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Occasional Insanity Outperforms Daily Misery: Day-Hiking Mt. Whitney, Fasted

“Why Are We Hungry?” will return next week. Meanwhile, I recommend you read it starting from Part I if you haven’t already, because Part III, and particularly Part IV, throw quite a bit of light on currently hot issues.

Adaptation to endurance exercise is important, because our ability to burn fat for energy is important:

J Appl Physiol. 1984 Apr;56(4):831-8.
Adaptations of skeletal muscle to endurance exercise and their metabolic consequences.
Holloszy JO, Coyle EF.

The major metabolic consequences of the adaptations of muscle to endurance exercise are a slower utilization of muscle glycogen and blood glucose, a greater reliance on fat oxidation, and less lactate production during exercise of a given intensity. These adaptations play an important role in the large increase in the ability to perform prolonged strenuous exercise that occurs in response to endurance exercise training.

However, one of the biggest problems with endurance training is diminishing returns. Holloszy and Coyle again:

Regularly performed endurance exercise induces major adaptations in skeletal muscle. These include increases in the mitochondrial content and respiratory capacity of the muscle fibers. As a consequence of the increase in mitochondria, exercise of the same intensity results in a disturbance in homeostasis that is smaller in trained than in untrained muscles.

Furthermore, though prolonged endurance exercise results in greatly increased fat oxidation, it also causes a period of decreased mitochondrial efficiency that lasts for at least 28 hours afterward…and probably longer.

Maria Fernström,1,2 Linda Bakkman,1,2 Michail Tonkonogi,2,3 Irina G. Shabalina,2 Zinaida Rozhdestvenskaya,2 C. Mikael Mattsson,1,2 Jonas K. Enqvist,1,2 Björn Ekblom,1,2 and Kent Sahlin1,2
Reduced efficiency, but increased fat oxidation, in mitochondria from human skeletal muscle after 24-h ultraendurance exercise
Journal of Applied Physiology May 2007 vol. 102 no. 5 1844-1849

The most important novel findings of the present study were that 1) mitochondrial efficiency decreased after ultraendurance exercise and remained reduced after 28 h recovery; 2) mitochondrial FA oxidation (state 3) and relative FA oxidation [PC/(PC + Pyr)] increased Post-Ex; and 3) noncoupled respiration rate (state 4) was reduced after 28 h of recovery.

Given these facts, we can easily see why “chronic cardio” produces more injuries than it does fitness. Continually pounding out the same mileage, day after day, quickly strands us on a performance plateau of diminishing returns—both in performance and in physique.

Here’s an alarming example, summarized from the above study by one of its authors:

Bakkman, Linda
Mitochondrial function adaptations to changed metabolic conditions
Department of Medicine, Solna, Karolinska Institutet, Stockholm, Sweden, 2010

“…The nine subjects were elite ultra-endurance performance athletes, all men. They had an impressive exercise background with 3-9 years of regular extreme endurance exercise and recent merits from national and international championships. … The group had a body fat content of an average 16.9% (range 10.8-26.1) of body weight, which is typical for males of their age.”

So much for the hypothesis that exercise, by itself, is enough to lose fat. If international ultra-endurance champions still carry a “typical” load of 17% bodyfat, how can the rest of us hope to attain the physique we’d like?

Beating The Law Of Diminishing Returns: Occasional Insanity Trumps Daily Misery

As Holloszy and Coyle make clear, the first feat of endurance at a given duration and intensity produces the greatest increase in respiratory capacity. So in order to bring ourselves to a high level of performance, it seems likely that occasional ridiculous efforts would produce the same adaptation as daily lower-intensity effort, for a much smaller time commitment and much less damage to our joints and heart. As I said in "Eat Like A Predator", “The only way to improve is to push your limits.”

To that end, I bring you…

22 Miles, 6200′ Up, 6200′ Down, Zero Calories: Mt. Whitney, Fasted

Inspired partially by Asclepius’ journey, I day-hiked Mt. Whitney—the tallest mountain in the 48 continental United States—on my way home, after the Ancestral Health Symposium. In other words, my training program involved sitting in a chair and listening to presentations…at sea level.

Would-be hikers start at 8,300 feet (2530 meters), and climb almost 6,200 feet (1890 meters) in 11 miles (17.7 km), on their way to the summit at 14,497 feet (4491 meters), before returning down the same trail for a total of 22 miles (35.4 km) and 12,400 feet (3780 meters) of elevation change. (Click here for relief maps, and all the information you could want about attempting it yourself.)

Most people take two or three days, camping at altitude to acclimate…but a substantial number attempt it as a day hike. Since I live at over 6000′ and am in reasonably good shape, I decided that it wasn’t enough of a challenge, and it would be a good test of my metabolic flexibility and ability to oxidize fat if I did the entire hike completely fasted. No breakfast, no energy bars, no sandwiches, no gorp, gels, blocks, shots, powders, or electrolytes. Water and my own fat would have to serve.

Did I mention I also used minimal shoes?

My hike started here, at the Whitney Portal parking lot, where delinquent bears had recently thrown a party.
Delinquent Bear Party at Whitney Portal

There is an apocryphal quote, usually attributed to a Yosemite park ranger, about designing bear-proof containers: “There is considerable overlap between the intelligence of the smartest bears and the dumbest tourists.”

These food storage boxes were installed so that people don’t leave food in their cars at the trailhead: even a small black bear can easily break into a car, using nothing but its own strength. I suspect what happened here is that some people didn’t properly close the “bear boxes” after stashing their own food. There are two kinds of bear box: one uses a simple hidden latch, but the ones pictured use a sort of Allen key on a chain and are much trickier to open and close.

I found one of the simple ‘hidden latch’ type, and my cooler was safe upon my return.

2000 feet of altitude and several miles later, Whitney Portal is barely visible, with the Owens Valley beyond.
Looking down at Whitney Portal

A record snow year meant the creeks were still running. Balance was required.
Agility puzzle on Whitney Portal trail
Agility puzzle on Whitney Portal trail

This is the last tree you’ll see. Note the saddle in the far distance: that’s where the previous picture of the Owens Valley was taken from, just a couple hours ago.
Treeline

Now we’re in the high alpine. Progress slows somewhat at 13,600′ altitude, and I admit to having felt somewhat lightheaded. I’m not sure whether it was a lack of air or lack of calories, but a short rest at Trail Crest solved my problems.
Trail Crest

Looking the other direction from Trail Crest:
High alpine from Whitney trail(The haze in the valley is due to a large wildfire to the south.)

This hike isn’t like running 22 miles on flat pavement: there are many miles of trail that look much like this:
Rough trail

And this:
Rough trail 2

But persistence and a steady pace soon placed me at the summit. Note the cheap skate shoes—which were actually quite functional, having both great ground feel and robust toe protection:
Summit plaque

Whereupon I enjoyed stunning views of the entire Eastern Sierra that photographs simply cannot convey, and a relaxed hour or so on top of the world.
View from Whitney summit

Life establishes itself anywhere it can, even at 14,000 feet:
Life hangs on at 14,000 feet

And on sheer granite walls, where every shelf and crevice supports a tree:
Life hangs on

The pictures end here, but the hike continued. I must admit that the final few miles, descending from Outpost Camp, were a grind…I wasn’t desperate or in pain, but I was quite ready to be back at my car, sitting down and eating the delicious gravlax, Greek yogurt, and blueberries I had stashed in a cooler.

Some notes on the journey and recovery, in no particular order:

  • I didn’t feel hungry at all during the entire six-hour descent from the peak—and my hunger was totally manageable on the way up. Eating a diet high in saturated fats, primarily from meat and coconuts, appears to have increased my ability to oxidize my own fat for energy.
  • I had to stop and rest a couple times on the ascent, but I never felt drained or helpless…just like I had got a bit ahead of my ability to produce energy.
  • Since I wasn’t eating, I didn’t need to drink much water. In fact, though I brought water bottles, I only ended up drinking water where it was naturally available—so I could have done the entire hike carrying nothing but a windbreaker! (Note: not recommended.)
  • Another benefit: Mt. Whitney is very heavily traveled, so hikers must pack out all their own poop. Not eating also meant not having to poop in a bag and carry it around with me all day.
  • I felt fine the next day, though not sprightly, and hiked perhaps another seven miles. Neither was my appetite out of control: my body only went into recovery mode once I did nothing for most of a day, whereupon my appetite and sleep deficit caught up with me. (It felt like I was ready to keep going as long as there was a crisis, and my body only demanded recovery once the crisis was over.)
  • I am not, to my knowledge, a gifted athlete. This is not a feat out of reach for any reasonably healthy human, given proper diet and a level of regular physical activity. (If you haven’t ever walked five miles on flat ground, Mt. Whitney is not the place to start.) What will stop you is injuries or degenerative disease, which are your real limitations.
  • I could have easily kept hiking if I had to. My feet hurt a little from walking on sharp rocks all day, but I still had energy left to keep going.

To elaborate on this last point: Our capacity for energy storage, as fat, is basically infinite as it applies to a single day of physical effort, or even multiple days: 3500 calories per pound of fat goes a long way. Our limitation is the rate at which we can burn it for energy…

…and that is what we increase by pushing the limits of our endurance: the base rate at which we can keep going all day, and all night if we must. Fat oxidation is the foundation atop which all our impressive feats of momentary strength and quickness are built.

Where Are Your Limits?

We’re all quite comfortable here at our computers, with a solid roof over our heads, central heating, clean running water, enough to eat, and an only mildly dysfunctional government and police force…

…but life isn’t always so easy. Earthquakes and tornadoes, floods and tsunamis, wars and revolutions, genocides and epidemics and famines. The Rape of Nanking, the Trail of Tears, the Indonesian Tsunami, the Spanish flu, the Cultural Revolution, … the death toll of natural and human-caused disasters is beyond all comprehension.

Ask yourself: would you be a victim, a refugee, or an emigrant?

Live in freedom, live in beauty.

JS


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The Science Behind The “Low Carb Flu”, and How To Regain Your Metabolic Flexibility

Caution: contains SCIENCE!

Important note! For a more up-to-date exploration of this subject, I strongly recommend my 2013 AHS presentation “What Is Metabolic Flexibility, And Why Is It Important?”

Most of us who eat a low-carbohydrate diet—Paleo, Primal, Atkins, or otherwise—experience anywhere from a couple days to a couple weeks of low energy as we adjust to it, an experience known informally as the “low carb flu”. And some people never seem to adjust.

Here’s why—and here are some ideas that might help you if you’re having trouble adjusting!

Note that low-carb isn’t an objective of a paleo diet: it’s just the usual consequence of eliminating grains and sugars.

It’s certainly possible to eat a higher-carb paleo diet—and it’s a good idea if you’re doing frequent, intense workouts like HIIT, Crossfit, or team sports after school—but you’d have to eat a lot of potatoes and bananas to get anywhere near the same amount of carbohydrate you used to get from bread, pasta, cereal, and soda.

Burning Food For Energy: Glycolysis and Beta-Oxidation

Our bodies have several ways to turn stored or ingested energy into the metabolic energy required to move around and stay alive. This is called cellular respiration.

The two main types of cellular respiration are anaerobic (which does not require oxygen) and aerobic (which requires oxygen). Anaerobic metabolism, also known as fermentation, is nineteen times less efficient—and we can only maintain it for short periods, because its waste products build up very quickly. This is why we can’t sprint for long distances.

We spend most of our time in aerobic metabolism. Our two primary aerobic sources of energy are glycolysis, which converts glucose to energy, and beta-oxidation, which converts fat to energy.

A Short Metabolic Digression Explaining The Above (Optional)

Strictly speaking, glycolysis is the start of both the aerobic and anaerobic oxidation of glucose: it converts glucose to pyruvate.

In the aerobic oxidation of glucose, the pyruvate is transported into the mitochondria, whereupon it is converted to acetyl-CoA and fed into the TCA cycle (aka the citric acid cycle or Krebs cycle, depending on how long ago you took your biology course.) This produces 19 times more energy than the original glycolysis!

In the anaerobic oxidation of glucose (“lactic acid fermentation”), the pyruvate is instead converted to lactic acid, which produces no more energy.

In the aerobic oxidation of fat (“beta-oxidation”), the fat is transported into the mitochondria, whereupon it is sliced up into individual acetyl-CoA molecules, each of which enters the TCA cycle.

Humans have no way to anaerobically oxidize fat.

I put this here because pictures of molecules are scientific!

A graphic flowchart of glycolysis. You know it's SCIENCE! because there are a lot of molecules and arrows.

Lots of fine print = SCIENCE!

And here's a flowchart of beta-oxidation.



Glucose is the simple sugar all cells use for glycolysis, and it’s the most common. The other simple sugars we can digest are galactose (found primarily in milk), which we convert to glucose—and fructose (found primarily in fruit, table sugar, corn syrup, and honey), which our liver converts directly to glycogen or fat.

Starch is just a bunch of glucose molecules stuck together. In fact, “complex carbohydrates” in general are just sugars stuck together…and we can only absorb them through the intestine once they are broken down into individual simple sugars by our digestive system. In other words, all “carbohydrates” are just sugar.

There is a lot more to talk about here, including glycogen storage and retrieval, gluconeogenesis, and de novo lipogenesis…but explaining all the pathways of digestion, energy storage, and cellular respiration would be an entire book in itself!

Moving on: while it’s OK for fat to hang around in our bloodstream for a while, high blood sugar is actively toxic to our tissues. (The long-term consequences of untreated diabetes—heart, kidney, nerve, eye, and muscle damage, leading to numbness, blindness, amputations, strokes, and death—are basically just long-term glucose poisoning.) So after we eat something containing any amount of carbohydrate, insulin ensures that the glucose is immediately taken into our cells and either burned for energy, stored, or converted into palmitic acid—a saturated fat!

This is why a “low-fat, high-carb” diet is really a high-fat diet. Unless your “high-carb” diet involves an intravenous glucose drip carefully metered to keep your blood sugar constant, most of the ‘carbohydrates’ (sugars) you eat will be converted either to glycogen or to palmitic acid (again, a saturated fat) before you use them. “Soluble fiber” and other indigestible carbohydrates are fermented into short-chain saturated fats, like butyric acid, in your colon. Fructose, of course, is converted directly to liver glycogen or to palmitic acid. And if you’re losing weight by burning your own fat, keep in mind that human fat has roughly the same composition as lard—approximately 40% saturated!

You might ask yourself if it makes sense that natural selection would select us to store energy in the form of something directly harmful to us. If saturated fat is really so terrible, and polyunsaturated fat is really so healthy, why doesn’t our body store energy as linoleic acid, like grains do?

Metabolic Flexibility and the Respiratory Exchange Ratio

If we have excess glucose in our bloodstream, our muscles will burn it first, because it’s toxic. But eventually we run out of glucose, and that’s when our bodies need to switch over to beta-oxidation—burning fat. The ability to switch back and forth between the two processes is called “metabolic flexibility” in the scientific literature.

Metabolic flexibility varies dramatically from individual to individual, which we would expect based on the widely varying experiences people report with low-carb diets. So how do scientists figure out what fuel our bodies are burning?

It turns out that beta-oxidation (fat-burning) produces less carbon dioxide than glycolysis (sugar-burning)—and we can measure that in our breath. The ratio of CO2 to O2 is 0.7 for beta-oxidation and 1.0 for glycolysis…so an RER (Respiratory Exchange Ratio) of 0.7 indicates pure fat-burning, and 1.0 and above indicates pure sugar burning. (You can read more about the RER here.)

Typical healthy people have a resting, fasting RER of approximately 0.8. Therefore, we can easily see that the frequent vegetarian and vegan claims of “Nothing else can provide any energy without first being converted to carbs” and “You can get plenty of energy from fat, but you have to go into ketosis to do it” are—like most nutritional claims made by veg*ans—complete bunk.

Metabolic Flexibility: The “Low Carb Flu” Is Not Your Imagination

It shouldn’t be a surprise that the obese and diabetic tend to have higher resting RERs, and that higher RER is a significant predictor of future obesity. If our ability to burn fat for energy is impaired, we’re going to have a hard time losing weight, and we’ll become ravenously hungry when our blood sugar runs out no matter how much fat we have available to burn.

Is this sounding familiar to anyone?

Sounds like the “low carb flu”, doesn’t it? When we talk about our metabolic “set point”, part of what we’re talking about is metabolic flexibility. It does no good to have a huge store of fat if we can’t burn it for energy!

Int J Obes Relat Metab Disord. 1992 Sep;16(9):667-74.
Fasting respiratory exchange ratio and resting metabolic rate as predictors of weight gain: the Baltimore Longitudinal Study on Aging.
Seidell JC, Muller DC, Sorkin JD, Andres R.

“…The adjusted relative risk of gaining 5 kg or more in initially non-obese men with a fasting RER of 0.85 or more was calculated to be 2.42 (95% confidence interval: 1.10-5.32) compared to men with a fasting RER less than 0.76.”

Furthermore, it turns out that people with a family history of type II diabetes, but who don’t yet have it themselves, have higher RERs and impaired metabolic flexibility.

Diabetes August 2007 vol. 56 no. 8 2046-2053
Impaired Fat Oxidation After a Single High-Fat Meal in Insulin-Sensitive Nondiabetic Individuals With a Family History of Type 2 Diabetes
Leonie K. Heilbronn1, Søren Gregersen2, Deepali Shirkhedkar1, Dachun Hu1, Lesley V. Campbell1

“…An impaired ability to increase fatty acid oxidation precedes the development of insulin resistance in genetically susceptible individuals.”

Also see:

AJP – Endo November 1990 vol. 259 no. 5 E650-E657
Low ratio of fat to carbohydrate oxidation as predictor of weight gain: study of 24-h RQ
F. Zurlo, S. Lillioja, A. Esposito-Del Puente, B. L. Nyomba, I. Raz, M. F. Saad, B. A. Swinburn, W. C. Knowler, C. Bogardus, and E. Ravussin

This is very important: we can see that impaired fat oxidation must be related to the causes, not the consequences, of obesity and diabetes. So we’ve struck another blow to “calories in, calories out”, and the idea that you’re fat just because you’re lazy.

In support of this theory, I note this paper, which contains the following graph of several individuals’ RER in response to a high-fat diet vs. a moderate-fat diet. Keep in mind that the change was only from 37% to 50% fat, which is relatively minor, and the paper doesn’t tell us what fats were being consumed…but this graph is still instructive:

The top graph is the average, the bottom graph is for each individual. Note that some adapted right away, some took several days, and some were still not adapted on day 4!

Higher RER isn’t all bad. It’s associated with having more fast-twitch muscle fibers, which are associated with a greater ability to build muscle mass. This fits the anecdotal evidence that people who gain fat easily also tend to gain muscle easily, whereas skinny people have a much harder time bulking up.

So maybe you’re lucky, or already in good health, and you adapt relatively quickly to a low-carb diet. But what if you’re not? What if you’re stuck with the “low carb flu”?

Regaining Your Metabolic Flexibility

Obviously we’d like to regain our metabolic flexibility. But how? Here’s one way:

Journal of Applied Physiology September 2008 vol. 105 no. 3 825-831
Separate and combined effects of exercise training and weight loss on exercise efficiency and substrate oxidation
Francesca Amati,1 John J. Dubé,2 Chris Shay,3 and Bret H. Goodpaster1,2

“…Exercise training, either alone or in combination with weight loss, increases both exercise efficiency and the utilization of fat during moderate physical activity in previously sedentary, obese older adults. Weight loss alone, however, significantly improves neither efficiency nor utilization of fat during exercise.

Diabetes September 2003 vol. 52 no. 9 2191-2197
Enhanced Fat Oxidation Through Physical Activity Is Associated With Improvements in Insulin Sensitivity in Obesity
Bret H. Goodpaster, Andreas Katsiaras and David E. Kelley

“Rates of fat oxidation following an overnight fast increased (1.16 ± 0.06 to 1.36 ± 0.05 mg · min−1 · kg FFM−1; P < 0.05), and the proportion of energy derived from fat increased from 38 to 52%." October 15, 2009 The Journal of Physiology, 587, 4949-4961. Improved insulin sensitivity after weight loss and exercise training is mediated by a reduction in plasma fatty acid mobilization, not enhanced oxidative capacity
Simon Schenk1, Matthew P. Harber1, Cara R. Shrivastava1, Charles F. Burant1,2 and Jeffrey F. Horowitz1

“…Resting fatty acid oxidation was unchanged after the intervention in WL [weight loss]. Consistent with an increase in maximal oxidative capacity, resting whole-body fatty acid oxidation was increased more than 20% after WL + EX [weight loss + exercise].”

In other words, despite the title, weight loss plus exercise increased resting fat oxidation…but just losing weight did not!

AJP – Endo April 2008 vol. 294 no. 4 E726-E732
Skeletal muscle lipid oxidation and obesity: influence of weight loss and exercise
Jason R. Berggren,1,2 Kristen E. Boyle,1,2 William H. Chapman,4 and Joseph A. Houmard1,2,3

“10 consecutive days of exercise training increased (P ≤ 0.05) FAO [fatty acid oxidation] in the skeletal muscle of lean (+1.7-fold), obese (+1.8-fold), and previously extremely obese subjects after weight loss (+2.6-fold)…These data indicate that a defect in the ability to oxidize lipid in skeletal muscle is evident with obesity, which is corrected with exercise training but persists after weight loss.”

How about that? It turns out that exercise is important after all…not because of the calories you burn by exercising, which you usually replace right away because you’re hungry, but because it helps you regain metabolic flexibility. Exercise stimulates your body to burn more fat, both during exercise and at rest.

And that’s what health is about: we’re not interested in losing weight if it just means losing muscle. We’re interested in losing fat.

There are other benefits beyond fat loss, too: exercise tends to normalize broken metabolisms.

Diabetes March 2010 vol. 59 no. 3 572-579
Restoration of Muscle Mitochondrial Function and Metabolic Flexibility in Type 2 Diabetes by Exercise Training Is Paralleled by Increased Myocellular Fat Storage and Improved Insulin Sensitivity
Ruth C.R. Meex1, Vera B. Schrauwen-Hinderling2,3, Esther Moonen-Kornips1,2, Gert Schaart1, Marco Mensink4, Esther Phielix2, Tineke van de Weijer2, Jean-Pierre Sels5, Patrick Schrauwen2 and Matthijs K.C. Hesselink1

“Mitochondrial function was lower in type 2 diabetic compared with control subjects (P = 0.03), improved by training in control subjects (28% increase; P = 0.02), and restored to control values in type 2 diabetic subjects (48% increase; P < 0.01). Insulin sensitivity tended to improve in control subjects (delta Rd 8% increase; P = 0.08) and improved significantly in type 2 diabetic subjects (delta Rd 63% increase; P < 0.01). Suppression of insulin-stimulated endogenous glucose production improved in both groups (−64%; P < 0.01 in control subjects and −52% in diabetic subjects; P < 0.01). After training, metabolic flexibility in type 2 diabetic subjects was restored (delta respiratory exchange ratio 63% increase; P = 0.01) but was unchanged in control subjects (delta respiratory exchange ratio 7% increase; P = 0.22).”

Did you catch that? “Metabolic flexibility in type 2 diabetic subjects was restored”?

Unfortunately, this study didn’t measure resting fat oxidation, like the others—but it does suggest that there’s no need to kill yourself with “Biggest Loser”-style misery. 30 minutes of cycling at 55% of maximum effort twice a week, and one session of weight training once a week, was enough to restore metabolic flexibility. That doesn’t sound very intimidating, does it? (And there are many better and more entertaining ways to get half an hour of moderate aerobic exercise than sitting on a stationary bike.)

“Aerobic exercise was carried out on a cycling ergometer twice a week for 30 min at 55% of a previously determined maximal work load (Wmax). Resistance exercise was performed once a week and comprised one series of eight repetitions at 55% of subjects’ previously determined maximal voluntary contraction (MVC) and two series of eight repetitions at 75% MVC and focused on large muscle groups (Chest press, leg extension, lat pull down, leg press, triceps curls, biceps curls, abdominal crunches, and horizontal row).”

…Yet You Must Take Advantage Of Your Newfound Metabolic Flexibility

Of course, our newly-regained flexibility won’t help if we stuff ourselves with the government-recommended 7-11 servings of “heart-healthy whole grains” (= “carbs”, = sugar) per day, because we will be constantly burning sugar. Only when we’re done burning glucose can we use our newfound flexibility to burn some fat.

That’s one reason, among many, why I eat a paleo diet—and why I don’t snack. (For more on that subject, read “Why Snacking Makes You Weak, Not Just Fat”.)

A Short Digression: Please Stay Off The “Faileo Diet”

Some ‘paleo’ books still insist that saturated fat is bad for you and paleolithic people didn’t eat much of it, which is absolute nonsense. But your calories have to come from somewhere…if not fat, then from protein or carbohydrates. And since those same books also usually disallow potatoes and other convenient sources of starch, you’re basically stuck eating lots of lean protein.

As a result, you’ll eat very few calories, because of the satiating effect of protein—which is fine if you’re just trying to lose weight, but disastrous if you’re physically active, because you’ll be perpetually exhausted. This is why fat-phobic ‘paleo’ is sometimes called the “Faileo Diet”.

The Difference Between Beta-Oxidation and Ketosis

Here’s where I say something that might be controversial: I think going cold-turkey VLC (very low carb) or zero-carb makes the transition much harder, particularly for people who are already physically active.

Beta-oxidation (fat-burning) occurs nearly continually, and produces much of our energy at rest once insulin has cleared any sugar spike out of our system. However, our body does have some requirement for glucose, which it satisfies in the short-term primarily by having the liver make it—a process called gluconeogenesis.

If we eat zero carbs, or very few, over a period of time, our body enters a state called ketosis, in which some of our tissues that used to require glucose shift over to burning ketone bodies, which are alternative products of fat metabolism. And while it is true that our brains and hearts actually run more efficiently on ketones, it takes several weeks for our bodies to fully adapt. Meanwhile, we lack energy for high-effort activities, because our muscles are depleted of glycogen, which is made from glucose.

So you might not have the “low-carb flu”—you might be stuck in an unnecessary multi-week rut of keto-adaptation.

Interested in learning more about ketosis? Read Stephen Phinney’s “Ketogenic Diets and Physical Performance” (Nut Metab 2004, 1:2) for more information about ketosis and the process of keto-adaptation. Once you’ve read that, if you’re deeply interested in the ketotic state, try ketotic.org…and if you’re interested in a ketogenic diet that isn’t nutrient-deficient or disgusting, try these articles from the Drs. Jaminet (Ketogenic Diets I, Ketogenic Diets II).

There is a persistent myth that ketosis is dangerous: it’s not. People (including some doctors) commonly confuse it with ketoacidosis, a pathological state usually only found in uncontrolled diabetics and (rarely) raging alcoholics.

Even worse, you might be stuck in the state informally known as “Low Carb Limbo”—in which you’re eating too few carbohydrates to fuel high-effort, glycolytic activity, but too many carbohydrates to ever keto-adapt.

If you’re active and determined to keto-adapt, read this excellent article from Primal North, “Keto-Adaptation vs. Low Carb Limbo”.

Conclusion: Stay Out Of The Muddy Middle

In summary, it’s much easier and quicker to burn fat via beta-oxidation than it is to adapt to ketosis…so unless ketosis is your goal, you might be making your transition to a healthy diet much harder by keeping your carb intake too low.

I think that if we keep our carbohydrate intake near our body’s requirement while not in ketosis, which is perhaps 15-20% of total calories—and only eat those carbohydrates with meals involving complete protein and fat, not by themselves—most of us should be able to gain the fat-burning benefits of metabolic flexibility without suffering the pain of trying to adapt to ketosis. So if you’re new to Paleo or low-carb eating, you’re stuck with long-term “low-carb flu”, and especially if you’re already physically active, try adding some root starches like potatoes or sweet potatoes to your meals. (Or white rice, if you’re following the Perfect Health Diet.)

(And if you’re determined to keto-adapt, go fully ketogenic, as per “Keto-Adaptation vs. Low Carb Limbo.”)

Live in freedom, live in beauty.

JS

For more information, continue reading my 2013 AHS presentation “What Is Metabolic Flexibility, And Why Is It Important?”


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