If you regularly fish on the Great Lakes, chances are you’ve heard stories about how good the fishing used to be. Stories passed down through generations about monstrous lake trout being caught in inconceivable numbers, typically starting with “back in my day.” Fact or fiction, one thing is for certain — there aren’t as many lake trout in the Great Lakes as there used to be.
For millennia, lake trout were an apex predator in the Great Lakes. Prior to European colonization, many Indigenous communities relied heavily on lake trout for sustenance. Post-colonization, lake trout supported one of the most successful freshwater fisheries in the world. However, by the 1940s, populations had declined dramatically, and by 1960, lakers were extirpated from lakes Ontario, Michigan, and Erie.
The introduction of invasive species, especially sea lamprey, and overfishing are thought to be the primary causes behind the lake trout collapse.
After the collapse
After the lake trout collapse, the Great Lakes ecosystem underwent immense change. Alewife and rainbow smelt (small, invasive fish) became the most abundant prey in many areas. Aiming to control them, fisheries managers began stocking Pacific salmon. By the 1970s, Pacific salmon were established and successful in decreasing alewife.
Populations of alewife became so low during the 1980s that large-scale salmon dieoffs followed, causing fisheries managers to re-think their management strategies. By the 1990s, the new focus was to find a balance between the demand of recreational Pacific salmon fishery and the rehabilitation of native fish.
Lake trout rehabilitation soon became a priority for agencies, with extensive sea lamprey control programs, restrictive fishing regulations, and increased stocking. Despite this, lake trout currently only have self-sustaining populations in Lake Superior and parts of Lake Huron. Other lakes rely almost entirely on hatchery stocking.
This lack of reproductive success sparked a wave of research to determine why lake trout were struggling.
What’s killing lake trout?
Early research eyed environmental contaminants as the culprit. However, researchers in the 1990s determined this was not the cause, as the concentration of contaminants in wild lake trout eggs were not high enough to explain the high mortality rates. Scientists shifted their focus to nutritional factors. In hatcheries, wild lake trout demonstrated uncoordinated movements, reduced growth, and lethargy — signs that resemble symptoms of Vitamin B deficiency in humans.
This led John Fitzsimons, a researcher at the Great Lakes laboratory of Fisheries and Aquatic Sciences, to the discovery that lake trout in the Great Lakes are deficient in Vitamin B1, also known as thiamine.
Why aren’t lake trout getting enough thiamine?
Well, it turns out alewife and rainbow smelt contain high concentrations thiaminase, an enzyme which breaks down thiamine in the predators that eat these fish.
Why do fish need thiamine?
Thiamine is an essential vitamin. Animals cannot produce it on their own, relying entirely on their diet for the daily dose. Like most B-vitamins, thiamine plays an important role in converting food into energy. In humans, low levels of thiamine can cause severe impairments to the nervous system, and also causes severe cardiac impairments —something that has not been studied in lake trout.
This is what I set out to explore in my graduate thesis work. It is well-known that the heart is an incredibly important organ for fish. It provides lakers with the ability to chase prey, avoid predators, and migrate to spawning grounds.
What’s lesser known is the relationship between heart function and thermal tolerance. This is how an organism survives heat stress.
Recent research has shown that fish with stronger hearts tend to have a greater ability to tolerate warmer water. If thiamine deficiency affects heart function in lake trout like it does in humans, it may not only affect their day-to-day activities, but also their ability to tolerate warmer water in the future — a worrying consequence with climate change. Recent results from my hatchery-based research support this theory. In a recently accepted article in the Canadian Journal of Zoology, lake trout raised on a diet containing the enzyme thiaminase had impaired cardiac function and were unable to tolerate warmer water temperatures.
With the help of the MNRF, the Natural Sciences and Engineering Research Council of Canada (NSERC), the OFAH, and Genome Canada, samples of wild lake trout are also being collected to test this theory.
Solutions
All of this may sound like the future doesn’t seem so bright for lake trout in the Great Lakes, but there are possible solutions. For one, management agencies should prioritize the reestablishment of native prey species. This has already started on Lake Ontario, where native cisco stocking was implemented in 2012. It might also be possible to start stocking types (strains) of lake trout that are more tolerant to thiaminase — something that my colleagues and I at Western University are also looking into.
With the collective effort of researchers, management agencies, and anglers, this cherished predator could once again flourish in the Great Lakes.
Originally published in the July 2023 issue of Ontario OUT of DOORS
“Lake Trout raised on a diet containing the enzyme thiaminase (that we were told break down in the fish body to thiamine) had impaired heart function…”
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