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).

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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).

Which Micro- & Macronutrients Intakes Are Associated With High HDL Levels? Study Shows Magnesium & Folate Are, High Carbohydrate & Total Animal Fat Intakes Are Not!

The advantage of HDL is its stability that reduces the risk of plaque build-up in the intestinal wall, which is clogged by the remnants of oxidized LDL and causes heart disease & co.

First things first: We are not talking about "hard experimental evidence" as you could generate it in a randomized controlled trial in a metabolic ward. The data I am reporting today is from a cohort with 1,566 participants with extensive lipid phenotype data completed the Harvard Standardized Food Frequency Questionnaire to determine their daily micronutrient intake over the past year - an epidemiological study that used stepwise linear regression was used to separately evaluate the effects of dietary covariates on adjusted levels of HDL-C, HDL-2, HDL-3, and apoA1.

Interestingly, this is the first study with a quality data-set that determined the association between specific dietary micronutrients with HDL-C, HDL-2, HDL-3, and apoA1, and how these dietary associations differ across the various measures of HDL - not just one.

Learn more about HDL, cholesterol, heart health & co at the SuppVersity

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Every other day fasting for your lipids

Dairy Protein Satiety Shoot-Out: Casein vs. Whey

Fish oil & oleic acid counter their ben. effects

Eggs increase cholesterol reverse transport

Does roasted coffee increase bad LDL?

To identify the HDL-promoters in the diet, the scientists use demographic and clinical variables in the base model. What they found was that numerous dietary intakes increased total HDL-C variance.
The results of their stepwise linear regression model in Table 1 indicate - probably for some people much surprisingly - that all alcohol intake levels were positively associated with HDL-C.

"In addition, magnesium, folate, and the saturated fat, myristic acid (14:0), were all positively and independently associated with HDL-C. Carbohydrate intake, iron, and % of fat derived from animal sources were each negatively additive for HDL-C." (Kim. 2014)

Similar effects from dietary intakes were observed for HDL-2, of which we know that it is decreased in women with rheumatoid arthritis (Arts. 2012) and individuals with other inflammatory diseases (including metabolic syndrom) and associated with a slightly higher reduction in acute myocardial infarction risk than "regular" HDL in several studies (Salonen. Salonen. 1991; Stampfer. 1991; Buring. 1992; Gaziano. 1993) for all alcohol intakes, magnesium, folate, and myristic acid (14:0), eicosapentaenoic acid (20:5, a ω-3 EPA), all of which were positively and independently associated with HDL-2 levels.

Table 1:  Best-fit model from stepwise linear regression predicting HDL-C levels using dietary intake data (Kim. 2014)

The opposite was the case for arachidonic acid (20:4, an ω-6 ARA), carbohydrate and iron intakes, which were both negatively associated with HDL-2 (see Table 1).

Don't forget to put things into perspective!

And just to make sure, I don't get angry emails from bulletproof coffee drinkers: Your coffee is fine, the content of the only "good" saturated fat, i.e. myristic acid, happens to be especially high coconut oil (41%; Sodamade. 2013) and relatively high in butter (12% independent of whether it's grass-fed or not; Couvreur. 2006) - surprised? Not really, I guess. As a SuppVersity reader you are by now aware that the bad reputation coconut oil and butter have for being mostly saturated fats is no longer supported by contemporary scientific evidence (Dias. 2014).

And with respect to the total animal fat intake - for the average Westerner that's a good measure of how much processed meat he / she eats, so I would not overrate the small negative association (1/80 of the one of having a ton of carbohydrates in your diet!) the scientists found in the study at hand.

Eggs are unquestionably and exception from the "animal fat" is bad for HDL rule | learn more.

Bottom line: With the exception of folate, which has previously not been reliably associated with increases in HDL, let alone speficic HDL subfraction, the improvements with alcohol, magnesium and EPA are not exactly news. The same is true for the decreases in response to increased intakes of (all) animal fat, arachidonic acid, carbohydrates and iron.

In the end, the study confirms what we already know: The way you eat (and train; see Leon. 2001) can directly affect the level of the heart-healthy HDL fractions in your blood.

One thing you should keep in mind, though, is that it's the ln = logarithmus of these macronutrients and micronutrients that's associated with increased / decreased HDL and its subfractions. This means that small changes are not really important. Things that would count are eating low carb vs. extreme high carb or eating no folate containing foods vs. a significant amount of these.

References:

• Arts, Elke, et al. "High-density lipoprotein cholesterol subfractions HDL2 and HDL3 are reduced in women with rheumatoid arthritis and may augment the cardiovascular risk of women with RA: a cross-sectional study." Arthritis Res Ther 14.3 (2012): R116.
• Buring, J. E., et al. "Decreased HDL2 and HDL3 cholesterol, Apo AI and Apo A-II, and increased risk of myocardial infarction." Circulation 85.1 (1992): 22-29.
• Couvreur, S., et al. "The linear relationship between the proportion of fresh grass in the cow diet, milk fatty acid composition, and butter properties." Journal of dairy science 89.6 (2006): 1956-1969.
• Dias, C. B., et al. "Saturated fat consumption may not be the main cause of increased blood lipid levels." Medical hypotheses 82.2 (2014): 187-195.
• Gaziano, J. Michael, et al. "Moderate alcohol intake, increased levels of high-density lipoprotein and its subfractions, and decreased risk of myocardial infarction." New England Journal of Medicine 329.25 (1993): 1829-1834. 
• Kim et al. "Effects of dietary components on high-density lipoprotein measures in a cohort of 1,566 participants." Nutrition & Metabolism 2014, 11:44.
• Leon, ARTHUR S., and OTTO A. Sanchez. "Response of blood lipids to exercise training alone or combined with dietary intervention." Medicine and science in sports and exercise 33.6 Suppl (2001): S502-15.
• Salonen, Jukka T., et al. "HDL, HDL2, and HDL3 subfractions, and the risk of acute myocardial infarction. A prospective population study in eastern Finnish men." Circulation 84.1 (1991): 129-139. 
• Sodamade, A¹, and O. S. Bolaji. "Fatty acids composition of three different vegetable oils (soybean oil, groundnut oil and coconut oil) by high-performance liquid chromatography." Chemistry and Materials Research 3.7 (2013): 26-29.
• Stampfer, Meir J., et al. "A prospective study of cholesterol, apolipoproteins, and the risk of myocardial infarction." New England Journal of Medicine 325.6 (1991): 373-381.

Switch From Chicken to Lamb to Rid Yourself of Belly Fat, Reduce Your Triglyceride and Basal Insulin Levels

If you consider this, i.e. you suprailaic body fat (here measured by a caliper, just as it was done in the study at hand), ditching the chicken for some lamb, may be one of the myriad factors that could help you "solve" the problem.

Chicken, rice and broccoli. That is still the dietary paradigm, most people have on their minds, when average Joes and Janes are talking (often with some disdain) about what "healthy eating must look like".

Now, a recent study from GENUD, the "Growth, Exercise, Nutrition and Development" Research Group at the Universidad de Zaragoza in Spain (Graffe. 2013) suggests that at least item #1 on that list, namely chicken, would have been better replaced with a protein source of which I suspect even most of you won't be consuming on a regular base: Lamb!

That a proper sleep hygiene is of utmost important for your health and body composition is something you, as a SuppVersity veteran will be highly familiar with (if you are a newbie read yourself smart, here).

"Switch out the light and dish up the lamb, bro!"

That the second part of the jovial imperative in the above headline could be another factor to take into consideration, on the other hand, is true news (even for me) and should - with only one study backing it up - be considered more of an empirically grounded hypothesis than a "100% certain scientific result".

Table 1: Cooking methods for both lamb and chicken (Graffe. 2013)

Nevertheless, the observations, María Isabel Mesana Graffe and her colleagues made, when they put a group of healthy 16-26-year old "men" and "women" (I know, when I was sixteen, I thought I was a man, too - little did I know ;-) from Teruel and Zaragoza on an 8-week dietary regimen containing either...

• 150 grams of chicken, three times per week, or
• 150 grams of boneless lamb, three times per week,

... are quite intriguing. The participants received their otherwise (roughly) identical diets in in their local university accomodation halls:

"To ensure harmonisation, product-rich diets were served during lunch time and with each chef of the designated university accommodation halls were given instructions on the cooking methods." (Graffe. 2013; cooking methods, see table on the right)

The whole study design was in fact pretty straight forward and resembles an ideal world, where the citizens obey to dietary recommendations like "eat at least three meals with 150g of lamb per week" as if their lives depended on it (is it ironic or just sad that it actually does depend on the pathetic advice people are given?).

After an initial visit at which the medical history of all participants was assessed, a first blood draw, as well as anthropometric, blood pressure and heart rate measures were undertaken. After an 8-week period, all subjects came in for a second visit and the second testing session and crossed over to the other other group, i.e. subjects who had been consuming chicken for the first 8-weeks were then assigned to eat lamb and vice versa.

2x 8 weeks + an intermediate 5-week washout later...

Thus, after 8 weeks on diet A, a 5-week washout and another 8-weeks on diet B, all subjects had been consuming one or the other diet for 8 weeks, when they eventually arrived for the third and last assessment of their cardiovascular risk markers, body composition, blood pressure and heart rate.

Figure 1: Changes in skinfold thickness (before vs. after) and corresponding arm, hip and waist circumferences in the participants after 8 weeks on the "chicken" vs. "lamb diets" (Graffe. 2013)

As I know that "looking good naked" is much sexier (in the literal, as well as the figurative sense), than being healthy, we'll take a look at the anthropometric data, first (see figure 1). It probably doesn't take much explaining on my side. The general trends speak for themselves and I guess, you won't complain that it is in the change of the amount of fat that's covering the abs, where the scientists observed the only significant inter-group differences - do you?

Figure 2: Changes in blood lipids cardiovascular parameters, glucose and insulin levels during the 8-week chicken / lamb diet phases; only non-pastel bars are statistically significant  (Graffe. 2013)

With the fat mass differences being most significant in the abdominal area, it is also no surprise that the major changes among the cardiovascular risk parameters were (a) reduced triglyceride levels and (b) improved insulin levels - exactly those parameters that are usually most closely related to abdominal obesity and "all things metabolic syndrome".

Not chicken or lamb, "chicken or egg" - that's the question!

These observation do obviously rise the usual SuppVersity question: "What's the mechanism, here?" What is certain is that the beneficial effects on abdominal fat, trigs and insulin are not due to the clenbuterol residues in chicken (up to 224ng/g; cf.Malucelli. 1994) cyclists love to use as an excuse, when they have once again been busted for the abuse of beta-agonists. Why? Well than eating chicken should help not hinder leaning out. Could it be the remnants of antibiotics in the chicken meat, as proposed by eg. Nicholson et al. (2005)? Or is it simply the bad arachidonic acid chicken common wisdom will tell you that it was so high in chicken meat?

Figure 3: Fatty acid composition of beef, lamb, pork, chicken, duck and turkey in % of total lipids (left) and arachidonic acid content in mg/100g (Li. 1998)

If you peek at the data in figure 3, which is obviously not based on the dietary intake of the subjects in the study at hand, but displays the general fatty acid composition of various meats, including lamb and chicken (both marked with grey boxes) as they were reported by Li et al. in 1998, it would appear as if "everybody's favorite devil", the essential omega-6 fatty acid arachidonic acid can hardly be blamed for the superiority of lamb - after all there is about the same amount of it in lamb as there is in chicken (for Ducks and dark poultry things are different!)

Did you know that lamb is the #1 dietary source of CLA?

Lamb contains 5.6 mg/g CLA, whereas beef and veal contain only 2.9–4.3 mg/g and 2.7 mg/g, respectively.

Non-ruminant meats such as chicken and pork, contain 0.9 mg/g and 0.6 mg/g, respectively (Mulvihill. 2001).

Eggs contain no CLA, at all - unless the chicken are fed with CLA enriched diets and the yolk between 3mg and 14-32mg/100g total fat (Jones. 2000; Raes. 2002).

Whether the CLA is at the heart of the effects in the study at hand is yet questionable, after all one of the side effects is insulin resistance and that's the opposite of what the sign. decrease in insulin would suggest.

What could be a culprit, though is the overall higher n-6/n-3 ratio of chicken. There is no debating that there is a statistically significant difference between chicken with 9.73g of omega-6 fatty acids per omega-3 vs. lamb in which every omega-6 fatty acid is "appropriately (?) buffered" with 0.57g of omega-3s (the corresponding n3/n6 ratios are 1.59, 1.78, 13.92, 9.73, 10.82 and 10.53 for beef, lamb, pork, chicken, duck and turkey, respectively; data based on Li. 1998).

But is it really that easy? The n3/n6 ratio - again!? I 'd say no. Also, or rather particularly in view of the relatively lose dietary control... I mean, if you have to eat chicken at least three times a week in the canteen, you are certainly more likely to grab a burger with "red meat" (or whatever it is they put in-between the patties) on the weekends or in the evening.

This and other confounding factors would obviously negate neither the previously mentioned n3/n6 ratio hypothesis, nor the scientists' very own hypothetical explanation that the "the presence of unsaturated fats [...], such as oleic acid and conjugated linoleic acid" which are naturally high in ruminant meat (see infobox on the right), can have figured here, as well. It should however remind you that there is, if anything, only one single reason that "we are fat" and that's the way "experts" base their advice on observations like these, cherry pick those they like and discard the ones they don't like until the various net result - call it the "XY diet" or the "dietary guidelines" - confuse the hell out of the poor average Janes and Joes who are looking up to those "experts" to rescue them before the obesity pandemic carries them off just like the 35.7% of the US adults who are already obese (the latest data is still based on figures from 2009-10; cf. Ogden. 2012)

---

If you work anyway similar to a male rodent, 4g/day Tongkat Ali, could help with the abs, your testosterone levels and "other issues", as well (learn more)

Bottom line: My personal take away message from the study at hand is not "never eat chicken again" or "eat lamb everyday", but rather: "Don't forget about how lucky we are that we have so many foods to chose from." So don't get stuck on only one of them - and that regardless of what common wisdom, recognized or unrecognized experts or individual studies may suggest would be "best" for the way you look and feel!

There is no magic bullet and no singular reason that "we" are fat and I am 100% sure that eating chicken instead of lamb is the smallest obstacle standing between your and a shredded set of abs.

 References:

• Jones S, Ma DW, Robinson FE, Field CJ, Clandinin MT. Isomers of conjugated linoleic acid (CLA) are incorporated into egg yolk lipids by CLA-fed laying hens. J Nutr. 2000 Aug;130(8):2002-5.
• Li D, Ng A, Mann NJ, Sinclair AJ. Contribution of meat fat to dietary arachidonic acid. Lipids. 1998 Apr;33(4):437-40.
• Malucelli A, Ellendorff F, Meyer HH. Tissue distribution and residues of clenbuterol, salbutamol, and terbutaline in tissues of treated broiler chickens. J Anim Sci. 1994 Jun;72(6):1555-60.
• Mulvihill, B. Ruminant meat as a source of conjugated linoleic acid (CLA). Nutrition Bulletin. 2001; 26: 295–299. 
• Ogden CL et al. Prevalence of Obesity in the United States, 2009–2010. NCHS Data Brief No. 82 January 2012.
• Nicholson JK, Holmes E, Wilson ID. Gut microorganisms, mammalian metabolism and personalized health care. Nat Rev Microbiol. 2005; 3:431–438.
• Raes K, Huyghebaert G, De Smet S, Nollet L, Arnouts S, Demeyer D. The deposition of conjugated linoleic acids in eggs of laying hens fed diets varying in fat level and fatty acid profile. J Nutr. 2002 Feb;132(2):182-9.

Science Round-Up Seconds: Optimal Health & Fitness Best Promoted W/ Intense Exercise. News on PUFAs & Thyroid Metabolism. Manganese the Anti-Sugar Glue Mineral!?

There may be a hitherto overlooked "enzymatic connection" between low thyroid function (spec. "low T3 syndrome" or starvation-/overtraining-induced reductions in thyroid levels) and "insufficient" levels of the long-chain varieties of both, omega-3 (EPA, DHA), as well as omega-6 (GLA, ARA) fatty acids.

I must admit that Carl & I did much to my own surprise cover more ground than I thought we would - and that despite his lengthy rant about the FDA ;-) That said, there is still enough for a second serving, aka the "Seconds", featuring news like:

• The optimal exercise for health and fitness is intense - SuppVersity readers & Superhuman Radio listeners knew it all along, the comfort zone won't enforce adaptation
• PUFAs and the thyroid - insufficient conversion of LA and ALA with low T3 levels; probably also relevant everyone who enjoys starvation and overtraining
• Manganese an anti-sugar glue mineral - study shows manganese protects blood vessels in a high glucose environment from the from monocyte adhesion and subsequent endothelial dysfunction

Contrary to previous shows it does not really matter, whether or not you have already or are still going to listen to the show. If you want, or your schedule doesn't allow otherwise, you can very well start with the Seconds, though - and that despite the fact that the author(s) of book of etiquette probably won't appreciate that ;-)

Scientists listen to the SuppVersity science round: Working out glycogen-depleted rules

8x Increase in "Mitochondria Building" Protein PGC1-Alpha W/ Medium Intensity Exercise in Glycogen Depleted Elite(!) Cyclists:- that's the headline of an October 2012 SuppVersity post

(Taanaka. 2013) -- The headline of this paragraph is obviously meant to be funny, but still. It's a funny coincidence that Hiroaki Tanaka, Kazuhiro Morimura and Keisuke Shiose from the f Fukuoka University in Fakuoka, Japan have just published a review on what the title tells us is An optimal exercise protocol for improving endurance performance and health and the protocol they suggest is basically very similar to the one(s) you will have heard about on the Science Round-Ups of December 8 and December 21, in which we broached the same issue of training in a glycogen depleted state, I also addressed in a post from October 2012 (see image on the right).

Obviously the review that has just been published in the The Journal of Sports Medicine and Physical Fitness has been written before my article, but it's still nice to see that the conclusions the Japanese researcher draw are virtual identical to what you read and heard on the SuppVersity and Super Human Radio, before:  

1. Tell me about efficacy: 4-6×30 s supramaximal sprint cycling Wingate tests are as effective as 40-120 min exercise session s at 65% of VO2Peak (Burgomaster. 2008); 7×30 s “all-out” bouts and 3×20 min bouts at approximately 87% of VO2peak could induce a similar increase in PGC-1α (Psilander. 2010); learn more about HIIT
   The optimal exercise protocol to improve health and endurance performance was discussed in re-lation to exercise-induced gene expression of PGC-1α.
2. Training intensity is a critical factor in PGC-1α gene expression and requires trainees to work out at a high(er) intensity broaching the lactate threshold (=no hours of endurance training, but glycolytic exercises such as sprinting or plyometrics)
3. HIIT does  not simply offer a way to meet the criteria in (2), it is also highly time efficient and improves aerobic capacity to a much greater extend than classic steady state cardio training
4. Training a glycogen depleted state renders submaximal continuous exercise a viable alternative to high intensity workouts.

Actually it would be ideal if I wouldn't have to repeat that whenever this issue comes up, but just to make sure: Do never forget that training  glycogen depleted is something like an intensity technique. Just like training past failure on every set, heavy eccentrics or planned phases of deliberate overreaching, it can set you up for overtraining and the Athlete's Triad, when your diet and / or recovery times are off.

PUFAs and the thyroid - insufficient conversion of LA and ALA with low T3 levels

(Swenne. 2013) -- This is not what the Peat-anians (or whatever you may call the friends of Dr. Ray Peat's theories may call), are now thinking about. At least at first sight, it would appear that it's quite the opposite of Peats anti-thyroid theory of polyunsaturated fatty acids (PUFAs).

Figure 1: Illustration of the role of the blocked (X) desaturase (DS) enzymes Delta-6 and Delta-5 in the formation of long-chain omega-6 (top) and omega-3 (bottom) fatty acids

After all, the results, Swenne and Vessby present in a paper that has been published only a couple of days ago in Acta paediatrica point towards an inhibitory effect of low thyroid function (specifically low triiodothyronine = T3 levels) on PUFA metabolism.

Stupid question of the day: "But Arachidonic Acid (ARA) is bad anyway, so why would I care - I mean, I take my fish oil" I am fully aware that the screwed up worshiping of omega-3 and the overgeneralized demonization of omega-6 fatty acids make questions like this appear logical, if not "smart". In fact, they do yet only reveal the public ignorance towards the complex interactions and the importance of proper ratios of both types of polyunsaturated fatty acids.

In an exercise scenario comprising a 4x/week classic body building strength training regimen, for example, the ingestion of 1g of arachidonic acid on a daily basis has been shown to have anti- not pro-inflammatory effects (-15% IL-6; Roberts. 2007)

Upon closer scrutiny of the actual data, it does yet turn out that the starvation induced alterations of omega-3 essential fatty acid (EFA) metabolism the Swedish scientists observed in 227 adolescents with eating disorders went hand in hand with the down-regulation of T3 levels. This observation alone does therefore not suffice to settle the "chicken or egg question" (i.e. what comes first?). The researchers' analysis of the activity of the desaturase enzymes (see figure 1), which convert the short chain omega-3/6 to long-chain omega-3/6 fatty acids would yet suggest a causative relationship between the reductions in active thyroid hormone and the subsequent deficiency of the long-chain polyunsaturated fatty acids EPA & DHA (omega-3) and GLA and arachidonic acid (omega-6). Now things become really interesting, when we also take into consideration that previous studies have shown that

"[i]nsulin appears to stimulate both desaturases, while hormones that increase blood sugar concentrations such as glucagon, adrenalin and corticosteroids are inhibitory for both enzymes." (Swenne. 2013)

This in turn brings us right back to the Athlete's Triad (read more about the Athlete's Triad in the respective SuppVersity Special) where the continuous lack of readily available energy results in low insulin levels and chronically elevated glucogon, adrenalin and corticosteroid levels, so that long-chain PUFA supplementation (and this includes the omega-6 fatty acids GLA and ARA) would appear to be indicated for (chronically) overtrained athletes, as well.

Manganese protects endothelial cells of diabetic rodents

(Burlet. 2013) -- In the latest issue of the Journal of Biological Chemistry, Elodie Burlet and Sushil K. Jain from the Louisiana State University Health Sciences Center report that administration of a whopping dose of 16 mg/kg body weight of manganese chloride (this equals ~4mg of elemental manganese) to Zucker diabetic fatty rats (standard model of diet-induced diabetes) significantly reduced the binding of immune cells to the endothelium and will thus have an ameliorative effect on the development of cardiovascular diseases.

As the data in figure 2 goes to show you the human equivalent of ~50mg/day elemental manganese did also induce statistically highly significant reductions in cholesterol and - what's probably of greater real-world relevance in view of the CVD-risk - a 60% reduction (!) in triglycerides in the diabetic rodents.

Figure 2: Relative expression of markers of binding of immune cells to the endothelium and cholesterol and triglyceride levels in diabetic rodents with or without additional 4mg/kg elemental manganese in their drinking water (Burlet. 2013)

Among the plethora of (trace-)minerals manganese certainly is one of the least known and that despite the fact that it plays an absolutely crucial role in blood glucose management. In view of the fact that it is known to raise not decrease blood glucose, it is however understandable that detailed information about this trace mineral the levels of which are tightly regulated by our bodies is scarce - I mean, the number of people suffering from hypoglycemic episodes is several magnitudes smaller than the number of (pre-)diabetics. Moreover, the beneficial effects on blood lipids have also been confirmed in different scenarios such as a rodent model of menopause (Bae. 2011)

Table 1: Average manganese content of selected foods (download full list from the USDA, here)

Since manganese also figures in  the enzymatic cascades which underly protein metabolism, bone formation, the synthesis of the neurotransmitter GABA and is an essential constituent of the eponymous manganese superoxide dismutase, one of the most important enzymes in the endogenous anti-oxidant system of the mitochondria, it is actually no wonder that manganese is officially considered one of the "essential trace minerals". With an adequate intake of 2.3mg for men and 1.8 mg for women (according to the Linus Pauling Institute) and it's abundance in Western type diets (>10mg/day), full-blown deficiencies are yet rare.

A 1987 study by Friedman et al. did yet show that a diet that contains insufficient amounts of manganese will result in skin rashes and pathologically low cholesterol levels. Since high levels of manganese are also implicated in the development of Parkinson's or rather a "Parkinson like disease" that's induced by manganese accumulation, but does not involve degeneration of midbrain dopamine neurons, supplementation with larger amounts of manganese without knowing one's dietary intake (better even tissue and serum levels), supplementation high(er)-dose supplementation is thus counter-indicated. Whether human type II diabetics can benefit from supplementation and which dosages are save and effective will still have to be elucidated.

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That's it already: In case you want more short news, even before the official installment of "On Short Notice" is posted tomorrow (don't as me what's going to be in there, I have no clue as of yet ;-), I suggest you visit the SuppVersity Facebook Page and check out these

• NON-ergogenic gadget of the week - Holographic wrist band meant to increase performance turns out to worsen performance compared to performance worse than "placebo"  (read more)
• The anti CVD taurine <> cholesterol connection - High serum taurine levels protect people with abnormally high cholesterol from cardiovascular disease (read more)
• Tennis elbow? Ultrasound and laser therapy show promise in treatment of medial and lateral epicondylitis, review says. (read more)
• Milk - What's good for the young ones can't be bad for the elderly, right? Right! Japanese 70+-agers' BMI and HDL levels benefit from milk consumption (read more)

as well as the other news I  have already posted + those that are going to appear within the next 24h and before the short news are even written (let alone published ;-).

References: 

• Bae YJ, Choi MK, Kim MH. Manganese supplementation reduces the blood cholesterol levels in Ca-deficient ovariectomized rats. Biol Trace Elem Res. 2011 Jun;141(1-3):224-31.
• Burgomaster KA, Howarth KR, Phillips SM, Rakobowchuk M, Macdonald MJ, McGee SL, Gibala MJ. Similar metabolic adaptations during exercise after low volume sprint interval and traditional endurance training in humans. J Physiol. 2008; 586: 151-160.
• Burlet E, Jain SK. Manganese supplementation reduces high glucose-induced monocyte adhesion to endothelial cells and endothelial dysfunction in zucker diabetic fatty rats. J Biol Chem. 2013 Jan 17.
• Friedman BJ, Freeland-Graves JH, Bales CW, et al. Manganese balance and clinical observations in young men fed a manganese-deficient diet. J Nutr. 1987;117(1):133-143.
• Psilander N, Niklas P, Wang L, Li W, Westergren J, Jens W, Tonkonogi M, Michail T, Sahlin K, Kent S. Mitochondrial gene expression in elite cyclists: effects of high-intensity interval exercise. Eur J Appl Physiol. 2010; 110: 597-606.
• Roberts MD, Iosia M, Kerksick CM, Taylor LW, Campbell B, Wilborn CD, Harvey T, Cooke M, Rasmussen C, Greenwood M, Wilson R, Jitomir J, Willoughby D, Kreider RB. Effects of arachidonic acid supplementation on training adaptations in resistance-trained males. J Int Soc Sports Nutr. 2007 Nov 28;4:21.
• Swenne I, Vessby B. Relationship of Δ(6) -desaturase and Δ(5) -desaturase activities with thyroid hormone status in adolescents with eating disorders and weight loss. Acta Paediatr. 2013 Jan 19.
• Tanaka, H, Morimura K, Shiose H. An optimal exercise protocol for improving endurance performance and health. J Phys Fitness Sports Med. 2013; 1(4): 595-604.