Standard American Diet Has 'Optimal' Fatty Acid Ratio to Induce Diabesity. Plus: Study Shows Doubling Saturated Fats Would Yield More Benefits Than Halving Them

Study confirms: The SAD diet yields 'optimal' results (img. forbes.com)

Since this post is already lengthy enough, I will spare you how saturated fatty acids have long falsely been accused as the sole driving force of the western obesity epidemic and how the tides appear to be slowly yet steadily appear to be turning, as scientists delve deeper and deeper into the interactions of the total fat content in the diet, its fatty acid composition and the interaction of both with the two other macronutrients and their specific forms and get right to the study at hand. A study that appears in the current issue of the Journal of Lipid Science and deals with the first of the aforementioned interactions. The one that focuses on the total fat content and the individual fatty acid make-up of the diet (Enos. 2012).

Fat shoot out: Saturated vs. mono vs. PUFA

As Enos et al. point out, the main purpose of their study was to examine the effects of three high fat diets differing only with respect to the percentage of total calories from saturated fats.

• SFA-6% - contained 6% saturated fats,
• SFA-12% - contained 12% saturated fats, and
• SFA-24% - contained 24% of saturated fats

While the the high fat diets were set to have an identical fat (40% of the energy), carbohydrate (45% of the energy) and protein content, the two control diets were low in total fat (12%/68%/20% of the energy from fat/carbs/protein). They did however likewise differ as far as their fatty acid composition is concerned, with the modified chow mirroring the ratios (!) not the amounts of mono- and polyunsaturated fatty acids of the high fat chow (see figure 1).

Figure 1: Fatty acid composition (left) and their sources (right) that were used in the different diets the rodents were fed for 16 weeks (based on Enos. 2012)

The diets were administered for 16 weeks. Body composition and metabolism (glucose, insulin, triglycerides, LDL-C, HDL-C, total cholesterol) were examined monthly.  Adipose tissue (AT) expression of marker genes for M1 and M2 macrophages and inflammatory mediators (TLR-2, TLR-4, MCP-1, TNF-α, IL-6, IL-10, SOCS1, IFN-γ) was measured and so on and so forth... and the results were... well, not exactly as you may have expected (the latter statement assumes that you expected the SFA to be either the savior or the doom of the human race, depending on which side of the LC/LF divide you are stading).

Figure 2: Body composition (left), adipocyte size (right) and fat pad weight (inset) of the rodents at the end of the study period (Enos. 2012) Values not sharing a common letter (abc) differ significantly over time within the given diet treatment (P≤.05)

If you take closer look at the data in figure 2, there are two things that will probably catch your eye right away. The first 'eye catcher' pertains to the influence of replacing a large amount of the omega-6 fatty acids by monounsaturared fatty acids, as you will find them in olive oil, for example.

• The rodents who received the modified standard chow, with a fatty acid composition identical to the high fat diets (SFA-6%, SFA-12%, SFA-24%) had the exact same body composition as their mates who received the standard chow with its 3.7x higher n6:n3 ratio. The removal of omega-6 fatty did thus not have any beneficial effects on adiposity in the low fat groups.

The second 'eye catcher' is the non-linear increase in adiposity with increasing amounts of saturated fatty acids in the diets. This does not mean that the expected increase in obesity and adipocyte size was totally absent (read the latest "Get Lean & Stay Lean" item for more information about the association of large fat cells and metabolic syndrome), though:

• The mice in the SF-6-24% did all gain significantly more body weight and body fat than their peers on the low fat diets, but there appears to be a turning point, when the saturated fat content exceeds 12%. After all the mice in the SFA-24% group had almost the same body composition as their peers on the SFA-6% diet.

So, what do we make of these 'eye catchers'? The first one, you could argue, shows that "omega 6 overload" is not a problem, as long as you are consuming a low fat diet, in the first place. Even with the major part of those 12.2% of energy your diet provides in form of various fatty acids belonging to the potentially inflammatory omega-6 fatty acids, that's still way too low to do any harm. It does, by the way, yet explain why low fat diets work so well in a society, where most high fat foods the public consumes are laden with omega-6 fatty acids - not an insignificant result, I would say.

The 12%-SF diet, most closely mimics the standard American diet

Apropos public, the second 'eye catcher' is even more telling in term of public health,... wait, I should write sickness. Why? Well, the 12%SFA high fat diet, which supplies ...

• 47% of energy in form of carbohydrates (380g sucrose, 100g maltodextrin, 50g cornstarch per 1kg of diet; identical for all SFA groups),
• 40% of energy in form of fats (of which 12% were saturated fats), and
• 13% of energy in form of protein (from casein),

... mimics, as the researchers point out, "most closely" (Enos. 2012) the standard American diet (SAD). And the result is obvious: Diabesity!

It's a fat balancing act of macro and micro ratios  - complex and far from being understood 

What's intriguing though, is that the adipogenic effects of the diet were ameliorated, when the SFA content was further increased and the diet contained 68.6g of lard per kg chow instead of just 35.4g and 96.7g of coconut oil instead of just 30g. Since this increase in SFA was at the expense of both mono- and omega-6 fatty acids, you could of course also argue that replacing at least the latter of the two with SFAs must be healthy. Unfortunately, even a brief glance back at figure 2 reveals that this is not necessarily correct. After all, the SFA-6% group was still better off than the SFA-24% group, although they had the highest amounts of oleic and omega-6 fatty acids in the diet.

By now you should actually have realized that this is once more a difficult balancing act. Where different baseline intakes of dietary fat and carbohydrates (total) are pair of setscrews and the individiual fatty acid composition of the diet is another one. And the way these setscrews are set will not just influence the body composition:

Figure 3: Serum IL-6, MCP-1, adiponectin and leptin levels, TNF-alpha mRNA expression in the adipose tissue (left), adipose tissue sample form the rodents receiving standard chow, the SFA-12% and the SFA-24% diet (Enos. 2012). The fat cells of the SFA-6% animals looked similar to those on the SFA-6% diets.

Based on the body composition data presented in figure 2 the marked increases in serum leptin and TNF-alpha mRNA expression in the adipose tissue of the rodents in figure 3 (left) should be about as unsurprising as the fact that the adipocytes of the SFA-12% group show the greatest macrophage infiltration and subsequent necrotic tissue.

If anything is surprising, it is the non-significance of the peak in IL-6 in the SFA-24% group (this was due to a very high standard deviation) and the fact that the serum level of MCP-1 a marker of increased macrophage activity was not elevated, while the adipose tissue mRNA expression was significantly higher (5-8x) in all SFA groups compared to both of the control diets. In the end this is yet only another clear sign that far more processes than we have previously thought happen locally and do not depend on circulating and thus endocrine signaling molecules.

Figure 4: Blood glucose and insulin levels of the mice over the course of the study period (Enos. 2012)

If you take the data from figure 4 into account as well, you will certainly agree with the statement Enos. et al. make pertaining to the negative effects of the SFA-12% diet, which is - just to remind you - the mirror image of the standard American diet:

"The 12%-SF diet, most closely mimicking the standard American diet, led to the greatest adiposity (absolute fat mass), macrophage infiltration, and IR [insulin resistance]." (Enos. 2012)

Figure 5: Total  cholesterol (TC, top) and LDL-C to HDL-C (bottom) ratios (Enos. 2012)

And I guess it would actually be about time to get to the bottom line, here, if it was not for the sentence that follows this assertion:

"Although the 24%-SF diet increased adiposity and produced IR, it did not significantly increase macrophage infiltration, it led to a lesser degree of AT inflammation, and it did not raise the TC/HDL-C ratio." (Enos. 2012)

Yep, you are reading right, as the data in figure 5 shows the total to HDL ratio of the SFA-24% group, which were those rodents who consumed the largest amount of "bad" saturated fat, was virtually identical to the one of the rodents on the standard and the modified standard chow and significantly lower than in those rodents who 'lived the American way of life' (SFA-12%). A similar trend was seen in the LDL:HDL radio and the triglyceride levels.

Bottom line: So, does that mean that we would just have to fry our potato chips in lard and all will be good? Not really, no. If we keep munching tons of plain sugar, even a saturated fat only diet is not going to save us from doom (I suspect there will be another inflection point at levels which exceed 50% SFA, anyway). What the study results do yet clearly implicate is that the macronutritent and fatty acid composition of the standard American diet is downright conspicuously obesogenic, pro-diabetic, inflammatory.

While the macronutrient ratio (high carb + high fat) appears to set the body into fat storage mode, the individual ratios of the fatty acids determine the efficacy of body fat storage, the negative effects on blood glucose management, and the degree of adipose tissue inflammation - and the standard American diet excels in all these disciplines.

As far as the saturated fats go (I wonder if it also plays a role that one of the main sources was coconut oil), the study suggests that you can achieve ameliorations of adiposity on both sides of the 'obesogenic optimum' of 12% saturated fats. If you take a last look at the data in figure 4, you will yet have to concede (or triumph?) that eating more not less saturated fat and thus frying your potatoes in lard, appears to be the more promising modification you could make, if the saturated fat content of the diet was your only set screw. Feels good to know it isn't right?

References:

• Enos RT, Davis JM, Velazquez KT, McClellan JL, Day SD, Carnevale KA, Murphy EA. Influence of Dietary Saturated Fat Content on Adiposity, Macrophage Behavior, Inflammation, and Metabolism: Composition Matters. J Lipid Res. 2012 Oct 28.

You Are What You Eat? Not Really! Rodent Study Shows Mice Are What the Salmon Ate That's in Their Chow

Image 1: Farmed Atlantic salmon - raised with & fried in soy *yummy*

Health conscious as you are, you will probably make sure to get grassfed beef, pay extra for the delicious Kerrygold butter and ask your farmer whether the chicken that lay the eggs you are just about to buy were pastured or received the standard feed and tons of antibiotics... right? Ok, but do you know what the fish that's lying there right in front of you had as his last supper? No? Well, after reading today's SuppVersity news, you will probably give your fish monger the third degree... but one thing after the other.

We are what that what we eat ate!

In a soon to be published study in the British Journal of Nutrition, Anita R. Alvheim and her colleagues from the National Institute of Nutrition and Seafood Research, the Department of Biomedicine  at the University of Bergen in Norway, the National Institute on Alcohol Abuse and Alcoholism in Rockville, USA, and the Department of Biology at the University of Copenhagen in Denmark, report which astonishing (or should I say frightening?) downstream effects it can have when the fish farmer who supplies your local fish monger with salmon wants to save a couple of bucks and replaces the fish oil in the diet of his farm-raised Atlantic salmon with some cheap (and hip / at least among vegans ;-) soybean oil.

Table 1: Fatty acid composition of rodent chow (top) and change in fa content of salmon due to soy oil feeding (rel. fish oil fed salmon, bottom; Alvheim. 2012)

To elucidate the downstream effects of this practice, the researchers raised Atlantic salmon on either soy or fish oil based diets (250g of each added to the diet), slaughtered the animals, filleted them and used the fillets to prepare two calorically identical rodent chows. A practice, by the way which was not as easy as it may sound, after all the salmon that had received the soy-based diet was significantly fatter (33% fat in the fillet of the soy fed vs. 26% fat in the fish oil fed salmon), so that the scientists had to make up for the lack of fat. The 6-week old mice were then randomly assigned to one of the two experimental diets to which they had ad libitum access for 6 weeks.

As the data in figure 1 goes to show the rodents on the "soy-salmon" diet had a significantly elevated hepatic alpha linoleic acid and arachidonic acid (AA) content in the hepatic phospholipids. After 9 weeks on the diet, there was a trend towards increased body weight gains that reached statistical significance in week 15 - and that in the absence of statistically significant differences in energy intake. 

Figure 1: Linoleic acid, Arachidonic acid and Arachidonoylglycerol (endocannaboid) content of liver phospholipids (left, data expressed relative to fish oil diet group), body weight development (right; Alvheim. 2012)

Moreover, compared to the rodents on the diet that contained the "normal" salmon the rodents on the soy fed salmon diet had significantly lowered EPA and DHA levels in the phospholipid fraction of their liver, erythrocytes and white adipose tissue. This lead to an overall decrease of the omega 3-index from 23 to 16 and increased the relative abundance of n-6 highly unsaturated fatty acids from 19 to 39 % percent. The histological analysis of the adipose tissue did also reveal that the rodents who received the diets with the soy fed salmon exhibited significantly more of the so-called crown-like structures which are remnants of macrophage (immune cells) invasion into the inflamed and partly necrotic (=dead) adipose tissue. The presence of this structures is associated with major increases in local and systemic inflammation and their has been implicated as one of the major driving forces of obesity induced metabolic disturbances in mice and humans (Bremer. 2011). Furthermore the adipocyte size in the groin area (=inguinal WAT) was increased.

Figure 2: I must admit I did not check if AP got the data in this chart right, but if they did, the increase in AA and AA-related endocannaboids is only part of the problem and you better stick to grass-fed beef if you can't afford wild salmon.

Implications: Overall, the weight gain may be negligible, the intricate differences in the phospholipid structure of various cells and even the presence of the crown-like structures relatively harmless and still, with the overall increase in soybean oil consumption in the US (from 2.2% of the total energy to 7.3% of the total energy intake) and the constant decline of natural (not supplemental!) DHA and EPA in the diet of the average US citizen, in the course of the 20th century (Blasbalg. 2011), the indirect or "second feed" assault from all sorts of animal products may well be the literal "last straw that brakes the camels back". After all, there is accumulating evidence for a direct relation between the diet-induced increase in arachidonic acid derived endocannaboids like 2-arachidonoylglycerol (cf. figure 1) in rodents and humans and the modulating effects of dietary fat intake on the latter.

With the study at hand, Alvheim et al. show pretty conclusively that the effect of certain foods, specifically oils, can be "handed down" in the food chain an effect that is hitherto largely ignored by scientists and nutritionists. In conjunction with reports that show that the DHA and EPA content of Atlantic salmon is already on the decline, while the linolic acid content has increased from 1.1 g/100 g in 2005 to 1.6 g/100 g in 2010  (NIFES. 2011), this raises the question of whether salmon, which is still considered to be the go-to protein and fat source for health-conscious customers, has not already been turned into another Frankenfood and puts another emphasis on the importance of knowing not just what you eat, but also what whatever you eat ate or grew on... but the latter is, I guess a topic for another blogpost ;-)

References: 

• Alvheim AR, Torstensen BE, Lin YH, Lillefosse HH, Lock EJ, Madsen L, Hibbeln JR, Malde MK. Dietary linoleic acid elevates endogenous 2-arachidonoylglycerol and anandamide in Atlantic salmon (Salmo salar L.) and mice, and induces weight gain and inflammation in mice. Br J Nutr. 2012 Aug 10:1-10.
• Blasbalg TL, Hibbeln JR, Ramsden CE, Majchrzak SF, Rawlings RR. Changes in consumption of omega-3 and omega-6 fatty acids in the United States during the 20th century. Am J Clin Nutr. 2011 May;93(5):950-62. Epub 2011 Mar 2.
• Bremer AA, Devaraj S, Afify A, Jialal I. Adipose tissue dysregulation in patients with metabolic syndrome. J Clin Endocrinol Metab. 2011 Nov;96(11):E1782-8. Epub 2011 Aug 24.
• Massiera F, Saint-Marc P, Seydoux J, Murata T, Kobayashi T, Narumiya S, Guesnet P, Amri EZ, Negrel R, Ailhaud G. Arachidonic acid and prostacyclin signaling promote adipose tissue development: a human health concern? J Lipid Res. 2003 Feb;44(2):271-9.
• NIFES. National Institute of Nutrition and Seafood Research. Research on nutrition;
  feed for fish and fish as food. < www.nifes.no/sjomatdata > retrieved Aug 14, 2012.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

---

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

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


References:

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

Rodent Study Confirms: GMO Soybean Oil is Pro-Inflammatory & Induces DNA Damage! Extra Virgin Olive Oil to the Rescue!

GMO Soybean oil? Better for cars only.

I am pretty sure there will be rebuttals to the results of this study... although, it's published in the OpenSource journal Nutrients and was conducted by scientists from Saudi Arabia and the UK who probably don't have the media-connections the scientists who conducted the GMO-corn study back in the day had.

Against that background it's unlikely that non-SuppVersity-readers will even hear about the paper El-Kholy et al. published in the June edition of Nutrients (El-Kohly. 2014) -- Well, that is - unless you spread the word, obviously ;-)

You better take creatine than ecdysteroids if you want to build muscle

Foods, not Macros Count!

Olive Oil Flavor is Healthy

Argan Oil as Test Booster

Oleic Acid ⇄ Microbiome

Tocotrienols? Red Palm Oil!

SAD Diet Analysis

Let's take a look at the methods and results, now. Needless to say that we are talking about preliminary rodent data, here - data from 40 adult male albino rats, to be precise. The rats were used in this study and divided into four groups.

• The control group of rodents was fed basal ration only. 
• The second group was given basal ration mixed with extra virgin olive oil (30%). 
• The third group was fed basal ration mixed with soybean oil from GM-soy (15%).
• The fourth group survived on a combination of EV olive oil, GM and the basal ration.

All rodents were kept on the respective diets for 65 consecutive days. On day 65, blood samples were collected from each rat for antioxidant enzyme analysis.

Figure 1: Lipid oxidation and glutathione levels (El-Kohly. 2014)

"In the group fed on basal ration mixed with GM soyabean (15%), there was a significant increase in serum level of lipid peroxidation, while glutathione transferase decreased significantly. [...] the amount of DNA and NCE were significantly decreased. [...] We can conclude that adding EV olive oil to the diet of rats appears effective in inhibiting oxidative damage and may act as a protective agent against chronic diseases such as liver fibrosis, hyperlipidemia and diabetes. In addition, EV olive oil may also have a protective function against carcinogenic processes." (El-Kohly. 2014)

That's an intriguing result and one of which I am asking myself if you'd see it with regular soybean oil, as well.

"True or False? Adding Fat to A Carby Meal Lowers Insulin Response. Muscle Hypertrophy Impairs Oxygen Diffusion. Reducing Carb Intake Improve Muscular Insulin Sensitivity" | more

Bottom line: Now, although we cannot tell for sure, whether it's the "GM", i.e. the genetic modification, or simply the fact that soy is devils excrement and not suitable for mammalian consumption *don't take this excursion to seriously*, we do know two ways to protect our DNA from the vegan assault:

1. Avoid soybean oil like a plague - easy for all of us who follow the SuppVersity-no-processed foods principle, but more or less impossible for everyone who buys products from the "food" industry
2. Add extra virgin olive oil to our diet  - the addition of EVO is simple and effective, but will only alter "the tested parameters towards normal levels" 

For me, personally, "towards normal" is not convincing enough. If you asked me, I'd thus suggest you chose option (1) - the switch to a "zero" processed foods diet is going to have a whole lot of other beneficial effects on your health, physique and performance, anyways.

Reference:

• El-Kholy, T.A.; Hilal, M.A.; Al-Abbadi, H.A.; Serafi, A.S.; Al-Ghamdi, A.K.; Sobhy, H.M.; Richardson, J.R.C. The Effect of Extra Virgin Olive Oil and Soybean on DNA, Cytogenicity and Some Antioxidant Enzymes in Rats. Nutrients 2014, 6, 2376-2386.