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

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

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"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?

Docosahexaenoic Acid (DHA) Blunts Negative Side Effects of Conjugated Linoleic Acid (CLA) W/out Hampering Its Effects on Body Fat Loss & the Expression of Obesity Genes

She already knew what scientists have recently discovered and now confirmed: You better stack CLA and DHA if you want lean and health offspring ;-)

Conjugated linoleic acid (CLA) is not only an omega-6 fatty acid, it's also a trans-fat (though a natural one) and still even scientists believe that it could contribute to the solution of the diabesity epidemic, if it (a) finally yielded the same extreme fat loss (yep, just the blubber, nothing else) results in human beings as in rodents (cf. "CLA Annihilates Body Fat and Increases Endurance") and (b) anywhere near appropriate doses would not hold he risk of inducing fatty liver disease and insulin resistance (Clément. 2002). At least with respect to (b) a "bodybuilding approach" to CLA supplementation which is based on the "if hammering your head against the wall hurts, you better make sure you wear a helmet" principle of stacking CLA and PUFAs, esp. the long-chain omega-3 fatty acid DHA, has already yielded some promising results in a study that has been published earlier this year (Fedor. 2012a).

Since, the deposition of fat in the liver in response to CLA supplementation is in the end only the logical consequence of CLA's lipolytic (=fat releasing) and anti-lipogenic (=inhibition of fat storage) effects in the adipose tissue, the absence of adequate data on the amount of fat in adipose tissue and muscle or the fatty acid composition of liver, adipose tissue, and muscle, nor did we monitor the changes in the expression of genes involved in fatty acid metabolism in adipose tissue and muscle in the respective study did not allow for the conclusion that the co-supplementation of DHA would not blunt the beneficial fat loss effects of CLA, as well.

Is it possible that high dose DHA blunts the negative and the positive effects of CLA?

In a paper that's going to be published in the next issue of Metabolic Syndrome And Related Disorders Dawn M. Fedor et al. describe the results of a follow up study, which dealt with this very question and I guess I am not giving away more than what you will already inferred from the headline of this post, when I tell you that the answer to the question in the subheading is "No, DHA does not blunt the beneficial effects of conjugated linoleic acid on adipose tissue!"

Figure 1: Relative body weight, liver weight, periuterine fat mass, muscle weigh, liver total lipid weight, adipose total lipid weight, and muscle total lipid content of the mice after 4 weeks on a 0.5% CLA, 0.5% CLA + 1.5% DHA or 1.5% DHA diets expressed relative to respective data from mice on the standard chow (Fedor. 2012b)

If you take a closer look at the data in figure 1 you will realize that the provision of a diet that contained 0.5% CLA (only the "active", but potentially hazardous t10, c12 isomer was used in the study) and 1.5% DHA did not blunt the beneficial effects on total and periuterine body fat mass in eight-week-old, pathogen-free female C57BL/6N mice. On the other hand, it did mitigate the negative effects on liver weight and (and this is actually quite remarkable) had identical beneficial effects on liver fat as the DHA only diet.

DHA + CLA = perfect synergists

Although the "equation" above may sound as if I had taken it right from one of those shiny adds in a muscle mags, it does in fact look, as if the combination of CLA + DHA was the silver bullet for healthy body fat (and I repeat only body fat not lean mass!) reductions in the absence of any dietary and/or exercise interventions.

Figure 2: Expression of selected genes involved in the synthesis, storage and release of fatty acids from the adipose tissue; the respective values (in a.u.) of the control group were all 100, so you can thing of these as percentages, as well (Fedor. 2012)

Moreover, the analyses of the expression of pro- and anti-obesity genes in the adipose tissue does actually support this claim:

"CLA significantly decreased the expression of LXRb, PGC1a, PPARg, SREBP1C, ACOX1, and CD36 adipose mRNA when compared to the control group. We also observed a trend for CLA to decrease the expression of HSL (P=0.08). DHA was not able to prevent any of these decreases in gene expression. CLA significantly increased UCP2 mRNA expression when compared to control group; DHA again had no effect." (Fedor. 2012b)

If we translate all these acronyms the scientists use to describe the data I've plotted for you in figure 2 into plain cause and effect relations, we could simply state: CLA induced changes in the expression of genes in the adipose tissue of the rodents that would prevent the maturation of adipocytes and the synthesis and accumulation of fatty acids, while increasing their release into circulation,  and DHA did not effect these changes.

DHA takes care of the energy that's released / not stored in fat cells

What the co-administration of DHA did, however, was to prevent the deposition of the energy that was released, respectively not even stored in the adipocytes in the liver -- and it did that so effectively that the overall weight of the liver of the mice in the CLA + DHA group was not greater than the the liver weight of the rodents in the control group.

Figure 3: Liver fatty acid composition (µmol/g) and omega-3 : omega-6 ratio after 4 weeks on regular (control), 0.5% CLA, 0.5% CLA + 1.5% DHA and 1.5% DHA diets (Fedor. 2012b)

In fact, the co-administration of conjugated linoleic acid and DHA did even reduce the total fatty acid content of the liver (not to a statistically significant degree, though) and brought about profound changes in its fatty acid content - most prominently, a whopping +975% increase in the omega-3 : omega-6 ratio (see small graph in figure 3) that were even slightly more pronounced in the CLA + DHA group than in the DHA only group (you do remember that CLA is an omega-6 trans-fat, right?).

Finally a stack that works -- but will it work in humans, as well? 

I don't know if it dawned on you, already, but dairy and butter from grass cows already has both CLA and DHA in it - what a lucky coincidence, isn't it? Still, there is one downside: You simply cannot eat enough of it to get anywhere close to the human equivalents of the amounts that are used in rodent studies.

Now, although both the changes in body fat levels in the CLA + DHA group were consistent with those observed in the CLA only group and the effects of the combination treatment on the changes in hepatic fatty acid composition were consistent with those observed in the DHA only group, there is still one question we have to answer: Are we going to see similar esults in humans?

To be honest, I still cannot answer this question, but if you take into consideration that no previous human trial used dosages in the 20-30g range simply because that would be unethical given the associated side effects, we may soon get an answer to this question - as soon as scientists dare to slowly escalate the dosage, trusting on the ability of supplemental DHA to blunt the negative, while conserving the beneficial effects of CLA.


References:

• Clément L, Poirier H, Niot I, Bocher V, Guerre-Millo M, Krief S, Staels B, Besnard P. Dietary trans-10,cis-12 conjugated linoleic acid induces hyperinsulinemia and fatty liver in the mouse. J Lipid Res. 2002 Sep;43(9):1400-9.
• Fedor DM, Adkins Y, Mackey BE, et al. Docosahexaenoic Acid prevents trans-10, cis-12-conjugated linoleic Acid-induced nonalcoholic Fatty liver disease in mice by altering expression of hepatic genes regulating fatty acid synthesis and oxidation.Metab Syndr Relat Disord. 2012a;10:175–180
• Fedor DM, Adkins Y, Newman JW, Mackey BE, Kelley DS. The Effect of Docosahexaenoic Acid on t10, c12-Conjugated Linoleic Acid-Induced Changes in Fatty Acid Composition of Mouse Liver, Adipose, and Muscle. Metab Syndr Relat Disord. 2012b Nov 21.

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 ;-)

Standard American Diet Has 'Optimal' Fatty Acid Ratio to Induce Diabesity. Plus: Study Shows Doubling Saturated Fats Would Yield More Benefits Than Halving Them

Study confirms: The SAD diet yields 'optimal' results (img. forbes.com)

Since this post is already lengthy enough, I will spare you how saturated fatty acids have long falsely been accused as the sole driving force of the western obesity epidemic and how the tides appear to be slowly yet steadily appear to be turning, as scientists delve deeper and deeper into the interactions of the total fat content in the diet, its fatty acid composition and the interaction of both with the two other macronutrients and their specific forms and get right to the study at hand. A study that appears in the current issue of the Journal of Lipid Science and deals with the first of the aforementioned interactions. The one that focuses on the total fat content and the individual fatty acid make-up of the diet (Enos. 2012).

Fat shoot out: Saturated vs. mono vs. PUFA

As Enos et al. point out, the main purpose of their study was to examine the effects of three high fat diets differing only with respect to the percentage of total calories from saturated fats.

• SFA-6% - contained 6% saturated fats,
• SFA-12% - contained 12% saturated fats, and
• SFA-24% - contained 24% of saturated fats

While the the high fat diets were set to have an identical fat (40% of the energy), carbohydrate (45% of the energy) and protein content, the two control diets were low in total fat (12%/68%/20% of the energy from fat/carbs/protein). They did however likewise differ as far as their fatty acid composition is concerned, with the modified chow mirroring the ratios (!) not the amounts of mono- and polyunsaturated fatty acids of the high fat chow (see figure 1).

Figure 1: Fatty acid composition (left) and their sources (right) that were used in the different diets the rodents were fed for 16 weeks (based on Enos. 2012)

The diets were administered for 16 weeks. Body composition and metabolism (glucose, insulin, triglycerides, LDL-C, HDL-C, total cholesterol) were examined monthly.  Adipose tissue (AT) expression of marker genes for M1 and M2 macrophages and inflammatory mediators (TLR-2, TLR-4, MCP-1, TNF-α, IL-6, IL-10, SOCS1, IFN-γ) was measured and so on and so forth... and the results were... well, not exactly as you may have expected (the latter statement assumes that you expected the SFA to be either the savior or the doom of the human race, depending on which side of the LC/LF divide you are stading).

Figure 2: Body composition (left), adipocyte size (right) and fat pad weight (inset) of the rodents at the end of the study period (Enos. 2012) Values not sharing a common letter (abc) differ significantly over time within the given diet treatment (P≤.05)

If you take closer look at the data in figure 2, there are two things that will probably catch your eye right away. The first 'eye catcher' pertains to the influence of replacing a large amount of the omega-6 fatty acids by monounsaturared fatty acids, as you will find them in olive oil, for example.

• The rodents who received the modified standard chow, with a fatty acid composition identical to the high fat diets (SFA-6%, SFA-12%, SFA-24%) had the exact same body composition as their mates who received the standard chow with its 3.7x higher n6:n3 ratio. The removal of omega-6 fatty did thus not have any beneficial effects on adiposity in the low fat groups.

The second 'eye catcher' is the non-linear increase in adiposity with increasing amounts of saturated fatty acids in the diets. This does not mean that the expected increase in obesity and adipocyte size was totally absent (read the latest "Get Lean & Stay Lean" item for more information about the association of large fat cells and metabolic syndrome), though:

• The mice in the SF-6-24% did all gain significantly more body weight and body fat than their peers on the low fat diets, but there appears to be a turning point, when the saturated fat content exceeds 12%. After all the mice in the SFA-24% group had almost the same body composition as their peers on the SFA-6% diet.

So, what do we make of these 'eye catchers'? The first one, you could argue, shows that "omega 6 overload" is not a problem, as long as you are consuming a low fat diet, in the first place. Even with the major part of those 12.2% of energy your diet provides in form of various fatty acids belonging to the potentially inflammatory omega-6 fatty acids, that's still way too low to do any harm. It does, by the way, yet explain why low fat diets work so well in a society, where most high fat foods the public consumes are laden with omega-6 fatty acids - not an insignificant result, I would say.

The 12%-SF diet, most closely mimics the standard American diet

Apropos public, the second 'eye catcher' is even more telling in term of public health,... wait, I should write sickness. Why? Well, the 12%SFA high fat diet, which supplies ...

• 47% of energy in form of carbohydrates (380g sucrose, 100g maltodextrin, 50g cornstarch per 1kg of diet; identical for all SFA groups),
• 40% of energy in form of fats (of which 12% were saturated fats), and
• 13% of energy in form of protein (from casein),

... mimics, as the researchers point out, "most closely" (Enos. 2012) the standard American diet (SAD). And the result is obvious: Diabesity!

It's a fat balancing act of macro and micro ratios  - complex and far from being understood 

What's intriguing though, is that the adipogenic effects of the diet were ameliorated, when the SFA content was further increased and the diet contained 68.6g of lard per kg chow instead of just 35.4g and 96.7g of coconut oil instead of just 30g. Since this increase in SFA was at the expense of both mono- and omega-6 fatty acids, you could of course also argue that replacing at least the latter of the two with SFAs must be healthy. Unfortunately, even a brief glance back at figure 2 reveals that this is not necessarily correct. After all, the SFA-6% group was still better off than the SFA-24% group, although they had the highest amounts of oleic and omega-6 fatty acids in the diet.

By now you should actually have realized that this is once more a difficult balancing act. Where different baseline intakes of dietary fat and carbohydrates (total) are pair of setscrews and the individiual fatty acid composition of the diet is another one. And the way these setscrews are set will not just influence the body composition:

Figure 3: Serum IL-6, MCP-1, adiponectin and leptin levels, TNF-alpha mRNA expression in the adipose tissue (left), adipose tissue sample form the rodents receiving standard chow, the SFA-12% and the SFA-24% diet (Enos. 2012). The fat cells of the SFA-6% animals looked similar to those on the SFA-6% diets.

Based on the body composition data presented in figure 2 the marked increases in serum leptin and TNF-alpha mRNA expression in the adipose tissue of the rodents in figure 3 (left) should be about as unsurprising as the fact that the adipocytes of the SFA-12% group show the greatest macrophage infiltration and subsequent necrotic tissue.

If anything is surprising, it is the non-significance of the peak in IL-6 in the SFA-24% group (this was due to a very high standard deviation) and the fact that the serum level of MCP-1 a marker of increased macrophage activity was not elevated, while the adipose tissue mRNA expression was significantly higher (5-8x) in all SFA groups compared to both of the control diets. In the end this is yet only another clear sign that far more processes than we have previously thought happen locally and do not depend on circulating and thus endocrine signaling molecules.

Figure 4: Blood glucose and insulin levels of the mice over the course of the study period (Enos. 2012)

If you take the data from figure 4 into account as well, you will certainly agree with the statement Enos. et al. make pertaining to the negative effects of the SFA-12% diet, which is - just to remind you - the mirror image of the standard American diet:

"The 12%-SF diet, most closely mimicking the standard American diet, led to the greatest adiposity (absolute fat mass), macrophage infiltration, and IR [insulin resistance]." (Enos. 2012)

Figure 5: Total  cholesterol (TC, top) and LDL-C to HDL-C (bottom) ratios (Enos. 2012)

And I guess it would actually be about time to get to the bottom line, here, if it was not for the sentence that follows this assertion:

"Although the 24%-SF diet increased adiposity and produced IR, it did not significantly increase macrophage infiltration, it led to a lesser degree of AT inflammation, and it did not raise the TC/HDL-C ratio." (Enos. 2012)

Yep, you are reading right, as the data in figure 5 shows the total to HDL ratio of the SFA-24% group, which were those rodents who consumed the largest amount of "bad" saturated fat, was virtually identical to the one of the rodents on the standard and the modified standard chow and significantly lower than in those rodents who 'lived the American way of life' (SFA-12%). A similar trend was seen in the LDL:HDL radio and the triglyceride levels.

Bottom line: So, does that mean that we would just have to fry our potato chips in lard and all will be good? Not really, no. If we keep munching tons of plain sugar, even a saturated fat only diet is not going to save us from doom (I suspect there will be another inflection point at levels which exceed 50% SFA, anyway). What the study results do yet clearly implicate is that the macronutritent and fatty acid composition of the standard American diet is downright conspicuously obesogenic, pro-diabetic, inflammatory.

While the macronutrient ratio (high carb + high fat) appears to set the body into fat storage mode, the individual ratios of the fatty acids determine the efficacy of body fat storage, the negative effects on blood glucose management, and the degree of adipose tissue inflammation - and the standard American diet excels in all these disciplines.

As far as the saturated fats go (I wonder if it also plays a role that one of the main sources was coconut oil), the study suggests that you can achieve ameliorations of adiposity on both sides of the 'obesogenic optimum' of 12% saturated fats. If you take a last look at the data in figure 4, you will yet have to concede (or triumph?) that eating more not less saturated fat and thus frying your potatoes in lard, appears to be the more promising modification you could make, if the saturated fat content of the diet was your only set screw. Feels good to know it isn't right?

References:

• Enos RT, Davis JM, Velazquez KT, McClellan JL, Day SD, Carnevale KA, Murphy EA. Influence of Dietary Saturated Fat Content on Adiposity, Macrophage Behavior, Inflammation, and Metabolism: Composition Matters. J Lipid Res. 2012 Oct 28.

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.