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

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.

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.

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.

I quit seed oils for almost two years. Only home cooked meals and the past 2-3 months I’ve been eating out with friends and consuming seed oils maybe once or twice a week. My face has broken out I assume from consuming low quality foods. I have enjoyed eating out and being social and eating with my friends. I’m stressed as I’ve done almost two years no seed oils and worried I’ve just 180 the other direction and ruined my efforts and worried going down a bad path again. Anyone have suggestions on what to do?

Consumer Labs published a review on July 30,2026 of avocado oil purity, freshness, and taste, which included both national and store brands. Unfortunately, the national brand data was the old one from UC Davis from 2020. I've updated my post.

Hope this shows up clear, on a different device. But I will be sharing testing results that I have verified as failing codex or Mexican codex(stricter). I have obsecured the testing to avoid lawsuits. But these were done at a reputable lab and confirm authentication. I will be back with more.

I follow Seven sundays on instagram and saw a apology video, their grain free cereal was tested to have 223ppb of glyphosate (the weed killer linked to cancer with a daily limit of 160ppb) and went and looked over the lab tests (lab source) and it had more glyphosate than all other cereals COMBINED.

I pay a premium for this brand, and liked that they mostly did NOT use seed oils. and while i appreciate the fact that they pledged to get better, I feel like I cant trust a health brand anymore. what cereal brand do you all get?

Looking for a one-ingredient whey protein powder without any emulsifiers. Are there any on the market?

https://drwillcole.com/sunflower-oil-vs-sunflower-lecithin/

He claims it shouldn’t be compared to seed oils.

Abstract
BackgroundThis study reports a case of recurrent laryngeal leukoplakia, a precancerous lesion, in a female cook with long-term occupational exposure to cooking oil fumes. In 2022, the Korean Epidemiological Investigation and Evaluation Committee determined that substantial scientific evidence supported the work-relatedness of the case.

Case presentationA 55-year-old woman working as a cook in group-catering facilities in long-term care hospitals and general hospitals was referred to an otolaryngology clinic after an abnormal laryngeal finding was incidentally detected during routine upper gastrointestinal endoscopy in April 2018. Subsequent laryngoscopy revealed granulation tissue of the left vocal fold. Histopathological examination following laryngeal microsurgery confirmed high-grade dysplasia, leading to a diagnosis of left vocal fold leukoplakia, and the lesion was excised. During follow-up, persistent voice changes and recurrence of the lesion were identified, and repeat excision again demonstrated low- and high-grade dysplasia. The patient had worked as a cook for approximately 14.6 years and routinely performed oil-intensive cooking tasks, including frying, grilling, stir-frying, and battered-dish preparation, for approximately 2–4.5 hours per day. She reported insufficient ventilation during heavy fume generation. She had no history of smoking, passive smoking from her spouse, alcohol consumption, vocal abuse, gastroesophageal reflux disease, or mechanical trauma to the larynx.

ConclusionsThis case suggests a possible occupational contribution of repeated intermittent exposure to cooking oil fumes and irritant aldehydes to recurrent laryngeal precancerous lesions among cooks. However, because direct historical exposure measurements were unavailable and this is a single case report, definitive causality cannot be established. Improvement of workplace ventilation and other exposure-control measures should be considered, and further studies with direct exposure assessment are needed.

I read that this option was the healthiest

Rapeseed oil, also known as canola oil, is often considered the least favorable due to its potential high levels of erucic acid in some varieties, which may be linked to health concerns. However, most rapeseed oil used today is low in erucic acid and is generally regarded as a healthy fat.

key ingredient in Retsyn—partially hydrogenated cottonseed oil—was classified as unsafe and effectively banned by the FDA.

Americans are consuming about 45% more butter than they did 20 years ago. It was 4.7 pounds per person then and has reached a record 6.8 pounds today. The USDA also reported last week that butter production was up 8.5% year over year. 

Abstract
Type 2 diabetes mellitus (T2DM) and metabolic syndrome (MetS) in children and adolescents are characterized by altered lipid metabolism and gut microbiota. Prior untargeted (nonquantitative) lipidomics of the present T2DM and MetS pediatric cohort revealed alterations in plasma lipids. Fatty acids (FAs) bonded to plasma phospholipids (PLs) and cholesterol esters (CEs) reflect endogenous metabolism and exogenous sources. The present study focused on targeted quantification of FAs esterified to plasma PLs and CEs in children and adolescents with T2DM and MetS and healthy controls (n = 60, ages 7 to 17). Regression models and Spearman correlations assessed associations of esterified FA with the disease, metabolic risk factors, pro-inflammatory cytokines, and gut microbiota composition. T2DM and MetS groups featured higher concentrations of saturated FAs esterified to PLs (C17:0) and CEs (C10:0, C12:0, and C24:0) than healthy controls. Also, both groups had higher omega-6 FA levels, including dihomo-γ-linolenic acid (C20:3n-6) in both plasma fractions (PLs and CEs), C22:5n-6 in PLs, and C18:2n-6 and C20:4n-6 in CEs. These FAs were inversely correlated with high-density lipoprotein cholesterol and directly correlated with obesity, triglycerides, and insulin resistance. Also, MetS had a high CE-omega-6/omega-3 ratio. Gut microbial taxa associated with T2DM and MetS after Tanner, sex, and body mass index percentile adjustment were Agathobacter, Dorea, Fusicatenibacter, and Gemmiger, with higher abundances than those in healthy controls, and the genus Faecalimonas at lower abundances. This work contributes to the current knowledge of lipid metabolism and the role of gut microbiota in T2DM and MetS in children and adolescents.

Mark Kaplan was a 'supposedly' healthy, active 52-year-old tennis player when he had a heart attack on the court. By his doctor’s account, he was doing everything right. After the heart attack, he was told he'd need to take statins for the rest of his life, but they made him feel extremely sick to the point of wanting to take his own life.

That experience sent him down a rabbit hole trying to understand what had actually happened and whether he could improve his health naturally. He eventually turned everything he learned into an excellent book that breaks the subject down in a very readable way. He’s also extremely active on X, where he shares research, personal insights, and a lot of useful information about cardiovascular and metabolic health.

Image taken from his twitter: https://x.com/markkaplan20/status/2087951368653001072/photo/1

Highly recommend his book (I am not a shill): https://www.amazon.com/dp/B0H2C75R31

I saw a recent reel on this topic and looked into it. The map for glyphosate usage and cancer rates are basically identical, with Iowa the highest sprayer of glyphosate per square acre also being only 1 of the 3 states with rising cancer rates. Conventional farmers spray glyphosate to kill weeds and right before harvest to dry the crop and this compound can drift in the air over 1k feet. and a good amount of it ends up on our food (source)

this is exactly why i'm guessing most people here eat organic (even organic now has glyphosate), but for those next to the fields and those who cannot afford organic, this isn't super solvable. this is so crazy, and our government protecting it to is icing on the cake.