Don’t want to put on weight as you get older? Try sweet chili peppers and cold spells.


Don’t want to put on weight as you get older? Try sweet chili peppers and cold spells .

Scientists say exposure to moderately cold temperatures and a chemical found in chilies have been shown to boost levels of ‘brown fats’ linked to staving off weight gain.

Scientists have discovered that prolonged exposure to cold temperatures and eating chili peppers can help to prevent people putting on weight as they get older.

In a ground-breaking study from Japan, it has been shown that both cold and a chemical found in the peppers have similar effects in building up levels of BAT (brown adipose tissue), which helps regulate the way the body expends energy.

BAT is a kind of tissue that exists in all babies, found around the neck and chest, but which gradually breaks down as adults get older. This rate varies between people, and previous studies have proven there is a link between BAT levels dropping off and age-related weight-gain setting in.

This is the first time anyone has been able to prove BAT levels can be made to recover once lost. Scientists exposed test subjects to moderately low temperatures, around 17°C, for two hours every day over six weeks.

When compared to a control group that went about their lives as normal, those subjected to cold showed increased levels of BAT – and also lost around 5 per cent of their body fat.

While this might seem a fairly obvious outcome as the test subjects’ bodies work harder to keep warm, what was really surprising was the similar effect on BAT of consuming “capsinoids”, found predominantly in sweet chili peppers.

Capsinoids have been shown to activate temperature sensors in the gut – similar to the way hot-tasting chilies impact sensors in the mouth.

Those studied who ate large quantities of peppers were also seen to experience increases in BAT tissue – though they didn’t, yet, lose body fat. Researchers speculated that a longer study would likely show genuine weight loss to go with the recovery of BAT.

Lead researcher and report author Takeshi Yoneshiro, from the Hokkaido University Graduate School of Medicine in Japan, said: “Our results showed that human BAT could be recruited even in individuals who had lost BAT, thereby contributing to body fat reduction. This is the first report of successful recruitment of BAT leading to reduced body fat in humans.”

He added that capsinoids appear to induce so-called “brown fat” in the same way as cold by “capturing” the same cellular system that the body’s nervous system uses to increase heat production.

Source: Journal of Clinical Investigation.

Study Suggests Oregano Oil Works for Weight Loss and Inflammation


 

A new animal study shows that carvacrol, the active component of oregano oil, can actually prevent diet-induced obesity by modulating genes as well as reducing inflammation in white adipose tissue. Carvacrol (2-methyl-5-isopropylphenol) is a monoterpene phenolic constituent of the essential oil produced by numerous aromatic plants and spices such as oregano oil.

The main objective of the study was to investigate effects of carvacrol in mice fed with a high-fat diet, which is an important model and cause of modern day obesity, and to study the potential underlying mechanisms focusing on the gene expression involved in adipogenesis, thermogenesis and inflammation.

Male mice were divided in three groups: 1) those who were fed a normal diet, 2) those fed a high-fat diet,  and 3) those fed with a 0.1% carvacrol-supplemented diet. Body weight, visceral fat-pads (known as organ fat or intra-abdominal fat) and biochemical parameters were determined. Adipose tissue (connective tissue which stores fat) genes and protein expression levels were also assessed.  The mice fed with the  carvacrol-supplemented diet exhibited significantly reduced body weight gain, visceral fat-pad weights and plasma lipid levels (trygliceride and cholesterol levels) compared with mice fed with a high-fat diet.  Furthermore, the high-fat-diet induced up-regulations of adipose tissue genes and protein associated with the signaling cascades that lead to adipogenesis and inflammation but were significantly reversed by dietary carvacrol supplementation.

In summary, under experimental conditions carvacrol prevented obesity in high fat-diet fed mice by decreasing body weight, visceral fat-pad weights and lowering plasma lipid levels. The evidence obtained in this study suggests that carvacrol appears to inhibit visceral adipogenesis most likely by suppressing bone morphogenic protein-, fibroblast growth factor 1- and galanin-mediated signaling, and it also attenuates the production of pro-inflammatory cytokines in visceral adipose tissues by inhibiting toll like receptor 2 (TLR2)- and TLR4-mediated signaling.

It is significant to note that the amount of carvacrol used in the study is a typical amount that one would use when supplementing with oregano oil.  A 1500 calorie diet would need approximately 1.5 calories of carvacrol and a 2000 calorie diet would need approximately 2 calories.  If one is consuming 1500 calories per day he or she would need 166 mgs of carvacrol, or 222 mgs for a 2000 calorie diet.

According Byron Richards, CCN, “a key part of the weight gain problem for any person is that immune cells start having an inflammatory party within white adipose tissue, attracting even more immune cells and causing progressive inflammation.  This problem locks in the dysfunction of white adipose tissue and contributes to stubborn weight issues.  This is the first study showing that carvacrol can directly improve this difficult problem, helping break a vicious cycle.”

Five Scientific Studies Demonstrating that Oregano Oil is Effective in Alleviating Inflammation

The first study, published in the journal Experimental and Toxicologic Pathology, discovered that oregano oil significantly improved rat colitis, or inflammation of the colon. When compared to the control group, the oregano-treated rats showed much greater success in terms of visual disease signs such as ulceration and swelling,

In a second study, reported in the journal Mediators of Inflammation, thyme and oregano oils were used in conjunction and found to benefit colitis in mice. The oils reduced the levels of cytokines, biochemical traditionally associated with inflammation. The results found oil treatment led to lower mortality and reduced tissue damage in the animals.

A third study an investigation reported in the journal Phytomedicine examined the effects of carvacrol on liver regeneration. Carvacrol is one of the key active ingredients in oregano oil. Rats with their livers surgically removed were assigned to two different groups. One group was treated with carvacrol and the other served as the control group. The carvacrol group experienced noticeably increased liver-weight gain.

A fourth study found in Phytomedicine discovered that carvacrol protected the livers of rats that also had blood supply restricted to those organs. The investigators found that carvacrol was nontoxic to rat livers used in the study.

In the fifth and final study, published in the Proceedings of the National Academy of Sciences, found that an active ingredient in oregano can cure additional instances of inflammation. This ingredient, known as beta-carophyllin (E-BCP), was administered to mice with inflamed paws. In seven out of ten experiments, there was a subsequent improvement in inflammation symptoms. Researchers believe E-BCP might be of possible use in treating osteoporosis and arteriosclerosis.  Beta-carophyllin works by docking on specific receptor structures in the cell-membrane – the so-called cannabinoid-CB2 receptors. The result is a change in cell behavior, inhibiting the cell’s production of phlogogenic signal substances. According to investigator Dr. Jürg Gertsch, E-BCP has been used to treat mice with swollen paws due to inflammations. In 70 percent of cases where the treatment had been administered, the swelling subsequently subsided.

Many of the oils available in today’s market are derived from non-oregano species, such as various types of marjoram as well as species of thyme. Julia Lawless, author of The Encyclopedia of Essential Oils, says that the vast majority of oregano oil is not labeled correctly, because it is derived from thyme, that is Spanish thyme.  I  highly suggest using a cold-pressed pharmaceutical grade formula of Wild Organic Mediterranean Oregano with at least 79-80% carvacrol content such as  Oregasil.  This is the oregano oil that I suggest to clients as well as the one that our family uses.

Source: oawhealth.com

The skinny on cocaine. Insights into eating behavior and body weight in cocaine-dependent men.


Abstract

There is a general assumption that weight loss associated with cocaine use reflects its appetite suppressing properties. We sought to determine whether this was justified by characterizing, in detail, alterations in dietary food intake and body composition in actively using cocaine-dependent individuals. We conducted a cross-sectional case-control comparison of 65 male volunteers from the local community, half of whom satisfied the DSM-IV-TR criteria for cocaine dependence (n = 35) while the other half had no personal or family history of a psychiatric disorder, including substance abuse (n = 30). Assessments were made of eating behavior and dietary food intake, estimation of body composition, and measurement of plasma leptin. Although cocaine users reported significantly higher levels of dietary fat and carbohydrates as well as patterns of uncontrolled eating, their fat mass was significantly reduced compared with their non-drug using peers. Levels of leptin were associated with fat mass, and with the duration of stimulant use. Tobacco smoking status or concomitant use of medication did not affect the significance of the results. Weight changes in cocaine users reflect fundamental perturbations in fat regulation. These are likely to be overlooked in clinical practice but may produce significant health problems when cocaine use is discontinued during recovery.

 

 

Fat Cells Feel the Cold, Burn Calories for Heat.


Transforming fat cells into calorie-burning machines may sound like the ultimate form of weight control, but the idea is not as far-fetched as it sounds. Unexpectedly, some fat cells directly sense dropping temperatures and release their energy as heat, according to a new study; that ability might be harnessed to treat obesity and diabetes, researchers suggest.

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Fat is known to help protect animals from the cold—and not only by acting as insulation. In the early 1990s, scientists studying mice discovered that cold temperatures trigger certain fat cells, called brown adipose tissue, to release stored energy in the form of heat—to burn calories, in other words. Researchers have always assumed this mechanism was an indirect response to the physiological stress of cold temperatures, explains cell biologist Bruce Spiegelman of Harvard Medical School, Boston. The activation of brown fat seems to start with sensory neurons throughout the body informing the brain of a drop in temperature. In response the brain sends out norepinephrine, the chief chemical messenger of the sympathetic nervous system, which mobilizes the body to cope with many situations. In experimental animals, stimulating norepinephrine receptors triggered brown adipose tissue to release its energy and generate heat, while animals bred to be missing these receptors were unable to mount the same fat cell response.

People also have brown adipose tissue that generates heat when the body is cold. And unlike white fat, which builds up around the abdomen and contributes to many disorders including heart disease and diabetes, this brown fat is found in higher proportions in leaner people and seems to actively protect against diabetes.

In brown fat, the heat-generating process depends on a protein called UCP1; the protein is also thought to be central in brown fat’s ability to prevent diabetes. Researchers are now exploring ways of activating this molecular pathway. But in trying to figure out exactly how fat cells respond to the body being cold, Spiegelman and colleagues discovered that plain old “white” fat cells have a few surprises left. In a study appearing online today in the Proceedings of the National Academy of Sciences, the researchers exposed various kinds of fat cells to cold temperatures directly. “We were a little surprised that no one had tried this before,” Spiegelman says.

The researchers cooled several types of lab-grown human fat cells—brown, white and “beige” (white adipose tissue with some brown cells mixed in)—to temperatures between 27˚ and 39˚C for four hours, eight hours, or up to ten days. White fat cells and beige cells responded to cooling in dramatic fashion. In these cells, levels of the UCP1 were doubled by 8 hours after the treatment. The change in UCP1 also proved to be reversible: Its levels returned to normal once the cells’ temperature was lowered to 37 degrees. But in brown fat cells, no induction of the protein was observed, indicating that cold temperatures don’t mobilize these cells by flipping this particular switch.

The researchers also found that white fat cells obtained from mice lacking receptors for norepinephrine were still able to respond to cooling by turning on UCP1—showing that the heat-generating pathway is both specific to those fat cells and independent of the sympathetic nervous system .

The finding won’t lead to an antifat pill any time soon, Spiegelman says, but it does give scientists new avenues to explore. “It’s a piece of the basic science, adding to an evolving awareness that fat cells have many lives that we never knew about. Now we know they can sense temperature directly. The next question is, how do they do it, and can that ability be manipulated?”

“The paper is filling in an emerging picture that adipose tissue can be a more flexible, adaptive organ than we once thought,” says Sven Enerbäck, a physician and adipose tissue researcher at the University of Gothenburg in Sweden. “The finding raises the question of whether this new pathway has widespread effects on the animal as a whole.”

Finding that white fat cells directly detect and react to cold is a surprising development, notes cell biologist Peter Tontonoz of the University of California, Los Angeles, because it shows that the sympathetic nervous system isn’t the whole story when it comes to heat generation by adipose tissue. He’s curious whether the heat-generating pathway in white fat is a routine part of everyday temperature regulation. “Even if it isn’t,” he adds, “it could still be targeted by small molecules or other drugs.”

Source: sciencemag.org

 

 

What Does It Mean to Be Fat Adapted?


When describing someone that has successfully made the transition to the Primal way of eating I often refer to them as “fat-adapted” or as “fat-burning beasts”. But what exactly does it mean to be “fat-adapted”? How can you tell if you’re fat-adapted or still a “sugar-burner”?

I get these and related questions fairly often, so I thought I’d take the time today to attempt to provide some definitions and bring some clarification to all of this. I’ll try to keep today’s post short and sweet, and not too complicated. Hopefully, med students and well-meaning but inquisitive lay family members alike will be able to take something from it.

As I’ve mentioned before, fat-adaptation is the normal, preferred metabolic state of the human animal. It’s nothing special; it’s just how we’re meant to be. That’s actually why we have all this fat on our bodies – turns out it’s a pretty reliable source of energy! To understand what it means to be normal, it’s useful examine what it means to be abnormal. And by that I mean, to understand what being a sugar-dependent person feels like.

Are You a Sugar-Burner?

  1. A sugar-burner can’t effectively access stored fat for energy. What that means is an inability for skeletal muscle to oxidize fat. Ha, not so bad, right? I mean, you could always just burn glucose for energy. Yeah, as long as you’re walking around with an IV-glucose drip hooked up to your veins.

What happens when a sugar-burner goes two, three, four hours without food, or – dare I say it – skips a whole entire meal (without that mythical IV sugar drip)? They get ravenously hungry. Heck, a sugar-burner’s adipose tissue even releases a bunch of fatty acids 4-6 hours after eating and during fasting, because as far as it’s concerned, your muscles should be able to oxidize them[1]. After all, we evolved to rely on beta oxidation of fat for the bulk of our energy needs. But they can’t, so they don’t, and once the blood sugar is all used up (which happens really quickly), hunger sets in, and the hand reaches for yet another bag of chips.

  1. A sugar-burner can’t even effectively access dietary fat for energy. As a result, more dietary fat is stored than burned. Unfortunately for them, they’re likely to end up gaining lots of body fat. As we know, a low ratio of fat to carbohydrate oxidation is a strong predictor of future weight gain.
  2. A sugar-burner depends on a perpetually-fleeting source of energy. Glucose is nice to burn when you need it, but you can’t really store very much of it on your person (unless you count snacks in pockets, or chipmunkesque cheek-stuffing). Even a 160 pound person who’s visibly lean at 12% body fat still has 19.2 pounds of animal fat on hand for oxidation, while our ability to store glucose as muscle and liver glycogen are limited to about 500 grams (depending on the size of the liver and amount of muscle you’re sporting). You require an exogenous source, and, if you’re unable to effectively beta oxidize fat (as sugar-burners often are), you’d better have some candy on hand.
  3. A sugar-burner will burn through glycogen fairly quickly during exercise. Depending on the nature of the physical activity, glycogen burning could be perfectly desirable and expected, but it’s precious, valuable stuff. If you’re able to power your efforts with fat for as long as possible, that gives you more glycogen – more rocket fuel for later, intenser efforts (like climbing a hill or grabbing that fourth quarter offensive rebound or running from a predator). Sugar-burners waste their glycogen on efforts that fat should be able to power.

The Benefits of Being Fat Adapted

Being fat-adapted, then, looks and feels a little bit like the opposite of all that. A fat-burning beast:

  1. Can effectively burn stored fat for energy throughout the day. If you can handle missing meals and are able to go hours without getting ravenous and cranky (or craving carbs), you’re likely fat-adapted.
  2. Is able to effectively oxidize dietary fat for energy. If you’re adapted, your post-prandial fat oxidation will be increased, and less dietary fat will be stored in adipose tissue.
  3. Has plenty of accessible energy on hand, even if he or she is lean. If you’re adapted, the genes associated with lipid metabolism will be upregulated in your skeletal muscles. You will essentially reprogram your body.
  4. Can rely more on fat for energy during exercise, sparing glycogen for when he or she really needs it. As I’ve discussed before, being able to mobilize and oxidize stored fat during exercise can reduce an athlete’s reliance on glycogen. This is the classic “train low, race high” phenomenon, and it can improve performance, save the glycogen for the truly intense segments of a session, and burn more body fat. If you can handle exercising without having to carb-load, you’re probably fat-adapted. If you can workout effectively in a fasted state, you’re definitely fat-adapted.

Furthermore, a fat-burning beast will be able to burn glucose when necessary and/or available, whereas the opposite cannot be said for a sugar-burner. Ultimately, fat-adaption means metabolic flexibility. It means that a fat-burning beast will be able to handle some carbs along with some fat. A fat-burning beast will be able to empty glycogen stores through intense exercise, refill those stores, burn whatever dietary fat isn’t stored, and then easily access and oxidize the fat that is stored when it’s needed. It’s not that the fat-burning beast can’t burn glucose – because glucose is toxic in the blood, we’ll always preferentially burn it, store it, or otherwise “handle” it – it’s that he doesn’t depend on it.

I’d even suggest that true fat-adaptation will allow someone to eat a higher carb meal or day without derailing the train. Once the fat-burning machinery has been established and programmed, you should be able to effortlessly switch between fuel sources as needed.

How Can You Tell if You’re Fat Adapted?

There’s really no “fat-adaptation home test kit.” I suppose you could test your respiratory quotient (RQ), which is the ratio of carbon dioxide you produce to oxygen you consume. An RQ of 1+ indicates full glucose-burning; an RQ of 0.7 indicates full fat-burning. Somewhere around 0.8 would probably mean you’re fairly well fat-adapted, while something closer to 1 probably means you’re closer to a sugar-burner.

The obese have higher RQs. Diabetics have higher RQs. Nighttime eaters have higher RQs (and lower lipid oxidation). What do these groups all have in common? Lower satiety, insistent hunger, impaired beta-oxidation of fat, increased carb cravings and intake – all hallmarks of the sugar-burner.

It’d be great if you could monitor the efficiency of your mitochondria, including the waste products produced by their ATP manufacturing, perhaps with a really, really powerful microscope, but you’d have to know what you were looking for. And besides, although I like to think our “cellular power plants” resemble the power plant from the Simpsons, I’m pretty sure I’d be disappointed by reality.

Yes?Then you’re probably fat-adapted. Welcome to normal human metabolism! No, there’s no test to take, no simple thing to measure, no one number to track, no lab to order from your doctor. To find out if you’re fat-adapted, the most effective way is to ask yourself a few basic questions:

  • Can you go three hours without eating? Is skipping a meal an exercise in futility and misery?
  • Do you enjoy steady, even energy throughout the day? Are midday naps pleasurable indulgences, rather than necessary staples?
  • Can you exercise without carb-loading?
  • Have the headaches and brain fuzziness passed?

Fat Adaption versus Ketosis

A quick note about ketosis: Fat-adaption does not necessarily mean ketosis. Ketosis is ketosis. Fat-adaption describes the ability to burn both fat directly via beta-oxidation and glucose via glycolysis, while ketosis describes the use of fat-derived ketone bodies by tissues (like parts of the brain) that normally use glucose.

A ketogenic diet “tells” your body that no or very little glucose is available in the environment. The result? “Impaired” glucose tolerance and “physiological” insulin resistance, which sound like negatives but are actually necessary to spare what little glucose exists for use in the brain. On the other hand, a well-constructed, lower-carb (but not full-blown ketogenic) Primal way of eating that leads to weight loss generally improves insulin sensitivity.

About the Author:

Mark Sisson is the author of a #1 bestselling health book on Amazon.com, The Primal Blueprint, as well as The Primal Blueprint Cookbook and the top-rated health and fitness blog MarksDailyApple.com. He is also the founder of Primal Nutrition, Inc., a company devoted to health education and designing state-of-the-art supplements that address the challenges of living in the modern world. You can visit Mark’s website by visiting marksdailyapple.com.

Source: Dr. Mercola

 

 

What Does It Mean to Be Fat Adapted?


When describing someone that has successfully made the transition to the Primal way of eating I often refer to them as “fat-adapted” or as “fat-burning beasts”. But what exactly does it mean to be “fat-adapted”? How can you tell if you’re fat-adapted or still a “sugar-burner”?

I get these and related questions fairly often, so I thought I’d take the time today to attempt to provide some definitions and bring some clarification to all of this. I’ll try to keep today’s post short and sweet, and not too complicated. Hopefully, med students and well-meaning but inquisitive lay family members alike will be able to take something from it.

As I’ve mentioned before, fat-adaptation is the normal, preferred metabolic state of the human animal. It’s nothing special; it’s just how we’re meant to be. That’s actually why we have all this fat on our bodies – turns out it’s a pretty reliable source of energy! To understand what it means to be normal, it’s useful examine what it means to be abnormal. And by that I mean, to understand what being a sugar-dependent person feels like.

Are You a Sugar-Burner?

  1. A sugar-burner can’t effectively access stored fat for energy. What that means is an inability for skeletal muscle to oxidize fat. Ha, not so bad, right? I mean, you could always just burn glucose for energy. Yeah, as long as you’re walking around with an IV-glucose drip hooked up to your veins.

What happens when a sugar-burner goes two, three, four hours without food, or – dare I say it – skips a whole entire meal (without that mythical IV sugar drip)? They get ravenously hungry. Heck, a sugar-burner’s adipose tissue even releases a bunch of fatty acids 4-6 hours after eating and during fasting, because as far as it’s concerned, your muscles should be able to oxidize them[1]. After all, we evolved to rely on beta oxidation of fat for the bulk of our energy needs. But they can’t, so they don’t, and once the blood sugar is all used up (which happens really quickly), hunger sets in, and the hand reaches for yet another bag of chips.

  1. A sugar-burner can’t even effectively access dietary fat for energy. As a result, more dietary fat is stored than burned. Unfortunately for them, they’re likely to end up gaining lots of body fat. As we know, a low ratio of fat to carbohydrate oxidation is a strong predictor of future weight gain.
  2. A sugar-burner depends on a perpetually-fleeting source of energy. Glucose is nice to burn when you need it, but you can’t really store very much of it on your person (unless you count snacks in pockets, or chipmunkesque cheek-stuffing). Even a 160 pound person who’s visibly lean at 12% body fat still has 19.2 pounds of animal fat on hand for oxidation, while our ability to store glucose as muscle and liver glycogen are limited to about 500 grams (depending on the size of the liver and amount of muscle you’re sporting). You require an exogenous source, and, if you’re unable to effectively beta oxidize fat (as sugar-burners often are), you’d better have some candy on hand.
  3. A sugar-burner will burn through glycogen fairly quickly during exercise. Depending on the nature of the physical activity, glycogen burning could be perfectly desirable and expected, but it’s precious, valuable stuff. If you’re able to power your efforts with fat for as long as possible, that gives you more glycogen – more rocket fuel for later, intenser efforts (like climbing a hill or grabbing that fourth quarter offensive rebound or running from a predator). Sugar-burners waste their glycogen on efforts that fat should be able to power.

The Benefits of Being Fat Adapted

Being fat-adapted, then, looks and feels a little bit like the opposite of all that. A fat-burning beast:

  1. Can effectively burn stored fat for energy throughout the day. If you can handle missing meals and are able to go hours without getting ravenous and cranky (or craving carbs), you’re likely fat-adapted.
  2. Is able to effectively oxidize dietary fat for energy. If you’re adapted, your post-prandial fat oxidation will be increased, and less dietary fat will be stored in adipose tissue.
  3. Has plenty of accessible energy on hand, even if he or she is lean. If you’re adapted, the genes associated with lipid metabolism will be upregulated in your skeletal muscles. You will essentially reprogram your body.
  4. Can rely more on fat for energy during exercise, sparing glycogen for when he or she really needs it. As I’ve discussed before, being able to mobilize and oxidize stored fat during exercise can reduce an athlete’s reliance on glycogen. This is the classic “train low, race high” phenomenon, and it can improve performance, save the glycogen for the truly intense segments of a session, and burn more body fat. If you can handle exercising without having to carb-load, you’re probably fat-adapted. If you can workout effectively in a fasted state, you’re definitely fat-adapted.

Furthermore, a fat-burning beast will be able to burn glucose when necessary and/or available, whereas the opposite cannot be said for a sugar-burner. Ultimately, fat-adaption means metabolic flexibility. It means that a fat-burning beast will be able to handle some carbs along with some fat. A fat-burning beast will be able to empty glycogen stores through intense exercise, refill those stores, burn whatever dietary fat isn’t stored, and then easily access and oxidize the fat that is stored when it’s needed. It’s not that the fat-burning beast can’t burn glucose – because glucose is toxic in the blood, we’ll always preferentially burn it, store it, or otherwise “handle” it – it’s that he doesn’t depend on it.

I’d even suggest that true fat-adaptation will allow someone to eat a higher carb meal or day without derailing the train. Once the fat-burning machinery has been established and programmed, you should be able to effortlessly switch between fuel sources as needed.

How Can You Tell if You’re Fat Adapted?

There’s really no “fat-adaptation home test kit.” I suppose you could test your respiratory quotient (RQ), which is the ratio of carbon dioxide you produce to oxygen you consume. An RQ of 1+ indicates full glucose-burning; an RQ of 0.7 indicates full fat-burning. Somewhere around 0.8 would probably mean you’re fairly well fat-adapted, while something closer to 1 probably means you’re closer to a sugar-burner.

The obese have higher RQs. Diabetics have higher RQs. Nighttime eaters have higher RQs (and lower lipid oxidation). What do these groups all have in common? Lower satiety, insistent hunger, impaired beta-oxidation of fat, increased carb cravings and intake – all hallmarks of the sugar-burner.

It’d be great if you could monitor the efficiency of your mitochondria, including the waste products produced by their ATP manufacturing, perhaps with a really, really powerful microscope, but you’d have to know what you were looking for. And besides, although I like to think our “cellular power plants” resemble the power plant from the Simpsons, I’m pretty sure I’d be disappointed by reality.

Yes?Then you’re probably fat-adapted. Welcome to normal human metabolism! No, there’s no test to take, no simple thing to measure, no one number to track, no lab to order from your doctor. To find out if you’re fat-adapted, the most effective way is to ask yourself a few basic questions:

  • Can you go three hours without eating? Is skipping a meal an exercise in futility and misery?
  • Do you enjoy steady, even energy throughout the day? Are midday naps pleasurable indulgences, rather than necessary staples?
  • Can you exercise without carb-loading?
  • Have the headaches and brain fuzziness passed?

Fat Adaption versus Ketosis

A quick note about ketosis: Fat-adaption does not necessarily mean ketosis. Ketosis is ketosis. Fat-adaption describes the ability to burn both fat directly via beta-oxidation and glucose via glycolysis, while ketosis describes the use of fat-derived ketone bodies by tissues (like parts of the brain) that normally use glucose.

A ketogenic diet “tells” your body that no or very little glucose is available in the environment. The result? “Impaired” glucose tolerance and “physiological” insulin resistance, which sound like negatives but are actually necessary to spare what little glucose exists for use in the brain. On the other hand, a well-constructed, lower-carb (but not full-blown ketogenic) Primal way of eating that leads to weight loss generally improves insulin sensitivity.

About the Author:

Mark Sisson is the author of a #1 bestselling health book on Amazon.com, The Primal Blueprint, as well as The Primal Blueprint Cookbook and the top-rated health and fitness blog MarksDailyApple.com. He is also the founder of Primal Nutrition, Inc., a company devoted to health education and designing state-of-the-art supplements that address the challenges of living in the modern world. You can visit Mark’s website by visiting marksdailyapple.com.

Source: mercola.com