HLLE and GAC: My dialogue with Hemdal

As you well may remember I have been highly critical of the study published by Jay Hemdal, curator of fishes at the Toledo Zoo, who is to release a study indicating GAC as a cause of HLLE. My primary critizisms were first and foremost that causation had not been shown, but merely a relationship, that the biosecurity of specimens obtained for the study was suspect, and not enough had been done to resolve the possibility of waterborne pathogens.
Admittedly my initial reaction was quite hyperbolic, mostly because of the public response of lay people to a non-scientific report (about a scientific report). I was interested in seeing the meat and bones of this paper before I made any decision, and I went on a rant to illustrate my contempt, cautioning aquarists to question the things that they read.
I responded publicly (somewhat less flamboyantly) to this report on AdvancedAquarist.com (originally from CORAL MAGAZINE) and was met in kind with a response from Jay Hemdal himself. Here is the conversation thus far:

by Jay Hemdal
Andy,

You'll definately want to read the full paper when it comes out. However, to address some of your points now:

1) The small amounts of water moved were specifically to address the issue of viral particles, and were deemed sufficient to induce transfer, if indeed they were the culprit (they weren't).

2) Chronic stress induced by the systems would have had an equal effect on the control fish - and they were fine. There is no metric to support your assertion that the fish were not housed properly...the control fish look beautiful to this day!

3) The live rock came from the same system, so controls and test fish were exposed equally.

4) The group size was kept to a minimum due to the trenchant effect the carbon had on the test subjects. I saw no reason to disfigure more fish with carbon than I needed to. Our resident research biologist selected the minimum sample size for me. My co-author ran the stats: "after four months, all of the fish in that system showed severe lesions (N=12). These results are statistically significant when compared to the control group, where none of the fish developed lesions (N=11) (Chi-Square p < 0.001)."

Finally, there are two other papers in press that implicate carbon as causing HLLE.

The only issue that I wish I had done differently was that I should have washed the lignite carbon. Too many people are focusing on that. I didn't wash the carbon because I wanted to be sure to see the effect. What I hear is, "you didn't wash the carbon, and everyone knows you are supposed to wash it!" These people lose sight of the fact that the intermediate system used washed pelleted carbon, and those fish ALSO developed HLLE.

Months after we removed the carbon, the test fish are starting to heal. How can that not support causation? I have not seen a clearer correlation for a cause of HLLE.

I'm looking forward to hearing what else Jay has to say. Jay also responded in the thread to a few other comments and on several other points which can be seen at AdvancedAquarist.com

 

Here's the latest. Jay has said that his newest suspicion is that GAC causes HLLE by binding organic waste that are normally bound to particulate metals which are thereby freed and agitate lateral line. My quesiton is why, and how are tang and angelfish later line's different from other species of fish. Also, what's the difference between unwashed lignite carbon and washed carbon? Obviously there is some difference there, and how does this explain this proposed cause. I'll ask him more of these questions in the future. For now, here's where the conversation stands:
by Jay Hemdal
Andy,

The history of HLLE research is muddled to say the least. Blasiola's work, that formed the basis of the "vitamin C link" to HLLE, was based on six fish, and had improper controls - yet everyone now "knows" that poor diet causes HLLE. Our sample size was five times larger, and had proper controls.

If ANY of our control fish had developed HLLE, or if ANY of the carbon treated fish had NOT developed HLLE, the statistics might not have been clear enough to make the conclusion we did. Since it was 0% versus 100%, a larger sample size would NOT have helped. In fact, in the first draft of the paper, my co-author calcuted the chi square P

 

I own the 2nd edition, we have made some reference to it in a separate dialogue. It is certainly not material for the lay person, it's an in depth collegiate level, you might even say post graduate level reference well suited for those with a background in biology, or medical lab science. That said, it's an incredible reference which includes review of disease conditions on many levels including pharmacopoeia, histology, cytology, microbiology, and more.