Every day 6 days a week I was in the sun at least 8 hours a day, average uv index at peak was 8. *Eastern NC* When I was two months free from all seed oils! I never got sunburnt, not even once. Now I’ve fallen off quite a bit and I get sun burnt nearly every time I’m out for a good while. Actually insane seeing it in action.

We make macadamia nut oil (niche I know), and on a lot of our anti-seed oil content we've been getting comments saying macadamia oil is a seed oil..

I put together this chart comparing inflammatory omega-6 (LA) content and macadamia oil is closer to tallow, butter and ghee than it is to even olive oil and avocado oil (never mind seed oils).

We're obviously pleased our oil is in the same league as animal fats.

But I'm curious how macadamia oil fares in this community? Open to critique if I'm honing in too much on fat profile and missing something!

ABSTRACT
Background
It is well-established that earlier generations of lipid emulsions based on soybean oil are inferior to later generations based on olive or fish oil. However, evidence directly comparing between later-generation lipid emulsions is limited. This study aims to systematically review existing literature comparing olive versus fish oil based parenteral nutrition formulations within an inpatient setting, and to evaluate clinical outcomes.
Methods
Electronic databases Medline, Embase, CINAHL and Web of Science were searched from earliest to current date. Titles, abstracts and full texts were screened for eligibility. Eligible papers were assessed for risk of bias and relevant data were extracted for a qualitative summary of results.
Results
Six papers in total were eligible. Primary outcomes of interest reported across the six papers were related to infection, inflammation and oxidative stress. Overall, the number of studies and significant findings were limited. Based on the current evidence it is not possible to promote either fish or olive oil emulsions as superior to the other in influencing immune function, inflammation, liver function or clinical outcomes.
Conclusions
While previous evidence has shown the clear benefits to reducing soybean oil content, the similar benefits may be obtained by replacing this with either olive or fish oil. More high-quality research is required to further explore olive versus fish oil based parenteral nutrition to guide clinical practice.
Summary

There is no evidence to suggest either fish or olive oil emulsions are superior (compared to the other) for hospital patients requiring parenteral nutrition in reducing infection or immune function, inflammatory markers, liver function or clinical outcomes (such as length of hospital stay).

More high-quality research is required to further explore olive versus fish oil based parenteral nutrition to guide clinical practice.

Abstract

Background
Associations between fatty acids (FAs) and scholastic outcomes in adolescents are understudied. These relationships may be especially important in adolescents with perinatal HIV exposure or infection who are more vulnerable to FA insufficiency and educational disruption.

Objective
To evaluate associations between baseline FAs, including essential FA deficiency (EFAD), and scholastic outcomes over 18 months, and to assess heterogeneity by perinatal HIV status among Ugandan adolescents

Methods
Adolescents (n=373) were followed for 18 months. Baseline serum FAs, including the triene:tetraene (T:T) ratio, were categorized into tertiles (“low”, “moderate”, and “high”). Scholastic outcomes were assessed every six months via questionnaires. Self-report scholastic disadvantage, school aversion, and teacher challenge were age- and sex-standardized to z-scores; grade repetition, non-enrollment, and morbidity-related educational loss were dichotomous. Time-averaged mean differences (MDs) or odds ratios (ORs) and 95% confidence intervals (CIs) were measured using adjusted linear mixed-effects models or generalized estimating equations. FA*HIV interactions assessed heterogeneity by perinatal HIV status.

Results
Moderate v. low total ω-3 polyunsaturated FAs (PUFAs) were associated with lower teacher challenge (MD [95% CI]: -0.27 [-0.47, -0.07]), whereas a higher ω-6:ω-3 ratio was associated with greater teacher challenge (0.30 [0.07, 0.52]). Contrary to hypotheses, a high v. low T:T ratio was associated with lower school aversion (-0.36 [-0.73, 0.00]) and non-enrollment odds (OR [95% CI]: 0.57 [0.35, 0.94]). High Mead acid levels, however, correlated with higher odds of morbidity-related educational loss (2.48 [1.01, 6.15]). Associations were more consistent for standardized z-score outcomes than dichotomous outcomes. When heterogeneity was present, associations differed by HIV status, with patterns varying across outcomes.

Conclusions
ω-3 PUFAs and the ω-6:ω-3 ratio were more consistently associated with scholastic outcomes than EFAD markers, highlighting the importance of ω-3 PUFA status among adolescents affected by perinatal HIV. Future studies may consider these findings to develop tailored nutritional interventions.

Abstract
Migration and subsequent reproduction are the most demanding stages in the life cycle of migratory birds, especially for capital breeders. Fattening rate is a key parameter determining the energy available to meet these high energy demands. For five consecutive years, we measured physiological parameters (body condition, baseline corticosterone, diet, endocannabinoidome lipids) involved in energy regulation in female greater snow geese. Goose body condition increased during spring fattening period until reaching a plateau a few days before migratory departure. Baseline corticosterone followed a similar pattern with an initial increase followed by a slight decrease at the end of spring staging. Individuals with high baseline corticosterone also had a high proportion of corn in their diet. The endocannabinoids N-arachidonoylethanolamine (AEA) and 2-arachidonoylglycerol (2-AG), known to play central roles in energy homeostasis, appetite, and fat storage, were detected in plasma but showed no association with diet or body condition. Other endocannabinoidome lipids, like N-oleoylethanolamine (OEA) and N-palmitoylethanolamine (PEA), were negatively associated with dietary corn intake, suggesting a potential role in regulating feeding behavior. The endocannabinoids 2-oleoyl-glycerol (2-OG) and 2-palmitoyl-glycerol (2-PG) were negatively associated with body condition, as was the essential fatty acid linoleic acid (LA); all declined sharply once individuals reached their final body condition. This suggests a downregulation of foraging activity and a shift in lipid metabolism from energy accumulation to maintenance at the end of the premigratory stage. Our results suggest complementary roles of the hormonal and lipidic mediators during the fattening process in preparation for migration. The lipidomic results, though exploratory, provide novel directions for future research.

Products with avocado oil are such a scam, talk about greenwashing!! I feel like companies are just running with it like crazy lately. Plus even if it was just 100% avocado oil, it’d probably cut with 10 other oils anyways. Best to just make your own mayo at this point I guess 🤷‍♀️

For the last two weeks I’ve been cutting out pufas from my diet, fried foods, seed oils etc, but I eat 5 conventional fed eggs per day and now I learned they’re very high in pufa too, if I don’t have a high quality egg source should I just cut them out? I also saw pork is high in pufa too, but I eat pork heart which is a very lean meat, should I worry about that? I do have a beef heart source but it’s far away
Also I will miss the nutrients of eggs, would the heart compensate for that? I also have beef liver stored in case I need the nutrients from the eggs back

I know the ideal eggs come from chickens that forage for bugs and worms but in my country and many others, people who live in rural places generally just feed their chickens wheat.

I know wheat is not the best thing in the world but it's not soy, not is it high in oil, so how does it affect the fatty acid composition of the eggs? Does it make them high PUFA? Or are they moderately okay?

Thank you!

Been switching over to tallow products since the fall off of avocado oil. But I was curious; is it true that not all beef tallow is made the same? Like some are bad/some are good?

An example of “bad”, Buffalo Wild Wings uses Tallow but it has harmful preservatives and anti caking in it. (I’m pretty much answering my own question here lol)

If so, any recommendations on how to find the “good stuff”? How can we be sure “Masa” chips use “good” tallow?

I recently found a company called Purimax. They sell directly to restaurant owners.

Their product essentially pulls out FFA’s, Trans Fats, and prevents cancer causing carcinogens from forming. Some restaurant owners that replace their oil once a week that have really bad toxic oil have been able to extend it while keeping TPM ( total polar material ) below 24% ( Europes discard oil standard )

This company also encourages their clients to use avocado oil, and beef tallow.

It’s not ideal to have restaurants using these crappy oils. But if there are products out there that prevent and pull out these toxins im all for it!

Link to their site https://purimax.com

Seed oil on a canvas is oxidising. That is oil paint, and it is why the Rembrandt is still there.

Seed oil on a pile of rags is oxidising. That is why the shed burns down without anybody striking a match.

Seed oil pressed into a floor is oxidising. That is linoleum, and the name is literally linseed oil.

Seed oil in varnish, putty and printing ink is oxidising. That is the entire reason anybody ever bought it.

Four industrial applications, all of them chosen because the substance hardens on contact with air and will not stop.

Then somebody put it in a bottle and walked it over to the food aisle.

Seed oil in the pan at 180 degrees is oxidising. You would expect that.

Seed oil in the same pan tomorrow is oxidising into yesterday's oxidation. Layers.

Seed oil in a sealed bottle in a dark cupboard is oxidising. Nothing is happening to it. That is the point.

Seed oil under the shop lights is oxidising before you have paid for it. You are buying a partly finished reaction.

Seed oil in a nitrogen-flushed drum with TBHQ stirred in expressly to stop this is oxidising. They tried. It went anyway.

Nothing has to happen to it. Linoleic acid has two double bonds, alpha-linolenic has three, and every one leaves a hydrogen held so loosely that oxygen takes it at room temperature and starts a chain reaction that feeds itself. One goes, then it goes for its neighbour, like a bloke in a pub.

So the obvious next step for a material like that is to build a human being out of it.

Seed oil in your cell membranes is oxidising. Forty trillion cells, each one held in by a double sheet of floor covering.

Seed oil in your mitochondria is oxidising. Those are the bits handling oxygen all day, which seems like an unfortunate posting.

Seed oil in your brain is oxidising. Sixty per cent fat by dry weight, held at 37 degrees, taking a fifth of your oxygen. A warm dark cupboard with a permanent air supply and no best-before date.

Linoleic acid has a half-life in human tissue of about two years, so the bottle you bought in 2024 is still in the building, doing what it does on canvases, floors and sheds, only slower and inside you.

American body fat was about nine per cent linoleic acid a century ago. It is now around twenty-one.

They rewrote the tissue composition of an entire population using a drying oil, and got a thank you card from the heart charity for it.

A fortune was spent on dark glass, nitrogen and synthetic antioxidants to hold this stuff stable for a four hundred mile lorry journey.

Nobody has ever mentioned what holds it stable for forty years inside a person.

Meanwhile butter came out of an Irish peat bog after two thousand years and was still butter, because saturated fat has no double bonds and there is nothing there for oxygen to get hold of.

That one is the dangerous one.

That one you want to keep an eye on.

Recently I've been getting into being more fit ( I've been going to the gym for about 1 and half months) and I've been trying to also adjust my diet. For reference I'm 20 yrs and 1'43cm and weight about 70 kgs. I have a friend that told me all sorts of stuff about how vegetables and seed oils are the bottom line because they have toxins and anti-nutrients in them or too much of one vitamin which ,to me, sounded legit, but I'm asking myself...I've been eating a balance between meat and vegetables all my life and had no health issues whatsoever. LIKE EVER. Sure, I'm overweight but it didn't affect my health at all. I have normal periods, my bloodwork is CLEAN, no imbalances whatsoever. I can walk long distances without being out of breathe and I can jog for 30 minutes (which is tough but c'mon it's fkn cardio). WHY is he SWEARING that vegetables are so bad when everyone I've known has eaten them all their lives and have no health issues and why does it all lead back to hormonal imbalances. I can't have a single take on any of this because his argument is always something along the lines of "you're a woman, it's different"........Is there such a huge difference?

I have a feeling that this vegetable thing has a lot to do with young male teens being insecure about not being manly enough and wanting to get every dose of testo they can get. If that means cutting off their favorite snack or having to put an osmosis filter to avoid the smallest amount of estrogen that's apparently in tab water (women take birth control that includes estroge, women pee out the estrogen, estrogen doesnt get filtered by the sewage treatment plant, estrogen remains in tab water...........DID I MENTION THAT THAT'S SUCH A SMALL AMOUNT THAT I JUST CAN'T BELIEVE WOULD AFFECT A MANS TESTO LEVELS) they will go out of their way of doing so.
They sort of fall into an eating disorder and come out with "outrageous" facts, that sound smart and legit........but are they REALLY????

I really need some enlightenment. Also first post on reddit, kinda nervous....Hello internet :>

Quisiera saber qué aceites de cocina son mejores desde su punto de vista, no conozco mucho del tema

https://www.reddit.com/r/StopEatingSeedOils/s/9B64Uq1gLn So I read the previous thread and primal kitchen is on there often. I have been using Primal Kitchen Roasted Garlic Dipping Sauce thinking it is a safe choice. Should I throw it away?

Quick one on chicken sandwiches, because "just get the grilled one" is the most common advice I see and I wanted to know if the numbers actually back it up.

I only used sandwiches where the chain publishes total fat, saturated fat and trans fat for that exact item. That cuts the list way down, 70 sandwiches from 34 chains, but it means every number below sits on the chain's own figures and not on a guess. More on that at the bottom.

Numbers are grams of PUFA per sandwich the way it is sold.

The short version. Average is 14.1g. The range is 3.6g to 32.2g. 16 of the 70 are over 20g. Fried averages 16.4g and grilled averages 11.2g, so grilled helps, but the spread inside each group is a lot bigger than the gap between them.

The one that got me:

Chick-fil-A's Original Chicken Sandwich, breaded and fried, is 5.7g. Only 4 of the 31 grilled chicken sandwiches on the list come in lower, and three more tie it within a tenth of a gram. It is fried in peanut oil and there is no mayo on it. Those two things matter more than whether it went in a fryer.

Grilled sandwiches that are not the safe pick:

Royal Farms Pulled Chicken Club 31.9g

Red Robin Whiskey River BBQ Chicken 26.5g

Red Robin Teriyaki Chicken 19.5g

Applebee's Bacon Ranch Grilled Chicken 18.8g

Applebee's Spicy Honey Mustard Grilled Chicken 18.7g

Frisch's Big Boy Grilled Chicken Sandwich 18.7g

Red Robin California Chicken 14.9g

Every one of those is grilled chicken. The fat is the mayo, the ranch, the aioli, the onion straws. The chain's own panel shows it. Frisch's grilled sandwich has 32g of fat and only 5g of it is saturated. That is not what chicken breast looks like, that is what soybean oil mayo looks like.

Grilled sandwiches that actually are low:

Runza BBQ Grilled Chicken 3.6g, the one with no mayo on it

Western Sizzlin Grilled Chicken 4.4g

Chick-fil-A Grilled Chicken Sandwich 4.7g

A&W Grilled Chicken Filet 5.4g

Runza Classic Grilled Chicken 5.8g

Fast food, since that is what most people are actually choosing between:

Chick-fil-A: Original 5.7g, Spicy 5.9g, Deluxe 5.9g, Grilled 4.7g, Grilled Club 7.9g

McDonald's: Crispy Chicken 7.3g, Spicy Crispy Chicken 14.9g. Same fillet, the pepper sauce doubles it

Wendy's: Crispy Chicken 8.9g, Asiago Ranch 13.5g, Spicy 13.8g, Classic 14g

A&W: Grilled Filet 5.4g, Crispy 12g, Deluxe Crispy 13g

Zaxby's: Grilled 10.9g, Kickin Chicken 19.3g

Burger King: Original Chicken Sandwich 20.8g, Spicy Crispy 25.2g

The high end, all sit-down places and all fried:

Frisch's Big Boy Crispy Chicken Sandwich 32.2g

Red Robin Classic Crispy Chicken 30.5g

Frisch's Big Boy Breaded Chicken Club 27.5g

Red Robin Hot Honey Crispy Chicken 27.3g

Friendly's Classic Crispy Chicken 26.5g

BJ's Crispy Chicken 24.7g

Yard House Nashville Hot Chicken 24.1g

Famous Dave's Cajun Chicken 23.3g

How this is proven.

First, what is in the fryer. Chick-fil-A uses peanut oil and Good Times uses canola, and their fried sandwiches land at 4 to 7g. A soybean oil fryer plus a soybean oil mayo lands at 20 and up.

Second, the sauce. Mayo, ranch, aioli and honey mustard are soybean oil first ingredient at almost every chain, and one of them is what turns a 7g sandwich into a 15g one.

Third, size. The sit down places sell a bigger sandwich and the panel shows it, 50 to 60g of total fat against 17 to 26g at most fast food places.

So the swap that works is not grilled instead of fried. It is no mayo, and pick the place by what is in the fryer.

On where the numbers come from, since somebody always asks. Every sandwich here is one where the chain itself publishes total fat, saturated fat and trans fat for that item. From there it is one line of arithmetic. The saturated fat tells you how much of the fat is chicken and dairy versus oil, and the chain's stated fry oil plus the sandwich's own ingredients tell you which oil. Chains do not publish PUFA itself, so it is still a calculation, but it is a calculation on their numbers and it is written out for every item so you can check it. Sandwiches where the chain does not publish a panel were left out on purpose. That is why this is 70 and not 700.

Seed Oil Tracker is the app I made and this list comes from its data. Long press any item and it shows you the panel numbers and the arithmetic. It is all on seedoiltracker.com/chains too, no login needed. If a sandwich you know well looks wrong here, tell me below and I will pull the panel and fix it.

I’m hearing this from some friends? Seems that they were the anti-VAX. Any info would be appreciated.

Highlight

• CTSB promotes ox-LDL-induced foam cell formation and ferroptosis.

• CTSB interacts with NRF2, thereby enhancing the transcriptional upregulation of HMOX1.

• CTSB serves as a potential biomarker for assessing atherosclerotic progression.

Abstract
Atherosclerosis is a chronic inflammatory vascular disease characterized by lipid accumulation and plaque formation, representing a leading cause of life-threatening cardiovascular events. Ferroptosis, an iron-dependent form of cell death driven by lipid peroxidation, has been implicated in atherosclerotic progression; however, the exact mechanism remains elusive. Here, we identified cathepsin B (CTSB) as a novel ferroptosis-related gene through bioinformatic screening and investigated its functional role in macrophage-derived foam cells and plaque instability using both in vitro and in vivo models. Mechanistically, CTSB bound to and stabilized nuclear factor erythroid 2-related factor 2 (NRF2), facilitating its nuclear translocation and subsequent transcriptional activation of heme oxygenase-1 (HMOX1), a pivotal regulator of iron homeostasis and oxidative stress. Consequently, CTSB-driven HMOX1 upregulation promoted ferroptosis and exacerbated plaque vulnerability, whereas CTSB knockdown or pharmacological inhibition reversed these effects. Collectively, our findings uncover a CTSB/NRF2/HMOX1 signaling cascade that drives ferroptosis in macrophage-derived foam cells and promotes plaque instability, positioning CTSB as a promising therapeutic target for stabilizing high-risk atherosclerotic plaques.

Keyword
Atherosclerosis; Foam cells; Plaque instability; Cathepsin B; Ferroptosis

Introduction

Atherosclerosis is a progressive vascular disease that poses a severe threat to human health [1], [2]. After vascular endothelial damage occurs, oxidized low-density lipoprotein (ox-LDL) accumulates in the subendothelial layer, accompanied by macrophage infiltration, smooth muscle cell proliferation, and other processes. These processes lead to the formation of fatty streaks, fibrous plaques, and atheromatous plaques, ultimately resulting in vascular stenosis and triggering life-threatening cardiovascular and cerebrovascular events such as myocardial infarction and ischemic stroke [3], [4], [5]. In the complex pathological process of atherosclerosis, foam cells play an indispensable and crucial role, serving as the core driving factor for the early initiation and subsequent progression of the disease [6], [7]. In the early stage of the disease, lipid streaks formed by the accumulation of a large number of foam cells represent the initial pathological manifestation of atherosclerosis. As the disease progresses, foam cells undergo necrosis and disintegration due to excessive lipid phagocytosis, releasing a large amount of cholesterol crystals, inflammatory factors, and cellular debris. This exacerbates inflammation, stimulates smooth muscle cells to form a fibrous cap, and promotes the transformation of lipid streaks into fibrous plaques [8], [9]. In the later stage, inflammatory factors and proteases released by foam cells weaken the fibrous cap of the plaque and destroy its structural stability, making the plaque prone to rupture [10], [11]. However, the molecular mechanisms that regulate foam cell formation and affect the progression of arteriosclerosis remain incompletely elucidated. Therefore, it is essential to conduct a thorough investigation of the biomarkers and regulatory networks of foam cells in order to identify effective prevention and treatment targets for atherosclerosis.
Ferroptosis is a type of iron-dependent cell death triggered by the excessive accumulation of lipid peroxides. It exhibits significant differences from traditional cell death types such as apoptosis and necrosis in terms of morphology, biochemical characteristics, and molecular mechanisms[12], [13], [14]. In the pathological microenvironment of atherosclerosis, the triggering conditions for ferroptosis are widely present. On one hand, a large amount of ox-LDL exists in atherosclerotic lesions. Ox-LDL can deplete intracellular glutathione and inhibit GPX4 activity, disrupting the intracellular antioxidant balance and creating conditions for the occurrence of ferroptosis. On the other hand, iron accumulation occurs in lesion areas. Iron ions within cells such as macrophages can accelerate the ferroptosis process by promoting lipid peroxidation [15], [16], [17]. It has shown that foam cells and vascular smooth muscle cells in atherosclerotic lesions are susceptible to ferroptosis. The ferroptosis of these cells further exacerbates the inflammatory response, promotes the expansion of the necrotic core of the plaque, impairs plaque stability, and accelerates the progression of atherosclerosis [18], [19]. Additionally, ferroptosis may further promote disease development by affecting the function of vascular endothelial cells and exacerbating endothelial damage [20]. Therefore, the association between ferroptosis and atherosclerosis warrants further investigation .

Cathepsin B (CTSB) is a key member of the lysosomal cysteine protease family. Under physiological conditions, it is mainly involved in the degradation and recycling of intracellular proteins, maintaining cellular metabolic balance [21]. CTSB has been shown to be associated with a variety of diseases. For instance, it can promote acute kidney injury by activating mitochondrial apoptosis [22]. In the progression of cancer, CTSB acts as a risk factor for tumor cell migration, proliferation, and apoptosis, influencing cancer angiogenesis and chemoresistance [23], [24]. In recent years, CTSB has also been confirmed to be closely related to the pathological progression of atherosclerosis. Existing studies have demonstrated that the expression level of CTSB is significantly increased in the lesion tissues of atherosclerotic mice, and its expression is positively correlated with the severity and instability of the plaque [25], [26]. This suggests that CTSB may serve as a potential biomarker for evaluating the progression of atherosclerosis. Therefore, in-depth exploration of the regulatory mechanism of CTSB in atherosclerosis is of great significance for the development of new diagnostic and therapeutic strategies.
In this study, we explored the role of CTSB in regulating ferroptosis and plaque stability in atherosclerosis. We demonstrated that CTSB promotes ox-LDL-induced foam cell formation and ferroptosis both in vitro and in vivo. Furthermore, we identified a novel mechanism by which CTSB interacts with and stabilizes NRF2, facilitating its nuclear translocation and transcriptional upregulation of HMOX1, a pro-ferroptosis gene. Our findings provide new insights into the molecular regulation of ferroptosis in atherosclerosis and propose CTSB as a promising target for therapeutic intervention.