Deep Fried Food, What Is Your Opinion?

[General Orange]

Other than AGE, is frying doing anything else that would be bad to get a lot of? Or could it be that the negative health association here is mainly due to PUFA use being so common in fried food?

Changes in food caused by deep fat frying - A review

...The process is based on the oil-food interaction at high temperatures, which cooks and dehydrates the food, leading to physical and chemical changes, such as starch gelatinization, protein denaturation, flavoring and color production via Maillard reaction. Some food and oil compounds are lost in the frying process, and potentially toxic compounds are developed in the oxidized oil. Although widely studied, many of these compounds have not been fully identified. The purpose of this study was to review literature findings on changes in food caused by the frying process....

 

[General Orange]

Biological Effects of Frying Oils Mediated by the Activation of Peroxisome Proliferator-Activated Receptors (PPAR)

"Feeding experiments using rats, mice, and pigs revealed that ingestion of frying oils, compared with fresh fats, provokes a wide array of biological effects in mammals including oxidative stress [1-4], impaired glucose tolerance [5], and thyroid function and lipid metabolism alterations [6-10]. At least some of these, in particular the alterations in lipid metabolism, are mediated by profound changes in gene expression. Recent studies clearly demonstrated that characteristic substances of frying oils such as 9-HODE, 13-HODE, and 13-HPODE as well as CFAM are potent ligands and activators of peroxisome proliferator-activated receptors (PPAR) [11-15]. These nuclear receptors, which include the three subtypes α, β/δ, and γ, are transcription factors that can be activated by FA and their metabolites (e.g. eicosanoids). However, the potency of different FA and FA metabolites to bind and activate PPAR varies greatly, and hydroxylated FA are stronger activators of PPAR than their respective nonhydroxylated counterparts. This probably explains why administration of fresh fats to animals causes only a weak activation of PPAR."

- It appears frying oils (vegetable) also have some positive effects also, from the article.

Positive effects:

Presumably, the PPARα activating property of frying oils also contributes to its preventive effect on alcoholic fatty liver development - a state in which hepatic FA catabolism is impaired owing to ethanol-induced blockade of PPARα function. Using a rodent model of alcoholic fatty liver it could be demonstrated that administration of a frying oil causes an activation of hepatic PPARα as evidenced by increased transcript levels of PPARα-regulated genes involved in FA catabolism in rat liver despite sustained feeding of ethanol [15]. This suggests that frying oil increases the capacity of the liver to oxidize FA and thus counteracts the elevated levels of triacylglycerols and the diminished PPARα function during ethanol-feeding.

French fries munchies goes well with binge drinking, I guess.
...

Reduced cholesterol concentrations in liver and plasma associated with feeding of frying oil [2,7] are probably due to negative regulation by frying oil of genes involved in cholesterol homeostasis.

...
Conclusions
Through the activation of PPAR, which have both stimulatory and inhibitory effects on gene transcription, components of frying oil are capable of regulating gene expression positively and negatively. Stimulatory (positive) effects on gene expression are largely responsible for regulatory effects of frying oil on lipid and lipoprotein catabolism as well as carnitine homeostasis, whereas the regulatory effects of frying oil on FA, triacylglycerol, and cholesterol synthesis are mediated by inhibitory (negative) effects of frying oil on gene expression.

 

[Glassy]

I must be about 6 months Peating now and I got a hankering for some hot chips (fries). I looked into finding a shop that uses tallow/lard as a base oil and just decided to make some myself. I rendered the tallow from a whole rump and made some chips. I couldn’t get them crispy without turning them a dark brown colour (I might have to trying cooking them in oil twice as I just blanched them in water).

The taste was amazing. Even the darkest ones which I would never have eaten normally were tasty. No weird after taste and didn’t leave me feeling disgusting afterwards. They felt more satisfying to my appetite.

The fat content alone is enough to not do it regularly but it’s nice to know it can be done while Peating and it’s worth the effort. I might have to start making beef stock again as buying tallow just seems wrong and the stock yields a lot. Most beef in Australia is raised on pasture and finished on grain. Not ideal but the other alternative was coconut oil and I’m not sure that would taste as great.

 

[lvysaur]

I've seen many people say that before, and I've always experienced worse symptoms after a bowl of sauteed restaurant fare than after a few pieces of fried chicken.

 

[postman]

Heat damages food and the more heat there is the more damage there will be. Acrylamides, heterocyclic amines, lipid peroxides, carbs and protein and fat all are damaged.

I would maybe have it as a treat every now and then but not as a staple of my diet. And palm oil is way too unsaturated.

 

[General Orange]

I must be about 6 months Peating now and I got a hankering for some hot chips (fries). I looked into finding a shop that uses tallow/lard as a base oil and just decided to make some myself. I rendered the tallow from a whole rump and made some chips. I couldn’t get them crispy without turning them a dark brown colour (I might have to trying cooking them in oil twice as I just blanched them in water).

The taste was amazing. Even the darkest ones which I would never have eaten normally were tasty. No weird after taste and didn’t leave me feeling disgusting afterwards. They felt more satisfying to my appetite.

The fat content alone is enough to not do it regularly but it’s nice to know it can be done while Peating and it’s worth the effort. I might have to start making beef stock again as buying tallow just seems wrong and the stock yields a lot. Most beef in Australia is raised on pasture and finished on grain. Not ideal but the other alternative was coconut oil and I’m not sure that would taste as great.

Animal fats with cholesterol heated above 120 degree celcius will oxidize the cholesterols. Cholesterol oxides get in tissue and can lead to atherosclerosis.

edit link: True or False? Butter, Ghee, Lard & Tallow - Are Saturated Animals Fats the Kings and Queens of the Frying Pan? - SuppVersity: Nutrition and Exercise Science for EveryoneTrue or False? Butter, Ghee, Lard & Tallow - Are Saturated Animals Fats the Kings and Queens of the Frying Pan? - SuppVersity: Nutrition and Exercise Science for Everyone

 

[Nicole W.]

Honestly I’ve just been craving fallafel lately. FWIW, AGE should be much higher in high protein foods than in low protein foods. Pre-blanching, and then breading and flash deep frying - in the right oil could potentially bring out some Maillard reaction flavor / with less risk then pan frying or roasting ( both which require longer cooking times). If I’m not mistaken, longer cook times and higher heats are both bad for AGE.

I think falafel might be the main driver of/ explanation for the Israeli Paradox, lol.

 

[Travis]

I think falafel might be the main driver of/ explanation for the Israeli Paradox, lol.

That's initially funny, but quickly loses all humor potential upon a few seconds' reflection. This is actually most likely true, and we should all have a moment of silence for all the falafel-induced tumors in Israel: [...] The Israelis generally eat a whole-food diet high in antioxidants and vitamins, yet also have a high mortality rate. From what I recall, the presumed 'paradox' had been derived from this fact yet also on account of Israeli cardiovascular disease incidence. The Israelis have the highest intake of omega−6 fatty acids on the globe, having a ω−6∶ω−3 ratio approaching 20∶1. Since the hopelessly-backwards partly line of modern cardiology predicts Israelis to have low cardiovascular disease, an apparent 'paradox' arises once it's realized they have one of the highest.

'Coincidence is what you have left over when you apply a bad theory.' ―Percy Bridgman​

The six-pointed Star of David had likely been created to signify to position of the first double bond of linoleic acid, the national fatty acid of Israel—one point for each carbon removed from the omega end. Long-chained omega−6 fatty acids displace omega−3 fatty acids from the cell membrane, leading to significant changes in physical properties. Dozens of physicochemical studies plainly indicate that DHA (22∶6ω−3) has the strongest propensity for excluding cholesterol from cell membranes, a capacity related to the degree of unsaturation yet particularly demonstrated by DHA. Docosahexaenoic acid has the greatest water solubility, kinetic energy, and volume of any membrane lipid; it also has a unique geometry, or 'kink.' Physicochemical studies plainly demonstrate that osbond acid (22∶6ω−6), the omega−6 product that mimics DHA, is much less capable in it's ability to exclude cholesterol from cell membranes and reconstituted micelles. Epidemiological studies and postmortem analysis confirm this trend, and so do long chain inhibitors of DHA synthesis such as erucic acid (22∶1ω−9).

The term 'cardiovascular disease' is somewhat generic one, and I contend there are a few distinct layers and mechanisms involved. Although Linus Pauling's paradigm of cardiovascular disease perfectly explains arterial weakness and embolisms, I think the cell membrane DhA∶ObA ratio is the most powerfully determinant of a vessel's cholesterol affinity. The idea that omega−6 fatty acids would contribute to cell membrane cholesterol affinity would be actually be predicted from the data gathered through in vitro cholesterol–lipid studies, such as this one.

 

[x-ray peat]

fwiw Dr Jennifer Daniels claims that fried food is extremely dehydrating on the body and that it ages you prematurely.
no way to verify

 

[raypeatclips]

The six-pointed Star of David had likely been created to signify to position of the first double bond of linoleic acid, the national fatty acid of Israel—one point for each carbon removed from the omega end.

If I ever had to choose a sentence that I know nobody else in the world had ever spoken, this would be my choice.

 

[yerrag]

Honestly I’ve just been craving fallafel lately. FWIW, AGE should be much higher in high protein foods than in low protein foods. Pre-blanching, and then breading and flash deep frying - in the right oil could potentially bring out some Maillard reaction flavor / with less risk then pan frying or roasting ( both which require longer cooking times). If I’m not mistaken, longer cook times and higher heats are both bad for AGE.

I like this. Deep frying is the fastest way to cook. It tastes the best as well. With the oil being hot enough, oil isn't absorbed so much as the water vapor from the meat is constantly oozing out, keeping the oil out.

I now start to appreciate the use of batter, which keeps the protein from being burned, and AGE products are minimized.

This is counter-intuituve, but the higher heat involved in deep frying makes the cooking time much shorter, and I could argue that deep frying is a healthy way to cook.

As long as it's the good oils that are used. For me, it has to be fully hydrogenated coconut oil or beef tallow, which is already fully saturated. And I say this giving a finger to CPSI, who ran a campaign against beef tallow, causing Mickey D's to ditch it for PUFA oil!

 

[General Orange]

As long as it's the good oils that are used. For me, it has to be fully hydrogenated coconut oil or beef tallow, which is already fully saturated. And I say this giving a finger to CPSI, who ran a campaign against beef tallow, causing Mickey D's to ditch it for PUFA oil!

"tallow (109mg of cholesterol / 100mg)" good luck frying with that.

""I always pour away the oil! I am safe, right?" If I had not heard this argument before I would certainly not mention that the oxidized cholesterol does make it into the fried products. In a study from 1991, Zhang et al. report that the average content of the measured forms of oxidized cholesterol in french fries that had been fried in fresh, previously unoxidized tallow at a fast food restaurant ranged from 1.6-3.8 mg/100g and thus 3-8x more than Pie et al. found in a rare steak (>0.5mg /100g after 3 minutes of cooking) or cooked pork (>0.56mg /100g) in 1991 or those reported by Al-Saghir et al. for cooked farmed salmon (0.33-0.9mg/100g; cf. Al-Saghir. 2004 -- the table on the left is a fully referenced overview of COP levels in various foods from Otaegui-Arrazola. 2010)."

 

[yerrag]

"tallow (109mg of cholesterol / 100mg)" good luck frying with that.

""I always pour away the oil! I am safe, right?" If I had not heard this argument before I would certainly not mention that the oxidized cholesterol does make it into the fried products. In a study from 1991, Zhang et al. report that the average content of the measured forms of oxidized cholesterol in french fries that had been fried in fresh, previously unoxidized tallow at a fast food restaurant ranged from 1.6-3.8 mg/100g and thus 3-8x more than Pie et al. found in a rare steak (>0.5mg /100g after 3 minutes of cooking) or cooked pork (>0.56mg /100g) in 1991 or those reported by Al-Saghir et al. for cooked farmed salmon (0.33-0.9mg/100g; cf. Al-Saghir. 2004 -- the table on the left is a fully referenced overview of COP levels in various foods from Otaegui-Arrazola. 2010)."

This isn't me trolling, but how can beef tallow, being a saturated fat, be oxidized and be also called oxidized cholesterol?

Can you oxidize what is already saturated?

 

[Travis]

Because tallow also has approximately...

...(109mg of cholesterol / 100mg)...

 

[Travis]

If I ever had to choose a sentence that I know nobody else in the world had ever spoken, this would be my choice.

You've seen that masonic triangle right? Well; what do you suppose their 'big secret' really is?

 

[yerrag]

Because tallow also has approximately...

Like water has 109/110mg of dihydrogen oxide? And that makes it very acidic with 2 hydrogen atoms?

 

[Travis]

Like water has 109/110mg of dihydrogen oxide? And that makes it very acidic with 2 hydrogen atoms?

Some would consider approximately one part cholesterol per hundred significant . . . and 110 milligrams of H₂O actually has 7.33 × 10²¹ hydrogen atoms and 8.53 × 10¹⁹ deuterium atoms.

 

[Captain_Coconut]

That's initially funny, but quickly loses all humor potential upon a few seconds' reflection. This is actually most likely true, and we should all have a moment of silence for all the falafel-induced tumors in Israel: [...] The Israelis generally eat a whole-food diet high in antioxidants and vitamins, yet also have a high mortality rate. From what I recall, the presumed 'paradox' had been derived from this fact yet also on account of Israeli cardiovascular disease incidence. The Israelis have the highest intake of omega−6 fatty acids on the globe, having a ω−6∶ω−3 ratio approaching 20∶1. Since the hopelessly-backwards partly line of modern cardiology predicts Israelis to have low cardiovascular disease, an apparent 'paradox' arises once it's realized they have one of the highest.

'Coincidence is what you have left over when you apply a bad theory.' ―Percy Bridgman​

The six-pointed Star of David had likely been created to signify to position of the first double bond of linoleic acid, the national fatty acid of Israel—one point for each carbon removed from the omega end. Long-chained omega−6 fatty acids displace omega−3 fatty acids from the cell membrane, leading to significant changes in physical properties. Dozens of physicochemical studies plainly indicate that DHA (22∶6ω−3) has the strongest propensity for excluding cholesterol from cell membranes, a capacity related to the degree of unsaturation yet particularly demonstrated by DHA. Docosahexaenoic acid has the greatest water solubility, kinetic energy, and volume of any membrane lipid; it also has a unique geometry, or 'kink.' Physicochemical studies plainly demonstrate that osbond acid (22∶6ω−6), the omega−6 product that mimics DHA, is much less capable in it's ability to exclude cholesterol from cell membranes and reconstituted micelles. Epidemiological studies and postmortem analysis confirm this trend, and so do long chain inhibitors of DHA synthesis such as erucic acid (22∶1ω−9).

View attachment 10119

The term 'cardiovascular disease' is somewhat generic one, and I contend there are a few distinct layers and mechanisms involved. Although Linus Pauling's paradigm of cardiovascular disease perfectly explains arterial weakness and embolisms, I think the cell membrane DhA∶ObA ratio is the most powerfully determinant of a vessel's cholesterol affinity. The idea that omega−6 fatty acids would contribute to cell membrane cholesterol affinity would be actually be predicted from the data gathered through in vitro cholesterol–lipid studies, such as this one.

Do you think getting DHA through diet or supplementation is important for optimal health? The omega3 to omega6 ratio...

 

[Travis]

Do you think getting DHA through diet or supplementation is important for optimal health? The omega3 to omega6 ratio...

I think it's practically unavoidable, and the bigger danger is ω−6 fatty acids displacing the small yet ubiquitous amounts of α-linolenic acid (18∶3ω−3) found naturally in leaves and grass-fed dairy. Practically all the DHA found in non-fish-eating mammals had initially been elongated and desaturated from α-linolenic acid. Omega−6 fatty acids such as linoleic (18∶2ω−6) and γ-linolenic (18∶3ω−6) acids compete with α-linolenic acid (18∶3ω−3) at the elongation/desaturation stage, the former two intending to become arachidonic (20∶4ω−6) and osbond (22∶5ω−6) acids while the latter vies to become eicosapentaenoic (20∶5ω−3) or docosahexanenoic (22∶6ω−3).

linoleic ⟶ γ-linolenic ⟶ dihomo-γ-linolenic ⟶ arachidonic ⟶ osbond​

α-linolenic ⟶ eicosatetraenoic ⟶ eicosapentaenoic ⟶ docosapentaenoic ⟶ docosahexanenoic​

The first step of elongation/desaturation outlined above yields the eicosanoids, shown in red. The omega−6 dihomo-γ-linolenic and arachidonic acids are directly analogous to omega−3 eicosapentaenoic acid and displace it from similar locations. These are the only three lipid precursors of prostaglandins:

dihomo-γ-linolenic ⟶ prostaglandin E₁

arachidonic ⟶ prostaglandin E₂

eicosapentaenoic ⟶ prostaglandin E₃
​

All three prostaglandin types have variable activity. Since humans had evolved equitorally, it could be fair to consider the 3-series prostaglandins the more natural ones. Studies indicate that prostaglandin E₃ has about ¹⁄₄ the potency of prostaglandin E₂, and the leukotrienes differ even more in potency: Neutrophils are attracted to leukotriene B₄ at concentrations 5000 × lower than leukotriene B₅. Leukotriene B₃, synthesized from Mead acid (20∶3ω−9), is about five times less potent.

Mead acid ⟶ leukotriene B₃

arachidonic ⟶ leukotriene B₄

eicosapentaenoic ⟶ leukotriene B₅
​

Mead acid is the omega−9 eicosanoid created during omega−6 restriction. Mead acid can form a leukotriene yet it cannot form a prostaglandin; cyclooxygenase will hydroxylate this lipid yet will not cyclize it. Unfortunately, the longer 22-carbon lipids do not seem to have a functional omega−9 analogue so we cannot make them ourselves. The docosanoids don't appear to have a hormonal function are are strictly functional membrane lipids.

linoleic ⟶ γ-linolenic ⟶ dihomo-γ-linolenic ⟶ arachidonic ⟶ osbond

α-linolenic ⟶ eicosatetraenoic ⟶ eicosapentaenoic ⟶ docosapentaenoic ⟶ docosahexanenoic
​

The sum of osbond + DHA in the brain appears to be a constant, always falling within the range of 14–17% in the grey matter. It appears as though we must choose one type or the other, and since omega−6 fatty acids are invariably associated with pathology I think we should choose 'the other.' Omega−6 fatty acids compete with omega−3 fatty acids during multiple stages during the four-carbon elongation/desaturation phase, making their dietary ratio of critical importance.

Despite its name, osbond acid will not make you feel like a secret agent. This lipid cannot exclude cholesterol from the cell membrane as well as DHA and its' presence there yields less glucose-permeable membranes. The substitution of DHA with osbond acid has implications in both insulin resistance and cardiovascular disease.

Unstable docosahexaenoic acid needs never to be consumed because its precursor α-linolenic acid is found in leaves and grass-fed dairy/beef. I am aware of the idea that 'all DHA is initially synthesized in the liver before it travels to the brain,' yet I somewhat doubt this because 18-carbon endogenous lipids are freely found there—i.e. linoleic acid. Radiolabeled oleic acid has also been shown to cross the blood brain barrier, so it could be wise to consume the more stable α-linolenic acid because its direct brain transport seems certain. Since we all eat this already, it makes more sense to simply avoid omega−6 with increased diligence. This way, we can ensure a proper DHA∶osbond ratio while keeping lipofuscin to a minimum. Lipofuscin increases with age in non-mitotic neurons, slowly lowering their metabolism until death. Postmortem analysis of centenarians reveal that lipofuscin can account for up to 75% of the internal volume in motor neurons.

 

[Captain_Coconut]

I think it's practically unavoidable, and the bigger danger is ω−6 fatty acids displacing the small yet ubiquitous amounts of α-linolenic acid (18∶3ω−3) found naturally in leaves and grass-fed dairy. Practically all the DHA found in non-fish-eating mammals had initially been elongated and desaturated from α-linolenic acid. Omega−6 fatty acids such as linoleic (18∶2ω−6) and γ-linolenic (18∶3ω−6) acids compete with α-linolenic acid (18∶3ω−3) at the elongation/desaturation stage, the former two intending to become arachidonic (20∶4ω−6) and osbond (22∶5ω−6) acids while the latter vies to become eicosapentaenoic (20∶5ω−3) or docosahexanenoic (22∶6ω−3).

linoleic ⟶ γ-linolenic ⟶ dihomo-γ-linolenic ⟶ arachidonic ⟶ osbond​

α-linolenic ⟶ eicosatetraenoic ⟶ eicosapentaenoic ⟶ docosapentaenoic ⟶ docosahexanenoic​

The first step of elongation/desaturation outlined above yields the eicosanoids, shown in red. The omega−6 dihomo-γ-linolenic and arachidonic acids are directly analogous to omega−3 eicosapentaenoic acid and displace it from similar locations. These are the only three lipid precursors of prostaglandins:

dihomo-γ-linolenic ⟶ prostaglandin E₁

arachidonic ⟶ prostaglandin E₂

eicosapentaenoic ⟶ prostaglandin E₃
​

All three prostaglandin types have variable activity. Since humans had evolved equitorally, it could be fair to consider the 3-series prostaglandins the more natural ones. Studies indicate that prostaglandin E₃ has about ¹⁄₄ the potency of prostaglandin E₂, and the leukotrienes differ even more in potency: Neutrophils are attracted to leukotriene B₄ at concentrations 5000 × lower than leukotriene B₅. Leukotriene B₃, synthesized from Mead acid (20∶3ω−9), is about five times less potent.

Mead acid ⟶ leukotriene B₃

arachidonic ⟶ leukotriene B₄

eicosapentaenoic ⟶ leukotriene B₅
​

Mead acid is the omega−9 eicosanoid created during omega−6 restriction. Mead acid can form a leukotriene yet it cannot form a prostaglandin; cyclooxygenase will hydroxylate this lipid yet will not cyclize it. Unfortunately, the longer 22-carbon lipids do not seem to have a functional omega−9 analogue so we cannot make them ourselves. The docosanoids don't appear to have a hormonal function are are strictly functional membrane lipids.

linoleic ⟶ γ-linolenic ⟶ dihomo-γ-linolenic ⟶ arachidonic ⟶ osbond

α-linolenic ⟶ eicosatetraenoic ⟶ eicosapentaenoic ⟶ docosapentaenoic ⟶ docosahexanenoic
​

The sum of osbond + DHA in the brain appears to be a constant, always falling within the range of 14–17% in the grey matter. It appears as though we must choose one type or the other, and since omega−6 fatty acids are invariably associated with pathology I think we should choose 'the other.' Omega−6 fatty acids compete with omega−3 fatty acids during multiple stages during the four-carbon elongation/desaturation phase, making their dietary ratio of critical importance.

Despite its name, osbond acid will not make you feel like a secret agent. This lipid cannot exclude cholesterol from the cell membrane as well as DHA and its' presence there yields less glucose-permeable membranes. The substitution of DHA with osbond acid has implications in both insulin resistance and cardiovascular disease.

Unstable docosahexaenoic acid needs never to be consumed because its precursor α-linolenic acid is found in leaves and grass-fed dairy/beef. I am aware of the idea that 'all DHA is initially synthesized in the liver before it travels to the brain,' yet I somewhat doubt this because 18-carbon endogenous lipids are freely found there—i.e. linoleic acid. Radiolabeled oleic acid has also been shown to cross the blood brain barrier, so it could be wise to consume the more stable α-linolenic acid because its direct brain transport seems certain. Since we all eat this already, it makes more sense to simply avoid omega−6 with increased diligence. This way, we can ensure a proper DHA∶osbond ratio while keeping lipofuscin to a minimum. Lipofuscin increases with age in non-mitotic neurons, slowly lowering their metabolism until death. Postmortem analysis of centenarians reveal that lipofuscin can account for up to 75% of the internal volume in motor neurons.

An extreme depth of knowledge. I will need to read this a few times over. In your opinion, what would be the best way to get good intake of DHA on a poor man's diet?