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.

High Fish, Soy, Lard & Low Fat Diets: How Do They Affect Body Composition, Lipid and Glucose Metabolism? Results From Study on Rats That Don't Get Obese on High Fat Chow

(Un!)Surprising results: The "healthy" soy oil is the only fat in the study at hand that causes NAFLD.

I know, it is not certain whether or not the results of rodent studies will transfer to human beings and believe me, I would rather have seen this study conducted on humans or at least pigs. And while the latter are simply to expensive, the former are unreliable and don't like to be caged in metabolic wards... well, unless they receive a monetary compensation that costs about as much as a whole pigsty ;-)

That being said, let's stick with what we have and take a look at the results, Yoko Hashimoto and her colleagues published in a recent issue of the medical journal Lipids (Hashimoto. 2013).

The "obesity resistant" wistar rat and it's reaction to different dietary fats

I promise, the results are interesting and probably highly relevant, because the strain of Wistar rats (Slc:Wistar/ST) used in this study does not become obese simply because there is some fat in their chow. In fact, this is exactly the reason why the Japanese researchers picked the Wistar/STs. They wanted to examine the effects of various high-fat diets on plasma and hepatic lipid parameters and lipid metabolism in an obesity "resistant" rodent strain (everyone and every rat can become obese, but these don't get obese just by feeding them fatty chow) who were kept on either standard low fat chow or 3 different high-fat diets for 4 weeks (45% of the energy from fat) .

Figure 1: Fatty acid composition of the different diets (Hashimoto. 2013)

The primary outcomes of the study were the body and tissue weights, total food consumption, fatty acid composition, and energy metabolism, as well as the plasma and liver lipid profiles of the rodents.

Figure 2: Food intake, organ/body weight (Hashimoto. 2013)

If you take a look at the first set of results, namely the energy intake and body/organ weights, and focus on the distribution of white and brown fat you will realize that all rats on the high fat chow were significantly fatter than their low fat fed peers. For the fish oil group, however, the fat gain was almost exclusively from metabolically active brown fat.

Figure 3: Serum an liver lipid profiles (Hashimoto. 2013)

Against that background it is actually not surprising that the "fish oil rats" were the ones with the most favorable blood lipid profile. The rats in the soy group, on the other hand carried the highest amount of white fat and that also shows up in their messed up liver lipids.

The changes in the blood lipid levels the researchers observed went hand in hand with a few, but statistically significant differences in the local expression of important epigenetic regulators of fatty acid oxidation Acat1 / Acox1, in particular in the "fish oil rats":

Suggested read on the effects of fish oil on liver fat: "TTA + Fish Oil - Fat Burning Superfats or Hepatoxic Pro-Oxidants?" (read more)

"Nineteen genes involved in inflammation response genes as well as lipid metabolism-related genes were selected and their mRNA expression levels were measured by qRT-PCR. No significant differences were detected between the groups in the expression levels of genes encoding microsomal triglyceride transfer protein (MTP), ACAT2, 3-hydroxy-3-methylglutaryl-Coenzyme A reductase (HMG- CoA R, EC 1.1.1.34), and prostaglandin-endoperoxide synthase 1 (PTGS1, COX-1). In contrast, the expression levels of Acat1 and Acox1 mRNAs were the most abundant (p < 0.01) in the livers of the [fish] group." (Hashimoto. 2013)

Interestingly enough, the fish oil group was yet not the only group with metabolically relevant changes in the genetic landscape of the liver:

"Lipogenesis was not significantly increased in the [soy] group [...] Moreover, the level of VLDL secretion in the [soy] group was lower than that in the [lard] group group, because the mRNA expression levels of Apob and Mttp were not up-regulated in the [soy] group. The normal levels of VLDL secretion contributed to hepatic lipid accumulation in the [soy] group"(Hashimoto. 2013)

Overall, the results of the study at hand do not simply highlight the differential effects of various forms of fatty acids on the development of metabolic derangements, they are also testimony to the fact that their effects on the metabolism of obesity-resistant Slc:Wistar/ST rats are much different from those of the obesity-susceptible animals that are usually used in studies like that. The latter become hyperphagic (ravenously hungry => overeating) and acquire hepatic lipid accumulation, almost irrespective of the source of dietary fat. The results of Hashimoto et. al. on the other hand demonstrate that "obesity-resistant Slc:Wistar/ST rats are isocaloric and do not exhibit hepatic lipid accumulation even when consuming high-fat diets, except one that includes soybean oil." (Hashimoto. 2013)

---

These results remind me of another SuppVersity article with the telling title "If You Go 'High Carb', You Better Go Really High! Seven Meals/Day, More than 800g of Carbs, Less Than 50g of Fat & 1000kcal Over Maintenance and Still Lean Gains!" (read more)

Bottom line: For me there are three messages to take away from this study. (1) The Slc:Wistar/ST rat could be a much better model to study the effects of high fat diets on human metabolism, than the regular rodents that are in fact actually selected for their high susceptibility to become obese on diets with 45% vs. just 11% of the energy in form of fat. (2) In a high fat diet scenario fish oil is the most effective way to keep the liver clean; the increase in body fat on the other hand is identical and the higher brown (=metabolically active) vs. white fat accumulation is probably irrelevant for humans. And what's more, if you take into consideration that all animals weighed the same at the end of the study, you just have to do the math to know that the "low fat rodents" were not just leaner, but also more muscular than their peers. (3) Lastly, there is the issue of omega-3 vs. omega-6 fatty acids where the comparison between the effects of lard and soybean oil do not contradict the importance of ratios, but still underline that the ratio interacts with the total PUFA (and omega-6) intake and that nothing compares to high soybean oil, when it comes to ruining your health deliberately.


References:

• Hashimoto Y, Yamada K, Tsushima H, Miyazawa D, Mori M, Nishio K, Ohkubo T, Hibino H, Ohara N, Okuyama H. Three Dissimilar High Fat Diets Differentially Regulate Lipid and Glucose Metabolism in Obesity-Resistant Slc:Wistar/ST Rats. Lipids. 2013 Aug;48(8):803-15

Half As Heavy, but Twice As Fat: "Atkins-Style" No-Carb Diet + Exhaustive Exercise Compromise Body Composition

Image 1: Your scale is a fat liar and putting too much trust in it is a potential hazard to your health.

In the past couple of months the shrine with the image of the Dr. Atkins has begun to totter. "Lower your carbs!" What sounds easy and works pretty well as a short- to medium-term intervention for the morbidly obese 100% insulin resistant sedentary slob is getting more and more "healthy" or "newly healthy" and active individuals into serious trouble. I have been blogging about the fallacy of athletes dieting like Biggest Losers and Biggest Losers training like athletes before and do not want to go through all the arguments again. What I do yet want to do is to point you to the intriguing results of recently published (unfortunately rodent) study from the Ludwig Maximilian University here in Munich, Germany (Caton. 2012)

Extreme "Atkins diet" minimizes weight gain, but induces a "skinny fat" phenotype in exercised rodents

If you take a cursory look at the results you see exactly what the disciplines of Dr. Atkins will tell you: "It is so easy to lose weight and/or maintain your weight on this diet! You just cut your carbs and are good to go!"

Figure 1: Change in body weight in mature and adolescent rodents on "Atkins" or standard diet after the initial 10-day phase without exercise and at the end of the 21-day period with daily running exercise (to exhaustion, max. 30min; data adapted from Caton. 2012)

And in fact, though a strictly controlled rodent study certainly is not the best model for the largely psychologically determined dietary patters of human beings, the results of the study at hand clearly show that a 94% fat diet does in fact reduce the diet induced weight gain in both adolescent and mature rodents (and the practical experience of thousand of people tells us that this works for humans, as well). Compared to the rodents on the standard diet (9% fat, 33% protein, 58% CHO, 3.04 kcal/g; fat from soybean oil!), the "Atkins rats" with their calorically more than twice as dense (7.5kcal/g) lard + butter diet exhibited a lower increase in body mass - specifically in the initial 10-day phase without exercise (the sedentary slob phenomenon I hinted at in the introduction).

Figure 2: Adipose tissue weight (mature animals, left) and volume (adolescent animals, right) at the end of the study period (data adapted from Caton. 2012)

The data on the exact body composition of the animals in figure 2 does yet confirm what I (and even the advocates of Atkins diets) have been reiterating time and again: The figure on the scale is only signficant if you ware still morbidly obese (cf. "Intermittent Thoughts on How to Measure Your Success"). After all, the  "Atikins rats" may have gained only ~50% of the body weight of their peers on the standard diet, but they had significantly more subcutaneous, visceral and total body fat (volume, adolescents) and heavier epididimal and inguinal visceral fat depots (% of body weight, mature rodents) - and that despite identical caloric intakes (due to pair-feeding) and a +38% higher post-exercise energy expenditure and in the presence of 2x and 6x lower insulin levels (adolescent and mature, respectively), ~25% reduced IGF-1 levels, 2x higher leptin levels, lower cholesterol levels and identical total serum protein.

"Was that grass-fed butter and lard from pastured pigs?"

I can already hear them, the voices complaining how "unfair" this study was, how the Atkins group got "omega-6 laden fats" from "conventionally raised pigs" and butter that was not made from milk of "grass-fed cows". This, the low protein content of this extreme interpretation of the "Atkins diet" and the mere fact that we are dealing with a rodent, not a human study, are certainly all valid arguments (the latter two more than the former, though), but they don't change the basic message that no-carbing (without regular carb-loads) and working out hard don't go well together, at least not if your goal is to improve your health and physical appearance.

Image 2: If your inside looks like that of adolescent rats on the high fat diet (A), you should better forget about what the scale is telling you and how much weight you may already have lost on whatever type of diet you have been following.

Practically this means that when you have come down 100lbs from morbidly obese to chubby and are starting a preferably intense (cf. HIIT) exercise regimen to finally get in "decent shape", you better make good use of your improved insulin sensitivity and reintroduce a reasonable amount of carbs. Starting with 10g per meal, or 30g per day (not counting veggies) and building up to a level that allows you to keep losing body fat, while gaining or at least maintaining all the muscle mass you have, will also enable you to consume a decent amount of protein (get 20g of quality protein with every meal) without running into problems related to the sudden occurrence of large amounts of amino acid derived glucose in the veins of your "fat adapted" body. If, on the other hand, you are already in "at least decent" shape, fit and metabolically healthy, but still cannot lose those unaesthetic love handles. It may be time to start "playing" a little with your macros, in the way, but not just 1:1 like Adelfo has done it. A 5-6 day lower carb (carbohydrate intake placed around workouts; veggies don't count) strategy + 1weekly re-feed, where the reduction in carb intake gets you into a <20% caloric deficit will keep your insulin levels lowish and steady, will gradually reduce your glycogen stores, will ramp up AMPK and insulin sensitivity and will force your body to come up with the missing 20% of the energy from your adipose tissue, could be one way to success - a way, which unquestionably won't work for everyone and a way which will have to be tweaked to your own demands, but also a way which is not going to leave you lean on the outside and fat from within (cf. image 2).

True or False? Butter, Ghee, Lard & Tallow - Are Saturated Animals Fats the Kings and Queens of the Frying Pan?

Even if animal fats were the best frying fats, this wouldn't 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 that's 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 today's 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* what's that? It's 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? It's easier to process and there are not tarry clouds floating in the pan, when you heat it.

"But don't we all know that cholestrol ain't 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 ain't 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, don't 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 Internet's 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.

"I always pour away the oil! I am safe, right?" If I had not heard this argument before I would certainly not mention that the oxidized cholesterol does make it into the fried products. In a study from 1991, Zhang et al. report that the average content of the measured forms of oxidized cholesterol in french fries that had been fried in fresh, previously unoxidized tallow at a fast food restaurant ranged from 1.6-3.8 mg/100g and thus 3-8x more than Pie et al. found in a rare steak (>0.5mg /100g after 3 minutes of cooking) or cooked pork (>0.56mg /100g) in 1991 or those reported by Al-Saghir et al. for cooked farmed salmon (0.33-0.9mg/100g; cf. Al-Saghir. 2004 -- the table on the left is a fully referenced overview of COP levels in various foods from Otaegui-Arrazola. 2010).

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 Alzheimer's disease (AD) and vascular dementia, as well as kidney failure (Sottero. 2009)

Total amounts of COPs (mg/100g) in the extracted fat of raw, fried w/out and w/ corn, olive and partially hydroge- nated vegetable oil, and steamed salmon (Al-Saghir. 2004).

Surprising interactions between frying oils and fried foods: I already mentioned that (a) oxidized cholesterol from frying oils migrate into the fried foods, and (b) the cholesterol in the foods is oxidized, as well. Now, the previously cited study by Al-Saghir et al. (2004) happened to compare the amount of oxidized cholesterol (COPs) in cooked farmed salmon for different cooking oils and found that the salmon that had been fried in partially hydrogenated vegetable oils had the lowest, the steamed salmon the highest content of oxidized cholesterol (0.98mg/100g) - luckily, frying with olive oil can protect you from both, the transfats in partially hydrogenated veg. oils and the COPs in steamed salmon.

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! What's the answer to our question, after all?

The best advice I can give you is to stop consuming fried foods.

We may not be able to trace obesity, diabetes, heart disease, cancer and dementia back to a specific frying oil - what we can do, though, is to draw the links between these and the general consumption of fried foods.

So, no more fried Big Macs or Snickers Bars, and all the other delicious "all American style" foods, folks!

Note: You may or may not have realized this, but at least with respect to the formation of oxidized cholesterol products, the "healthy" steaming turned out to be even worse than frying in Al-Saghir's 2004 study (see light-blue infobox)

Are butter, ghee, lard & tallow the best or the worst frying fats? While it stands out of question that the cholesterol oxidation products (COPs) are bad for you, we don't have a study that proves that the amount you'd consume if you were frying your eggs in butter in the morning will cause all sorts of ailments from "A" as "Alzheimer's" to "Z" as in "diabeteZ" ;-)

The previously cited animal studies have - as usual - been conducted with very high amounts of oxidized cholesterol in the diet and the "Ghee is the reason for increased heart disease in British Indians" hypothesis Jacobson et al. proposed in their 1982 article in The Lancet would not explain, why Indians who live in India didn't have a similarly high heart disease risk at that time... that being said, from 1960 to 1995 the prevalence of heart disease in urban areas of India increased from a meager 1% to almost 10% (Gupta. 1995; compare that to "only" 8.7% in US citizens aged 50years or older; Alexander. 2003). Moreover, US Indians who use >1kg of ghee to fry their foods have a record-breaking 4x increase in atherosclerosis risk compared to their non-ghee eating peers (Gupta. 1997).

You see, we can go back and forth on this and still won't make any progress. Personally, I would not use ghee, tallow or lard for frying; and whether coconut oil, or maybe olive oil, of which you know that it is cholesterol-free and learned that it reduces the rate of cholesterol oxidation (Al-Saghir. 2004) are better alternatives is going to be a topic for another installment of True or False - so stay tuned for more!

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. 
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