrose, whatever) to trigger their genetic susceptibility to type2 diabetes - and medical capability couldn't save the babies born with type1 diabetes. (An early death is a useful way of slowing the spread of defective genes!)
But nowadays the "rich" countries have sugars galore - whether as alcohols, carbohydrates, cordials, "energy drinks", fats, "health drinks", KFC-etc, "soft drinks", and the biscuits & cakes & chocolates galore - so that many of us have our children then slow down and develop the type2 diabetes was latent in us - I was in my late 40s before I felt "slow" enough to seek a diagnosis.
It might well be that the poor survive, the rich die early!


[susie] 30.5.2016 - 18:05
Google was good enough to translate the headings as
Hip Joint Dysplasia in German Shepherd Dogs
Influence of Parents on the HD Level of Offspring
but I wish you had informed us what the numbers from 1 up to 2 at the left signify.

Und nein, mein Liebchen ßuzie - ich nicht sprechen sie Deutsche. But in the days when computers ran on DOS I programmed a database to produce a near-enough translation of Körscheinen or whatever the plural of Körschein is.


[Hundmutter] 30.5.2016 - 19:05

● "Of course, as far as Bubba and America is concerned, one could ask questions about why OFA took the route it has, with the gradings it has, when it could have had a scheme which sat easier with other countries' way of reckoning hip status and made it less difficult to work out the comparisons."
The main reason is that they are USAmericans, and in 1935 their G.B. Schnelle, an American veterinarian, discovered hip dysplasia in dogs; but it attracted little attention until, in 1956, the American Aninvale Kennels publicised that their dogs are affected. Followed by the 1958 Swedish study, the Swedish KC setting up a 1959 HD scheme for just GSDs, and THEN, in autumn 1964 John M Olin gathered a group of individuals - representatives of the Golden Retriever Club of America, German Shepherd Dog Club of America and the veterinary community - to discuss means of limiting hip dysplasia. This led to the formation of the Orthopedic Foundation for Animals (OFA), incorporated as a non-profit corporation by the state of Illinois on July 7, 1966.

So OFA was second into the field, first of the English-speaking nations (if one can accept Cornish, Gaelic, Glaswegian, Irish, Welsh, Yanklish as English...). The KC (UK) began its first scheme in 1965. The SV started "investigating" in 1966 but didn't set up the 'a'-stamps until 1967. My nation's veterinary university began its study in 1967 but the NZVA didn't make the scheme nationwide until 1972.
ALL of those schemes - including the FCI's - are blunt "category" schemes.

The Breed Information Foundation's system was the first (and so far ONLY, unless you count PennHIP's single 0-to-100 scale) scheme to use actual MEASUREMENTS instead of "trained eyes", to report on all 18 aspects, and to introduce a fine scale - BIF-scoring gives numbers from 0 to 106, which makes mathematical analysis MUCH easier. And being able to see the aspect scores of all 18 aspects warns intelligent breeders as to which mates are getting close to "POOR" on the same aspects as each other.


[Swarnendu] 30.5.2016 - 22:05
Two Wongs certainly COULD make a White! If Lawrence Wong and Penny Wong produced a daughter, in my country there is nothing to stop them registering her as Patsy White. If they happen to be members of a Christian church they could also have her christened as Patsy White.

Wodderyameen, that's not what you meant?


[bubbabooboo] 31.5.2016 - 00:05

● "Then there is the SV, OFA and all of the phoney baloney experts looking at x-rays which are simply a hard to observe phenotypic trait and do not reflect underlying genetics at all since we don't have a clue what if any genetic factors influence HD, DM"

You ARE determined to slander experts and exaggerate outrageously!
YOU apparently "don't have a clue what if any genetic factors influence HD, DM" but almost anyone who can be bothered can work out both the logical genetic MODE and logical environmental factors producing HD. IDENTIFYING the actual alleles is taking longer - but have you bothered to find out how many genes and how many alleles there are in the canine genotype? Without starting to count the mDNA?
IDENTIFICATION WILL TAKE TIME.

As for DM:
Dr Roger Clemens thought he knew, with the Jack Flash Test (named for Marjorie's sufferer).
Now there are perhaps 476,000 labs around the world claiming to be able to identify the alleles for non-DM versus DM. That OFA admits
"Among the hundreds of dogs studied so far at the University of Missouri, only two dogs with test results of N/N (Normal) have been confirmed to have DM"
is a little bit unfortunate, but not enough to totally discredit the test - maybe time will prove that DM is polygenic. I've had my bitch tested - N P, damnit! - and so her breeders have tested her relatives and found that the sire and every one of his offspring is a carrier. And gossip-line "research" found that both of Bea's dam's grandsires were either producers of or died of DM. IF I can get Bea pregnant to an N N stud I am going to have to test every pup in the first 3 weeks (the Australian lab is VERY slow getting results back), and endorse the registrations of the carriers that they are NOT to be bred from unless their owner can produce an adult N N certificate (quite possible: As Bea's milk includes her own DNA, milk in a pup's mouth could produce a false Positive from swabbing while the pups are still suckling - and no, I am NOT going to starve my pups and wash their mouths out. Nor am I going to hold the whole litter back until they are well & truly no longer attempting to suckle). But again, this is Off Topic to the hip-check thread, although relevant to your rants....

As for your
● "That is why identical twins raised in the same home will often have different diseases and medical conditions late in life when environment has had time to change there genetic expression"
- you DO insist in using language so loosely that you end up stating untruths. Sadly, many vets with USA web-sites ALSO misuse words.
To make your thoughts CLEAR you must use word pedantically.
☆ DISEASES are "caught" from the environment - whether bacteria, "germs", parasites, poisons, pollutants, snake-bites, toxins, viruses, or whatever other infectious agents you care to name.
☆ Genes produce DEFECTS, DISORDERS or SUSCEPTIBILITIES (as with type2 diabetes).


And bloody HELL - as soon as I posted that at 06:46 on Thursday morning (NZTime), the pdb declared that "something was left behind at the vet's". Ditto 2nd & 3rd tries. So I had to try a FOURTH time to paste & format & post this - the damned thing failed again at 9.45pm, accepted an unformatted unspaced text-only version at just before 10pm. And again at 10:15pm Thursday. So I finakky get this seconf half poisted at 03:15am on Friday, then find that I cannot edit my plain-text post becuase it was pio=sted mire tha  3 hiuyrs agi. Grrrrrrrrrrrr! And now it is after 3:17 am here - but the bed should be well warmed by now.

Yeah, Les, I didn't say I thought Malcolm considered
himself infallible ! I think he was probably a tad more
interested in the genes for HD than those for colour;
when you consider the amount of attention colour
genetics has always got and the continuing interest,
the 'naming' (letter allocation), etc, he probably thought
any outstanding questions would resolve sooner rather
than later. The fact that he could say he was wrong re:
Jena only strengthens my conviction that he did not have
the sort of massive ego which prevents people admitting
error, and therefore would have widely mentioned new

findings in the gene structure for HD well before he got

sick / had finished Book #3.  (I wonder if Helen has

a draft that could be posthumously published ?)

My apols to our American cousins about their earlier work
on HD - I should have realised. Nonetheless, I do think
OFA's system is (remains, if it goes back to the start) less
clear than it could be, thus does not help these discussions.
Personally I have always favoured the UK version over the
States AND the German A Stamp.

[Hundmutter] 2.6.2016 - 16:06

● "I think" (Malcolm Willis) "was probably a tad more interested in the genes for HD than those for colour; when you consider the amount of attention colour genetics has always got and the continuing interest, the 'naming' (letter allocation), etc, he probably thought any outstanding questions would resolve sooner rather than later."

Never forget that "colour" (and "Patterns") are relatively EASY to study, because we can SEE the effects and most of them are purely at the Mendelian level that can be easily demonstrated using a Punnett Square. (In NZ we were more interested in identifying bulls whose calves produced more milk. And rams whose progeny were more resistant to facial eczema spores.)  The craving for simplicity is probably why the early HD research plumped for the "dominant with limited penetration" theory, without troubling to explain HOW that "penetration" could be "limited" - Tinkerbell's magic is delightful to easily-confused minds.

● "would have widely mentioned new findings in the gene structure for HD well before he got sick / had finished Book #3.  (I wonder if Helen has a draft that could be posthumously published ?)"
I'm pretty sure I've asked Helen that during  2012, but if you need help contacting her to find out, just ask me.
I forget how long he was ill, but his life-span was 1935-2011. No doubt he was very interested in the 2008 announcement, but too ill to do much about it. As of today 2016, the DNA situation remains frustrating.
The 09.05.2014 article at:
http://www.tiho-hannover.de/en/news-press/press-releases/press-releases-2014/press-release/article/canine-hip-dysplasia-genes-ide/
links you to 3 other papers from 2012- to 2014, the first PLOS "paper" explains that «five SNPs of 843 GSDs (277 unaffected, 566 affected) explained 20 to 32% of the  phenotypic variance of CHD in GSD» - which is very promising, but a long way from being the total picture needed for DNA profiles to be able to avoid us mating carriers to carriers. Those who have successfully minimised their stock's risk by using an xray scheme with statistical analyses probably won't find DNA-profiling worth-it yet, but for those to whom the difficulties of getting the DATA from which to assess how risky will be the matings they are considering would find that reducing their stock's risk of HD by 20 to 32% is worthwhile - especially when buyers successfully SUE breeders of dysplastic pooches, as happened in the UK several years ago (I'm not sure whether Dr Willis was the one who was an expert witness telling the Court that at present breeders cannot be SURE that their stock will be free of HD) and in NZ. I'm surprised that we haven't heard of successful suings in the USA - perhaps the sheer FLOOD of suing there for trivial things has overwhelmed the media's interest.
Note that that PLOS paper states "each CHD-associated SNP on CFA24, 26 and 34 is located within or in close proximity of genes involved in bone formation and related through a joint network". Good ole proximity-linkage.

For those "alligators" who float motionlessly amid unwanted information until FOOD is within reach:
From that VERY long PLOS article I copy this patch as a demonstration  of just how many candidate genes are still being studied in a single university:
"Complex segregation analyses demonstrated involvement of a major gene for the German Shepherd Dog. Genome-wide linkage studies showed nine genome-wide significant quantitative trait loci (QTL) for CHD in German Shepherd Dogs. A linkage study in a Labrador Retriever-Greyhound cross-bred family revealed twelve dog chromosomes (CFA) with chromosome-wide significant markers for CHD. In Portuguese Water Dogs, QTL for signs of CHD were demonstrated on CFA1 and 3. A genome-wide association study (GWAS) for CHD and osteoarthritis (OA) across several dog breeds including Labrador Retriever-Greyhound crosses identified four CHD-associated and two OA-associated SNPs. The CHD-associated SNPs were located on CFA3, 11 and 30, but not within QTL of the Labrador Retriever-Greyhound crossbred linkage study. In 174 Bernese Mountain Dogs, two different CHD-regions were identified on CFA14. A third CHD-associated region was located on CFA37. A Dutch study on 48 CHD-affected and 30 CHD-free Labrador Retrievers revealed significant SNPs on CFA8 within a previously reported quantitative trait locus (QTL) in German Shepherd Dogs. A 10-bp intronic deletion haplotype within FBN2 on CFA11 was shown to be associated with CHD. Dogs homozygous for this haplotype had significantly less FBN2 mRNA in their femoral head articular cartilage. The mutant FBN2 haplotype was identified in 49 different breeds, but homozygous mutant haplotypes were prevalent in only Labrador and Golden Retrievers."

● "I do think OFA's system is (remains, if it goes back to the start) less clear than it could be, thus does not help these discussions. Personally I have always favoured the UK version over the States AND the German A Stamp."
I HOPE that that " favour " goes back only to when the detailed BIF-scoring was accepted for ALL breeds (about 1978? - I've asked the BVA for some facts, but too recently for them to have supplied it yet) and not the dreadful 1960 League and 1965 BVA/KC "category" schemes which had something like 1 Pass and 2 or 3 Fails.I periodically state that the 'a'-scheme is too blunt and that only the ZW analysis gives it any credibility. However, our friend Dr Willis was helpful with the 'a'-stamps, too, arranging with the SV's Dr Brass to take a BIF-reader to Germany and read the stored plates of the 'a'-stamped GSDs imported to the UK.
Dr Willis's analysis showed:
│       SV       │ BIF average │ BIF range │
│ 'a'-1 / 'a'-n  │     2.86    │   0-10    │
│ 'a'-2 / 'a'-fn │     4.14    │   0-15    │
│ 'a'-3 / 'a'-nz │     7.79    │   1-25    │
Those foreign to BIF-scoring need to remember that all the "blunt category" schemes rely on the reader's "eye", whereas BIF-scoring MEASURES 9 aspects per hip on the xray then converts each measurement to a 0-6 or 0-5 scale, producing a 2-hips total range from 0 for "Flawless" to 106 for "Oh my GOD!". Done properly, 2 radiologists do the measuring independently, and if their totals vary by more than about 3 a third radiologist does the measuring again to check which of the original radiologists is becoming careless/mean/over-generous. Which all takes time, of course.

My preference for the current UK HD numbering system dates
only back to the 80s (which seems ancient history now by the
standards of most !); I know little about the earlier method(s)
employed by the BVA, as in the 60s I was still a teenager just
getting involved with the breed. I'm aware of the "Breeders
Letter" stuff (Glenteall Iris, tail female for Trudi, and Taz, had
one) but due to my age and as a non Breeder I have never
had to concern myself with anything other than the Breed Mean.

On the point about trying to make predictive sense out of the
whole DNA gathering / phenotypic varience, as I pointed out
to Bubbabooboo in an earlier post, knowing individual dogs
scores is only PART of the picture. As Malcolm wrote:
"It is generally accepted by most workers involved that HD is
a polygenic trait. It should therefore have a heritability. Estimates of heritability of HD are not numerous and any attempt to seek a median value or best estimate is complicated by the fact that different diagnostic

systems exist throughout the world. It does not follow

that an estimate made from OFA data is necessarily

relevant to British data. ...There is ample evidence that

dogs with better hips will, on average, produce better hips regardless of the nutritional and environmental situation

in which the progeny are kept. ...Certainly one cannot guarantee that having both parents and 3 grandparents normal will lead to 100% normality in hip status.
But the principle that the better the hips in the pedigree the better the hips in the decendants is clear." He also used to argue frequently what others have often posted: that you

get the clearer results the more dogs' scores are recorded, and that ALL the scores, bad as well as good, ought to be publicised. (I do miss his updates to those tables !)

But I suppose Bubba will find this "unreadable" too ! It's an odd disease that regularly strikes some posters on here, that when they stand a chance of having their POV undermined, they stop reading the posts of their opponents ... has happened to me quite a few times recently.  

[Hundmutter] 3.6.2016 - 07:06

● "My preference for the current UK HD numbering system dates only back to the 80s (which seems ancient history now by the standards of most !)"
Sure is, compared to Sheila R, and especially Percy E. I think Chris H is "pushing it", too.

● "due to my age and as a non Breeder I have never had to concern myself with anything other than the Breed Mean."
Which was rather atrocious at 18 until fairly recently.

● "On the point about trying to make predictive sense out of the whole DNA gathering / phenotypic varience, as I pointed out to Bubbabooboo in an earlier post, knowing individual dogs scores is only PART of the picture."
And a SMALL part!

● "As Malcolm wrote:
"It is generally accepted by most workers involved that HD is a polygenic trait. It should therefore have a heritability. Estimates of heritability of HD are not numerous""
And as the FOUNDATION of HD is in the genetics, the more in-bred a population, the higher the heritability reported. The reports I've read put it from 40% where there is little intense line-breeding, to 60% where there is intense line-breeding to in-breeding.

● "He also used to argue frequently what others have often posted: that you get the clearer results the more dogs' scores are recorded,"
As long as you don't merely think that TOTAL numbers across the breed are what count. What is important is the number for each "popular" stud. Regrettably, few broods have enough progeny scored to make calculating data from their progeny results. (On the other hand - in many cases ONE litter per bitch is a litter too many!)

● "and that ALL the scores, bad as well as good, ought to be publicised."
Of course. Absolutely ESSENTIAL once you accept that the foundation of HD is lots of recessives.

● "But I suppose Bubba will find this "unreadable" too ! It's an odd disease that regularly strikes some posters on here, that when they stand a chance of having their POV undermined, they stop reading the posts of their opponents ... has happened to me quite a few times recently."
Of course. Just as he dropped out of the animal genetics class because the profs wouldn't accept HIS beliefs as being "truth". One of my interested fans informed me that he has already attempted to impress an easier audience by starting a new thread:
http://www.pedigreedatabase.com/community.read?post=867586-mendelian-genetics-lies-we-have-been-told--incomplete-penetrance-and-variable-expressivity#867640
No, I DON'T wish him luck. As in YahooAnswers, the struggling ignorant get horribly confused by the trolls-with-an-agenda prowling in the pdb.

Yes it was because I already read that 'new' topic, including his remarks
about you, that I mentioned it.

If you read all the research to date on HD everyone has a theory and none of them have any valid proof that their theory has even a glimmer of predictive value. These unproven genetic theories work for a very small subset of the human or canine population. A recent proclamation of scientist finding a genetic cause for MS stated that their findings held great hope for less than 1% of the 15% of MS cases that are familial while 85% are sporadic and their finding held out hope for a future blah, blah, blah. They all involve correlation and not causation. Environment is the factor that the OFA, SV, Malcolm Willis, and the Kiwi Burger Boy are keen to ignore. In fact everyone selling dog food, pet pesticides, and OFA x-rays are eager to say that genetics causes HD or DM because that means they don't have to face the truth that the food and environment our dogs are exposed to plays a much bigger role in 90% of our dog's health than genetics. Only a few very simple genetic disorders involving at most a few genes are predictable using Mendelian genetics. Like the cigarette companies those profiting from poisoning our dogs want genetics to be the "bad guy" and not their poisons. In the 1950's and 1960's the cigarette makers had an army of geneticists who proclaimed that lung cancer was not affected by smoking .. lung cancer was said to be a genetic disorder by these classical Mendelian geneticist on the payroll of Big Tobacco. Those profiting professionally or monetarily from a theory tend to cling to it like a tick.

To the Kiwi Burger King .. your grammar checking and self importance are becoming a bit confusing. The USA as a former British country took a different path from the British surrogates. There are a majority of the world's population for whom English is not their mother tongue and also a large number of English speakers for whom the UK variant of the English language is not sacred. Being GSD king of Kiwi land ( even if it were true ) does not seem so important in light of the fact that New Zealand has a population equal in numbers to Alabama and an economy equal in value to Kentucky. Those are recent references but perhaps you would prefer 1990 numbers?? I do not claim to be an expert on genetics or GSD breeding but I do have a skill set based on many years in biological research and the pesticide industry that allows me to spot the lies, deceit and important omissions in biological research ( and there are lots of them ) and to also understand how those lies profit those telling them.

Re the environment, I don't think Willis was 'ignoring' it at
all, there was (is) just insufficient evidence of IT providing
causation. Given that what you are claiming is hardly news
either, as far as opinions on HD go, he was looking at that
question - he just wasn't finding it as even a partial answer.
But he WAS finding the correlation between hip status and
parentage. He didn't have any invested preferences, he just
wanted the truth.

You also have to remember that HD (and "clicky hips" in human children) isn't a recent phenomenon. Instances of

its occurrence well pre-date most of the dog foods & pet products, (and other things eg chemicals), you seek to

wholly blame. Nobody is arguing that such things never

do damage; they may well lead to more or worse
cases in those genetically predisposed to this condition, as with so many others, but we will never find the actual cause, or cure, if we insist on looking in the wrong places just because we want to kick the manufacturers.

As for sales tactics, I cannot speak for those involved in OFA or even for the Panel members used by the BVA - but your remark about the SV versus the experience of breeding 5 generations made me giggle - who the hell do you think

runs the SV, if not established and experienced German breeders ?

Meanwhile those breeders who want to excuse their lack

of attention to the breeding methods they are using continue to enjoy the smokescreen.

[bubbabooboo] 3.62016 - 15:06

● "To the Kiwi Burger King .."
Trust YOU to write to someone who doesn't exist.

Confusion about grammar is YOUR problem.
▫ I know a chap in India for whom English is a third language - and who copes better in English than you do.

▫ I know an AmerIndian in Aridzona for whom English is a fourth language (Yanklish being her third) - who copes better in English than you do.

▫ I know a blind person in Texas who has Yanklish & Braille as her first two languages, yet her mastery of English grammar is excellent. She recently obtained software that allows her to dictate her messages instead of hurting her wrists & shoulders (yes, she has a painful auto-immune disorder) and BOY does that tool make much of her messages incomprehensible. I imagine that the problem is because computer programmes in their early stages require EXACT matches, and so varying enunciation and accents (especially pronunciation of vowels) "trick" them until the software develops by "learning" the user's speech modes.

● "a large number of English speakers for whom the UK variant of the English language is not sacred."
#1: There is no such thing as "the UK variant of the English language". Where do you think the USA got most of its linguistic variety from? You MIGHT manage to understand a Cockney who is willing to make allowances for your poor comprehension. The Yorkshire pair who used to be our breeding partners took some effort to follow the flow of, but we got there. Try following a Cornishman or a Glaswegian (such as Billy "the big yin" Connolly) in full flow - if you watch any of Billy's video clips, admire his tie & clipboard but realise that in those sessions he was trying to imitate an Edinburgian, not being his Glaswegian self
#2: The people you refer to are NOT using English - they are using mostly-English WORDS, but in ways that resemble a collage such as "collage weighs that inn reassemble a butt" more than actual English. My preferred version of English was known as "BBC Received", until the BBC gave up and hired users of various patois.

There cannot be complete comprehension until ALL people have the same language as their natural speech, and give each word the SAME meaning as does everyone else. I'd rather that the spellings they used revealed the etymology of the root-words their speech is based on. And I DO wish that vowel sounds would stay FIXED!

● "does not seem so important in light of the fact that New Zealand has a population equal in numbers to Alabama"
Not "equal" - which is a word with a precise meaning. The populations are numerically "approximate", within about 5%.
However many people have been known to state that "It's not the SIZE that matters - it's what you DO with it". In that respect, I doubt that Alabamans have DONE as much as NZers. 
http://www.nzedge.com/legends/   will point out such as the Maori Tohunga who (during the era of the American Uncivil War) invented ways to defend fortresss against cannons & riockets that were later used in WW1; our farmer who MIGHT have flown before the Wright brothers (Ohio, not Alabama) did; our farm boy who developed the science that produced the atomic bomb and nuclear-power; our Dunedin-then-Whanganui sportsman who developed the plastic surgery techniques that made life worthwhile for the victims of horrific burns during WW1, followed by the Dunedin lad who took those reconstructive techniques even further for WW2 victims, and created "The Guinea Pig Club"; our Thames-then-Otago lad who became a fighter ace in WW1 then, in WW2, defended Malta as long as possible then successfully controlled Britain's defence against the Luftwaffe, and who recently became the only 20thC person to have a statue in Trafalgar Square (hey - without HIM, the USA mightn't have needed to join WW2!); our Wellington lad who enabled your JPL to put the first human on the Moon. Not to forget our cultural and linguistic leaders. To use an expression from 1-on-1 fighting: NZers have always "fought above their weight".
Remember February 1985, when NZ Prime Minster David Lange refused entry to the USS Buchanan because the USA would "neither confirm nor deny that the ship had nuclear capability"?
http://www.nzhistory.net.nz/media/photo/uss-buchanan-cartoon
And March 1985 when he resoundingly beat the Rev. Jerry Falwell in the Oxford Debate about nuclear weapons?
https://www.youtube.com/watch?v=OeHTziiFVx0

The NZ attitude COULD be why last year Burger King NZ reported a $7,500,000 loss
BOY there are a lot of Burger King outlets in the USA!


[Hundmutter] 3.6.2016 - 16:06
● "Re the environment, I don't think Willis ...(snip)... But he WAS finding the correlation between hip status and parentage. He didn't have any invested preferences, he just wanted the truth."
But it was whatever GENETIC causes were (or were not) involved that were his speciality. I suspect that he was also intelligent enough to realise that people living in heavily industrialised nations have VERY little they can personally control in their environment, although photos of mask-wearing Japanese are often seen.
Although you are a pullet rather than an old hen, as a Pommie you should be aware of the reports from Nem Elliott and Madeleine Pickup in roughly the 60s & 70s about the mental consequences of pups licking the lead-painted pillars of old barns they were housed in during the weather that Flanders & Swann sang about: https://www.youtube.com/watch?v=_eT40eV7OiI

● "You also have to remember that HD (and "clicky hips" in human children) isn't a recent phenomenon."

Sure isn't. Dinosaur skeletons show HD. But I don't think that their species did pelvic replacements, etc.