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marylin monroe
Showing posts with label MUFA. Show all posts
Showing posts with label MUFA. Show all posts

The Quest for the Optimal Cooking Oil: Heat Stable, Low PUFA & Cholesterol Free - High MUFA Sunflower / Canola, Olive, Coconut & Avocado Oil Qualify for the TOP5

The oil is not he only thing that's damaged, when you're frying foods; and acrylamide is only the most prominent of these nasty compounds.
Alright, it's about time to acquit myself of a longstanding promise: the promise to finally write the unofficial second part to my article on cooking oils & fats from February 2014 that busted the myth of the "healthy" saturated cooking oils and fats (read more). It's an "unofficial" part II, because the previous article was actually intended to be "just" a rebuttal to the unwarranted craze about using butter, lard & co to fry in order to protect yourself from developing heart disease and other nasty ailments.
Needless to say that this part is going to focus on purportedly healthier alternatives ranging from high-oleic acid sunflower and canola oil to another often hyped dietary fat: coconut oil.
Lean more about frying & co at the SuppVersity

Std. US Diet Has "Optimal" Obesogenic Fat

MUFA Modulates Gut Bacteria → Weight Loss

The Healthy Taste of Olive Oil - Flavor's Enough!

GMO Soybean Oil Proven to Be Pro-Inflammatory

"Pimp My Olive Oil" - W/ Extra Antioxidants

Frying Does not Just Oxidize Oils, It Does Fat More!
Before we delve deeper into the discussion lets briefly recap what exactly we are looking for in the "optimal" frying oil: The optimal frying oil should...
  • ... either contain a low amount of readily oxidizable PUFAs or contain significant amounts of antioxidants that protect these important, but sensitive fatty acids from being oxidized,
  • ... be cholesterol-free, because dietary cholesterol can be a problem, if it's consumed in large amounts in its pro-atherogenic (=tending to promote the formation of fatty deposits in the arteries) oxidized form,
  • ... have a high smoke point, i.e. can be heated to very high temperatures before enough volatile compounds such as water, free fatty acids, and short-chain degradation products of oxidation emerge from the oil that a bluish smoke becomes clearly visible.
All three suppositions are important because, the consumption of oxidized PUFAs, oxidized cholesterol (Valenzuela. 2003) and other volatile compounds from "burnt" oils and fats have consistently been associated with negative health effects.
  • Figure 1: The consumption of soy bean oil that was heated for 3h is associated with an increase in body fat that is independent of an increased intake of food (Penumetcha. 2013)
    The consumption of oxidized PUFAs has been associated with an increased cardiovascular disease risk and increases in body fat, of which recent studies indicate that it is not caused by an increase in food intake (Penumetcha. 2013).

    Some scientists in fact believe that the association between the consumption of high amounts of (high omega-6) seed oil is associated with heart disease & co not due to the fatty acid composition of these oils per se, but rather due to extensive use of these products in highly processed (convenient) foods, which in turn contain high amounts of oxidized polyunsaturated fatty acids and will thus drive the development of heart disease, diabetes & co.
  • Oxidized cholesterol as it occurs at relatively high amounts un highly processed foods, has the potential cytotoxic, mutagenic, atherogenic, and possibly carcinogenic effects (Peng. 1985; Kumar. 1991; Valenzuela. 2003; Orczewska-Dudek. 2012). In that it's important to point out that not all heated animal products (e.g. eggs) will contain significant amounts of oxysterols, because the formation of these potentially unhealthy byproducts of the heating process depend on (a) temperature, (b) heating time and (c) storage & packaging.

    Against that background, soft-boiled eggs are healthier than hard-boiled eggs or fried eggs and a hot chocolate milk is less of a problem than repeatedly heated and extensively processed eggs, meats & co.
    Figure 2: Overview of the effects of storage, processing and heating on the levels of oxidized cholesterol in various food items (various sources).
    Why? Easy: They contain significantly lower amounts of the potentially unhealthy oxidized cholesterol - a dietary ingredient that can become a serious problem only if you consume high quantities on a regular basis, though.
  • Figure 3: Changes occurring during deep fat frying (Fritsch. 1982).
    Oxidized fatty acids and cholesterol are actually part of the volatile compounds that arise, when a cooking / frying oil starts to "smoke". In his 1981 paper in the Journal of the American Oil Chemists’ Society, Fritsch published a neat graphical illustration of what happens during the frying process (see Figure 3).

    As you can see, it's a complex series of changes and reactions that produce numerous decomposition products. As Fritsch points out, "the functional, sensory and nutritional quality of frying fats are changed and may reach a point where high quality foods can no longer be prepared," as these reactions proceed. In the end, the oil will be unpalatable.

    Unfortunately, the negative effects on your health will occur way before you will be able to detect the changes in viscosity, color or taste (specifically if the oils are used in processed products, where any off tastes would be covered by (artificial) flavorings, anyways) or see the smoke. That's also why the smoke point of a given fat  / oil is not exactly the best criterion to judge its suitability as "optimal frying oil".
Now that you're aware that checking it's not enough to look at the "Smoke Point" in the unreferenced Wikipedia article, let's get to the question that's been praying on your minds ever since I posted my article on cooking oils & fats on February 2014 (read more): Which oil, if not the allegedly superior animal fats, shall I use for cooking and frying?

Q: What's the optimal frying oil, now? A: It depends!

Now that we know that we want an oil that's relatively low in PUFAs, high in (natural) antioxidants, cholesterol-free and has a high smoking point, a few candidates come to mind:
  • High oleic acid canola (or rapeseed) or high oleic acid sunflower oil - Both contain a low amount of PUFAs, no cholesterol, and have relatively high a smoking points of 194°C  and 200°C, respectively.
    Table 1: Ranking of the oils tested by Bertrand Matthäus; 1 indicates rank #1 = first place, 4 indicates rank #4 = last place (Matthäus. 2006).
    Accordingly, it's not surprising that high oleic acid rapeseed and sunflower oils come out on top of a comparison by Betrand Matthäus, in which the researcher compared the formation of  oligomer triacylglycerols, polar compounds and free fatty acids, as well as the results of a sensory evaluation of the oil itself and the French fries that were fried with high oleic acid rapeseed (HORO), high oleic acid sunflower (HOSO), partially hydrogenated rapeseed oil (PHRO) and, the worst choice, palm olein (PO).

    If you compare the high oleic acid varieties of sunflower and rapeseed oil that are made from seeds with a low PUFA and high MUFA content, you will yet realize that the the often derided sunflower oil is actually the most stable one. The rapeseed oil, on the other hand, produced the tastiest fries (according to the full text of the study). Since "only small differences in the chemical parameters of all oils were found" and "[o]nly the total result of the assessment of PO was significantly worse than the results of the other oils (p < 0.01)" (Matthäus. 2006), the rapeseed oil comes out on top of this comparison.
Using high MUFA rapeseed oil not just for frying, but as a major fat source in the diet leads to significant improvements in blood lipids in hypercholesterolaemic subjects (Gillingham. 2011)
You cannot seriously be suggesting sunflower and canola oil! Yes, I can! I know that both have quite a bad reputation, but if you look at the scientific evidence that's mostly unwarranted.

If you look objectively at the existing evidence, it is debatable whether this may not be superior to using olive oil or other high MUFA oils, but certainly superior to using other frying oils or animal fats. Plus: It works it cholesterol lowering and glucose metabolism improving magic not just in patients with high cholesterol levels (see figure on the left), but also in healthy young women (Uusitupa. 1994; Jones. 2014).
  • Now, being resistant to oxidation is one thing. Having overall beneficial effects on one's health, however, is a totally different thing. A "thing" that was tested in a 2005 study, by Allman-Farinelli et al. in which the researchers were able to show that replacing saturated fats in the diet with high-oleic-acid oils like sunflower oil will favorably alter the low-density lipoprotein cholesterol, triglycerides, and factor VII coagulant activity" of healthy men and women and thus present "another useful source of MUFA for diets aimed at prevention of heart disease"(Allman-Farinelli. 2005).
    Figure 4: Evidence of the effect of canola oil on health-related risk factors.
    In a similar vein, canola aka eruchic acid free rapeseed oil, which is also available as high oleic acid cooking oil, has been shown to reduce TC concentrations in healthy or hypercholesterolemic individuals, compared with high-SFA or typical Western diets. Studies also indicate that it "may potentially promote immune and cardiovascular health through its antithrombic and antioxidative effect" (Lin. 2013). For the other benefits listed in the overview in Figure 4, the results are sometimes less equivocal. Overall, Lin et al. whose review of literature was obviously funded by the canola industry still claims that "canola oil can now be regarded as one of the healthiest edible vegetable oils in terms of its biological functions and its ability to aid in reducing disease-related risk factors and improving health" (Lin. 2013) - a claim that sounds a bit hyperbolic, in spite of the fact that their review of the literature supports many of the claims.

    Against that background I would stick to using canola, or if you live in Europe or can acquire it overseas rapeseed oil only in its high oleic acid variety and specifically for frying foods at high temperature, when you cannot live with the taste they would acquire if you used extra virgin olive oil, instead.
  • The coconut miracle not ideal for frying!? -There is little doubt that virgin coconut oil belongs to the "healthy oils" - despite, or rather due to its low PUFA content. The question is: Is it also ideal for frying? If we go through our checklist, as prevoiusly said...
    • it contains only 1.7% PUFAs, 85.2% saturated and 6.6% monounsaturated fats, which means it's more or less PUFA free and thus not prone to heat induced oxidation
    • it's cholesterol free, so the problem with oxidized cholesterols that is rampant in fats from animal products is not a problem,
    • it's smoke point is relatively, low though, at only 163°C even the deodorized, bleeched coconut oil will form enough volatile compounds for the ugly bluish smoke to rise from your pan (Man. 1998).
    The question we have to answer is thus: Is the comparatively low smoke point reason enough to abstain from using coconut oil as a frying oil? For virgin coconut oil, the answer may be yes, for the refined, bleached, and deodorized version of coconut oil, however, the peroxide levels remains stable within the relatively narrow time window (smaller than 1h) you would use when you fry foods (see Figure 5).
    Figure 5: After a 30 hours of frying (not shown) the US' favorite health killer, soybean oil, has peroxide values that exceed the measuring capacity of the assay, Yuki & Ishikawa used in their 1979 study (Yuki. 1979)
    As you can see in Figure 5 this is in stark contrast to soybean oil, of which you probably know that it is heavily abused as frying oil in the US.

    Unfortunately, its comparatively low peroxide values don't tell you the full truth about the usefulness of coconut oil. Compared to similarly bleached and deodorized palm oil, coconut oil will have higher %FFA levels, which are indicative of an increased oxditation & hydrolysis of fatty acids and are responsible for the "soapy" flavor that made the test product in a 1998 study by Man, et al. hardly palatable. From a product quality perspective, frying with palm oil would thus be (and for most companies is) the preferable choice. From a mere health perspective, though, frying with coconut oil - especially at lower heats that do not exceed the smoke point of 163°C (vs. 229° for palm oil), is yet a good and tasty choice.
  • Avocado oil, the exotic alternative - There is unfortunately little research on the long-term health effects of using avocado oil for frying.
    Table 2: The fatty acid composition of cold-pressed and refined avocado oil does not differ (Haiyan. 2007)
    As you can see in Table 2, avocado oil, irrespective of whether it is refined or cold-pressed ("virgin"), has a high omega-9 fatty acid content. In conjunction with the similarly oxidation resistant saturated fatty acids, it makes up roughly 84.7% of the fatty acids.

    Table 3: Comparison of selected properties, like baseline FFA and peroxide value (PV | both indicative of the presence of unwanted byproducts of storage or processing induced oxidation), antioxidant content,  persticides & co in avocado oil and olive oil (Reed. 2001)
    The risk of consuming exuberant amounts of oxidized fatty acids is thus relatively low, despite the 12.6% of fatty acids with a higher susceptibility to oxidation (note: lard contains 13.6% or more of those highly volatile fatty acids | Enig. 1983).

    There is no cholesterol in avocado oil, so oxidized cholesterols are not an issue. Compared to olive oil, avocado oil contains an increased amount of beneficial antioxidant, is naturally lower in peroxides and free fatty acids (this does not mean that there will be necessarily less after processing) and is usually, just as olive oil, pesticide free (Reed. 2001).

    Against that background it's worth taking a look at the results of a 2012 study from the University of Navarra in Spain, which found that ...
    "Avocado oil was richer than olive oil in total phytosterols at time 0 h (339.64; 228.27 mg/100 g) and at 9 h (270.44; 210.30 mg/100 g) of heating. TBARs was higher in olive oil after 3 h, reaching the maximum values in both oils at 6 h of heating treatment. Vitamin E was higher in olive oil (35.52 vs. 24.5 mg/100 g) and it disappeared earlier in avocado oil (at 4 vs. 5 h). The stability of avocado oil was similar to that of olive oil." (Berasategi. 2012 | my emphasis)
    Since no regular consumer will fry his foods for more than 3h, the previously presented evidence clearly indicates that avocado oil is an allegedly more expensive, albeit slightly superior alternative to olive oil, the last oil on our list (see below).
  • Olive oil, refined or, even better, extra virgin - If it was not for the price and the taste, the whole world would probably long have switched over to olive oil as their go-to oil for everything. I am not going to (re-)cite the plethora of epidemiological evidence in favor of its beneficial health effects, here. Instead I will briefly go through our three items from the initially presented list.

    Olive oil has a relatively low omega-6 and virtually no omega-3 fatty acids (10.5g PUFA total per 100g). It's fatty acid profile, alone, does therefore tell us that it could be a suitable candidate for the "optimal" frying oil.
    Figure 6: Effect of air, light and deep-frying on p-AV of olive, corn and soybean oil (Naz. 2004). Please not that improper storage will also increase the oxidative damage to your cooking oils.
    Olive oil is cholesterol free, so the oxidation of cholesterol during the frying process is not an issue, either; and when it is heated it turns out to produce a relatively low amount of unwanted peroxidation products (see Figure 6). This would render olive oil or, as I examined previously, extra virgin olive oil (read more | see red box in particular) the perfect cooking oil, if it was not for its taste, which is not compatible with every dish you may be cooking.
Figure 7: Rice bran oil, despite a high PUFA content is pretty heat stable. It still didn't make the top list in this article - also to keep the article from turning into an ebook ( Debnath. 2012 ;-)
Bottom line: It's still 2014 and I have finally managed to put out the unofficial part II to my article on cooking oils & fats from February 2014 that busted the myth of the "healthy" saturated cooking oils and fats (read more). I have to admit. It's far from being as all-encompassing as I would have liked it to be, but even though I did not list ricebran oil (a relatively high PUFA content, but with a smoke point at 258°C for refined rice bran oil still pretty heat stable (De. 1999) | cf. Figure 7), which is an excellent cooking oil, as well and skipped many of the details on the oils I did discuss, the main message is clear: If you want to fry foods there is a range of cholesterol-free low PUFA oils you can choose from, with the high MUFA canola/rapeseed and sunflower oil being the cheapest and probably still most commonly used frying oils and avocado oil being the most expensive and I would guess least used of the candidates investigated in this article | Comment on Facebook!
    References:
    • Allman-Farinelli, Margaret A., et al. "A diet rich in high-oleic-acid sunflower oil favorably alters low-density lipoprotein cholesterol, triglycerides, and factor VII coagulant activity." Journal of the American Dietetic Association 105.7 (2005): 1071-1079. 
    • Berasategi, Izaskun, et al. "Stability of avocado oil during heating: Comparative study to olive oil." Food Chemistry 132.1 (2012): 439-446.
    • Chan, Shu-Hui, et al. "Cholesterol oxidation in whole milk powders as influenced by processing and packaging." Food chemistry 47.4 (1993): 321-328. 
    • De, B. K., and D. K. Bhattacharyya. "Deacidification of high-acid rice bran oil by reesterification with monoglyceride." Journal of the American Oil Chemists’ Society 76.10 (1999): 1243-1246. 
    • Debnath, Sukumar, et al. "Effect of frying cycles on physical, chemical and heat transfer quality of rice bran oil during deep-fat frying of< i> poori:</i> An Indian traditional fried food." Food and Bioproducts Processing 90.2 (2012): 249-256.
    • Enig, M. G., et al. "Fatty acid composition of the fat in selected food items with emphasis on trans components1." Journal of the American Oil Chemists’ Society 60.10 (1983): 1788-1795.
    • Fritsch, C. W. "Measurements of frying fat deterioration: a brief review." Journal of the American Oil Chemists’ Society 58.3 (1981): 272-274. 
    • Gillingham, Leah G., et al. "High-oleic rapeseed (canola) and flaxseed oils modulate serum lipids and inflammatory biomarkers in hypercholesterolaemic subjects." British Journal of Nutrition 105.03 (2011): 417-427.
    • Haiyan, Zhong, et al. "Endogenous biophenol, fatty acid and volatile profiles of selected oils." Food chemistry 100.4 (2007): 1544-1551. 
    • Jones, Peter JH, et al. "High-oleic canola oil consumption enriches LDL particle cholesteryl oleate content and reduces LDL proteoglycan binding in humans." Atherosclerosis (2014).
    • Osada, Kyoichi, et al. "Oxidation of cholesterol by heating." Journal of Agricultural and Food Chemistry 41.8 (1993): 1198-1202. 
    • Kumar, Naresh, and O. P. Singhal. "Cholesterol oxides and atherosclerosis: a review." Journal of the Science of Food and Agriculture 55.4 (1991): 497-510.
    • Lercker, G., and M. T. Rodriguez-Estrada. "Cholesterol oxidation: presence of 7-ketocholesterol in different food products." Journal of Food Composition and Analysis 13.4 (2000): 625-631.
    • Lin, Lin, et al. "Evidence of health benefits of canola oil." Nutrition reviews 71.6 (2013): 370-385. 
    • Man, YB Che, and WR Wan Hussin. "Comparison of the frying performance of refined, bleached and deodorized palm olein and coconut oil." Journal of Food Lipids 5.3 (1998): 197-210.
    • Matthäus, Bertrand. "Utilization of high‐oleic rapeseed oil for deep‐fat frying of French fries compared to other commonly used edible oils." European Journal of Lipid Science and Technology 108.3 (2006): 200-211.
    • Morgan, J. N., and D. J. Armstrong. "Quantification of Cholesterol Oxidation Products In Egg Yolk Powder Spray‐dried with Direct Heating." Journal of food science 57.1 (1992): 43-45.
    • Missler, S. R., B. A. Wasilchuk, and C. Merritt. "Separation and identification of cholesterol oxidation products in dried egg preparations." Journal of Food Science 50.3 (1985): 595-598.
    • Naz, Shahina, et al. "Oxidative stability of olive, corn and soybean oil under different conditions." Food Chemistry 88.2 (2004): 253-259.
    • Orczewska-Dudek, Sylwia, et al. "Cholesterol and lipid peroxides in animal products and health implications-A review." Annals of Animal Science 12.1 (2012): 25-52.
    • Paniangvait, P., et al. "Cholesterol oxides in foods of animal origin." Journal of Food Science 60.6 (1995): 1159-1174.
    • Peng, Shi-Kaung, et al. "Cholesterol oxidation derivatives and arterial endothelial damage." Atherosclerosis 54.2 (1985): 121-133.
    • Penumetcha, Meera, et al. "A diet containing soybean oil heated for three hours increases adipose tissue weight but decreases body weight in C57BL/6 J mice." Lipids in health and disease 12.1 (2013): 26. 
    • Pie, Jae Eun, Khira Spahis, and Christine Seillan. "Cholesterol oxidation in meat products during cooking and frozen storage." Journal of Agricultural and Food Chemistry 39.2 (1991): 250-254.  
    • Reed, A. B., et al. "New Zealand extra virgin olive oils." Food New Zealand Feb/March 2001 (2001): 20-24. 
    • Uusitupa, Matti, et al. "Effects of two high-fat diets with different fatty acid compositions on glucose and lipid metabolism in healthy young women." The American journal of clinical nutrition 59.6 (1994): 1310-1316.
    • Valenzuela, Alfonso, Julio Sanhueza, and Susana Nieto. "Cholesterol oxidation: health hazard and the role of antioxidants in prevention." Biological research 36.3-4 (2003): 291-302. 
    • Valsta, Liisa M., et al. "Effects of a monounsaturated rapeseed oil and a polyunsaturated sunflower oil diet on lipoprotein levels in humans." Arteriosclerosis, Thrombosis, and Vascular Biology 12.1 (1992): 50-57. 
    • Yuki, E., and Y. Ishikawa. "Tocopherol contents of nine vegetable frying oils, and their changes under simulated deep-fat frying conditions." Journal of the American Oil Chemists’ Society 53.11 (1976): 673-676.

    The Fat Truth Behind the Dairy Weight Loss Miracle: MUFA and PUFA Impair, Saturated Fat and Plenty of Micronutrients Drive Full-Fat Dairy-Powered Fat Loss.

    Image 1: Kids who drink more milk, tend to be leaner... and that despite (?) the fact that this stuff comes out of an animal and is full of bad cholesterol and fat - outrageous ;-)
    Plenty of interesting news, lately, so this one - just like the recently released hypertrophy / hormone correlation study by Stuart Phillips, about which I have been talking in yesterday's installments of the Intermittent Thoughts got somewhat delayed. With the Christmas holidays and the approaching and all those New Year's weight loss resolutions (I would prefer the term "fat loss resolution", though ;-) already on your mind, I do yet think that it is about time to break the news on the "fat" reason for the purported beneficial effects an increased consumption of dairy products during periods of caloric restriction appears to have on weight and more specifically body fat loss (Linn. 2000; Peirara. 2002; Shahar. 2010).

    Dairy, calcium or simply the right macronutrient composition?

    The scientific results I am going to present are taken from a study that was published in the Journal of Nutrition and Metabolism a few weeks ago (Smilowitz. 2011). In a randomized, placebo-controlled study Jennifer T Smilowitz and her colleagues from the USDA-funded (keep that in mind, when interpreting the results, or rather the scientists interpretation of the latter ;-) Western Human Nutrition Research Center assigned their 62, against the background of the rampant obesity epidemic, only slightly overweight young subjects (mean age: 25y; BMI ~28) to a calorically restricted diet (-500kcal) that was specifically designed to "provide comparable levels of macronutrient and fiber, to approximate the average consumption in the US" (35% fat, 49% carbohydrate, 16% protein and 2-3g fiber), which contained either
    • 0-1 servings of dairy, with 500mg dietary calcium (from the whole diet) + placebo,
    • no dairy (still 500mg calcium from diet), 900mg of supplemental calcium carbonate, or
    • 3 servings of dairy, with 1400mg of dietary calcium (from the whole diet) + placebo
    Thusly, the study basically mimicked, what would happen if you told the average American to just keep their usual sedentary life-style (the subjects were instructed not to start to exercise or anything like that) and either just reduce his caloric intake by 500kcal, to do the former and to make sure to have three servings of dairy per day, or to just take an additional "healthy" calcium carbonate supplement.

    Eat dairy + whatever you want and lose weight?

    Now, interestingly, the subjects were not only free to chose whether they wanted to consume the dairy from low or normal fat cheese, milk and/or yoghurt, they were also relatively free as far as the rest of their dietary choices were concerned so that the detailed analysis of their food-logs allowed for conclusions to be drawn that went beyond the initial scope of the study... but let's take one thing after the other.
    Figure 1: Dietary intake (macronutrients in kcal/day) of the subjects before and at the end of the 12-week study period and relative changes in carbohydrate, protein and fat intake (data calculated based on Smilowitz. 2011)
    If you take closer look at the analysis of the dietary records the subjects had to keep, you will notice that the minor differences in the dietary prescriptions induced quite profound changes as far as the macronutrient composition of the respective diets was concerned. While the subjects in the non-dairy groups, regardless of whether they received a calcium supplement or placebo, cut back on all the three major macronutrients, the requirement to incorparate three servings of dairy into their meal-plan, alone appeared to suffice to keep the protein intake of the dairy group at a reasonably high level (~72g; which would be 0.96g/kg body weight). The protein intake of the two non-dairy groups, on the other hand dropped to 57g (0.75g/kg) and 54g (0.7g/kg) for the calcium and placebo supplemented groups, respectively.
    Figure 2: Changes in body composition and measures of insulin sensitivity after 12-weeks on the high dairy, calcium supplemented or placebo supplemented diets (data calculated based on Smilowitz. 2011)
    In view of the facts that the subjects had to stick to the calorically restricted diet for 12 weeks, it should not surprise you that all of them lost a statistically significant amount of body weight (cf. figure 1) and improved their insulin sensitivity (as indicated by reduced insulin levels and HOMA-IR values).What should yet strike your eye are the increased reductions in body fat and waist circumference and the greater increase in lean mass-% in the high dairy group. Now, you will probably assume that this was a result of the higher protein intake, and that may in fact have been the case, as one of my beloved model calculations by which scientists "adjust" their data for whatever they want (usually until the result is in accordance with their hypothesis ;-) revealed that
    Dairy product consumption was found to be significantly associated with reduced WC [waist circumference] and %BF [percent body fat], however, these relationships were no longer significant after adjustment [my emphasis ;-] for protein and energy intake and physical activity.
    Figure 3: Scatterplot of the partial correlations between reported 12-week mean dietary fat intake expressed as % of total energy and changes in lean body mass (LM) and body fat % (taken directly from Smilowitz. 2011)
    Assuming that this "adjustment" yielded valid results it is all the more interesting what a subsequent analysis of the "adjusted" data revealed:
    When expressed as a percent of total energy, dietary fat composition was correlated with changes in anthropometrics. Reported MUFA at 12 wk was inversely and positively associated with changes in % LM and % BF, respectively.
    Or, in the words of the layman: The greater the relative monounsaturated fatty acid (MUFA) content of the subjects' diets, the more lean mass was lost and the more body fat was retained during the study period (cf. figure 3). Similarly, a higher intake of polyunsaturated fatty acids (PUFA) was associated with lower reductions in waist circumference, and while  the scientists claim that the n3:n6 ratio did not matter, it should make you wonder if it could actually be coincidental that the n6:n3 ratio in the dairy group was 6.6, while the ones in the calcium and placebo groups were 8.7 and 7.9, respectively.

    And what about saturated fats? 

    Moreover, the USDA scientists mention only "in the small print" that most fundamental (and statistically significant) distinguishing feature of the dairy group, who unquestionably had more favorable weight loss results despite an overall greater caloric intake, was (and I am quoting this from the paper) "a significantly higher intake of SFA [saturated fats] and lower intakes of MUFA and PUFA compared with the calcium supplement and placebo groups". Now, guess where this "bad" saturated fat came from? Well, probably from full-fat dairy! And guess why those "good" MUFAs and PUFAs were missing from the diets of the high dairy group. Well, probably because the subjects ate less "healthy vegetable oils"... ah, and did I already mention that the dairy group also ingested disproportionally (relative to their caloric intake) higher amounts of biotin, vitamin B12, vitamin D and - God forbid! - cholesterol?
    Image 2: Even if you like animals, eating their eggs and full-fat dairy products won't hurt them.

    So, while the scientists do their best to conceal that all those "bad things", like a high protein intake and nutrient dense real non-processed animal products with their original (saturated) fat, cholesterol and micronutrient content left untouched, are the true driving forces of successful weight loss (and, you bet, also maintenance), I am quite confident that you, as a diligent student of the SuppVersity, would not have needed the doctored... ah, pardon me, ... I obviously meant the well-adjusted results of this study to know that. After all, you are probably just enjoying a rib-eye steak with some delicious melted butter from grass-fed cows, right?

    Pimp My Olive Oil! When Virgin is not Phenol-Rich Enough: The Pharmacokinetics of Phenol-Enriched Virgin Olive Oil.

    Image 1:  "If we have not somehow pimped it, it can never be good enough!" appears to be one of the credos with which mankind approaches almost every health-remedy nature has provided for us. In the past this approach was not particularly healthy, though... is phenol-enriched olive oil going to be the exception to the rule?
    Being the health-conscious person you obviously are (why else would you visit the SuppVersity ;-), chances are that olive oil, or, to be specific, extra virgin olive oil is one if not primary source of of mono- and polyunsaturated fats in your diet. But do you actually know why? I mean why olive oil? And why extra virgin? What? "Mediterranean diet", "high MUFA content", "lower incidence of coronary heart disease and cancer"? All right, you have done your homework on olive oil, but what about the "extra virgin"? The polyphenols, right. The phenolic content is in fact what distinguishes a "good" olive oil. The phenolic alcohols, the secoiridoid derivatives, the phenolic acids, the lignans and the flavonoids in concert have been reported to have anti-oxidant, anti-inflammatory, anti-atherogenic and anti-carcineogenic properties and are probably as, if not more important for the beneficial health effects of the Mediterranean gold than its fatty acid profile (Covas. 2007; Covas. 2008).

    So, if those polyphenols are the "active ingredients" in olive oil, wouldn't it be nice if we had an oil that had even more of these beneficial healthy secondary plant metabolits in our oils, right?

    Now we have tons of polyphenols, but does that make a difference?

    The thought, that a souped up version of the already phenol-rich virgin olive oil would be an even more potent health promoter must have occurred to a group of researcher from Spain, as well. Back in 2010 already, Manual Suárez and his coworkers published a paper in the Journal of Argiculture and Food Chemistry in which they describe the development of a "phenol-enriched olive oil with phenolic compounds from olive cake" (Suárez. 2010). In essence, the scientists just put back some of the pulp (an extract to be precise) that is produced when the oil is squeezed from the olives into the end-product. In a more recent study the scientists did now try to evaluate how much of these (additional) health promoters in 30ml of regular virgin olive oil (VO) and the enhanced virgin olive oil (EVOO) actually make it into the blood of 16 (8 men, 8 women) healthy subjects in a randomized, controlled, cross-over trial (Suárez. 2011).
    Figure 1: Compositional differences (phenol-enriched vs. standard virgin olive oil) in polyphenol content (data calculated based on Suárez. 2011)
    If you take a look at the compositional differences between the regular and the "phenol-enriched" virgin olive oil, it is quite obvious that, from a mere quantitative point of view, Suárez' product with on average 3.3x more secondary plant metabolits should be the more potent health promoter. After all, numerous previous studies have shown that those olive oils with (naturally!) particularly high phenol-content exhibit the most pronounced beneficial health effects (Samanego Sanchéz. 2007). This would yet require adequate absorption of the respective compounds from a now obviously more dense solution, which, according to the results of this study, does not seem to be the case for all compounds - and more importantly, all subjects:
    The in vivo study showed that the concentration of fourteen of twenty-four compounds detected was higher in the plasma samples from the EVOO than after ingestion of VOO. Among these, two of them, hydroxytyrosol sulphate and vanil-lin sulphate, were statistically significant in attending their pharmacokinetic parameters, demonstrating the suitability of enrichment. In general, a displacement of the time to reach the maximum concentration is observed in the samples, which indicates that more time is needed to absorb the higher phenolic content. However, inter-individual variabilityin the concentration of the plasma phenol metabolites shows that it is difficult to show statistically significant differences between the VOO and the EVOO.
    The scientists thusly conclude that the "metabolism of phenols is affected first by the individual". So until we actually know which influence these are, the label "phenol-enriched" on olive oils and other products has little meaning for you as an individual. And even if you belong to the "lucky" high-absorbers, only two, namely vanillin sulphate and hydroxytyrosol sulphate will reach what the scientists call "pharmocokinetic" levels, if you ingest two tablespoons of the super-potent "phenol-enriched" virgin (and still relatively natural) olive oil.
    Figure 2: Changes in total antioxidant activity (TAA) of experimental oils subsequent to heat treatment (from Pellegrini. 2001)
    Note: Common Internet wisdom would suggest that you have to be particularly cautious with those "phenol-enriched virgin olive oils", when respective products hit the market (and I bet this won't take long). After all, you will all have heard how heating those oils damages the healthy polyphenols - and while that may to some extend be the case, a 2001 study by Nicoletta Pellegrini et al. found that the total antioxidant value of olive oil does not only increase with increased polyphenol content, but that those polyphenols are also "stabilizers of R-tocopherol during olive oil heating, thus contributing to the nutritional value of cooked foods" and "the prevention of antioxidant activity decay in olive oil during realistic heating conditions" (Pellegrini. 2001), which ranged from 30min at 160°C to 120min at 190°C. The latter happens to be at the upper end of the regular deep-frying temperature and would thus suggest that the commonly heard recommendation not to use extra virgin olive oil for frying is not valid, at least when we focus exclusively on its total antioxidant capacity as measured by Trolox essays (cf. figure 2). In that it should be mentioned that, with its relatively high content of highly oxidizable omega-6 fats, olive oil still isn't the "ideal" frying oil - notwithstanding that frying does not constitute the healthiest way of preparing your food anyways ;-)
    And though a recent study has shown that the latter conjugates with LDL and thusly protects it from oxidative damage (González-Santiago. 2010), it remains to be verified whether the consumer variety of the olive oil in this study will actually provide any health benefits. And this is particularly true in view of the fact that the food giants will, as they already do it in the case of "normal" virgin olive oil, minuscule amounts this probably expensive ingredient into their otherwise unhealthy convenient products, just to be able to put the highly marketable "contains phenol-enriched virgin olive oil" on the label... but, hey! I guess, this is just the never-ending story of complete nutritional idiocy ;-)

    On Short Notice: Nucleotide Supplementation Increases Performance & Fortifies Immune Response. Plus: Oleic Acid Increases, SFA Lowers E2, Testosterone & DHT Binding

    Are nucleotides a useful supplements for intensity maniacs and can olive oil reduce your free testosterone levels?
    If you have been visiting the SuppVersity for a while now, you were probably surprised to see that the "Short News" (aka "On Short Notice") are back. The reason, I changed my mind and reintroduced this assembly of short news items is that I realized that there is an intemediate category of news and infos between the very short Facebook news that (a) disappear in the oblivion of the SuppVersity Facebook Wall, (b) don't allow me to post graphics that would illustrate the study results and (c) still take some time to write and the detailed analysis in the "original" SuppVersity articles.

    So, if you disagree and can give me a good reason why I should not post news compilations like the one at hand more regularly, speak now or forever hold your peace ;-)

    Nucliotide supplementation counters immune suppressive effects of exercise

    (Ostojic. 2013) - I think I mentioned a similar study a couple of weeks ago in the SuppVersity Facebook News, but since this most recent investigation into the ergogenic effects of the small organic nitrogen-based combinations of a five-carbon sugar and a phosphate group that
    • form the building blocks of nucleic acids, such as DNA and RNA, and 
    • participate in cellular signaling and metabolism
    deals with in young, healthy, fit men and their response to the provision of a supplement that looks similar to something you are probably goint to see on the market pretty soon, I thought it may be interesting enough to make it into this "news" article-format.
    Figure 1: Illustration of the molecular structure of nuleotides (Sadava. 2000)
    The supplement we are talking about is a combination of different nucleotides, i.e. cytidine 5′-monophosphate, uridine 5′-monophosphate, guanosine 5′-mono-phosphate and adenosine 5′-mono-phosphate from partially purified (90%) germinated barley seeds extracted during sporulation and the reason it's worth knowing what was in it, because it was able to ...
    • Want a quick performance fix? Use sodium bicarbonate | learn more
      significantly increase time to exhaustion (+7%)
    • ramp up serum levels of immunoglobulin A and
    • elevate the NKC cytotoxic activity
    in the blood of the 14 recreationally active participants (age 22; BMI 24kg/m²; body fat 11%) who participated in a standardized incremental exercise test on the treadmill ("Run till you drop") after taking 50mg/day of this product for 2 weeks.

    Oleic Acid Increases E2, Testosterone & DHT Binding

    Not from Greece, the land of olive oil and eve's cheese, but from Spain comes a study that links Oleic acid, the mono-unsaturated fat from Olive oil to increases in SHBG. The researchers from the Universitat Autònoma de Barcelona analyzed the lab reports and nutrition data of a total of 315 men and observed that
    "SHBG serum levels were significantly higher in subjects using olive oil for cooking in comparison with subjects using sunflower oil. The SHBG levels correlated positively with MUFA (p < 0.001) and negatively with saturated fatty acids (p = 0.003)." (Sáez-López. 2013)
    Based on multiple regression analysis of the data, the scientists calculated that the amount of MUFA in the subjects' diets accounted for 20.4% of SHBG variance. Despite the fact that this means that your MUFA intake determines "only" 20% your SHBG levels, the data in Figure 1 (left), clearly indicates that these 20% show pretty significant correlations with important health markers.
    Figure 2: Correlation between SHBG levels and BMI, MUFA intake (in % total fat) and fasting blood glucose - left; correlation between phospholipid MUFA and SFA content and SHBG - right (Sáez-López. 2013)
    In order to elucidate the underlying mechanisms, the scientists conduced an additional in-vitro study, in the course of which Sáez-López were able to confirm that oleoyl-CoA, a metabolite that's produced, when oleic acid is metabolized, downregulates PPAR-γ in the liver (HepG2 cells).

    As a SuppVersity veteran, you'll know that any reduction in PPAR-gamma in the adipose tissue will result in a decreased propensity of fat storage (read up on it). In the liver, PPAR-gamma is  responsible for the production of SHBG, as well. In view of the fact that SHBG binds and deactivates* androgens and estrogens (*this is not essentially correct for all tissues!), your MUFA intake could thus be one of the set-screws that determine the level of unbound sex-steroids in your blood.
    With 60-80% olive oil is one of the best sources of oleic acid and this is not a reason to stop consuming it - irrespective of T-binding (read more)
    Bottom Line: Based on the currently available evidence it appears as if nucleotide supplements could have a future as immune and performance booster for intense training athletes.

    Despite the fact that it is unlikely that there will be any side effects, (a) the increased immune activity, which could be a problem for people with auto-immune disease and (b) the non-existence of scientific evidence to support their long-time efficacy (and safety), I would wait and see how things develop before investing significant amounts of money in supplemental RNA / DNA precursor.

    Something very similar is true for results of the Sáez-López study that investigated the "SHBG raising" effects of oleic acid. In view of the negative association between SHBG levels BMI and fasting blood glucose, which have, by the way, been observed in previous studies: Phillips & Gerald, for example, observed a significant negative correlation between SHBG and the waist / hip ratio in 55 obese men aged 21 to 70 (Philips. 1993). And while SHBG binds testosterone the small change will not render all your testosterone useless, so that you don't have to be afraid of sudden olive oil induced anti-virility effects ;-)

    References:
    • Ostojic, Sergej M., Kemal Idrizovic, and Marko D. Stojanovic. "Sublingual Nucleotides Prolong Run Time to Exhaustion in Young Physically Active Men." Nutrients 5.11 (2013): 4776-4785.
    • Phillips, Gerald B. "Relationship between serum sex hormones and the glucose-insulin-lipid defect in men with obesity." Metabolism 42.1 (1993): 116-120.
    • Sadava, D. et al. Life: The Science of Biology, 9th ed. 2009
    • Sáez‐López, Cristina, et al. "Oleic acid increases hepatic sex hormone binding globulin production in men." Molecular nutrition & food research (2013).

    PUFA Increases Postprandial Thermogenesis in Healthy Premenopausal Women & Beyond - 14% Increase Over MUFA & SFA Sounds Huge, But Does it Matter?

    Is there something to the good vs. bad fat shenanigan, after all?
    Only recently scientists from the Texas Tech University report that a PUFA-rich high-fat meal led to a greater diet-induced thermogenesis in normal-weight premenopausal women compared with SFA- or MUFA-rich high-fat meals.

    Reason enough to take a closer look at this and previous studies investigating the diet-induced thermogenic effects of PUFA-, MUFA- and SFA-rich meals and to conduct a reality check wrt to the question whether these differences actually matter - I mean, will you get and stay lean by upping your PUFA intake? Let's take a look!
    You can learn more about fat at the SuppVersity

    Are Men Fat- & Women Sugar-Cravers?

    Fat, not Fructose Cons. Increased in the US
    Adding Fats to Carbs Does not Reduce Insulin

    The Forgotten Pro-Insulinogenic Effects of SFAs

    Margarine Not Butter Incr. EU Waists

    Low Fat to Blame for Low Vitamin D Epidemic?
    In the initially mentioned study, Hui C. Clevenger, Amanda L. Kozimor, Chad M. Paton and Jamie A. Cooper explored the effect of three HF meals enriched with different fatty acids (MUFAs, PUFAs or SFAs) on metabolism in premenopausal women of normal weight. In that, the metabolic parameters of interest included postprandial energy expenditure (EE), which is then used to calculate DIT, and substrate oxidation, which included respiratory exchange ratio (RER), fat oxidation and carbohydrate (CHO) oxidation.

    Based on previous research in men of normal weight, the Texas Tech researchers hypothesized that the diet induced thermogenesis (DIT) and fat oxidation would be the highest after the PUFA- and MUFA-rich meals and lowest after the SFA-rich meal in premenopausal women - a result of which you already know that it was only partly confirmed.
    Figure 1: Diet-induced thermogenesis and respiratory exchange rate (higher RER = lower fatty acid oxidation vs. higher CHO oxidation) in the 5h after the test meal (Clevenger. 2014)
    The data in Figure 1 does after all tell you that the expected MUFA-induced increase in diet-induced thermogenesis did not occur. PUFAs, on the other hand did the job, Clevenger et al. expected them to do. They increased the DIT by an ostensibly whopping 14% over the DIT the scientists observed in response to the ingestion of the high MUFA and SFA liquid meals that had been prepared with the same base of 8 fl oz (237 ml) of chocolate Ensure(R) with soy lecithin and Nesquik (R, but contained different additional dietary fatty acids added depending on the treatment condition:
    • Table 1: Liquid meal nutrient composition
      breakdown (Clevenger. 2014).
      The PUFA-rich meal was ‘base’ plus sunflower oil and flaxseed oil, with 42% of total energy coming from PUFA.
       
    • The MUFA-rich meal was ‘base’ plus canola oil and extra virgin olive oil, with 42% of total energy coming from MUFA.

    • Finally, the SFA-rich meal was ‘base’ plus butter, coconut oil and palm oil, with 40% of total energy coming from SFA. 
    As the data in Table 1 indicates, the nutrient profiles didn't differ much. The fatty acid composition, on the other hand did, with the SFA meal being the only one with measurable amounts of Butyric, Caprioc, Caprylic, Capric, Lauric, Myristic and Hepatedic acid. Fatty acids of which previous research indicate that they induces an obesity-linked proinflammatory gene expression profile in adipose tissue of subjects at risk of metabolic syndrome (van Dijk. 2009).

    High MUFA diets, on the other hand, have been shown to potentiate the effects of weight loss in obese NIDDM patients (Low. 1996). They are the major group of fatty acids in the one oil, everyone appears to agree that it's health (Olive oil). And last but not least, even the allegedly unhealthy omega-6s have been shown in randomized controlled to reduce liver fat and modestly improve metabolic status, without weight loss, when compared to high saturated fat diets (Bjermo. 2012).

    All of these effects / this evidence could potentially be more important than the increase postprandial thermogenesis in the study at hand - so the ultimate question is: Does DIT even matter?
    Now, does this increase in DIT matter? Westerterpet et al. who found a negative correlation between body fat levels and the diet induced thermogenesis in their 2008 study (Westerterpet al. 2008), certainly believe it matters. If we look at the total extra diet-induced energy expenditure in 5h after the test-meal in the study at hand, on the other hand, I cannot but ask myself, whether those 1.4kcal can actually make a difference.

    I am not sure what you think, but considering the fact that you can burn those 1.4 extra calories in less than one minute in the gym, it's hard to believe that the increased thermogenesis alone warrants the layman's conclusion that the study at hand would provide evidence for the superiority ot PUFAs over MUFAs and saturated fats ... what do you think?
    References:
    • Bjermo, Helena, et al. "Effects of n− 6 PUFAs compared with SFAs on liver fat, lipoproteins, and inflammation in abdominal obesity: a randomized controlled trial." The American journal of clinical nutrition 95.5 (2012): 1003-1012.
    • Clevenger, Hui C., et al. "Acute effect of dietary fatty acid composition on postprandial metabolism in women." Experimental physiology (2014): expphysiol-2013.
    • Westerterp, Klaas R., et al. "Dietary fat oxidation as a function of body fat." The American journal of clinical nutrition 87.1 (2008): 132-135.

    The Female(?) Athlete Triad - Part III/III: Road to Recovery! Step #2 = Accept There is No Magic Macronutrient Ratio

    No need to raid another tomb, Lara, the quest for the one and only ideal macronutrient composition that will yield optimal results for the rest of your life ends here (img courtesy of Paramount)!
    I am not planning to bore you with a longish summary of the previous installment(s) of this series, here. Still, I don't want to head on to the 2nd step of the "Road to Recovery", which is going to deal with the quest for the "optimal" macronutrient ratio, without a brief reminder of the central role of nutrient availability in both the etiology, as well as the recovery from the athlete triad - or, as Dr. Zanker from the Carnegie Research Institute at the Leeds Metropolitan University in the United Kingdom puts it, the simple fact that the "exercise associated reproductive dysfunction in women is attributable to deficits of readily available energy" (Zanker. 2006)

    In a couple of more general remarks some of you have recently (not without good reason, by the way) criticized my excessive and in parts random use of mark-ups like bold print or underlining. In the introductory paragraph to today's post the word "readily" is however so important that the underlining is obligatory.

    Your hypothalamus does not like to wait, therefore "readily" is the keyword, here!

    It is after all the lack of appropriate readily available energy, primarily in the form of circulating glucose, liver glycogen, and adipose tissue triacylglycerol that precedes the low plasma insulin concentration and reductions in total body fat content and corresponding disturbance of leptin secretion, ghrelin, cortisol, thyroid and of course luteinizing hormone (see data in figure 1; the absolute levels from the healthy group may also serve as a reference to compare your own labwork to; mind the units!).
    Figure 1: Hormonal and glucose metabolism (* indicates 24h values) of women with functional hypothalamic amenorrhea (not necessarily exercise induced) expressed relative to values in eumenorrheic control; values above the bars indicate the total values of the respective markers in healthy controls and may provide you with some orientation, when you are looking at your own bloodwork (data based on Loughlin. 1998)
    In order to avoid / counter the reproductive and associated problems and break out of the vicious circle of the athlete's triad, Zanker proposes the following three steps (based on Zanker. 2006; yet with a couple of additions from my side): 
    • Avoid abrupt and rapid weight loss and maintain an “adequate” body fat content, which may be individually specific, but coincides with regular reproductive function.
    • Consume adequate amounts of energy to fuel your increased metabolic demands; never go below your resting energy expenditure, regardless of whether you  want to or even have to lose weight.
    • Make sure you get an adequate amount of carbohydrates either on a continuous (low GI carbs with every meal) or in a cyclic manner as part of a low(er)* carbohydrate diet with a baseline intake of 90-120g/day and additional carbs after every workout.
      *compared to the RDA of ~60% carbs
    "Carbohydrates? But aren't those just making you fat?" With this very question that's now probably on the mind of one or two (or three ;-) of you, we did eventually arrive at the topic of this episode of the Athlete's Triad Series:
    Is there a ideal macronutrient ratio that will prevent the onset
    and help you get rid of the athlete's triad?
    To be honest, I don't know the answer to this question... and although I had almost typed the word "yet" win the place where you now see the "..." , I must admit that I am not even sure if there actually is a definitive answer to this question. What I do have to offer, though, is a couple of things to keep in mind, when it comes to the macronutrient make-up of your diet.
    1. There is no such thing as a "bad" nutrient. There are about as many good arguments to vilify the overconsumption of protein, as there are arguments against the usual scapegoats, carbohydrates and fats.
    2. Glucose and saturated fats can be essential, too. Just because your body can produce carbs and saturated fats on its own, this does not mean that you do not have to, let alone should not eat them.
    3. The optimal macronutrient ratio will change over time - just like and in response to the way your physique, conditioning, lifestyle, training and general stress levels  will be changing. This implies that diet X, which may have worked magically for you, when you got rid of slabs of body fat is now that you are finally in the "normal range", let alone already so lean that your body's alarm bells are constantly ringing, hampering your progress.
    And even if the previous comments on the importance of readily available energy and glycogen repletion would suggest that carbohydrates should make up the lion's share of the diet of any athlete trying to recover from the triad (or not to fall victim to it), an extreme high carbohydrate alone is neither guaranteed to solve the problem nor is it a sustainable way of eating you could stick to once you've "carbed" yourself out of the dark hole you have been digging over the past months.

    Readily available energy? Does that mean I have to eat sugar all day?

    Figure 2: Cortisol (left) and testosterone (right) levels in healthy men after 10 days on high protein vs. high carbohydrate diets (based on Anderson. 1987). Tegelman et al. report similar results from Swedish elite male Ice Hockey players after a reduction of fat and an increase in carbs (Tegelman. 2007)
    On the one hand, we've known for over two decades that a high carbohydrate diet based on bread, vegetables, fruit, juices, pastry, and candy having a protein / carb / fat ratio of 10% / 70% / 20% will result in lower cortisol and higher testosterone levels (in men) than a high protein diet with a protein / carb / fat ratio of 44% / 35% / 21% that's based on lots of meat, fish, poultry, egg whites, and a liquid dietary supplement protein supplement (Anderson. 1987; see figure 2). On the other hand, a closer analysis of the data I compiled based on the tabular overview of pertinent studies on amenorrheic from the review by Manore (see figure 3 in the last installment) suggests that real.world advantage of carbohydrates depends on the deepness of the whole you already dug (the deeper the more advantageous) and your willingness / ability to cover or even surpass your daily energy requirements (the more you eat on a daily basis and in at least three square meals spread equally across the day, the less you will depend on the readily available energy from carbs).

    Against that background, the high carbohydrate intake (62% of total energy from carbohydrates; nutrient ratio in grams 16% protein, 71% carbs, 14% fats) was probably necessary for the women in the eumenorrheic group with an energy intake of slightly less than 30g/kg body weight (figure 3, R5).
    Figure 3: Macronutrient compositions (in kcal!) of amenorrheic and eumenorrheic women from 15 different studies (based on an overview in Manore. 2002)
    For the eumenorrheic female athletes who were at, or way above the average mean energy intake of 35g/kg body weight, the "high" carbohydrate intake of 265g/day probably wasn't detrimental. On the other hand, it appears questionable, whether an increase in protein intake from 1.2g protein per kg of body weight to 1.5-2.0g/kg and a corresponding protein to carbohydrate ratio of 25% / 62% would not have been more facilitative to their goals (specifically if those include strength training). The same goes for both, the replacement of yet another part of the carbohydrate ration with an isocaloric amount of fats and the overall role of fats in the etiology of and the recovery from the athlete's triad.

    The fat-phobia still loomed large, when the majority of studies was conducted

    Part of the problem of reconciling theoretical considerations, such as the "availability advantage" of carbohydrates and the scarce and almost exclusively observational data based on which I compiled the overview in figure 3 of this, as well as the last installment of this series, is that eating patterns of both the eumenorrheic, as well as the amennorheic athletes was geared towards the dietary paradigm of the day. With "the day" being the late 1980s and 1990s, i.e. those years in which the fat-phobia literally climaxed, it should be obvious that the baseline diet was low in fat and high in carbs.

    Against that background it should also be clear that anyone trying to "cut calories" would reduce the amount of fats, the "bad energy dense heart killers" and keep the intake of carbohydrates constant (=high). This is probably also, the reason that the ostensible disproportionate lack of fats in the diets of the amenorrheic women vanished, once I weighted the data with the number of participants.
    Figure 4: Total dietary intake of protein, carbohydrates and fats (in g; left) and differences between women with and without regular menses (right); data expressed either as simple group averages or weighed for the number of study participants (same sources as figure 3)
    The picture that emerges after this adjustment has been done (figure 4, right, light bars) is clear and stands in line with my initial remarks on the primary of readily available energy in the form of circulating glucose, liver glycogen, and adipose tissue triacylglycerol, of which at least the former are way more readily derived from carbohydrates than fats.

    And even the triacylglycers do, as the name implies, require a certain amount of glucose for the glycerol backbone (could be produced in the liver from amino acids and/or fats, though) and a minimal amount insulin to be stored in the fat cells (can be secreted in response to high amounts of protein and fat, as well, though).

    So no fats? Just carbs and some protein?

    Yet though carbohydrates have the availability bonus and proteins are necessary to maintain, better even build muscle mass, you would be ill-advised to steer clear of all dietary fats and, even more so the many good foods that contain them. Not so much because of the "essential" polyunsaturated fatty acid, though. According to a study by Tomten and Høstmark the dietary intake of PUFAs in 20 female runners with regular (n=10) and irregular (n=10) menses (LH levels of 7.6 vs. 2.9 IU/l!) was not statistically different. The intake saturated fats (-28%) and even more the intake of MUFAs (-38%), on the other hand was (Tomten. 2009) and the corresponding total fat-intake of 1.1g/kg body weight was obviously not sufficient to maintain optimal hormonal levels in the presence of a training volume of 7.5h per week.

    What about vegetarianism? I know a few of you won't like this, but unless you are at least ovo-lacto vegetarian, i.e. a person who eats dairy and eggs, you are going to have a hard time fueling your athletic endeavors appropriately. After all, vegetarianism is associated with hormonal and menstrual abnormalities even in the non-athletic population, when they are dieting (Pirke. 1986). If you combine a mild energy deficit, as it is often seen in vegetarian, let alone vegan athletes, simply because it's harder for them to cover their energy and specifically protein and fat requirements without guzzling omega-6 oils and soy shakes all day (both not advisable, by the way), it is actually not surprising that Benson et al. mention vegetarianism right along low calorie intakes, nutritional inadequacies and low body fat stores as one of the main contributers to the (female) athlete triad (Benson. 1996).
    Now you can certainly argue that all this comes down to the energy density and the correspondingly lower overall energy intake and could have been compensated for, if the women with menstrual irregularities had simply eaten more carbohydrates. In view of the fact that they didn't do so, I can hardly refute this argument. On the other hand, we have seen in the previous installment that an overexpression of GH and ghrelin is in as much part of the problem as too little insulin and a pathologically high insulin sensitivity. And some more fat in the diet (alongside carbs / not as the sole energy source!) couId in fact come handy to get that back in check.

    Moreover, having a carb to fat ratio of ~2:1 (in energy equivalents) and a baseline fat intake in the range  of 80-100g (total) as the female runners with regular menses in the Tomton sudy had, has the beauty of never having to throw away the egg yolks, being able to get your share of fatty fish, full fat dairy, Kerrygold butter, virgin coconut and olive oil and beef or better calf liver as well as nuts once in a while. This in turn will allow you not just to stay sane and flexible with your diet, but also to satisfy your need for all those vital micronutrients you won't find in any of E-number laden fat-reduced garbage from the "low fat" shelves at the supermarket.

    You see, in the end it all comes back eating simply more of the usual suspects, many people would probably file under "a paleo diet with lots of (safe) starches & fruit to fuel the energetic demands of a hard working athlete", these days.

    If we think of the hypothetical daily energy requirement of 2000kcal/day which is often used as a reference for the nutrition information on those products of which you are going to buy less in the future (most real foods don't have nutritional information printed on them, you know ;-), the corresponding "numbers" could be anywhere on a continuum
    • from 110g protein / 190g carbs / 100g fats, for someone without an endurance component in his workouts*, 
    • to 100g protein / 240g carbs / 80g fats for someone who has a major endurance component and / or follows a high volume lifting routine*
      *pre- and post workout nutrition are not included, here!
    This approach would ensure that you get enough protein, appropriate amounts of readily available energy, mainly in the form of safe starches and fruit, quasi unlimited amounts of vegetables and so much fat that you don't have to resort to the devastating "chicken breast, rice and broccoli diet", which will only worsen your situation.


    References:
    • Anderson KE, Rosner W, Khan MS, New MI, Pang SY, Wissel PS, Kappas A. Diet-hormone interactions: protein/carbohydrate ratio alters reciprocally the plasma levels of testosterone and cortisol and their respective binding globulins in man. Life Sci. 1987 May 4;40(18):1761-8.
    • Benson JE, Engelbert-Fenton KA, Eisenman PA. Nutritional aspects of amenorrhea in the female athlete triad. Int J Sport Nutr. 1996 Jun;6(2):134-45.
    • Laughlin GA, Dominguez CE, Yen SS. Nutritional and endocrine-metabolic aberrations in women with functional hypothalamic amenorrhea. J Clin Endocrinol Metab. 1998 Jan;83(1):25-32.
    • Manore MM. Dietary recommendations and athletic menstrual dysfunction. Sports Med. 2002;32(14):887-901.
    • Pirke KM, Schweiger U, Laessle R, Dickhaut B, Schweiger M, Waechtler M. Dieting influences the menstrual cycle: vegetarian versus nonvegetarian diet. Fertil Steril. 1986 Dec;46(6):1083-8.
    • Tegelman R, Aberg T, Pousette A, Carlström K. Effects of a diet regimen on pituitary and steroid hormones in male ice hockey players. Int J Sports Med. 1992 Jul;13(5):424-30.
    • Tomten SE, Høstmark AT. Serum vitamin E concentration and osmotic fragility in female long-distance runners. J Sports Sci. 2009 Jan 1;27(1):69-76.
    • Zanker CL. Regulation of reproductive function in athletic women: an investigation of the roles of energy availability and body composition. Br J Sports Med. 2006 Jun;40(6):489-90; discussion 490.