Schaff Valley Angus-thoughts?

[EAT BEEF]

like OT and Sam posted, about my breed of cattle on an internet discussion board.
Frankie

Get over yourself and your breed.

 

[robert]

Either one of them could have taken some time and found what I found:

Unfortunately, at this stage, we only have reports on about 30 animals that have produced FCS syndrome progeny....

http://www.angusaustralia.com.au/geneti ... TopicThree

Thirty (30) animals and these are the people who OT says have been researching Fawn Calf for years! Thirty (30) animals that Sam says may destroy the Angus breed. :roll:

If FC is a problem, we need to fix it. Personally, I have a hard time not challenging the posting of gossip and innuendo, like OT and Sam posted, about my breed of cattle on an internet discussion board.

there were only about 40 AM cases too, how much damage has that done? Honestly, much more could have been done on that front too. If reports from Dr. Beever are correct we might only be looking at a couple percent or so of AI sires, I surely hope so. Discussion about a defect when there is ample evidence of its existence is not gossip, perhaps if a few more folks had 'gossiped' about AM years ago we might not be dealing with what we have now?

 

[angus9259]

There is a huge FCS topic on Advantage, you can see where a couple of well respected doctors have reported a bad taste, you can also go to the Australian Angus site and find info on FCS.

You're making the claim that FC beef is bad and will ruin the breed based on an internet discussion board! That's the basis of your comment? Why do I bother being surprised?

An internet discussion board made up of some of the Australian Veterinarians and scientists that discovered it years ago- and first made it public over here- and that have been studying it for years... If we were waiting for the AAA -- we still wouldn't know it existed as they have been in denial....
Those Australians studying it have so far shown much more credibility than the semen pimps and breeders that covered it up...

If discussion boards are revealing, below you'll find a link from another discussion board with a post quoting Dr. Denholm. The post was actually put up by someone named "oldtimer". Dr. Denholm's suggestion in this quote is that suggestion of poor taste are based on "anectdotal reports" and is "speculative at this stage" though requiring further investigation.

http://www.ranchers.net/forum/about34878-36.html

It seems there are probably no actual "reports" on either side of the issue. There is most probably speculation worthy of investigation.

 

[Frankie]

there were only about 40 AM cases too, how much damage has that done? Honestly, much more could have been done on that front too. If reports from Dr. Beever are correct we might only be looking at a couple percent or so of AI sires, I surely hope so. Discussion about a defect when there is ample evidence of its existence is not gossip, perhaps if a few more folks had 'gossiped' about AM years ago we might not be dealing with what we have now?

There's nothing wrong with discussion of genetic defects. We've had several of them about Angus genetic defects right here on this board. It's important that the commercial cattleman understand the problems and how to avoid them. We've also talked here about other black breeds that could carry the same genetic defects. But without a spec of validation, SAM tells us there's a "whole pile" of Fawn Calves here in the US. That's gossip and innuendo. It says a lot about his character.

 

[RD-Sam]

Frankie, you are in denial.

 

[RD-Sam]

Frankie, I guess you think this is just another plot to destroy the angus breed too? :roll: http://www.advantagecattle.com/forum/to ... IC_ID=4634

 

[Oldtimer]

Frankie, I guess you think this is just another plot to destroy the angus breed too? :roll: http://www.advantagecattle.com/forum/to ... IC_ID=4634

Yeah- I just saw that...I thought it was ironic while Frankie was promoting a stick your head in the sand, poo poo it away stance-- many progressive angus breeders are concerned enough about the size and potential of the problem to want to try and find out more so they can do something about it....

 

[Oldtimer]

Interestingly- Dr. Denholm just posted again today about this subject- and his research...

As previously stated on this site, I have been planning this research on possible meat quality defects in Fawn Calf Syndrome (FCS) for some time.

The 5 surviving FCS calves in my small FCS research herd are now between 2 and 6 months of age and all are available for this research involving both biomechanical and organoleptic (taste panel) testing.

I was therefore not only surprised but also very pleased when Prof. Switzer contacted me a few days ago suggesting he could assist with some funding for this work. I subsequently gave him a rough estimate of the anticipated cost of this research.

Costing of any research that I am able to participate in personally will ultimately have to be undertaken using the NSW Government's Department of Industry and Investment R&D Project Costing Program. The FCS cattle that I work with all belong to the NSW Government and the costing of any research involving them must be done according to the Department's established R&D costing formulae. This is a mandatory and fixed costing protocol that covers all departmental R&D projects.

To ensure adequate sensitivity in the trial and appropriate statistical analysis, replicates are necessary. This replication involves not only the need for several animals in each group (test and control) but also several muscle sites within each carcase because some muscles could be affected but not others, depending on their different myofibre types and the endomycial connective tissue composition.

A comparison of meat from one FCS affected and one normal animal from different backgrounds would not be useful, given the extent of normal variation in the population and the many factors affecting meat quality that would not be controlled in that type of comparison. I therefore do not believe a "proof of concept" or pilot trial involving only one FCS affected and one normal animal would be worthwhile, but it would reduce the number of FCS cases subsequently available for a properly designed trial and hence would compromise the potential power of that proper trial.

In a way, the suggested "proof of concept" has already been completed. An informal comparison between FCS meat and the FCS meat eater's prior experience of grocery store beef in an uncontrolled situation appears to be exactly what has been reported here on ACS and elsewhere, involving more than one FCS animal and many normal animals.

Unless we assume that the people who have reported FCS meat to be abnormal are all deliberately misleading us, which seems unlikely, then I think an adequate "proof of concept" is already to hand.

As the FCS affected calves are still unweaned, this proposed trial on FCS meat quality is still about a year off. I am advised by the meat science experts in my Department that meat quality comparisons involving tenderness and flavour parameters should not be undertaken with cattle less than 15 months of age. So, even if funding is obtained, we are still some time off from an answer to this question about the consumer acceptability of FCS meat.

In my view, it is unlikely that FCS meat will be entirely inedible, but it may be suitable only for certain lower grade manufacturing purposes. If this is shown to be the case, it might be appropriate to ensure that carcases from FCS affected animals are diverted to such manufacturing purposes and do not enter the normal fresh meat chain. Whilst not wishing to prejudge the results of the proposed research, I doubt that the meat quality of young feedlot fed FCS affected cattle would be any worse than meat from some other animals in the human food chain, notably meat from older cull breeding animals with low body condition scores. We need to be careful not to create an impression that the quality of meat from FCS affected animals might be completely outside the normal range of meat quality in the human food chain. That is very unlikely. What is more likely is a finding that the meat quality from young feedlot finished FCS cases is outside the normal range for other well finished young animals.

The situation with heterozygous FCS carriers also needs to be assessed as there is some possibility of a lesser effect on meat quality in heterozygotes. I hope to be able to identify any abnormality in the meat from heterozygotes in the proposed trial.

With respect to the discussion above about publication of results from this proposed research, whatever the source of funding, the R&D contract will be made between my Department and the funding agency. I will not personally be a party to the R&D contract, just the Principal Investigator appointed to the project by my Department. Publication of the results in a referreed scientific journal is the expected outcome of all such R&D contracts. The R&D contract would not include any right for the funding agency to influence publication of the results. For me personally, that would be anathema. I have worked for several years now to bring the FCS phenotype and its heritability out into the light of day in the international Angus world (and I have succeeded thanks to Brian Weaver and ACS members) and I certainly do not intend to begin or allow some cover-up of details of the phenotype now, albeit that these details might involve commercially important meat quality traits. If there is an effect of FCS on meat quality, the results will be published in full in the scientific literature, probably after an initial disclosure of the results on this site.

Angus breeders on both sides of the Pacific will benefit from this proposed research, whatever the results. It seems that some North American Angus breeders do recognise this and are now attempting to raise the funds necessary for the work to progress here in Australia. I will continue to do this myself here in Australia, but I do acknowledge and very much appreciate the thoughtful assistance of colleagues in the U.S.A., in particular Prof. Switzer, who also see this research as a priority for Angus breeders.


LD50

 

[Brandonm22]

They need to do the research and AAA ought to pay for it; however this

"An informal comparison between FCS meat and the FCS meat eater's prior experience of grocery store beef in an uncontrolled situation appears to be exactly what has been reported here on ACS and elsewhere, involving more than one FCS animal and many normal animals"

is proof of absolutely nothing. You have to do this scientifically to draw any kind of conclusions.

 

[Oldtimer]

They need to do the research and AAA ought to pay for it; however this

"An informal comparison between FCS meat and the FCS meat eater's prior experience of grocery store beef in an uncontrolled situation appears to be exactly what has been reported here on ACS and elsewhere, involving more than one FCS animal and many normal animals"

is proof of absolutely nothing. You have to do this scientifically to draw any kind of conclusions.

Unless we assume that the people who have reported FCS meat to be abnormal are all deliberately misleading us, which seems unlikely, then I think an adequate "proof of concept" is already to hand.

Thats exactly what he said...It is a "proof of concept" that there is a need for a full blown study to prove or disprove the reports and determine extent...

 

[Brandonm22]

More testing is definitely warranted; but one guy saying that he incidentally and unscientifically "proved" a concept isn't any sort of proof. If I killed one myself (or got the butcher down the road to do it) THEN went to Food Giant and bought some steaks off of the shelf to compare against, the difference is more likely to be in the differing butchering, feeding, transporting, and handling process. To do this right, you need to identify ~25 fawn calves and throw them in to a feedlot with 25 fcs negative Angus calves feed and handle everybody the same way. Process the whole pen identically on the same day and then do blind test panel testing, fawn calf versus non carrier calf.

 

[VanC]

More testing is definitely warranted; but one guy saying that he incidentally and unscientifically "proved" a concept isn't any sort of proof. If I killed one myself (or got the butcher down the road to do it) THEN went to Food Giant and bought some steaks off of the shelf to compare against, the difference is more likely to be in the differing butchering, feeding, transporting, and handling process. To do this right, you need to identify ~25 fawn calves and throw them in to a feedlot with 25 fcs negative Angus calves feed and handle everybody the same way. Process the whole pen identically on the same day and then do blind test panel testing, fawn calf versus non carrier calf.

Dr. Denholm hasn't said that anything has been proven yet. In this context the term "proof of concept" simply means that enough evidence exists to warrant a controlled study. It's somewhat like a judge determiming that enough criminal evidence exists to put someone on trial.

 

[novaman]

I don't normally get involved in these sort of discussions but its bugging me. I was at a meeting today and a professor at NDSU was talking about genetic defects. He did some research and he is guessing "wildly", as he put it, that somewhere between 2 and 23% of Angus cattle registered in the past few years have the genetic defect AMS. He didn't get into Fawn calf much at all. Now here's my problem. These scientists are wanting to study these fawn calves to see if there is a difference in taste. Who cares if there is a difference in taste? It is a defect and should be eradicated should it not? Maybe I'm missing something but there are lots of people who lost a great deal of money with all this genetic defect stuff. I would think the best route to take would be elimination of the problem animals ASAP.

 

[Frankie]

I don't normally get involved in these sort of discussions but its bugging me. I was at a meeting today and a professor at NDSU was talking about genetic defects. He did some research and he is guessing "wildly", as he put it, that somewhere between 2 and 23% of Angus cattle registered in the past few years have the genetic defect AMS. He didn't get into Fawn calf much at all. Now here's my problem. These scientists are wanting to study these fawn calves to see if there is a difference in taste. Who cares if there is a difference in taste? It is a defect and should be eradicated should it not? Maybe I'm missing something but there are lots of people who lost a great deal of money with all this genetic defect stuff. I would think the best route to take would be elimination of the problem animals ASAP.

Remarkably, I agree with you. Why spend $50,000 to find out if the meat is good or bad? Some meat tastes better than some and always will. From a scientific standpoint, it would probably be interesting, but from a beef production standpoint, we need to get those animals out of the Angus gene pool. And any other breed that has included Bando 598 in their gene pool should, too. Lots of better things to spend the money on, IMO.

No, Fawn Calf isn't always a terminal defect. The name comes from them looking like a fawn at birth. Some of them have a difficult time getting up and nursing. But if they make it to yearling, they don't look much different than normal calves.

Dr. Beever has been studying the problem since 2008. While we've registered close to 500,000 Angus calves in the last two years, he says

...only 27 calves were consistent with the pathology landmarks that we associate exclusively with FCS.

http://www.angus.org/Pub/FC/FC_Notice_122109.aspx

 

[lakading]

This has got to be THE BIGGEST thread hijacking in CT history. Nice work. :clap:

If anyone still wants to talk about SAV, I'd love to hear comments from anyone who has seen and/or used the Heritage bull.

 

[Brandonm22]

I don't normally get involved in these sort of discussions but its bugging me. I was at a meeting today and a professor at NDSU was talking about genetic defects. He did some research and he is guessing "wildly", as he put it, that somewhere between 2 and 23% of Angus cattle registered in the past few years have the genetic defect AMS. He didn't get into Fawn calf much at all. Now here's my problem. These scientists are wanting to study these fawn calves to see if there is a difference in taste. Who cares if there is a difference in taste? It is a defect and should be eradicated should it not? Maybe I'm missing something but there are lots of people who lost a great deal of money with all this genetic defect stuff. I would think the best route to take would be elimination of the problem animals ASAP.

A good cow lives for 15 years. If you have a 100 Angus cows, you have ~$110,000 invested out there and some registered herds can have many times that. It is asking an awful lot to expect that guy to do blood work on his whole herd and then cull 10-80% of them for a genetic defect he likely has never seen and in the case of FCS isn't even lethal.

 

[Anonymous]

If anyone wants to continue this genetic defect discussion, please start another thread under a different name.