ONLINE DRIVERS MEDIA

This add is a perfect example of how saturated fat, in this case lard has always been blamed for the "lard" on ones hips.

Any hypothesis that tries to blame for our "fat misery" on a single nutrient is short-sighted. After years of fat-bashing, carbophobia and fructose hating in the course of which the situation progressively, we are now seeing the first studies which investigate what the Polish researchers, Adam Jurgo?ski, Jerzy Ju?kiewicz and Zenon Zdu?czyk from the Institute of Animal Reproduction and Food Research at the Polish Academy of  Sciences call the "biological interactions among these dietary factors" in their latest paper in the peer-reviewed open-source journal Nutrients (Jurgo?ski. 2014).

With the publication of the data of a their latest rodent study, the scientists have already taken the first step to a new, an "interactionist" perspective on the obesogenic effects of saturated vs.unsaturated and simple vs.complex carbohydrates and their interaction with another previously overlooked factor that has gotten quite some attention in the past months: The gut and its inhabitants.

Goodbye! Nutritional scapegoatism 

It goes without saying that this model study is nothing but a first step on a long road we still have to travel, but the differential effects the four diets (see Table 1)...

• Table 1: Composition of the diets.

  the soybean powered high cornstarch diet (OS),
• the lard-laden high cornstarch diet (LS), 
• the soybean-powered high fructose diet (OF), and
• the lard-laden high fructose diet (LF)

...had on the health, caecal short-chain fatty acid concentrations, cholesterol and triglyceride levels are revealing, to say the least.
If you take a closer look at the actual study outcomes, you will see that the answer(s) the study provides are about as complex as its design.

In contrast to the dietary fat which had no independent effect on any of the measured markers of gut function, the carbohydrate source, i.e. cornstarch vs. fructose lead to significant differences in total small intestinal mass, mean pH of the ileal digesta and the mucosal activity of sucrase, all of which were increase on the high fructose diet.

Figure 1: Serum lipid levels of the rodents after 4 weeks on obesogenic diets containing different forms of dietary fat and carbohydrate (Jurgo?ski. 2014)

Interactive effects were observed for the mass of the cecum itself (the tissue) and the digesta with opposing effects of fructose on when it was administered in conjunction with lard (reductions) vs. soybean oil (increases in cecum mass). Slightly different effects were observed for the short-chain fatty acid composition (SCFA):

"Both the dietary fats and carbohydrates contributed to changes in the total SCFA concentration in the caecal digesta of rats (p < 0.05 and < 0 0.001, respectively). The highest total SCFA concentration was in group LS, while group OS had a significantly lower concentration (p ?0.05). Similarly, the acetate concentration in the caecal digesta was influenced both by dietary fats and carbohydrates (p < 0.05 and p < 0.001, respectively) with a similar span of differences among particular groups (p ?0.05). The type of dietary carbohydrate had significant influence on the propionate and isobutyrate concentrations in the caecal digesta (p < 0.001 and p < 0.05, respectively); however, both dietary factors had an interactive effect on their concentrations (p < 0.05). The highest propionate concentration was observed in the LS and OS group, whereas significantly lower concentration was found in the OF group. The lowest isobutyrate concentration was in group OF and it was significantly higher in group OS (p ?0.05)." (Jurgo?ski. 2014)

The serum lipid profiles were influenced by both, the types of fats and carbohydrates as shown in Figure 1. Whats particularly striking, here, is the nasty effects of a combined lard + fructose feeding on the triglyceride levels.

A similar fat-dependence as for the fructose induced triglyceride boost can be observed for the levels of total and HDL cholesterol, which were increased only by the combination of fructose + saturated fat. In the rodents that received soybean oil with their coke, ... ah, I mean with their fructose, the researchers observed the exact opposite trend and a 5x lower yet similarly increased artherosclerosis risk (as evidenced by the 5x higher atherogenic index).
References:

• Gajda, Angela M. "High fat diets for diet-induced obesity models." A Report for Open Source Diets (2008).

Asian foods are low in SFAs. So the researchers had to add it to the pan.

From a physiological perspective, the observation researchers from the Nakamura Gakuen University, the  Akita University, the Chiba University and the University of Copenhagen appear counter-intuitive, why should fat increase the insulin response to a meal. The presence of fat in a meal should slow down the absorption of glucose, right?

Obviously you havent read my previous article on the fallacies of adding fat to glucose in the false believe that the reduced digestive speed would reduce the post-prandial insulin spike ("True or False? Adding Fat to A Carby Meal Lowers Insulin Response." | read more) - a highly suggested read you may want to read either, before or after you devour todays SuppVersity article.
Dont worry, todays article still has something new to offer. While the previously reported data dealt with acute responses to high(er) fat meals, Itoh et al. (2014) whose study is available as an "ahead of print paper" on the website of Nutrition Research, looked at the effects of sub-chronic, not acute high saturated fat intakes.

Figure 1: Graphical overview of the procedure  (Itoh. 2014)

In that, they conducted an intervention study to investigate the insulin and plasma GIP responses in 11 healthy women, including a dietary control. Subjects were provided daily control meals (F-20; saturated fatty acids/monounsaturated fatty acids/polyunsaturated fatty acids [S/M/P] ratio, 3:4:3) with 20 energy (E) % fat, followed by 2 isoenergetic experimental meals for 7 days each. All meals were standard Japanese meals, the recipes for both experimental meals were identical, only a different cooking oil was used.
Talking about "test meals" (I dont like to call them thus, as they were consumed for a couple of days and not just for a "test), these meals comprised 60 E% carbohydrate, 15 E% protein, and 30 E% fat with the fat being distributed as follows:

• in the high saturated fatty acid meal (FB-30): S/M/P, 5:4:1; 
• in reduced saturated fatty acid meal (F-30): S/M/P, 3:4:3

Tests were conducted after two days on the FB-20 meal (pre) and at the end of the FB-30 and F-30 phases (see Figure 1), before and 30, 60, and 120 minutes after a meal tolerance test.

Figure 2: Comparison of glucose, insulin, and C-peptide levels after the control, F-30, and FB-30 meals (Itoh. 2014)

Interestingly, the plasma glucose responses did not differ between F-20 and FB-30 or F-30. The insulin levels, on the other hand, were higher after the FB-30 than after the F-20 (P<.01).

The GIP response, i.e. the response of the non-satiating non-fat burning insulin release triggering brother of GLP-1 (learn more) that does neither reduce hunger, not appetite nor improve glucose control (increased amount of insulin used to store away the same amount of glucose; cf. Edholm. 2010), after the FB-30 was higher than that after the F-30 (P< .05).

"In addition, the difference in the incremental GIP between FB-30 and F-30 correlated significantly and positively with that of the insulin." (Itoh. 2014)

The scientists believe that their results clearly prove, what scientists have believed for quite some time, now: "a high saturated fatty acid content stimulates postprandial insulin release via increased GIP secretion." (Itoh. 2014)
References:

• Boden, Guenther, et al. "Mechanisms of fatty acid-induced inhibition of glucose uptake." Journal of Clinical Investigation 93.6 (1994): 2438.
• Edholm, T., et al. "Differential incretin effects of GIP and GLP?1 on gastric emptying, appetite, and insulin?glucose homeostasis." Neurogastroenterology & Motility 22.11 (2010): 1191-e315.
• Itoh, Kazue, et al. "High saturated fatty acid intake induces insulin secretion by elevating gastric inhibitory polypeptide levels in healthy individuals." Nutrition Research (2014).
• Nuutila, P., et al. "Glucose-free fatty acid cycle operates in human heart and skeletal muscle in vivo." Journal of Clinical Investigation 89.6 (1992): 1767.
• Roden, Michael, et al. "Mechanism of free fatty acid-induced insulin resistance in humans." Journal of Clinical Investigation 97.12 (1996): 2859.

Even if animal fats were the best frying fats, this wouldnt turn  doughnuts into "health food" and french fries into raw carrot sticks.

If you "liked" the SuppVersity on Facebook (www.facebook.com/SuppVersity) you will probably already have seen the controversies and questions my post "Scientists on the Quest for the Perfect Frying Oil" (read more) has triggered. Eventually, it all revolves about yet another of those nutritional wisdoms thats circulating on the Internet: "Ghee, tallow, lard, ... saturated animal fats and the coconut micacle, of course, are the best and only frying oils you should use." (next best Internet source)

How on earth could F. Aladedunye, and R. Przybylski, the authors of the previously cited study even dare stating that high-oleic low-linolenic rapeseed, high-oleic sunflower oils are good frying oils?

But enough of the sarcasm: In todays installment of "True or False" (read previous installments) we will focus solely on the cholesterol-containing animal fats, and save the one and only "coconut miracle" (Coconut oil - virgin, of course - must be good for everything, right? There have after all (E)-Books been written about it ;-) for another installment of this series. So, where do we start then? I guess, we could start by rendering down a big packet of butter in my frying pan... but *wtf* whats that? Its turning tar black!? Can that really be the ideal frying fat? Probably not, but if regular butter sucks, what about clarified butter aka "ghee", then? Its easier to process and there are not tarry clouds floating in the pan, when you heat it.

"But dont we all know that cholestrol aint bad for us?"

Unfortunately, there are other problems with ghee;  problems that are related to the heat-induced oxidation of cholesterol and the presence of large amounts of cholesterol oxides in commercially available "clarified butter" even before you even start heating it as it was reported by Kubow et al. in 1993 (12.3% w/w of total sterols).

If rancid fish full of oxidized PUFA aint bad for us (read previous article), why would we want to use saturated animal fats for frying then? Please note that the overwhelming evidence says that oxidize PUFAs are bad for you.

Not a problem? We all know the whole cholesterol thing is a hoax that was made up just to put everyone on statins? Well, even if that were the case, the "whole cholesterol thing" is about the effects of intact, not oxidized cholesterol on heart health. The oxidized sterols in your "healthy" clarified butter, on the other hand, dont just make it into the bloodstream (Staprans. 1994 & 2003), they will also be incorporated in various tissues (Vine. 1997) and lead to a rapid (+100%) increase the formation of fatty streak lesions in the aorta of lab animals (Staprans. 2000) and have been linked to the unexplained high risk of atherosclerosis in Indian immigrant populations in the US (Jacobson. 1987) as well as the occurrence and progression of atherosclerosis in general (Leonarduzzi. 2002; Gargiulo. 2011).

As mentioned before, butter is unfortunately, not the only high cholesterol item on the Internets list of "best, because highly saturated, frying oils". Next to butter (215mg of cholesterol / 100g) you will also find lard (95mg of cholesterol / 100mg) or tallow (109mg of cholesterol / 100mg) on these lists.
Needless to say that neither tallow nor lard or any other of these animal fats contain enough antioxidants to protect their cholesterol from being oxidized (Ryan. 1981; Park. 1986a,b).

Figure 1: Even if you believed that cholesterol was bad for you, the ~50% reduction in intact cholesterol that occurs, when you heat tallow at temperatures of 155°C and 190°C should not be a reason to celebrate (Park. 1986a)

Interestingly, Park et al. have been able to show that this process starts at temperatures as low as 135°C (the recommended frying temperature for most products is 160°C+) and does not increase with higher temperatures. For pure cholesterol Osada et al. determined 120°C as the lowest temperature that induces oxidative changes (Osada. 1993).

In 1986, a group of researchers who conducted research for the French government found that 78% of the total cholesterol that was lost (23% of total cholesterol) from beef tallow during deep frying was recovered in form of the four best known forms of oxidized cholesterol, i.e. Triol-, 7a-, 7/3-, and 7-Oxo-cholesterol (Bascoul. 1986).

The latter have been shown to decreases barrier function of cultured endothelial cell monolayers (induce leaky gut; Hennig. 1987) and smooth muscle cells (Zwijsen. 1992).

Aside from their previously mentioned effect on the progression of atherosclerosis and their direct effect no the gut lining and other protective barriers in your body. These cholesterol oxidation products (COPs) have also been shown to promote the growth of colon (Kendall. 1992) and other forms of cancer (Sevanian. 1986; Gabitova. 2014), figure in the development of type II diabetes (Mol. 1997), block the production and blood pressure lowering effects of nitric oxide (Brown. 1999) and have been implicated in the development and progression of Alzheimers disease (AD) and vascular dementia, as well as kidney failure (Sottero. 2009)
And while all the non-enzymatically produced COPs in fried (and other) foods are  "bad guys", the enzymatic conversion of cholesterol in the body (see Figure 2, bottom) can produce compounds of which Otaegui-Arrazola, Menéndez-Carreño, and Ansorena write in their 2010 review that they play important biological role.

Figure 2: Not all oxysterols are created equal. Those your body creates by enzymatic reactions figure in cholesterol homeostasis (Otaegui-Arrazola. 2010)

In fact, certain oxysterols can suppress the activation of the master transcriptional regulators of lipid homeostasis (SREBPs) by binding to an oxysterol sensing protein in the Endoplasmic Reticulum, while others accelerate the degradation of the key cholesterol biosynthetic enzyme, HMG-CoA reductase, and/or serve as natural ligand activators of a nuclear receptor (LXR) involved in coordinating many aspects of reverse cholesterol transport (Gill. 2008).

These "good oxysterols" do thus appear(!) to play a subtle but important role in the control of cholesterol homeostasis. In the context of this true or false question, their existence, functions and benefits are however irrelevant. Apropos, question! Whats the answer to our question, after all?
Reference:

• Al-Saghir, Sabri, et al. "Effects of different cooking procedures on lipid quality and cholesterol oxidation of farmed salmon fish (Salmo salar)." Journal of Agricultural and Food Chemistry 52.16 (2004): 5290-5296. 
• Alexander, Charles M., et al. "NCEP-defined metabolic syndrome, diabetes, and prevalence of coronary heart disease among NHANES III participants age 50 years and older." Diabetes 52.5 (2003): 1210-1214.
• Bascoul, J., et al. "Autoxidation of cholesterol in tallows heated under deep frying conditions: evaluation of oxysterols by GLC and TLC-FID." Lipids 21.6 (1986): 383-387. 
• Brown, Andrew J., and Wendy Jessup. "Oxysterols and atherosclerosis." Atherosclerosis 142.1 (1999): 1-28.
• Gabitova, Linara, Andrey Gorin, and Igor Astsaturov. "Molecular Pathways: Sterols and receptor signaling in cancer." Clinical Cancer Research 20.1 (2014): 28-34.
• Gargiulo, Simona, et al. "Plaque oxysterols induce unbalanced up-regulation of matrix metalloproteinase-9 in macrophagic cells through redox-sensitive signaling pathways: Implications regarding the vulnerability of atherosclerotic lesions." Free Radical Biology and Medicine 51.4 (2011): 844-855.
• Gill, Saloni, Renee Chow, and Andrew J. Brown. "Sterol regulators of cholesterol homeostasis and beyond: the oxysterol hypothesis revisited and revised." Progress in lipid research 47.6 (2008): 391-404. 
• Gupta, R., and V. P. Gupta. "Meta-analysis of coronary heart disease prevalence in India." Indian heart journal 48.3 (1995): 241-245.
• Hennig, Bernhard, and Gilbert A. Boissonneault. "Cholestan-3gb, 5?, 6?-triol decreases barrier function of cultured endothelial cell monolayers." Atherosclerosis 68.3 (1987): 255-261.
• Jacobson, MarcS. "Cholesterol oxides in Indian ghee: possible cause of unexplained high risk of atherosclerosis in Indian immigrant populations." The Lancet 330.8560 (1987): 656-658. 
• Kendall, Cyril W., et al. "Effect of dietary oxidized cholesterol on azoxymethane-induced colonic preneoplasia in mice." Cancer letters 66.3 (1992): 241-248.
• Kubow, Stan. "Lipid oxidation products in food and atherogenesis." Nutrition reviews 51.2 (1993): 33-40.
• Leonarduzzi, Gabriella, Barbara Sottero, and Giuseppe Poli. "Oxidized products of cholesterol: dietary and metabolic origin, and proatherosclerotic effects (review)." The Journal of nutritional biochemistry 13.12 (2002): 700-710.
• Mol, Marc JTM, et al. "Plasma levels of lipid and cholesterol oxidation products and cytokines in diabetes mellitus and cigarette smoking: effects of vitamin E treatment." Atherosclerosis 129.2 (1997): 169-176. 
• Osada, Kyoichi, et al. "Oxidation of cholesterol by heating." Journal of Agricultural and Food Chemistry 41.8 (1993): 1198-1202. 
• Otaegui-Arrazola, A., et al. "Oxysterols: a world to explore." Food and Chemical Toxicology 48.12 (2010): 3289-3303.
• Park, S. Won, and Paul B. Addis. "Identification and quantitative estimation of oxidized cholesterol derivatives in heated tallow." Journal of agricultural and food chemistry 34.4 (1986a): 653-659. 
• Park, S., and P. B. Addis. "Further investigation of oxidized cholesterol derivatives in heated fats." Journal of Food Science 51.5 (1986b): 1380-1381.
• 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.
• Ryan, Thomas C., J. Ian Gray, and Tan D. Morton. "Oxidation of cholesterol in heated tallow." Journal of the Science of Food and Agriculture 32.3 (1981): 305-308. 
• Sottero, Barbara, et al. "Cholesterol oxidation products and disease: an emerging topic of interest in medicinal chemistry." Current medicinal chemistry 16.6 (2009): 685-705.
• Sevanian, A., and A. R. Peterson. "The cytotoxic and mutagenic properties of cholesterol oxidation products." Food and Chemical Toxicology 24.10 (1986): 1103-1110.
• Staprans, Ilona, et al. "Oxidized lipids in the diet are a source of oxidized lipid in chylomicrons of human serum." Arteriosclerosis, Thrombosis, and Vascular Biology 14.12 (1994): 1900-1905. 
• Staprans, Ilona, et al. "Oxidized cholesterol in the diet accelerates the development of atherosclerosis in LDL receptor–and apolipoprotein E–deficient mice." Arteriosclerosis, thrombosis, and vascular biology 20.3 (2000): 708-714.
• Staprans, Ilona, et al. "Oxidized cholesterol in the diet is a source of oxidized lipoproteins in human serum." Journal of lipid research 44.4 (2003): 705-715.
• Tsai, Lee Shin, and Carol A. Hudson. "Cholesterol oxides in commercial dry egg products: quantitation." Journal of Food Science 50.1 (1985): 229-231.
• Vine, D. F., et al. "Absorption of dietary cholesterol oxidation products and incorporation into rat lymph chylomicrons." Lipids 32.8 (1997): 887-893.
• Zwijsen, Renate ML, Ingeborg MJ Oudenhoven, and Laura HJ de Haan. "Effects of cholesterol and oxysterols on gap junctional communication between human smooth muscle cells." European Journal of Pharmacology: Environmental Toxicology and Pharmacology 228.2 (1992): 115-120.