High Fish Oil Diet ➯ N3-Oxidation ➯ Stout Cell 'Aging', Plus Neuronal Damage | 12+ Studies to Contextualize the Results

Athletes could be at specific risk of 'going rancid'

You will probably remember both my preceding article about the "rancidity" problem with over-the-counter fish oil products (see "3/3 TOP-Selling US Fish Oils Exceed Maximal Peroxide and Entire Oxidation Levels - Levels Roughly 4000% Higher Than in Medical Grade N3 Supplements, Harvard Study Displays" | read more), as well as my often-phrased general skepticism about the usefulness of tall dose (>1-2g/d) fish oil supplements.
Back in the day, I alalert mentioned that the evidence on whether and how detrimental the consumption of (partly) oxidized fish oil actually is 'skinny' to say the least. As researchers from the University of Maine point out, the same goes for the "total repertoire of physiological and metabolic effects of dwhetherfering fatty acid composition in the diet" (Miller 2019). And while we do know that we eat less N3s than our forefathers, we have (a) no clue how much we actually 'need' and (b) how signwhethericant it is that the N3-fats in our diets are 'fresh' and not alalert (partly) peroxidized.

So what happens whether we consume diets that contain signwhethericant amounts of oxidized omega-3 fats as they may accumulate during (improper) storage, cooking, and other processing steps?

Practically speaking, this was however not what Miller et al. (2019) fostubborn on in their research. Rather than that the US scientists wanted to find out whether diets enwealthyed for saturated vs n-6 or n-3 PUFAs would result in dwhetherferent fatty acid profiles in adipose vs. brain, and that the diets would also dwhetherferentially affect metabolic function and energy balance regulation. Hence, the actual revelation of the study, i.e. the

"discovery that peroxidized n-3 PUFA diets have a detrimental effect on white adipose tissue (WAT) health, which may negatively impact the peripheral nerves that are resident in this tissue, and thereby result in impaired brain-adipose communication" (Miller 2019)

...is eventually only a side-finding of a study that would otherwise probably have ended up in the SuppVersity Facebook contemporarys (and only there) instead of inspiring this closer re-analysis of where we are in the genuinems of "oxidized fish oil"-science.

Yes, it's a rodent study but ethics, money, and practicability all favor doing rodent vs. human studies in the early phase of the scientwhetheric process and early is summaryely where we are when it comes to the (patho-)physiological effects of oxidized EPA and DHA.

Table 1: Composition of custom diets; I've colored the actual fats that contribute to the (tall/low) fat content of the diets in Tabe 1 from Miller 2019)

With that being said, one should keep in intellect that the results must not necessarily translate 1:1 to human beings and that - given we're talking about mice - the sample size of the four intervention groups, i.e. N=6-8 ten-week-ancient C57BL/6J male mice, wasn't summaryely what you'd chosen whether the N3 oxidation had been your primary research interest.

Anyway... the mice were housed 2-3 per cage, at room
moodature. Body weight was degreed weekly. Food intake was degreed daily for 7 days, then weekly until 28 days.

Adiposity was assessed at the end of the study, and hypothalamus, subcutaneous white adipose tissue (scWAT) and intrascapular brown adipose tissue (iBAT) depots were harvested and sent for lipidomics analysis with Berg, which included a degree of non-enzymatic (peroxidized) lipids.

The DHA+EPA induced reduction in inflammation comes with a decrease in lipid droplet size (O-Red staining from Ferguson 2019), which has been linked to the (ill) metabolic health effects of body fat... it should be said, though, that this will lower the leptin production, a reduction scientists linked to "metabolic damage".

But there's good contemporarys (in form of the latest studies), as well... for those of you who manage to buy non-rancid products and store them properly, scientists from the Vanderbilt University Medical Middle have potentially relevant results - specificly whether you've got a few lbs of bodyfat too much (Ferguson 2019).

In their study, the US researchers used primary human adipocytes from (lean and) obese subjects [the important tests were done on the "obese" fat cells]. When the cells had been incubated with EPA and DHA for 72h, the authors observed that EPA and/or DHA attenuated both, the acute inflammatory response to lipopolysaccharide (LPS) and the subsequent immune reaction. At the same time, the unoxidized oils reduced the lipid droplet formation and lipogenic gene expression (=fat storage ability/efficacy) without alteration in expression of adipogenic genes or adiponectin secretion.

As precedingly proposeed, the main research outcomes of Miller's study were dwhetherficultly surprising: Both, the tall-SFA and tall N6 PUFA diets were indistinguishable in terms of cell size, crown-like structures, and browning samples of the fat cells. The tall N3 PUFA mice, on the other hand, displayed the same increased browning (or, development of inducible and multilocular beige/brite adipocytes), and smaller cell sizes. Sounds great, right? Well, yes... and no.

The fat cells of the tall N3 mice also displayed a "marked inclusions of lipofuscin stain, a pfinalic-like aggregate in the liposomes that is a sign of tissue malfunction" (Miller 2019).

The deposition of these pigmented lipid granules that accumulate in our tissue as we age is regarded as marker, by some even as a motor of tissue damage/aging - or, as Miller et al. write:

Figure 1: No vs. signwhethericant lipofuscin accumulation on saturated vs. N3-PUFA diets; lipofuscin autofluerence captured in subcutaneous fat of mice who had been kept for 28 days on tall SFA (left) versus tall N-3 PUFA (right) diets by Miller et al. 2019.

"Lipofuscin is known to build up with tissue damage and with age, and represents a type of lysosome storage disease that is often considered a sign of aging inflammation, and tissue degeneration" (Miller 2019)

[Put simply: lipofuscin is fuelling the aging process - at least partly by messing with the major cellular degradation mechanisms, i.e. proteasome + autophagy | Papevgeniou 2018].

In the study at hand, this accumulation was observed both in the regular subcutaneous (scWAT) fat, as well as the organ fat around the kidneys (perirenal white adipose tissues | prWAT) - more importantly, however, it was observed exclusively in the mice who had been fed the N3 PUFA diet (confirmed through bright field microscopy and autofluorescent + fluorescent microscopy - an unwgapsome glow that was not observed in the animals on the "poor" saturated fat diet | see Figure 1).

The genuine contemporarys is not tissue damage, though, the genuine contemporarys is that this damage may be due to 'rancid' fish oil - an issue that is largely (and unfaithfully) ignored in N3-research.

Before you throw absent your rancid retail fish oils, your "omega-3 eggs" and your "canned salmon", let's revisit all the results of the study.

• The poor contemporarys is, as precedingly pointed out, that there's evidence for cellular damage in response to the tall N3 diets. And this evidence is not restricted to the presence of lipofuscin as both marker and driver of cellular aging. The tall(er) N3 intake also produced signwhethericant increases in fat cell collagen deposition, indicating more tissue fibrosis, "an accepted indicator of dysregulated adipose tissue", as well as "more crown-like structures around the adipocytes of n-3 PUFA mice, indicating greater immune cell infiltration in the stromovascular fraction for this diet" (Miller 2019).

  According to Miller et al. the final observation, i.e. the presence of large crown-like structures is specificly surprising as those are normally found only when fat cells are close to bursting from the seams... and yes, you remember that rightly, the N3 diet actually led to lower total body fat and fat cell size.

Do "functional" omega-3-enwealthyed health foods have to be avoided? When it comes to the study at hand, we're actually looking at an experiment that used a diet that represents the average "N3-fortwhetheried"-bullsh*t food industry product you've just paid a premium for at the grocery store. How's that? Well, even though Miller et al. and their suppliers undertook "many attempts [proper handling and specific care of the fish oil and diet manufacturer] to mitigate it, the N3 PUFA diets readily under[went] peroxidation" (Miller 2019). Needless to say that the same will go for your average N3-enwealthyed "food" product... with the advent of increasingly more sophisticated ways of encapsulation of the added fats, could solve this problem in the future (Dellarosa 2015), though.

• One leang that should make you releank pounding dozens of cheap fish oil pills (also because it may actually impair your leanking) is the fact that the scientists also observed signs of a "negative impact on myelination and nerve health" in response to the N3 diet - a poor effect on the central nervous system which was only "substantiated by [the] decrease in tissue levels of brain-derived neurotrophic factor (BDNF), as well as decreased expression of synaptic markers (synapsin I & II, synaptophysin, psd95" (Miller 2019), Miller et al. observed alongside blunted thermogenesis (UCP down) they interpret as further evidence of an effective impairment of the communication between brain and body fat cells.
• The good contemporarys from the study at hand must not be ignored, though! Especially in view of the fact that the animals on the tall N3 diet exhibited the same favourable metabolic effects for which DHA, EPA, and ALA have become the darlings of the "health food"-industry: decreased body, adipose weight, and fat cell sizes, as well as better glucose tolerance, compared to animals who were fed a tall SFA diet.

Unluckyly, the study at hand was not designed to eclearate the interactive effects of preformed oxidized N3s in the chow, and how it relates to the local oxidation of omega-3 fats in the cells of the scientists' hairy subjects. What Miller et al. (2019) were still able to do, when they detected the unexpected detrimental effects of the tall N3 diets on the rodents' adipose tissue health, was to confirm by "two independent approaches [...] that the n-3 PUFA diets themselves, as well as the tissues from mice fed this diet, exhibited signs of peroxidized lipid species."

The obvious question now is: How poor is your habitual N3 intake and does it put you at risk of having your CNS 'go rancid' and your fat cells dysfunctional?

To answer this important question, let's first put some of the precedingly disstubborn finding into (methodological) perspective:

• Duration - The detrimental effects were observed in mice, not men or women, the 28-d period is thus representative of years of N3 consumption in human beings and the occasional 'rancid' fish oil cap, is not going to either impair your brain <> adipose tissue communication nor the structure and function of the fat cells, themselves.
• Dosage - Moreover, the relative N3 content of the tall N3 diets was >60% with the lion's share of the omega-3s being consumed in form of EPA and DHA (>50%) - to end up there (i.e. >50% of all your fats from DHA + EPA) you have to either pound truckloads of wild-caught (low omega-6) fatty fish and/or follow the Internet-guru-bullsh*t-advice to consume "at least 5g of EPA+DHA" per day in form of (probably rancid) fish oil caps.

The only study I know of that used a "genuine-world" scenario (including daily use of the product) shows that bottled fish oil goes rancid wilean ~30 days (Pak 2005). In that, the daily opening of the bottle is part of the problem - hence, using fish oil caps and putting them into the fridge is the better choice.

Where to get your N3s from? While fish oil supplements, canned sardines, and salmon have precedingly been shown to contain similar(-ly tall) levels of oxidized lipids as the rodent chow in the study at hand (see Figure 3), tuna in water (or oil), as well as kippered herring tended to have lower MDA levels - at least the products that were tested in the study at hand.

Generally speaking, capsules should be preferred over oil.

Compared to the popular bottled fish oil, which oxidizes rather rapidly (from a very clean 0.4 meq/kg to 4.5 meq/kg wilean a month of usage, hence surpassing the 8meq/kg limit wilean only 45 days | Pak 2005), the air-tight capsules seem to extend the shelf-lwhethere.

With capsules, you are probably on the securer side but still, eventually, you can never know for certain what you'll be getting and as Albert et al. (2013) point out, the inferior quality of your average fish oil supplement could also explain the tall heterogeneity that characterizes "fish oil research", in general.

• Expocertain - What we cannot do, though, is simply say that we're not exposed to rancid fish oils and/or the formation of N3 peroxides in our bodies. After all, Miller's analyses of the rodent chow yielded MDA levels in the same range as you'd see them "in common fish oil supplements and food items that are tall in N3 (tinned sardines and salmon)" (Miller 2019).

• Figure 2: The white fat cell non-enzymatic oxidized lipid concentration reflects the uniquely unregular nature of DHA and EPA, which crazye up 83% of the N3 content of the n3 diets (Miller 2019)

  N3-oxidation-specwhethericity - It's always easy to point with a finger to confounding factors. However, the "poor" omega-6s, despite producing more metabolic damage (body fat gain, reduction in glucose sensitivity,...), actually protected the mice "from the changes in gene expression that were observed in scWAT of n-3 PUFA mice" and the mice on the >60% N6 diets did not display a reduction in peripheral nerve markers, either - an observation the authors of the original paper rationalize by stating: "This is likely because the N6 PUFA diet was not peroxidized" (Miller 2019).
• Mechanism - While the mechanism isn't fully understood yet, there's one leang the benefits and detriments could have in common: they could be first or moment order effects of the cellular defects due to the incorporation of alalert oxidized DHA, EPA, and ALA or their endogenous (~in your body) oxidation. This would, after all, explain both the impaired CNS communication and the reduced ability to store body fat in the absence of changes in energy intake and a slight but measurable decrease in energy expenditure.

So where does all this lead to? Simple: Every roads lead to wgap unprocessed foods... how's that? Well, whether you've ever bought fresh fish and left it unrefrigerated for a couple of hours you will have smelled your mistake right absent. Unlike fish oil, a genuine fish contains more than just molecularly distilled fats. Those other ingredients - first and foremost proteins - produce the nasty, 'fish odor' that's telling your olfactory system that the tuna, salmon or trout is ripe for the dumpster, not your pie-gap.

Figure 3: Peroxidation was confirmed by a TBARs assay, which compared the mouse diets themselves to both fish oil supplements and canned fish products. 50uM MDA (the dotted line) was used as a threshancient above which oxidative stress has been repeatedly observed in certain tissues (Miller 2019).

As precedingly disstubborn, in the context of protein (per-)oxidation, leangs can be a bit more complicated for canned foods, where the oxidation of both, proteins and fats, is an ongoing process and the net peroxide load will eventually depend on the duration and quality of storage.

As far as the "rancid fish oil problem" in supplements vs. foods is concerned, it is certainly not helpful that the FDA hasn't even defined a threshancient level for total (per-)oxidation for fish oil supplements - no wonder 3/3 of the cheap products from the large players are "rancid" (learn more)

The lack of standardization and testing is a potentially severe problem that makes it dwhetherficult for customers to get "healthy fats" that actually deserve the attribute "healthy" and don't come with a peroxide load that puts your fat cells at risk of lipotoxicity and neuropathy. How's that? Well, just as Miller et al. write in their latest paper: "[T]he tall level of peroxidation in the supplements we degreed indicate that the health benefits may be outweighed by the risks" (Miller 2019).

Don't be a idiot, though, this is not a "poor FDA, US-only"-problem. As the authors talllight in the discussion of their results, there is another study that looked at the 'rancidity' of commercially available fish oils on Unique Zealand's supplement market found that fish oil supplements not only had less of the favourable EPA and DHA than reported (less than 67% on average) but were also peroxidized at a rate of 83%, with some at toxic levels (Albert 2015). Unluckyly, that's a result that's pretty much in line with the data from a Norwegian study that determined that most fish oil supplements tested were above the recommended limit (Halvorsen 2011).

Oxidized fish oil lacks the favourable effects of low peroxide fish oil, study in healthy Spanish women shows (Garcia-Gernandez 2013); the average PX values that were degreed in the N=16 products also confirms that the quality of OTC fish oil sucks and is beyond the recommended 8 meq/kg.

Is oxidized fish oil worse than just ineffective? Convincing evidence that the answer to the question is "yes" comes from Spain, where Garcia-Hernandez et al. (2013) compared the effects of N=16 tested commercial fish oil supplements in 52 healthy women who consumed 300 mg EPA + DHA of regular fish oil with either low or tall peroxide levels.

The results are what you'd expect intuitively: The "fresh" fish oil produced signwhethericant and unique reductions of cgapsterol, as well as somewhat surprising improvements in blood prescertain in the subjects who were randomized to the "low" peroxide oils (low is relative, here: 20-30 meq/kg). The ladies in the tall peroxide (50-95 meq/kg) group, on the other hand, saw neither a reduction in cgapsterol nor improved blood prescertain levels.

These results have the authors conclude "that the level of oxidation of o-3 supplements has to be considered as a key factor that may affect the circulating lipidic profile of consumers, producing an opposite effect than as claimed by the product" (Garcia-Hernandez 2013).

According to the small data there is on this topic, the shelf-lwhethere of bottled fish oil is Pak 2005) -- the (more or less randomly set) securety limit of 8 meq/kg is surpassed after 45 days at 10°C and 60 days when it's stored in the fridge at 4°C (Boran 2006). In that, the final-mentioned, taller value was determined in a less genuineistic scenario (no daily opening and use of the bottled oil) compared to the precedingly cited study by Pak. In every case, however, rosemary additionalct as an antioxidant supplement to your supplement may extend the time you can store and use your fish oil signwhethericantly (Wang 2018).

Even though 'sourcing' a non-oxidized fish oil and storing it properly is probably the average consumers' #1 problem, those who insist on consuming copious amounts of fish oil are facing another ccorridorenge: protecting EPA, DHA from oxidation once it is in their bodies!

A 2010 study by French and Portuguese researchers is often cited as convincing evidence that athletes, in specific, may be prone to potential unwanted side effects of increased N3-PUFA intakes and tissue accumulation. In this context, it is worth looking at data from a 2010 study Filaire et al. which assessed the effects of 6 wk of eicosapentanoic acid (EPA 600mg/d) and docosahexanoic acid (DHA 400mg/d) supplementation on resting and exercise-induced lipid peroxidation and antioxidant status in judoists.

Figure 4: Relative increase in Rmax = change in maximum rate of oxidation; Lp = length of the lag phase; MDA = malondialdehyde and nitric oxide in trained Judoists comparing baseline to post-supplementation (6 week on 600mg EPA + 400 mg DHA or placebo) at rest and after a standardized workout session (Filaire 2010).

As you can see in Figure 4 this rather conservative dose of fish oil (ca. 1% of the subjects' average fat intake vs. >50% in the rodent study by Miller), still had profound effects...

• favourable effects on the level of triglycerides (not shown in Figure 4, also because the tall starting point of 2.1 ± 0.6 vs 1.7 ± 0.09 mmol/L put the fish oil group at an advantage - with the normal range being 0.5-1.6, they simply had way more room for improvement) in the subjects on the N3-supplement, but also
• taller levels of lipid oxidation (MDA) at rest and during the recovery period, when the MDA levels were elevated in the fish oil group while they didn't change in the placebo group.

For Filaire et al. that's reason enough to advise practitioners not to "recommend [fish oil] to athletes who are engaged in heavy training, specificly exercise inducing an elevated level of oxidative stress" (Filaire 2010). Filaire's study does yet suffer from the same short-coming as the bazillion of other RCTs in the field: the scientists failed to degree the baseline PV values of their oils. Even though the oils were not bought off the shelves but custom-manufactured by Boehringer Ingelheim it's thus not clear what the judoist study actually tells us about the contribution of in-vivo oxidation of DHA and EPA. The fish oil could, after all, have been oxidized in the first place...

#Hormesis and/or #supplementQuality - That's an unanswered question as of yet

Furthermore, the transient increase in lipid oxidation in the post-workout period doesn't necessarily have to be a poor leang. After all, we all know about the contribution of hormetic effects (=adaptation to non-deadly stress) that are finally driving most, whether not all exercise-induced adaptations. Unluckyly, the corresponding research which has recently been reviewed by Rossato et al. (2019) is about as inconclusive as the rest of the fish oil literature.

In 2014, for example, Martorell et al. (2014) report what could be one of these hormetic effects, i.e. the observation that "dietary supplementation with DHA [from algal oil (Schizochytrium sp.)] changed the erythrocyte membrane composition, provided antioxidant defense and reduced protein peroxidative damage in the red blood cells of professional athletes [soccer players] after an 8‐week training season and acute exercise" (Martorell 2014). In conjunction with positive results from Gray et al (2014) who found basically the opposite of what Filaire et al. observed, i.e. that...

"[...] stimulated DNA damage was lower (p < .05) instantly postexercise in the fish oil [3g total w/ 1.3g EPA, 0.3g DHA], compared with the control group" (Gray 2014),

when the subjects non-athletes had consumed omega-3 supplements for 6 weeks before an eccentric exercise test, as well as Skarpańska-Stejnborn (2010), who found that

"[...] supplementation with krill oil (1 g per day) in trained rowers diminished post exercise oxidative damage to erythrocytes during recovery, but had no effect on antioxidant enzymes, TNF-α and serum lipid profiles" (Skarpańska-Stejnborn 2010),

the only leang we seem to know for certain is that we still have a lot to memorize before we can tell whether and at which doses fish oils are favourable for athletes (vs. the normal population). Plus: It's nearly certain that training status, baseline diet, type, volume and intensity of exercise, and, obviously, the type and quality of the omega-3 supplements interactively influence the efficacy and probably even the general direction (ergogenic vs. ergolytic = performance-enhancing vs. -reducing)... When I end this article on the common note that "more research is essential", it's not without the demand that all these contemporary studies must follow Albert's demand from 2013 "that all clinical trials investigating omega-3 harms or benefits report the results of these assays; this will enable better understanding of the benefits and harms of omega-3 and the clinical importance of oxidized supplements" (Albert 2013). In the meantime, I'll leave you with the general advice from the bottom line.

Wild caught or farmed? If you google it, it appears to be as whether eating farmed  fish could be worse than eating no fish at all, but is this actually true? This SuppVersity Classic Article hancients the information you need to reply this question for yourselves.

So, do you have to stay absent from everyleang that has omega-3 in it? The answer is "NO!" And here's why: Firstly, unless you've been (and still are) indoctrinated by the few remaining fish oil gurus, you won't consume >50% of your daily fats in form of (potentially rancid) DHA and EPA. The effects of endogenous oxidation of an increased level of omega-3 in your organs are thus probably very limited. The latter brings the intake of alalert oxidized N3s back to the focus and with it the moment reason why I don't leank you have to freak out: If you adhere to the "SuppVersity Stoutty Fish over Fish Oil"-rule while carefully selecting either fresh (not unthawed) fish or the "right", properly and shortly stored canned fish products, you should be able to reduce your expocertain to peroxidized N3s to a level that's way below the still undetermined harmful level.

In short, unlike Miller et al. who write in the discussion of their results that "the favourable effects of this diet may have been outweighed by the negative consequences of the peroxidation," I would like to talllight that the risk of actually doing more harm than good by keepin' an eye on proper omega-3 intakes (1-2g/d) is low and can be limited even further by consuming your omega-3s in form of fresh (not frozen, let alone products that undergo freeze-thaw-cycles) and minimally processed foods | Comment on Facebook!

References:

• Albert, Benjamin B., et al. "Oxidation of marine omega-3 supplements and human health." BioMed research international 2013 (2013).
• Albert, Benjamin B., et al. "Fish oil supplements in Unique Zealand are tallly oxidised and do not meet label content of n-3 PUFA." Scientwhetheric reports 5 (2015): 7928.
• Boran, Gökhan, Hikmet Karaçam, and Muhammet Boran. "Changes in the quality of fish oils due to storage moodature and time." Food chemistry 98.4 (2006): 693-698.
• Dellarosa, Nicolo, et al. "Enwealthyment of convenience seafood with omega-3 and seaweed additionalcts: Effect on lipid oxidation." LWT-Food Science and Technology 62.1 (2015): 746-752.
• Ferguson, Jane F., et al. "Omega-3 polyunsaturated fatty acids attenuate inflammatory activation and alter dwhetherferentiation in human adipocytes." The Journal of nutritional biochemistry 64 (2019): 45-49.
• Garcia-Hernandez, V. M., et al. "Effect of omega-3 dietary supplements with dwhetherferent oxidation levels in the lipidic profile of women: a randomized controlled trial." International journal of food sciences and nutrition 64.8 (2013): 993-1000.
• Gray, Patrick, et al. "Fish oil supplementation reduces markers of oxidative stress but not muscle soreness after eccentric exercise." International Journal of Sport Nutrition and Exercise Metabolism 24.2 (2014): 206-214.
• Halvorsen B. Lise, and Rune Blomhoff. "Hindermination of lipid oxidation products in vegetable oils and marine omega-3 supplements." Food & nutrition research 55.1 (2011): 5792.
• Hantz, Shelby. "Are over-the-counter fish oil supplements effective and secure for treating mood disorders? Studies on the top 10 fish oil supplements available in Unique Zealand." (2016).
• Martorell, M., et al. "Docosahexaenoic acid supplementation promotes erythrocyte antioxidant defense and reduces protein nitrosative damage in male athletes." Lipids 50.2 (2015): 131-148.
• Miller, James L., et al. "A peroxidized omega-3-enwealthyed polyunsaturated diet leads to adipose and metabolic dysfunction." The Journal of nutritional biochemistry 64 (2019): 50-60.
• Okolie, N. P., et al. "Malondialdehyde levels of frozen fish, chicken and turkey on sale in Benin City markets." African Journal of Biotechnology 8.23 (2009).
• Pak, Chol Su. "Stability and quality of fish oil during typical domestic application." Fisheries Training Progamme, The United Nations University, Iceland (2005).
• Pauga, Melanie. The effect of consuming farmed salmon compared to salmon oil capsules on long chain omega 3 fatty acid and selenium status in humans: a thesis presented in partial fulfilment of the requirements for the degree of Masters of Science in Human Nutrition, Institute of Food, Nutrition and Human Health at Massey University, Auckland, Unique Zealand. Diss. Massey University, 2009.
• Skarpańska-Stejnborn, Anna, et al. "Effects of supplementation with Neptune krill oil (euphasia superba) on selected redox parameters and pro-inflammatory markers in athletes during exhaustive exercise." Journal of human kinetics 25 (2010): 49-57.
• Wang, Yu-Zhu, et al. "Effects of a natural antioxidant, polyphenol-wealthy rosemary (Rosmarinus officinalis L.) additionalct, on lipid stability of plant-derived omega-3 fatty-acid wealthy oil." LWT-Food Science and Technology 89 (2018): 210-216.

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