No Magic Numbers: The Omega-3:Omega-6 (N3/N6) Ratio - Higher is Better, But as Part of the Standard American Diet Even a 1:1 Ratio Won't Protect You Against Diabesity

Eating "like an American" makes you fat and sick. No matter what the omega-3 to omega-6 ratio of your diet may be.

It is a pity. Yeah, if the latest study from the University of South Carolina was a human study, it would finally provide a definitive answer to the question how much omega-3 we actually need. Well, I should clarify: It would provide an answer to the question how much omega-3 we need with a given baseline omega-6 intake.

In view of the fact that the study duration was 20 weeks, it would yet take more than 60 (human) years to find out, whether the ratio of n-3/n-6 in the diet is in fact as irrelevant as the reslts Reilly T. Enos et al. present in their latest paper would suggest.

You can learn more about omega-3 & co at the SuppVersity

Fish Oil Makes You Rancid?

Are All Fats Bad For You?

Fish Oil & GLA vs. Acne

MUFA & Fish Oil Don't Match

Fish Oil Doesn't Help Lose Weight

Rancid Fish Bad 4 Health

Over those 20 weeks the scientists from the Departments of Pathology and Chemistry and Biochemistry fed their previously healthy C57BL/6 mice diets that contained either the regular rodent chow or one out of four high fat diets with omega-3 to omega-6 ratios of 1:1, 5:1, 10:1, and 20:1. As the scientists point out, the percentage of calories provided by each of the three macronutrients and the ratio of monounsaturated FAs (MUFAs) to PUFAs (MUFA:PUFA) were identical for the HFDs and were designed to be similar to the standard American diet.

Table 1: Diet composition of treatment diets.SFAs, Saturated Fatty-Acids; MCSFAs, Medium-Chain Saturated Fatty Acids; LCSFAs, Long-Chain Saturated Fatty Acids; USFAs, Unsaturated Fatty Acids; MUFAs, Monounsaturated Fatty Acids; PUFAs, Polyunsaturated Fatty Acids (Enos. 2014)

The only significant difference among the HFDs was the omega-6:omega-3 (The control diet (AIN-76A Mod) was used in order to match the MUFA:PUFA and omega-6:omega-3 of the 20:1 HFD.)

Ok, the rodent thing is not the only problem

None of the diets contained any long-chain omega-6 or omega-3 FAs. In human terms this would mean that we are not testing a high fish, high grass-fed beef, but a high omega-3 vegetarian diet with tons of alpha linolenic, but no Docosahexaenoic acid (DHA) or Eicosapentaenoic acid (EPA), which is the "stuff" (=long-chain omega-3 fatty acids) you would find in meats of grass-fed beef and, of course, fish.

Figure 1: Changes in body weight, visceral fat weight and adipocyte size during 20 weeks on modified "standard American diet" w/ different ratios of omega-3 to omega-6 fatty acids (Enos. 2014)

And still, based on the current paradigm, the scientists expected to see significant differences in metabolic health parameters between the high and low omega-3 to omega-6 ratio groups - at best even a complete revision of the metabolic damage the rodents suffered due to consuming a high energy + high fat diet.

It does not always work that way.

In reality, though, any therapeutic benefit produced by reducing the omega-6:omega-3 was evident only when comparing the 1:1 to 20:1 HFD. Yep, that's true, the mice on the 1:1 HFD had a lower total to HDL (TC:HDL-C) ratio and a decreased adipose tissue CXCL14 gene expression and adipose tissue macrophage infiltration, both of which would indicate that they had a lower risk cardiovascular disease.

As a SuppVersity reader you know very well that "A Meta-Analysis Says: Fish Oil Does Not Help You Lean Out!" you do yet also know that the there are also a bunch of arguments "Why It's Still Worth Having Fatty Fish 1-2x/Week" | more

But there were benefits, weren't there? Yes, there were! In fact, there was even a direct link between higher EPA:AA (AA: arachidonic acid, the allegedly inflammatory and thus "bad" long-chain omega-6 fatty acid) and DHA:AA in the adipose tissue phospholipids. 

The net outcome on the other hand, was profoundly disappointing: "[...]despite these effects, and independent of the omega-6:omega-3, all HFDs, in general, led to similar levels of adiposity, insulin resistance, and AT [adipose tissue] inflammation" (Enos. 2014) - in short, it's a sad, but actually not surprising fact that the standard American diet (SAD) will make you fat and diabetic, no matter how much omega-3 fatty acids you are shoveling down.

References

• Enos, Reilly T., et al. "Reducing the Dietary Omega-6: Omega-3 Utilizing α-Linolenic Acid; Not a Sufficient Therapy for Attenuating High-Fat-Diet-Induced Obesity Development Nor Related Detrimental Metabolic and Adipose Tissue Inflammatory Outcomes." PLOS ONE 9.4 (2014): e94897.

Protein Power - Study Suggests: 40%+ is Where True Magic Happens. Plus: If Protein is King, Whey is the Emperor

It's not just about more protein it's about significantly more protein and - possibly - also about whey!

Just to make sure: Yes, I know the study I am about to discuss in today's SuppVersity article is a rodent study - a rodent study by researchers from the University College Cork and the University College Dublin (Mc Allan. 2014).  And yes, I know that you ain't no fury little mouse or rat...

... but I do also know that the beneficial metabolic effects of high protein intakes appear to be even more, not less pronounced in human beings and will thus not mention 500x that the assumption that we'd see similar benefits in men and women would obviously require experimental confirmation... alright?

Now that we are clear, dear non-dams and non-bucks...

... you are probably already drooling at the sought of reading yet another "high protein is good for you" study. Don't worry I am not going keep you on the tenderhooks longer than absolutely necessary. What is necessary, though is a very brief summary of the study design, which was designed to elucidate the effects macronutrient quality and composition on energy balance and the gut microbia - probably two of the hottest topics in today's discussions on the health and fitness bulletin boards of this world.

You can learn more about protein intake at the SuppVersity

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Spread or waste your protein?

Protein requ. of athletes

High EAA intra-workout fat loss

Fast vs. slow protein

Too much ado about protein?

As the Irish researcher point out, their goal was to investigate how changes to protein quality (casein versus whey protein isolate; WPI) and the protein to carbohydrate (P/C) ratio within a high fat diet (HFD) impacts on the aforementioned parameters. The questions the experiment was supposed to answer were thus:

• Protein Quality ➲ Would adding whey protein on top of an obesogenic high fat rodent diet yield to a different weight and microbiota response than casein protein?
• Protein Quantity ➲ Would diets with 20%, 30% or 40% of the total energy intake from protein have different effects on body weight and microbiota in the rodents?

In view of the fact that casein is the standard protein in many of the high fat diets that are used in experiments like this, the study would thus also be able to give us an idea of whether or not the use of the slow-releasing IGF-1 boosting dairy protein contributes to the obesogenic effects.

As it turned out, the analysis of issues related to question #2, i.e. "Would diets with 20%, 30% or 40% of the total energy intake from protein have different effects on body weight and microbiota in the rodents?" did produce the more intriguing results, though.

Figure 1: Weight gain, fat and lean mass, as well as energy intake and respiratory exchange ratio (RER) after 21-weeks on diets with different amounts of whey protein in them (McAllan. 2014),

If you take a look at the data in Figure 1, it's easy to see that (a) in comparison to casein (data from casein experiment not shown, because it was not discussed in detail | maybe there will be a follow up paper!?), WPI at a similar energy content normalised energy intake, increased lean mass and caused a trend towards a reduction in fat mass (P= 0.08). You may find that surprising, but it's actually been known for quite some time now that whey buffers many of the ill-health effects of high fat diets in rodents.

Figure 2: Adipose tissue mRNA expression of selected genes (McAllan. 2014)

Although the addition of whey protein did not alter the oxygen consumption or locomotor activity, it was able to ...

• reduce the plasma leptin and liver triacylglycerold levels, and...
• attenuate the reduction in adipose FASN mRNA 

in HFD-fed mice (compared to what the researchers observed in rodents on the casein chow). Moreover, a high throughput sequence-based analysis of faecal microbial populations revealed that the

"[...]microbiota in the HFD-20% WPI group clustering closely with HFD controls, although WPI specifically increased Lactobacillaceae/Lactobacillus and decreased Clostridiaceae / Clostridiumin HFD-fed mice." (McAllan. 2014)

To understand the potential implications of these changes we will have to take a closer look at the recent evidence linking Clostridiaceae and Lactobacillaceae to the diabesity epidemic:

• 

  Lactobacillus reuteri has anti-breast-cancer effects as well  (Lakritz. 2014).

  certain types of clostridiaceae are characteristic for obesity prone animals; their transplanation to normal mice will make them similarly vurnerable to the obesogenic effects of HFDs (Duca. 2014); similar differences, i.e. higher levels of clostridiaceae in obese individuals, have been observed in human studies, as well (Ferrer. 2013)
• lactobacilli, above all those of the reuteri type, have recently been used in several studies for their anti-obesogenic (Million. 2013a, b), anti-autoimmune (Forsberg. 2013), anti-caries (Stensson. 2013), anti-helicobacter plyori (Francavilla. 2013), pro-vitamin-D (Jones. 2013), and a whole host of other beneficial effects; for other types of lacutobacilli researchers have observed that they exert similar anti-obesity effects that may be mediated by the intestinal productino of the anti-obesity isomer of CLA, i.e. trans‐10, cis‐12‐conjugated linoleic acid (Lee. 2007)

If we look at the previously listed metabolic effects, these changes in the make-up of the gut microbiome obviously correspond with the remarkable health improvements that occured in the whey-fed rodents.

High protein, low carb - What does it do?

Table 1: Plasma amino acid levels (mmol/L); blue bars to the right indicate sign. inter-group difference (McAllan. 2014)

Contrary to what you'd expect based on appetite increasing effects researchers ascribe to high protein diets (Weigle. 2005), the increase in protein-to-carbohydrate ratio (P/C) did not lead to measurable reductions in energy intake, but ....

"[...]the highest ratio [40% of the total energy intake from protein] reduced HFD-induced weight gain, fat mass and plasma triacylglycerol, non-esterified fatty acids, glucose and leptin levels, while it increased lean mass and oxygen consumption." (McAllan. 2014)

As the scientists point out, similar effects were observed on adipose mRNA expression, where the highest ratio of protein to carbohydrates reduced HFD-associated expression of UCP-2 (a protein that has the fat stores eat themselves up), the inflammatory marker TNF-alpha and CD68 a gylcoprotein that messes with LDL cholesterol.

On the other hand, the (really) high protein diet increased the diet-associated expression of the b3-adrenergic recepto (b3-AR), lipoprotein lipase, a water soluble enzyme that hydrolyzes triglycerides in lipoproteins, such as those found in chylomicrons and very low-density lipoproteins (VLDL), as well as the expression of insulin receptors and the glucose transporters GLUT4 - all of which should be old acquaintances of loyal SuppVersity readers.

Bottom line: The beneficial metabolic effects the addition of 40% whey protein isolate to a highly obesogenic baseline diet produced in the study at hand are remarkable and highly specific. "Specific", in that they don't occur with "an increase in protein intake".

Figure 3: Body weight development over the 21-week study period. The 40% whey diet clearly sticks out (McAllan. 2014)

In other words, the anti-obesogenic, anti-diabetic and anti-hyperlipidemic effects occurred not in response to "any type and amount of additional protein" that was added on top of what can be considered a model of a high fat version of the Western Diet. The previously discussed benefits were observed only, when this protein was whey protein and comprised a whopping 40% of the total energy intake of the rodents. The casein-based diets, as well as diets with lower amounts of whey protein isolate were ineffective, or - as you can see in Figure 3 - they "clustered together and away from the 40% WPI group", whose body weight - and this unquestionably quite remarkable - was hardly different from that of those 10 mice who were fed a regular, low fat diet for the whole 21-week study period.

References: 

• Duca, Frank A., et al. "Replication of obesity and associated signaling pathways through transfer of microbiota from obese prone rat." Diabetes (2014): DB_131526.
• Forsberg, Anna, et al. "Pre‐and post‐natal Lactobacillus reuteri supplementation decreases allergen responsiveness in infancy." Clinical & Experimental Allergy 43.4 (2013): 434-442.
• Jones, Mitchell L., Christopher J. Martoni, and Satya Prakash. "Oral Supplementation With Probiotic L. reuteri NCIMB 30242 Increases Mean Circulating 25-Hydroxyvitamin D: A Post Hoc Analysis of a Randomized Controlled Trial." The Journal of Clinical Endocrinology & Metabolism 98.7 (2013): 2944-2951.
• Lakritz, Jessica R., et al. "Beneficial bacteria stimulate host immune cells to counteract dietary and genetic predisposition to mammary cancer in mice." International Journal of Cancer (2014).
• Lee, K., et al. "Antiobesity effect of trans‐10, cis‐12‐conjugated linoleic acid‐producing Lactobacillus plantarum PL62 on diet‐induced obese mice." Journal of applied microbiology 103.4 (2007): 1140-1146.
• McAllan, Liam, et al. "Protein Quality and the Protein to Carbohydrate Ratio within a High Fat Diet Influences Energy Balance and the Gut Microbiota In C57BL/6J Mice." PLOS ONE 9.2 (2014): e88904.
• Million, M., et al. "Correlation between body mass index and gut concentrations of Lactobacillus reuteri, Bifidobacterium animalis, Methanobrevibacter smithii and Escherichia coli." International Journal of Obesity (2013a).
• Million, Matthieu, and Didier Raoult. "The role of the manipulation of the gut microbiota in obesity." Current infectious disease reports 15.1 (2013b): 25-30.
• Stensson, Malin, et al. "Oral Administration of Lactobacillus reuteri during the First Year of Life Reduces Caries Prevalence in the Primary Dentition at 9 Years of Age." Caries research 48.2 (2013): 111-117.
• Weigle, David S., et al. "A high-protein diet induces sustained reductions in appetite, ad libitum caloric intake, and body weight despite compensatory changes in diurnal plasma leptin and ghrelin concentrations." The American journal of clinical nutrition 82.1 (2005): 41-48.

Fructose-Nation: No Change in Fructose Availability in the US Since the Early 1970s. So Why Are We Fat, Then?

From fat to Fructose - just another scapegoat for a fundamental problem?

Over the past 5 years or so, the idea that that fructose is to blame for the ever-increasing rates of diabesity has become so popular that hypotheses such as "the fructose consumption has exploded over the past decade" are usually accepted as scientifically verified facts.

A recent paper from the Department of Nutrition and Health Sciences at the University of Nebraska did now remind me that not all things that appear logical and consistent with our believes are necessarily true.

Do we even consume that much fructose?

As Trevor J Carden and Timothy P Carr point out, "the consumption pattern of fructose and other key nutrients" in the past 4 decades, "remains a topic of debate" (Carden. 2013). To determine whether fructose consumption in the US has increased sufficiently to be a casual factor in the rise in obesity prevalence Carden and Carr analyzed the USDA Loss-Adjusted Food Availability Database.

The researchers found that the food availability of glucose and fat, but not fructose, increased in the US between 1970 and 2009.

To calculate the percent change in energy from food groups and individual nutrients, Carden and Carr started initially compiled the available data on the per capita loss-adjusted food availability for 132 individual items were. In a second step they analyzed the corresponding nutrient profiles and used their findings to determine the availability of energy as well as macronutrients and monosaccharides during the years 1970-2009. By comparing the values for a given year to the baselinen in 1970, they did eventually determine the percent change in energy from food groups and individual nutrients.

Figure 1: Change in food energy availability per capita, 1970-2009 (Carden. 2013)

If you take a glance at the data in Figure 1 it's easy to see that their findings indicate that during this 40 year period the total energy availability increased by +10.7%. In that, the main "offenders" were grains and oils, the net change in total fructose availability, on the other hand was 0% - in other words, the added sweeteners (1%) were not even fructose based. Furthermore, Carden and Carr observed that the ...

"[e]nergy available from total glucose (from all digestible food sources) increased 13.0% [and ended up being] more than 3-times greater than fructose." (Carden. 2013)

With 14.6%, the amount of fat increased to a very similar extend as that of glucose. That's a 3x higher increase than for protein (+4.7) and am 1.6x higher increase in energy availability than for carbohydrates ,in general (+9.8).

So, it's the fat and sugar that's to blame? Not the fructose?

Despite the fact that I am not particular fond of the "fructose theory of everything evil", I believe that we got to be cautious about the significance of Trevor J Garden's and Timothy P Carr's conclusion, that their data would "suggest" that fructose is "unlikely to have been a unique causal factor in the increased obesity prevalence". If you take a look at the supplemental data they provided you will find, that their list of 132 foods used to calculate USDA food availability, i.e.

• Head Lettuce
• Kale
• Lima Beans
• Whole flavored milk
• Buttermilk
• Lowfat flavored milk
• Plain 1-percent milk
• Plain 2-percent milk
• Skim milk
• Eggnog and Half and Half (dairy and fat share of)
• Sour cream
• Yogurt
• Cheeses
• Lowfat cottage cheese
• Reg. cottage cheese
• Frozen yogurt and other misc
• Ice cream
• Lowfat ice cream
• Condensed bulk and canned skim milk
• Condensed bulk whole milk
• Condensed canned whole milk
• Dry buttermilk
• Dry whole milk
• Nonfat dry milk
• Barley products
• Corn flour and meal
• Corn hominy and grits
• Corn starch
• Durum flour
• Oat products
• Rice
• Rye flour
• White and whole wheat flour
• Beef
• Lamb
• Pork
• Veal
• Chicken
• Turkey
• Fish and Shellfish
• Eggs

• Great N. Beans
• Butter
• Edible beef tallow
• Lard
• Margarine
• Other edible fats and oils
• Salad and cooking oils
• Shortening
• Beer
• Wine
• Distilled Spirits
• Garlic
• Frozen Veggies
• Mushrooms
• Mustard Greens
• Navy Beans
• Okra
• Onions
• Canned Veggies
• Other Dry Beans
• Peas and Lentils
• Pinto Beans
• Potatoes
• Pumpkin
• Radishes
• Red Kidney Beans
• Lettuce
• Snap Beans
• Spinach
• Squash
• Sweet Corn
• Sweet Potatoes
• Tomatoes
• Turnip Greens
• Peanuts
• Tree Nuts
• Coconuts
• Refined sugar
• Dextrose
• Glucose
• HFCS
• Edible syrups
• Honey
• Plain whole milk
• Green Peas

• Collard Greens
• Avacado
• Bananas
• Blackberries
• Blueberries
• Canteloup
• Cherries
• Cranberries
• Dates
• Figs
• Grapefruit
• Grapes
• Honeydew
• Kiwifruit
• Lemons
• Limes
• Mangos
• Olives
• Oranges
• Frozen Berries
• Papayas
• Peaches
• Pears
• Pineapple
• Plums and Prunes
• Raisins
• Raspberries
• Stawberries
• Tangerines
• Watermelon
• Artichokes
• Asparagus
• Bell Peppers
• Black Beans
• Broccoli
• Brussel Sprouts
• Cabbage
• Carrots
• Cauliflower
• Celery
• Cucumbers
• Eggplant
• Apples
• Apricots
• Chili Peppers
• Escarole & Endive

... is representative of the variety of foods US citizens eat, but it does not tell you which of these foods, they will eventually select. Let's take apples, coconuts, and white and whole wheat flour as an example triplet. I guess if you had to rank them according to their contribution to the total energy intake of the average US citizen, none of you would hesitate to give me an answer like this: "White and whole wheat flour > apples > coconuts". Without the corresponding "weights" that would tell the scientists that white and whole wheat flour has a 10x higher impact on the average macronutrient composition of the average American diet, we be talking about the nutrient and fructose availability, not the actual intakes.

Better treat the data with the appropriate caution

Unfortunately, the scientists provide only rudimentary information about the impact of food choices, i.e. how much of the items listed above, the average US citizen actually consumes, namely:

• The food categories that increased the most during this time were grains and fats/oils, having increased 24.2% and 25.3%, respectively. 
• Caloric sweeteners (including both sucrose and HFCS) increased a modest 1.3%. 

With respect to the sweeteners Carden and Carr emphasize that the "sugar" availability, or as they put it the "monosaccharides available for metabolic absorption" is more than 3x higher than that of fructose.

In other words: Despite the fact that fructose appears to have become ubiquitous, overeating on plain sugar is still 3x easier. That this does not imply that you cannot do so, is the main and in my humble opinion crucial problem Carden and Carr fail to address. The result of their study do after all not exclude that a significant parts of the US population increased their fructose intake, in spit of the fact that its availability remained essentially the same.

The availability of a given nutrient on the shelves of US supermarket may provide a realistic image of the diets of a society of identical clones, who wheel their carts back and forth through the whole supermarket and buy foods from all each and every shelf. The "real" American, however, is no clone. On the contrary! He has his preferences and for a large part of the society these preferences can be found in the "highly processed, high sugar, high fat"-shelves of the super market. He does not care about the coconuts, apples, kale, mushrooms, olives and all the other foods in the "whole foods" section of the supermarket. They are available, but not what he is looking for.

Figure 2: The increase in total energy intake is one of the most fundamental contributers to the obesity epidemic (adapted from Carden. 2013)

Bottom Line: Despte the disconnect between availability and consumption you will be hard pressed to debate the scientists' conclusion that "increased total energy intake, due to increased availability of foods providing glucose (primarily as starch in grains) and fat" are the major contributors to the increased obesity in the US.

What is annoying, though, is the fact that a vast majority of the researchers fails to realize that their studies already account for the obesogenic effects of nutrient density. The average "high fat diets are bad for ..." is after all based on experiments, where animals or humans are fed diets that are high in both fat and carbohydrates.

Despite the fact that these studies provide a realistic portrayal of the average Western diet, the messages people infer, when they read about these results in the mainstream media is flawed.

It's not about eating less, fat, fructose, sugar or whatever scapegoat the author of the corresponding article believes was to blame for our misery. It's about nothing else than turning our whole way of eating upside down. It's about the right foods, not the right macros and it's about moderation and mindfulness.

References:

• Carden, T. J., & Carr, T. P. (2013). Food availability of glucose and fat, but not fructose, increased in the US between 1970 and 2009: analysis of the USDA food availability data system. Nutrition journal, 12(1), 130.

Science Round-Up Seconds: The Macro-Mineral Alphabet & the Potential Health Hazards of Diet-Induced Latent Acidosis

You lose 600x more sodium than magnesium during a workout. The RDA is yet only ~3-4x higher (Montane. 2007).

If you already listened to the podcast of yesterday's installment of the SuppVersity Science Round Up (if you have not already done so, you can dowload the podcast, here), you may have noticed that I confused the minimal potassium (K) to sodium ratio (Na), which is probably ~1:1, and the "original" K:Na ratio in the "paleo diet".

According to Sebastian et al. (2002) the latter is ~8-9:1 in other words: 8-9 mols of potassium per mol of sodium. That's miles apart from the 1:2-3 ratio the average Westerner (the exact ratio varies depending on which study you refer to) uses as a springboard to hypertension ;-)

The (un-)definite mineral synergism/antagonism chart

Another thing you may have noticed with yesterday's show is the fact that the show was pretty "topic centered". My personal feeling is that it has a much better flow this way and that not despite, but because Carl and I did not cover such a broad range of topics. I cherish the hopefully non-futile hope that you feel the same but am obviously open for any constructive criticism from your side

The SuppVersity macro mineral chart provides a general overview of the complex interactions that exist between calcium, phosphorus, magnesium, sodium, chloride, and potassium (compiled based on various sources)

. This, by the way, does also apply to the corresponding installment of the Seconds, of which you will soon realize that it is not a non-related add-on, but will expand, explain and summarize interesting aspects we've covered in the live show (note: from next week on the Science Round-Up will air at 12 PM EST, the same URL as usual).

On that note, let's start with an "expansion" I already promised to deliver towards the end of the show: some information on the synergism and antagonism of the macro minerals. It's a pretty complex matter and the following illustration is based on generalizations. Some of them, like the low-level exception to the antagonism between calcium and magnesium, of which I believe that it is important to know are explicitly mentioned, others are not.

A very good example of the former, i.e. the important second order interactions is the influence sodium has on the antagonism between potassium and magnesium. The latter disappears, when sodium levels are high and magnesium is needed as a sodium antagonist. Similarly, the often-touted antagonism between magnesium and calcium is actually a co-factor relation, where any "antagonism" is only the result of imbalances between the two.

The good, the bad and the ugly: Just a question of the "wrong" perspective

One thing that should actually be obvious, but is often ignored in all the hoopla about the "good" and "bad" guys among the macro-minerals is that "antagonisms" do not contradict the essential nature of all of the electrolytes, which are - antagonistic or not - in the end, all actors in the same metabolic play.

Figure 1: Average ratio of mineral content (new:old) of 20 vegetables and 20 fruit: data based on comparison of  UK Government’s Composition of Foodsdata at two-time points separated by approximately 50 years (Mayer. 1997)

I mean, take calcium and phosphorus as an example, they are both essential for the structural integrity of your bone and the fact that calcium has a reputation of being the "good guy", while phosphorus is the "bad guy" is just a necessary consequence of the overabundance of the latter, i.e. phosphorus from grains, soft drinks, dairy products, meats, fish, seeds, nuts, eggs and due to the change in mineral ratios (cf. figure 1) even most fruits and vegetables in the food chain of Mr. Joe Average, these days.

According to a 2009 paper by Dana Cordell et al. this may well change in the not all too distant future, after all "the quality of remaining phosphate rock is decreasing and production costs are increasing" (Cordell. 2009). With estimates saying that the demand for phosphorus is going to double within the next 40 years, it stands to reason that the decried overabundance of phosphorus, which is, among other things, also responsible for lowering the zinc content of the produce (cf. Peck. 1980) may be partly reversed within the next decades... I mean, we all know that nothing is as "convincing" as with financial interests, right?

The strong ion difference determines your pH levels

What's the difference between macro-minerals and their "little brothers" the trace minerals? Calcium, sodium, potassium, phosphorus, magnesium, chloride and sulfur are macro-minerals because you need them in amounts that are greater than 100mg per day. Of the trace minerals, on the other hand, you need less (in most cases much less) than 100mg per day. That does not mean though that Iron, zinc, copper, chromium, fluoride, manganese, iodine, molybdenum and selenium were less important - it's merely a quantitative distinction.

While it stands to reason that there is a reason, calcium, sodium, magnesium, and potassium are also called "electrolytes", astonishingly few people can actually give an ad hoc explanation why this is the case - and that despite the fact that their lives depend... no, not on the answer, but on the existence and physiological function of electrolytes ;-)

If you have listened closely to your physics teacher, you will yet probably be aware that an "electrolyte" (electro- ~ charge, -lyte ~ carrier) is a positively or negatively charged molecule (ion) and nothing out of the ordinary in nature.

In your body electrolytes are used to establish ionically charged gradients, similar to the gradient that exists between the positive and negative pole of a battery. These gradients are situated on the cell membranes in excitable tissues, such as muscle and verve, where they facilitate or hinder the influx/efflux of other charged particles.

One of these gradients, in fact probably the physiologically most significant one, by the way, is established by positive sodium (Na+) and potassium (K+) ions and their negative counterpart chloride (Cl-) - exactly those electrolytes you've heard about in yesterday's show (remember: whenever you hear "salt" it actually means Na + Cl).

The electrolytes are not the only charged particles ...

From your chemistry lessons, you may remember that there are not just ionic atoms, but also ionic molecules and that the electron configuration of these particles will determine how they bind, interact and react. But I guess, we have had more than enough complicated theory for today, so if you want to know how the anions and how the strong ion difference (SID) is calculated, check out this brief overview over at acid-base.com.

Rather than going into the details of the mechanism, I decided that it would probably of greater value to wrap the Seconds up with a brief overwiev of the downstream effects of a metabolic state, of which Pizzorno, Frassetto and Katzinger point out that it is not necessarily characterized by acedemia, i.e. pH levels below the "magic" (if we were honest, we'd you'd have to write arbitrary, here) cut-off limit of pH 7.35:

High intensity exercise can also lower your blood pH, an effect you can counter with sodium bicarbonate

"Acidosis only becomes acidaemia when compensatory measures to correct it fail. To illustrate the difference between acidosis and acidaemia, take the following example: two processes occurring simultaneously in the same individual, such as a respiratory acidosis combined with a metabolic alkalosis. In this case, if the respiratory trend toward acidosis is greater than the metabolic trend, a pH of less than 7·35 may be reached, and would be considered acidaemia, despite the presence of a metabolic alkalosis. The intensity of each ‘process’ will determine the pH, but the terms themselves (acidosis, alkalosis) do not indicate a certain pH." (Pizzorno. 2009)

In other words, you don't have to suffer from diabetic or otherwise pathogenic "acidosis", to suffer from one of the following ill health-consequences:

• 

  Hip fracture incidence per 100,000 study participants; aggregated data from cohorts from 33 countries (Frassetto. 2001)

  Calcium loss, bone loss, osteoporosis - Unfortunately, this is not only the best-known side effect of "being too acidic", it's also the only one people take seriously. In that, scientists and lay press alike have zoned in on the high intake of animal proteins as the main confounding factor. But despite the fact that the high sulfur content (methionine, cysteine & co) does certainly contribute to the problem, the data in the figure at the right should make it quite clear that the stuff we eat and don't eat with our meats is at least as much to blame for the misery. In view of the fact that
  

  "[...] cereal grains themselves are net acid-producing and alone accounted for 38% of the acid load yielded by the combined net acid-producing food groups in the contemporary diet" (Sebastian. 2002)

  the average (processed) grain addicted US citizen with his/her quasi-non-existent vegetable intake would end up way on the left side of the x-axis of the graph on the right-hand side, even if he ate not a single gram of animal protein - we would just have to relabel the axis to vegetable/acidd forming food intake (including grains!)".
• Increased renal nitrogen excretion and hampered protein synthesis - One of the less known effects of an increased acid/base ratio is an increase in nitrogen excretion that will obviously not simply hamper your gains, but can also set you up to sarcopenia (age-induced muscle loss).
  
  

  

  Correcting a diet-induced low grade metabolic acidosis with K-bicarbonate reduces the nitrogen loss of 750mg - 1000mg per day (per 60kg BW) in post- menopausal women (Frassetto. 1997)

  In the end, the excretion of nitrogen is nothing, but an adaptive mechanism and a consequence of the catabolism of tissue protein. It is, if you will, a basic necessity for your body to rob your muscle and other tissue of glutamine and all other amino acids, that can be convert to glutamine in the liver, from where it is delivered to the kidney where it's used to synthesize ammonia and excrete the potentially toxic acid load. This will obviously mitigate the severity of the acidosis, it does yet also entail a net loss in muscle and organ protein that cannot be compensated for by an increase in acid forming protein in your diet.
  
  As the data in the figure to the right goes to show you this is a process that's regulated on a day to day basis and the relief in nitrogen loss (data in mg/day/60kg) provided by bicarbonate supplementation (days 0-18) is transient and disappears as soon as you return to your regular low-base, high acid diet (days 19-30).
• Impairments of the growth hormone / IGF-1 axes - Brunnger et al. tested in 1997 whether experimental acidosis would have an effect on the growth hormone / IGF-1 axis and observed a "significant decrease in serum IGF-1 concentration without a demonstrable effect on IGF binding protein 3", which points towards an acid induced "primary defect in the growth hormone/IGF-1 axis" that occurs "via an impaired IGF-1 response to circulating growth hormone with consequent diminution of normal negative feedback inhibition of IGF-1 on growth hormone" (Brunger. 1997). Interestingly, Mahlbacher et al. were able to show that the administration of IGF-1 can in turn ameliorate acidosis and thus correct the previously discussed nitrogen wasting (Mahlbacher. 1999).
  
  

  

  Learn more about the effects of GH, IGF1 and it's splice variants MGF & co and their influence on skeletal muscle hypertrophy in the respective part of the Intermittent Thoughts on Building Muscle (go to the overview).

  In fact, potential physiological effects of the acid-induced impairment of the GH / IGF-1 axes had been observed much earlier, already. McSherry et al. for example report in a 1978 article in the Journal of Clinical Investigations that children with short stature and classic renal tubular acidosis developed normally, when they were treated with adequate amounts of alkalizing agents.
  
  That similar negative effects can be observed even in the presence of "low-grade 'tonic' background metabolic acidosis" was confirmed by Frassetto et al. who observed statistically significant increases (+11%) in 24-hour mean growth hormone secretion in post-menopausal women with diet-induced low-grade metabolic acidosis, when their dietary acid load was neutralized with adequate amounts of potassium bicarbonate (Frassetto. 1997).
  
  In a subsequently published study the scientists argue that the concomitantly observed increases in osteocalcin and bone metabolism would confirm the physiological significance of these changes (Frassetto. 2001). The effects on bone add to the well-known beneficial metabolic effects of growth hormone ( and line up with the recently reported association between low growth hormone levels and memory impairments (Wass. 2010).
  
  In view of the bad press GH and IGF1 are getting, it is important to point out that we are talking about a normalization of the GH/IGF-1 axis, here. It is therefore unlikely that the restoration of a normal acid-base balance will have any of the anti-longevity and pro-cancerous (see next bulletin point) effects of growth hormone and IGF-1 you may have read about in the pertinent literature.
• Potential protective / anti-cancer effects - While conclusive scientific evidence for the involvement of low-grade acidemia in the etiology of cancer is still missing, it has long been speculated that the genetic and epigenetic perturbations, which will turn normal cells into cancer cells may be triggered (among other factors) by disturbances in the acid-base equilibrium. As Ian Forrest Robey points out in his 2012 review of the literature, a diet induced
  

  "[a]cid-base disequilibrium has has been shown to modulate molecular activity including adrenal glucocorticoid, insulin growth factor (IGF-1), and adipocyte cytokine signaling, dysregulated cellular metabolism, and osteoclast activation, which may serve as intermediary or downstream effectors of carcinogenesis or tumor promotion." (Robey. 2012)

  If you want to learn more about the "state of the art research" on the potential link between latent dietary acidosis and the development of cancer, I suggest you simply read the free fulltext of the paper on PubMed. 

I guess, now that you've learned about some of the intricacies of adequate mineral intakes and balances, the acid / base balance, nitrogen and bone loss, growth hormone and cancer, and listened to the interactions of sodium blood pressure, blood glucose and insulin on yesterday's show, it's about time to come back to the simple things that work - the bottom line, so to say...

"What was that about the nutrient sufficiency of the vegetarian / vegan diet, you said on the air?" The above figure shows the % of omnivores, vegans and vegetarians who meet the RDAs  for protein and fiber and selected vitamins and minerals (DiMarino. 2013)

Bottom line: A whole foods convenient-"food" free with the right balance of vegetables, protein, and a reasonable amount of complex largely unprocessed carbohydrates, fats and fruits - call it "ancestral" or "paleo", if you will - is going to provide you with all the minerals you need, it will contain them in the right ratios and supply your body with all the co-factors it needs to use them. It will stabilize your pH levels, normalize your growth hormone / IGF-1 axis and is beyond any doubt the most effective way to get and stay in shape, to reduce your cancer risk, ward off diabetes and lead a life that's not simply long, but also worth living.

If you adhere to these simple rules, there is no reason to be worried about "not getting your minerals" and other essential nutrients. After all, this is what distinguishes you from the "average" western omnivore, vegetarian or vegan who fails to meet most of his or her nutrient requirements.

References:

• Brungger M, Hulter HN, Krapf R. Effect of chronic metabolic acidosis on the growth hormone/IGF-1 endocrine axis: new cause of growth hormone in sensitivity in humans. Kidney Int. 1997; 51:216–221
• Cordell D, Drangert J-, White S. The story of phosphorus: Global food security and food for thought. Global Environ Change. 2009;19(2):292-305.  
• DiMarino A. A Comparison Of Vegetarian Diets And The Standard Westernized Diet In Nutrient Adequacy And Weight Status. The Ohio State University. A Thesis Presented in Partial Fulfillment of the Requirements for Graduation with Distinction from the School of Health and Rehabilitation Sciences of The Ohio State University. 2013. 
• Frassetto L, Morris RC, Jr., Sebastian A. Potassium bicarbonate reduces urinary nitrogen excretion in post-menopausal women. J Clin Endocrinol Metab. 1997: 82:254–259.
• Frassetto L, Morris RC Jr, Sellmeyer DE, Todd K, Sebastian A. Diet, evolution and aging--the pathophysiologic effects of the post-agricultural inversion of the potassium-to-sodium and base-to-chloride ratios in the human diet. Eur J Nutr. 2001 Oct;40(5):200-13.
• Mahlbacher K, Sicuro A, Gerber H, Hulter HN, Krapf R. Growth hormone corrects acidosis-induced renal nitrogen wasting and renal phosphate depletion and attenuates renal magnesium wasting in humans. Metabolism. 1999; 48:763–770
• May RC, Kelly RA, Mitch WE. Metabolic acidosis stimulates protein degradation in rat muscle by a glucocorticoid-dependent mechanism. J Clin Invest. 1986. 77:614–621.
• Mayer AM. Historical changes in the mineral content of fruits and vegetables. British Food Journal. 1997; 99(6):207 - 211
• McSherry E, Morris RC, Jr. At tainment and maintenance of normal stature with alkali therapy in infants and children with classic renal tubular acidosis. J Clin Invest. 1978; 61:509–527. 
• Montain SJ, Cheuvront SN, Lukaski HC. Sweat mineral-element responses during 7 h of exercise-heat stress. Int J Sport Nutr Exerc Metab. 2007 Dec;17(6):574-82.
• Peck NH, Grunes DL, Welch RM, MacDonald GE. Nutritional Quality of Vegetable Crops as Affected by Phosphorus and Zinc Fertilizers Agron. J. 1980; 72: 528–534.
• Pizzorno J, Frassetto LA, Katzinger J. Diet-induced acidosis: is it real and clinically relevant? Br J Nutr. 2010 Apr;103(8):1185-94.
• Sebastian A, Frassetto LA, Sellmeyer DE, Merriam RL, Morris RC Jr. Estimation of the net acid load of the diet of ancestral preagricultural Homo sapiens and their hominid ancestors. Am J Clin Nutr. 2002 Dec;76(6):1308-16.
• Wass JA, Reddy R. Growth hormone and memory. J Endocrinol. 2010 Nov;207(2):125-6.
• Williams B, Layward E, Walls J. Skeletal muscle degradation and nitrogen wasting in rats with chronic metabolic acidosis. Clin Sci. 1991; 80:457–462

Inulin & Beta Glucan Reduce Body Fat Gain By -50% & -33%! Both Have Similar Effects on the Gut Microbiome, But Only Inulin Appears to Be More Than An Appetite Suppressant

What do these Jerusalem artichokes, agave, bananas, burdock, camas, chicory, coneflower, costus, dandelion, elecampane, garlic,jicama, Leopard's-bane, mugwort, onion, wild yams, yacon and a whole host of other foods have in common? Right! They contain inulin. Whether you will be able to get a whopping amount of 10% inulin in your diet w/out the use of supplements or "enriched" foods, is yet as questionable as how beneficial this actually is for friends of physical culture.

The gut microbiome is not just one of the hottest topics in the (health-)blogosphere, it is also a subject of ongoing research. Research, however, that is, if we are honest, still very much in its infancy. As impressive as the results from the latest studies into the metabolic downstream effects of the administration of fermentable fiber to rodents may be and as obvious as their relation to certain changes in the gut microbiome of the animals may appear - in the end, our understanding of the underlying mechanisms does not allow any reliable prognoses like "double the amount of lactobacilli and you will eventually be able to lose that pouch of body fat you've been carrying around for years now". And yet, if the results from the latest rodent experiments at the Imperial College in London, could be reproduced in humans, I can already foresee that both, the consumption and use of the foods I listed in the caption of the image to the right, as well as related products, extracts and supplements, which contain more or less significant amounts of the naturally occurring polysaccharides, we usually refer to as inulin, will increase in the months and years to come.

Fermentable fiber and the gut-brain-axes: The key to lifelong leanness?

If this is not your first visit to the SuppVersity, you will certainly be aware that the idea of a magic pill (or fiber) that will allow you to eat whatever, whenever and in whichever amounts without having to cope with the metabolic consequences is illusive. When the addition of 10% inulin (or beta glucan) to the diets of 36 male C57BL/6 mice had an "anti-obesogenic" effect, this does not mean that the poor critters who were kept on a hypercaloric high fat (41.8%) diet for 8 weeks did not get obese. What it does mean, though, is that the addition of 10% fermentable (=being food for certain gut bacteria) fiber in the form of

*the producers of these products did not fund or support the study (at least the scientists don't mention that in the respective disclosure ;-)

• inulin from Synergy(TM)*, a fructan based preparation containing both long and short chain
  fructooligosaccharides, or
• beta-glucan from Glucagel(TM)* a highly rich (,80%) barley derived b-glucan preparation

to their otherwise iso-caloric diet (the HFD control contained cellulose) was not without helped to mitigate the negative effects of this diet - a fact the majority of you, of whom I would expect that they are not on a fast-food diet should keep in mind, before they head over to their favorite online supplement vendor and type "Synergy inulin" into the search box.

Figure 1: Effect of addition of 10% fermentable fiber as inulin or beta glucan to the high fat diet of male mice on cumulative weight gain (left), body composition and fatness (middle) and food intake (right) over the course of 8 weeks (data adapted from Arora. 2012)

In spite of that, the results are simply too impressive not to think about their implications in otherwise healthy and even more so previously obese individuals. This is particularly true, because the same microbial changes about which the authors write in a previously published paper from May 2012 that the ...

"[...] increases in both Bifidobacteria and Lactobacillius and a significant increase in short chain fatty acids (SCFA) [went hand in hand with] increase in neuronal activation within the arcuate nucleus (ARC) of animals that received In [inulin] supplementation" (Anastasovska. 2012)

do not (and this is a result of the researchers very latest experiments) simply blunt the rodents appetite. If that was the case, the rodents that received the beta glucan supplemented chow and consumed 12% less energy should have had the most favorable body composition. A cursory glance at figure 1 will yet tell you that this was not the case, though.

Inulin beats beta glucan when it comes to body fat reduction / repression

If we take a closer look a the differential effects of inulin and beta glucan, there yet only one figure that really sticks out and that's the accumulation of fat within the musculature of the animals. The "beautiful marbling" people are looking for in their steaks, however, usually is a harbinger of impeding or even existing skeletal muscle insulin resistance. A muscle fat content above the high fat control (it's certainly a weakness that we don't have a "real" control group on standard rodent chow, here) as Arora et al. observed it in the tissue samples of the beta glucan group, does thus tell you something about its potential usefulness, or rather uselessness of this specific type of fermentable fiber.

Figure 2: Effects of the different types of fermentable fiber on cecal microflora groups (figures are in scientific notation, this means "1E+6" equals 1mio, "1E+9" would be 1 billion etc.; data based on Arora. 2012)

In conjunction with the information about the corresponding changes in the gut microbiome (see figure 2), which appear virtually identical in both groups (specifically the extreme increasesin in both Bifidobacteria (BIF) and Lactobacillius (LAB) really stick out), this does however suggest that the modulatory effect on the composition of the gut flora, or at least the part of it the scientists evaluated in the study at hand, cannot be the only driving force behind the beneficial metabolic effects of inulin.

Inulin or beta glucan? This is not a question... 

While the latter, i.e. inulin, which has by the way been found to directly suppress lipogenesis in a 2011 study by Belgian scientists in a similar HFD rodent model (Dewulf. 2011), appears to be promising for everyone, regardless of whether he or she is poisoning him- or herself with the standard American diet (which is, with its high fat and high carbohydrate content de facto an identical twin of the so-called "high fat diet" in rodent studies), the ingestion of larger amounts of the former, i.e. beta glucan, does at least appear questionable.

If you want to use inulin to your metabolic advantage, you better make sure you get your self a more comfortable place to answer the call of nature - it could call thrice as often! Moreover, large amounts of inulin and other fermentable fiber can induce gastrointestinal distress-

The question is therefore not so much whether it's worth supplementing (it's certainly worth to incorporate some of the initially mentioned foods into your diet, as most of them contain a whole list of other advantageous micronutrients) with inulin or beta glucan - the answer would obviously be inulin - but rather whether it's worth adding larger amounts of inulin to an already healthy diet. And while we cannot answer this question based on the results of the previously cited rodent studies, we could argue that Marwa Zenhom and her colleagues from the Christian Albrecht University in Kiel have already supplied relevant evidence that this would be the case (Zenhom. 2011). After all, the German researchers have been able to show that the PPAR-gamma related anti-inflammatory effects (significant reductions IL-12 secretion in Caco-2 cells and gene expression of IL-12p35, IL-8, and TNFa as well as NF-kB) of oligosaccharides are not (exclusively) brought about by their effects on the gut microbiome, because bacteria simply were not present in their in-vitro study with human Caco-2 cells (cells from the gut lining). Bassaganya-Riera et al. even argue that this effect could be beneficial for IBS patients (Bassaganya-Riera. 2011).

Whether having 10% of your diet in form of inulin, or to make this more conceivable, having 1 tablespoon of plain inulin for every 9 tablespoons of whatever else you eat is either feasible or reasonable, is a whole different story (to put that into perspective: The average inulin intake of Westerners is 1-10g per day (van Loo. 1995). Even 10g would yet only be enough if you ate only 100g of food within 24h!)... and I must forewarn you, if you go by the fecal volume of the mice in the Arora study, it is possible that you will spend >3x more time on the toilette than usual ;-)

References:

• Arora T, Loo RL, Anastasovska J, Gibson GR, Tuohy KM, Sharma RK, Swann JR, Deaville ER, Sleeth ML, Thomas EL, Holmes E, Bell JD, Frost G. Differential effects of two fermentable carbohydrates on central appetite regulation and body composition. PLoS One. 2012;7(8):e43263.
• Anastasovska J, Arora T, Sanchez Canon GJ, Parkinson JR, Touhy K, Gibson GR, Nadkarni NA, So PW, Goldstone AP, Thomas EL, Hankir MK, Van Loo J, Modi N, Bell JD, Frost G. Fermentable carbohydrate alters hypothalamic neuronal activity and protects against the obesogenic environment. Obesity (Silver Spring). 2012 May;20(5):1016-23.
• Astegiano M, Pellicano R, Terzi E, Simondi D, Rizzetto M. Treatment of irritable bowel syndrome. A case control experience. Minerva Gastroenterol Dietol. 2006 Dec;52(4):359-63.
• Bassaganya-Riera J, DiGuardo M, Viladomiu M, de Horna A, Sanchez S, Einerhand AW, Sanders L, Hontecillas R. Soluble fibers and resistant starch ameliorate disease activity in interleukin-10-deficient mice with inflammatory bowel disease. J Nutr. 2011 Jul;141(7):1318-25.
• Dewulf EM, Cani PD, Neyrinck AM, Possemiers S, Van Holle A, Muccioli GG, Deldicque L, Bindels LB, Pachikian BD, Sohet FM, Mignolet E, Francaux M, Larondelle Y, Delzenne NM. Inulin-type fructans with prebiotic properties counteract GPR43 overexpression and PPARγ-related adipogenesis in the white adipose tissue of high-fat diet-fed mice. J Nutr Biochem. 2011 Aug;22(8):712-22.  
• van Loo J, Coussement P, de Leenheer L, Hoebregs H, Smits G. On the presence of inulin and oligofructose as natural ingredients in the western diet. Crit Rev Food Sci Nutr. 1995 Nov;35(6):525-52.
• Zenhom M, Hyder A, de Vrese M, Heller KJ, Roeder T, Schrezenmeir J. Prebiotic oligosaccharides reduce proinflammatory cytokines in intestinal Caco-2 cells via activation of PPARγ and peptidoglycan recognition protein 3. J Nutr. 2011 May;141(5):971-7.

Red Meat and Even Pork is Good for You!? Reduced Weight Gain, Improved Insulin Sensitivity and No Adverse Side Effects from "Red Meat Supplementation" Even in Rodents!

Image 1: Must be the red meat between those healthy grain based burger buns that makes this rodent fat, right? What? Yeah... of course epidemiologists count this as a "red meat meal" - it has "red meat" in it... wait, ah yeah: More likely pink slime, with some totally benign ammonia in it, you are right ;-)

Those of you who have been around here at the SuppVersity for some time, may have remembered the "Additional(!) 200g of Pork a Day Build Lean Mass, Improve Blood Lipids & Glucose Levels" from September 2011, when a couple of weeks ago yet another "anti-meat study" hit mainstream media news. You will probably have read enough of the certainly accurate, but in a way pointless criticism of the study, elsewhere in the bloggosphere, so that I decided not to repeat the argumentation, which basically discards the value of all epidemiological data (as long as it is not interpreted in accordance with the respective blogger ;-)... now, not all scientists are epidemiologists, some, like Petzke et al. (see the post I mentioned before) or, more recently Haiyan Chen and his (or her?) Chinese co-workers actually care to conduct experiments on the health effects of red meat consumption and their results are by no means as unequivocal (Chen. 2012), as the introductions and dead-certain conclusions of the epidemiologist would suggest.

If you want to lose weight and ward off diabesity, you "supplement" with red meat!

In their 24 week trial, Chen et al. kept a group of 24 male Wistar rats, who had been pre-fattened on the standard SAD-like "high fat diet" for 14 weeks (an interesting side note: only 24 of the 46 rats who received the HFD diet got actually obese, i.e. they gained +20% more body-fat than their peers - so what does that tell you about the "general" fattening effect of the "high fat diet"?) on either

• regular rodent chow with 67.8% of energy from carbohydrates, 12.8% fat and 19.4% protein, or
• red-meat enriched "high" protein diets with 46.6% of energy from carbohydrates, 16.7% fat and 36.7% protein

The "high protein" (I am putting the term "high" between inverted commas, because I am well aware that for many of you the "medical high protein diet" contains about the least imaginable amount of protein you believe you could get along with; suggested read "20g or 40g of Whey? That is NOT the Question!") contained 780g of lean pork powder per kg. With the other components from the standard chow being added at ratios that would make sure that the rodents from both groups would have an identical caloric intake of 336 kJ/day (=normal caloric intake for adult rats). In the course of the 24-week study period (for rodents with their 2-3 year life expectancy this is like 10-15 human years!), the scientists measured the body weight and fasting  blood glucose levels weekly and every 4 weeks, respectively.

Figure 1: Body weight (in g) during and visceral fat (in g) after 24 weeks on high protein meat or normal protein chow diets (data adapted from Chen. 2012)

As you can see in figure 1 the addition of the "unhealthy red meat" (remember: neither was this "healthy chicken" nor grass-fed beef, but Chinese pork meat - similar to the lean cuts of pork that made the women in the Petzke study lean out and build muscle) reduced the weight gain of the already obese 17-week old rodents by more -57% (!) and left them with 44% less of pro-inflammatory visceral fat mass than their peers on the healthy "meat-less" standard chow. Despite an increase in BUN, the creatinine levels of both groups were identical and there were no signs of kidney damage in any of the rodents kept on the meat-supplemented high protein diet.

Figure 2: Insulin AUC during intravenous glucose tolerance test (IGGT) and fasting GLP-1 levels
(data adapted from Chen. 2012)

The insulin response during an intravenous glucose tolerance test (a measure of insulin resistance), on the other hand, was reduced, just as fasting GLP-1 levels were (P < 0.05; for more information on the intricate relationship between GLP-1, insulin and obesity / fat loss, check out my previous post on WMHDP).

Why the different results? Don't tell me meat is not bad for me!

Aside from the questionnaire based epidemiological studies, where "Pizza Salami" is a "red meat food", I mentioned earlier, there definitely is experimental data (on which the working hypothesis of many of the epidemiological studies are founded, by the way) that would suggest that feeding red meat to rodents is not the best thing to do... now, if we discard species-specific issues for the time being, how can those differences be explained? Chen et al. provide a pretty straight-forward set of potential confounding factors in their discussion, which I am going to summarize for you:

• meat is an energetically denser protein source than dairy - this may explain why, compared to dairy products, meat has been found to be positively associated with weight gain in rats (eg. Belobrajdic. 2003)
• the longer experimental duration - in previous studies there were already "tendencyies toweight loss" at the end of the mostly 10-12 week study periods 
• the age of the animals may have a profound effect on the weight gain; for rats that are younger than the ones in the study at hand, an increased weight could would in fact indicate a healthy effect during the most active growth period of the rodents rats; this would not preclude, though that the same diet would facilitate weight loss in mature rats

Still, aside from the lack of blood lipid profiles, blood calcium and phosphorus levels, which as the scientists concede would have been "important [to judge the] safety of the high-protein diet", there is another factor, I would really insist on, if it had not been for the repeatedly mentioned human trial by the German scientists and that would be that the use clenbuterol, salbutamol and sibutramine - "weight loss adjuvants", or the Chinese would probably say dietary supplements to ensure lean livestock *rofl* - is still daily fare in China, so that - theoretically speaking - we cannot exclude that the rodents received a whopping dose of any, if not all of these drugs in their "meat-supplemented" high protein diets ;-)

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 ;-)