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.

Vitamin D & PUFA - Is There an Overlooked Antagonism Between Polyunsaturated Fatty Acids and Vitamin D3?

Image 1: Do not write off all the "good"
foods until you read the full blogpost,
including my comment at the end
(image by ADAM)

Hah... I knew a newsitem the title of which joins everybody's contemporary "pet supplements", would get your attention. Quasi as a byproduct of one of the hilarious vitamin D + calcium trials in which scientists seek to prevent bone loss and fracture in men and women age 65 and older by supplementation with 700IU (no I am not missing a "0", here) and 500mg calcium per day, Sathi Niramitmahapanya and his colleagues from the  U.S. Department of Agriculture Human Nutrition Research Center on Aging at Tufts University found an interesting and previously not thought of negative correlation between their subjects' plasma levels of 25-hydroxyvitamin D (25OHD) levels and the ratio of poly- to monounsaturated fatty acids in their diets (Niramitmahapany. 2011). Could it be that you have to choose, when it comes to high vitamin D or PUFA intake?

Since this was not a specifically designed experiment, Niramitmahapany et al. had to rely on the data that had already been gathered in a 3-year, randomized, double-blind, placebo-controlled trial, originally designed to determine the effect of supplemental vitamin D + calcium on rates of  bone loss and fractures in 152 men and women (age >65years). Consequently, the study relies heavily on the accuracy of complex regression analysis, by the means of which the Tuft researchers tried to figure out which of the handful of confounding variables they had surveyed, had the greatest influence, or I should say statistically measurable explanatory value for the effect of vitamin D3 supplementation on serum 25-hydroxyvitamin D levels in their elderly subjects.

In essence a regression model consists of a system of several sets of loosely predefined partial differential equations (e.g. logarithmic, linear, polynomial, etc.), the scientists, or rather their computers (in this particular study, the SPSS software package was used for statistical analyses) solve using the experimentally established data. Although statistical analyses like this allow for literally unlimited adjustments for confounding variables, such as body weight, total energy intake, etc., the underlying models are still in and out of themselves theoretical constructs that are based on certain hypothesis and assumptions. Thus, any "associations" of parameter A and outcome B, which are usually expressed in the form of regression coefficients (larger coefficient = greater explanatory power), are valid only if all the underlying assumptions hold true.

Out of the parameters Niramitmahapany et al. evaluated, the only independent variable with a significant impact on the effect of supplemental vitamin D3 on serum levels was the composition (not the absolute amount!) of the fats in the subjects' diets.

Figure 1: Statistically modeled regression coefficients of total fat intake and MUFA/PUFA ratio; adjusted for baseline BMI, 25OHD levels, total energy intake (data adapted from Niramitmahapany.. 2011)

As the regression coefficients in figure 1 clearly show, neither the absolute amount of fats nor the absolute amount of an individual type of dietary fat (monounsaturated, MUFA; polyunsaturated, PUFA; saturated fatty acids, SFA) are adequate predictors of serum 25OHD levels. The ratio of monounsaturated to polyunsaturated fatty acids (MUFA / PUFA ratio) on the other hand turned out to be a pretty reliable predictor of the amount of active vitamin D in the sera of the study participants. This was all the more the case if possible influences of saturated fatty acids were taken into account in the model, as well.

Now, statistics and "associations" are one thing, mechanisms and "causations" are yet another; and obviously the latter, i.e. cause-and-effect relations and determinisms, are what humans, in general, and natural scientists, in particular, have been striving for even before the early days of natural science in the ancient times. Thus, I assume you will be interested to hear, what the scientists have to say with regard to the underlying mechanisms of the statistical "association" they observed:

The mechanisms by which fatty acid intake may influence vitamin D3 absorption have not been completely delineated. Most of the available evidence comes from early work by Hollander and colleagues (Hollander. 1981). Their gut perfusion studies in the rat revealed that vitaminD3 is absorbed by passive diffusion in the proximal jejunumand the distal
ileum (10). Absorption of physiological doses of vitamin D3 in rats was reduced by 30%in the presence of a 4-fold increase in luminal fat (Hollander. 1978; 1981), and consistent with our findings, the PUFA, linoleic and linolenic acids, were particularly effective in decreasing vitaminD3 absorption (Hollander. 1978). Hollander offered several potential explanations for why these fatty acids impaired vitamin D3 absorption. They may have increased the solubility of vitamin D3 in the micelles and changed the partition coefficient such that the vitamin D3 stayed in the micelle. Alternatively, they may have increased the size of the micelle and thereby reduced its diffusion rate and increased its difficulty in crossing the unstirred water layer lining the intestinal mucosa. 

I suppose, what you just read about how dietary fat impairs the absorption of vitamin D goes against all you have hitherto heard from the same "experts" and "gurus" who have been telling you to take 20g of fish oil and 20.000IU of vitamin D, each day. Well, in their defense, it should be said that small amounts of dietary fat are actually beneficial, probably even essential for the uptake of the so-called "fat-soluble" vitamins A, D, K (and probably even E), BUT its obviously not the fat that "drives" or "carries" the vitamins into your blood stream, but the bile acid that is secreted in order to digest the former, which helps with / is necessary for the absorption of these, in the true sense of the word, vital nutrients. Moreover, as Niramitmahapanya et al. state, even evidence for the general accepted claim that vitamin D from small amounts of fish oil "produced a greater increment in 25OHD than vitaminD3 as a powder or dissolved in ethanol" is "inconclusive", ...

because the starting 25OHD levels, study durations, and dosing schedules in the available studies weren’t matched and because increment in 25OHD rather than absorption of parent vitamin D3 was measured.

And studies by Holvik (2007) and Maalouf (2008) which compared identical doses of vitamin D as a powder or in ethanol vs. vitamin D in oil found no difference.

The authors of the study at hand obviously did not look close enough at the data of the Maalouf study, because they state that Maalouf had "found the serum 25OHD increment to be greater with the oil vehicle", which may be correct, but the difference was small and mainly the result of a single 'hyperresponder' within the small study population (N=9 in the respective group). The "greater increment" in the oil group of the Maalouf study is thus statistically irrelevant.

So, while it appears quite clear that the general effect of large amounts of fat taken with physiological doses of vitamin D is a negative one, the scientists cannot explain why mono-unsaturated fatty acids seem to be an exception to the way the other fats (and PUFAs in particular) appear to negatively affect micelle content or migration rate of fat-soluble vitamins in the intestines. Yet, whatever the mechanism may be, an increase or, after all, a reduced decrease in vitamin D3 absorption from the gut may yet be another of the hitherto established health benefits of the long-overlooked mono-unsaturated fatty acids.

Dr. Andro's comment: If you want my personal assessment of these results, take them with an appropriate amount of skepticism. After all, eating meat, fish, liver, eggs, dairy etc., all rich sources of dietary fat and fat soluble vitamins, is the way nature intended us to get part (remember we would synthesize most of our vitamin D from sun exposure) of our vitamin D. So, the only way it would make sense that fat reduces its absorption would be the close association of cholesterol, which is the building block our body uses to manufacture vitamin D, and fatty foodstuff. It would thus be more prudent to say that "fat starvation", which would naturally be associated with low cholesterol intake, is a signal for you body to increase vitamin D uptake, in order to save the valuable cholesterol for the production of other hormones. Instead of avoiding fatty foods, you should thus rather get your lazy ass off the couch and into the sun to put the cholesterol from your 10-egg-breakfast-omelet to good use ;-)

Scientists Probe the Interaction Between Saturated and Unsaturated High Fat Diets and Their Corresponding Carbohydrate Sources (Cornstarch vs. Fructose)

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 Jurgoński, Jerzy Juśkiewicz and Zenon Zduńczyk 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 (Jurgoński. 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.

World premiere! I know it sounds hilarious, but this is actually the first study I have seen that focused on nutrient interactions, instead of individual (macro-)nutrients in diets that are not even suitable to isolate the effects of the nutrient of interest - most prominent example the "high fat diet"  which is high in fat (45% of the energy is the standard; there are yet also "high fat" diets with only 32% of the total energy from fat; Gajda. 2008) but leaves enough room for carbohydrates to complement, some would say "trigger" the obesogenic effects by providing a pro-insulinogenic stimulus that will blunt the oxidation of the dietary fat and help drive it into the cells.

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 (Jurgoński. 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)." (Jurgoński. 2014)

The serum lipid profiles were influenced by both, the types of fats and carbohydrates as shown in Figure 1. What's 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).

Suppversity Suggested Read: "EGGS - A Four-Letter Food Improves Both Cholesterol Particle & Phospholipid Profile + HDL-Driven Lipid Reverse-Transport" | read more

The results are still difficult to place. The complementary increases in total and HDL cholesterol in the lard + fructose group for example could be interpreted as unproblematic in view of the contemporary social media trend to depict high cholesterol as absolutely irrelevant. In view of the concomitant 2.3x increase in the ratio of triglycerides to HDL-cholesterol, of which we do know for sure that it predicts extensive coronary disease (Luz. 2008), it is still warranted to conclude that the combination of fructose and saturated fats is even worse than the combination of a high fructose intake with unsaturated fats, which had almost no effect on the triglycerides to HDL ratio and left the rodents in the corresponding group with a trig:HDL ratio what was >2.5x lower than that of the lard + fructose rodents.

Yes, I know - that's only rodent data, there is no information on body weight, or the gut microbiome and even the impact on glucose metabolism wasn't measured (you can predict from the triglyceride levels, though, that the animals lard + fructose diet had the lowest insulin sensitivity), the reason I still spent a whole article on this paper is that this is the kind of study, we'd need if we actually want to understand "why we are fat" from the inexplicably popular (macro-)nutrient perspective... I mean, let's be honest: On the level of food items, the complexity is not a problem and we all know the food items that propel the obesity epidemic, don't we?

References:

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

Saturated Fat Makes You Fat! You Read the Press Release - Here is the Whole Story: A Story of Muffins, SFA, MUFA, PUFA, Body, Liver & Visceral Fat and N6s & Lean Mass

I have to admit: Whether a conclusion as general at this is warranted based on the data from a recent study is questionable.

Somehow I knew that people would freak out, about a press release I reposted on the SuppVersity Facebook page earlier today (read it!). Next to saying that you can eat fructose and not get obese saying that you can eat PUFAs without getting fat is probably as heretic as saying that saturated fat makes you fat... what? Oh yes! You're right, it can be even worse. I mean, imagine you'd say that unsaturated fatty acids are less obesogenic than saturated fats.

Ah, come on! That's so mainstream it must be propaganda from the "pharmaceutical enteprise/ cholesterol lowering drug entreprise" [sic!], right?

Well, I am just looking at the acknowledgements of the study the press release refers. Let's see: "None of the authors have any conflicts of interest to disclose" and "This study was funded by the Swedish Research Council (project K2012-55X-22081-01-3)." No, I wouldn't say this sounds like there had been a "pharmaceutical enteprise/ cholesterol lowering drug entreprise" funding the study

Just as an aside: Discarding the results, because the results are not inline with your own indoctrictinat like the guys who sponsored it, is pretty pathetic. If you want to argue that the results Fredrik Rosqvist and his colleagues from the Uppsala University, and the Center for Clinical Research Dalarna are b*s*, you better take a look at the study design to identify flaws and shortcomings - and guess what?! That's what we are about to do now.

Now that we have all calmed down a bit, let's see what exactly we could freak out about - or, to put it differently, let's take a closer look at the study design, the results, and their interpretation.

I - The Research Question

I know that many of you don't care about questions. That's a mistake. In science, questions are everything. Answers are secondary. The motto of a true researcher is thus - just as the Greek philosopher Euripides had it -  "Question everything. Learn something. Answer nothing." In the end, we've already made a very good start by questioning the scientists' conclusion that

"[...] overeating SFA promotes hepatic and visceral fat storage whereas excess energy from PUFA may instead promote lean tissue in healthy humans." (Rosqvist. 2014)

What we are interested in part I of our analysis are not our questions, though. What we want to look at now, is the question that worried the researchers, the questions, whether ...

"[...]liver fat accumulation during moderate weight gain could be counteracted if the excess energy originate mainly from PUFA rather than from SFA." (Rosquist. 2014)

This question, as logical as it may seem for the average individual who has been sucking up the "good fat (PUFA) vs. bad fat (SFA)" mantra with his PUFA-enriched formula ever since he was born, is obvious a reason to freak out for the meanwhile almost as average black-and-white thinking inhabitant of the blogosphere.

Don't interpret this article as incentive to follow all dietary recommendations to the "T" before you've read my 2012 article on the effects of an allegedly heart healthy low fat diet on the LDL particle profile of healthy volunteers | read more

What this question is not, though, is pure invention. The idea to investigate whether liver fat accumulation during moderate weight gain could be counteracted if the excess energy originate mainly from PUFA rather than from SFA was born, when the researchers observed an isocaloric diet rich in PUFA given for 10 weeks reduced liver fat content and tended to reduce insulin resistance compared with a diet rich in SFA in individuals with abdominal obesity and type 2 diabetes (Bjermo. 2012) - the differences were not earth-shattering, but statistically significant (-1% total fat in PUFA vs, +0.6% body fat in SFA); and the "improvements" in the visceral fat to subcutaneous fat ratio (a marker of a healthier fat distribution) in the PUFA group of the Bjermo study were brought about (mainly) by increases in subcutaneous body fat in the PUFA group.

In view of the fact that the alleged improvements (in many cases the values simply worsened less) of the blood lipids, glucose and insulin levels, the hypothesis that "liver fat accumulation during moderate weight gain could be counteracted if the excess energy originate mainly from PUFA rather than from SFA" (Rosquist. 2014) is legitimate, but probably optimistic.

II - Study Design

So, if the underlying hypothesis is valid, the next thing we could target to debunk the claim that saturated fats are more fattening / unhealthier than unsaturated fats would be to have a closer look at the design of the LIPOGAIN study:

• 

  Figure 1: Rel. changes in liver, visceral and subcutaneous fat in subjects over-consuming a high vs. low (white) saturated fat diet.

  the subjects were randomly allocated to the two intervention groups
• the scientists made sure that the subjects gained weight at identical rates (3%) (the amount of muffins consumed per day was individually adjusted weekly, i.e. altered by +/- 1 muffin/day depending on the rate of weight gain of the individual)
• the dietary intervention was based on highly standardized food items 
• muffins containing sunflower oil (high in the major dietary PUFA, linoleic acid, 18:2 n-6) or 
• muffins containing palm oil (high in the major SFA, palmitic acid, 16:0). 
• the muffing were baked in large batches under standardized conditions in a metabolic
  kitchen at Uppsala University
• except  for  the type of fat, the  muffins  were  identical  with  regard  to  energy,  fat (51%),  protein (5%), carbohydrate (44%; sugar to starch ratio 55:45), and cholesterol content, as well as taste and structure.

I guess you will agree that there are no major design flaws, here. If anything, you could speculate that the changes in SFA and PUFA intake (-1.6% and +4.9% SFA intake and +7.9% and +0.3% PUFA intake in the PUFA and SFA group, respectively) were pretty pathetic and insufficient to produce significant results.

Figure 2: Relative contribution of saturated (SFA), monounsaturated (MUFA) and polyunsaturated (PUFA) fatty acids to the total energy intake of the subject before and after the study (Rosquist. 2014)

If you take a look at my plot of these differences (you should be aware that they are expressed in terms of the total energy intake), you will have to concede, though, that the difference between SFA/PUFA ratios, i.e. 0.9 and 3.6, is pretty significant.

Figure 3: There is a distinct correlation between the relative amount of omega-6 fatty acids in the blood and the change in lean mass - a beneficial one!

More or less flawless, but still questionable: Whether that's enough for you to accept that the Rosquist et al. used their results to make a general statements about the effects of saturated vs. unsaturated fat intake is up to you. The same goes for the real-world significance of the different body and liver fat trajectories in Figure 1.

In view of non-negligible increases in total, liver and visceral body fat and the absence of the often-touted pro-anabolic effects of saturated fats (mind the proportionality of an increase in the allegedly bad omega-6 concentration in the blood and the lean mass increases / decreases in Figure 3), it's difficult to keep nibbling on a chunk of bacon without at least taking into consideration that the "bad PUFAs" may not be as bad after all.

"Whut?" Calm down, I am not suggesting that you have to go back to the "saturated fat is bad for you" mantra, but I would like to invite you to take a parting look at Figure 2 (right) and note that the main characteristic of the "PUFA" diet is not its high PUFA content, but it's balanced fat content. Maybe the sentence "The optimal diet is characterized by a balanced intake of all three main types of dietary fat" would thus be a conclusion we can agree on - ha?

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.
• Rosqvist, Fredrik, et al. "Overfeeding Polyunsaturated and Saturated Fat Causes Distinct Effects on Liver and Visceral Fat Accumulation in Humans." Diabetes (2014): DB_131622.