Which Fats Should Mothers-to-Be Consume if They Don't Want Their Kids to be Obese as Early as With 2-7 Years?

Fat is an important nutrient for the unborn child. Accordingly, the question is not if pregnant women should consume fat, it's rather how much and at which ratios saturated, monounsaturated (MUFA) and polyunsaturated (PUFA) fatty acids should be consumed. A new study does now go even one step further and tries t assess the optimal amount of individual fatty acids like arachidonic acid (ARA), Eicosapentaenoic acid (EPA) or Docosahexaenoic acid (DHA).

It should be obvious: Out of ethical reasons, the question from the headline can only be answered based on rodent or epidemiological studies. Now, I am not exactly a fan of epidemiology, but in this important case, I wouldn't like to rely on rodent data, which tends to deviate significantly from human data in long-term trials spanning several developing periods.

As you will probably know, a high-intake ratio of n -6/n-3 polyunsaturated fatty acids (PUFAs) has been suggested to contribute to excess fetal adipose tissue development - a hypothesis that is, as Alihaud et al. pointed out in their 2004 review, "supported by epidemiological data from infant studies as well as by the assessment of the fatty acid composition of mature breast milk and formula milk" and allegedly a consequence of the fact that n6 fatty acids are "potent promoters of both adipogenesis in vitro and adipose tissue development in vivo" (Alihaud 2004).

High-protein intakes during pregnancy are linked to higher lean mass (Tielemans 2016).

Practical Protein Oxidation 101

5x More Than the FDA Allows!

More Protein ≠ More Satiety

Protein Oxidation = Health Threat

Protein Timing DOES Matter!

Keto for Superior Weight Loss?

In contrast to what the previously referenced review may suggest, we know very little about the differential effects of PUFAs, MUFAs, and SFAs - what is even worse, though, is that know almost nothing about the individual fatty acids, with the only previous study investigating individual fatty acids being Donahue et al.'s 2011 US cohort study, which found what you've probably read previously:

"An enhanced maternal-fetal n−3 PUFA status was associated with lower childhood adiposity."

The problem, however, is that this conclusion is based on a cohort of which we all know that it is chronically deficient in N-3 fatty acids and laden with pro-inflammatory N-6s - the American Diet. Since you're not stupid enough to believe that N3s are good, while N6s are bad, you will also know that perfect health in adults, babies and even unborns will not be achieved by avoiding one and consuming another essential nutrient in excess (the n-6/n-3 ratio in the Donahue study is 12:1, in the more recent study by Hakola et al. that's based on the Finnish birth cohort with 3807 mother–child pairs it is 10:3, i.e. 58% lower).

Why is modeling better than linear analysis? If we talk about the effects of foods, behavior, and whatnot on our weight, health, or other parameters, it is unrealistic to assume that the relationship between, say, food intake and health outcome X is linear. Rather than that it seems logical to assume that it is U-shaped with a happy medium and problems resulting from both, eating too much and too little food. The statistical analysis of the data from Hakola et al. (2017) can identify these relationships, the multivariate linear analysis in Daonahue (2011) can not.

Figure 1: It is important not to forget the really important modulators of your kids' obesity risk for boys (1st) and girls (2nd value): your BMI, how much weight you gain during pregnancy (keyword: piggin' out), and highly correlated your child's birth weight (data based on Hakola 2017). 

The general lack of data and the geographic specificity, alone, would warrant another study, the possible existence of nonlinear relationships is yet another important reason to do another study, a study that does not rely solely on multi-variable linear analyses as the Donahue study did. The most recent study by Hakola, et al. did just that. Here, a nonlinear modeling approach was used:

"[...] generalized estimating equation (GEE) models [were used] to study the associations of covariates and maternal dietary variables on the repeatedly measured offspring overweight and obesity[; an] autoregressive working correlation structure was used to model the correlation of the repeated outcomes" (Hakola 2017). 

Furthermore, Hakola et al. (2017) conducted separate analysis for boys and girls and tracked the children from year 2-7 and thus beyond the 3-year mark of the Donahue study.

Low EPA and high ARA are obesity protective according to Hakola 2017.

It's also revealing to look at what didn't matter and more: The protein intake, for example, didn't matter. The intake of saturated fat didn't matter. The amount of individual saturated fats (myristic, palmitic, stearic acid) didn't matter. The total MUFA content didn't matter, the total amount of PUFA didn't matter.  And the amount of CLA or total trans-fats didn't matter, either. What did matter, though, and that in a way you may not have expected were high arachidonic acid and low EPA intakes. Both, the allegedly unhealthy n-6 and the purportedly healthy n-3, were, as you can see in the Figure to the left, obesity protective (-50% risk ; p = 0.02 and p = 0.03, respectively) in 2-7-year-old boys.

This doesn't necessarily mean that their results are "better", but it does certainly warrant taking a very close look at that the authors found (quoting from Hakola 2017):

• In girls, maternal intake ratio of n-6:n-3 PUFAs had a U-shaped association with obesity (adjusted OR for the lowest 2.0 [95% CI 1.27–3.20] and the highest 1.7 [1.03–2.73] vs. the two middle quartiles of n-6:n-3 PUFAs, p = 0.01).
• In boys, arachidonic acid (20:4n-6): docosahexaenoic acid + eicosapentaenoic acid ratio was associated with obesity (adjusted OR for the lowest 1.0 [0.60–1.57] and the highest 0.5 [0.26–0.88] vs. the two middle quartiles, p = 0.02). 
• Saturated fatty acids and monounsaturated fatty acids were not associated with overweight or obesity in either sex.

In layman's terms: Both a very high ratio of n-6 to n-3 ratio, a result of eating too much high n-6 foods and eating too few n-3 foods, is just as bad as avoiding the allegedly "bad" n-6 foods, such as vegetable oils, nuts and seeds, and also conventional meat. This is particularly obvious for boys, in whom Hakola et al. found that the often supplemented n-3 fatty acids DHA and EPA were associated with increased obesity if they were not compounded by high intakes of their n-6 counterpart arachidonic acid.

In girls, the n-6/n-3 ratio showed a U-shaped relationship w/ obesity; in boys avoiding n-6s and thus their long-chain variety arachidonic acid while prioritizing DHA+EPA (n-3) will even increase the boys' risk of overweight and obesity at age 2-7 by 50%!

That there's a sex-difference with respect to the pro-/anti-obesity effects of dietary fat consumption during pregnancy has been known for years, the specificity for certain fatty acids, on the other hand, is a novel result - just like the nonlinearity of the link between the n-6-to-n-3 ratio and its effects on overweight/obesity in girls (the data for linoleic acid/linolenic acid is virtually identical).

Figure 2: Overweight and obesity risk according to quartiles (the higher the quartile, the greater the ratio) of n-6/n-3 intakes in male (left) and female (right) offspring; based on Finnish birth cohort (3807 mother–child pairs; Hakola 2017).

This does also imply that, for boys, the simple ratio of n-6/n-3 fatty acids is irrelevant - at least in Finland; and that's in contrast to the dreaded, allegedly inflammatory and unhealthy arachidonic acid (the long-chain n-6 counterpart to DHA and EPA) which has to be balanced with its n-3 counterparts DHA and EPA to achieve and optimal (low) overweight/obesity risk when your baby boy is 2-7 years old - optimal, at least in the Finnish birth cohort study, was...

...unfortunately, I cannot tell you the exact optimal numbers, because it was neither in the full text of the study nor in the supplemental data.

Now that may sound "bad", but an "optimum" calculated based on a single prospective study that was conducted in a country you don't even live in (my Finnish friends: please ignore the last argument, but acknowledge that a single study cannot identify the "optimum", anyway).

Figure 3: Overweight and obesity risk according to quartiles of arachidonic acid (ARA) to DHA+EPA ratio in male (left) and female (right) offspring; based on Finnish birth cohort (3807 mother–child pairs; Hakola 2017)

What appears to be certain, though, is that this ratio is greater than the ratio of medium intakes of ARA/DHA+EPA of the subjects in the study at hand, i.e. 10.32 [to put that into perspective, the ratio of the average supermarket egg is ca. 50, the ratio of "omega-3 eggs" is ca. 0.5, the one of free-ranging chicken ca. 0.7 (Simopoulos 1992)].

Figure 4: The metabolic processing and effects of n-6 and n-3 metabolism on selected exemplary physiological processes ranging from inflammation and immunity to vascular and brain health (Uauy 2006).

What does all that mean? If childhood obesity is the relevant study outcome, the notion that you can hardly get enough omega-3 fatty acids is simply false. That's not news, but it is commonly forgotten with all the hype about fish oil and omega-3 fatty acids.
Yes, DHA and EPA are healthy, yes, they are essential (at least for mothers to be / their unborn offspring), and yes, they are a deficiency nutrient in the average western diet. That a given nutrient is healthy and essential, however, does not imply that its physiological/nutritional counterpart is unhealthy and non-essential. Both, N3- and N-6 fatty acids are essential for the normal development of unborn babies.

It is thus hardly surprising that the study at hand emphasizes the importance of ratios and the inadequacy of the assumption that the link between the n-6/n-3 ratio and/or individual fatty acids was necessarily linear.

It would be a huge mistake to use the data from the study at hand to estimate "optimal" intakes for mothers, for at least three reasons: Firstly, we are (a) talking about a single study, even if it was the perfect study, that wouldn't be enough to make reliable general statements. Secondly, the study was (b) conducted in a population that has one of the highest intakes of plant n-3 PUFAs in the world and an above average intake of seafood n-3 PUFAs (Pietinen 2010; Micha 2014). Women from Finland and a country like the US will thus differ not only with respect to their fatty acid intakes but also with respect to the levels of n-6s and n-3s in their blood and cells. It is thus not surprising that US-studies like Donahue et al. (2011) found inverse linear associations between n-3 intakes and childhood weight that turned out to be U-shaped in the Hakola study, with subjects with significantly higher n-3 intakes. Third- and lastly, childhood obesity is (c) a huge problem and contributes to the diabesity epidemic with all its unhealthy consequences, it is yet by no means the only factor we'd have to consider if we wanted to recommend "optimal" ratios for n-6/n-3 and, more specifically, ARA/DHA+EPA intakes in pregnant women.

What we can already say with some certainty is that mothers-to-be should consume a balanced diet, a diet that contains both, n-6 and n-3 fatty acids in a ratio that cannot be determined based on the limited database we have, today - a ratio that will probably differ according to at least three parameters: offspring sex, maternal baseline diet, and, obviously, the health parameter we're looking at (e.g. obesity at age 2-7 vs. IQ at age 2-7 vs. insulin sensitivity, etc.) | Comment!

References:

• Ailhaud, G., and P. Guesnet. "Fatty acid composition of fats is an early determinant of childhood obesity: a short review and an opinion." Obesity reviews 5.1 (2004): 21-26.
• Donahue, Sara MA, et al. "Prenatal fatty acid status and child adiposity at age 3 y: results from a US pregnancy cohort." The American journal of clinical nutrition 93.4 (2011): 780-788.
• Hakola, L., Takkinen, H-M., Niinistö, S., Ahonen, S., Erlund, I., Rautanen, J., Veijola, R., Ilonen, J., Toppari, J., Knip, M., Virtanen, S. M., and Lehtinen-Jacks, S. "Maternal fatty acid intake during pregnancy and the development of childhood overweight: a birth cohort study." Pediatric Obesity 12 (2017): 26–37. doi: 10.1111/ijpo.12170.
• Micha, Renata, et al. "Global, regional, and national consumption levels of dietary fats and oils in 1990 and 2010: a systematic analysis including 266 country-specific nutrition surveys." Bmj 348 (2014): g2272.
• Pietinen, Pirjo, et al. "FINDIET 2007 Survey: energy and nutrient intakes." Public health nutrition 13.6A (2010): 920-924.
• Simopoulos, Artemis P., and Norman Salem. "Egg yolk as a source of long-chain polyunsaturated fatty acids in infant feeding." The American journal of clinical nutrition 55.2 (1992): 411-414.
• Tielemans, Myrte J., et al. "Protein intake during pregnancy and offspring body composition at 6 years: the Generation R Study." European journal of nutrition (2016): 1-10.
• Uauy, Ricardo, and Alan D. Dangour. "Nutrition in brain development and aging: role of essential fatty acids." Nutrition reviews 64.s2 (2006).

Low Carb(-ing) Reduces Fat & Fast Food (10-20%) Cravings Plus 60% Less Hunger After Meals in Obese Men/Women

You always crave the foods you must not eat, right? No, ... a recent study finds decreases in sweet and starch cravings in obese individuals on low-carb diets.

If the calorie intake is standardized, low-carb dieting has no proven metabolic weight loss benefit compared to any other dietary weight loss intervention. In the real-world, as well as less tightly controlled studies in obese individuals, however, they tend to outperform their American Heart Association inspired bogus low fat, low protein, high carbohydrate counterparts.

The reason? No, still no "metabolic advantage": reduced hunger and food cravings and the subsequently increased adherence and reduced energy intake - an assumption that isn't proven, but at least supported by Colette Heimowitz' latest paper. A paper based on a study that was sponsored by Atkins Nutritionals and smells of bias, but a study that's in line with millions of N=1 reports on the internet.

Would be interesting to compare keto to high-protein, not western diets, right?

Practical Protein Oxidation 101

5x More Than the FDA Allows!

Low Carb Unfit for Crossfit(ters)

Protein Oxidation = Health Threat

Keto Diet ⇒ Perform. ↓

Keto for Superior Weight Loss?

As the authors explain, "[...m]any individuals entering weight loss programs may believe that restriction of a certain type of food (e.g., carbohydrate, CHO) may increase their cravings for that food" (Heimowitz 2017). With their vested interest in making the low-carb diet and their low-carb convenience food look good, the scientists' goal was to prove that these carbohydrate cravings don't exist. Obviously, that's not what you will read in the paper which phrases things significantly less suspiciously stating that "the present study was to assess motivation for entry into a weight loss program, acceptability of low-CHO commercially-prepared foods, and changes in food cravings during rapid weight loss associated with high-fat, low-CHO dietary consumption" (Heimowitz 2017). "The foods provided for the first 2 wks included Atkin’s products (frozen dinners, bars and shakes), and some freshly-prepared meals (total fat was 54±4% of energy (%E), protein, 28±2 %E, and CHO 14±1 %E; fiber intake, 26±8 g/d) and resulted in an energy deficit of 1198 ± 655 kcal/d, then...

Figure 1: Macronutrient composition of the energy-reduced diets (intended deficit of ~1200kcal/day | Heimowitz 2017)

"[f]or the next 2 wks, subjects prepared their own meals with the goal of achieving a similar food intake. Subjects were surveyed regarding reasons for enrolling in the program, and at baseline (BL) and 4 wks, completed the Food Craving Inventory (cravings for foods that were fatty, sweet, high in CHO (starches), or categorized as fast foods), and the Three Factor Eating Questionnaire (TFEQ) to assess food intake motivation" (Heimowitz 2017).

All N=20 subjects (10 men and 10 women with a mean age o 40±8y, and a BMI in the red obesity zone of 34±3 kg/m²) completed the study with their main goal being to look better - not to be healthier, which ran as a poor second, along with family issues.

Figure 2: Plot of the most relevant anthropological and psychological study outcomes (Heimowitz 2017).

Over the course of the intervention, of which you should by now have realized that its non-controlled nature significantly reduces its meaningfulness, the subjects lost a highly significant amount of bod weight (5.7±0.6 kg, P<0.00001) and, more importantly, were able to reduce their waist circumference by 5.6±0.9 cm (P<0.00001). Unsurprisingly, "subjects stated that consumption of [the authors' company's] pre-made meals aided them in meeting their weight-loss goals" (Heimowitz 2017).

• 95% of subjects reported being somewhat satisfied to very satisfied with the meals, 
• 60% felt less hunger after meals, and 
• 75% reported reduced 'eating when bored'

With regard to the underlying research question, the scientists' statistical analysis of the data from the questionnaires, the authors observed a high baseline craving for sweet foods (45% of subjects reported frequent cravings for sweets) that did not increase with low-carb dieting. In fact, after weight loss, cravings for sweets and starchy foods were reduced by significant 12±10% (P=0.02 | low effect size, though) and 12±6% (P<0.01 | medium effect size), respectively.

What is particularly interesting is that the reduction in sweet cravings tended to be associated with a reduction with significant reductions in disinhibition and increases in cognitive restrained: over time, the subjects were thus more and more able to control their food intake and less susceptible to fall victim to their (now reduced) cravings - reduced cravings for sweets and starches and reduced cravings for fatty foods (11±7% | P<0.03) and fast food cravings (19±5% | P=0.0006), all without the often-heard-of difference between men and women (you know how women are supposed to crave sweets, and men fatty foods).

Different Study Population = Different Goals, Different Outcome: "Low Carb Diets and Physical Performance - Recent Studies Show Performance Decrements in Average Joes + Athletes" | read  more

Bottom line: The study provides valid evidence for the commonly heard claim that low-carbing would reduce food cravings. It does not, however, prove that a similar effect wouldn't have been observed simply due to weight loss with other diets. Do the scientists mention that in the conclusion to the abstract, the only part of a paper many people read? Obviously not.

Without a follow-up study that compares the effects of a low-carb to an energy-equivalent control diet (ideally one that's high(er) in satiating proteins), the study at hand must be considered preliminary evidence.

Evidence that is, however, in line with the reports of many (formerly) obese low-carb fans all around the world - reports from lean individuals and athletes, as well as the results of studies comparing low- and high-carb diets head to head (e.g. Brehm 2003; ), on the other and, are much more inconsistent and suggest that metabolic, genetic and/or lifestyle differences may determine whether low-carbing will curb your appetite | Comment!

References:

• Brehm, Bonnie J., et al. "A randomized trial comparing a very low carbohydrate diet and a calorie-restricted low fat diet on body weight and cardiovascular risk factors in healthy women." The Journal of Clinical Endocrinology & Metabolism 88.4 (2003): 1617-1623.
• Heimowitz, Colette, et al. "Changes in Food Cravings during Dietary Carbohydrate-restriction." The FASEB Journal 31.1 Supplement (2017): 643-23.

Eating 75-100g Fat (M-/PUFA) in the AM Improves Glucose (7-8%), Insulin (40-60%), Trigs (4-16%), GSH & MDA (40-75%)

If we assume that the protein fried eggs with its comparatively low insulinogenicity is not a problem (unlike your whey, for example), avocado and eggs fried in olive oil is the perfect breakfast to replace the liquid test meal used in the study.

There's no debating that increased amounts of free fatty acids in the blood will impair your insulin sensitivity, as they should be there only, when your supply of carbohydrate is running out, AMPK and with it the expression of lypolytic enzymes increase and the triglycerides from your fat stores are broken down into free fatty acids and released into your bloodstream where they can be used by liver, muscle and other organs as an alternative energy source.

Now, the word "alternative" is of paramount importance, here, because you'll find yourself being in (diabetic) trouble if those FFAs pile up on top of high glucose levels. This is what happens with the SAD diet and its high carbohydrate and fat content (and energy!) content.

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?

It's a vicious circle: When the levels FFAs are up, insulin sensitivity goes down (after all, with a normal diet you'd have to burn the fat and spare the precious glucose | Bodne. 1997; Koves. 2008). Since there's more and more glucose spilling in over the portal-vein, though, insulin will keep increasing to a point where it does no longer simply impair, but almost block the oxidation of free fatty acids. Now, without insulin working its glucose shuttling magic, however, the cells begin to starve for glucose and... right, more FFAs are being released, the insulin resistance increases, still hardly more glucose is being shuttled into the cells to restore AMP to ATP and the process continues.

What does all of that have to do with eating more MUFAs and PUFAs to control your glycemia? Well, nothing and everything. First- and most importantly, it should remind you that this is not about eating fat with your carbohydrates. That's exactly not what the latest study from the Hospital Clínico Universitario Valencia in Spain would suggest, even though I bet you will have some idiot already have misinterpret the study in this way "for your" online. Rather than that the study was, as the abstract already tells you, conducted to ...

"[...] evaluate the changes in glycemia, insulinemia, and oxidative stress markers during an oral fat load test in nondiabetic subjects with abdominal obesity and to analyze the association between postprandial oxidative stress markers and postprandial glucose and insulin responses" (Martinez-Hervaz. 2016)

This quote also contains another important information you will have people with an agenda forget to mention: the subjects in whom the fats worked their magic were abdominally obese! Later on we will see why this is relevant and why the same rules won't apply to lean individuals, but for the time being let's firstly take a look at the exact characteristics of the N = 40 (total) subjects in the study in Table 1.

Table 1. General characteristics, fasting lipids and lipoproteins, glucose, insulin and HOMA index values in the studied groups (Martinez-Hervas. 2016); ^a control vs abdominal obesity group (p<0.01).

Even though the discriminating feature, i.e. the characteristic the scientists used to find subjects for the two groups was their waist circumference (>102/88 cm for men and women, respectively vs. <102/88 in the control group), it shouldn't surprise you that the scientists have also observed sign. differences in other anthropometric and metabolic markers such as the BMI, the level of triglycerides, blood lipids and postprandial glucose levels after an oral glucose tolerance test (OGTT | see Table 1).

Is it a problem that the male / female ratio differed? That is difficult to tell. We do know that men and women handle nutrients, esp. fat and carbs slightly differently, but I doubt that the difference between an 11/9 ratio in the control group and a 7/13 ratio in the abdominal obesity group will ruin the results of the study at hand. Nevertheless, this should be addressed in future studies.

After initial testing, the subjects from both groups ingested the same commercial liquid preparation of high-fat meal of long chain triglycerides. The product is called SuperCal and must not be confused with a vitamin D + calcium product with the same name that is being sold on the US market. From a previous European study, I've got some extra-information about its composition, namely that

"[...] 125 ml contains 60 g fat, of which 12 g are saturated, 35.35 g are monounsaturated, and 12.75 g are polyunsaturated. Each 100 ml contains <1 g lauric acid, <1 g myristic acid, 4.8 g palmitic acid, 1.4 g stearic acid, 27.7 g oleic acid, 9.6 g linoleic acid, 1.4 g behenic acid, and 0.5 g lignoceric acid" (Fernández‐Real). 

The detailed fatty acid composition of the SFAs, MUFAs and PUFAs emulsion that was administered at a dosage of 50 g fat per m² of body surface (calculate your body surface if you want to know your individual equivalent dose = result of your calculation in m² x 50g g/m²; e.g. 1.78 m² x 50 g/m² = 89 g of fat) at 8:30 after an overnight fast is not mentioned in the Martinez-Hervas study. What the authors of the study at hand tell us, however is that the likewise relevant ratio ω6/ω3 is > 20/1 - similar to the average diet, by the way; a fact that excludes that this is an omega-3 effect we are seeing, here. Similarly, exercise or previous meals, shouldn't have messed with the results, either. After all, in both groups, only water was permitted during the "eating" or rather "drinking" process, and no physical exercise was undertaken before or during the "fasted" fat loading test in the AM.

Figure 1: Overview of the rel. levels of glucose, insulin, HOMA-index, trigs, the GSSG/GSH ratio and MDA, a byproducs of lipid oxidation (Martinez-Heras. 2016); levels expressed relative to control at baseline (T = 0), see explanation below

In order to make the data more accessible (compared to the tabular overview of absolute values in thee FT) for you, I've standardized each of the measurable variables to match 100%. This means that all the fasting bars at T = 0h will be at the 100% mark, because they are what the effects of fat loading are compared to. Let's take a look at two examples:

• 

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

  Insulin: In contrast to what you will see if you co-administer fat and carbohydrates (learn more), the administration of the high MUFA + PUFA fat supplement in the absence of carbohydrates lead to a sign. reduction of the initially 3.8-fold increased insulin levels. Not to normal levels, but at least to 158% (i.e. 1.6-fold elevated) of the fasted value of the lean subjects. Ah, but remember: All that happened with the fat load, alone, and in the absence of CHOs. In the presence of carbs the results would have been much different.
• GSSG/GSH ratio: The effects on the ratio of 'used' glutathione (GSSG) to the amount of the 'fresh' master anti-oxidant (GSH) were quasi the opposite of what the scientists observed for insulin. Here, the abdominally obese group had 2.4x elevated levels to begin with. This tells you that, compared to the normal controls, their anti-oxidant status was a mess. After only 8h, however, their GSSG/GSH ratio had not just declined, it was actually lower than the fasted value of the control group.
  
  And again, likewise similar to the effects on insulin, the control group saw benefits as well, with a 64% decrease in the GSSG/GSH ratio their antioxidant defenses did also benefit from the MUFA + PUFA load in the AM.

For other parameters you will see similar, for many of you probably surprising benefits. Things to keep in mind, though, is that we are talking non diabetic subjects in both groups, even if the abdominally obese subjects had fasting HOMA index values fourth fold higher than controls, higher fasting triglyceridemia and higher fasting oxidative stress markers. If that sounds like you, then the acute ingestion of ~75-120g (depending on your body surface) of fat on empty in the AM, when hyperlipidemia is not that much of an issue, you can benefit from a high MUFA + PUFA fat load as you would find it in an avocado + egg fried in olive oil, for example... or, as the authors of the study at hand have it:

"[O]ur study has demonstrated a significant reduction of postprandial glycemia, insulinemia, c-peptide and oxidative stress markers using an acute oral overload of unsaturated fat. We have found a significant correlation between oxidative stress markers and postprandial lipemia. There is an increase of TG achieving the maximum peak four hours after the beginning of the test. However, although postprandial lipemia has been implicated in the development of insulin resistance and oxidative stress, and despite the increase of TG, there are significant reductions of the HOMA index and oxidative stress markers" (Martinez-Hervas).

Even though you may think otherwise, the authors are also right, when they point out that "[t]he influence of dietary macronutrients in insulin sensitivity is not well known" (ibid.) This is especially true, when we begin mixing proteins, carbohydrates and fats and start to take into consideration that we can have a dozen of types of the three in a single meal.

What about me? I am not abdominally obese, will I benefit, too? If we assume that you deprive yourself of any carbohydrates (and proteins?), you should see the same benefits as the subjects in the control group - those are lower than what we see in the big belly group and may simply be a result of the moderate energy intake (that's < 900kcal before an 8h fast even for many bigger guys), it would appear as if the answer to your rightly asked question would be "Yes, you can benefit, as well." Whether this will also require you to abstain from all, not just insulinogenic dairy proteins, however, will have to be tested in future studies.

It may thus depend on the food-matrix whether the results of previous studies, most of which clearly indicate that saturated fat will increase in fasting and postprandial insulin resistance would have yielded different results if the meals were administered in the absence of carbohydrates, for example - even though, additional evidence traced these effects back to increased levels of saturated fat in the cells' phospholipids that can alter their phyco-chemical properties and decrease the glucose transporters (while MUFA and PUFA have been shown to do the opposite | Borkman. 1993). Martinez et al. who have not actually tested the effect of SFAs in their studies provide additional evidence in their discussion:

Will the additional butter on top of the potatoes reduce the insulin response? You can find the answer to this and the other questions in today's episode of "True or False?" | Learn the answer

"Iggman et al demonstrated in elderly men that palmitic acid, the major saturated fatty acid found in adipose tissue, inversely correlates to insulin sensitivity measured by euglucemic-hyperinsulinemic clamp. However, they also found a positive relation of insulin sensitivity with the content of linoleic acid in adipose tissue (Iggman. 2010). It is in accordance with our results because our commercial liquid preparation of high-fat meal of long chain triglycerides is composed in the majority by linoleic acid (59%). Furthermore, in line with our findings, the replacements of dietary saturated fat by unsaturated fat also improved fasting insulin sensitivity (Vessby. 2001).

Several other studies have demonstrated that unsaturated fat improves fasting and postprandial IR, although the mechanism is largely unknown (Wang. 2015). Moreover the PREDIMED study has recently demonstrated that unsaturated fat can improve fasting insulin sensitivity and prevent the incidence of type 2 diabetes (Salas-Salvadó. 2011).

Another thing the study could not address is the chicken or egg question: After all, you can argue athat the significant reduction in oxidative stress markers the scientists throughout the fat load test could - as a result - have improved the subjects insulin sensitivity, but - at least in theory - it is imaginable that this worked the other way around... by an unknown feedback loop.

Figure 2: Relative in-group reduction in the parameters from Figure 1 from 0h to 8h (Martinez-Hervas); in contrast to the previous figure the one at hand shows the in-group difference, i.e. the change in control at 0 vs 8h, etc.

As you see, there's still lots to be learned about dietary fat out there - including the fact that a "high fat" diet that combines high energy with high fat and high carbohydrate intakes is always detrimental for your health and should no longer be used in studies, unless the goal is to mimic the Western diet (and I beg scientists to then call it what it is, and that's not a "HFD").

Beware of dairy proteins, especially whey, but also casein are highly insolinogenic and may reduce if not reverse the effects of fat loading in the AM on glucose management and inflammation | learn more.

Bottom line: Before you get addicted to the previously suggested avocado + eggs fried in olive oil breakfast, please keep in mind that this is not what the scientists tested. Especially in view of the relatively high protein level in eggs, another study would have to make sure that the latter won't interfere with the benefits... even if that's much less likely for eggs, meat or fish than for the highly insulinogenic dairy proteins.

Furthermore, the study at hand cannot tell us anything about the long-term effects, because it is an acute intervention (not even lasting for 24h, there could have been a rebound at 12h or 24h or with the ingestion of another meal at noon, etc.) that suffers from another methodological problem.

Without a control supplement containing high(er) amounts of saturated fat, the assumption that the results were MUFA + PUFA specific is simply based on the scientists' review of the existing research (see previous elaborations + quotes). And as the scientists add, last- and [f]inally, oxidative stress markers analyzed could be also altered by others players regulating the postprandial state" (Martinez-Hervas. 2016) | Leave a comment, praise or criticism on Facebook!

References:

• Boden, Guenther. "Role of fatty acids in the pathogenesis of insulin resistance and NIDDM." Diabetes 46.1 (1997): 3-10.
• Borkman, Mark, et al. "The relation between insulin sensitivity and the fatty-acid composition of skeletal-muscle phospholipids." New England Journal of Medicine 328.4 (1993): 238-244.
• Fernández‐Real, José M., et al. "Fat overload induces changes in circulating lactoferrin that are associated with postprandial lipemia and oxidative stress in severely obese subjects." Obesity 18.3 (2010): 482-488.
• Iggman, David, et al. "Adipose tissue fatty acids and insulin sensitivity in elderly men." Diabetologia 53.5 (2010): 850-857.
• Koves, Timothy R., et al. "Mitochondrial overload and incomplete fatty acid oxidation contribute to skeletal muscle insulin resistance." Cell metabolism 7.1 (2008): 45-56.
• Martinez-Hervas, Sergio, et al. "Unsaturated Oral Fat Load Test Improves Glycemia, Insulinemia and Oxidative Stress Status in Nondiabetic Subjects with Abdominal Obesity." PloS one 11.8 (2016): e0161400.
• Vessby, Bengt, et al. "Substituting dietary saturated for monounsaturated fat impairs insulin sensitivity in healthy men and women: The KANWU Study." Diabetologia 44.3 (2001): 312-319.

Nigella Sativa Quadruples Fat Loss Success: 8% vs. 2% Rel. Body Fat Reduction in 8 Weeks With NS Before Every Meal

Nigella sativa is not well known in the West.

You may remember the SuppVersity special on Nigella sativa from January 2015. A special, in which beneficial metabolic effects of nigella sativa aka black cumin were only one item on a long list of health benefits, of which many had unfortunately been observe in rodent studies.

With a recent study from the Tabriz University of Medical Sciences, there's now evidence for humans that the fat loss benefits of the oil from nigella sativa are real - at least when it is ingested before meals by dieting overweight individuals.

Learn more about the effects of your diet on your health at the SuppVersity

Only Whey, Not Soy Works for Wheytloss

Taste Matters - Role of the Taste Receptors

Protein Satiety Shoot-Out: Casein vs. Whey

How Much Carbs Before Fat is Unhealthy?

5 Tips to Improve & Maintain Insulin Sensitivity

Carbohydrate Shortage in Paleo Land

We are talking about a double-blind, placebo-controlled, randomized, clinical trial, with 50 obese women. The participants were randomly divided into an NS oil group (n=25) and a placebo
group (n=25). All subjects received the same standardized diet, the scientists describe as follows:

"All the participants received a moderate fat, nutrient-balanced reduction diet. A dietician designed an individual diet by using the Mifflin equation to determine resting energy expenditure (Namazi et al., 2015). After adding the estimated physical activity coefficient (based on International physical activity questionnaire) and thermic effect of food coefficient (1.1), 500 kcal from the amount of total required daily energy calculated for each subject was subtracted. The resulting diet was composed of 15% protein, 55% carbohydrates, and 30% fat. A 24-hour dietary recall (one weekend day and two weekdays) was applied for assessing the level of patients’ compliance with the diet" (Mahdavi. 2016).

The diet was supplemented with either nigella sativa (NS) oil soft gel capsules (3g/day) with one capsule a 1g being taken 30 minutes before meals or a sunflower oil (SF) placebo capsules for eight weeks, total.

Does timing matter and what about the seeds? While it is difficult to tell, whether the effects would vanish if the oil was timed differently (i.e. not 30 minutes before meals), the mix of active ingredients, including thymoquinone (TQ), thymol, nigellone, nigellicine, alpha-hederin, unsaturated fatty acids, vitamins (B1, B3, B6, E) and minerals (Fe, Zn, Cu) may in fact have to be present in the digestive tract before / during a meal. It is similarly questionable, whether simply eating the seeds will have the same effect. If we assume that they don't "got through" (soaking, grinding or chewing them may help), they should. After all, the seeds contain the same (if not more) of the active ingredients as the oil - even if they are probably less concentrated.

To assess the success of the intervention, the scientists analyzed their subjects' BMI, and anthoprometric indices (body fat by bio-impedance), serum levels of insulin, adiponectin, peroxisome proliferator-activated receptor γ (PPAR-γ) and insulin sensitivity in obese women. Secondary outcomes were effects of NS oil supplementation with a low-calorie diet on liver enzymes and other health parameters. Dietary intake and physical activity were controlled.

Figure 1: Changes in body composition during the 8-week study in the treatment and placebo group (Mahdavi. 2016).

The first somewhat surprising result of the study is that all 50 participants completed the trial - an observation that suggests that both the diet and the consumption of the oil weren't difficult to adhere to. Accordingly, it is not surprising that all women lost a significant amount of boy weight. Especially in terms of body fat, however, the benefits differed according to treatment: While the NS oil group lost -3.6% of their total body fat mass (that's a relative reduction of ~8%), the control group lost only -0.8% (a relative reduction of ~2% | note: I used the values from the table in FT and not the questionable percentages the scientists provide in the abstract, which are even higher, but not in line with the recorded absolute changes in body fat).

These benefits went hand in hand with significantly more pronounced improvements in basal insulin levels, which were reduced by -29.3% in the treatment group and by only -8.6% in the placebo group. In conjunction with the +87.5% vs. 39.4% increase in adiponectin levels, and a significantly higher relative visceral fat loss, it is save to conclude that the addition of nigella sativa did also affect the subject's metabolic disease risk significantly.

Reader Question: Are Black Seeds (Nigella Sativa), Their Oil, Ointments & More Good For Me? What do the Studies Say?

Bottom line: Black cumin or Nigella sativa has been used in traditional oriental medicine as a weight loss aid for centuries. With the study at hand and similar studies in rodents, we are now finally able to confirm what has been "best practice" elsewhere forever.

With that being said, you cannot expect weight / fat loss miracles. No weight loss without dieting, no dieting without effort... taking black cumin oil as weight loss support may accelerate the progress, but eventually it's the energy reduced diet that had the women shed 8% of their superfluous body fat in 8 weeks, not the Nigella sativa oil | Agreed? If not, leave a comment on FB!

References:

• Mahdavi, Reza, et al. "Changes of body composition and circulating adipokines in response to Nigella sativa oil with a calorie restricted diet in obese women." Journal of Herbal Medicine (2016).
• Namazi, Nazli, et al. "Oxidative Stress Responses to Nigella sativa Oil Concurrent with a Low‐Calorie Diet in Obese Women: A Randomized, Double‐Blind Controlled Clinical Trial." Phytotherapy Research 29.11 (2015): 1722-1728.

Path to Fat-Induced Obesity is Sprinkled With Salt - Sodium Boosts Food & Energy Intake & Reduces Fat's Satiety Effect

Think you cannot eat the whole pizza? Add salt - this should "help" with the hardest all-you-can-eat challenges.

I am not telling you something new if I tell you that excess fat consumption has been linked to the development of obesity. I hope that it's also not news to you that the consistent association between high(er) fat intakes and weight gain in epidemiological studies cannot be reproduced in human studies where the diet is just high in fat and doesn't have the perfect "potato chips"-combination of fat and carbohydrate that has not just been proven to increase food intake, but also to have pro-addictive effects on the brain (Hoch. 2015).

The fat to carbohydrate ratio Hoch et al. identified as a crucial determinant of snack food intake and brain reward responses in their 2015 study is yet not the only characteristic feature of potato chips.

Learn more about the effects of your diet on your health at the SuppVersity

Only Whey, Not Soy Works for Wheytloss

Taste Matters - Role of the Taste Receptors

Protein Satiety Shoot-Out: Casein vs. Whey

How Much Carbs Before Fat is Unhealthy?

5 Tips to Improve & Maintain Insulin Sensitivity

The Overfeeding Overview - What Makes You Fat?

Another similarly striking feature chips share with a couple of other highly addictive foods is their salt content. The same salt content of which Bolhuis et al. write in their soon-to-be-published paper in The Journal of Nutrition that we don't know yet how it interacts with the appetitive effects of fat. Apropos fat, whether fat will increase or decrease your appetite is actually highly individual question. Some studies even suggest that a high fat content has appetite reducing effects - at least in those individuals with a high fat taste sensitivity.

Unfortunately, the results of pertinent studies are inconclusive; and that even in people with intact fat taste sensitivity. In view of previous research showing similar associations between the salt content of snack foods and their appetizing effects as they were observed for high carbohydrate + high fat foosds, Bolhuis et al. speculated that our fat taste sensitivity may be influenced by the co-ingestion of salt. To test this hypothesis, the researchers recruited forty-eight healthy adults [16 men and 32 women, aged 18–54 y, body mass index (kg/m2): 17.8–34.4]. After an initial assessment of their individual fat taste sensitivity, the subjects participated in a randomized 2 x 2 crossover design trial, in which each participant attended 4 lunchtime sessions after a standardized breakfast.

Figure 1: The high salt meals were generally rated as more pleasant, while fat had no effect on the perceived pleasantness of the meal (Bolhuis. 2016).

The meals seemed to be identical elbow macaroni (56%) with sauce (44%); the sauces, however, were manipulated to be

• low-fat (0.02% fat, wt:wt)/low-salt (0.06% NaCl, wt:wt),
• low-fat/high-salt (0.5% NaCl, wt:wt), 
• high-fat (34% fat, wt:/wt)/low-salt, or 
• high-fat/high-salt.  

Ad libitum intake (primary outcome) and eating rate, pleasantness, and subjective ratings of hunger and fullness (secondary outcomes) were measured.

The results indicate that salt increased food (= food weight) intakes by 11%, independent of fat concentration (P = 0.022), while increasing the fat intake had no independent effect of fat on food intake (P = 0.6 for the amount of food, not its energy content).

Figure 2: This is what really counts, the effects of modfiying fat and salt content of the meals on total energy intake during the meals; data in kcal per meal (Bolhuis. 2016).

A slightly different picture emerges for the total energy intake, though. Here, the salt intake still mattered (significant with high vs. low salt meals), the main determinant of the total energy intake, however, was the fat content of the meal, with the high-fat meals triggering a whopping +60% (P < 0.001) increase in energy intake in the average subject.

Figure 3: When the diet was high in salt, the mediating effect of fat taste sensitivity on food intake (in g) is lost (Bolhuis. 2016)

Unlike the amount of fat in the meals, the sex of the participants had an effect on the food intake (P = 0.006), with women consuming 15% less by weight of the high-fat meals than the low-fat meals.

More importantly, however, the fat taste sensitivity appeared to decrease signifi-cantly with increasing amounts of salt in the high-fat meals (fat taste x salt interaction on delta intake of high-fat - low-fat meals; P = 0.012), which tended to trigger a satiety effect in the fat sensitive subjects only if they were also low in salt (see Figure 3).

The Overfeeding Overview: High Fat, Carb, Protein, MCTs, Leptin, Testosterone, T3 & Reverse T3 - Get an Overview of the Consequences of Short- & Long-Term Overfeeding - Yes, the existing research shows that high fat intakes (in the presence of carbo-hydrates) are the most fattening.

Bottom line: As the authors of this intriguing study rightly point out, their results "suggest that salt promotes passive overconsumption of energy in adults" (Bolhuis. 2016) and as if that was not bad enough, even those who are sensitive to a higher fat content of food will be fooled into overeating when the high salt content of said foods overrides the fat-mediated satiation.

Ah,... before you rejoice and start eating tons of unsaltet potato chips - there's one thing I should remind you of: even though an excessive increase in dietary fat (from 0.6 to 15.5 g/100g) did not have a main effect on food intake by weight, it led to a 60% higher energy intake, irrespective of the salt content of the meal - an observation that should remind you of the "volume hypothesis" of satiety | Comment!

References:

• Bolhuis, Dieuwerke P. et al. "Salt Promotes Passive Overconsumption of Dietary Fat in Humans." The Journal of Nutrition (2016): Ahead of print.
• Hoch, Tobias, et al. "Fat/carbohydrate ratio but not energy density determines snack food intake and activates brain reward areas." Scientific reports 5 (2015).