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Why Snacking Makes You Weak, Not Just Fat

Caution: contains SCIENCE!

All of us want to stay as strong and fit as we can, with as little effort as we can…and the profusion of ridiculous exercise gadgets and workout books testifies to our desire to look like fitness models, while living and eating like Homer Simpson.

What we want...

...and what we get.


However, the government-recommended “food pyramid”—and its inevitable consequence, sugar (‘carbohydrate’) addiction—sabotages our efforts to be healthy and strong. Snacking doesn’t just make us fat…it makes us weak.

To explain why, we need to review some metabolic facts.

Insulin: The Storage Hormone

Our bodies strongly regulate ‘blood sugar’, which is just the amount of free glucose in our bloodstream. Under normal circumstances, this is about a teaspoon.

If we don’t have enough glucose in our blood, our cells start dying very quickly, starting with our brain. If we have too much, it slowly poisons the kidneys, eyes, heart, and circulatory system—and we experience all the complications of untreated diabetes, such as numbness, blindness, muscle wasting, gangrene, renal failure, and heart failure.

When we eat and digest food, its nutrients are absorbed into our blood, through our intestines. If that food contains glucose (‘starch’, ‘carbohydrate’, ‘sugar’)—or certain amino acids (‘protein’)—our pancreas secrete a hormone called insulin, which signals cells all over our bodies to take these nutrients out of our bloodstream and store them. This keeps our blood sugar from getting too high.

Since there’s a lot more than a teaspoon worth of glucose in most foods (look on the ingredient label: most of “Total Carbohydrate” is glucose), it’s obvious that both our pancreas’ production of insulin, and our cells’ response to insulin, has to be solid and well-regulated, or we will have major health problems—which we call diabetes.

(Diabetes is just long-term glucose poisoning. Type I diabetes is when your blood sugar stays high because your pancreas can’t make insulin. Type II diabetes is when your blood sugar stays high because your body stops responding to insulin.)

Here’s another important metabolic fact: unlike body fat, which is a dedicated organ for storing energy in the form of…fat, our body has no dedicated storage organ for protein. (Recall that “protein” is just chains of amino acids.) Our body’s tissues—primarily our muscles—do double duty here. Muscles move our bodies, and they provide a storage reserve for our body’s daily protein needs.

This is why long-term fasting, or protein deprivation, causes you to lose muscle: your body disassembles it for the amino acids it needs every day to maintain itself.

Insulin, Proteolysis, and Protein Synthesis: It’s Not Just About Blood Sugar

Insulin has many effects in the body, not all of which are completely understood. Click the image for a long discussion.

Now we are getting to the meat of the story.

There is an interesting fact about insulin: it doesn’t just cause our bodies to store fat, and it doesn’t just cause our bodies to try and build muscles and tissues. It also tends to inhibit proteolysis, which is the process by which our bodies break down our own tissues (again, primarily our skeletal muscles) for protein.

But it doesn’t always do this.

Am J Physiol. 1993 Nov;265(5 Pt 1):E715-21.
Acute hyperglycemia enhances proteolysis in normal man.
Flakoll PJ, Hill JO, Abumrad NN.

Skipping to the middle of the text:

“Previous studies from our laboratory have indicated that the effect of insulin on suppressing proteolysis is highly dependent on the availability of plasma amino acids. […] At maximal insulin levels…protein breakdown was suppressed by approximately 90% when amino acids were available compared with 45% when hypoaminoacidemia was allowed to develop. These studies were performed with glucose fixed at euglycemic levels.”

So we know that insulin + available protein = 90% reduction in proteolysis, while insulin + no available protein = 45% reduction in proteolysis. Now we return to the abstract:

“ABSTRACT: The influence of hyperinsulinemic-hyperglycemia on protein and carbohydrate homeostasis was assessed using L-[1-13C]-leucine and [3-3H]glucose combined with open-circuit indirect calorimetry. After a 30-min basal period, healthy human volunteers were subjected to two sequential experimental periods (150 min each) during which insulin was continuously infused at a rate to elicit maximal effects (10.0 mU.kg-1 x min-1, resulting in 220-fold basal levels) in conjunction with an infusion of L-amino acids to maintain euleucinemia. Plasma glucose was maintained near basal (94 +/- 2 mg/dl) during period I and at twofold basal (191 +/- 4 mg/dl) during period II. The endogenous rate of leucine appearance (index of proteolysis in mumol.kg-1 x h-1) dropped by 80% from basal during period I (P < 0.01) but only by 44% during period II. […] The present study demonstrates that, during hyperinsulinemia, acute elevations of plasma glucose to two times basal levels result in a marked stimulation of whole body proteolysis during hyperinsulinemia.”

And now we also know that normal blood sugar + maximal insulin = 80% reduction in proteolysis, whereas high blood sugar + maximal insulin = 44% reduction in proteolysis.

These are two very interesting sets of facts. Here’s the summary:

  • Insulin increases whole-body protein synthesis…but the protein has to come from somewhere.
  • If protein is available in the bloodsteam and your blood sugar is normal, insulin almost completely stops the process of breaking down your muscles for your protein needs. This makes sense: why break down muscle when protein is already available?
  • If protein is unavailable in the bloodstream, insulin only halfway stops this process. This also makes sense: if protein is unavailable from the food you ate, you still need to get it from somewhere.
  • If your blood sugar is high (twice normal), insulin stimulates whole body proteolysis.

And here’s the takeaway:

Every time you stimulate insulin production by eating carbohydrates, you need to eat some complete protein with it—or instead of rebuilding your muscles and tissues, your body will continue to disassemble itself to get that protein. And the higher your blood sugar spikes, the more your body will disassemble itself anyway.

Are you seeing the problem? When you eat, insulin signals your body to stop eating itself…but only if you’ve eaten protein, and only if your blood sugar isn’t spiking.

Every time you eat candy or drink a soda by itself, not only are you signaling your body to store fat…you’re disassembling your own muscle.

It’s even worse. That ‘healthy’ mid-afternoon apple or orange, to keep your blood sugar up? Same problem. And remember the food pyramid? Those “7-11 servings of heart-healthy whole grains” we’re all supposed to be eating every day? How are you going to stuff eleven servings into three meals?

You’re not: you’re going to snack.

That’s what we’re advised: never, ever let yourself get hungry. Keep your bloodstream filled with sugar and insulin at all times! So that’s what we do. Crackers, bagels, muffins, corn chips, rice cakes, cookies, danishes…all low-fat, of course.

And, even worse, low-protein. Being grain and sugar-based, snack foods contain little protein—and the protein they do contain is incomplete. (Corn and wheat are deficient in lysine, one of the essential amino acids.) If your body is short on any essential amino acid, it will still have to disassemble itself to get the one it needs, regardless of how much of all the others are available.

Every time you eat high-sugar, protein-deficient food—even whole fruit and “heart-healthy complex carbohydrates”—you’re making yourself fatter and weaker.

In support of this theory:

Ann Surg. 2005 Feb;241(2):334-42.
Influence of metformin on glucose intolerance and muscle catabolism following severe burn injury.
Gore DC, Wolf SE, Sanford A, Herndon DN, Wolfe RR.

Metformin administration was also associated with a significant increase in the fractional synthetic rate of muscle protein and improvement in net muscle protein balance. Glucose kinetics and muscle protein metabolism were not significantly altered in the patients receiving placebo.

CONCLUSIONS: Metformin attenuates hyperglycemia and increases muscle protein synthesis in severely burned patients, thereby indicating a metabolic link between hyperglycemia and muscle loss following severe injury.”

Why would giving a diabetes drug to burn victims cause them to heal more quickly? Because metformin stops the liver from making glucose—lowering blood sugar.

Conclusion: Snacking Makes You Fat, And Snacking Makes You Weak

This explains a lot, doesn’t it? Why so many joggers can pound out hundreds of miles and still squeeze up muffin tops? Why so many cyclists can spin for thousands of miles and still have to stuff a beer gut into their Lycra? Why even the skinny ones often look like famine victims—not like strong, healthy, capable humans? And why you never look like the people in the magazine ads, no matter how long you spend on the hamster wheels at the gym?

This helps explain why so many vegans (especially raw vegans) appear scrawny and malnourished. Fruit might have some nutrients in it, but it’s still essentially protein-less sugar.

It also helps explain why obesity with Type II diabetes is so difficult to recover from: high blood sugar keeps you from building muscle like a normal person. (There are many other positive feedback loops in obesity and diabetes…this is just one of them.)

Not only does that post-workout bran muffin contain more calories than you burned—it’s making you fat, and you’re still losing the muscle you’re trying to build.

It’s not the “food pyramid”—it’s the “fat pyramid.”

Stop eating birdseed (‘grains’) and diesel fuel (‘vegetable oil’).
Start eating real food.
Live in freedom, live in beauty.

JS


Postscript: How Do I Stop Snacking, And What Do I Eat Instead?

Answer: eat real food and you won’t need to snack. Here’s how I stay lean and strong with very little effort.

For more information, you can read my three-part series on carbohydrate addiction: Mechanisms of Sugar Addiction, “Adjacent To This Complete Breakfast!”, and The Myth Of Complex Carbohydrates.

Important note! Forwarding this article using the buttons below makes you 17% sexier.

The Lipid Hypothesis Has Officially Failed
(Part 1 of many)

In 1977, the US Government issued its first dietary recommendations: eat less fat and cholesterol, and more carbohydrates.  Yeah, that worked.

Feel free to hotlink this image so long as you also make the image a link to http://www.gnolls.org, or put a visible link to gnolls.org under it.

Thanks to George McGovern and the “United States Senate Select Committee on Nutrition and Human Needs” for killing millions of people via the consequences of obesity—diabetes, heart disease, depression, cancer, dementia, stroke, osteoarthritis, and a host of other totally preventable maladies.

Seriously: we let a Senate committee decide what was healthy to eat? I guess we got what we deserved.

“Low-Calorie” Foods Made Us Fat

To forestall the inevitable cascade of reflexive defenses of the status quo, which are “We started eating more junk food”, “We started eating more food generally. Calories in, calories out” and “People got lazy and stopped exercising”, I’ll point the skeptics to the following study, which uses the same data set (NHANES) as the graph:

The American Journal of Medicine Volume 102, Issue 3 , Pages 259-264, March 1997. Divergent trends in obesity and fat intake patterns: The american paradox. MD Adrian F. Heini, MD, DrPH Roland L. Weinsier

RESULTS: In the adult US population the prevalence of overweight rose from 25.4% from 1976 to 1980 to 33.3% from 1988 to 1991, a 31% increase.
    [WIth a 55% increase in obesity and a 214% increase in extreme obesity. See the original NHANES data.]
During the same period, average fat intake, adjusted for total calories, dropped from 41.0% to 36.6%, an 11% decrease.
    [We were doing exactly what we were told to do: eat less fat.]
Average total daily calorie intake also tended to decrease, from 1,854 kcal to 1,785 kcal (−4%). Men and women had similar trends.
    [Look at that! We weren’t eating any more food…but, somehow, we got fatter anyway.]
Concurrently, there was a dramatic rise in the percentage of the US population consuming low-calorie products, from 19% of the population in 1978 to 76% in 1991.
    [Again, we were doing exactly what we were told to do: eat low-fat, high-carb products.]
From 1986 to 1991 the prevalence of sedentary lifestyle represented almost 60% of the US population, with no change over time.
    [So we weren’t exercising any less, either.]

In other words, we were eating the same number of calories, eating dramatically more low-calorie, low-fat ‘health food’, and exercising the same amount…but we got dramatically fatter!

Why does the “low-fat, high-carb” weight loss strategy fail? Start here with “Why You’re Addicted To Bread”. And here’s how I eat: “Eat Like A Predator, Not Like Prey”.

Then, continue to Part 2!

Live in freedom, live in beauty.

JS

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Fat And Glycemic Index: The Myth Of “Complex Carbohydrates”

(This article is Part III of a series on carbohydrate addiction. Each part stands alone, but I recommend starting with Part I, “Why You’re Addicted To Bread“, as it explains the fundamentals. Part II is here.)

The Mystery of the Flour Tortilla

This article started when I asked a simple question: “Why do flour tortillas have such a low glycemic index?”

The humble flour tortilla tops any list of low glycemic index grain products, with a GI of only 30. Yet whole-wheat bread has a GI of 71! (Source.)

Why is that?

“Complex Carbohydrates”…Not So Complex After All

Most low-fat diet pushers (from Pritikin, to Ornish, to the ADA and US government, to vegan fronts like the PCRM) make a big noise about “complex carbohydrates”. The theory goes like this: Table sugar is made of just two simple sugars, glucose and fructose. That’s bad, because it digests too quickly for our body to use all of it—whereupon the excess is turned into fat, stored as fat, and we’re hungry again. In contrast, the ‘complex carbohydrates’ in whole-grain products are good because they digest more slowly, allowing our body to use all of them. Right?

Wrong.

As described in Part I, whole wheat bread (71) has the same glycemic index as white bread (72), and both of them have a higher GI than white table sugar (62)! This fact alone proves that the theory of “complex carbs” is flawed: our bodies absorb the sugar from that ‘healthy’ whole wheat bread more quickly than…pure table sugar.

Low Glycemic Index: What’s Responsible?

So what’s the real story behind glycemic index? Why do we digest some ‘carbohydrates’ (sugars) so much more slowly than others? And how does a flour tortilla top the list?

Answer: it’s the fat.

  • Mexican flour tortillas have a GI of 30, whereas American whole wheat bread has a GI of 72. Remember, you need plenty of lard (or, at least, grain oil) to make a nice, flat, chewy tortilla.
  • A plain French baguette has a sky-high glycemic index of 95: spread some butter and jam on it, and the GI declines to 65.
  • Cooked white rice has 0.2% fat and a GI of 64; a meal of white boiled rice, grilled hamburger, cheese, and butter has a GI of 24.
  • A Pizza Hut Super Supreme pizza (13.2% fat) has a GI of 30, whereas a Vegetarian Supreme (7.8% fat) has a GI of 49.
    (Source.)

This is common sense once we think about it for a minute. As anyone who’s taken a freshman nutrition class can tell you, fat inhibits gastric emptying and slows digestion. For example:

Pierre Thouvenot, C Latge, M-H Laurens, and J-M Antoine. Fat and starch gastric emptying rate in humans: a reproducibility study of a double-isotopic technique. Am J Clin Nutr 1994;59(suppl):781S.

Executive Summary: A high-fat mixture of egg yolks, olive oil, and butter left the stomach over 50% slower than spaghetti…and that doesn’t even count the time taken to digest it in the intestine. (Also note that spaghetti has a glycemic index of 38-61, depending on cooking time—much lower than bread or cereal at 70-80.)

In conclusion, the theory of “complex carbs” is a red herring. The primary driver of glycemic index is fat content. The more fat, the slower the sugars (‘carbohydrates’) are digested, and the lower the glycemic index.

(Yes, it is possible to make lower-GI pure carbohydrates: a wheat ‘bread’ containing 80% intact kernels gets down to a GI of 52…just under a Snickers bar at 55. But wait…80% intact kernels? That’s not bread…that’s a cake of birdseed! I’ve never even seen that sold in a store, let alone watched someone actually try to eat it.)

Conclusion: A Low-Fat Diet Means A High Glycemic Index Diet

When we take fat out of our diet and replace it with ‘carbohydrates’ (sugars), the glycemic index of the food we eat goes up dramatically.

This has obvious negative consequences for our health and weight, and I’m going to highlight it, because it’s the key to this article:

High-GI ‘carbohydrates’ (sugars), simple or complex, are digested far more quickly than we can burn them for energy, whereupon our bodies convert them into fat and store them as fat—leaving us hungry, even though we are gaining weight!

Then, we get a transient dopamine rush and subsequent serotonin high before our blood sugar crashes, but that decreases over time as we get fatter—meaning that we are chemically as well as metabolically addicted to sugar (‘carbohydrates’).

Does this situation sound familiar? You’re told to take those ‘unhealthy’ fatty foods out of your diet—and suddenly you’re either hungry and miserable, or you’re gaining weight uncontrollably. Ever wonder why you don’t feel full no matter how many plain bagels, glasses of skim milk, cups of low-fat yogurt, and boxes of fat-free Fig Newtons you eat…yet you still have the compulsion to keep eating?

Even worse, if this vicious cycle of goes on long enough, you become insulin-resistant, and then diabetic. Isn’t this what’s happening to all of America? Our ‘obesity epidemic’ started once we told people to avoid fat at all costs…

…and now you know why. It’s because by removing fat from your diet, you’re turning everything you eat into candy.

Incredible but true fact: a medium Jamba Juice fruit smoothie (‘Berry Lime Sublime’) has substantially more calories (487) than a Quarter Pounder (417)—and a large has almost as many calories (610) as a Double Quarter Pounder (647)!

Which one will leave you feeling like you ate a meal, and which one will leave you still hungry?

...than the Quarter Pounder!

This has more calories...


But Isn’t Fat Bad For You? Science Says “No.”

We’ve been told for decades that fat and cholesterol are bad, and saturated fat will kill you. That is, stated baldly, a lie.

There is no association between saturated fat intake and heart disease, and there is no association between egg intake (the largest source of dietary cholesterol) and heart disease.

Patty W Siri-Tarino, Qi Sun, Frank B Hu, and Ronald M Krauss. Meta-analysis of prospective cohort studies evaluating the association of saturated fat with cardiovascular disease. Am J Clin Nutr Jan 2010

“A meta-analysis of prospective epidemiologic studies showed that there is no significant evidence for concluding that dietary saturated fat is associated with an increased risk of CHD or CVD.
[…]
“The pooled relative risk estimates that compared extreme quantiles of saturated fat intake were 1.07 (95% CI: 0.96, 1.19; P = 0.22) for CHD, 0.81 (95% CI: 0.62, 1.05; P = 0.11) for stroke, and 1.00 (95% CI: 0.89, 1.11; P = 0.95) for CVD. Consideration of age, sex, and study quality did not change the results. “

Here’s the layman’s version, from Scientific American:

Carbs Against Cardio: More Evidence that Refined Carbohydrates, not Fats, Threaten the Heart“, Scientific American, May 2010

“…The quintile of women who ate the most easily digestible and readily absorbed carbohydrates—that is, those with the highest glycemic index—were 47 percent more likely to acquire type 2 diabetes than those in the quintile with the lowest average glycemic-index score.” … “women who were overweight and in the quartile that consumed meals with the highest average glycemic load, a metric that incorporates portion size, were 79 percent more likely to develop coronary vascular disease than overweight women in the lowest quartile.”

“The next time you eat a piece of buttered toast, [Ludwig] says, consider that ‘butter is actually the more healthful component.'”

Moving on to eggs:

Public Health Nutr. 2010 Jul 16:1-10. Egg consumption and CHD and stroke mortality: a prospective study of US adults. Scrafford CG, Tran NL, Barraj LM, Mink PJ.

“We did not find a significant positive association between egg consumption and increased risk of mortality from CHD or stroke in the US population. These results corroborate the findings of previous studies.”

So: eat fatty meats, eat eggs, eat avocados. Cook with butter, tallow, and coconut oil, and perhaps some extra-virgin olive oil for taste. And if you absolutely must eat candy in the form of bread, cereal, or potatoes, eat them with plenty of butter, olive oil, cream, and whole milk.

Sounds a lot better than rice cakes and dry toast, doesn’t it?

Live in freedom, live in beauty.

JS


Postscript: if you want to know how we got bamboozled into believing that foods we’ve eaten for millions of years (meat) were bad for us, but industrial products that didn’t even exist until this century (‘vegetable oil‘) were good for us, you can watch Tom Naughton’s entertaining presentation “Big Fat Fiasco”, available here and on DVD here.

(This is Part III. Go back to Part I, Part II.)

“So what do YOU eat?” you ask. Click here for my classic article “Eat Like A Predator”.

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