Gene-ial or Dan-Gene-rous? Better Make Sure You Are Made For Every Other Day Fasting, If You Don't Want to Ruin Your Glucose + Lipid Metabolism and Become Viscerally Obese

Yes! I freely admit that I do have a problem with the subliminal "binge and starve" of the popular every other day fast, because it paves the not so royal road to binge eating disorders.

Only 2 years ago, there was hardly anyone but the followers of Martin Berkhan's "Lean Gains" regimen who knew what intermittent fasting would be. Ironically, now that mainstream is catching on, the hype within the fitness community is slowly abating  - maybe part of the reason is that it's no longer "cool" enough now that your fat neighbor does it ;-).

It goes without saying that the mainstream version comes without an obligatory exercise component and - what's probably even worse - in the absence of macronutrient, let alone food prescriptions that would make sure that the every other day fasts that are becoming increasingly popular these days become "binge and starve" protocols.

The every other day fast, a gateway to eating disorders?

I could probably write a whole article about the potential of feast and fast strategies to function as a gateway to binge-eating disorders, but I know that most of you will discard that by stating: "Pah, that's happening only to the psychologically labile person who can't control his-/herself"... I will argue against that in another article, but I want to let you know here and now, that you could hardly be more off.

Did you know that eggs can improve the lipid profile of most of us?

Stay calm! In view of the fact that rodents in the wild-type control group, who had fully functional LDL receptors did not show a similar negative response to the well-meant dietary intervention, the results of the study at hand are hopefully irrelevant for most of you. If you do have friends and relatives with inexplicably high cholesterol levels, you would however be ill-advised to encourage them to battle their problems with every other day fasting.

Anyway... What this article is actually about is a paper from the British Journal of Nutrition. It was written by Dorighello et al. and has been published online ahead of print. The corresponding study was designed to test the hypothesis that alternate day fasting, which has previously been shown ... 

• to decrease established metabolic risk factors of CVD and diabetes in human subjects and rodents (Varady. 2007),
• to reduce the production of liver mitochondrial reactive oxygen in mice (Caro. 2008), and 
• to increases the lifespan of rodents (Martin. 2006)

would ameliorate tissue mitochondrial oxidative stress and glucose intolerancr in LDL-receptor knockout mice. The LDL-receptor negative mouse is a common, or rather the scientific model of familial high cholesterol (these are the people who are put on a statin the very moment, they enter their doctor's office).

What the scientists expected and what they found were two pair of shoes

I guess you don't have to be a rocket scientists to see what the data in Figure 1 is telling us: In spite of a 20% reduction in energy intake (over the whole week), the rodents in the Dorighello study did not benefit from their every other day fasting regimen (EODF)

Figure 1: Changes in lipid and blood glucose levels (relative to control on ad libitum diet; left) and carcass composition in % of total weight (right; data based on Dorighello. 2013)

Accordingly, the Brazilian scientists who had expected that the fasting induced energy restriction, (-20%), alone, should ameliorate the metabolic disturbances in LDL-receptor knockout mice, and reduce their susceptibility to atherosclerosis, had to acknowledge that their clever every other day fasting regimen can have unexpected and, in the last consequence, eventually fatal effects on the heart health of the laboratory mice:

• Epididymal and carcass fat depots and adipocyte size were significantly enlarged by 15, 72 and 68 %, respectively.
• Pasma levels of leptin were 50 % higher in the EODF mice than in the ad libitum-fed mice.
• EODF mice showed increased plasma levels of cholesterol -  total cholesterol (37 %), VLDL-cholesterol (195 %) and LDL-cholesterol (50 %). 
• The glucose homeostasis of the "EODF mice" also disturbed. The scientists observed a +40 % increase in glycemia and a +50% increase in insulinaemia. In short, the mice became glucose intolerant and insulin resistant.
• The significant increases in systemic inflammatory markers, TNF-a and C-reactive protein, only topped the list of negative side effects of the every other day fast off.

Overall this lead to a 3-fold increase in spontaneous atherosclerosis development, an effect of which it cannot be said often enough that it was observed exclusively in the LDL-receptor negative mice.

Practically speaking... In spite of the fact that the main take home message of the study at hand may be relevant only for those who harbor a certain genetic disposition, I do not recommend a zero calorie every other day fast to anyone - irrespective of whether he or she does or doesn't have LDL receptors  ;-)

If you are not aware of cases of familiar hyper-cholesteraemia and want to improve your lipid metabolism by fasting and eating clean, I suggest you re-read my previous article about the "Two Day High-Protein, Low-Carb Fast" and try this, or a classic intermittent fasting routine with a 6-8h feeding window to shed some body fat and get in better metabolic shape.

So what does this mean? The results of the study at hand are exemplary of something regular SuppVersity readers have encountered a dozen of times, already. A fact that vindicates the often-heard, but rarely understood notion that "we are all different". As the study at  hand clearly shows, our gene's and their consequences on our physiology determine not just what we should eat, but also when we shoult eat it. 

You got to be wary, though! Contrary to what you may read in some shiny magazines and on banners on the Internet, the often advertized "gene type diet" is not even on the horizon, yet.

Yes, we can (theoretically) identify each and every gene in our bodies, but in contrast to a general LDL receptor dysfunction, many of the more subtle genetic differences are as of yet totally unknown. Any list of foods, or, as this study shows, suggest food frequency rules you may get are up to know about as accurate as the names of the man or woman of your dreams you will get if you follow the friendly advice the music television advertisement gives you and "send an SMS with the keyword 'love' and your name" to a random number. Even for the well-studied APO-E polymorphisms, scientists are time and again surprised to find that their results are not in line with data from previous studies. Contemporary accepted implications, such as "people whose apolipoproteins belong to the APO-E4 class will do more harm than good if they consume larg(er) amounts of fish oil" could thus be as flawed as the idea that only fat can make you fat - likewise the result of premature conclusions that seemed logical in view of the contemporarily available, highly insufficient data, by the way.

References:

• Caro P, Gómez J, López-Torres M, Sánchez I, Naudi A, Portero-Otín M, Pamplona R, Barja G. Effect of every other day feeding on mitochondrial free radical production and oxidative stress in mouse liver. Rejuvenation Res. 2008 Jun;11(3):621-9.
• Martin B, Mattson MP, Maudsley S. Caloric restriction and intermittent fasting: two potential diets for successful brain aging. Ageing Res Rev. 2006 Aug;5(3):332-53.
• Varady KA, Hellerstein MK. Alternate-day fasting and chronic disease prevention: a review of human and animal trials. Am J Clin Nutr. 2007 Jul;86(1):7-13. Review.

Obese Vegan Salmon!? Vegetable Oils and Proteins Reduce DHA and EPA Content by -28% and Increase Overall Adiposity and Triglyceride Levels in Atlantic Salmon.

Image 1: Could this be made of obes vegan
salmon? (img from littlesteps.eu)

If you listened to yesterday's episode of Carl Lenore's Super Human Radio, you may remember that I repeatedly pointed out that "not all milk is created equal" and that milk quality is determined by food quality (if you want to read more about milk in general and colostrum in particular, I suggest you read last week's Ask Dr. Andro, as well). Today I am going to tell you about another of the industry's economic (in the monetary sense) ways of reducing the quality of animal foods in our foodchain - and we are talking about a food with a much better reputation than milk or beef: Salmon, the "heart-healthy cold-water fish" that is literally in on (or rather between) everyone's lips, lately.

Note: Salmon is explicitly mentioned in the "sample one-day menu" scientists at Colorado State developed according to the USDA dietary guidelines (Dietary Guidelines for Americans), so don't tell me you are not supposed to eat Norwegian fish, anyway, because you, my American friends, are supposed to have Grilled salmon, steamed broccoli, barley pilaf, low-fat milk and cake with fresh berries for dinner ;-)

Bente E. Torstensen and his (her?) collegues from the National Institute of Nutrition and Seafood Research and the Skretting Aquaculture Research Centre in Norway conducted an interesting experiment (Torstensen. 2011). For about a year, the researchers fed 6,000 smolt of Atlantic salmon (mean weight 355g) which had previously been randomly assigned to one out of three experimental + one control groups with diets containing...

• maximal amounts of fish meal and fish oil (Control)
• the "safe maximum replacement" of both fish meal and fish oil with plant meal (80% plant protein) and vegetable oil (70% vegetable oil) (80PP70VO)
• half the maximum replacement with plant meal (40%) and maximal replacement with vegetable oil (70%) (40PP70VO)
• maximum replacement with plant protein (80%) and half of the maximal replacement with vegetable oil (35%) (80PP35VO)

While the control diet obviously resembles what salmon, which primarily feeds on other fish, would naturally eat, the diet composition of group 2 remotely reminds me of what the food-industry has been feeding the less health-conscious masses in the US and Europe over the last decades. What... as a animal-loving vegan you are more interested in the fate of the poor salmon than in that of your sick and obese fellow human beings? Ok, here is what happened:

Maximum dietary VO [vegetable oil] and PP [plant protein replacements] increased visceral lipid stores, liver TAG, and plasma VLDL and TAG concentrations. Increased plasma TAG correlated with an increased expression of apoB100, indicating increased VLDL assembly in the liver of fish fed the high-plant protein- and VO-based diet.

Veganism, it turns out, ain't the preferable diet for salmon. Depending on which end of the dietary spectrum you belong to - the carnivorous hunter or the vegan gatherer -  you will probably now be asking yourselves one of the following questions:

1. Hunter: "What does that have to do with me? I always knew plant proteins and oils are bad for you!"
2. Gatherer: "What does that have to do with me? I don't eat salmon and the results from a 'fish-model' certainly won't apply to human beings!"

In isolation both the carnivorous hunter as well as the vegan gatherer appear right, when they ignore a prick like me citing the results of an insignificant fish study, the amalgam of both of these trains of thought does yet bring up a more unsettling question: What happens to the average health-conscious customer on a budget who thinks he is doing him/herself good by frying his economically raised, i.e. vegetable oil and protein fed, salmon in "healthy" vegetable oils and finishes dinner with a tofu dish? To be honest, I don't think we really need a study to answer that question. You just have to look at your peers to see the health consequences of eating sick animals and other vegetables that were either never intended for human consumption or have been (over-)processed beyond all recognition.

Figure 1: Relative changes in the fatty acid profile compared to "real", i.e. fish-fed, salmon after 1 year on vegetable oil and protein (data calculated based on Torstensen. 2011)

A pros pos "beyond recognition" if you have a closer look at the combined effects of vegetable oils and proteins on the fatty acid (figure 1) of the fish you will notice that industrially produced salmon fed with the "safe maximum replacement" dose of vegetable oils and proteins has little resemblance with the healthy food most consumers believe they were eating, when they buy "salmon" at the grocery store. Most obviously, the beneficial n3:n6 ratio of 7.6 in "real" salmon changed for the worse and ended up at roughly 3.0 after one year on a 80% plant protein 70% vegetable oil diet. Moreover, the individual composition of the fatty acids changed, as well. These changes include -28% reductions in EPA and DHA levels. After all, customers are left with something that looks like salmon, because it has been artificially colored, and tastes like "salmon", simply because 99% of the customers do not even know how "real" salmon would taste, because since the 1980s the ratio of wild-caught (real) salmon to farmed (fake ;-) Atlantic salmon has declined from 10:13 to 1:480 and fewer and fewer people have even had the chance to taste non-industrially produced salmon.

Spicing Up Fat Loss: Structural Similarity to Melanocortin-4 Agonists Powers Piperine's (Black Pepper Extract) Fat Loss and Lipid Lowering Effects

Image 1: The molecular structure of
piperine makes it a potential
melanocortin-4 (MC4) agonist.

Despite the fact that the American fast food mentality has long conquered the Indian subcontinent, and obesity and diabetes are on a rise, the ideal of the curry eating, spicy food loving, lean Indian still figures in the minds of people in the "old" (Europe) and "new" world (America). Maybe this is part of the reason  why many of us willingly believe(d) in the ability of black pepper and other spice extract to literally "burn away" unwanted body fat, when we read about it in the latest supplement advertisement. Other than in the cases of Goji berries, Acai and co, a recent study (Shah. 2011) coming from, you guessed it, India, was not only able to confirm the validity of these claims (at least for rodents / more on that later), it also gives a reasonable explanation for the fat-burning effect of piper nigrum.

Using the standard rodent model of obesity-induced dyslipedemia (the high fat diet fet male Sprague Dawley rat), Shah et al. found that treatment with 40mg/kg (human equivalent dose: 6.5mg/kg)

significantly reduced not only body weight, triglyceride, total cholesterol, LDL, VLDL, and fat mass, but also increased the HDL levels, with no change in food intake.

In that, it is important to note, that both, weight loss, as well as the improvements in blood lipids occurred despite continuous intake of the fattening "high fat" diet (which was obviously also relatively high carb, just like the typical western diet), of which the rats kept eating about the same amount as before the initiation of treatment. A silbutramine treated control group, on the other hand, "exhibited a significant reduction in food intake as compared to the HFD-control group". In contrast to the prominent weight loss drug, piperine's effect on body weight, fat mass and blood lipids are thus not partly mediated by a simple reduction of caloric intake.

Figure 1: Epididymal (white adipose tissue, WAT) and interscapular (brown adipose tissue, BAT) fat mass in % of unsupplemented rats on a high fat diet (HFD) after administration of either sibutramine or piperine along with HFD for 11 weeks (data adapted from Shah. 2011)

In view of an unmistakable structural similarity of piperine to other selective melanocortin receptor agonists such as piperazine, piperidine, pyridazinone, tetrahydropyran, thiadazole, and diazole derivatives, the scientists propose direct melanocortin-4 receptor agonism at the level of the arcuate nucleus and thus "increased energy expenditure, and increased Insulin sensitivity" as an underlying mechanism for the anti-obesity, anti-hyperlipidemic effects of black pepper extract. Coupled with its thyrogenic activity, which "modulates apolipoprotein levels and insulin resistance" piperine turns out to be one of the few really promising fat loss adjuvants available on the vast supplement market.

To all that has been said, there is however one major caveat: Humans are not rodents, and whenever you read of thermogenic effects that have been observed in rats or mice, you must remember that human beings, other than those little critters lose most of their already negligible brown fat depots (BAT) within the first month of their lives. An organism lacking this type of thermogenic fat will obviously react very differently to compounds that speficitcally target thermogenic pathways. Whether the results from this study can be transfered to humans, or in other words, whether piperine will burn your love handles away, still warrants confirmation in human studies.

On a side note: The smaller reduction in BAT (cf. figure 1) observed in this study does not imply that the thermogenic effect of brown adipose tissue thermogenesis would not play a fundamental role in the metabolic effects of piperine. In order to raise the animal's body temperature, BAT actually uses white adipose tissue as a "fuel source".

High Dose Caffeine + Non-Alcoholic Fatty Liver Disease = 355% Increased Very Low Density Lipoprotein (VLDL)

Image 1: Already in "pill form" - Coffee beans

Caffeine, the world's #1 drug certainly is a remarkable substance. It does not only have myriads of well-established physiological effects, already, but it seems that - if you wanted to - you could identify another one everyday. It is thus not really surprising that a recently published study by Abd El-Ghany, M.A., Rasha, M. Nagib and Hagar, M. El-Saiyed from the Mansoura University in Egypt casts yet another, in this case, however, pretty scary light on the lifeblood of the average Starbucks junkie (El-Ghany. 2012).

Caffeine prevents weight gain - whohooo! Or not?

The scientists set out to investigate the differential effects the oral administration of 10mg/day of pure caffeine, or dose-equivalents from coffee, (black) tea, cacao and Nescafe (note: this is my understanding of the somewhat sloppy English translation of the methods) would have on the lipid levels of rats who had been pretreated with a lard-based high fat diet and CCl4 for three months. This treatment had elucidated the expected inflammatory response and fatty acid deposition in the livers of the animals that were then randomly assigned to either one of the 5 treatment or a non-treated control group.

Figure 1: Weight gain (relative to initial weight) and food intake in non-treated, caffeine, cacao, Nescafe, coffee, or black tea treated rodent model of NAFLD (data adapted from El-Ghany. 2012)

And when you peak at the study outcome in figure 1 I would bet that your first reaction is: "Hey, cool! I must ramp up my caffeine intake even more, then!" We are in fact so conditioned to believe that weight loss, or the absence of weight gain is a "good thing" that I made the same stupid mistake, when I first looked at the (in the study) tabular data of the El-Ghany study. Then, I began to wonder: "How come that coffee and cacoa, of which I have repeatedly read that they help with weight loss, did increase the weight gain to levels that were higher than those in the non-treated control group." Finally, it dawned on me: What we are dealing with, here, is not weight loss or ameliorated weight gain, what we are seeing in all the groups is more of a special form of "failure to thrive"! After all, the non-CCL4 treated 'real' control group (data not shown in figure 1) did gain 45% of their initial body weight and thus still 15% more than the coffee group, of which I was mislead to believe that they "performed" worst.

High dose caffeine is for NAFLD sufferers not!

Looking at the rest of the data it became increasingly clear, the whopping dose of 10mg of caffeine per rodent per day, a dose, by the way, which happens to translates into a human equivalent dose of 10mg/kg (i.e. 800mg for an 80kg adult), did a pretty decent job in liberating fatty acids from the adipose tissue. So "decent", in fact, that the already compromised weight gain in those sick creatures was further attenuated.

Figure 2. Lipid levels in the treatment groups expressed relative to non-treated NAFLD rodents (left); selected liver slices (right; based on El-Ghany. 2012)

But it gets even worse, the sudden influx of fatty acids from the adipose tissue was so overwhelming that the already damaged livers of the NAFLD rodents started to spill out copious amounts of very low density lipoprotein (VLDL) - those nasty little cholesterol molecules of which researchers believe that they are the cause of cardiovascular disease. And despite the fact that we do not have any tissue images of the heart, the congested vein in the liver slice from one of the caffeine guzzling rodents appears to confirm the causal relationship of VLDL and clogging of the blood vessels; an effect, by the way, which could neither be countered by the -71% reduction in triglyceride levels, nor the -44% reduction in total lipids (compared to non-treated NAFLD control). 

Figure 3: Total cholesterol (CHO) and LDLc to HDL-c ratios in the non-treated, as well as the treated groups expressed relative to non-NAFLD control (data calculated based on El-Ghany. 2012)

In a 1985 letter to the editor of the Journal of the American Medical Association (Jama) William and Simpson explain the sudden occurrence of enormous amounts of VDLD in response to the lipolytic (=fat liberating) effects of caffeine as follows:

Upon liberation from the adipocyte, fatty acids are transported to the liver, where they are reesterified and the resultant triglycerides packaged for release in very-low-density lipoprotein (VLDL), which also contains apolipoprotein B.

If we assume that this hypothesis is correct, coffee, cacao and even Nescafe must obviously contain substances which help the liver to cope with the additional influx of fatty acids, as the animals in the respective groups do not only have significantly lower VLDL levels than the poor critters in the caffeine group, but also exhibit the most beneficial total cholesterol-to-HDL and LDL-to-HDL ratios (cf. figure 3) of all groups.

Say no to stims, energy drinks and coke and chose natural caffeine sources

In view of the ameliorative effects all the caffeine containing preparations had on the pathological features of NAFLD (cf. figure 2, right), and based on the results from previous studies and the assumption that the VLDL increase in the tea group was similarly well-handled in the rest of the body as it was in the liver, which did not present any of the congested veins that were so characteristic of the livers of the animals in the caffeine only group, the take home message of this study is one every SuppVersity student should be familiar with, by now: Nature knows best!

Image 2: I don't have to tell you that the study at hand suggests that those sugary caffeine bombs people call "energy drink" could give many of their livers their quietus.

Note: If you live in Dallas County, it does take no more than three attempts to identify a neighbor, friend, someone from your family or simply a pedestrian being in the early stages of NAFLD. And given the fact that the 33.6% NAFD rate in Dallas County was measure in 2005 already (Szczepaniak. 2005), it is almost certain that your neighbors' liver, which may still have been comparably healthy in 2005 has caught meanwhile. The results of this study could thus have greater implications on public health than you may initially have thought and it clearly suggest that the use of high dose "fat burners" and / or pre-workout supplements, as well the regular consumption of caffeine and sugar laden "energy drinks" or even coke is absolutely contra-indicated; and that not just in the obese, but also in the insulin resistant normal weight, whose liver is often similarly clogged with fat as the one of his 200lbs heavier comrade in crime.

If the caffeine is ingested in the absence of its natural adjuvants bad things happen. If they remain where they belong, however, the same whopping dose of caffeine that makes things worse could actually turn into a decent "liver fat burner".

While Coffee, tea and cacao drinkers can thus breathe a sigh of relieve, the average stim junkie who is already squirreling caffeine laden, geranium (DMAA) intoxicated pre-workout supplements and fat burners for the days after the DMAA ban, should better watch his liver health. Otherwise it may well be that he or she will end as a "case study" in the library of the FDA - filed under "death by fulminant liver failure induced by geranium + caffeine containing pre-workout supplement" - btw. isn't it strange that the FEDs don't have such a case study for one of the commercially available energy drinks, or even plain Coke, already?

Working Out 45 Min After Dinner Improves Post-Meal Blood Glucose & Trigs More Effectively Than Working Out Before

Resistance training alone won't make up for a sloppy diet - no matter if you do it before or after meals.

I am not sure how feasible this is going to be for you, but if you are a type II diabetic or anyone concerned about the potential detrimental health effects of the rise in glucose and triglycerides after a meal, working out 45 minutes after dinner is the way to go.

Abnormally elevated postprandial glucose and triacylglycerol (TAG) concentrations are strong risk factors for cardiovascular disease (CVD) in patients with type-2 diabetes. Therefore, scientists expect that interventions that reduce postprandial glucose and TAG concentrations should lower the risk of CVD (Krook. 2003; O'Gorman. 2008).

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

Only Whey, Not Soy Works for Wheytloss

Taste Matters - Role of the Taste Receptors

Dairy Protein Satiety Shoot-Out: Casein vs. Whey

How Much Carbs Before Fat is Unhealthy?

5 Tips to Improve & Maintain Insulin Sensitivity

Carbohydrate Shortage in Paleo Land

Previous studies have shown that acute exercise typically lowers postprandial glucose and TAG concentrations (Tobin. 2008) in patients with type-2 diabetes, but as Timothy D. Heden et al. point out, there is considerable heterogeneity in the responses with some individuals not experiencing beneficial changes in these risk factors (Gill. 2007; van Dijk. 2012).

"One potential explanation why some patients with type-2 diabetes do not have beneficial changes in postprandial glucose and TAG with acute exercise is because of the timing of the acute exercise session relative to meal consumption. Limited evidence suggests that the timing of aerobic exercise around a meal may be important and might explain why some individuals are exercise “insensitive” or “non responders”." (Heden. 2014) 

The only study to directly compare the effect of pre-meal and post-meal aerobic exercise on postprandial glucose concentrations in patients with type-2 diabetes showed that post-dinner, but not pre-dinner walking, lowered postprandial glucose concentrations (Colberg. 2009).

Figure 1: Previous studies indicate that aerobic workouts after meals have more beneficial effects on the potentially unhealthy increases in glucose or triglycerides (Collberg. 2009)

Although no study has directly examined the effect of exercise timing on postprandial TAG in patients with type-2 diabetes, there is evidence that exercise performed the day prior to a high fat meal has no effect on postprandial TAG responses (Dalgaard. 2004; Gill. 2007), while post-breakfast aerobic exercise reduced the postprandial TAG response (Tobin. 2008). Taken together, it appears that aerobic exercise may have its most powerful effect to lower postprandial glucose and TAG responses when performed after a meal, possibly because of slowed gastric emptying and/or greater skeletal muscle glucose and TAG uptake and utilization at this time.

The question that remained was: Is the same true for resistance training?

Since resistance exercise (RE) has a more pronounced long(er)-lasting effect on ones metabolism than aerobic training, the researchers from the University of Missouri tested the hypothesis that post-dinner RE, compared to pre-dinner RE, would in fact be more effective at improving two clinically important postprandial risk factors (glucose and 109 TAG) for CVD at a time of day when they are typically highest in obese patients with type-2 diabetes.

The standardized test workout consisted of the following exercises (in this order): leg press, seated calf raises, seated chest flyes, seated back flyes, back extensions, shoulder raises, leg curls, and abdominal crunches. All exercises were performed for three sets (1-2 min rest between sets) of 10-repetitions for each RE. During this session, the first set for each exercise was a warm-up set and the weight used was 50% of the participants 10-RM. After the warm-up set, the weight for the next two sets was the participants previously determined 10-RM.

Figure 2: Postrandial lipid response in the obese type II diabetics (Heden. 2014)

As you can see in Figure 2 the scientists suspicion was right, the postprandial workout (M-RE) had significantly more pronounced beneficial effects on the lipid metabolism of the type II diabetic subjects who consumed a standardized breakfasts (English muffin, cheddar cheese, one large egg, ham, hash brown, ketchup, and apple or orange juice) lunch (white bread, ham, mayonnaise, cheddar cheese, a granola bar, and apple or orange juice) and dinner meals (spaghetti noodles, spaghetti sauce with beef added, garlic bread, a lemon lime flavored soda, and 1.5 g of acetaminophen (to assess gastric emptying)) containing ~50% carbohydrate, 35% fat, and 15% protein.

Similar effects were observed for the insulin and glucose responses (see Figure 3) which were significantly improved and should thus complement the beneficial effects of the reduced triglyceride and very low density lipoprotein (VLDL) levels.

Figure 3: Changes in postprandial insulin and glucose levels (Heden. 2014)

Bottom line: Before we get to the actual interpretation of the result let me briefly point out that it would probably have been at least as effective if the subject had not been fed bull**** like ketchup, mayonnaise, granola bars, and purportedly healthy, but de facto obesogenic fruit juices. The unfortunate truth, however, is that 99% of the type II diabetics still eat like this. For them, the use of resistance training after each meal may be a possible, but unquestionably not practical way to ameliorate the unwanted cardiovascular side effects.

In view of the fact that most diabetics don't work at all, I am 100% convinced that the results of the study at hand have zero practical significance - even I wouldn't go work out after dinner only to lie in bed hungrily, thereafter, And if I did, I would raid the fridge later at night - certainly not a practice that's heart healthier than working out before dinner.

Speaking of which: Working out before dinner would also mean working out after lunch and could thus effectively help the increase in triglycerides and glucose after lunch. Not too bad either, right? | Comment on Facebook!

References:

• Colberg, Sheri R., et al. "Postprandial walking is better for lowering the glycemic effect of dinner than pre-dinner exercise in type 2 diabetic individuals." Journal of the American Medical Directors Association 10.6 (2009): 394-397. 
• Dalgaard, Marian, Claus Thomsen, and Kjeld Hermansen. "Effects of one single bout of low-intensity exercise on postprandial lipaemia in type 2 diabetic men." British Journal of Nutrition 92.03 (2004): 469-476.
• Gill, Jason MR, et al. "Effect of prior moderate exercise on postprandial metabolism in men with type 2 diabetes: heterogeneity of responses." Atherosclerosis 194.1 (2007): 134-143.
• Heden, Timothy D., et al. "Post-dinner resistance exercise improves postprandial risk factors more effectively than pre-dinner resistance exercise in patients with type 2 diabetes."
  Journal of Applied Physiology (2014). Ahead of print.
• Krook, Anna, et al. "Reduction of risk factors following lifestyle modification programme in subjects with type 2 (non‐insulin dependent) diabetes mellitus." Clinical physiology and functional imaging 23.1 (2003): 21-30.
• O'Gorman, Donal J., and Anna Krook. "Exercise and the treatment of diabetes and obesity." Endocrinology and metabolism clinics of North America 37.4 (2008): 887-903.
• Tobin, L. W. L., Bente Kiens, and Henrik Galbo. "The effect of exercise on postprandial lipidemia in type 2 diabetic patients." European journal of applied physiology 102.3 (2008): 361-370.
• van Dijk, Jan-Willem, et al. "Exercise and 24-h glycemic control: equal effects for all type 2 diabetic patients?." Medicine and science in sports and exercise (2012).

SAD - Human Study Shows: Three Days on "High Fat" Standard American Diet Produce Heart Healthier LDL Particle Profile Than NCEP-Approved Low Fat Diet

Image 1: SAD or just mad? It does in fact look like you better stick to Royal TS, French fries & co instead of following a low fat diet according to the guidelines of the National Cholesterol Education Program if you care about your heart health.

In view of the fact that millions of lives depend on it (literally, not just figuratively!) it is actually quite surprising, some would probably say "scandalous" that the experimental evidence (and I am talking about controlled experiments on real, healthy human beings, not about epidemiological and thusly statistical) for the purported beneficial effects of a non-calorically restricted "healthy low fat diet" in the absence of additional exercise interventions is... scarce, to say the least. I was thusly positively surprised, when I hit on a study from a group of researchers from the Institute of Nutraceuticals and Functional Foods at the Laval University and the Lipid Research Center at the CHUL Research Center in Québec, Canada, the title of which suggested that it could provide exactly that - experimental evidence in support of the purportedly healthy low fat diet (Guay. 2012).

Scientists and their interpretation of a "high fat" diet...

I guess, those of you for whom this is not the first visit to the SuppVersity will be aware that I have made a habit of looking at the data first, to make up my mind, before I even take a closer look at the scientists interpretation of the latter (this is what is usually called the "conclusion"). And, geez! The "high-fat diet", the Valérie Guay and her colleagues advertise in the title of their paper turned out to be another case of the standard American diet, the relative fat content of which (32% of total calories) is not exactly, what's on my mind, when I think of a "high fat" diet.

Figure 1: Relative macronutrient composition of the baseline and the isocaloric test (high and low fat) diets (left); total fiber, cholesterol and phytosterol content, as well as polyunsaturated to saturated fatty acid (PUFA/SFA) ratio and total fat in % of total calories (right; data calculated based on Guay. 2012)

The fact that this paper still made into the news, although the researchers' interpretation of a "high fat" diet was designed to "reflected as closely as possible current North American men averages", does yet already tell you that the results were not that the "healthy low fat diet bet the crap out of the standard American one".

SAD! Standard American Diet beats the nasty small LDL particles out of a healthy low fat diet

In fact, a closer look at the somewhat cryptically presented study results revealed that, at least as far as the measured outcome variables of this particular study are concerned, the exact opposite was the case: It was not the purportedly healthy low-fat diet which was designed according to the recommendations of the National Cholesterol Education Program Adult Treatment Panel III (cf. JAMA. 2001) which induced favorable changes in the lipid profile of the twelve initially healthy normal-weight male volunteers (~27.1y; BMI 25.2kg/m²) who took part in this 3-day randomized, double-blind, crossover study, but the calorie-, fiber- and vegetable- and animal-protein-wise identical "high fat" diet, which had been designed in the image of the infamous "standard American diet" (SAD).

Figure 2: Lipid profile (left) and its relative changes (compared to baseline, right) in response to the 3-day dietary intervention (data calculated based on Guay. 2012)

If you look at the data in figure 2 through Pfizer-ish-blue glasses you will probably say: "Wait a minute! The cholesterol level did decrease in the low fat group! So this must be the better diet." And yes, this may actually be the case, if you define better according to the same fundamentally "cholesterol is bad for you"-paradigm which has been flushing billions of dollars (and of course Euros ;-) into the coffers of Pfizer & Co over the last decades. If you have yet been following the by no means "latest" scientific research on the correlation of cholesterol and heart disease, you will be aware that neither total cholesterol, nor total LDL levels, but rather the amount of highly oxidizable small LDL particles is a relatively reliable marker of the risk of heart disease (Lamarche. 1997)- and, fortunately, Guay et al. are aware of that, as well, and measured the characteristics of LDL particles by the means of electrophoresis.

Figure 3: Relative distribution of LDL particle sizes (left), cholesterol content (mmol/L) of LDL fractions (middle), and mean LDL particle size and LDL peak particle diameter (LDL-PPD; right); * indicates p < 0.05; ** indicates p < 0.001 (data adapted from Guay. 2012)

The results of the LDL-particle analysis shown in figure 3, show quite neatly, that the unquestionably unhealthy standard American diet (Attention: Do not misinterpret these study results as a carte blanche to stick to eating your regular crappy diet!) did not only result in more favorable triglyceride (1.48 vs 1.01mmol/L, p = 0.0003) and HDL levels (1.29 vs 1.41 mg/L, p = 0.05; cf. figure 2), than its allegedly "healthy" low fat counterpart, it was ...

[...] also associated with a significant increase in LDL particle size (255.0 vs 255.9Å; p = 0.01) and a significant decrease in the proportion of small LDL particle (<255.0 Å) (50.7% vs 44.6%, p = 0.01).

And although Guay et al. are quick to point out that "because the present study was only conducted in men, the results cannot be generalized to the whole population", I would say that these results should at least.make you reconsider if following a "healthy low fat diet" in accordance with the dietary guidelines of the National Cholesterol Education Program will help you lower your risk of heart disease... unless, of course, you have already popped so much Lipitor & co that the chronic lack of cholesterol is already hampering your cognitive abilities -.what? Ah, yes... of course, the favorable results occur only if you take you daily dose of statins with your low fat meals... right, how could I forget that ;-)