Category Archives: Fructose

the opposite of food, Op. 76

Processed non-junk food

or

as close to “non-junk” as processed food can be

Notice the inverse relationship between fat content and the number of ingredients in these three commercially available sour cream products.  This is processed food.

Regular:
Cultured pasteurized grade A cream and milk, enzymes.

Low-Fat:
Cultured Milk, Cream, Nonfat Dry Milk, Whey, Modified Corn Starch, Sodium Phosphate, Guar Gum, Carrageenan, Calcium Sulfate, Locust Bean Gum, Gelatin, Vitamin A Palmitate.

Fat Free:
Cultured Low-fat Milk, Modified Corn Starch, Whey Protein Concentrate, Propylene Glycol Monoester, Artificial Color, Gelatin, Sodium Phosphate, Agar Gum, Xanthan Gum, Sodium Citrate, Locust Bean Gum, Vitamin A Palmitate.

 

 

Fat-Free Half & Half

not cream

In general, “Half & Half” refers to a 50:50 blend of whole milk and cream.  People think it’s better than cream because it has less fat.  Whole milk is about 3% fat by weight, while cream is about 30%.  Mix ‘em together and you end up with Half & Half, which is somewhere in between (12-14%).  Fat has a profound effect on flavor and texture… so how exactly does “Fat-Free Half & Half” taste and feel just like regular Half & Half?!?  Muah ha ha ha haaaa!

divide and conquer

From what I can gather, the fat is replaced with corn syrup and pharmaceutical grade thickeners, emulsifiers, etc., scientifically engineered to mimic the precise flavor and texture of Half & Half.  There are even artificial colors added to make it look like cream.  There are artificial colors added to make it look like cream?  AYFKM?  For some reason, I find this oddly offensive.  It is to these artificial colors which I object.  I want this concoction (that is advertised as better than cream) to look like whatever “corn syrup, carrageenan, sodium citrate, dipotassium phosphate, mono and diglycerides, and vitamin A palmitate” looks like.  And it should release a pale green mist upon contact with coffee.

The sugar in Fat-Free Half & Half comes from corn syrup, while that in real dairy is lactose.  Glucose is sweeter than lactose, and there’s 2-3x more sugar in Fat-Free Half & Half.  Does this mean people use less of it?  I doubt it, because the additional sweetness is probably necessary to compensate for the lack of fat.

And what about all the other additives in Fat-Free Half & Half?  This is reminiscent of the introduction of trans fats into our diet by way of replacing butter and lard with margarine and shortening…

Carrageenan is partially responsible for improving the mouthfeel and texture of Fat-Free Half & Half.

carrageenan. Looks scary, right?

At high doses, it’s an inflammatory gut irritant.  Given coffee’s not-so-gut-friendly reputation, do you really want to push it with carrageenan?

On another note, carrageenan is used to design some of the most beautifully artistic desserts.

In this context, I’m reminded of the phrase: “the dose makes the poison.”  In other words, those dishes are a dietary rarity, reserved for the most special of occasions.  At that level of exposure, it could be a blend of carrageenan, trans fat, sucrose, and Red #40, you could eat 5 of them at a time, and you’d never experience any malevolent effects.  But what about a few tablespoons in your coffee every morning for 30 years???  (alternatively, perhaps I’m underestimating carrageenan exposure a bit) (other, more sordid uses of carrageenan)

Avoid processed foods, especially when they’re no more convenient or healthy their conventional counterparts.

 

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P.S.  Perhaps I was a little too hard on Fat-Free Half & Half.  It’s not as bad as microwave popcorn, or this classic:

One 43 gram Twinkie contains 5 grams of fat, 25 grams of sugars, 1 gram of protein, no fibre, 150 kcal, and over 35 ingredients:

  • Enriched Wheat Flour – enriched with ferrous sulphate, B vitamins (niacin, thiamine mononitrate, ribofavin and folic acid).
  • Sugar
  • Corn syrup
  • Water
  • High fructose corn syrup
  • Vegetable shortening – containing one or more of partially hydrogenated soybean, cottonseed or canola oil, and beef fat.  [trans fat]
  • Dextrose
  • Whole eggs
  • Modified corn starch
  • Cellulose gum
  • Whey
  • Leavenings (sodium acid pyrophosphate, baking soda, monocalcium phosphate)
  • Salt
  • Cornstarch
  • Corn flour
  • Corn syrup solids
  • Mono and diglycerides
  • Soy lecithin
  • Polysorbate 60
  • Dextrin
  • Calcium caseinate
  • Sodium stearol lactylate
  • Wheat gluten
  • Calcium sulphate
  • Natural and artificial flavours
  • Caramel colour
  • Sorbic acid (to retain freshness)
  • Colour added (yellow 5, red 40)

 

 

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a novel gut health diet paradox, Op. 75

The low FODMAPs diet

FODMAPS  – Fermentable Oligosaccharides, Disaccharides, Monosaccharides, and Polyols.  Basically, FODMAPs are a bunch of sugars that are poorly digested in some people and cause a fantastic variety of health problems ranging from bloating and abdominal pain all the way to chronic fatigue and anxiety.  AND a low FODMAPs diet seems to provide some relief (Ong et al., 2010; Staudacher et al., 2011).

Just like it’s weird name, it’s difficult to simplify the rules of the low FODMAPs diet, so here it is graphically:

FODMAPs vs. GFCF

Grains are excluded from GFCF due to gluten and from FODMAPs due to oligosaccharides.  Dairy is excluded from GFCF due to casein and from FODMAPs due to lactose (not sure where FODMAPs stands on fermented dairy like kefir or FAGE).  Thus, both GFCF and FODMAPs exclude grains and dairy.  However, GFCF doesn’t restrict fructose, which is excluded in FODMAPs (monosaccharide).  And last but not least, GFCF but not FODMAPs allows polyols, but as I’ll explain later, I don’t think polyols belong on this list (perhaps “FODMAPs” was just more pleasant-sounding than “FODMAs”).

“polyols”

FODMAPs vs. low carb

A low carb diet is low in both FODMAPs and gluten.  But perhaps similar to polyols, some leniency should also be applied to casein, as standard low carb diets don’t restrict casein but still improve a variety gastrointestinal symptoms (and quality of life in IBS patients; Austin et al., 2009).  Alternatively, a dairy-free low carb diet would cover all your bases.

or you could bring a gun to a knife fight, part I.

Alterations in gut bacteria are frequently associated with gastrointestinal problems, and two classes of nutritional supplements aimed at modifying the gut flora seem to help.  “Probiotics” contain the buggers themselves, while “prebiotics” contain their fuel.

divide and conquer

Bifidobacteria

With regard to the former, “bifidobacteria” seem to be the major player.  Bifidobacteria are the highest in the gut of breast fed babies and lowest in elderly folk.  They are lacking in IBS sufferers (Kerckhoffs et al., 2009; Parkes et al., 2012), and supplementation with bifidobacteria-containing probiotics improve a variety gastrointestinal symptoms (B. infantis 35624 [Whorwell et al., 2006]; B. animalis DN-173 010 [Guyonnet et al., 2007]; B. bifidum MIMBb75 [Guglielmetti et al., 2011])

B. infantis 35624 is found in Align.

B. animalis DN-173 010 is found in Dannon’s Activia yogurt.  But as with most yogurt products, it comes unnecessary added sugars.

Personally, I’d recommend a blend like that found in Jarrow Bifidus Balance (which comes preloaded with its own stock of prebiotics, to be discussed later).

Back to the paradox (or a shameless teaser for next week’s episode): the low FODMAPs, GFCF, and low carb diets all have beneficial effects on gut health but reduce bifidobacteria.  Bifidobacteria supplements and bifidogenic prebiotics are also good for the gut.

a far more enigmatic paradox than the French one, IMO, to be continued…

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Candy in disguise, Op. 73

on the chopping block:To recharge between hunting, gathering, and avoiding predation, our Paleolithic predecessors snacked on gluten-free energy bars comprised of a variety of fruits nuts, and vegetable oils all stuck together with Mother Nature’s sweet sticky honey and dates.  <end sarcasm>

For the record, I’m not a card-carrying member of the Paleo community; just looking out for a respectable nutrition movement.

NoGii No Gluten Paleo Bars” should not be confused with anything healthy.

INGREDIENTS: Dates, Honey, Organic Cashews, Almonds, Apple Juice Sweetened Cranberries (Cranberries, Apple Juice Concentrate, Sunflower Oil), Sesame Seeds, Dried Unsweetened Tart Cherries, Sunflower Seeds, Unsulphured Dried Apples, Freeze-dried Strawberries, Strawberry Juice Concentrate, Organic Sunflower Oil. ALLERGENS: Contains Tree Nuts (Almonds and Cashews).

Full disclosure:

Case closed.

On a more positive note, NoGii No Gluten Paleo Bars have no added sugars.  Indeed, those were saved for their “NoGii Kids Bar.” 

INGREDIENTS: Soy Protein Crisps (Soy Protein Isolate, Tapioca Starch), Marshmallow Creme (Sugar, Brown Rice Syrup, Crystalline Fructose, Invert Sugar, Water, Egg Albumen, Agar, Gum Arabic, Natural Flavor), Brown Rice Syrup, Organic Brown Rice Crisps (Organic Brown Rice, Organic Brown Rice Syrup, Sea Salt), Rice Syrup Solids, Maize Dextrin (Dietary Fiber), Organic Canola Oil, Organic Agave Syrup, Whey Protein Isolate, Organic Palm Oil, Vanilla Yogurt Drizzle (Sugar, Fractionated Palm Kernel Oil, Whey Powder, Nonfat Dry Milk Powder, Cultured Whey, Soy Lecithin [emulsifier], Vanilla), Vegetable Glycerine, Natural Flavors, Sea Salt, Soy Lecithin, Mixed Tocopherols (Natural Vitamin E), Purified Stevia Extract, Lo Han Extract.

NoGii proudly advertises “NO HIGH FRUCTOSE CORN SYRUP” and “ALL NATURAL,” but this is despicable, ESPECIALLY because these are targeted at children.

Divide and conquer

  1. Agave syrup has MORE fructose than high fructose corn syrup (it’s like higher fructose corn syrup).  Why brag about “no high fructose corn syrup” if you’re only going to include a higher fructose substitute?
  2. Crystalline fructose.  (yes, that would be 100% fructose).
  3. Invert sugar is chemically virtually identical to high fructose corn syrup.  This is deceitful… it wouldn’t be so bad if they didn’t advertise (in all capital letters) “NO HIGH FRUCTOSE CORN SYRUP” directly on the website.
  4. Lastly, there’s nothing “Brown Rice” about “Brown Rice Syrup.”  It’s just plain syrup.  It may not have fructose, but it’s still just a blend of simple sugars.

NoGii is pulling no punches, so neither am I: they are trying to trick parents into feeding their kids something that they may not have had they known what was really in it.

NoGii.  Worst company of the week.  No, of the month, because they are targeting children.

A superior alternative:

Quest Low Carb Gluten Free Protein Bars

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Non-sequiter nutrition

(or another over-caffeinated soapbox rant)

Taxing junk food?  If I thought the government had a clue what constituted “junk,” maybe I’d view this more favorably.  But my gut says no.

 

 

“Bad food? Tax it, and Subsidize Vegetables”  Mr. Bittman, we subsidize the hell out of corn; what good has that done?   I don’t think controlling diet via junk food taxes is the right way to healthify America, but if I had to choose I’d say shift subsidies away from corn and soybean, and toward things like organic spinach and grass fed beef.   This would impact a lot of foods containing ingredients that are [IMO] barely suitable for human consumption like high fructose corn syrup and trans fats (and corn & soybean oils).

 

 

Denmark and Romania taxing saturated fat?  Really?  we already went through this when we traded saturated fat-rich butter for diabesogenic trans fat-rich margarine-  (“saturated fat”).  A tax on saturated fat is non-specific; it hits many healthy foods and not enough junk food.  And it is, by definition, a tax NOT on the deceptively unsaturated trans fats.  Alternatively, subsidizing corn and soybeans is just making soda and junk food cheaper.

 

 

do NOT eat at KFC in Hungary, Peru, or Poland.  or anywhere.  that’s microwave popcorn levels of trans fat.

Better nutrition education and evidence-based recommendations are far better solutions, IMHO, but we aren’t a country of philosopher’s.  I’ve touched a bench on which the sign “wet paint” was taped, and I probably also touched a red hot stove despite my mother’s warning against it.  oh well.

 

 

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Insulin per se

This recent manuscript nearly slid beneath the radar… almost stopped reading at the abstract until the word “nifedipine” appeared (among its widely pleiotropic effects, nifedipine also lowers insulin).

The series of experiments described below demonstrate one aspect of the scientific method reasonably well.  None of the individual experiments, when viewed in isolation, really prove the hypothesis.  But the researchers tested it with a variety of widely different methods and all of the results went in the same direction.  The hypothesis in question: insulin causes fat gain, and hyperinsulinemia per se, not macronutrients or calories, is the root cause.

This group has previously shown that sucrose is more detrimental than fish oil is beneficial toward obesity and glycemic control.

High glycemic index carbohydrates abrogate the anti-obesity effect of fish oil in mice (Hao et al., 2012 AJP)

Divide and conquer
Mouse study.  Lots of diets, in brief:
Pair fed: high fish oil (180 g/kg) plus 13%, 23%, 33%, and 43% sucrose (by weight, switched out for casein [a poor choice IMO])
High fish oil (180 g/kg) plus sucrose, fructose, glucose, low GI carbs, and high GI carbs.
That’s a lot of diets.  Kudos.

As expected, higher sugar and lower protein intakes enhance weight gain (yes, even when pair-fed similar calories [i.e., a calorie is not a calorie]) and this is at least partly due to reduced metabolic rate (as per the poor man’s energy expenditure test- measuring body weight before and after 24 hours starvation [higher weight loss = higher metabolic rate]):High sucrose-fed mice also had more inflamed adipose tissue and less thermogenic brown fat, which likely contributed to their glycemic dysregulation and elevated adiposity.

Sucrose is comprised of glucose and fructose, so to determine which component was causing obesity, they fed mice high fish oil diets plus either sucrose, glucose, or fructose.  Interestingly, the glucose group gained as much weight as the sucrose group.  Since the fructose group gained the least amount of weight, the researchers attributed the sucrose-induced obesity to insulin! (fructose doesn’t elicit an insulin response; and insulin levels were lowest in the fructose group).

Body weight, plasma insulin, and glucose tolerance:

I. Thus far: glucose and sucrose cause obesity by stimulating insulin secretion.  Glycemic deterioration is worst in the glucose-fed group because they were consuming most of the most insulinogenic sugar: glucose.  It was lower in the sucrose and fructose groups because sucrose contains only half as much glucose as pure glucose, and fructose contains no glucose.  IOW, these data suggest hyperinsulinemia per se causes obesity and insulin resistance.  Gravitas.

They further tested this by comparing high and low GI diets which cause higher and lower insulin levels, respectively.  As expected, the low GI diet led to less weight gain, and significantly lower insulin levels and adipose tissue accumulation compared to the high GI diet:

II. Thus far: high insulin levels, whether induced by glucose, sucrose, or high GI starch, lead to obesity.

They next took a non-dietary approach by artificially increasing insulin levels with glybenclamide in fish oil-fed mice to see if hyperinsulinemia could still cause obesity.  The results weren’t robust, but the higher insulin levels tended to increase adiposity even in mice fed the anti-obesogenic fish oil diet. 

In the experiment, the opposite approach was taken: nifedipine was used to lower insulin.  The use of octreotide and diazoxide has been used in a similar context with similar results in humans, discussed HERE and HERE.Again, the results were not robust, but when viewed collectively a picture begins to emerge: raising insulin levels, whether it is with a high glucose or sucrose diet, a high GI diet, or glybenclamide increases adipose tissue growth; and conversely, lowering insulin levels, whether it is with a less insulinogenic sugar diet (fructose), a low GI diet, or nifedipine decreases adipose tissue growth.  Oh yeah, and low carb works too.

 

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USDA vs. nutrition, round II

The school lunch program is screwed.

First the USDA modifies the definition of a vegetable to include pizza.  Now they significantly altered their standards for school lunches to include fewer healthy foods and more USDA-approved ones (see report at the USDA’s website).  In brief, this move further reduces the nutrition of school lunches and will likely do more harm than good.  Here’s why:

In this cross-sectional Swedish study, parents recorded 7-day food diaries for their 4-year old children who then went in for a regular checkup.

Metabolic markers in relation to nutrition and growth in healthy 4-y-old children in Sweden (Garemo et al., 2006 AJCN)

On a 1,400 kcalorie diet, these children were consuming roughly 15% protein, 33% fat, and 52% carbs (about 20% of which came from sucrose).  That seems like a lot of calories, but besides playing all day, 4 year old children are also growing at an incredible rate.

Interesting finding numbers 1 & 2:  Children who got most of their calories from fat had the lowest BMI (i.e., they were the leanest), and the opposite was observed for carbs.

When divided into groups of normal weight vs. overweight and obese, some interesting and non-intuitive patterns emerged.  For example, lean kids don’t eat less food; but they do eat fewer carbs and less sucrose (and make up the difference by eating more fat and saturated fat).

Some of the weaker correlations showed:
-total calorie intake was associated with growth (logical)
-total carbohydrate intake was associated with increased fat mass (unfortunate yet also logical)
-total fat intake was associated with decreased fat mass (interesting)

And those who ate the most saturated fat had the least amount of excess body fat. (more on this below)

Fortunately, in a young child, a poor diet hasn’t had enough time to significantly impact their metabolic health; as such no macronutrient was associated, either positively or negatively, with insulin resistance [yet].

In a more appropriately titled follow-up, Swedish pre-school children eat too much junk food and sucrose (Garemo et al., 2007 Acta Paediatrica), Garemo reported that most of their carbs came from bread, cakes, and cookies, while most of the sucrose came from fruit, juices, jam, soft drinks, and sweets.  And WOW, go figure- most of the fat came from meat, chicken, sausage, liver, eggs, and dairy; NOT vegetable oils.

And in a mammoth dissertation, Eriksson (2009) confirmed many of these findings in a larger cohort of 8-year old Swedish children and had this to say about dairy fat:

The open boxes represent overweight kids, the closed boxes are lean kids.  Going from left to right, in either the open or closed boxes, BMI declines with increasing intake of full fat milk (perhaps parents should reconsider skim milk?).  Eriksson also confirmed that saturated fat intake was strongly associated with reduced body weight.  Interestingly, she mentioned that food intake patterns are established early in life, so it might be prudent to remove sugars and other nutrient poor carb-rich foods, and introduce nutritious whole foods as early as possible.  I’m not exactly sure how she assessed patterns of food intake establishment, but it seems logical.  Especially in light of the following study… we’ve seen 4 year olds, 8 year olds, and now we have 12-19 year olds.  The relationship between diet and health is consistent across all age groups.

Virtually all of the above data in Swedish children seem to suggest dietary saturated fat, whether it’s from beef, sausage, eggs, whole fat dairy, or liver (i.e., WHOLE food sources; NOT hydrogenated vegetable oils), is associated with reduced fat mass.  Metabolic abnormalities were not present, probably because the children were simply too young (although body weight seems to respond relatively quickly, other downstream effects of poor nutrition take years to accumulate before symptoms develop).

An American study about nutrient density and metabolic syndrome was recently published.  These kids were exposed to poor nutrition for just long enough to experience some of those malevolent effects.

Dietary fiber and nutrient density are inversely associated with the metabolic syndrome in US adolescents (Carlson et al., 2011 Journal of the American Dietetic Association)

The figure below divides fiber (a proxy for good nutrition; i.e., leafy vegetables, beans, etc.) and saturated fat into groups of least and most amounts comsumed. The lowest fiber intake was 2.9 grams for every 1,000 kcal, and 9.3% of these kids already had metabolic syndrome; the highest fiber intake was 10.7 grams / 1,000 kcal and 3.2% had metabolic syndrome.  Thus, consuming a fiber-rich [nutrient dense] diet is associated with a significantly reduced risk of metabolic syndrome.

The next rows are saturated fat.  The lowest saturated fat intake was 6.9 grams / 1,000 kcal and 7.2% had metabolic syndrome; the highest saturated fat intake was 18 grams / 1,000 kcal and 6.7% had metabolic syndrome…. huh?  While it didn’t reach statistical significance, the trend for saturated fat paralleled that of a “nutrient dense” diet.  Is it possible that saturated fat might be part of a nutrient dense diet?   if saturated fat comes in the form of red meat, liver, eggs, etc., then yes, it is part of a nutrient dense diet.  This conclusion evaded both the study authors and the media.

In 4 and 8 year old Swedish children, those who ate the most saturated fat had the least excess fat mass.  In 12 – 19 year old American adolescents, those who ate the most saturated fat had the lowest risk for metabolic syndrome.

Is it too much of a stretch to connect these ideas by saying that in the short run, a low saturated fat (nutrient poor, carb-rich) diet predisposes to obesity; and in the long run it predisposes to metabolic syndrome  ???

Collectively, these data suggest a diet based on whole foods like meat and eggs, including animal fats, with nutrient dense sources of fiber (e.g., leafy vegetables) but without a lot of nutrient poor carb-rich or high sugar foods, may be the healthiest diet for children.  

Flashback: recap of “USDA vs. nutrition, round I”
USDA: 1
Nutrition: 0
They made pizza a vegetable and insiders suspect that next they’ll try to make it a vitamin.

USDA vs. nutrition, round II

USDA: replacing normal milk with low fat milk
nutrition: full-fat milk was associated with lower BMI in both lean and obese children (see the Eriksson figure above)

USDA: increasing nutrient poor carb-rich options
nutrition: this was associated with increased fat mass in children (Garumen et al., see figures above)

USDA: reducing saturated fat as much as possible
nutrition: reduced saturated fat was associated with excess fat mass in children and metabolic syndrome in adolescents.

Such changes will have an immeasurable long-term impact if children grow up thinking these are healthy options.  Finally, this blog post does not contain a comprehensive analysis of saturated fat intake and health outcomes in children, but the USDA’s new regulations should have been accompanied by one.  In other words, these regulations should not have been based on the studies discussed above, but the studies discussed above should have been considered when the USDA was crafting their recommendations.  Obviously, they weren’t.

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sucrose, visceral fat, et al.

Sugar-containing beverages vs. visceral fat

or

The malevolence of regular (non-diet) soda

 

Background: visceral fat is an ectopic lipid storage site which is associated with a host of problems.  The amount of visceral, but not subcutaneous fat correlates very well with insulin sensitivity.  The figure below is from a classic paper which showed just that (Banerji, Lebovitz, et al., 1997 AJP).  On the left is a plot of subcutaneous fat vs. glucose disposal (a measurement of insulin sensitivity), and there is no clear relationship.  On the right, however, shows a strong negative correlation of visceral fat and insulin sensitivity.

Visceral fat is associated with insulin resistance, which is a precursor to type II diabetes.  So, what causes fat storage in visceral adipose tissue (besides hyperinsulinemia)?

Sucrose-sweetened beverages increase fat storage in the liver, muscle and visceral fat depot: a 6-mo randomized intervention study (Maersk, Richelsen, et al., 2011 AJCN)

If you just started drinking a few cans of soda per day without intentionally changing anything else, this is what would happen.  The control groups got milk (isocaloric), diet soda, or water.  Food intake and physical activity was similar at baseline and during the intervention.

Figure 1 takes the cake:

Visceral fat, the most unhealthy fat depot, increased markedly in the group consuming regular cola, while it decreased in those drinking milk.  Diet soda or water had no effect.  A similar trend occurred with liver fat, probably the second-most unhealthy fat depot.  Same thing for muscle fat.

And from what we can infer, these effects were independent from energy balance (similar food intake and physical activity before and during the intervention).  Food intake data weren’t presented, but we’re told it was similar in all four groups.  Given these food intake-independent changes in body weight, energy expenditure data would have been a great addition to this manuscript.

The exoneration of diet soda?  In this study, the diet soda group seemed to win, with the best overall changes in body composition as per percent body fat.

And while those consuming milk gained the most weight, they gained muscle (possibly due to the higher protein content of milk).  AND the diet soda group gained the second highest amount of muscle (possibly due to the nutrient partitioning effects of caffeine, although that explanation is admittedly a bit of a reach).  The only differences in macronutrient intake were due to the beverages in question.

Food intake data should’ve been presented and measurements of energy expenditure would’ve added a lot.  The composition of the beverages and resulting changes in body weight/composition suggest no major deviations in the Laws of Energy Balance, and the changes in muscle mass make sense with what we know about dietary protein and sugar.  Furthermore, there is good reason to believe the observed malevolent effects of regular non-diet soda are true.

Similar results were seen in a well-controlled study where isocaloric glucose or fructose-containing beverages were given to overweight/obese humans for 10 weeks (Stanhope, Havel, et al., 2009 JCI):

Also similar to 3 weeks of 80 grams sucrose per day given to healthy young men (Aeberli, Berneis, et al., 2011 AJCN):

(waist circumference is a reasonably good marker for visceral fat)

The former studies have been of the [stronger] intervention type, but the same thing is seen in observational studies (Pollock, Dong, et al., 2011 AJCN).  This next study is of particular importance because it is in children.  The major sources of fructose were fruit juice and regular soda.  Elevated visceral fat is observed as early as 14-18 years of age!

What is most relevant about this study is that kids who drank the most fruit juice and soda were beginning to show signs of pre-diabetes and elevated inflammatory markers.  In kids.

there’s nothing redeeming about sucrose or its partner in crime fructose.

 

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Fructose vs. The Laws of Energy Balance

Exclusively from literature featured in past blog posts, e.g. HERE and HERE, excessive fructose consumption seriously deranges metabolism.  Furthermore, fructose pre-disposes to and exacerbates leptin resistance, which is one of the most proximal causes of obesity viz. overeating.  However, this doesn’t exonerate processed foods, modern grain-based diets, or trans-fats because they frequently co-exist.  Many popular breakfast cereals contain all three, and IMO a fructose-free breakfast cereal wouldn’t do much in the treatment and/or prevention of obesity.  Just eat better.  And we might even get “low-fructose” foods on grocery store shelves in the near future (but don’t hold your breath, food companies LOVE their fructose).

Consuming fructose-sweetened, not glucose-sweetened, beverages increases visceral adiposity and lipids and decreases insulin sensitivity in overweight/obese humans (Stanhope et al., 2009 Journal of Clinical Intervention)

Consumption of fructose-sweetened beverages for 10 weeks reduces net fat oxidation and energy expenditure in overweight/obese men and women (Cox et al., 2011 European Journal of Clinical Nutrition)

Metabolic responses to prolonged consumption of glucose- and fructose-sweetened beverages are not associated with postprandial or 24-h glucose and insulin excursions (Stanhope et al., 2011 American Journal of Clinical Nutrition)

These studies came out in a few separate publications, were ultra-high budget, and used very advanced techniques to quantify energy expenditure and body composition.  AND much care was taken to ensure the subjects were truly weight stable when appropriate (inpatients for two weeks in the beginning and end of the study so all of their food intake and anthropological measurements could be assessed accurately).  The experiment consisted of feeding subjects a sugar-sweetened beverage, either glucose or fructose, equivalent to 25% of their daily energy requirements.

During the inpatient portions, subjects were fed a standardized diet of 15% protein, 20% fat, and 55% carb:

Note the differences in GI & GL (bottom two rows).   Fructose has a negligible impact on glycemia because, well, it’s fructose (not glucose), and it doesn’t magically transform into glucose after ingestion.

When left to their own free will, the patients pretty much ate the same:

In general, after a period of adaptation, their intake of other foods should have declined by 25% to compensate for the additional calories from the sugar drinks, but sugar seems to hijack the appetite set point – first row in the table above; calories were 20-25% higher, almost the exact amount of calories in their sugar drinks – therefore all subjects gained a few pounds (1% of initial body weight) (and then they went back on good behavior when they were being observed in the metabolic ward):

Herein we have the first unexpected pearl: the fructose group gained visceral fat (VAT) whereas the glucose group gained subcutaneous fat (SCAT) (eerily similar to what is seen with trans-fats!).

Exhibit A:

The glucose group actually gained slightly more fat mass than the fructose group, but most of the excess weight was deposited in the relatively inert SCAT, or “extraabdominal” regions.  The fructose group, on the other hand, gained it all in VAT (apple, not pear).  Abdominal fat and waist circumference increased significantly in the fructose drinkers.  FYI that is very interesting.  And it wasn’t caused by individual differences- it’s not like some people were more predisposed to gain more VAT than SCAT; these subjects were randomized.  Diet, or more specifically, dietary sugars caused this differential fat storage.  Amazing.

Exhibit B:

This figure shows the differences in fat gain.  The glucose group gained less VAT than SCAT, while the fructose group did the opposite.  Genetics had nothing to do with this.  It is diet.  It is nutrition.  For the love of God people, it is nutrition.

In lieu of the recent publication by Dr. Bray, it is interesting to note the second pearl: an example of the irrelevance of the laws of thermodynamics (universal) with respect to the Laws of Energy Balance (conjured up by yours truly).  Namely, energy expenditure is affected by the diet… IOW, the laws of thermodynamics are not violated, but all calories are not equal (THERE. I said it… on the record, in cyberspace, for all of eternity).

This nuance is introduced in figure 2:

Divide and conquer

On the left, fat oxidation is slightly lower in the glucose group.  This is expected, because carb oxidation should have increased due to the increased carb consumption (in the form of the glucose drink).  But as seen in the right panel, fat oxidation declined significantly in the fructose group.  From this, we would expect fat gain to be greater in the fructose group compared to the glucose group … but it wasn’t.  Artefact?  Error in measurement?  I don’t know how, but this appears to be a violation of the Laws of Energy Balance (which is impossible).  UNLESS energy expenditure declined more in the fructose group than in the glucose group.

Exhibit C:

And it did!  Both groups increased their sugar consumption (by design), and energy expenditure declined in both groups (they all gained weight).  The fructose group gained about a pound less than the glucose group, but consumed slightly fewer calories on average.  So the reduced fat oxidation didn’t enhance fat gain in the fructose group because food intake declined proportionately; and they maintained energy balance relative to the glucose group because energy expenditure was slightly lower (this is complicated).

To be clear, the fructose-induced VAT deposition is not explained by reduced fat oxidation as that would imply less fat gain overall, relative to the glucose group (which didn’t happen).

Fructose-induced VAT deposition is a product of the deranged nutrient partitioning caused by fructose itself.  It’s a dangerous lil’ bugger.  How does fructose conspire with the metabolic machinery to selectively enhance visceral adiposity?  Not sure, but it might have something to do with insulin.  Glucose but not fructose stimulates insulin secretion, and SCAT is more sensitive to the anti-lipolytic effects of insulin than VAT.  The overall fat gain was similar in both groups, in accord with the Laws of Energy Balance.   But insulin tends to drive fat into metabolically safer SCAT.  An example of this concept in practice can be seen by looking at obese insulin resistant people.  In this population, SCAT is less responsive to insulin, relativeto lean people, and indeed, they have significantly greater visceral fat mass.  So fructose doesn’t trigger an insulin response, which means excess calories are less likely to be stored in SCAT, but since this can’t violate the Laws of Energy Balance the calories must go somewhere…  deposited into the notorious VAT bank where they not only still make you fat but also initiate a storm of metabolic abnormalities.

 

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Nutrition under attack

Global nutrition is in a state of emergency

Tax this:

Not this:

 

If you catch a whiff of anyone talking about a dietary fat tax here in the states, attack!  Hold no bars.

Passage of the Danish saturated fat tax confirms the shit hit the fan.  They should’ve taxed people for being fat (to offset the increased medical and healthcare costs associated with obesity), or sugars (for making people fat).  Instead, the food companies, famous for crafting thousands of varieties of Danish pastries, lobbied for the taxes to be levied against dietary fat.  This “inadvertently” encourages people to consume more Danish pastries with only 7 grams of saturated fat yet 39 grams of sugar!  The tax will favor Pop Tarts over eggs, and this is supposed to make people healthier?

A dietary fat tax is particularly troublesome because it strikes an expensive blow against real whole foods like eggs, butter, and meat, while leaving unscathed processed foods like doughnuts, refined grains, and SUGAR.  This disproportionately affects healthy foods that are in no way responsible for the obesity epidemic.

My suggestions:

1)      Leave people alone.

2)      A better target, which would entail markedly less collateral damage, is “added” sugars.  Taxing “added” sugars would hit soda, processed food-like products, snacks, and junk food… lots of bad guys, few good guys

3)      Make a tax based on empty calories: foods with a higher ratio of calories to nutrients get taxed more than nutrient-dense foods… thus, people would be eating fewer calories but more nutrients!  That wasn’t too hard?

4)      Tax food in direct proportion to its shelf-life.

5)      The revenue from any of these alternative options should be put toward nutrition education programs in elementary schools.  And a portion of the money saved in healthcare costs should be redirected into funding research in the nutritional sciences.  And the rest can be used to pay off the National debt.

 

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Hedonism, take II

 

More on the relationship between obesity, delicious food, and the magic of gastric bypass.

Roux-en-Y gastric bypass surgery changes food reward in rats (Shin et al., 2011 Intl Journal of Obesity)

I wish I knew how, but this study definitely shares a theme with the remarkable effects of a bland diet and spontaneously reduced caloric intake in obese but not lean subjects, (from the first post in this series, found here).

In brief, there were 3 groups of rats in this study: 1) diet-induced obese (“sham”); 2) diet-induced obese rats that underwent gastric bypass surgery (“RYGB”); 3) chow-fed lean controls (“lean”).  The dietary regimen was a kerfuffle, but that wasn’t really the point of the study; to make the rats obese, they were given standard chow, a purified high sugar high fat diet, and chocolate-flavoured Ensure all at once…  and we have no idea how much of each they were consuming :/    But here’s the nutrient breakdown of each anyway, by calories: 

and here is a rough ingredient list:

HFD, high fat high sugar diet

They performed a battery of psychological evaluations designed to empirically measure how much an animal “wants” or “likes” a rewarding food.  Call me simple, but I would’ve rather just seen how much of each of the above diets the rats consumed when presented with all 3 simultaneously.  If most of their calories came from the sweet chocolate-flavored Ensure, then I’d say they still liked rewarding foods.  If on the other hand they selected more of the sugar-free chow, then they probably don’t care as much for rewarding food.  Maybe this wouldn’t fly in psychonutrition circles, but I don’t really think such circles exist.  Alternatively, would RYGB rats have lost more weight if they were fed exclusively chow compared to those given Ensure?  Fortunately, this question was addressed in an earlier manuscript by Zheng (Meal patterns, satiety, and food choice in a rat model of Roux-en-Y gastric bypass surgery [Zheng, Berthoud, et al., 2009 AJP])

When given the sugar-free chow diet, the control rats eat less.  When given a high sugar high fat diet, the control rats eat more.  RYGB rats don’t seem to care.  But that’s kind of exactly what Shin showed by complicated psychological tests:

Lean and sham (obese) rats like a very sweet beverage (1.0 M sucrose) significantly more than a more bland solution (0.01 M sucrose).  RYGB rats don’t seem to care.  This was repeated to a tee in another group of “obesity-prone” rats suggesting it might be a true product of the gastric bypass surgery:

And oddly enough, human subjects that have undergone roux-en-Y gastric bypass surgery seem to be able to detect much lower concentrations of sucrose but not like it as much (they can “taste” it more, but might not “like” it more)  (they are satisfied with less-sweet foods) (Changes in patients’ taste acuity after Roux-en-Y gastric bypass for clinically severe obesity [Burge et al., 1995 JADA])

 

 

Are these findings related to obese humans who spontaneously consume significantly less of a bland diet?  (recall obese but not lean human subjects lost weight on the bland diet).  Similarly, rats consume significantly more of a tasty junk-food cafeteria diet.  There is definitely something magical about roux-en-Y gastric bypass surgery; it is the single most effective treatment [cure] for obesity.  Obese humans eat less of a bland diet, roux-en-Y gastric bypass surgery decreases the “liking” of a sugar-rich beverage (but enhances one’s ability to detect sucrose)… RYGB and that bland diet caused massive weight loss in their respective [obese] subjects…   These things just have to be related, my spidey-sense is going wild

 

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