Believe it or not raw food vegans, it takes scrambled (whole) eggs to turn your veggie salads into a "superfood", or rather, to have the "super effects" of all its "super vitamins" on your health . The photo shows an egg-recipe from The Organic Dish, take a look; and don't worry if you're afraid of healthy oats, you can leave out the out cakes under the eggs ;-)
I still see people throwing the good yolk of their eggs away. Shame on you! You're not just throwing the most nutrient dense (also in terms of nutrients per energy content) away, you also sacrifice the beneficial effects of the co-ingestion of eggs with other nutrient dense foods - benefits which have only recently been recognized by the scientific community when people finally starting looking beyond individual foods and nutrients and started to investigate the actual and practically more relevant effects of food matrices.
This trend that began with the negative effects of pesticides and/or heavy metals in "real meals" (which are always food matrices | Wilkowska. 2011) is something I have written about in the Facebook News and individual articles before and I plan to re-address, whenever scientists like Kim, Ferruzzi & Campbell (2016) give them the deserved attention.
You aren't interested in vitamns? Maybe in fasting for health and fatloss, then?
Breakfast and Circadian Rhythm
Does Meal Timing Matter?
Habits Determine Effects of Fasting
Fasting Works for Obese, Too!?
Alternative Day Fasting "Rulez"!
Intermittent Fast-ing + Weights!?
Why's that? Well, as it turns out and has just been confirmed for beta-carotene and vitamin E (Kim. 2015 & 16) by the aforementioned authors from the Purdue University (Kim. 2016) the way you combine your foods is as important for your nutrient sufficiency as the micronutrient content of the individual foods.
Let's do some math, together: For the fat-soluble vitamins E, which are obviously relevant in the context of Kim et al.'s latest studies (2015 & 16), the RDA is 14 mg/day. That's the amount of vitamin E you'd get from a relatively small quantity of each of the randomly chosen high vitamin E foods in Figure 1.
Figure 1: Yes, you can get your vitamin E from a single food, but that's not wise - for several reasons (Kim. 2016).
The bad news is that for all for of them it is not clear whether you will actually absorb all the vitamin E, so that it can do its anti-oxidant magic in your bloodstream. Yes, for wheat germ oil, sunflower seeds, and almonds, the relatively high fat content is one out of many potentially relevant cofactors (including cooking methods, the type of dietary lipids, and interactions with digestive enzymes or other dietary | Eitenmiller. 2004) compounds for the optimal uptake of fat-soluble vitamins such as vitamin E (learn more).
The paprika powder from Figure 1, no matter how nutrient dense it may be, will probably get only small amounts of its vital (=vitamin and other beneficial micronutrients) carriage (including, but not restricted to beta-carotene and vitamin E) delivered into your blood... unless, obviously, you combine it with the right foods and thus form a nutrient absorption optimizing food matrix.
Figure 2: Kim's 2015 study showed a similarly pronounced increases of the accumulated area under the curve (AUC), i.e. the total uptake of various carotenes when 3 eggs were added to vegetable salad (made with 3g of canola oil).
A food matrix consisting of three scrambled eggs and vitamin-(A)-rich vegetable salad of which Kim's previous study showed that it increased the bioavailability of beta-carotene 8-fold (see Figure 2). In the current study (Kim. 2016), the authors did thus speculate that...
"[b]ecause carotenoids and vitamin E are both fat-soluble nutrients, we expected cooked whole eggs to also increase the absorption of vitamin E contained in the same salad" (Kim. 2016).
to evaluate the accuracy of their hypothesis, the scientists recruited 16 healthy male participants for a randomized, single-blind, crossover-design experiment:
"[All] participants completed 3 trials that each included consuming a controlled diet for 7 d followed by a testing day. In addition, 1-wk dietary washout periods were scheduled between each of the trials. [...] The investigators were fully blinded to the participants test-day meals until after all testing and sample analyses were completed, but the participants and dietitians were not blinded to the meals" (Kim. 2016)
Obviously, I am not giving away any secrets, when I tell you that the experiment confirmed the authors' hypothesis. Interestingly enough, with practically relevant increases in vitamin E absorption being achieved with both, the "low egg" (LE - 1.5 cooked scrambled eggs) and the "high egg" (HE - 3 cooked scrambled eggs) vegetable salads, which contained, just as in the previous study, 100 g tomatoes, 62 g shredded carrots, 70 g baby spinach, 25 g romaine lettuce, and 5 g Chinese wolfberries, and was served with 3 g of canola oil (note: all vegetables and eggs were purchased from the same local market and brand throughout the study period, thus we can assume that the contents of alpha-tocopherol and gamma-tocopherol in the test salad were 2.1 and 2.0 mg/serving, respectively, for all three trials).
Figure 3: Relative increase (per vitamin E intake in mg) in TRL levels of alpha- and gamma-tocepherol in response to the ingestion of the vegetable salad alone, the salad with 1.5 or 3 cooked scrambled whole eggs (Kim. 2016)
In fact, the increase in the levels of alpha- and gamma-tocopherol in the subjects' triacylglycerol-rich lipoprotein fractions (TRLs) was even more pronounced than that of the carotenes in Kim et al.'s 2015 study. Since eggs contain sign. amounts of vitamin E, themselves (they don't contain, alpha-, beta-carotene and lycopene), we do yet have to look at the relative (i.e. relative uptake of amount of vitamin E that was ingested) uptake levels I have plotted for you in Figure 3. For these, the increases for alpha- and gamma-tocopherol were 'only' 107%, 144%, 441% and 358% in the 1.5 egg LE and the 3 egg HE group, respectively.
That the former, i.e. the increase in the LE = 1.5 egg trial didn't reach statistical significance is, as the authors rightly point out, most likely "due to the small sample size and low statistical power" (Kim. 2016) - a phenomenon that has been observed previously in small-scale studies that compared the nutrient availability of vitamin E with different doses of fat (Mah. 2015 | this study also used a less preferable marker of vitamin E absorption, namely plasmo not triacylglycerol-rich lipoprotein fractions (TRLs) levels, which mainly represent newly absorbed dietary vitamin E, as the studies by Kim et al.).
Highly Suggested Read: "Egg-Ology Today: The Underappreciated Health Benefits of Egg Phospholipids, Prote-ins & Antioxidants in the Yolk" | more.
Bottom line:Whole eggs are good for you! If you want to know what, i.e. which substance or nutrient (many of which I've discussed in the article you can read by clicking on the three eggs to the right) it is that gives eggs this ability, you will yet have to continue getting your EOD dose of SuppVersiy articles and Facebook News, because Kim's latest study was not designed to "assess the specific impact of [different] components of egg yolk on vitamin E absorption" (Kim. 2016)... after two studies showing significant benefits, however, we can be almost sure that a follow up study will be conducted; and if so, I can guarantuee that I will address it here or in the SV Facebook News, where you can also comment on this article!
References:
Eitenmiller, Ronald R., and Junsoo Lee. Vitamin E: food chemistry, composition, and analysis. CRC Press, 2004.
Kim, Jung Eun, et al. "Effects of egg consumption on carotenoid absorption from co-consumed, raw vegetables." The American journal of clinical nutrition 102.1 (2015): 75-83.
Kim, Jung Eun, Mario G. Ferruzzi, and Wayne W. Campbell. "Egg Consumption Increases Vitamin E Absorption from Co-Consumed Raw Mixed Vegetables in Healthy Young Men." The Journal of Nutrition (2016): First published ahead of print September 21, 2016 as doi: 10.3945/jn.116.236307
Mah, Eunice, et al. "a-Tocopherol bioavailability is lower in adults with metabolic syndrome regardless of dairy fat co-ingestion: a randomized, double-blind, crossover trial." (2015).
Wilkowska, Angelika, and Marek Biziuk. "Determination of pesticide residues in food matrices using the QuEChERS methodology." Food Chemistry 125.3 (2011): 803-812.
Some butter on top of the broccoli would allow for the assimilation of the absorption of the 101.6μg vitamin K
623IU vitamin A (various).
There are a handful of very basic questions in nutrition science, no one appears to have an answer to. One of these questions, which is directly related to the well-known fact that the vitamins A, D, E & K are "lipid soluble". This means that they are "solved" and thus made absorbable by fats and oils. The general assumption is thus that the vitamins A, i.e. the retinol and carotenoids, all forms of vitamin D, the tocopherols and -trienols (vitamins E) and the two major forms of vitamin K, i.e. phylloquinone (K1) and menaquinone (K2) will only be absorbed, if you consume them with a sufficient amount of dietary fat. Now, the questions obviously are (a) is this correct and (b) how much is sufficient.
Is there a rule of thumb? Well, I guess if there was one, it would be to consume 5-10g of low PUFA fats with every meal to maximize the absorption of fat-soluble vitamins. Needless to say, that this does not imply that you'd have to start adding olive oil to your post-workout shake ;-)
In view of the fact that the answers to (a) and be are not necessarily identical for all four vitamins of interest, it appears sensible to tackle them one after the other.
A
Starting with vitamin A and the various forms of carotenoids, we can already confirm that (a), i.e. the assumption that we need dietary fats to optimally absorb vitamin A is correct. As Karin van het Hof and her colleagues point out, the "amount of dietary fat required to ensure carotenoid absorption [does yet] seem low (∼3–5 g per meal), although it depends on the physicochemical characteristics of the carotenoids ingested." (van het Hof. 2000) In spite of the fact that 5g of fat are not exactly much, the classic uncooked vegetarian orthorexic salad often comes with a total of only 5g of fat of which 95% remain at the bottom of the salad bowl. If that sounds like your favorite dish, you should be aware that you are risking that all the good beta- and other carotenoids in the salad will pass right through.
Red Palm Oil is an excellent carotene source that comes with tons of fat for optimal absorption | learn more
With carotenes you should keep in mind that they have individual and "vitamin A"-related effects that occur after their conversion to retinol and the uptake of the latter through the lymphatic system in the gut. For this to take place the presence of a couple of ~5g of fat (Jayarajan. 2013) in the intestinal lumen is paramount importance. Even more than preformed vitamin A, carotenes do thus rely on the presence of dietary fat in your meals to be optimally converted (Goodman. 1966) and absorbed.
Figure 1: Changes in hepatic vitamin A (retinol) and carotenoid stores in gerbils after 14 days on high fat (30%) vs. low fat (10%) diet (Deming. 2000)
In that, the concomitant presence of both dietary fat and carotenoids in a meal is a necessary prerequisite for the absorption of vitamin A, also because the fatty acids will trigger the conversion of of beta-carotene into vitamin A and its subsequent absorption via the lymphatic system (Ribaya‐Mercado. 2002). It is thus not surprising that animal studies by Lakshman et al. (1996) and Deming et al. (2000; see Figure 1) suggest that low fat diet can lead to a depletion of the vitamin A tissue stores even if the serum levels remain constant. The amount of fiber in the diet, on the other, has no influence the absorption of vitamin A (Mills. 2009).
Interestingly enough, the provision of the fat blocker Orlistat reduces the absorption of vitamin A only insignificantly, as a 1996 paper by Angela T. Melia, Susan G. Koss‐Twardy, and Jianguo Zhi would suggest (Melia. 1996).
E
Which takes us right to vitamin E, the absoprtion which is - in spite of being "blocked" by the fat blocker orlistat (Melia. 1996) - less susceptible to the absence of dietary fat than you may think. Annet JC Roodenburg, Rianne Leenen, Karin H van het Hof, Jan A Weststrate, and Lilian BM Tijburg do in fact argue that the optimal intake of vitamin E requires only "a limited amount" of dietary fat (Roodenburg. 2000).
Figure 2: Vitamin E serum levels after 7 days on control (low fat, 3g) or high(er) fat (36g) diet with and without supplemental vitamin E (Roodenburg. 2000)
As you can see in Figure 2. A minimum intake of only 3g per day was sufficient to keep the vitamin E levels stable. The short study period of 7-days (each) and the absence of measures of tissue concentration of vitamin E do yet reduce the practical relevance of the data, Roodenburg et al. present in their Y2k paper in the American Journal of Clinical Nutrition.
The PUFA advantage: Aside from the issue of serum vs. tissue levels, there is yet another experimentally verified fat vitamin E and fat carotenoid interactions we should take into consideration, when we are talking about "optimizing" our dietary vitamin E supply; and that's the type of fat we consume: Dietary fats with increased ratio of unsaturated to saturated fatty acids enhance absorption of carotenoid and vitamin E by increasing both efficiency of micellarization and lipoprotein secretion (Chitchumroonchokchai. 2010).
If you take a look at the high prevalence of vitamin E dieficiency among the fat (and PUFA) "loving", or at least eating, majority of Americans, it does yet become obvious that a lack of dietary fat is not just theoretically, but also practically not exactly the #1 reason you may become deficient in tocopherols and -trienols. That the latter is an increased demand due to chronic inflammation and the (over-)consumption of exactly those PUFAs that come with a shitload of vitamin E in nature, for a reason would yet be a topic for another SuppVersity article and thus something we will skip to fast forward to ...
K
...Vitamin K, obviously. Vitamin K is a relative newcomer to the public's understanding of the alphabet soup. Aside from being it a good tool to rip customers vitamin K, or rather K1 (plant sources) and K2 (animal sources) are thus also the only fat soluble vitamins not everyone knows. The fact that the amount of phylloquinone (K1) that makes it into your blood stream is ~70% reduced if you eat your spinach without fat (Gijsbers. 1996).
And if we take the results researchers from the Gifu University School of Medicine present in a 1996 paper in the Journal of Pharmacological Sciences, as a reference, the amount of fat you need to optimally absorb your K2 (menaquinones), is not exactly low.
Figure 3: For optimal absorption of K2, there has got to be a huge amount of fat in the meal - but who wonders. K2 comes with a high amount of fat (Uematsu. 1996)
Uematsu et al. had to supply their subjects, who consumed otherwise identical test meals with 8.8, 20.0 and 34.9g of fat in them with the maximal (i.e. 35g) of fat before the K2 absorption maxed out. In that the total area under the curve did not really differ between those subjects who consumed the K2 before and those who took it immediately after the test meal.
That's a pity, 'cause a high intake of vitamin K (menaquinone from animal sources) has been associated with a 27% reduced risk of developing heart disease (Geleijnse. 2004), an ailment of which many still believe that it was brought about by the fat they need to optimally absorb their vitamin K.
D
For vitamin D, our last "V" on the list, things look differently. For one, everybody knows about this miracle vitamin and for two, it may be "fat soluble", but the amount of fat that's required to optimally absorb it turned out to be much lower than previously thought (see "A Fat D-Ficiency! Do You Really Need More Vitamin D or Simply More Fatty Foods? Study Shows, Even 50.000 IU of Vitamin D3 Useless, When You Ingest It Without Fat. " | read more).
Actually you could argue that it's not fat, but cholesterol that should be essential for optimal D levels. It's not necessary to absorb supplements you should not be taking, but rather as a raw material that's used to produce vitamin D in the skin, once the latter is exposed to the sun. The allegedly logical assumption that statins which lower the production of endogenous (=your body's own) cholesterol would lower vitamin D levels, however, has been refuted in study investigating the effects of fluvastatin and rosuvastatin, of which the latter actually increased the 25-OHD levels (probably due to anti-inflammatory effects and a reduced use of vitamin D as an acute phase reactant | learn more)
In fact, Niramitmahapanya et al. found in 2011 that it's not necessarily a high amount, but rather the right type of fat that determines if and how much of the vitamin D you take in capsule form or find in comparably low amounts in your foods that determines how much of the vitamin D actually makes it into your bloodstream:
"The change in plasma 25OHD (nanograms per milliliter) during vitamin D
supplementation was positively associated with MUFA, (β = 0.94; P = 0.016), negatively associated with PUFA, (β = −0.93; P = 0.038), and positively associated with the MUFA/PUFA ratio (β = 6.46; P = 0.014)."
In plain English this means, that the "good" seed and vegetable oils with their high PUFA content will effectively inhibit the absorption of vitamin D - an observation that adds to the many reasons the modern sedentary, sun-avoiding, sun-screen using, soybean oil (MUFA:PUFA = 0.4) guzzling American is low in or quasi devoid of vitamin D.
Figure 4: 25(OH)D
levels of 30 healthy men and women after ingestion of 50.000IU vitamin
D3 supplement in conjunction with a normal or low fat breakfast (Raimundo. 2011)
Against that background it's not surprising that you will not find a conclusive answer to the question how much fat you actually need. In a study that used a fatty meal with soybean oil in it, the effect would be totally different from one in which the subjects consumed meals that were made with sunflower oil, an oil with a MUFA:PUFA ratio >1. In view of the results Gnadinger et al present in a recent appear it does still seem appropriate to consume at least some fat alongside your vitamin D supplements. As far as the food-borne vitamin D is concerned, you don't have to worry, anyways. Foods that are high in D3 usually come with all the fat you need to absorb it.
How much fat, exactly you would need to make the most of dietary and supplemental vitamin D, on the other hand, is still not known. The previously mentioned data from the study by Raimondo et al. (see Figure 4, to the right) I wrote about in "A Fat D-Ficiency" is obviously still valid. The extremely high amount of vitamin D (50,000IU!) could yet require a correspondingly high amount of fat to be optimally absorbed and the fact that the fat in the study came from a "vegetable margarine" with an undisclosed ratio of MUFA:PUFA does not make the real-world effects any more predictable.
So what do I need to optimally absorb my "fat soluble" vitamins?
Vitamin A & carotenes require relatively high amounts of fat for optimal absorption.
Vitamin D absorption benefits from additional fat in the diet. While we don't know the optimal amount, we do know the optimal type: A high MUFA, low PUFA fat (the effects of saturated fat are unknown, but I gather they will be positive, as well).
Vitamin E requires only minimal amounts of fat (~3g) for optima absorption.
Vitamin K appears to be most fat hungry. The more fat you have in a meal, the better it is absorbed. If you supplement, always take the pills with your highest fat meal in the day.
Bottom line: If you take a look at the natural sources, it should be obvious. The fat soluble vitamins are meant to be consumed with fat... well, not really. Carotenes (pre-vitamin A), one of those vitamins for which the presence of dietary fat in a meal is most important do not necessarily come with their own "absorb me better"-portion of fat. Your carrots, pepper, and other high carotene veggies and fruits do thus require a butter, olive oil or cream topic not just to be absorbed, but - more importantly - to get converted to retinol aka "active vitamin A".
Vitamin E, on the other hand, requires much lower amounts of fat to be absorbed than many of you may have thought. In fact, you could argue that good vitamin E sources are not high in fat to facilitate the absorption of vitamin A, but rather the other way around: Soybean oil (my absolute favorite poison ;-) is high in vitamin E to make sure that whoever consumes it does not die immediately from the pro-inflammatory omega-6 load it contains.
Which takes us right to the 18-20g and 12-15g of PUFAs the average US man and woman consume on a daily basis (Kris-Etherton. 2000) and their negative impact on the absorption of the already low amounts of dietary vitamin D in a diet that rarely contains the optimal amount of 35g of fat in meal that actually has a significant amount of vitamin K the absorption of which would be improved by the presence of this allegedly unhealthy and fattening macronutrient.
References:
Chitchumroonchokchai, Chureeporn, et al. "Dietary fats with increased ratio of unsaturated to saturated fatty acids enhance absorption of carotenoid and vitamin E by increasing both efficiency of micellarization and lipoprotein secretion." FASEB J 24 (2010): 539-3.
Deming, Denise M., et al. "Amount of dietary fat and type of soluble fiber independently modulate postabsorptive conversion of β-carotene to vitamin A in Mongolian gerbils." The Journal of nutrition 130.11 (2000): 2789-2796.
Geleijnse, Johanna M., et al. "Dietary intake of menaquinone is associated with a reduced risk of coronary heart disease: the Rotterdam Study." The Journal of nutrition 134.11 (2004): 3100-3105.
Gijsbers, Birgit LMG, Kon-Siong G. Jie, and Cees Vermeer. "Effect of food composition on vitamin K absorption in human volunteers." British Journal of Nutrition 76.02 (1996): 223-229.
Goodman, Dew S., et al. "The intestinal absorption and metabolism of vitamin A and beta-carotene in man." Journal of Clinical Investigation 45.10 (1966): 1615.
Jayarajan, P., Vinodini Reddy, and M. Mohanram. "Effect of dietary fat on absorption of β carotene from green leafy vegetables in children." Indian journal of medical research 137.5 (2013).
Kris-Etherton, P. M., et al. "Polyunsaturated fatty acids in the food chain in the United States." The American journal of clinical nutrition 71.1 (2000): 179S-188S.
Lakshman, M. R., et al. "The effects of dietary taurocholate, fat, protein, and carbohydrate on the distribution and fate of dietary β‐carotene in ferrets." (1996): 49-61.
Melia, Angela T., Susan G. Koss‐Twardy, and Jianguo Zhi. "The effect of orlistat, an inhibitor of dietary fat absorption, on the absorption of vitamins A and E in healthy volunteers." The Journal of Clinical Pharmacology 36.7 (1996): 647-653.
van het Hof, Karin H., et al. "Dietary factors that affect the bioavailability of carotenoids." The Journal of nutrition 130.3 (2000): 503-506.
Raimundo, Fabiana Viegas, et al. "Effect of high-versus low-fat meal on serum 25-hydroxyvitamin D levels after a single oral dose of vitamin D: a single-blind, parallel, randomized trial." International journal of endocrinology 2011 (2011).
Ribaya‐Mercado, Judy D. "Influence of Dietary Fat on β‐Carotene Absorption and Bioconversion into Vitamin A." Nutrition reviews 60.4 (2002): 104-110.
Roodenburg, Annet JC, et al. "Amount of fat in the diet affects bioavailability of lutein esters but not of α-carotene, β-carotene, and vitamin E in humans." The American journal of clinical nutrition 71.5 (2000): 1187-1193.
Uematsu, Toshihiko, et al. "Effect of dietary fat content on oral bioavailability of menatetrenone in humans." Journal of pharmaceutical sciences 85.9 (1996): 1012-1016.
All nuts are good tocopherol (T) sources, but α- T is predominantly found in peanuts, almonds and sunflower seeds, while γ-T is the major vitamin E in walnuts, pecans and pistachios.
Over the past week I've been questioning the potency of various supplement superstars with respect to their ability to improve your, my or any one else's glucose metabolism. We've dealt with protein, peptides, fats, vitamin D, calcium, a whole host of B-vitamins and even the underrated vitamin A (go back and review all of them).
Today I am going to take a look at a "fallen star", vitamin E, once thought of as a panacea and universal protector of your cells, it has, at the latest with publication of the disappointing, if not shocking results of the SELECT trial in 2013 and the mass-media reverberations about increased prostate cancer risk, become the centerpiece (literally) of every anti-vitamin supplement rant.
You can learn more about this topic at the SuppVersity
Proteins, Peptides & Blood Glucose
SFA, MUFA, PUFA & Blood Glucose
Vitamin D & Diabetes
Glucose Manager Calcium?
Flush & No-Flush Niacin & Diabesity
Vitamin C & Glucose Control
Table 1: Tocopherol / -trienol compo-sition of select oils (Juang. 2014); mind the association of PUFA + γ- and MUFA + α-tocopherol.
You will probably remember that I have criticized the design and interpretation of the results of the often- and in my eyes over-cited SELECT trial on several occasions. And even if there was a +17% increase in cancer risk in young men who are stupid enough to take 400 IU of all rac-α-tocopheryl acetate, everyday (Klein. 2011), this does not necessarily exclude that the same effects occur if the vitamin E comes from a natural source and contains the whole vitamin E alphabet from alpha- over gamma to delta-tocopherol.
Not in spite of, but rather because of the existing evidence that vitamin E could cause prostate cancer and, when it's consumed with vitamin C, inhibit the beneficial adaptation processes that are triggered by the "eu-stressor" (=good stress) exercise, it is yet even more important that we take a closer look at the actual negative effects vitamin E supplements exert on your ability to control your blood sugar levels.
Vitamin E ➫ insulin resistance ➫ cancer?
I mean, think about it: What is the best growth environment for cancer? Right, sugar coated cells - a study by Stattin et al. (2007) has after all been able to show that to an the risk of developing any form of cancer increases almost linearly from the bottom to the top quartiles of fasting and postprandial glucose levels.
Figure 1: Risk increase for various cancer if fasted [F] and post-glucose load [P] blood glucose levels are in the fourth vs. first quartile; the hazard ratios were calculated based on data from the 33,293 femal and 31,304 male subjects of the Västerbotten Intervention Project of northern Sweden (Stattin. 2007)
If we assume that vitamin E does inhibit the anti-diabetic adaptations to exercise (in conjunction with vitamin C, it does just that; cf. Ristow. 2009), it would increase the risk of having extreme blood sugar excursions, of which the data in Figure 1 reveals that they, in turn, could be the reason vitamin E was found to be associated with an increased cancer risk.
Prostate cancer and high glucose levels? Unlike other forms of cancer, prostate cancer does not appear to flourish in high glucose environments. At least that's what the epidemiological evidence suggests. Evidence which may be flawed by the existence of a genetic variant with opposite effects on risk of type 2 diabetes and prostate cancer (Gudmundsson. 2007), which could partly explain the null association between glucose and prostate cancer in our study as well as the consistently reported reduced risk of prostate cancer in men with type 2 diabetes (Kasper. 2006).
The question we have to answer in today's installment of the "There is More to Glucose Control Than Low Carb", would thus be: Does vitamin E a protective, a detrimental, or no influence on the development of insulin and type II diabetes ... and the answer is: As usually, complicated.
First things first - What actually is vitamin E?
I have already hinted at the fact that "vitamin E" is a generic term that is usually falsely applied to alpha-tocopherol, only. When we are talking about vitamin E, we do yet have to look at the whole spectrum of vitamins E, which include the three tocopherols, as well as their rare tocotrienol buddies.
Tocopherols - α-, γ, and δ- and relates substances
Tocotrienols - α-, γ, and δ- and related substances
They are a class of chemical compounds many of which have vitamin E activity. This series of organic compounds consists of various methylated phenols. Because the vitamin activity was first identified in 1936 from a dietary fertility factor in rats, it was given the name "tocopherol" from the Greek words "τόκος" [birth], and "φέρειν", [to bear or carry] meaning in sum "to carry a pregnancy," with the ending "-ol" signifying its status as a chemical alcohol.
α-Tocopherol is the main source found in supplements and in the European diet, where the main dietary sources are olive and sunflower oils, while γ-tocopherol is the most common form in the American diet due to a higher intake of soybean and corn oil.
There is no RDA or other recommendation for the intake of the three most common tocopherols, i.e. α-, γ, and δ- tocopherol. The currently recommended intake for "vitamin E" is thus based on the concept of alpha-tocopherol equivalents. A very sketchy idea that's probably flawed due to significant differences in the metabolism and uptake of the various tocopherols between rodents and humans.
In view of the fact that dietary vitamin E provides - assuming you don't follow the standard American diet - a balanced mix of tocopherols, you don't really have to care about the accuracy of the conversion factors.
Tocotrienols are members of the vitamin E family. An essential nutrient for the body. The slight difference between tocotrienols and tocopherols lies in the unsaturated side chain having three double bonds in its farnesyl isoprenoid tail.
Tocotrienols are natural compounds found in select vegetable oils, including rice bran oil and palm oil, wheat germ, barley, saw palmetto, anatto, and certain other types of seeds, nuts, grains, and the oils derived from them. This variant of vitamin E typically only occurs at very low levels in nature.
At the moment we still know too little about this form of vitamin E to be able to tell how much of them you actually need. It is in fact not even sure that they are necessary at all.
Contemporary evidence does yet appear to suggest important functional differences between tocopherols- and -trienols that have the latter appear as the more potent cousins of the good old tocopherols. Furthermore, emerging evidence suggest that some long-chain vitamin E metabolites have even stronger anti-inflammatory effects than their vitamin precursors.
Unless you plan to live on artificial foods, alone, the rare tocotrienols will yet never fully replace the omnipresent tocopherols.
Table 2:Brief overview of some of the basic fact about the two main forms of vitamin E (partly based on the Wikipdia entries and on information from a soon-to-be-published review by Jiang)
This is unfortunately, where things get complicated. For one, 99% of the studies have been conducted with alpha-tocopherol, only. For two, the vast majority of the few studies that investigate potential effects of other "vitamins E" on glucose control use either another form of tocopherol, or tocotrienols. A study that would investigate the effects of the whole spectrum of vitamins E, let alone their interactions, on the other hand, has still to be conducted.
☇ Let's start with epidemiological evidence, today
That being said, out best and most realistic starting point is not the classic randomized controlled trial, but "epidemiological guesswork". As long as we are talking about food-borne vitamin E, we are always talking about a natural mix. A mix, which was (unfortunately) often measured in alpha-tocopherol units, but would, in the absence of supple of which studies show that the following associations (remember: epidemiology cannot prove cause-effect relationships)
Low vitamin E intakes (<10mg/day, i.e. 15IU) have been associated with and correspondingly low serum levels have been associated with 3.9x increased diabetes risk back in 1995, when vitamin E was still everybody's darling (Salonen. 1995). In view of the relatively low threshold level, this is yet rather a study that supports the notion that vitamin E is, just as the word "vitamin" implies, so vital for your health that you better make sure you get enough of it from your diet (the RDA is 15mg/day).
Table 3: The
number of studies that distinguishes the different forms of vitamin E is
low. A 2004 study by Montonen et al. does yet appear to confirm what I
wrote before - they are all relevant and the the 34% reduced diabetes
risk with a high dietary alpha-tocopherol intake is by no means
meaningless.
Significantly and borderline significantly reduced type II diabetes risks
with all forms of tocopherols and tocotrienols in a cohort consisting
of 2,285 men and 2,019 women 40–69 years of age who were free of
diabetes at baseline when they were recruited for a 23-year follow-up in
1967–1972 (Montonen. 2004).
What is particularly interesting is that the data in Table 3
clearly indicates that the good old, often ridiculed alpha-tocopherol
does still have the most potent anti- diabetes effect of all 6 forms of
vitamin E.
Moreover, with beta-tocotrienol, the 2nd place is
however occupied by a form of vitamin E you will find in very high
amounts (30µg/g; cf. Nielsen. 2008) in whole wheat grain - is this the
reason whole grains are associated with lower type II diabetes risk in
epidemiological studies (Cho. 2013)?
High intakes (>20mg/day, i.e. only 30IU!) of vitamin E are associated with a ~20% reduced risk of developing type II diabetes in the participants of the Insulin Resistance Atherosclerosis Study (IRAS) that involved 895 nondiabetic adults at baseline (including 303 with impaired glucose tolerance [IGT]), 148 of whom developed type 2 diabetes according to World Health Organization (WHO) criteria during the 5-year follow-up (Mayer-Davis. 2002)
Epidemiology, dietary vitamin E and high dose supplementation: Most epidemiological studies still measure the alpha-tocopherol intake and serum levels. As long as there are no supplements involved, the results will yet still be representative of dietary vitamins E intake. It's after all more or less impossible to get only one form of vitamin E from whole foods.
That being said, "officially" the consumption of alpha-tocopherol-only supplements is save - at least in amounts of 60, 200, or 800 IU/day (55, 182, or 727 mg) all-rac-a-tocopherol/d will not produce noticeable side effects, changes in body weight, plasma total proteins, albumin, glucose, plasma lipids or the lipoprotein profile, the whole set of measures of organ health, as well as the levels of antioxidant vitamins and minerals (including the other forms of vitamin E; Uchida. 2013), glutathione peroxidase, superoxide dismutase, or total homocysteine of healthy elderly individuals (Meydani. 1998). Bendich & Machlin even state that vitamin E was safe up to doses of 3,200IU/day. Personally I do yet strongly advice against using more than 1,200IU of E per day (Bendich. 1988) - irrespective of whether it's alpha tocopherol or a tocopherol and -trienol blend.
Liver Enzymes the #1 Marker of Insulin Resistance | learn more
Patients with non-alcoholic fatty liver disease consume on average only half the amount of vitamin E, their healthy peers do (Musso. 2003). As a SuppVersity reader you know about the intricate relation between NAFLD and diabetes, and are thus aware that this is another "pro" argument with respect to the consumption of high vitamin E foods. If this is your first visit to the SuppVersity check out my previous article "Liver Enzymes the #1 Marker of Insulin Resistance!? Plus: What Does the Correlation Bettwen HbA1C & ALT, AST and GPT Tell Us About Diabesity?" to learn more about the relationship between obesity, diabetes and non-alcoholic fatty liver disease.
On the other hand of the "foods vs. supplement divide" things are less black or white, though. While the previously cited epidemiological evidence clearly suggests that food-borne vitamin E will protect you against diabesity. On the "supplement side of things", we have both extremely promising positive experimental evidence:
42% increased glucose disposal in elderly study participants in response to mediated stimulation after 4 months on a 900 mg d-alpha-tocopherol, i.e. 1350IU (!) of supplemental vitamin E per day. The fact that Paolisso et al. also observed that the "net changes in plasma vitamin E concentrations correlated with net changes in insulin-stimulated whole-body glucose disposal (r = 0.60 P < 0.003)" makes their results even more amazing (Poalisso. 1994)
Low vitamin E intakes early in pregnancy have been found to set women up to insulin resistance and hyperglycemia later in pregnancy by Ley et al. who write in their recent paper in the European Journal of Clinical Nutrition that (Ley. 2013) even after adjustment for serum adiponectin among women consuming daily, higher dietary vitamin E intakes were associated with lower fasting
glucose, lower HOMA insulin resistance (long term measure of blood glucose), and higher Matsuda insulin
sensitivity index (standard measure to quantify insulin sensitivity) among women who consumed a faily multivitamin supplement with "adequate", albeit probably synthetic vitamin E (dl-alpha-tocopherol).
The specificity principle: I am not sure if you remember the "Three Simple Rules of Reasonable Supplementation" (re-read them), but if you do, you will remember that specificity is one of the most important principles to follow, if you want to make the most of your supplement regimen. In the case of alpha-tocopherol this may mean that benefits will be seen in people with high baseline inflammation, while people without chronic inflammation, will see no, or even experience negative effects from (high) dose vitamin E supplements.
Modest vitamin E supplementation (100 IU/day) can significantly lower blood glycated hemoglobin and TG levels and does not have any effect on red cell indices in Type I diabetic patients (Jain. 1996). In view of the inflammatory underpinnings of type I diabetes, this study is yet not exactly representative of the benefits a healthy individual may derive from the same amount of vitamin E... although, I have to admit that a 100IU supplement looks much more rational to me than one with 400-1,200IU - specifically if it's pure alpha-tocopherol.
High dose (800-1200 IU/day) vitamin E supplementation improves fasting blood glucose and HbA1c levels in obese subjects - eighty overweight individuals (BMI >27 kg/m²), to be precise, who were randomly allocated to receive either 800 IU vitamin E per day or a matching placebo for 3 months. The dose of vitamin E was increased to 1,200 IU per day for a further 3 months (Manning. 2006).
On the other hand, we have experimental evidence that refutes the previously reported beneficial effects of supplemental vitamin E on blood glucose management. Examples? Here you go:
And what about exercise: Aside from the previously mentioned negative effects on the adaptation triggering exercise induced eustress, there are no good reasons to avoid vitamin E supplements for athletes. In fact, my previous analyses of corresponding studies here at the SuppVersity would suggest that people with a high baseline inflammation that overrides the exercise-induced locally confined increase in inflammation, may have good reason to take up to 400 IU/day of mixed tocopherols (opt. -trienols) - specifically if their vitamin E intake from foods is low, like on a diet, for example.
600 IU/day of vitamin E taken every other day provided no significant protection against type 2 diabetes in initially healthy women in the Women’s Health Study randomized trial (Liu. 2006). A study that appears to confirm that supplementing additional antioxidants is, just like keeping your omega-3/omega-6 ratio up (learn more), useless, unless it's part of an overall healthy life-style - and in that case, there is still the nasty question: Will it negate the beneficial effects of exercise or not?
In general, vitamin E supplementation does not decrease all-cause mortality or cardiovascular disease risk in type II diabetes. This is at least what a 2003 meta-analysis of studies with 81,788 concluded. As Vivekananthan et al. point out, "the lack of a salutary effect was seen consistently for various doses of vitamins in diverse populations" (Vivekananthan. 2003)
Of particular interest for us is the conclusion Vivekananthan et al. draw based on the results of their meta-analysis: If their results "do not support the routine use of vitamin E" this does after all mean that we don't have to argue about whether or not antioxidants negate the beneficial effects of exercise or whether "high-dosage vitamin E supplementation may increase all-cause mortality" as Miller et al. (2005) suggest in a 2005 meta-analysis in the Annals of Internal Medicine - Why? Well, why would we care about negative side effects, if it's not worth using them, anyways!?
γ-tocopherol:tomotoes, tuna; eggs; walnuts, pecans, pistachios and sesame seeds, pine nuts; dark chocolate or baking chocolate; seeds & grains, flax, peas, lentils; corn, soybean & canola oil, margarines, all sorts of shortenings and fried foods that are prepared with high γ-tocopherol oils
δ-tocopherol:peppers, onions, tomato seeds; raspberries, black- berries; tuna, mol- lusks, eggs; edamame; orega- no; rice germ oil, soy- bean oil, all sorts of shor- tenings and fried foods that are prepared with high δ-tocopherol oils
Don't supplement, eat your vitamins E: Not using vitamin E supplements (for glucose management) does yet also imply that you have to get your vitamins E from dietary sources. In view of an RDA of only 15mg and evidence that 100mg of vitamin E is already plenty, this does not appear to be difficult, but if you look at the total amount of vitamin E in the average American diet, you will be surprised that (a) gamma- and not α-tocopherol is the major form of vitamin E in the vegetable oil laden US diets (~60-70 % γ- vs. 20-25% α-tocopherol; cf. McLaughlin. 1979) and that (b) more than 80% of the Americans who don't supplement and still 45% of those who take supplements are effectively vitamin E deficient (McBurney. 2014).
There is little doubt that McBurney's observations are partly related to the increase vitamin E requirements of a lifestyle that is characterized by junk-food diet, sedentarism and chronic inflammation. They are yet also a result of a lack of foods that are naturally high in vitamin E, and supply you with both, the full spectrum of tocopherols and -trienols and the necessary co-factors to make the most of your dietary vitamins E intake - in short, it's a lack of the foods in the list on the right. Foods of which I assume that I will find the healthy ones (in italics) on your plate regularly, right?
What? Oh, yes. Well, the tocotrienols are in fact a problem. With the exception of red palm oil (50-75mg/100g) you will find only trace amounts (all values in mg/100g) of them in various fats/oils like rice wheat germ oil (18.9), coconut oil (2.1), and cacao butter (0.2) and grains like barley (91) and oats (21).
Reference:
Bendich, A., and L. J. Machlin. "Safety of oral intake of vitamin E." The American journal of clinical nutrition 48.3 (1988): 612-619.
Cho, Susan S., et al. "Consumption of cereal fiber, mixtures of whole grains and bran, and whole grains and risk reduction in type 2 diabetes, obesity, and cardiovascular disease." The American journal of clinical nutrition 98.2 (2013): 594-619.
Gudmundsson, Julius, et al. "Two variants on chromosome 17 confer prostate cancer risk, and the one in TCF2 protects against type 2 diabetes." Nature genetics 39.8 (2007): 977-983.
Jain, Sushil K., et al. "Effect of modest vitamin E supplementation on blood glycated hemoglobin and triglyceride levels and red cell indices in type I diabetic patients." Journal of the American College of Nutrition 15.5 (1996): 458-461.
Jiang, Qing, et al. "γ-Tocopherol, the major form of vitamin E in the US diet, deserves more attention." The American journal of clinical nutrition 74.6 (2001): 714-722.
Jiang, Qing. "Natural forms of vitamin E: Metabolism, antioxidant and anti-inflammatory activities and the role in disease prevention and therapy." Free Radical Biology and Medicine (2014).
Kasper, Jocelyn S., and Edward Giovannucci. "A meta-analysis of diabetes mellitus and the risk of prostate cancer." Cancer Epidemiology Biomarkers & Prevention 15.11 (2006): 2056-2062.
Klein, Eric A., et al. "Vitamin E and the risk of prostate cancer: the Selenium and Vitamin E Cancer Prevention Trial (SELECT)." Jama 306.14 (2011): 1549-1556.
Ley, S. H., et al. "Lower dietary vitamin E intake during the second trimester is associated with insulin resistance and hyperglycemia later in pregnancy." European journal of clinical nutrition (2013).
Liu, Simin, et al. "Vitamin E and risk of type 2 diabetes in the women’s health study randomized controlled trial." Diabetes 55.10 (2006): 2856-2862.
McBurney, Michael, et al. "Vitamin E status of the US adult population by use of dietary supplements (1041.7)." The FASEB Journal 28.1 Supplement (2014): 1041-7.
Manning, Patrick J., et al. "Effect of high-dose vitamin E on insulin resistance and associated parameters in overweight subjects." Diabetes Care 27.9 (2004): 2166-2171.
Mayer-Davis, Elizabeth J., et al. "Plasma and Dietary Vitamin E in Relation to Incidence of Type 2 Diabetes The Insulin Resistance and Atherosclerosis Study (IRAS)." Diabetes Care 25.12 (2002): 2172-2177.
McLaughlin, P. J., and John L. Weihrauch. "Vitamin E content of foods." Journal of the American Dietetic Association 75.6 (1979): 647-665.
Meydani, Simin Nikbin, et al. "Assessment of the safety of supplementation with different amounts of vitamin E in healthy older adults." The American journal of clinical nutrition 68.2 (1998): 311-318.
Miller, Edgar R., et al. "Meta-analysis: high-dosage vitamin E supplementation may increase all-cause mortality." Annals of internal medicine 142.1 (2005): 37-46.
Montonen, Jukka, et al. "Dietary antioxidant intake and risk of type 2 diabetes." Diabetes Care 27.2 (2004): 362-366.
Nielsen, Merete Møller, and Åse Hansen. "Rapid high-performance liquid chromatography determination of tocopherols and tocotrienols in cereals." Cereal chemistry 85.2 (2008): 248-251.
Paolisso, Giuseppe, et al. "Pharmacological doses of vitamin E and insulin action in elderly subjects." The American journal of clinical nutrition 59.6 (1994): 1291-1296.
Salonen, Jukka T., et al. "Increased risk of non-insulin dependent diabetes mellitus at low plasma vitamin E concentrations: a four year follow up study in men." Bmj 311.7013 (1995): 1124-1127.
Stattin, Pär, et al. "Prospective study of hyperglycemia and cancer risk." Diabetes care 30.3 (2007): 561-567.
Uchida, Tomono, et al. "α-Tocopherol does not Accelerate Depletion of γ-Tocopherol and Tocotrienol or Excretion of their Metabolites in Rats." Lipids 48.7 (2013): 687-695.
Vivekananthan, Deepak P., et al. "Use of antioxidant vitamins for the prevention of cardiovascular disease: meta-analysis of randomised trials." The Lancet 361.9374 (2003): 2017-2023.
The anti-long-term health, but pro short term fat loss effects of vitamin C + E
I must admit that I filed the study by Paulsen et al. (2014; accepted manuscript) under "further evidence that high doses of anti-oxidants do more harm than good to active individuals" the very moment I posted the information from the corresponding press release in the SuppVersity Facebook News (read it!).
A couple of days ago, I wanted to cite the paper in a different context and took a closer look at the actual results (yeah, even I sometimes only read the abstract) and as it turns out,...
...the scientists left out some information, you may be interested in, ...
...even though it may not be relevant from a statistical perspective. How I know things about your interests?Based on the visitor statistics of the SuppVersity. I just have to take a brief look at them to know that the vast majority of you will be intrigued to hear that the "daily vitamin C and E supplementation" (1000mg vitamin C and 235mg vitamin E per day), although it may have "attenuated increases in markers of mitochondrial biogenesis following endurance training", led to an albeit non-significant, but highly conspicuous 60% increase in body fat reduction.
Figure 1: Pre- & post-levels of body fat mass (left, in kg) and relative changes in type I and type II muscle fiber size (right; in % of baseline) in the subjects in the vitamin C + E and placebo arm of the study (Paulsen. 2014)
Yes, I know. The inter-group difference did not reach statistical significance. If you look at the exact figures, though you will have to concede that the intra-group difference did. In other words: While the subjects who took the anti-ergogenic anti-oxidants lost a significant amount of body fat, those who took the placebo did not. This is because the fat loss in the supplementation groups was much more evenly distributed than in the placebo group (the corresponding standard deviations were "only" 1.6x, not 3.6x (placebo) higher than the average fat loss of -5.3kg).
Table 1: Overview of the exercise component of the study (Paulsen. 2014)
Due to the minimal loss or marginal gain of lean body mass (and fiber size; see Figure 1) in the vitamin and placebo group, respectively, the relative difference of the change in body fat % (-4.6% in the vitamin and -2.0% in the placebo group) is even more pronounced.
This does not mean that these effects on the body composition are "real", i.e. actually due to the provision of vitamin C + E. What it does mean, though is that the occurred, although there was no visible training effect on the mitochondrial capacity and thus in the absence of any visible / measurable training effects.
The fat loss effects are not significant and my ad hoc hypothesis to explain them merely speculative. Therefore I still advice against the use of high dose "kamikaze" antioxidants (mere ROS-scavenger) like vitamin C + E - not just in the vicinity of a workout, but in general.
The absence of structural changes and the corresponding long-term health benefits that will always outweigh those of temporary reductions of body fat, should be reason enough to understand that someone who is not sick and chronically inflamed as the animals and human subjects in the studies you will see referenced in the write-ups of the supplement industry not to consume copious amounts of vitamin C, vitamin E or NAC.
Bottom line: I am certainly no advocate of high dose vitamin supplements and there is accumulating and in my humble opinion convincing evidence that they blunt the adaptive response to exercise training - including the potentially life-saving changes in mitochondrial capacity.
Still, the data from the Paulsen study does also support the conventional wisdom that a high level of baseline inflammation hampers the loss of body fat and that in spite, or rather because of the fat-burning prowess of IL-6, of which Knudsen et al. (2014) have recently been able to show that it is responsible for the exercise induced increase in UCP1 expression in subcutaneous white adipose tissue that will have your love handles melt away.
That does not make sense? Well, maybe it does. If you think about it as a vitamin-induced alleviation of the IL-6 analog to insulin resistance that allows the fat cells to finally "see" the IL-6 again and would thus propel the loss of body fat in those of the 14 women and 13 men in the supplement arm of the study who had a high baseline inflammation and correspondingly low "IL-6 sensitivity", this would be similar to the beneficial effects of ALA on weight loss int he obese and their absence in lean people.
References:
Knudsen, Jakob G., et al. "Role of IL-6 in Exercise Training-and Cold-Induced UCP1 Expression in Subcutaneous White Adipose Tissue." PloS one 9.1 (2014): e84910.
Paulsen, G, et al. "Vitamin C and E supplementation hampers cellular adaptation to endurance training in humans: a double-blind randomized control trial." Journal of Physiology (February 2014; accepted manuscript).
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 wouldsuggest 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.
Image 1: Ever thought why your granny had to take her cod-liver oil, whenever there she suffered from an ailment as a child? Probably not due to the rancid omega-3 oils which were partly responsible for its awful taste. That its high vitamin A content may not just have helped her to ward off the colds and infections, but also to stay lean, is yet a potential "side-effect" of dietary retinol for clear-cut which evidence is emerging only recently.
Facebook followers of mine have probably seen my post on the beta carotene metabolites called β1-apocarotenoids - recently discovered naturally occurring vitamin A receptor antagonist (block the activity or "real" vitamin A = retinol) about two to three days ago (Eroglu. 2012). As a SuppVersity regular, you will also be aware that vitamin A in its active form is not simply a dangerous substance that is to be avoided at all costs. And though beta carotene has long lost its image as (yet another) super-vitamin, with both direct supplementation and food-enrichment being scrutinized, the aforementioned results yield a couple of interesting hypothesis that may be worth investigating - if we also take into account the results of another recently published study that was conducted by researchers from the Department of Biophysical Chemistry at Kyoto Pharmaceutical University in Kyoto, Japan (Tsuchiya. 2012), you could even make an argument that the combined overconsumption of beta carotene (mostly from supplements and enriched convenience foods) and the conditioned avoidance of the high fat foods that contain 'real' vitamin A may in fact be another maybe non-negligible contributer to the current obesity epidemic.
2.5x more all-trans-retinoic acid in chow reverse diet induced weight gain
In their manuscript that has been published online in advance, Tsuchiya et al. followed up on the results of a previous trial, in which genetically modified mice with almost no functioning vitamin A receptors showed a profound decrease in hepatic insulin-like growth factor-1 production and profound hepatic steatosis (fatty liver) - a pathology the scientists ascribed to profound insulin resistance as a direct consequence of the lack of vitamin A signaling. In their latest study, that was financed with a national research grant, and is soon to be published in the international journal Hepatology (Tsuchiya. 2012), Tsuchiya et al. fed C57BL/6J mice, which had been pre-fattened on the same high-fat, high-fructose diet many of our fellow human beings are indulging these days, diets containing either standard amount of vitamin A or 50mg of all-trans-retinoic acid per kg of chow.
Figure 1: Body weight (left) and glucose and insulin management (right) in normal and diabetes and obesity prone mice receiving control diet, standard high fat high fructose diet (HFHFr) or HFHFr + 50mg all-trans-retinoic acid (ATRA); data in the right is expressed relative to non-supplemented control (data calculated based on Tsuchiya. 2012)
Not much to the researchers surprise, the administration of the high fructose high fat diet that contained 50mg/kg (normal chow has 20mg/kg), i.e. 2.5x more all-trans-retinoic acid, than the standard HFHFr chow, did not only stop the almost linear weight gain the animals had experienced in the course of the 16-week pre-fattening phase in normal mice (cf. figure 1, left), it did also have statistically significant beneficial effects on the blood glucose (diabetes prone) and insulin (obesity prone) levels of mice that are genetically predisposed to develop diabetes (KK-Aγ) and obesity (ob/ob), in a second experiment.
The all-trans-retinoic acid (ATRA) <> leptin connection
And although the aforementioned results are certainly impressive, this is not an essentially novel finding - what was yet observed for the fist time in this study, is the reversal of the diet-induced reduction of hepatic leptin receptor expression in the HFHFr group receiving additional all-trans-retinoic acid in their diets (cf. figure 2, left).
Figure 2: Effects of additional ATRA in diet on leptin receptor expression (left) and relative diet- and diet + supplementation induced changes in selected makers of non-alcoholic fatty liver disease (right; data adapted / calculated based on Tsuchiya. 2012)
The latter went hand in hand with a restoration of IGF-1 BP2 and ameliorative effects on the measured markers of non-alcoholic fatty-liver disease markers (liver weight, lipid content; cf. figure 2, right).
Vitamin(s) A - obesity and beyond
These still "incompletely understood" (Bonet. 2011) metabolic effects of 'real' vitamin A and its metabolites are yet only the tip of an iceberg of the largely ignored health effects of the first micronutrient in the vitamin alphabet. Other only partly related effects are
Table 1: Vitamin A functions, major roles in the immune system and effects of vitamin A deficiency in undernutrition and obesity (Th1, T-helper type 1 response; Th2, T-helper type 2 response; UCP, uncoupling protein; BAT, brown adipose tissue; directly adapted from Garcia. 2012)
a coordinating / controlling effect of the enzyme that converts dietary vitamin A into the active form (ATRA) on lipid metabolism (Kiefer. 2012)
a genetic blockade of adipocyte growth and thusly a direct inhibitory effect on die-induced obesity (Berry. 2012)
a facilitative role in the maturation and replenishment of muscle progenitor cells (Ryan. 2011)
an ability to prime pluripotent stem cells to become myocytes (muscle cells; Le May. 2011)
protective effects on cardio-myocytes against damage due to hyperglycemia (Guleria. 2011)
systemic anti-inflammatory and immune regulatory effects via inhibition of interferon-gamma, TNF-alpha, NF-kappa-beta, IL-12, and promoting "an anti-inflammatory environment and adequate Th1:Th2 ratios" (Garcia. 2012)
more general metabolic functions and immune-specific+ obesity-specific deficiency effects are summarized in table 1 (Garcia. 2012)
If we use the study at hand as a guide and the respective human equivalent dose of the ATRA contained in the 5g of chow/day the rodents consumed, the anti-NAFLD + anti-obesity effects would require a daily vitamin A intake of ~833IU for a mouse and 1,930IU /kg body weight for a human being, which is - I guess I don't have to tell you that - hilariously much and potentially hazardous.
How much vitamin A and where do you get it from?
If we let ourselves be guided by the 2.5x amount of the standard dose (which was what the mice were actually fed), take the RDA as a reference for the latter and assume that the conversion of dietary vitamin A to all-trans-retinoic acid works properly, the corresponding human doses do actually seem pretty reasonable, with 11,250IU for men and 8,750IU for non-pregnant women and can in fact be achieved relatively easily by eating, e.g.
25g chicken or pig liver or 30g of beef liver
100g butter + 300g cream + 300g cheddar cheese
200g of bluefin tuna + 3 eggs + tbsp of cod liver oil
In many cases it should thus suffice to simply forget your fat- and organ-meat phobia, to satisfy your retinol requirements - after all, the foods listed above may have the highest vitamin A content, but are by no means the only valuable sources of vitamin A and reasonable amounts of its natural, plant-derived precursor beta carotene in a whole-foods diet.
Image 2: I don't know if you realize this, but all the good sources of vitamin D in this illustration also contain significant (measured in IU mostly way more) vitamin A.
Unresolved issues with vitamin D: There was a time, when people used vitamin A to counteract vitamin D toxicity. Hard to imagine in the days of D-phoria, where everybody is advised to supplement, when a recent paper on the common measurement methods for vitamin D concluded that "several studies demonstrated that current 25(OH)D measurement methods do not meet" the prerequisite of being "sufficiently accurate over time, location and laboratory procedures" (Tienpont. 2012). Recent research on the underlying physiological relation / antagonism of vitamin A and D is almost non-existent. The handful of rodent trials I am aware of that actually compared the effects of co-supplementation were conducted in the mid 20th century and yield no conclusive results as far as an 'optimal' A to D ratio would be concerned - mostly because they only elucidated how much vitamin A it would take to keep the rodents on vitamin D enriched diets alive for a few more days. A recently published study does yet suggest that the often heard recommendation to take 1,000IU of supplemental vitamin D3 per day does not effect vitamin A or leptin levels. Whether the -14% and -19% reductions in serum alpha- and gamma-tocopherol (vitamin E) levels that were observed in this trial (800IU D3 + 2g calcium) are physiologically significant would yet warrant further investigation (Chai. 2012). The same is true for higher doses of vitamin D3, specifically, when those are - as it is often suggested taken in conjunction with those few fatty meals that actually contain 'real' vitamin A.
Assuming that you avoid supplementing high doses of beta carotene (don't care about the various forms of carotenes in real food), as well as highly fortified convenience food (yeah, cereals belong to this category, as well, and may in fact be among the worst offenders) and do not fall for the idea that you need at least 10,000-20,000IU of supplemental vitamin D3 per day, simply because your skin is supposed to be capable of producing 10,000IU within less than 1h of sun exposure, you should get more then enough "raw material" for your body to produce ATRA from your diet.
