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.
From Meal Timing Over Broccoli & Full-Fat Dairy to Anti-Diabetic Sweeteners
Based on the number of visitors you like a number of short news that will bring you up to speed on a certain topic better than a longer in-depth analysis of just one study. This and the fact that the number of recent papers that would be worth being discussed at length is not exactly huge are the reason today's SuppVersity article falls into the "short news" category again.
Basically the title says it all. All of the individual items in today's news article are from the latest issue of Nutrition Research and thus related to the effects the stuff that enters your body through your mouth is going to have on your health and overall well-being.
You can learn more about meal frequency at the SuppVersity
Grazin' Bad For the Obese!
Breakfast Keeps You Lean?!
Frequent Protein Consumption
Myth: Few Meals More Bodyfat
8 Meals = Stable, But High Insulin
Int. Fasting & Exercise
Meal timing matters, but only because it has a significant effect on the amount of food we eat. According to the latest study by Kathryn J. Reid, Kelly G. Baron, and Phyllis C. Zee, factors that correlate with an increased energy intake in 59 individuals, whose rest/activity patterns were assessed using 7 days of wrist actigraphy, and whose caloric intake was evaluated using 7 days of diet logs, are:
eating more frequently ,
later timing of the last meal, and
a shorter duration between last meal and sleep onset
Again, none of these factors will mechanistically make you store more body fat. What they will do, however, is to make you eat more. Basically this is also what the scientists imply, when they say that "In a mediational model, eating frequency explained the relationship between eating closer to sleep onset and total caloric intake" (Reid. 2014).
Table 1: Associations between total calories, BMI, meal timing, meal frequency, and measures of sleep (Reid. 2014)
It is thus not, as you may assume based on the latest studies on the intricate relationship between meal timing and the workings of your biological clock, the timing that makes late eaters more prone to obesity, but simply the fact that they're eating more than the early birds.
Whole fat dairy intake is associated with lower obesity risk, findings from the Observation of Cardiovascular Risk Factors in Luxembourg study show. Bear in mind that we are dealing with observational data with all its usual flaws and shortcomings, before you start shoveling down extra amounts of whole fat dairy or throw all your low fat dairy products out of the window.
Figure 1: Multivariate adjusted (Model 1: M1 | Model 2: M2, details see text) difference in risk of being abdominally obese (WC ≥102 cm for men and 88 cm for women) in men and women consuming 3 vs. 1 serving of the given type of dairy per day (Crichton. 2014).
Although the data in Figure 1 has been adjusted for age, education, sex, smoking, physical activity (in min/wk), total carbohydrate (in g/d), total protein (in g/d), total fat (in g/d), total fiber (g/d), alcohol (in g/d), calcium (in mg/d), and total energy intake (in kcal/d), and in model 2 even for HDL (in mg/dL), LDL (in mg/dL), triglycerides (in mg/dL), and systolic and diastolic BP (in mm Hg), this is still statistical shenanigan and could well be messed up by a correlation between being fat and choosing fat foods in the (false?) believe that they would help you lose weight.
D-sorbose as an anti-diabetes sweetener. In an attempt to develop d-sorbose as a new sweetener that could help in preventing lifestyle-related diseases, scientists from the University of Nagasaki Siebold investigated the inhibitory effect of d-sorbose on disaccharidase activity, using the brush border membrane vesicles of rat small intestines - put simply they checked if d-sorbose would inihibt the breakdown of disaccharides into monosaccharides and thus have the ability to slow down the absorption of glucose from "complex" carbs.
Figure 2: Effects of adminstration of sucrose, the same amount of sucrose and + 10% d-sorbose or l-sorbose on the glucose and insulin response in rodents (Oku. 2014)
I've marked the "benefits", i.e. the decrease in blood glucose (left) and the reduced insulin spike (right) in Figure 2. As you can see the effect is - at least in rodents - physiologically relevant, so that it is reasonable that Oku et al. assume that
"[...] d-sorbose might also suppress postprandial elevation of levels of glucose and insulin due to ingestion of sucrose or maltose in humans and could be used as a sweetener that may reduce risk for lifestyle-related diseases but requires more research" (Oku. 2014).
In view of the fact that the technology that is necessary to produce large amounts of d-sorbose has become available only relatively recently it is yet unlikely that you will be able to buy this stuff at the health food store next door, already.
Green veggies like broccoli have also been shown to reduce postprandial glycemia + insulin and noost the production of the anti-obesogenic satiety hormone GLP-1 | learn more
Broccoli may ameliorate "brainflammation" in the eldery. That's at least what the latest rodent study from the University of Illinois would suggest.
The study that was conducted by Brigitte E. Townsend, Yung-Ju Chen, Elizabeth H. Jefferya, and Rodney W. Johnson showed marked reductions in age-elevated cytochrome b-245 β, an oxidative stress marker, and reduced glial activation markers in aged mice who were fed a diet containing 10% broccoli diet for 28 days. Overall the effects are obviously modest; and yet, the study still provides good evidence to keep broccoli on your "foods I consume regularly" list.
Does eating veggies reduce inflammation? Yes, it does, 8 servings per day will significantly reduce CRP (Watzl. 2000), 68g of avocados will reduce IL-6 & NF-kappaBeta (Li. 2013), high intakes of alpha- and beta-caro- tene containing foods is associ- ated with decreased coronary heart disease risk and CHD mortality (Osganian. 2003 ; Bujisse. 2008), tomatos may protect against prostate cancer (Etminan. 2004), tomato juice makes LDL molecules resistant to oxidation (Upritchard. 2000), toma- to paste protects your skin from UV radiation (Rizwan. 2011), etc.
You want more? Well I have another study for you. One that attempts to explain why fruits an veggies in general and plant carotenoids in particular are good for you. It's a study from the Environment and Agro-biotechnologies Department in Luxemburg (Kaulmann. 2014) that analyzed the effect of carotenoids on intracellular signaling cascade and the corresponding effects on gene expression and protein translation and found that (1) carotenoids are able to interact with the nuclear factor κB pathway and thus inhibit the downstream production of inflammatory cytokines, (2) carotenoids can block oxidative stress by interacting with the nuclear factor erythroid 2–related factor 2 pathway and activating phase II enzymes and antioxidants, such as glutathione-S-transferases, and concludes that we (3) still have an incomplete understanding of what exactly carotenoids and other phytochemicals can do for our health | Any comments? If so, leave them on Facebook!
References:
Buijsse, Brian, et al. "Both α-and β-carotene, but not tocopherols and vitamin C, are inversely related to 15-year cardiovascular mortality in Dutch elderly men." The Journal of nutrition 138.2 (2008): 344-350.
Crichton, Georgina E., and Ala'A. Alkerwi. "Whole-fat dairy food intake is inversely associated with obesity prevalence: findings from the Observation of Cardiovascular Risk Factors in Luxembourg study." Nutrition Research (2014).
Etminan, Mahyar, Bahi Takkouche, and Francisco Caamaño-Isorna. "The role of tomato products and lycopene in the prevention of prostate cancer: a meta-analysis of observational studies." Cancer Epidemiology Biomarkers & Prevention 13.3 (2004): 340-345.
Kaulmann, Anouk, and Torsten Bohn. "Carotenoids, inflammation, and oxidative stress—implications of cellular signaling pathways and relation to chronic disease prevention." Nutrition Research (2014).
Li, Zhaoping, et al. "Hass avocado modulates postprandial vascular reactivity and postprandial inflammatory responses to a hamburger meal in healthy volunteers." Food Funct. 4.3 (2013): 384-391.
Oku, Tsuneyuki, et al. "D-sorbose inhibits disaccharidase activity and demonstrates suppressive action on postprandial blood levels of glucose and insulin in the rat." Nutrition Research (2014).
Osganian, Stavroula K., et al. "Dietary carotenoids and risk of coronary artery disease in women." The American journal of clinical nutrition 77.6 (2003): 1390-1399.
Reid, Kathryn J., Kelly G. Baron, and Phyllis C. Zee. "Meal timing influences daily caloric intake in healthy adults." Nutrition Research (2014).
Rizwan, M., et al. "Tomato paste rich in lycopene protects against cutaneous photodamage in humans in vivo: a randomized controlled trial." British Journal of Dermatology 164.1 (2011): 154-162.
Upritchard, JANE E., W. H. Sutherland, and J. I. Mann. "Effect of supplementation with tomato juice, vitamin E, and vitamin C on LDL oxidation and products of inflammatory activity in type 2 diabetes." Diabetes care 23.6 (2000): 733-738.
Watzl, Bernhard, et al. "Prolonged tomato juice consumption has no effect on cell-mediated immunity of well-nourished elderly men and women." The Journal of nutrition 130.7 (2000): 1719-1723.
Even if you don't get burned tanning beds pose a risk factor!
I am not aware who invented the myth, but I am quite sure it's the tanning bed industry that propagates it: Tanning in what Germans call the "Asi-Toaster" (literal translation "a toaster for nackers") is safe!
If we put some faith into the results of a recent study from the Department of Dermatology at the University of Minnesota this is a fatal error. "Toasting" yourselves on a tanning bed increases your risk of developing skin cancer by 287%! Or, if you like that better, it almost quadruples (4x) it!
The results Rachel Isaksson Vogel and her colleagues from the University of New Mexico Cancer Center and the Brown University present in their latest paper in the Journal of the National Cancer Institute (JNCI) will probably be quite shocking for some of you who relied on the ability of the UV-filters in tanning beds to reduce the increase in cancer risk (Vogel. 2014).
There are better ways to get your vitamin D than tanning beds, learn more the SuppVersity
How Much To Take?
Leucine, Insulin & Vitamin D
Vit. D Speeds Up Recovery
Overlooked D-Sources
Vitamin D For Athletes!
Vitamin D Helps Store Fat
If you look at the data that's based on an analysis of the tanning practices of 1852 subjects, it becomes pretty obvious: The protection the filters appear to offer against sunburns does not translate into cancer protection! On the contrary!
Figure 1: Risk of melanoma by ever use of indoor tanning among individuals who tanned indoors without burning and never users stratified by lifetime burns from sun as estimated using logistic regression (n = 1852; cf. Vogel 2014).
If you scrutinize the data in Figure 1 you will have to admit that it is obvious that those of the subjects who were cautious enough not to expose themselves to "real sun" to avoid getting burned, were the ones with the highest melanoma risk due to tanning bed radiation! Those who avoid the sun like a plague have a 4x higher risk even after adjustment for
What else can protect you? Peer reviewed evidence for skin cancer protective effects exist from:
milk thistle (Katiyar. 2005)
melatonin (Janjetovic, 2014)
calcium (1g) + 400IU vitamin D3 (-37% in women with increased risk; Tang. 2011)
retinol (25,000IU/day; cf. Moon. 1997)
retinol and zinc +riboflavin and niacin + vitamin C and molybdenum (at 1-2x the RDA; cf. Blot. 1993)
Too much antioxidants, on the other hand have been shown to increase cancer risk in women (#68%; cf. Hercberg. 2007). Against that background, a reasonable amount of controlled sun exposure and a coretene rich diet offer probably the best protection.
sex, age at reference date (in years),
eye color (gray/blue, green, hazel, or brown),
hair color (red, blond, light brown, or dark brown/black),
skin color (very fair, fair, light olive, vs dark olive, brown, very dark brown, or black),
freckles (none, very few, few, some/many),
moles (none, very few, few, some/many),
income (≤$60,000, >$60,000, missing),
education (completed college, did not complete college),
family history of melanoma (yes, no, missing),
lifetime routine sun exposure (continuous),
lifetime sun exposure from outdoor activities (continuous),
lifetime sun exposure from outdoor jobs (continuous), and
lifetime sunscreen use (continuous)
using propensity score methods in two-sided statistical tests. In other words, while the raw data on the left hand side is confounded by being at high risk and avoiding the real sun, the data on the right hand side (orange bars) is not!
Now you want a supplemental alternative / adjunct, right?
Against that background the promised "supplemental tanning formula" which consists of pretty ordinary supplements, you can find on the shelves of every larger Internet-retailer will probably become even more interesting, right?
Table 1: Tanning of different body regions before and after treatment with the supplement combo ()
I have to admit, the results scientists from the Laboratoire OENOBIOL in Paris recorded are not very impressive (see Table 1), but the difference was significant and - and this may be even more important - the ingredients, i.e. 3mg beta carotene,
3mg lycopene. 5mg vitamin E (alpha tocopherol), and 30mg vitamin C (ascorbic acid) were ingested in a no-tanning scenario.
You want to kill two birds with one stone? Try "Tomatorade(R)" and get your daily tanning (Postaire. 1997) and cancer protective (Aust. 2005) dose of lycopene right from nature.
Bottom line: The fact that the "supplemental tanner" worked even in a no-sun-exposure scenario is interesting, because lycopene, in particular has been shown to be preferentially destroyed by UV radiation, in the course of the tanning process. The slight tan the subjects developed upon it's supplement restoration is thus only the cosmetic side of the benefits one can derive from this combo. What makes it really interesting, though, is that it will simultaneously build the skins defenses against UV-radiation and could thus be used in conjunction with reasonable (=partial shade) sun exposure to develop a beautiful and healthy tan without havin' to resort to the aforementioned "Asitoaster" and/or drugs like melanotan.
Reference:
Aust, Olivier, et al. "Supplementation with tomato-based products increases lycopene, phytofluene, and phytoene levels in human serum and protects against UV-light-induced erythema." International journal for vitamin and nutrition research 75.1 (2005): 54-60.
Blot, William J., et al. "Nutrition intervention trials in Linxian,
China: supplementation with specific vitamin/mineral combinations,
cancer incidence, and disease-specific mortality in the general
population." Journal of the National Cancer Institute 85.18 (1993):
1483-1491.
Green, Adèle, et al. "Daily sunscreen application and betacarotene supplementation in prevention of basal-cell and squamous-cell carcinomas of the skin: a randomised controlled trial." The Lancet 354.9180 (1999): 723-729.
Hercberg, Serge, et al. "Antioxidant supplementation increases the risk of skin cancers in women but not in men." The Journal of nutrition 137.9 (2007): 2098-2105.
Janjetovic et al. "Melatonin and its metabolites ameliorate UVB-induced damages in human epidermal keratinocytes." Journal of pineal research (2014). Ahead of print.
Katiyar, Santosh K. "Silymarin and skin cancer prevention: anti-inflammatory, antioxidant and immunomodulatory effects (Review)." International journal of oncology 26.1 (2005): 169-176.
Lappe, Joan M., et al. "Vitamin D and calcium supplementation reduces cancer risk: results of a randomized trial." The American journal of clinical nutrition 85.6 (2007): 1586-1591.
Moon, Thomas E., et al. "Effect of retinol in preventing squamous cell skin cancer in moderate-risk subjects: a randomized, double-blind, controlled trial. Southwest Skin Cancer Prevention Study Group." Cancer Epidemiology Biomarkers & Prevention 6.11 (1997): 949-956.
Postaire, Eric, et al. "Evidence for antioxidant nutrients‐induced pigmentation in skin: Results of a clinical trial." IUBMB Life 42.5 (1997): 1023-1033.
Tang, Jean Y., et al. "Calcium plus vitamin D supplementation and the risk of nonmelanoma and melanoma skin cancer: post hoc analyses of the women's health initiative randomized controlled trial." Journal of Clinical Oncology 29.22 (2011): 3078-3084.
Vogel, et al. "Exposure to Indoor Tanning Without Burning and Melanoma Risk by Sunburn History." JNCI J Natl Cancer Inst (2014) 106(7): dju112 doi:10.1093/jnci/dju112
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.
I would not expect "red palm olein wonders", but more RPO and less corn oil in the American diet may at least buffer the liver disease burden in the US (the figure is based on data provided by the American Liver Foundation)
On Turesday, November 19, 2013, you've learned from a study by Subermaniam et al. about the "anti-rust" effects of coconut oil (if you missed that, you can catch up here), today, we are going back to Malaysia and the Universiti Kebangsaan Malaysia and the results of another team of researchers to learn about the effects the various oils have on the "oiling of the liver" (Dauqan. 2013).
I guess most of you will remember my previous comments about the critical role of the liver (and its health or disease) in the development of the metabolic syndrome (read it up). It is thus by no means irrelevant, whether the chronic ingestion of a certain type of oil will result in MDA levels of 92µmol/g or 27.3µmol/g.
Boring!? No, rather surprising!
If you think this sounds boring and are by no means surprised that the malondialdehyde levels of the liver samples the researchers harvested after 4 weeks were 27.3µmol/g, 92µmol/g, 54µmol/g, 47.4µmol/g and 72.6µmol/g for the control diet with mixed fats, red palm oloein (RPO), regular palm oil (PO), corn oil (CO) and the previously celebrated coconut oil (COC), respectively, I would suggest you have a closer look at the the "magic" that happened over the following 4 weeks of on 15% RPO, PO, CO and COC diets.
Figure 1: MDA levels (µmol/g) of liver tissue as a marker of lipid oxidation after four and eight weeks on control diet or control diet with 15% of red palm olein, palm oil, corn oil or coconout oil (Dauqan. 2013)
Well, you see, the way the effects of red palm olein came full circle after another months on the 15% RPO diet is hardly "boring", is it? The MDA levels, a relatively reliable indicator of local lipid oxidation, of the rodents on the 15% red palm olein diet is now, 4 weeks after peaking at 92µmol/g down to 25.2µmol/g, indicating that the level of lipid peroxidation in the livers of the RPO group is now significantly lower than that of any other group (43.4µmol/g, 50.1µmol/g and 48.3µmol/g for control, palm oil, corn oil and coconut oil).
Short term detriments, long term benefits!
I know it sounds more than awkward, but eventually every SuppVersity student should be aware of the fact that the extrapolation of long-term effects from short-term data is a 'risky' business. Unfortunately, even 'experts' often disregard this fundamental rule, when they formulate their recommendations on nutrition, supplementation and exercise.
Table 1: Carotenoid and vitamin E composition (in %) of crude palm oil and red palm olein; the data is from a different study by Bonni & Choo who tested commercially available products (Bonni. 2000)
The statement, "Prefer coconut oil and avoid red palm olein!", for example would have been a reasonable dietary if we did not know about the turn-around in the second part of the study, when the beneficial effects of the saturated fat content of the coconut oil begin to fade and the absence of natural anti-oxidants in refined coconut oil begins to show its ugly face. At this point, the moderate amount of unsaturated fats in red palm olein (13% omega-6, 0% omega-3; see Bonnie. 2000), of which I am honestly not sure if it is the actual reason of the initial increase in lipid peroxidation (remember: corn oil has more PUFAs!), or whatever other underlying cause of the initial rise in inflammation is overriden by the accumulating amounts of vitamins E and carotenoids from the red palm olein, which rendered the liver of the oxidation-proof, or "rustless" if you will - similarly rustless as the hearts of the rogents in the previously cited study by Subermaniam et al. (learn more).
200g of palm fruits have the same amount of tocotrienols as 4kg of oats. Learn more "tocotrienol" and red palm oil facts in "Tocotrienols: What They Are, What They Do & How They Work + Why the RDA of Palm Olein is NOT 1xCup Per Day " | more
Bottom line: I would like to formulate two take home messages for today's SuppVersity article. Firstly, a theoretical one, which shall remind you of the fact that you can do more harm than good, if you (accidentally) terminate a study in a transitional state and formulate long-term dietary recommendations based on short-term observations, because the study at hand clearly indicates that some effects - in
this case the antioxidant effects of the tocopherols, -trienols and
carotenoids - take their time to become measurable. And seconfly a very practical one, which is eventually only a reminder of the existence of red palm oil (see article referenced on the right) - an excellent source of dietary antioxidants and probably your only chance to get your tocotrienols and high(er) amounts of some of the rarer carotenoids from regular foods.
References:
Bonnie, T. Y. P., & Choo, Y. M. (2000). Valuable minor constituents of commercial red palm olein: carotenoids, vitamin E, ubiquinones and sterols. Journal of Oil Palm Research, 12(1), 14-24.
Dauqan, E., Abdullah, A., & Sani, H. A. (2013). LIPID PEROXIDATION
IN RAT LIVER USING DIFFERENT VEGETABLE OILS. Malaysian Journal of
Analytical Sciences, 17(1), 300-309.
Valls, V., Goicoechea, M., Muniz, P., Saez, G. T., & Cabo, J. R. (2003). Effect of corn oil and vitamin E on the oxidative status of adipose tissues and liver in rat. Food Chemistry, 81(2), 281-286.
