Frying Does not Just Oxidize Oils, It will Also Decimate the Tocopherol & Tocotrienol Content of the Oils and Can Thus More Than Double the Oxidative Burden on Your Body

Fried butter on a stick - I bet there are more peroxides in the crust than in the butter beneath it.

Yesterday we have taken a look at the saturated fat content of the diet and its effects on body composition, insulin resistance and inflammatory markers (see "Study Shows Doubling Saturated Fats Would Yield More Benefits Than Halving Them"). Today, we are going to look at the effects of a way not just Americans, but more or less half of the globe likes to process their foods on the oils and subsequent health of someone who would consume these oils on a regular basis. By now, you will probably already know into which direction this post is heading. Right, we are talking about frying, about lipid oxidation and about the health effects of oxidized soy bean and palm oil the #1 "choices" in processed foods.

Oxidized frying oils and their effects on our health

The paper by Jaarin and Kamisah, two researchers from the Department of Pharmacology at the Universiti Kebangsaan Malaysi in Malaysia is certainly not the only, maybe not even the latest study dealing with this issue, what I like about it though, is the fact that they don't use some sort of standardized oxidized oil, but actually went through the following unquestionably not unrealistic procedure to obtain their frying oils:

"A kilogram of sweet potato slices were fried in a stainless steel wok containing two and half litres of palm oil or soy oil for 10 minutes at 180°C. Upon completion of the frying process, once heated oil was obtained. The process was repeated four times to obtain five times heated oil with a cooling interval of at least five hours. The food quantity was proportionately adjusted with the amount of vegetable oil left. No fresh oil was added between the frying processes to make up for the loss due to uptake by the frying materials." (Jaarin. 2012)

After the oils had been heated, a small quantity was extracted and the peroxide value, fatty acid composition and vitamin E content measurements (another strength of the study, most other studies discard the fatty acid composition and vitamin E content).

Figure 1: Peroxide levels (data expressed relative to fresh palm oil) of palm and soy oil after frying at 180°C for 10minutes once or five times (based on Jaarin. 2012)

If you take a look at the peroxide values in figure 1 you see that the peroxide values in both the palm and the soy oil increased significantly after only one heating process (10min at 180°) already and -- at least in the case of soy oil -- exceeded the established maximally allowed value (red line). The palm oil, on the other hand is slightly below the margin. Now that obviously does not mean that the palm oil was still 100% healthy, while the soy oil was toxic waste - it's rather an artifice due to the arbitrarily set 10meq/kg limit for lipid peroxides in oils that are meant for human consumption (the Japanese must by the way be 'peroxide proof' because their laws allow concentrations up to 30meq/kg!).

Figure 2: Relative fatty acid composition of the fresh, once or five times heated oils (based on Jaarin. 2012)

A mechanistic explanation for the fact that the soy oil presents a higher total peroxide level than the palm oil can easily be derived from the data in figure 2. As you can see,...

"[...t]he fresh soy oil contained about five times more polyunsaturated fatty acid compared to the palm oil. It seemed that five times heating had reduced about 10% of the polyunsaturated fatty acid content in the soy oil. The content of monounsaturated fatty acid in the fresh palm oil was higher than that of the fresh soy oil. Palm oil had a quite balanced ratio of saturated and unsaturated fatty acids, whereas more than 70% of soy oil fatty acid was unsaturated (polyunsaturated and monounsaturated). This unique fatty acid composition of palm oil renders its stability against oxidative insult." (Jaarin. 2012)

Now, both the oxidation process during heating as well as the in vivo oxidative effects of the consumption of those oils does not depend on their fatty acid makeup and oxidation status, only, but is also affected by the amount of antioxidants, in particular vitamin E, the respective oil brings to the table.

Figure 3: Relative amount of tocopherols and tocotrienols that remained in the oils after frying (left) and effects of the consumption of a diet containing 15% of the oils + 85% standard rodent chow for 4 months on male and ovariectomized rats that received additional +2% cholesterol in their diets on thiobarbituric acid reactive substances (TBARS), astandard marker of lipid oxidation (right;(based on Jaarin. 2012)

In that, the vitamin E content is not only important to protect you from the effects of the peroxides that are already in the oil, they are at least as important to protect the polyunsaturated fatty acids you consume from being oxidized in your body.

Against that background, is should be obvious that the profound reductions in both tocopherols and tocotrienols will augment the negative effects, so that it is actually not that surprising that the amount of thiobarbituric acid reactive substances (TBARS = standard marker of lipid oxidation) in the blood of the rodents which consumed the diets with 15% of the five times heated palm and soy oil more than doubled.

Figure 4: While olive oil is more stable than corn and soy, it's not 'oxidation proof either' what's also intriguing is the amount of oxidation that is induced just by exposing the oil to air or air and light for 30 days! (Naz. 2012)

Putting things into perspective: While I would hope that no one of you will use the same oil for frying twice or thrice, let alone five times, I am not so sure about the foods you would be served at the university canteen, let alone the fast food store around the corner. Against that background, it is however still at least unsettling to see that even when you are frying potatoes or meats in a pan at home, the T-BAR levels rise significantly.

I assume that no one of you will use soy oil and only few will be cooking with palm oil, but I know that many people still use olive oil in a hot pan for several minutes. And while I do not have data from the same study, the data in figure 5 would suggest that olive oil is probably as susceptible to heat as palm oil (if you go by the relations of palm:soy in the study at hand and olive:soy in the study by Naz et al.). If we go by this rule of thumb estimate, baking your potatoes in olive oil may not kill you, but clearly isn't the best way either.

Coconut oil!? No, unfortunately even the wonder oil does not come to a rescue. At least if we go by the data Matthäus obtained in 2007, it produces about as much peroxides as palm oil during the frying process (Matthäus. 2007). That's better than soy, and way below the critical margin, but still not without consequences on the overall oxidative burden you are exposing yourself to, when you consume significant amounts of fried foods on an everyday basis - and since I know that you do only have your occasional piece of fried grass fed butter on a stick, you won't have to be afraid anyway ;-)

Suggested reads:

• Pimp my virgin olive oil - Discusses among other things how the polyphenols stabilize the vitamin E and render EVOO more heat stable than regular olive oil.
• Vitamin(s)! E - A brief reminder that there is more than alpha-tocopherol + some evidence that delta tocopherol is king, when it comes to protect dietary oils

References:

• Matthäus, B, Use of palm oil for frying in comparison with other high-stability oils. Eur. J. Lipid Sci. Technol. 2007;109: 400–409. 
• Jaarin K, Kamisah Y. Repeatedly Heated Vegetable Oils and Lipid Peroxidation. Intech. 2012.
• Naz S, Siddiqi R, Sheikh H, Sayeed SA. Deterioration of olive, corn and soybean oils due to air, light, heat and deep-frying  Food Research International, Volume 38, Issue 2, March 2005, Pages 127–134.

Tocotrienols: What They Are, What They Do & How They Work + Why the RDA of Palm Olein is NOT 1xCup Per Day

Image 1: If you wanted to get the tocotrienol levels a producer of respective supplements says are  "required", you would have to eat at least 200g palm fruits a day. Alternatively, you can resort to 4kg of oats, if you like those better... What? you are wondering that you are not dead by now? After so many years of tocotrienol deficiency from not getting your 4kg of oats?

The long lists of pathologies related to vitamin E deficiency include, among others, all sorts of degenerative diseases from ataxia over general muscle degeneration to degeneration of sperm and subsequent infertility. But despite the fact that there is a pretty substantial amount of evidence that would suggest that a diet rich in vitamin E could not just prevent the aforementioned pathologies, but would also protect us from many of the currently prevalent ailments of western society such as obesity and coronary vascular disease (Mishra. 2003; Rimm. 1993), respective trials with dietary supplements usually show no, or even negative effects. I have already addressed a couple of  reasons why the benefits of dietary vitamin E intake often cannot be replicated with supplements in previous posts. The most significant one, probably is the absence of the "right" mixture and ratio of alpha-, beta-, gamma- and delta-tocopherols and, as an emerging contributer, the total absence of tocotrienols in the vast majority of vitamin E supplements and almost 99.9% of the pertinent trials.

What are tocotrienols? And what do they do?

I could now rant about the structural differences between the two, with the tocotrienols being an unsaturated variety of the tocopherols with a isoprenoid side chain, but I guess it is enough to know that due to  differences in their molecular structure, they also differ in their effects on the human body, of which you may already have apprehended that their cholesterol lowering effects were the first to attract the attention from researchers (Qureshi. 1986). Within the last 26 years researchers from all around the world have identified additional health benefits, the most prominent of which are...

• Anti-cancer effects (Kato. 1985; Sundram. 1989; Weng. 2009),
• General antioxidant effects (Newaz. 1999),
• Brain specific antioxidant effects (Khanna. 2003),
• Exercise-specific antioxidant effects (Lee. 2009),
• Cardiovascular disease (Shibata 2009)
• Diabetic neuropathy (Kuhad. 2009)
• Bone health (Ahmad. 2005)
• Metabolic syndrome (Weng. 2011)
• Antithrombotic effects (Qureshi. 2011)
• Endocrine health (Yu. 2005)
• Liver health (Patel. 2012)

The purpose of today's SuppVersity article is yet not so much to compile the most extensive list of potential, purported or demonstrated benefits of tocotrienols, the major dietary sources of which are (Kobayashi. 1975; Tan. 2011)

• rice bran oil (50:50 tocopherol:tocotrienol ratio), 
• palm oil (25:75 tocopherol:tocotrienol ratio), and 
• annatto (0.1:99.9 tocopherol:tocotrienol ratio) oil
• human breast milk (!) [though this is probably no major source for you ;-]

but rather to take a look at an intriguing chart of the various molecular targets (Aggarwal. 2010) and discuss the implications:

Figure 1: Molecular targets (left) and proteins that directly interact with tocotrienols (right; adapted from Aggarwal. 2010)

As you can see  without even looking really close at the above graphic, the number of those targets is vast. Another thing you should see right away is that the effect of the tocotrienols is mostly inhibitory (red ovals in the left) and include a couple of old foes, such as:

• the inflammatory cytokines & transcription factors: IL-1, IL-6, TNF-alpha, nf-kappabeta, IL-8 (probably involved in auto-immune reactions), PF-A4 (increases platelet aggregation and thus thrombosis risk)
• factors involved in angiogenesis and cardiocascular disease: VEGF (vascular growth factor, involved in CVD) and its receptor VEGF-r, VCAM-1 (increases adhesion of immune cells to the endothelial wall)
• kinases involved in the cell cycle and apoptotic regulators: CDK's, PKC, pERK, etc. & survivin, IAP-1 & 2 etc., but also telomerase, which are all involved in the proliferation of cancer
• enzymes involved in inflammatory processes: eNOS, iNOS, COX-2, etc.

On the upregulatory side of things, we have

• enzymes from the CYP cascade, which are among other involved in the clearance of estrogen, and other hormone like substances and the metabolism of drugs,
• MAPK and JNK, which exert anti-catabolic effects on muscle tissue, or 
• GPX and SOD, two of the major enzymes involved in the antioxidant defenses

Now, if we take a look at all these, you may remember that low COX-2 levels have only recently been identified with profound overtraining (cf. "Overtraining inflammation insufficient repair"), that AKT (not mentioned above, but in figure 1) is one of the driving forces of skeletal muscle anabolism and telomerase, extends cell life in general, not just in cancer cells. Which brings us back to the issue of ...

...how much anti-oxidants do we actually need?

Figure 2: Total tocopherol and tocotrienol content of high vitamin E foods / oils (top) and tocopherol ratios (bottom) , data based on Whittle. 1967 and Slover. 1971

Or, in this particular case, how much tocotrienols are still beneficial? Neither I, nor anybody else knows the exact answer to this question. And against this fact, the recommendations I came across on the website of a major producer of respective supplements, which state that you would need

• 80g of palm oilen (cooking oil),
• 160g of rice bran oil,
• 3kg of barley,
• 1.5kg of wheatgerm, or 
• 4kg of oats

to (I quote) "achieve the required [my emphasis] level of tocotrienols" should tell any reasonable person that those "required" levels (~150mg) are probably required to generate the target revenue of the said company, yet probably not required for you or any other human being to thrive.

Do not stack one more, but take one out!

Instead of adding another overpriced (and probably overdosed) tocotrienol supplement to your regimen, it is thus probably wiser to simply drop any superflous and potentially harmful alpha-tocopherol only supplements which do would offset the alpha- to gamma- and delta- tocopherol ratio (this could potentially be ameliorated by taking a natural blend) and limit the total tocopherol intake to reasonable levels, as the latter has also been shown to hamper the absorption and retention of tocotrienols (Ikeda. 2003). In this context it is also noteworthy that Ping Tou Gee writes in a 2011 paper with the aptly chosen title "Unleashing the untold and misunderstood observations on vitamin E" that this fact alone would suggest that "there is a need to review critically on the dietary reference intakes recommendations" for alpha tocopherol (α-T). His bold statement that

[i]t is not known whether α-T is still essential to humans in long terms, α-T₃ [alpha tocotrienol] diet appeared to produce healthy rats over five generations.

is yet probably an attribution to Palm Nutraceuticals Sdn. Bhd. (which is not the aforementioned company which wants to force-feed you either their supplements or 2 cups of rice bran oil), of which he states in the acknowledgments that he thanks them "for permission to publish this paper" and further evidence for how pathetic parts of the research in the medical field is - awful this science business, isn't it?

References:

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2. Ahmad NS, Khalid BA, Luke DA, Ima Nirwana S. Tocotrienol offers better protection than tocopherol from free radical-induced damage of rat bone. Clin Exp Pharmacol Physiol 2005;32:761–770 
3. Gee PT. Unleashing the untold and misunderstood observations on vitamin E. Genes Nutr. 2011 Feb;6(1):5-16. Epub 2010 Jul 20.
4. Ikeda S, Tohyama T, Yoshimura H, Hamamura K, Abe K, Yamashita K. Dietary alpha-tocopherol decreases alpha-tocotrienol but not gamma-tocotrienol concentration in rats. J Nutr. 2003 Feb;133(2):428-34.
5. Kato A, Yamaoka M, Tanaka A, Komiyama Ka, Umezawa I. Physiological effect of tocotrienol. J
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6. Khanna S, Roy S, Ryu H, Bahadduri P, Swaan PW, Ratan RR, et al. Molecular basis of vitamin E
   action: tocotrienol modulates 12-lipoxygenase, a key mediator of glutamate-induced
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7. Kobayashi H, Kanno C, Yamauchi K, Tsugo T. Identification of alpha-, beta-, gamma-, and delta-
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8. Kuhad A, Chopra K. Attenuation of diabetic nephropathy by tocotrienol: involvement of NFkB
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11. Newaz MA, Nawal NN. Effect of gamma-tocotrienol on blood pressure, lipid peroxidation and total antioxidant status in spontaneously hypertensive rats (SHR). Clin Exp Hypertens 1999;21:1297–1313.
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