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[TNAngler]

Well I don't know how 2 fish from the same section of a river, often within a few yards,  returning in the same year could have been exposed to ocean conditions so different that one is 25% to 35% bigger, better conditioned for it's length and when hooked, pulls harder, jumps more often and higher and take longer to land than another and the only other observable difference is the presence or lack of an adipose fin.

I'd also add that studies such as those done by Dr Dick Beamish and others have found that hatchery smolts once released from the hatchery have survival rates from 50% to 10% of their wild counter parts in current ocean conditions

I think the survival rate thing I listed a main culprit in my previous post.  I wouldn't say it is ocean conditions, it is knowing what to do with those conditions.  When we raised fish, we took the eggs from the other hatchery operating on the same system.  Their fish would come back smaller, weaker, and softer than their wild counterparts.  We had eggs from the same group and ours were not so it wasn't genetic.  It had to be something else.

[RalphH]

Beamish concluded his paper on the topic with 2 thoughts about the poor survival rates of salmon smolts released from DFO hatcheries relative to wild fish;

1) we have to find out why they are so different

2) we need to rethink how hatcheries in BC operate.

[wildmanyeah]

https://marinesurvivalproject.com/research_activity/list/hatchery-wild-interactions/

[wildmanyeah]

Seen this posted on a different site.

https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0221956

To increase the abundance of Coho salmon and enhance fishing opportunities along the coast of Canada, the Salmonid Enhancement Program was established in 1970s by Fisheries and Oceans Canada (DFO) and hatchery production of these species was initiated [8]. Hatcheries were considered to be effective because the egg-to-smolt survival in hatcheries was significantly higher than that in wild stocks [9]. However, in the marine environment, lower survival of hatchery-origin fish compared to wild fish has been reported [10]. It has been suggested that due to domestication, hatchery fish generally show reduced swimming ability [11] and lower resistance to stress and diseases than their wild counterparts [12]. There is even evidence that a single generation of hatchery production can reduce the genetic fitness of wild fish [13,14]. Given these findings, the continued use of enhancement hatcheries to produce large numbers of fish for exploitation has been debated. Genetic introgression, overcrowding, competition, predation, predator attraction, and transfer of pathogens and disease are all factors that may carry negative consequences from hatchery to wild fish [15–17]. Although infectious diseases are theoretically considered to pose higher risk in high-density rearing environments like hatcheries, there is still no study showing that hatchery-origin Coho salmon increase the transmission of infectious agents to sympatric wild populations [16,18]. Infectious diseases can disrupt salmon’s normal behaviour and physiological performance (e.g. swimming and visual acuity), immunological function, feeding and growth, and can cause mortality in severe cases [7,19]. There is a clear knowledge gap regarding pathogens that can adversely affect the performance and survival of Coho salmon. Out-migrating juveniles are particularly vulnerable to environmental stressors, including infectious agents, during their early marine life, and >90% of them may die in this limited period [4,20,21].

High rearing densities in hatchery environments increase the potential for enhanced transmission of pathogens, but the use of antibiotics and other mitigation measures, such as broodstock selection to minimize vertical transmission of Renibacterium salmoninarum, may reduce the incidence and spread of diseases. Alternatively, as many hatcheries use ground rather than river water, hatchery fish may be less exposed to myxozoan parasites that have an alternate invertebrate host in natural freshwater systems. Previous research by our group suggested that naturally occurring myxozoan parasites may be a risk for wild salmon in the ocean [22,23]. Given the observed lower survival of hatchery fish compared to wild fish in the ocean [4], if infection is driving this difference, we would expect that hatchery fish be more vulnerable to infection. As such, we undertook the present cross-sectional study to test the hypothesis that hatchery-reared Coho salmon smolts carry a higher burden of infectious agents at the time they are released from the hatchery compared to their wild counterparts, and that they continue to carry higher agent burdens in the early marine environment. To test this hypothesis, we applied a high throughput microfluidics system to detect and quantitate 36 infectious agents in juvenile Coho salmon sampled in BC, and compared the prevalence, diversity, and overall infection burden of detected agents between hatchery-origin and wild fish over the last 11 years (2008–2018).

Various Studies related to topic

9.Sweeting RM, Beamish RJ, Noakes DJ, Neville C. Replacement of wild Coho Salmon by hatchery-reared Coho Salmon in the Strait of Georgia over the past three decades. North Am J Fish Manag. 2003;
View ArticleGoogle Scholar

10.Beamish RJ, Sweeting RM, Neville CM, Lange KL, Beacham TD, Preikshot D. Wild chinook salmon survive better than hatchery salmon in a period of poor production. Environ Biol Fishes. 2012;
View ArticleGoogle Scholar

11.Bams RA. Differences in performance of naturally and artificially propagated sockeye salmon migrant fry, as measured with swimming and predation tests. J Fish Res Board Canada. 1967;
View ArticleGoogle Scholar

12.Salonius K, Iwama GK. Effects of early rearing environment on stress response, immune function, and disease resistance in juvenile coho (Oncorhynchus kisutch) and chinook salmon (O. tshawytscha). Can J Fish Aquat Sci. 1993;50: 759–766.
View ArticleGoogle Scholar

13.Araki H, Berejikian BA, Ford MJ, Blouin MS. SYNTHESIS: Fitness of hatchery-reared salmonids in the wild. Evol Appl. 2008;
View ArticleGoogle Scholar

14.Araki H, Cooper B, Blouin MS. Genetic effects of captive breeding cause a rapid, cumulative fitness decline in the wild. Science. 2007; pmid:17916734
View ArticlePubMed/NCBIGoogle Scholar

15.Weber ED, Fausch KD. Interactions between hatchery and wild salmonids in streams: differences in biology and evidence for competition. Can J Fish Aquat Sci. 2003;
View ArticleGoogle Scholar

16.Naish KA, Taylor JE, Levin PS, Quinn TP, Winton JR, Huppert D, et al. An evaluation of the effects of conservation and fishery enhancement hatcheries on wild populations of salmon. Advances in Marine Biology. 2007.
View ArticleGoogle Scholar

17.Christie MR, Marine ML, French RA, Waples RS, Blouin MS. Effective size of a wild salmonid population is greatly reduced by hatchery supplementation. Heredity (Edinb). 2012; pmid:22805657
View ArticlePubMed/NCBIGoogle Scholar

[Roderick]

... so it wasn't genetic.  It had to be something else.

They have the same genes but the "expression" of the genes is different. Raising them in tanks at high density causes some genes to be turned on that are not turned on in the wild, and others to be turned off that would otherwise be on.  It's like the situation when human twins are raised separately. They can turn out quite different even though their genes are identical.

[wildmanyeah]

Kinda sounds like gene manipulation to me... Took coho from 3 distinct groups and bread them all together...

http://www.fishingwithrod.com/fishy_news/file/051005.pdf

2. History of Coho Production at the Chilliwack Hatchery

The Chilliwack River Hatchery accommodates the freshwater life history of Pacific Salmon. Adults
are trapped, held and spawned. Eggs are fertilized, incubated and hatched. The juveniles are then
reared until they are sea-ready. The hatchery infrastructure consists of engineered incubation,
juvenile rearing, and adult holding ponds.
The hatchery, completed in 1980, is located on the Chilliwack River, centered in a section of the
river that is accessible to migrating salmonids. At the time of hatchery construction there were only a
few, very small coho populations spawning in this stretch of the Chilliwack River, while the largest
natural spawning areas were in the upper Chilliwack watershed and within the Vedder River
tributaries. The hatchery started its coho enhancement program with broodstock taken from three
tributary populations representative of the three main spawning areas within Chilliwack watersheds:
Dolly Varden Creek (upper watershed, early spawn timing), Post Creek (middle watershed and middle
spawn timing) , and Salwein Creek (Vedder tributary population with a late spawn timing). Since
1985, the broodstock has been taken exclusively from adults returning to the hatchery, and the run
has built up to about 65,000 adults, of which about 6,000 are intercepted along the adult migration,
about 10,000 are caught in the local recreational fisheries, about 10,000 spawn naturally elsewhere
in the watershed, and about 40,000 return to the hatchery. This results in a substantial surplus over
the up to 2,000 spawners needed for full hatchery production, and this surplus provides fish for First
Nation’s communal use, as well as economic opportunities when possible.
Although the coho program at the Chilliwack River Hatchery started as a rebuilding and
production initiative rather than a conservation effort, DFO is now evaluating the relative benefits and
risks of different production targets (i.e. different numbers of smolt to be released) in the light of wild
salmon conservation, protection, and preservation.

[RalphH]

They have the same genes but the "expression" of the genes is different. Raising them in tanks at high density causes some genes to be turned on that are not turned on in the wild, and others to be turned off that would otherwise be on.  It's like the situation when human twins are raised separately. They can turn out quite different even though their genes are identical.

called epigenetics:

Epigenetics is the study of heritable changes in gene expression (active versus inactive genes) that do not involve changes to the underlying DNA sequence — a change in phenotype without a change in genotype — which in turn affects how cells read the genes. Epigenetic change is a regular and natural occurrence but can also be influenced by several factors including age, the environment/lifestyle, and disease state.

https://www.whatisepigenetics.com/fundamentals/