SNP2: Quack Asylum – “Fish is Bad For You”

Overview of Claims

In this episode, we focused on four claims made in a particular video (although heard elsewhere too), namely:

• Claim 1: “Eating fish does not improve your health”
• Claim 2: By Cooking Fish, you’re already eliminating a lot of the omega-3
• Claim 3: “Farmed fish are not fed the algae that normally have, and so instead of omega-3 they make mainly omega-6, so they are inflammatory”
• Claim 4: “When you are eating fish, you are eating pollution, which is toxic”

Claim 1: “Eating fish does not improve your health”

The first point to note is that such a statement is essentially meaningless, given that it does not give the context of ‘relative to what?’

• What is the baseline diet?
• What is the current fish intake?
• What will the fish intake be replacing?
• Or if removing fish, what will replace it?
• What is someone’s omega-3 index?

When trying to work on the impact of consuming fish (particularly if focusing on it as a source of EPA and DHA), then we need to think about this on multiple levels:

1. What impacts are there on nutritional status?
   • e.g. how does it change omega-3 status? Or levels of other nutrients?
2. What impacts are there on intermediary markers?
   • e.g. is there a change in blood lipids?
3. What impacts are there on outcomes?
   • e.g. is there a change in risk of cardiovascular disease (CVD) or other outcomes of interest?

While the original claim is, as discussed above, quite meaningless, we can perhaps raise an interesting point of debate if we try and create the best “steelman” version of the claim…

Steelman version: If eating a diet with zero fish, that provides high n-3 intake via ALA (e.g. in chia and flaxseed), then addition of fish to the diet won’t improve health outcomes.

As discussed in epsiode 418 (Should We Consume a Direct Source of DHA?), while this is a hypothesis that should be continued to be investigated, we should be careful in discounted the potential benefits of a direct dietary source of EPA and DHA, even in those with high ALA intakes. Consider:

• If not getting a direct source of EPA and DHA, then ALA needs to be converted to these fatty acids in body. However, there are issues with how much actually gets coverted.
• ALA may be able to provide enough EPA (although conversion is still likely only in the single digits percentage wise), but most evidence suggests it doesn’t increase DHA levels.
  • • Stable isotope studies show that conversion to EPA occurs but is limited, and that conversion to DHA is even lower (Baker et al., 2016)
• Oily fish is the best direct source of DHA.
• Given that the omega-3 index is a well validated health marker, and that DHA has a significant impact on the O3I value, then direct sources of DHA are more likley to elevate O3I than ALA alone.

But to look at whether fish intake can lead to improved health outcomes, we can look at the consistent finding of epidemiology. One good review by Mozaffarian & Rimm (2006) that appeared in JAMA showed:

1. Consumption of 1-2 servings/wk of fish:
   • Reduces risk of coronary death by 36%
   • Reduces risk of total mortality by 17%
   • [Note: Lower risk is more strongly related to intake of oily fish (e.g, salmon), rather than lean fish (e.g., cod)]
2. Across different studies (see image below), compared with little or no intake, modest consumption (~250-500 mg/d of EPA + DHA) lowers relative risk of CHD mortality by 25% or more.
   1. Higher intakes do not substantially further lower CHD mortality, suggesting a threshold of effect.

When looking at the image of increasing omega-3 (or oily fish) intake in a population, it is crucial to consider the background level of intake. This is especially the case given point 2 above; i.e. there seems to be a threshold of effect.

• Japanese populations tend to have high background fish intake, with an average of 900 mg/d of EPA and DHA being commonly reported.
• These populations also tend to exhibit very low CHD death rates (87% lower than comparable Western populations).
• In such population, additional omega-3 intake does not seem to lead to a further reduction in CHD death. This would indicate that most of the population is already above the threshold for maximum mortality benefits.

Dietary recommendations support fish intake as being part of a health-promoting diet:

• Dietary Guidelines for Americans 2020 – 2025: 8-10 oz per week of seafood (average intake in US population is well below this)
• Eatwell Guide (UK): Eat 2 portions of sustainably sourced fish per week, one of which is oily
• EAT-Lancet: Fish is an “emphasized food”, with 1-2 servings per week being recommended

Claim 2: “By cooking fish, you’re already eliminating a lot of the omega-3”

A study by Bastias et al., 2017 that appeared in PLoS One compared raw salmon and mackerel to 4 different types of cooking methods:

1. oven
2. steam
3. microwave
4. canning

As seen from the above results table, the omega-3 content (as a percentage of fatty acids) in the different cooking methods of the salmon was approximately:

• Raw = 15.9%
• Canning = 19.0%
• Oven = 17.8%
• Microwaving = 16.6%
• Steaming = 21.0%

There was no change in omega-6 content.

Another study (Zotos et al., 2013) examined the impact on omega 3s in baked sardines and fried anchovies, with different cooking durations for each:

• Oven-baking of sardines for 20, 40, 50 and 60 min
• Anchovies were deep-fried in either sunflower or olive oil, for durations between 2-5 minutes

The Zotos study found that the omega-3 content of all the sardine samples (oven-baked) were basically the same. For the anchovy deep fried in sunflower or olive oil (2-5 mins), there was a significant drop off in omega-3 content. So it seems that, at least in this case, if the cooking method is high heat, deep frying then anchovies can lose a good amount of their omega-3.

Beyond individual studies of specific fish and cooking methods, we can think about this claim rationally. If indeed all cooking of fish “elminated a lot of the omega-3”, then given that people cook fish when they eat it, we probably wouldn’t expect to see fish consumption reliably increase omega-3 status, right? However, consistently (and wholly unsurprisingly) we see that people who eat more fish have a higher omega-3 index.

Claim 3: “Farmed fish are not fed the algae that normally have, and so instead of omega-3 they make mainly omega-6, so they are inflammatory”

Within this statement, there are really two separate claims that we can question:

1. Is farmed salmon low in omega-3?
2. Does more omega-6 make them “inflammatory”?

1) Is farmed salmon low in omega-3?

Going back to the Maozzifarian & Rimm review, we can find a compilation of data based on that from the Environmental Protection Agency (EPA), the Food and Drug Administration (FDA), and U.S. Department of Agriculture (USDA). This shows, for different types of fish:

1. the amount (in ounces) per week needed to reach the EPA + DHA recommendations
2. the cost (in dollars) to consume that amount

These data show how farmed salmon compares very favorably to other fish in respect of omega-3 content. The paper also detailed how, on average, a 6oz serving of farmed salmon contains 4,504 mg of EPA+DHA, in comparison to 1,774 mg per 6oz serving of wild salmon.

Given that farmed salmon is generally higher in total fat content, then even if EPA+DHA content (as a percentage) were less, it still translates to greater EPA+DHA content in the farmed salmon. This is backed up by a study by Jensen et al. (2020) comparing farmed vs. wild caught salmon:

1. It found that the amount of omega-3 fatty acids were a substantially lower in the farmed (8.9%) vs. in the wild (24.1%).
2. However, given that they found that the fat content of farmed salmon (18%) was three times that of the wild salmon(6%), this meant that the absolute amount of omega-3 per 100g of fish was much higher in the farmed salmon (4.3%) vs. the wild salmon (1.4%).

2) Does more omega-6 make them “inflammatory”?

The theory that omega-6 fatty acids are “inflammatory” is typically based on mechanistic reasoning relating to the omega-6 fatty acid: linoleic acid (LA). So it is known that LA is a precursor to arachidonic acid (AA), and that AA is the compound used to produce pro-inflammatory eicosanoids (e.g. Eicosanoids are important for the early stages of inflammation that we need after an injury).

However, the problem with this theory is that wide variations in LA intake do not in fact change AA levels in the body. So, increasing LA levels will not increase the ‘pro-inflammatory’ capacity of eicosanoids. This is confirmed in experimental human studies. A pro-inflammatory effect of LA has never been shown experimentally, and increasing LA levels results in no change in pro-inflammatory markers.

While some very limited animal-experimental data suggests that linoleic acid (an omega-6 fatty acid) may counteract potential benefits of omega-3 fatty acids, this hypothesis has not been supported by any clinical trials or prospective studies in humans.

If you’re interested in a deeper dive on diet and inflammation then see episode 329 of the podcast.

Claim 4: “When you are eating fish, you are eating pollution, which is toxic”

There are two main groups we can look at here in relation to fish and contaminants/pollutants:

1. Mercury
2. PCBs and Dioxins

Why is Mercury an Issue?

• Mercury is well known as a potential harm to human health, when exposure is very high.
• It can be produced natural sources such as volcanoes, but more commonly is a by-product on industry processes; power plants, mining, waste incineration, etc.
• Mercury can exist in several forms, a number of which aren’t seen as much of a problem. If inorganic mercury is ingested by an animal for example, absorption is pretty poor. While elemental mercury doesn’t easilt cross tissue barriers.
• But mercury can also appear in lakes and oceans (via rainwater) and there it can be converted into methylmercury by microbes. And this form of mercury can be absorbed and transported into tissues.
• Therefore methlymercury can accumulate in fish who inhabit these lakes and oceans. And as humans may eat these fish, there have been concerns of potential harm raised.
• Despite very high exposure being a known hazard, the health impacts of a chronic, low-exposure to mercury (e.g. via eating fish) has not been as clearly determined.

What Levels are a Problem? What is in Fish?

1. The European Food Safety Authority (EFSA) has established Tolerable Weekly Intakes (TWIs), or ‘safe levels’ of 1.3 µg/kg bodyweight for methylmercury.
2. Joint FAO/WHO Expert Committee on Food Additives (JECFA) set it’s TWI at 1.6 µg/kg boyweight.
3. Due to particular risks in the peri-pregnancy period, the Environmental Protection Agency set methylmercury intake of 0.1 ug/kg per day as the allowable upper limit
   • This is equivalent to a 50 μg/wk for a 70-kg woman
   • This is calculated by taking the lower 95% confidence limit at which gestational exposure to mercury may produce abnormal neurologic test scores, and then multiplying that by a 10-fold uncertainty factor.
4. Cross-sectional analyses done by Dr. Martha Clare Morris & colleagues (2016) examined brains in autopsies, and compared that to habitual fish intake in the years pre-death. They found that despite seafood consumption being correlated with higher brain levels of mercury, higher seafood consumption was correlated with less (not more) Alzheimer disease neuropathology.

Guidelines for Fish Consumption

1. Mercury levels in fish are primarily dependent on species, with the highest concentrations in large predators (e.g. shark and swordfish), and very low levels in smaller or shorter-lived species (e.g. salmon and shellfish).
2. Very high mercury exposure from prolonged high intakes of mercury-containing fish can produce sensorimotor symptoms in adults (as per this case study), most commonly ] a burning or prickling sensation that is usually felt in the hands, arms, legs, or feet,
   • A “prolonged, high intake” would be considered 1-2 servings of fish (including species high in mercury) per day, for a period of 10 years or more.
   • These sensorimotor symptoms are normally reversible when mercury exposure is reduced.
   • Whether lower exposures produce neurologic abnormalities in adults is not clear.
3. EPA advises women of childbearing age, nursing mothers, and young children:
   • To avoid shark, swordfish, golden bass, and king mackerel (each of these fish contain more than 50 μg of methylmercury per serving)
   • To eat up to 12 oz/wk (~2 typical servings) of a variety of fish and shellfish lower in mercury, with a limit of 6 oz/wk of albacore tuna (30 μg methylmercury per serving)
4. For CVD risk in the general population:
   • Two studies (Guallar et al., 2002 and Virtanen et al., 2004) found that higher mercury intakes could increase risk. However…
   • The net effect of fish consumption was still beneficial: i.e. the benefit associated with consumption of fish (or omega-3 fatty acids) was reduced the greater the mercury exposure was, but the higher mercury intakes did not wipe out the benefit.
   • Therefore, consuming fish still has a net risk reduction for CVD.
5. A variety of seafood should be consumed and in cases where someone is consuming a lot of fish (i.e. more than 4 servings per week) they should make sure to limit intake of the species that are higher in mercury.

Risks of PCBs and Dioxins

1. PCBs = polychlorinated biphenyls
2. Manufacture and processing of PCBs was prohibited in 1977.
3. Regulation has largely led to dioxin emissions decreasing by more than 90% since the late 80s.
4. But as PCBs and dioxins can persist in the environment for a long time, they continue to be present in low concentrations in many foods.
5. Mozzafarian & Rimm review: “Levels of dioxins and polychlorinated biphenyls in fish are low, and potential carcinogenic and other effects are outweighed by potential benefits of fish intake and should have little impact on choices or consumption of seafood”

Conclusions on Contaminants and “Toxic” Polltants

Gil & Gil, 2015: “Despite risks of mercury, PCBs and Dioxins “for major health outcomes among adults, the vast majority of epidemiological studies have proven that the benefits of fish intake exceed the potential risks with the exception of a few selected species in sensitive populations.”

Mozzafarian & Rimm, 2006: “Based on strength of evidence and potential magnitudes of effect, the benefits of modest fish consumption (1-2 servings/wk) outweigh the risks among adults and, excepting a few selected fish species, among women of childbearing age. Avoidance of modest fish consumption due to confusion regarding risks and benefits could result in thousands of excess CHD deaths annually and suboptimal neurodevelopment in children.”

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