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Specifically for teenagers it may be important to work out in both aerobic and anaerobic workouts. So, this would be another reason to favor the combined over the other regimen.

You will probably have overheard the "knowledgeable" trainers at the gym tell their credulous clients, who just told them they "want to lose that belly fat", that the best thing they could do was to "stop spending that much time with weight training" and to do some more (steady state) cardio. Well, in general, there's nothing wrong about steady state cardio - in fact, many studies show that it is superior to resistance training when it comes to "merely" shedding body weight (in the obese). If "weight loss" is still everything you're aspiring, though, you are either new to the waredownloadsoft or another of the "headline skimmers" who happen to ask questions that are answered not just in the article, but actually in one of the red boxes... ah, I am digressing.

So, what I actually wanted to tell you is that a recent study from the Universities of Ottawa and Calgary (Alberta. 2015), clearly contradicts the average commercial gym chain trainer's recommendation and shows that belly fat loss is better achieved with diet + resistance training.
The subjects of the study were youngsters, 304 (! the high number of participants is a huge plus of the study) 14-18 year-old overweight and obese teenagers (mean body fat almost 50%!), to be specific, who were randomized to four different treatments for 22 weeks:

Table 1: Training progression in the Aerobic and Resistance group (Alberga. 2015)

• aerobic training (Aerobic), 
• resistance training (Resistance),
• combined aerobic + resistance training (Combined) or 
• non-exercising control group (Control)

Adolescents,... ok, but unless they're too sarcopenic (=suffer from pronounced age-induced muscle loss) to hit the weights, your overweight clients or you, yourself, should be able to follow the same training programs the adolescents did and see similar results if you fully adhere to the following training prescriptions:

• Resistance: The duration of each session progressed to a maximum of about 45 min. Exercises were primarily performed on weight machines, and when required with dumbbells (lateral raise, shrugs, bicep curls, front raise, preacher curl, dumbbell pullover) or by using one's own body weight as resistance (lunges, sit-ups and abdominal crunches).
  

  Table 2: Overview of the individual workouts in the Resistance group (Alberga. 2015).

  Participants alternated among exercises from groups A1, A2, B1 and B2 shown in Table 2. Participants were asked to rest for ~ 2 min between sets and were instructed on proper breathing techniques.
• Aerobic: Participants randomized to the aerobic training group underwent a 22-week program (Table 1, left) wherein the exercise intensity and duration increased progressively to a maximum of 45 min per session. Exercise was performed on a cycle ergometer, elliptical or treadmill and participants were free to vary the machine(s) used. Exercise intensity was standardized using heart rate monitors (Polar Electro Oy, Kempele, Finland).
• Combined: This group performed the full exercise programs done by both the aerobic and resistance training groups (Table 1, left + right) during each session for a total of 4 times per week for a maximum of 90 min per session.

Figure 1: Changes in subcutaneous (SAT) and visceral (VAT) body fat at different regions; L4L5 represents area between 4th and 5th Lumbar vertebrae; * indicates sign. difference to control; # sign. difference to aerobic (Alberga. 2015).

References:

• Alberga, A. S., et al. "Effects of aerobic and resistance training on abdominal fat, apolipoproteins and high-sensitivity C-reactive protein in adolescents with obesity: the HEARTY randomized clinical trial." International journal of obesity (2005) (2015).
• Dansinger, Michael L., et al. "Comparison of the Atkins, Ornish, Weight Watchers, and Zone diets for weight loss and heart disease risk reduction: a randomized trial." Jama 293.1 (2005): 43-53.
• Thompson, A., and J. Danesh. "Associations between apolipoprotein B, apolipoprotein AI, the apolipoprotein B/AI ratio and coronary heart disease: a literature‐based meta‐analysis of prospective studies." Journal of internal medicine 259.5 (2006): 481-492.
• Walldius, G., and I. Jungner. "The apoB/apoA‐I ratio: a strong, new risk factor for cardiovascular disease and a target for lipid‐lowering therapy–a review of the evidence." Journal of internal medicine 259.5 (2006): 493-519.

The yolk is where almost all the "good" stuff in the eggs resides. Throwing the yolk of the 1-2 eggs you eat per day away, as people have been doing it for decades is thus madness.

For decades eggs have been falsely accused of being the drivers of the heart disease epidemic (cardiovascular disease claims upwards of 17 million lives worldwide each year | WHO. 2011). More recently, however, the small "cholesterol bombs" have been acquitted of all charges and scientists begin to (re-)evaluate their already know, but largely ignored health benefits. Health benefits that are not solely related to their high protein content, by the way.

As a waredownloadsoft reader you will know that eggs are valuable protein sources, but don't worry: This is not what today's waredownloadsoft article is about. Rather than that I would like to highlight a much less-known egg constituent, the egg phospholipids.
Studies indicate that eggs are the major source of phospholipids (PL) in the Western diet; the same phospholipids that "have emerged as a potential source of bioactive lipids that may have widespread effects on pathways related to inflammation, cholesterol metabolism, and HDL function" (Blesso. 2015).

Table 1: Typical Composition of Egg Phospholipids | FA, fatty acid; LysoPC, lysophosphatidylcholine; LysoPE, lysophospha-tidylethanolamine; PC, phosphatidylcholine; PE, phospha-tidylethanolamine; PI, phosphatidylinositol; PL, phospholipid; SM, sphingomyelin. (Blesso. 2015)

"PL are key components of all biological membranes and are abundantly found in the diet, primarily as glycerophospholipid and sphingolipid classes. Dietary glycerophospholipids are made up of two fatty acids (FA), a glycerol backbone, a phosphate group, and a polar organic molecule (choline, serine, inositol, or ethanolamine).[...] The average large egg contains approximately 1.3 g of PL, which are almost exclusively found in the yolk. 

A typical Western diet contains about 2–8 g of dietary PL per day. Estimates of average egg intake in the U.S. indicate that egg-derived PL contributes 10%–40% (or 0.8 g) of daily consumed PL. The major PL species found in egg include PC, phosphatidylethanolamine (PE), SM, and phosphatidylinositol (PI). The typical PL composition of egg is shown in Table 1, which reveals PC as the predominant species making up almost three quarters of the total PL. The typical FA compositions of egg PL species vary and are shown in Table 1" (Blesso. 2015).

Alongside carotenoids lutein and zeaxanthin, two potent anti-oxidant agents in eggs, and the previously mentioned phospholipids which have also been shown to

• Eggs have beneficial effects on cholesterol in your cells | learn more

  decrease serum cholesterol levels in rats (Murata. 1982) and a reduction of the intestinal absorption of cholesterol (Jiang. 2001), 
• improve memory retention and increase acetylcholine concentrations, a neurotransmitter that decreases in concentration in cases of Alzheimer’s disease (Masuda. 1998;  Favreliere. 2003), as well as 
• improve liver function, and cancer prevention (Gutierrez. 1997),

there are also a hand full of peptide / proteins and related agents - mostly in the yolk of eggs - that make eggs a totally underestimated health food:

• Table 2: Biological acitivities of egg proteins (Kovacs-Nolan. 2005)

  yolk proteins - ovalbumin, ovotranserin, ovucoid, ovomucin, lysozyme, as well as ovoinhibitor, vomacroglobulin, ovomacroglobulin and avidin have antibacterial activity and antihypertensive, immunomodulating, antiadhesive (=interferes with a key step of inflammation), antitumor, and antiviral activities (to find out what does what, check out Table 2 from Kovacs-Nolan. 2005);
• immunoglobulins - specifically immunoglobolin Y from egg yolk which has been shown to have antibacterial activity, antiviral activity, can reduce the incidence of dental caries, is used in anti-venoms, acts as an anti-inflammatory agent, and serves as a carrier for anti-cancer drugs (Mine. 2004);
• other components of the yolk - including phosvitin, sialyloligosaccharides and sialylglycopeptides, as well as the yolk lipids, lipoproteins, fatty acids, and cholesterol have scientifically proven antioxidant and antibacterial activities, as well (Kovacs-Nolan. 2005)

References:

• Abdullah, Mohammad MH, Peter JH Jones, and Peter K. Eck. "Nutrigenetics of cholesterol metabolism: observational and dietary intervention studies in the postgenomic era." Nutrition reviews (2015): nuv016.
• Ballesteros, Martha Nydia, et al. "One Egg per Day Improves Inflammation when Compared to an Oatmeal-Based Breakfast without Increasing Other Cardiometabolic Risk Factors in Diabetic Patients." Nutrients 7.5 (2015): 3449-3463.
• Blesso, Christopher N. "Egg Phospholipids and Cardiovascular Health." Nutrients 7.4 (2015): 2731-2747.
• Clayton, Zachary S., et al. "Influence of Resistance Training Combined with Daily Consumption of an Egg-based or Bagel-based Breakfast on Risk Factors for Chronic Diseases in Healthy Untrained Individuals." Journal of the American College of Nutrition 34.2 (2015): 113-119.
• Favreliere, S., et al. "DHA-enriched phospholipid diets modulate age-related alterations in rat hippocampus." Neurobiology of aging 24.2 (2003): 233-243.
• Goldstein, Joseph L., and Michael S. Brown. "A Century of Cholesterol and Coronaries: From Plaques to Genes to Statins." Cell 161.1 (2015): 161-172.
• Gutierrez, M. A., H. Takahashi, and L. R. Juneja. "Nutritive evaluation of hen eggs." Hen eggs, their basic and applied science. 2nd ed. CRC Press, New York (1997): 25-35.
• Herron, Kristin L., et al. "The ABCG5 polymorphism contributes to individual responses to dietary cholesterol and carotenoids in eggs." The Journal of nutrition 136.5 (2006): 1161-1165.
• Jiang, Yongzhi, Sang K. Noh, and Sung I. Koo. "Egg phosphatidylcholine decreases the lymphatic absorption of cholesterol in rats." The Journal of nutrition 131.9 (2001): 2358-2363.
• Kovacs-Nolan, Jennifer, Marshall Phillips, and Yoshinori Mine. "Advances in the value of eggs and egg components for human health." Journal of agricultural and food chemistry 53.22 (2005): 8421-8431.
• Masuda, Y., et al. "Egg phosphatidylcholine combined with vitamin B 12 improved memory impairment following lesioning of nucleus basalis in rats." Life sciences 62.9 (1998): 813-822.
• McNamara, Donald J. "The impact of egg limitations on coronary heart disease risk: do the numbers add up?." Journal of the American College of Nutrition 19.sup5 (2000): 540S-548S.
• Mine, Yoshinori, and Jennifer Kovacs-Nolan. "Biologically active hen egg components in human health and disease." The Journal of Poultry Science 41.1 (2004): 1-29.
• Murata, Masakazu, Katsumi Imaizumi, and Michihiro Sugano. "Effect of dietary phospholipids and their constituent bases on serum lipids and apolipoproteins in rats." The Journal of nutrition 112.9 (1982): 1805-1808.
• Nakamura, Yasuyuki, et al. "Egg consumption, serum total cholesterol concentrations and coronary heart disease incidence: Japan Public Health Center-based prospective study." British Journal of Nutrition 96.05 (2006): 921-928.
• World Health Organization. Global Status Report on Noncommunicable Diseases 2010; World Health Organization: Geneva, Switzerland, 2011.

If you cannot decide: Oatmeal or eggs, try oatmeal with sunny-side up eggs, avocado, cheddar and chives | more

In spite of the fact that it's true that epidemiological studies still report controversies on the effects of dietary cholesterol and egg intake on the risk for heart disease in patients with diabetes (Shin. 2013; Qureshi. 2006), you as a waredownloadsoft reader will know that convincing experimental evidence for the causative relation between eating eggs and a worsening of health-relevant lipid-markers is more or less simply "non-existent" (read more).

In fact, more recent evidence suggests that "an egg a day" may keep the doctor away about as reliable as the proverbial "apple" of which Alex taught you that it'll keep the doc away.
In contrast to average Joes and Janes, though, individuals with type II diabetes (T2DM) whose metabolic state is characterized by impaired glucose metabolism, atherogenic dyslipidemia, and chronic low-grade inflammation, could be at a disadvantage of which some scientists still speculate that it was not compatible with a high(er) cholesterol diet.

To test whether that's correct and diabetics should better stay away from eggs, researchers from the Centro de Investigacion y Desarrollo in Mexico compared two breakfasts with perceived differences in effects on heart disease risk, eggs and oatmeal, by conducting a randomized, crossover clinical trial in subjects with T2DM.

Figure 1: Effects of eggs and oatmeal breakfast on glucose control and inflammation in type II diabetics (Ballesteros. 2015).

We evaluated the effects of consuming one egg per day for a relatively extended period (five weeks) versus 1/2 cup (40 g) of oatmeal per day on plasma glucose and inflammatory markers, our primary endpoints. Our secondary endpoints included plasma lipids, markers of oxidative stress, and parameters of glucose metabolism, such as glycosylated hemoglobin (HbA1c). We hypothesized that eating one egg per day would not adversely affect primary or secondary endpoints when compared to an oatmeal breakfast. 

We further hypothesized that eggs would reduce inflammatory markers in this population, likely due to the presence of highly bioavailable carotenoids" (Ballesteros. 2015).

Twenty-nine subjects, 35–65 years with glycosylated hemoglobin (HbA1c) values <9% (this means they were diabetic, but not really "sick") were recruited and randomly allocated to consume isocaloric breakfasts containing either one egg/day or 40 g of oatmeal with 472 mL of lactose-free milk/day for five weeks.
Following a three-week washout period, subjects were assigned to the alternate breakfast. At the end of each period, we measured all primary and secondary endpoints. Subjects completed four-day dietary recalls and one exercise questionnaire for each breakfast period.

Figure 2: Markers of liver health were improved (reduced), as well.

There were no significant differences in plasma glucose, our primary endpoint, plasma lipids, lipoprotein size or subfraction concentrations, insulin, HbA1c, apolipoprotein B, oxidized LDL or C-reactive protein, which is a bummer and would go against the statement that eggs are more than just "less inflammatory" (i.e. actually anti-inflammatory foods).

However, after adjusting for gender, age and body mass index, aspartate amino-transferase (AST) (p < 0.05) and tumor necrosis factor (TNF)-α (p < 0.01), one of our primary endpoints were significantly reduced during the egg period.
References:

• Ballesteros, Martha Nydia, et al. "One Egg per Day Improves Inflammation when Compared to an Oatmeal-Based Breakfast without Increasing Other Cardiometabolic Risk Factors in Diabetic Patients." Nutrients 7.5 (2015): 3449-3463.
• Katz, David L., et al. "Effects of egg ingestion on endothelial function in adults with coronary artery disease: A randomized, controlled, crossover trial." American heart journal 169.1 (2015): 162-169.
• Rong, Ying, et al. "Egg consumption and risk of coronary heart disease and stroke: dose-response meta-analysis of prospective cohort studies." Bmj 346 (2013): e8539.
• Shin, Jang Yel, et al. "Egg consumption in relation to risk of cardiovascular disease and diabetes: a systematic review and meta-analysis." The American journal of clinical nutrition (2013): ajcn-051318.
• Qureshi, Adnan I., et al. "Regular egg consumption does not increase the risk of stroke and cardiovascular diseases." Medical Science and Technology 13.1 (2006): CR1-CR8.

Can you pump them up w/ silicon and to negate their atherosclerotic effects!?

In today's installment of the Nutrition Research Update in the Short News, I am going to tackle three studies that deal with the surprisingly pronounced, yet practically potentially irrelevant benefits of eating a high protein breakfast, silicon... not in breasts, but sausages as a means to protect you from heart disease and the fact that calories count so much that even on a "healthy diet" only those who eat in moderation will age healthily.

That sounds interesting? Fine! I am not going to waste any more time and will fast forward to the first study...

• Breakfasts Higher in Protein Increase Postprandial Energy Expenditure, Increase Fat Oxidation, and Reduce Hunger in Overweight Children from 8 to 12 Years of Age - In the eponymous study, Baum et al. determined whether consumption of a protein-based breakfast (PRO) increases postprandial energy metabolism and substrate oxidation, reduces hunger, and reduces food intake at lunch compared with a carbohydrate-based breakfast (CHO) in normal weight (NW) vs. overweight/obese (OW) children. Both, the normal and over-weight children participated in the same randomized, crossover protocol that arranged for all participants to be served a
  • high PRO [344 kcal, 21% protein (18 g), 52% carbohydrate, and 27% fat] or 
  • high CHO [327 kcal, 4% protein (3 g), 67% carbohydrate, and 29% fat]
  breakfast, after which the energy expenditure (EE), substrate oxidation, appetite, and blood glucose were measured over a 4 h period. To access whether the high protein intake would also affect the participants appetite, the subjects had free access to a lunch buffet and food intake was recorded.
  

  Figure 1: Energy expenditure, fat and carbohydrate oxidation in the 4h post breakfast (Blum. 2015).

  The results were unambiguous: After breakfast, OW children in the PRO group had higher (P < 0.0001) EEs and fat oxidation over the 4 h period than did the NW children in the CHO and PRO groups. Of these, the increase in energy expenditure was transient and didn't last for the full 4h period. The increase in fat oxidation in response to the high protein intake, on the other hand, lasted for the full 4 h period (+16%; P < 0.05) and went hand in hand with a surprisingly pronounced 32% increase in carbohydrate oxidation in the PRO vs. CHO (P < 0.01) trial.
  

  Table 1: Despite decreased hunger and increased fullness, the protein breakfast did not reduce the total energy intake or modify the macronutrient ratio of the foods the kids selected at the lunch buffet (Baum. 2015).

  Now, all this sounds great, but even though the subjects experienced decreased feelings of hunger (−14%; P < 0.01) and increased fullness (+32%; P < 0.05) after the PRO than the CHO breakfast, the lack of effect on the intake at the subsequent ad-libitum lunch is disappointing to say the least. This and the lack of long-term data make it very difficult to predict if a similar increase in protein during breakfast only would actually help the subjects lose weight.  
• Silicon ... not breasts, but enhanced meat may protect older individuals against atherosclerosis - That's at least what a recent rodent study by Garcimartin et al. (2015) suggests.

  "Research has shown that silicon can play an important role in protecting against degenerative diseases. Restructuring pork by partially disassembling meat would permit the incorporation of active components with potential functional effects. However, there has been no research to date on the impact that silicon, as a functional ingredient in restructured pork (RP), has on lipoprotein composition, metabolism, and oxidation" (Garcimartin. 2015).

  In order to find out whether the addition of silicon would actually have a meaningful effect, the scientists added 1.3g/kg silicon to sausages that were then fed to one group of old rodents while the rest received regular, non-enriched sausages as part of regular and pro-atherogenic cholesterol-enriched diets.
  
  The results were quite astonishing, as is partially normalized the changes induced by the high cholesterol diet. Compared with the rodents who received the regular sausages, those on the silicon sausages had lower VLDL compound concentrations (P < 0.001; e.g., 75% less VLDL cholesterol) and a significantly reduced VLDL oxidation (65% less conjugated dienes and 85% less TBARS) that went hand in hand with an increase in LDL-receptor expression (200% more).
  

  Figure 1: The silicon in the sausages increased the LDL receptor density to (almost) normal, the amount of cholesterol protecting AE in the blood and liver, as well as its ratio to the amount of cholesterol. The result is obvious: With as little oxidized VLDL in the blood as the control, we can safely assume that the rodents that consumed the silicon enriched sausages have a sign. lower atherosclerosis risk (Garcimartin. 2015).

  In spite of the fact that there are differences in the susceptibility of mouse and man to the pro-atherogenic diets of the results do - just as the authors point out - still suggest that silicon added to restructure pork can strongly counterbalanced the negative effect of high-cholesterol-ingestion and, as I would like to add, the negative effects of endogenous cholestrol (by increasing its uptake by LDL receptors and decreasing its susceptibility to oxidation) thus "functioning as an active hypocholesterolemic, hypolipemic, and antioxidant dietary ingredient" (Garcimartin. 2015).
• Healthy eating requires a controlled (not restricting) energy intake to increase one's chance of "aging healthily" by almost 50% - If you question if eating "healthy" and not eating everything in sight is even worth it, you will like the results of a recent study from the Sorbonne in Paris (Essmann. 2015).
  
  In her latest study Karen E Essmann and her colleagues analyzed the diets of a subgroup of 2769 participants of the SU.VI.MAX (SUpplémentation en Vitamines et Minéraux AntioXydants) trial. They identified subjects consuming "healthy" and those on the "standard Western diet", adjusted the data for a large number of potential confounders and the influence of high(er) and low(er) energy intakes.
  

  Table 2: Overview of the criteria the scientists applied to identify "healthy eating" - CES-D, Center for Epidemiologic Studies–Depression Scale; DKTMT, Delis-Kaplan version of the Trail Making Test; IADL, instrumental activities of daily living; MMSE, Mini-Mental State Examination; RI-48, 48-item cued recall test; SF-36, Medical Outcome Study Short Form 36; SPPB, Short Physical Performance Battery.

  In that, the scientists found that the association between "healthy eating" and "healthy aging" was mediated by low(er) energy intakes. Only in subjects with median or lower energy intakes, the association between "healthy eating" and "healthy aging" reached statistical significance, so that the non-gluttonous "healthy eaters" were 49% more likely to age healthily.
  
  Since we are already talking "healthy eating", let's briefly mention that scientists from the University of Eastern Finland just confirmed the obvious (Haapala. 2015): A poorer diet quality is associated with worse cognition in children. What is a bit surprising, though, is that the relationship was stronger in boys than in girls.

References:

• Assmann, et al. "A Healthy Dietary Pattern at Midlife, Combined with a Regulated Energy Intake, Is Related to Increased Odds for Healthy Aging." J. Nutr. first published on 5 August 2015 doi:10.3945/jn.115.210740
• Baum, et al. "Breakfasts Higher in Protein Increase Postprandial Energy Expenditure, Increase Fat Oxidation, and Reduce Hunger in Overweight Children from 8 to 12 Years of Age." J. Nutr. first published on 12 August 2015 doi:10.3945/jn.115.214551
• Garcimartín, et al. "Silicon-Enriched Restructured Pork Affects the Lipoprotein Profile, VLDL Oxidation, and LDL Receptor Gene Expression in Aged Rats Fed an Atherogenic Diet." J. Nutr. first published on 5 August 2015 doi:10.3945/jn.115.213934
• Haapala, et al. "Associations of diet quality with cognition in children – the Physical Activity and Nutrition in Children Study." British Journal of Nutrition (2015): FirstView Article.

There are more than a dozen of options for virgin coconut oil on the market and there's no way the normal custumer can tell which one is actually "virgin" and which is a fraud and maybe even adulterated with palm oil - the technology to identify adulterations is there (Manaf. 2007), but I haven't heard of a label that would prove that the products were tested.

You are probably as fed-up with the hype around coconut oil as I am, right? Coconut oil here, coconut oil there. For this, for that and "did you know that coconut oil will also ..." Yes, you can even argue that a new branch of broscientists and snake oil vendors is dealing with little else than coconut oil.

In spite of that, I consider it at least remotely possible that the data from a recent rodent study that was published in the UK Journal of Pharmaceutical and Biosciences (Sharig. 2015) will catch your attention. I am sure you won't catch fire, though, but maybe at least some sparks, when you read that a relatively low dose of virgin coconut oil slowed down the weight gain, even if the oil was added to a non-obesogenic diet. Not excited? Well what about its triglyceride and total cholesterol lowering prowess and it's ability to keep LDL and VLDL in check while increasing HDL significantly - that's at least news-worthy isn't it?
But first things first - here's what the scientists did: The scientists bought a bunch of 2 months old rats. After 2 weeks of acclimatization, they randomly assigned them to one of the following diets:

• Group 1 was fed the normal pellet diet (control),
• Group 2 was administered normal diet with VCO (1 ml/day),
• Group 3 named as HCD received bread with pellet,
• Group 4  animals received HCD bread and pellet with VCO (1 ml/day),
• Group 5 called as HLD animals received cheese with pellet,
• Group 6 named HLD animals received cheese and pellet with VCO (1 ml/day)

All groups had free access to diets and water ad libitum for 10 weeks. To make sure the virgin coconut oil was actually consumed, the VCO was administered by oral gavage at a dose of 1.42 ml/kg. That's the rodent equivalent of ~3 tablespoons of coconut oil which is what Fife recommends in "Coconut Cures" (2005) you should take everyday to - as the title of the book says - prevent and treat common health problems with coconut (not all of the claims made in the book can be considered scientifically proven, btw).
The rodents remained on their respective diets for 8 weeks before... no, not before they were sacrificed, but before the scientists from the Managemant and Science University in Malaysia used a spectrophotometer and commercial enzymatic kits to determine the lipid parameters by enzymatic endpoint method, as well as the plasma total cholesterol (TC), triglyceride (TG) and high-density lipoprotein (HDL) levels were measured using commercial enzymatic kits.

Figure 1: Effect of Virgin coconut oil on plasma lipid profile of albino Wistar rats after 8 weeks (Shariq. 2015).

A brief glimpse at the data in Figure 1 shows that the addition of virgin coconut oil did in fact have a not exactly life-saving, but still health-relevant effect on the lipid metabolism of the rodents. What I personally consider most intriguing is that this was the case for all diets, including the normal one.
References:

• Feranil, Alan B., et al. "Coconut oil predicts a beneficial lipid profile in pre-menopausal women in the Philippines." Asia Pacific journal of clinical nutrition 20.2 (2011): 190.
• Liau, Kai Ming, et al. "An open-label pilot study to assess the efficacy and safety of virgin coconut oil in reducing visceral adiposity." ISRN pharmacology 2011 (2011).
• Manaf, Marina Abdul, et al. "Analysis of adulteration of virgin coconut oil by palm kernel olein using Fourier transform infrared spectroscopy." Journal of Food Lipids 14.2 (2007): 111-121.
• Shariq, B., et al. "Evaluation of Anti-Atherosclerotic Activity of Virgin Coconut Oil in Male Wistar Rats Against High Lipid and High Carbohydrate Diet Induced Atherosclerosis."