Category Archives: Fructose

CARBOTOXICITY [screaming face emoji]

Noxious Effects of Exaggerated Carbohydrate Intake (Kroemer et al., 2018)

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This blog post is about the above mentioned article. Disclaimer (qualm #1): it is very pro-low carb and refused to include any neutral or negative points about low carb. For example, had it been within the scope of the article, the authors may have said despite excluding the majority of carbohydrate-containing foods, low carb diets actually aren’t restrictive at all. In other words, this is not an unbiased review article.

 

 

Qualm #2: the authors say people have long-recognized the problems of lipid excess and it even has a name, “lipotoxicity.” But these revolutionaries thought the problems of carbohydrate excess need to be recognized so they coined the term “carbotoxicity.” Are we to believe these dorks never heard of “glucotoxicity” even though it was coined before lipotoxicity even was?!

The review is about the molecular, cellular, and neuroendocrine mechanisms that link a prolonged energy surplus to disease and accelerated aging. It doesn’t really distinguish how the energy surplus is established, specifically, but every now and then they throw out there “carbz.” Ignoring that, there are actually some pretty good points.

The history of dietary carbs had three major, transformative steps. The first was the transition from hunter-gatherers to agriculture which shifted the carbs from fruits, seeds, tubers, nuts, roots, and bulbs to a range of cereals (in Europe), rice (in Asia), corn (in Mesoamerica), and potatoes (in South America). And in Weston Price fashion, this was associated with an increase in dental cavities (probably more cause than correlation here).

Acarbose blocks carb digestion, D-glucosamine blocks glycolysis.

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Keto myths & facts

:::begin rant:::

Trigger warning?  Maybe.

Disclaimer: I’m pro-LC (P<0.05), but not anti-LF because LF works better than LC for some people.  And with the exception of things like keto for neurological issues, I think macros take a back seat to many other factors.

Myths: carbs cause insulin resistance (IR), diabetes, and metabolic syndrome.  Carbs are intrinsically pathogenic.  If a healthy person eats carbs, eventually they’ll get sick.

And the only prescription is more keto.

cowbell

And of course all of this could’ve been prevented if they keto’d from the get-go.

Proponents of these myths are referring to regular food carbs, not limited to things like Oreo Coolattas (which would be more acceptable, imo).  Taubes, Lustig, Attia, and many others have backed away from their anti-carb positions, yet the new brigade proceeds and has even upped the ante to include starvation.  Because “LC = effortless fasting?”

Does this sound sane?

“No carbs ever,
no food often…
otherwise diabetes.”

oreo-coolatta

no one in their right mind would say lentils & beans cause diabetes

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Summer is fattening. Don’t do it in winter.

Seasonal eating proper

More on seasonal eating in what appears to be the primary model for its justification for use in humans – hibernating mammals.

How it goes, or so they say: in summer, hibernators massively overeat, including carb-rich foods, in order to generate muscle and liver insulin resistance, so as to promote body fat growth.  The long light cycle reduces evening melatonin, which pushes back the usual nighttime peak in prolactin, which causes an abnormal resistance to leptin, which induces hypothalamic NPY and subsequent carbohydrate craving.  Ergo, summer is fattening.  In today’s day, increased artificial lights guarantee year-round pseudo-summer; and we no longer experience the benefits of the short light cycle: longer sleep times (akin to hibernation) and fasting – either complete fasting as in hibernation, or pseudo-fasting, ie, a ketogenic diet.

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Silent Leptin Resistance

Conventional leptin resistance has something do with obesity.  It is known.  Silent leptin resistance is … err … complicated. 

Divide and conquer

Fructose-induced leptin resistance exacerbates weight gain in response to subsequent high-fat feeding (Shapiro, Scarpace, et al., 2008 AJP)

A remarkable 60% fructose diet fed to rats for 6 months had absolutely no effect on energy balance.  Nil. QED.
Fig 1

Food intake and body weight were unaffected because the levels of and sensitivity to endogenous leptin were identical in both groups.

Enter the Dragon

Enter the Dragon

“Silent Leptin Resistance” – The fructose-fed rats are, however, profoundly resistant to the satiating effects of Metreleptin (a pharmaceutical grade injectable leptin analog):

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salt makes you thirsty, soda makes you hungry.

As previously discussed, DRINK was a randomized intervention study that gave children either regular or diet soda for a year and surprise surprise, the regular soda drinkers gained about more body fat than the diet soda drinkers (de Ruyter et al., 2012).  And in the follow-up, with an opposite study design, overweight & obese children who continued to drink regular soda gained twice as much weight as those who cut their intake (Ebbeling et al., 2012).  There was no apparent black box in the latter study as the kids who stopped drinking soda also decreased their intake of other foods…

-does not compute-fructose

wait a minute … By switching from regular soda to diet, you just end up compensating by eating more of something else, right?  My initial response to that has always been that it doesn’t matter – ANYTHING else is better than a straight shot of 100% HFCS (+ some other chemicals).  But those kids didn’t do that.  they ate less of other foods.

 

Does HFCS soda make you eat more?

A recent study has put a little more fuel on this fire.  Similar to the abovementioned two, it’s not a sophisticated study designed to accurately assess the impact of regular soda on appetite, satiety, hunger, etc., but it supports the theory that diet soda negative calories are NOT compensated for by eating more of something else.


Food and beverages associated with higher intake of sugar-sweetened beverages (Mathias et al., 2013)

It was another big cross-sectional NHANES study that simply asked how much regular soda, diet soda, and other foods kids were eating.Mathias data 1

They showed that as soda intake increased, so did total calories, which could simply mean the soda was adding calories to their diets.  This would indirectly support the opposite of the above mentioned theory, namely, that soda calories aren’t compensated for.  But it gets better (or worse, depending how you look at it):Mathias data 2

soda didn’t simply add to the total calorie intake.  More often than not, calorie intake increased above and beyond that contributed by the soda.  And it wasn’t just that bigger kids were drinking more soda and eating more food – these data were controlled for body weight.  The authors estimated that for every 100 kcal of soda drank, an additional 36 – 86 kcal of food was eaten.

salt makes you thirsty, and now soda makes you hungry?

 

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Corn. A riddle, wrapped in a mystery, inside an enigma.

Utterly.  Shocked.  is how I feel gazing upon the ingredients listed on one particular popular snack food.  And it isn’t one of those fancy gourmet all-natural whole food snacks, it is a classic that is probably in the kitchen of every child-wielding household.

Corn, corn oil, and salt.  And salt doesn’t even count, so it might just as well have said corn and corn oil, which could be summarized as “corn.”  Ladies and gentlemen, I present to you, the reigning champion of snack food sorcery, the red-headed stepchild (no offense) of international superpower PepsiCo… Fritos.  Using only corn, the wizards of Frito-Lay are turning this:into this:

and that’s without the use of trans fat, gluten, artificial additives, dairy, msg, onions, or soy.  They’re Kosher too.

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what is our proper “natural” diet?

Figuring out how best to eat, physiological insulin resistance, and an homage to pioneering nutrition research.

Insulin resistance, as we know it today, is associated with poor nutrition, obesity, and the metabolic syndrome.  But it’s FAR more interesting than that.  Indeed, it could even save your life.  At the time when the pioneering studies discussed below were occurring, the researchers had no idea insulin resistance was going to become one of the most important health maladies over the course of the following century.  Furthermore, these somewhat-primitive studies also shed some light, possibly, on how we should be eating.  hint: it might all come down to physiological insulin resistance.

The reduced sensitivity to insulin of rats and mice fed on a carbohydrate-free, excess fat diet (Bainbridge 1925, Journal of Physiology)

Rats were fed either a normal starch-based diet (low fat), or a high butter diet (low carb) for one month, then fasted overnight and injected with a whopping dose of insulin (4 U/kg).  First, take a guess, what do you think happened and why.  Then, click on the table below.

To make a long story short, all the starch-fed rats died while all the butter-fed rats lived.

On a high-fat zero-carb diet, plasma insulin levels are low.  Insulin is low because there no carbs (i.e., it’s supposed to be low).  Under conditions of low insulin, unrestrained adipose tissue lipolysis leads to a mass exodus of fatty acids from adipose tissue.  These fatty acids accumulate in skeletal muscle and liver rendering these tissues insulin resistant.  But this doesn’t matter, because insulin sensitivity is unnecessary when there aren’t any carbs around.  So if that rogue research scientist who’s always trying to jab you with a syringe filled with insulin actually succeeds, you won’t die.  The high-fat diet prevents insulin-induced hypoglycemic death.  This is physiological and absolutely critical insulin resistance.

To determine if this was specific to dairy (butter) or a general effect of a high fat zero carb diet, Bainbridge repeated the experiments with lard.  Lo-and-behold, lard-fed rats were just as fine as those dining on butter.  

To be sure, these studies exhibited a high degree of animal cruelty… but their simplicity is laudable.  And Bainbridge’s findings are not an isolated case.

Studies on the metabolism of animals on a carbohydrate-free diet.  Variations in the sensitivity towards insulin of different species of animals on carbohydrate-free diets (Hynd and Rotter, 1931)

Instead of starch, lard, and butter, Hynd and Rotter used milk and bread, cheese, and casein.  And their findings were essentially identical to Bainbridge’s: mice, rats, or rabbits fed carbohydrate-free diets were insulin resistant and protected against insulin-induced tragedies.

The interesting finding was in kittens, who sadly maintained insulin sensitivity when fed fish (high protein) or cream (high fat).

You’re probably thinking: why would I say any state of heightened insulin sensitivity is “sad?”  WELL, I say “sad” because we’re talking about physiological insulin resistance; a condition when resistance to the hypoglycemic effect of insulin is essential, and lack thereof is incompatible with survival.  To be clear: 1) kittens remain insulin sensitive on high fat and protein diets; and 2) this is OK because there aren’t any rogue research scientists running around trying to jab them with insulin.  While I can’t say for sure, this might have something to do with what kittens are supposed to eat, i.e., their natural diet.  High protein and fat diets won’t make them insulin resistant because unlike rodents, that is their normal diet.  (real mice eat fruits and seeds; laboratory mice eat pelleted rodent chow; cartoon mice eat cheese.)   Lard causes ectopic lipid deposition in insulin sensitive tissues in rodents because they aren’t accustomed to it.  Mice are optimized to eat a high carb diet.  Kittens eat protein and fat, usually in the form of mice.  But when given bread, kittens develop insulin resistance.  There is no bread in mice.

While we shouldn’t base our diet around the possibility of turning a corner and being jabbed with a syringe filled with insulin, perhaps we are simply more similar to kittens.  Hypercaloric diets loaded with sugar, excess carbohydrates, and empty calories cause [pathological] insulin resistance (which could theoretically save your life if a rogue research scientist jabbed you with insulin), whereas the opposite is true for diets high in fat and protein.  This is repeatedly demonstrated in diet intervention studies, most recently in the notorious Ebbeling study (Missing: 300 kilocalories).  When people were assigned to the very low carbohydrate diet, insulin sensitivity was significantly higher than when they were on low fat diets:Soapbox rant: I’m not saying low carb is what we are supposed to eat.  Nor am I saying it is the optimal diet.  IMHO any diet which excludes processed junk food and empty calories is “healthy.”  The Paleo diet isn’t healthy because some nutritionista says it’s what we are supposed to eat; Paleo is healthy for the same reason as Atkins, Zone, South Beach, and a million others: no junk food.

Maybe the diet we’re supposed to eat has nothing to do with the healthiest diet.  Maybe not.  But it probably isn’t bad for you.  just sayin’

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Non-sequiter nutrition II, a sugar-thought experiment

The average western diet contains about 50 grams of fructose from a variety of sources ranging from beneficial fibrous fruits to the more insidious sugar-sweetened beverages, soda and juice.  50 grams of fructose.   2 1/2 cans of Coca-Cola.

50 grams x 4 kcal/g = 200 kcal

200 kcal / 2,000 kcal = 10%

10% of your calories are provided by fructose

Even the very high end of fructose intake rarely exceeds ~85 grams, which is still < 20%.  My point?   This is nowhere near the 60% used in mouse diet studies.  Disclaimer: I think fructose causes leptin resistance because of data from such studies.  60% fructose is the fructose that causes leptin resistance and increased susceptibility to obesity.  What does this say about “normal” levels of fructose intake?  Toxic doses cause leptin resistance and obesity susceptibility in mice, well, because they’re toxic, and fructose toxicity just so happens to manifest like that (in mice).   60% is toxic.  15 cans of Coca-Cola per day (depending on who’s counting); but is it relevant?

39 grams of sugar, roughly half of which is fructose

In mouse studies, toxic doses are used for practical reasons- it’s cheap.  The animals can be rendered leptin resistant, glucose intolerant, and susceptible to obesity within a few months of feeding this expensive purified synthetic diet.  This probably (probably) takes over 100 times longer in humans simply because it’s nearly impossible for humans to ingest mouse-toxic-levels of fructose.

1. If the dose was based on body weight (like a drug; e.g., mg/kg or mpk):

60% fructose x 12 kcal/d = 7.2 kcal.  Divided by 4 kcal/g = 1.8 grams per day.

1.8 grams for a 40 g mouse = 45 g/kg.  For a 70 kg (154 lb) human = 3,150 grams of fructose or roughly 12,600 kcal.  I.e., 150 cans of soda or about a week’s worth of calories.  In other words, you’d have to eat a hypercaloric fructose-only diet for months.

2. If the dose was based on calories:

60% fructose x 2,000 kcal/d = 300 grams = 15 cans of soda or doughnuts per day.   News flash: that’s gross, but it won’t kill you.

fructose: still not as dangerous as playing in traffic

How about just lowering your lifetime sugar exposure.  39 grams of sugar is worse than 0.01 grams of stevia or sucralose.  Anyone remember “water?”  Even if you believe “a calorie is a calorie,” exclusively, it’s still really hard to burn off 39 grams of sugar.  Try running 2 miles.  Skinny kids might do this automatically after drinking a can of soda or eating a doughnut.  Not most adults.

Don’t play in traffic either.

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Decepticon Promicor (soluble corn fiber), Op. 81

I heard a comedian say he wished exercise was like high school; once you get your diploma, that’s it.  You never need to do high school again.  Unfortunately, the same isn’t true with artificial nutrition.  the mad food scientists are at it again.

Enter: Soluble corn fiber (SCF), mass produced by Megatron Promitor

Over a decade ago, Atkins released low carb bars.  Well, they weren’t actually low carb per se, they were low sugar.  This was accomplished by replacing sugar with glycerol (a sugar alcohol) and polydextrose (a pseudo-fiber).  While their bars are made from cheap ingredients and low quality protein, sugar alcohols and pseudo-fibers are certainly better than sugar.

Later, sugar alcohols took off in popularity, appearing in Met-Rx Protein Plus, Detour Lean Muscle, Dymatize Elite Gourmet, etc., etc.  Glycerol was prominent in Labrada and Pure Protein bars.  Supreme Protein bars use glycerol and maltitol, and a LOT of ‘em.  Quest took a stand against glycerol and uses the lower calorie and more stomach-friendly erythritol (if it ends in “-ol,” its probably an alcohol).

More recently, the field took a considerable philosophical leap forward and starting using real fiber, good fiber.  Inulin appeared in some Atkins bars, VPX Zero Impact, and the original Quest bars.  Quest has since switched to another good fiber, isomalto-oligosaccharides.  Unfortunately no one is using GOS, yet, but they will … mark my words (that’s a prediction, or stock tip… not a threat).

But now the field has taken a turn and we have another artificial ingredient, a pseudo-fiber, with which to deal.  “Soluble corn fiber (SCF)” first appeared in Splenda Fiber packets and then in Promax LS bars.

If you’re like me, you’re asking yourself: what is this stuff?  Is it real fiber?  Is it like the super fibers inulin and GOS?  Hello Pubmed

Divide and conquer

Stewart (2010) compared SCF to 3 other fibers and maltodextrin, 12 g/d x 2 weeks =

Pullulan, a rather potent fiber, is not well-tolerated.  Resistant starch (an insoluble fiber), soluble fiber dextrin, and SCF were all OK.  The gut microbiota seemed to have no preference, as short chain fatty acid production was similar in all groups (perhaps 12 grams is subthreshold?).  Similarly, health biomarkers, hunger levels, and body weight were unaffected.

Boler (2010) compared a commercially available SCF preparation to polydextrose, 21 grams per day for 21 days in 21 healthy men (cute.)

NFC, no fiber control; PDX, polydextrose; SCF, soluble corn fiber

In this study, however, SCF didn’t do so well.  It caused gas and reflux.  Perhaps this wasn’t observed in Stewart’s study because of the lower dose (12 vs. 21 grams).  Furthermore, polydextrose reduced while SCF increased short chain fatty acid production, both of which resulting in a higher acetate:butyrate ratio.  So unlike 12 grams of any of Stewart’s fibers (including SCF), the gut microbiota seems to respond to 21 grams of SCF.  And they pooped more (both fiber groups).

Data are expressed as log cfu/g feces.

Interestingly, SCF was remarkably bifidogenic.  Much more so than PDX, MOS (see Yen et al., 2011), and inulin (see Menne et al., 2000), but WAY less than GOS (see Silk et al. 2009).

the holy grail

This same group reported a more detailed analysis of the gut microbiota which unfortunately did NOT exactly confirm their earlier finding (Hooda et al., 2012):

Data presentation is different in the two publications, and if both are true, then SCF selectively increases a few specific strains of bifidobacteria but reduces many others (enough to increase the total amount but decrease the variety).  The functional implications of this are unclear (to me).

In the meantime, SCF appears to be at most an OK pseudo-fiber substitute.  Megatron Promitor is not likely to test it against the super fibers (e.g., inulin, GOS, etc.) any time soon, so we won’t know if it’s an advance or simply a side-step.  Such is life.

 

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XL soda ban, Op. 80

People have been warned about the dangers of excess sugar consumption, but compared to the anti-smoking campaign, the recent proposal to ban XL soda’s is like bringing a cup of water to a forest fire.

In an ideal world, a proper health initiative designed to provide people (kids too) with good nutrition information would work. The new proposal takes a different route: it bans the sale of soda’s larger than 16 ounces (but you can still buy 2-12 ouncers).  I see two possible outcomes: 1) someone who would’ve bought one 24 ouncer of soda might settle for 16 ounces; 2) the one in a million customer who wanted 24 ounces will walk away with two 12 ounce sodas instead.  Win-win, right?  In the first case, the toxic sugar burden is lessened by a third.  In the second, a potentially valuable lesson on “serving size” will be on display.   Serving size 2.0, in 3-D, spelling-it-out for all to see.

It might actually work.  From a nutritional perspective, 90 grams of highly bioavailable sugar (HFCS) is a biological disaster.  Pound for pound, there aren’t many worse things you can consume… it’s the anti-thesis of “moderation.”  Regardless of your stance on the calorie debate, no one can argue that 90 grams of sugar all-at-once is more detrimental than it’s caloric content would imply.  Even for skinny people (metabolic obesity?).  It’s worse than dietary fat, and  might be THEE cause of leptin resistance.

This isn’t a TPMC original, but this graph of soda, diabetes, and obesity is just about as compelling as epidemiology can be:

 

douse those sugar cubes with artificial flavors, colors, and preservatives, and we’re good to go

If the ban goes into effect and actually impacts sales, will there be a backlash? more food company lobbying?  increased government subsidies (reduced HFCS consumption -> more taxpayer dollars used to cover the losses)?  Who knows.  If it teaches people a lesson about serving size or empty calories it might be worth it.

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