Is Lard More Fattening Than Hydrogenated Vegetable Oil!? 17% Extra Weight, 32% Extra Fat Gain + Increased Appetite

Not all fats are created equal and lard and hydrogenated vegetable oils are not on the top-list of "healthy fat choices".

Our perspective on fat has changed significantly over the last decade. While some people still propagate that "fat is bad" and "should be generally avoided", most experts have stopped bashing fat in general and are now focusing on saturated fats. Saturated fats as they occur in lard,.. but wait! If you take a closer look at the fatty acid composition of lard, it turns out that it contains "only" 39.2% saturated, but 45.1% mono- and 11.2% polyunsaturated fats. That's actually not too far off of the average vegetable shortening with a saturated to monounsaturated to polyunsaturated fat ratio of 25.0 / 41.2 / 28.1% (nutritiondata.com)

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Frying Does not Just Oxidize Oils, It Does Fat More!

In contrast to said even more dreaded partially hydrogenized vegetable fats, which contains a whopping 13.2g of transfats per 100g, lard is yet mostly trans-fat free. That's a good thing, right? After all, high trans-fat intakes have been associated with increased inflammation and cardiovascular disease  (Hu. 1997; Lopez-Garcia. 2005. Now, while experimental evidence confirming negative effects in humans is non-existent, negative effects have also been observed in controlled animal experiments. It is thus more than reasonable to assume that of two of the most commonly used fat sources for cooking, i.e. lard and hydrogenated vegetable-shortenings, the former, the trans-fat free 100% "natural" fat source should be the healthier one.

Figure 1: Fatty acid content (g) of the three test diets (Kubant. 2015)

To check the validity of this hypothesis, scientists from the University of Toronto fed male Wistar rats for 14 weeks diets which contained either (1) high vegetable fat (HVF, 60 kcal% from vegetable shortening) or (2) high lard fat (HLF, 60 kcal% from lard). A group of rats that received the normal-fat chow (NF, 16 kcal% from vegetable shortening) served as control (see Figure 1). Body weight, food intake, adipose tissue mass, serum 25[OH]D3, glucose, insulin and fatty acid composition of diets were the scientists' main outcome data - data that confirm that not everything we take for granted will actually stand the test of science.

Figure 2: Body weight and fat gain over 12 weeks on control (low fat) or high fat diets w/ lard (HLF) or hydrogenated vegetable oils (HVF) as main fat sources (Kubant. 2015).

In contrast to what common sense would dictate, the rodents in the lard group were not leaner and healthier. In fact, the data in Figure 2 tells you that the exact opposite was the case: The rodents on the high lard diet gained significantly more body weight and - more importantly - body fat and did not, as some may now speculate, simply store the extra energy away instead of having it float around in the blood and ruin their insulin sensitivity (see Figure 3).

Figure 3: Markers of glucose metabolism at the end of the study (data expressed relative to control | Kubant. 2015)

So, basically, the scientists, who had even speculated that lard, due to its naturally high vitamin D content "may act to reduce the metabolic consequences associated with obesity, as suggested by other investigators" (Kubant. 2015), had to realize that their prediction was wrong. Whether lard is simply unhealthier or whether the effect was a results of the comparably lower food intake of the vegetable shortening group is difficult to say. What we do know, however, is that the animals who were on the lard diet consumed more calories than the HVF group. That 1g/day of extra food, however, was enough to have the scientists conclude that the rats have a strong preference for the taste of fat sources containing long-chain fatty acids (that is, oleic and linoleic), but by no means enough, to fully explain the significant difference in weight and body fat gain.

The Quest for the Optimal Cooking Oil: Heat Stable, Low PUFA & Cholesterol Free - High MUFA Sunflower / Canola, Olive, Coconut & Avocado Oil Qualify for the TOP5 | Learn more!

So lard is much worse than transfats? I wouldn't dare making a general statement about lard vs. vegetable shortenings based on this study. One thing I would like to remind every saturated animal fat worshipper of, however, is that his beloved "saturated fat sources" like lard are in fact hardly saturated at all. The common lard, the scientists used in the study at hand, for example, has higher amounts of polyunsaturated fatty acids in it than the average vegetable shortening. Its (by the saturated fat lovers dreaded) content of omega-6 fatty acids in the form of linoleic acid, which is currently everybody's favorite scapegoat for being obese, diabetic or whatnot, is even three times higher!

What we must not forget, either, are the divergent results about the fattening effects of transfats from monkey and rodent studies. While the one existing monkey study showed higher levels of intra-abdominal adiposity and insulin resistance in monkeys fed trans fatty acids (TFAs) for 6 years under a controlled feeding regimen (Kavanagh. 2007), a more recent study in rats found that dietary TFAs fed ad libitum (as much as the rodents wanted) did not influence food intake or body fat accumulation (Ochiai. 2013). Now, monkeys are more reliable than rats, right? Well, yes, but if the monkeys are on an energy restricted and the control diet was no lard diet, but rather the "perfect monkey diet", the rodent study with its realistic ad-libitum access to food and a diet composition that was more akin to what people eat these days becomes increasingly attractive. Overall, however, it doesn't really make sense to use any of these studies to speculate about the practical significance Kubant's rodent study has for men. If you asked me, it is not even relevant, anyways, because neither lard nor hydrogenated vegetable oils should be a regular part of your diet | Learn why in a previous SuppVersity Article or tell me what you think on Facebook!

References:

• Hu, Frank B., et al. "Dietary fat intake and the risk of coronary heart disease in women." New England Journal of Medicine 337.21 (1997): 1491-1499.
• Kavanagh, Kylie, et al. "Trans fat diet induces abdominal obesity and changes in insulin sensitivity in monkeys." Obesity 15.7 (2007): 1675-1684.
• Kubant, R., et al. "A comparison of effects of lard and hydrogenated vegetable shortening on the development of high-fat diet-induced obesity in rats." Nutrition & Diabetes 5.12 (2015): e188.
• Lopez-Garcia, Esther, et al. "Consumption of trans fatty acids is related to plasma biomarkers of inflammation and endothelial dysfunction." The Journal of nutrition 135.3 (2005): 562-566.
• Ochiai, Masaru, et al. "Effects of dietary trans fatty acids on fat accumulation and metabolic rate in rat." Journal of oleo science 62.2 (2013): 57-64.

Is There A Simple Marker on Your Standard Labs That Can Tell You Whether You're at High Risk of Heart Disease & Insulin Resistance? If So, How High / Low Should It Be?

Apples are more likely to be insulin resistant than pears... no, we are not talking about the fruits and neither about their effects on insulin resistance, but rather about the areas where you carry most of your body fat. If it's on the buttocks and thighs, your risk of being insulin resistant is much lower than if the lion's share of your passive energy store resides right on your abs.

If you've read the headline of today's SuppVersity article you are already in the know what this is going to be all about. I am yet not sure, whether you actually understand why doing a study like this makes sense... don't worry if you don't I have to admit I had to thing about it for quite some time, until looking at the various measures until it dawned on me that the main advantage is - you guessed it - of monetary nature!

I mean, if you could tell simply by looking at the standard labtests, most of which do include both triglycerides and HDL levels, you could save a lot of money on HOMA-IR or QUICKI tests and still be certain you suffer or don't suffer from insulin resistance and concomitantly increased cardiovascular disease risk.

Now the $64,000 question is: "Were Miguel Murguía-Romero et al. able to save your insurance company a lot of money, or not?"

The truth about cholesterol and heart disease...

... turned out to be more complex than the "pioneers" believed and complex "truths" have the nasty tendency to be self-contradictory and difficult to understand -- too difficult, in fact, to make it to the mainstream media and as it turned out obviously even too difficult for the average general practitioner, who is still easily convinced by the pharma reps that it was "best practice" to prescribe a statin and send the patient, who would be "unwilling and unable to change his dietary habits and increase his amount of physical activity, anyway" home with a script and patient information full of known side-effects most of the patients like to ignore.

Table 1: Talking about "metabolic syndrome" (MetS) what are the criteria to diagnose MetS? (Grundy. 2004)

That being said, the most prominent of the currently heralded alternative indicators of increased risks of cardiovascular disease are...

• a high level of low-density lipoprotein (LDL),
• a low level of high density lipoprotein (HDL),
• exuberant amounts of triglycerides (TRIGS),

... as well as all sorts of combination of the the two, respectively three bad guys (TC, TRIG, LDL)  and the one good guy (HDL). Research has also suggested that pre-existing co-morbidities like diabetes will increase the significance of the predictive effects of high triglycerides to high-density lipoprotein (TRIG/HDL) total cholesterol to high-density lipoprotein (TC/LDL), and LDL to high-density lipoprotein (LDL/HDL) ratios.

With their recently conducted experiment, the scientists from the Stanford University Medical School did now try to elucidate whether the triglyceride / HDL ratio, which has been emerging in trials with old(er) individuals as one of the best markers of cardiovascular disease, would predict the CVD risk in 2244 healthy college students  (17-24  years  old) of Mexican Mestizo ancestry  (1545 women and 699 men) and be able to identify younger individuals that are not merely at high risk of heart disease, but in whom this increased risk is direct consequence of being insulin resistant, as well.

Figure 1: Prevalence of insulin resistance ("objectively" confirmed by HOMA-IR data) as identified by the TG/HDL-C ratio or the criteria for "mebabolic syndrome" listed in table 1 (Murguía-Romero. 2013)

If you take a look at the data in figure 1 you can see that the "kill two birds with one stone"-, or rather "determine two medical problems with one parameter"-method the scientists wanted to establish is not exactly reliable. In fact the, chance of identifying people who had overtly high HOMA-IR values (=were effectively insulin resistant) just by the fact that their TRIG/HDL ratios were >3.5 for men and >2.5 for women is only 50/50.

A closer statistical analysis did still reveal a slightly higher sensitivity for the TRIG/HDL ratio (53% / 55% in women / men) than for the criteria catalog that's used to "diagnose" metabolic syndrome (see table 1), which ended up at a meager sensitivity of 36% for women and 46% for men. 

So where should your TRIG / HDL ratio be then?

In view of the results presented in the study at hand, the triglyceride-to-HDL ratio (TRIG / HDL) although it may not qualify as a diagnostic tool, is is a good indicator that there is something metabolically off. If that's your TRIG / HDL ratio that looks bad. Based on the figures in the study at hand this means:

• Your ratio of triglycerides to HDL-C should be < 3.5 if you are a man, or 
• Your ratio of triglycerides to HDL-C should be < 2.5 if you are a woman

If that'S not the case, this alone should be reason enough to investigate whether and how insulin resistant you actually are, what your real heart disease risk is like and what the underlying reasons of your potential health problems could be. You could start out by doing a glucose tolerance test and/or by tracking your glucose levels with a glucometer, for example, to gain some certainty with respect to your current insulin sensitivity. On the cholesterol side of things, however, a particle size analysis may be the next thing on your list (learn why particle size matters).

And don't forget that for most of the health-conscious victims of CVD, stress, not bad eating habits, or a lack of exercise, is the main problem - and that goes for both psychological and physiological stress (including overtraining; learn more).

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Bottom line:

Suggested Read: "Eat Whole Eggs All Day and Throw Your Statins Away? 375x Increased Dietary Cholesterol Intake From Eggs Reduces Visceral Fat & Promotes Healthy Cholesterol Metabolism" - For most people eggs boost, not lower HDL and they are certainly not the reason for the ever increasing heart disease risk (learn more)

In view of the fact that the majority of general practictioners is not going to run HOMA-IR or QUICKI tests on their patients on a regular basis, this ratio is certainly one of the best indicators you will find on your standard labs - and what's most appealing: It's better than the set of criteria for "MetSyn" (see table 1), which would, for example, per se overlook all the skinny fats out there.

In fact, the main message associated with the low sensitivity of the "MetSyn" criteria as a benchmark for insulin resistance, may well be that the mere absence of "above normal" levels for abdominal circumference, blood pressure and even blood glucose are not reliable criteria to determine, whether you are insulin resistant, or not. I'd say this is a message with public importance, especially for the skinny fats, who may well be the 15% and 13% of young men and women in the "no metabolic syndrome, but still insulin resistant"-group in the study at hand (see figure 1).

References:

• Grundy SM, Brewer HB Jr, Cleeman JI, Smith SC Jr, Lenfant C; American Heart Association; National Heart, Lung, and Blood Institute. Definition of metabolic syndrome: Report of the National Heart, Lung, and Blood Institute/American Heart Association conference on scientific issues related to definition. Circulation. 2004 Jan 27;109(3):433-8.
• Murguía-Romero M, Jiménez-Flores JR, Sigrist-Flores SC, Espinoza-Camacho MA, Jiménez-Morales M, Piña E, Méndez-Cruz AR, Villalobos-Molina R, Reaven RM. Plasma triglyceride/high-density lipoprotein cholesterol ratio, insulin resistance, and cardio-metabolic risk in young men and women. Journal of Lipid Research. 2013 [epub ahead of print]

Less Than 15mg of DHEA Exert Identical Beneficial Effects on Insulin Sensitivity as 1h of Cardio 5x Per Week. Both Effects Mediated Via Increases in Intra-Muscular DHT

Image 1: It has long been established that diabetics have particularly low DHEA levels (Loviselli. 1994), but what's the chicken and what's the egg here?

It is quite funny, sometimes you don't hear about certain supplements, (pro-)hormones, exercise-modalities etc. in years and then, all of a sudden, there are two studies on the respective topic in one week; and moreover, two pretty interesting ones! Last Friday, exactly 7 days ago, you've read here at the SuppVersity about the muscle-protective effects of low-dose dehydroepiandrosterone (DHEA) supplementation during a 5-day intense multiple-type exercise protocol (cf. "DHEA Blunts Muscle Damage During 5 Days of Combined Endurance, Strength and HIIT Training in Young Men"). Today, I have another interesting set of data for you - data which could not just shed some light onto the underlying mechanisms of the said protective effects against skeletal muscle damage, but also on DHEA's beneficial effects on insulin sensitivity.

Not younger, but leaner with a minimalist dose of DHEA?

In a 6 week trial, and thus over a more than eight times longer timespan than in the previously mentioned human study on skelatal muscle damage, Koji Sato and his (or her?) colleagues from the Ritsumeikan University, the Senshu University and the University of Tsukuba (all in Japan, as you probably already suspected) investigated the effects a low dose of DHEA (human equivalent: 0.16mg/kg per day => 10-15mg/day) supplementation on the insulin, QUICKI (=quantitative insulin-sensitivity check index) and intramuscular DHEA and DHT (dihydrotestosterone) levels in sedentary or exercised dietary obese male rodents.

Figure 1: Relative insulin levels, QUICKI, intramuscular DHEA and DHT content in obese male rodents after 6 weeks of DHEA or combined DHEA + exercise (1h, 5days/week) treatment (data adapted from Sato. 2012)

As you can see in figure 1 the effects of both 5x/week running on a treadmill (ETA: 1h) and orally administered DHEA were profound. If you compare the "exercise only" group (red) to the two DHEA groups (green and violet), you will yet notice interesting parallels. Not only were the decreases in serum insulin and the increases (=improvements of insulin sensitivity) in the QUICKI test very similar, the exercise regimen alone yielded a +56% increase skeletal muscle DHEA content and a +71% increase in DHT.

Exercise increases intramuscular DHEA & DHT...
 

Figure 2: Hormonal cascade from DHEA to DHT; all enzymatic conversions can take place on a systemic and intra-cellular level!)

At least the latter, i.e. the increase in DHT should not be news to you if you have been following the in-depth articles at SuppVersity over the past couple of months. From the Intermittent Thoughts on DHT you know that exercise in general and HIT endurance exercise in particular has been found to boost intramuscular dihydrotestosterone levels, as well. The bros, or friends of bros among you, will probably also have heard the horrific stories about creatine monohydrate leading to increased levels of DHT (van der Merve. 2009), of which every reasonable person must actually assume that they are nothing but a downstream effect of increased training loads and/or improved adaptation... I mean, think about it "paleo style": Why would the mammalian body (rodent and human appear to react alike here) increase the DHEA and, via 5-alpha reductase (cf. figure 2), the dihydrotestosterone levels in response to high volume exercise, if not as a means of adaptation?

Oral DHEA + exercise = double-whammy against obesity

The combined treatment, or I should say the exogenous support of the exercise induced changes had - and this is not visible from the data in figure 1, astonishingly profound effects on the diet induced weight gain of the lab animals. While all other rodents became fatter, those in the exercise + DHEA group remained at a steady body weight level; an observation the researchers comment as follows:

Although DHEA administration and exercise training each produced beneficial effects, 6-weeks of combination treatment were more effective for obesity. The precise mechanisms that reduced abdominal fat weight in the combination group remain unclear, yet we can propose several plausible hypotheses. 2 weeks of DHEA administration has been shown to activate fatty acid metabolism-related enzymes, such as long-chain fatty acyl-coenzyme A synthase, and to increase free CoA levels in liver (Mohan. 1998; Mohan. 1990). In addition, exercise training is  known to reduce adipogenesis via upregulation of fatty acid metabolism and increased energy expenditure (Hou. 2003). Therefore, 6-weeks of combination treatment may have promoted additive reductions in abdominal fat volume.

In other words, while DHEA increases the efficacy of fatty acid oxidation, exercise takes care of the increase in energy expenditure which is - all convictions wrt to "calories don't count" and the "calories in vs. calories out"-hypothesis aside - still a fundamental prerequisite that the fatty acids do actually get burned and are not released into circulation to be restored or replaced a couple of hours later.

"Ok, I am just ordering some DHEA, how much should I take?"

Before you head over to the online vendor of your choice to make sure you get your share of DHEA before the FDA hears that it could hamper the sales of diabetes drugs and removes it from the OTC market, I would like to remind you that despite the fact that Sato et al. rightly claim that a "combination treatment [with DHEA and DHT] may be more beneficial than either therapy alone", a cursory glance on the data in figure 1 should suffice to tell you that those additional benefits as statistically significant as they may be are just that "additional" and that exercise alone yielded about equal results, is free of negative and full of beneficial side effects (update: as long as you don't overtrain; thanks Stapedius for this important note) and does not have the same host of studies refuting its efficacy as DHEA has (Clore. 1995).

It is nevertheless intriguing that a hormone the medical orthodoxy has, more or less all of a sudden, dropped like a hot potato and declared "questionable" and "ineffective" is now, roughly 15-20 years being rediscovered... and I am pretty sure that this was not the last DHEA study you will see and read about here at the SuppVersity ;-)

References:

1. Clore JN. Dehydroepiandrosterone and body fat. Obes Res. 1995 Nov;3 Suppl 4:613S-616S. Review.
2. Hou CW, Chou SW, Ho HY, Lee WC, Lin CH, Kuo CH. Interactive effect of exercise training and growth hormone administration on glucose tolerance and muscle GLUT4 protein expression in rats. J Biomed Sci. 2003 Nov-Dec;10(6 Pt 2):689-96.
3. Loviselli A, Pisanu P, Cossu E, Caradonna A, Massa GM, Cirillo R, Balestrieri A. [Low levels of dehydroepiandrosterone sulfate in adult males with insulin-dependent diabetes mellitus]. Minerva Endocrinol. 1994 Sep;19(3):113-9.
4. van der Merwe J, Brooks NE, Myburgh KH. Three weeks of creatine monohydrate  supplementation affects dihydrotestosterone to testosterone ratio in college-aged rugby players. Clin J Sport Med. 2009 Sep;19(5):399-404.
5. Mohan PF, Cleary MP. Effect of short-term DHEA administration on liver metabolism of lean and obese rats. Am J Physiol. 1988 Jul;255(1 Pt 1):E1-8.
6. Mohan PF, Ihnen JS, Levin BE, Cleary MP. Effects of dehydroepiandrosterone treatment in rats with diet-induced obesity. J Nutr. 1990 Sep;120(9):1103-14.
7. Sato K, Iemitsu M, Aizawa K, Ajisaka R. Testosterone and DHEA activate the glucose metabolism-related signaling pathway in skeletal muscle. Am J Physiol Endocrinol Metab. 2008 May;294(5):E961-8. Epub 2008 Mar 18.
8. Sato K, Iemitsu M, Aizawa K, Mesaki N, Ajisaka R, Fujita S. DHEA administration and exercise training improves insulin resistance in obese rats. Nutr Metab (Lond). 2012 May 30;9(1):47. [Epub ahead of print]