How fried food causes cellulite, aging and skin looseness

Oxidised fatty acids in Fried food are major causes of cellulite, skin aging and skin laxity

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• Oxidised fatty acids in Fried food are major causes of cellulite and skin laxity

• Frying, Lipid Peroxidation, glycation, inflammation and cellulite

• Saturated fat peroxidation and coconut oil

• “I only go to expensive restaurants where they use good oil for frying”

• So, shouldn’t I eat fried food ever again?

• To avoid cellulite and cardiovascular disease, fry rarely

• Advanced lipid peroxidation end products in oxidative damage to proteins. Potential role in diseases and therapeutic prospects for the inhibitors

• Check our professional consultancy in radiofrequency, ultrasound cavitation, cellulite and skin tightening

Fried food, the no2 dietary cause of cellulite, after sugar

When to comes to cellulite, skin looseness and even overall health, fried food is one of the worst type of foods you can possibly put in your mouth.

As a cause of cellulite, it is second only to sugar, not because it is better than sugar but because most people eat much more sugar than fried food.

Of course, fried sugary foods, as in the case of doughnuts and pure evil - for your thighs as well as your heart blood vessels.

Fried oils/fats are damaged fats which accumulate in cell membranes, causing chronic, low-grade, whole-body inflammation and damage to all organs and tissues in the whole body, including blood vessels and skin.

Chronic, low-grade, whole-body inflammation and the consequent blood vessel, skin and other tissue damage are hallmarks of cellulite and skin looseness.

So it is no surprise that fried food is one of the three most important dietary causes of cellulite, together with hydrogenated/trans fats and sugar.

Frying, Lipid Peroxidation, glycation, inflammation and cellulite

The high temperatures used during all forms of frying - including sautéing, shallow frying, deep frying and stir frying - leads to Advanced Lipid Peroxidation End-Products (ALEs) and Advanced Glycation end products (AGEs).

Frying to smoking point is even worse, as smoke coming out of food/oil simply means damaged, peroxidised fatty acids. Examples include:

• Using coconut oil to fry "because coconut oil is saturated and therefore stable” (no, isn’t)

• When your kitchen fills with smoke after charring a fatty steak or burger

• Frying at high temperature with smoke being produced from the oil/fat, regardless if it is deep frying, shallow frying or wok frying

Both ALEs and AGEs are proven by multiple studies to cause cell damage, tissue damage and inflammation. One of them clearly states:

“Reactive carbonyl compounds (RCCs) formed during lipid peroxidation and sugar glycoxidation, namely Advanced lipid peroxidation end products (ALEs) and Advanced Glycation end products (AGEs), accumulate with ageing and oxidative stress-related diseases, such as atherosclerosis, diabetes or neurodegenerative diseases.”

The authors of the above study were of course not interested in cellulite but overall human health.

However, given that skin, adipose tissue and blood vessels, are especially vulnerable to glycation, inflammation and oxidative damage, I would definitely add cellulite to the list of the above ageing and oxidative stress-related diseases.

In fact there is a huge overlap between the causes and manifestations of civilisation diseases such as diabetes, cardiovascular disease, cancer and cellulite.

Saturated fat peroxidation and coconut oil

Indeed, saturated fat is less prone to lipid peroxidation, but not always. Coconut oil is a good example of an oil with low smoke point that is easily damaged.

Ideally if you want a healthy, acne-free, cellulite-free, less prone to ageing skin you should minimise the consumption of fried and charred food.

“I only go to expensive restaurants where they use good oil for frying”

Great, I am happy for you that you’re rich. But when it comes to fried food, “expensive” does not mean “healthy”.

Indeed, some restaurants advertise that they use quality oil for frying, so apparently their food is “healthy” 😂

However, the fact is that no restaurant in the entire world fries their tempura or chips or other food with quality oil, used only once, as any health-conscious person would, and should, do at home (once a month or less).

In the best case scenario they would use monounsaturated, high-oleic sunflower oil (which is more stable than the normal polyunsaturated sunflower oil) and in the worst case scenario it could be anything they baptise as “healthy”.

And no street food stall, fast food shop, pub or restaurant would use any sort of cold-pressed, extra virgin, unrefined, organic, non-GMO, “innocent” oil contained in a glass bottle, that health conscious consumers buy. Forget about extra virgin olive oil, of course. It ain’t gonna happen.

It’s more like cheap oil, often from GMO soya or corn, contained in a BPA-lined drum and filled with chemical additives in order to be able to be fried twenty times over - even at upmarket restaurants.

Perhaps at some little traditional restaurant in some forgotten village in Crete, southern Spain or southern Italy they might use locally cold-pressed extra virgin olive oil, because they have so much of it and it is made locally. However, even that is still used - and peroxidised - multiple times.

So, shouldn’t I eat fried food ever again?

“This is extreme, how can I live without fried food or sugar?”, I can hear some saying. To which my answer is “No problem, cellulite or skin ageing doesn’t kill”.

Of course, I could not say that for the “atherosclerosis, diabetes or neurodegenerative diseases” mentioned in the above study, which do indeed kill.

So perhaps the answer is moderation. To minimise oxidative damage, inflammation and glycation from fried food, avoid eating fried food at restaurants or aim for home cooked meals (restaurant food is 90% based on pan frying, shallow frying, deep frying, wok frying, sautée frying etc). And do not fry often at home either.

To avoid cellulite and cardiovascular disease, fry rarely

And when you RARELY do fry:

• Use high quality monounsaturated oil or saturated fat (NOT coconut oil), which are more stable. Do not use ANY other oil, including “saturated fat which is stable”. Saturated fat is indeed stable but it is not that good for you even unfried, despite what instagram says.

• Do not allow the oil/food to smoke - fry at lower temperatures

• Do not over-fry, as in brown/dark brown fries

• Do not reuse any oil after frying with it (yes, it gets very expensive, which takes us back to the previous point of “fry rarely”)

• Do not double-fry or triple-fry (as in refried beans or triple-cooked chips). Who the hell ever thought of this? The crispiness from triple cooked chips comes with extensive peroxidised lipids which a few hours after eating will be incorporated in your heart blood vessel lining cells. Do you want that?

• And do not cover the food with sugar-based marinades (such as BBQ sauce), which will add a lot of AGEs to the ALEs produced by frying. Fried sugar is the worst thing you can put in your mouth.

• Do not fry carbs, as in doughnuts, which will also add a lot of AGEs to the ALEs produced by frying. And as mentioned twice above, never fry sugary food.

Advanced lipid peroxidation end products in oxidative damage to proteins. Potential role in diseases and therapeutic prospects for the inhibitors

• Research paper link: https://pubmed.ncbi.nlm.nih.gov/17643134/

• Abstract: Reactive carbonyl compounds (RCCs) formed during lipid peroxidation and sugar glycoxidation, namely Advanced lipid peroxidation end products (ALEs) and Advanced Glycation end products (AGEs), accumulate with ageing and oxidative stress-related diseases, such as atherosclerosis, diabetes or neurodegenerative diseases. RCCs induce the 'carbonyl stress' characterized by the formation of adducts and cross-links on proteins, which progressively leads to impaired protein function and damages in all tissues, and pathological consequences including cell dysfunction, inflammatory response and apoptosis. The prevention of carbonyl stress involves the use of free radical scavengers and antioxidants that prevent the generation of lipid peroxidation products, but are inefficient on pre-formed RCCs. Conversely, carbonyl scavengers prevent carbonyl stress by inhibiting the formation of protein cross-links. While a large variety of AGE inhibitors has been developed, only few carbonyl scavengers have been tested on ALE-mediated effects. This review summarizes the signalling properties of ALEs and ALE-precursors, their role in the pathogenesis of oxidative stress-associated diseases, and the different agents efficient in neutralizing ALEs effects in vitro and in vivo. The generation of drugs sharing both antioxidant and carbonyl scavenger properties represents a new therapeutic challenge in the treatment of carbonyl stress-associated diseases.

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