Redox

Radioactive contamination spreading within Hanford plant.

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Radioactive contamination is spreading within one of Hanford’s huge processing plants, and the problem could escalate as the plant, unused since the 1960s, continues to deteriorate.

A new report on the Reduction-Oxidation Complex, more commonly called REDOX, recommends that $181 million be spent on interim cleanup and maintenance of the plant. REDOX is not scheduled to be demolished until about 2032, or possibly later because the nearby 222-S Laboratory in central Hanford will be needed to support the Hanford vitrification plant for another 30 to 40 years.

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The REDOX plant, one of five large processing plants at Hanford, is deteriorating and radioactive waste within it is spreading.

Doing some work on the building soon could reduce the threat of contamination spreading outside the building, including by animals, a break in a utility pipe or a fire, according to the report. Recommended work also would help protect Hanford workers.
 REDOX was used from 1952-67 to process about 24,000 tons of irradiated uranium fuel rods to remove plutonium for the nation’s nuclear weapons program and also to recover uranium to reuse in new fuel rods. It is highly contaminated, after processing eight times more fuel per day than earlier processing plants.

The main building is huge, measuring 468 feet long, 161 feet wide and 60 feet tall, with additional underground processing area.

Each annual inspection of some parts of the plant from 2012-15 found an escalation in the spread of radioactive contamination, including by precipitation that has leaked through the roof and joints of the concrete building.

Spread of contamination has been observed throughout the buildings and will intensify as the facilities continue to degrade.

DOE report on REDOX

Salt used to neutralize the contaminated processing system after it was shut down in 1967 appears to have corroded through some of the stainless steel process piping, according to an earlier Defense Nuclear Facilities Safety Board staff report.

Plastic bags were taped on one processing line to catch any drips of residual plutonium nitrate in places where leaks were anticipated. Two of the bags hold significant amounts of plutonium nitrate, which will spread if the bags leak, the DOE report said.

Signs of animal intrusion and deteriorating asbestos have been found in inspections of several areas.

 The main part of the plant — a long, high “canyon” — has not been entered since 1997. But “based on current conditions in areas where surveillance inspections are performed, water accumulation, animal intrusion, structure deterioration and contamination spread are expected,” the report said.

REDOX was used from 1952-67 to process about 24,000 tons of irradiated uranium fuel rods to remove plutonium for the nation’s nuclear weapons program and also to recover uranium to reuse in new fuel rods.

The report considered three plans to slow down deterioration and take action to confine contamination and reduce its spread, recommending the most extensive of the three alternatives. The plans range in cost from $148 million to $181 million.

Actions would include tearing down the plant’s radioactively contaminated Nitric Acid and Iodine Recovery Building and the main plant’s attached annexes. Two underground, single-shell tanks used to hold up to 24,000 gallons each of hexone also would be removed, if possible. Hexone was used in the process to extract plutonium from fuel rods.

Elsewhere in the plant, steps would be taken to reduce current hazards, which also could help prepare for the eventual demolition of the plant. Waste could be stabilized by isolating it or covering it with a fixative. Piping out of the plant could be plugged, fluids could be drained from piping and equipment, and some equipment could be removed.

Modifications to the plant’s ventilation system would be needed for some of the work.

The actions also target maintaining a skilled workforce at the Hanford Site that is experienced in contaminated deactivation and decommissioning work, which will be needed when major funding becomes available in the future.

DOE report on REDOX

Doing the proposed work would help retain workers experienced in decommissioning nuclear facilities at Hanford. They will be needed as more federal money becomes available for central Hanford environmental cleanup in the future, the report said.

DOE will consider public comments before a decision is made to proceed with work. Work would be done over the next several years as money is available and as the need for the work at REDOX is balanced against other Hanford cleanup priorities.

Low-dose testosterone induced protein anabolism in postmenopausal women

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Low-dose testosterone therapy could be a promising treatment option for reducing protein breakdown and oxidation in elderly men and postmenopausal women, according to researchers.

“Oral testosterone administration resulted in a significant reduction in the rate of leucine appearance, an index of protein breakdown, and the rate of Lox, an index of irreversible loss of protein,” Vita Birzniece, MD, PhD,senior lecturer at the University Western Sydney, clinical researcher in endocrinology and metabolism at the Garvan Institute of Medical Research and St. Vincent’s Hospital, Sydney and a senior lecturer at the University New South Wales, and colleagues wrote.

The researchers studied eight healthy postmenopausal women (mean age: 64.2 years; BMI: 26.8 kg/m2) administered 40-mg oral testosterone daily. Treatment effect was examined based on the concentration of testosterone, markers of hepatic function, resting energy expenditure and fat oxidation, as well as whole-body leucine turnover. Evaluations of liver transaminases, sex hormone-binding globulin (SHBG) and insulin-like growth factor 1 (IGF-1), in addition to all other measurements, were collected at baseline and after 2 weeks of treatment.

Data indicate testosterone therapy significantly decreased the leucine rate of appearance by 7.1% and the leucine oxidation by 14.6% (P<.05). Although SHBG remained within normal range (16.8%), IGF-1 increased by 18.4% (P<.05), researchers wrote. However, there were no significant changes to liver transaminases. Peripheral testosterone concentrations increased from 0.4 nmol/L to 1.1 nmol/L (P<.05), according to data.

“In the post-absorptive state, oral testosterone administration did not significantly affect resting energy expenditure and carbohydrate and fatty acid oxidation in healthy postmenopausal women,” the researchers wrote.

These findings add to the literature that low-dose oral testosterone may be beneficial for both men and women, they wrote.

Source: Endocrine Today

 

 

Sodium Reduction in PopulationsInsights From the Institute of Medicine Committee.

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The recent Institute of Medicine (IOM) report regarding dietary sodium1 has generated considerable interest and debate, as well as misinterpretation by advocates on both sides. Further discussion is necessary to inform the public and the health care community and to inform public health strategies for sodium reduction.

CURRENT PUBLIC HEALTH RECOMMENDATIONS REGARDING DIETARY SODIUM

Dietary sodium intake averages approximately 3400 mg/d in US adults, far in excess of the Dietary Guidelines for Americans (DGA) recommendation of less than 2300 mg/d for those older than 2 years and less than 1500 mg/d for certain high-risk subgroups, including African Americans, individuals with hypertension, diabetes, or chronic kidney disease (CKD), or those older than 50 years.2 In contrast, the 2005 IOM Panel on Dietary Reference Intakes (DRI) for Water, Potassium, Sodium, Chloride, and Sulfate3 found insufficient evidence to derive a “recommended dietary allowance” for sodium. Instead, an “adequate intake” of 1500 mg/d of dietary sodium was determined, reflecting the minimum needed to achieve a diet adequate in essential nutrients and to cover sweat losses. Additionally, the 2005 IOM panel established a “tolerable upper intake level,” using projections from available data on the effects on blood pressure, that consumption up to 2300 mg/d was unlikely to cause harm.

Based on the strength of the blood pressure data, various US (eg, American Heart Association [AHA]) and international (eg, World Health Organization [WHO]) organizations published recommendations for sodium consumption.4– 5 Although these recommendations were somewhat different from the DGA, there was general agreement that sodium consumption is excessive worldwide and should be reduced. Despite these recommendations, more than 90% of US adults consume more than 2300 mg of sodium per day, and among the high-risk subgroups more than 98% consume more than 1500 mg of sodium per day.6

A substantial body of evidence supports efforts to reduce sodium intake. This evidence links excessive dietary sodium to high blood pressure, stroke, and cardiovascular disease (CVD).1However, effects of sodium on blood pressure cannot always be disentangled from effects of total dietary modification, and effects of other electrolytes on blood pressure remain unresolved.7Concerns have been raised that a very low sodium intake may adversely affect lipids, insulin resistance, renin, and aldosterone levels and potentially may increase risk of CVD and stroke. Some studies link sodium intakes of less than 2300 mg/d to increased risk of CVD, at least in subpopulations. Thus, debate emerged about the sodium intake target that best improves health outcomes.

In response, the US Centers for Disease Control and Prevention commissioned the IOM to convene an expert committee to examine the designs, methods, and conclusions of literature published since the 2005 DRI report.3 Specifically, the committee was asked to review and assess potential benefits and adverse outcomes of reducing sodium intake in the population, particularly in the range of 1500 to 2300 mg/d, with emphasis on the high-risk subgroups. The committee was asked to focus on studies of direct health outcomes (vs surrogate end points such as blood pressure), to comment on implications for population-based strategies to reduce sodium intake, and to identify methodologic gaps and ways to address them. The committee’s full report is published elsewhere.1

SODIUM AND DIRECT HEALTH OUTCOMES

The committee searched literature published through 2012 for relevant publications. Information also was gathered from an open public workshop. Although not its primary emphasis, the committee summarized studies published since 2003 evaluating intermediate markers, particularly blood pressure. Focusing on CVD outcomes, the committee’s assessment of evidence was guided by factors such as study design, quantitative measures of dietary sodium intake, confounder adjustment, and number and consistency of available studies.

FINDINGS AND CONCLUSIONS

General US Population. Studies linking dietary sodium intake with direct health outcomes were highly variable in methodological quality; limitations included overreporting or underreporting of sodium intake. However, when considered collectively, the evidence on direct health outcomes indicates a positive relationship between higher levels of sodium intake and risk of CVD, consistent with the known effects of sodium intake on blood pressure. Furthermore, in some studies, the association between sodium and CVD outcomes persisted after adjusting for blood pressure, suggesting that associations between sodium and CVD may be mediated through other factors (eg, effects of other electrolytes) or through pathways other than blood pressure.

Studies evaluating sodium intake in the range of 1500 to 2300 mg/d demonstrate evidence of blood pressure lowering, but no studies have examined sodium intake in that range in the general population and direct CVD outcomes. The committee found that studies on direct health outcomes were of inconsistent quality and insufficient quantity to conclude whether sodium intake of less than 2300 mg/d was associated with either a greater or lesser risk of CVD.

Population Subgroups. The committee reviewed multiple randomized trials conducted by a single team that indicated low sodium intake (up to 1840 mg/d) may lead to greater risk of adverse events in patients with heart failure (HF) with reduced ejection fraction who received aggressive therapeutic regimens. Because these therapeutic regimens were different from standard US practice, trials using regimens that more closely resemble standard US clinical practice are needed. Of note, due to allegations of duplicate publication in 2 of these trials, a meta-analysis including them was recently retracted, after the IOM report’s completion.8 Another recently published small randomized trial involving patients with acute decompensated HF showed no benefit on weight or clinical stability from a combination of sodium and fluid restriction.9

The committee reviewed 2 related studies in individuals with prehypertension that suggested benefit from lowering sodium intake to 2300 mg/d and perhaps lower, although these studies were based on small numbers of persons with sodium intake in the less than 2300 mg/d range. In contrast, for patients with diabetes, CKD, or preexisting CVD, the committee found no evidence of benefit and some evidence suggesting risk of adverse health outcomes at sodium intake of 1500 to 2300 mg/d. In studies that explored statistical interactions, race, age, hypertension, and diabetes did not modify associations of sodium with health outcomes. The committee concluded that, with the exception of heart failure, evidence of both benefit and harm is not strong enough to indicate that these subgroups should be treated differently from the general US population. Thus, the committee also concluded that evidence on direct health outcomes does not support recommendations to lower sodium intake within these subgroups to or even less than 1500 mg/d.

IMPLICATIONS FOR POPULATION-BASED STRATEGIES TO GRADUALLY REDUCE SODIUM INTAKE

Although not asked to specify targets for dietary sodium, the committee noted factors that precluded establishing these targets. These include lack of consistency in methods for defining sodium intakes at both high and low ends of typical intakes and extreme variability in intake levels across studies. The committee could only consider sodium intake levels within the context of each individual study because there were impediments to calibrating sodium assessment measures across studies.

After release of the IOM report, several news outlets highlighted disagreement among health agencies about targets for dietary sodium intake and reported that experts disagreed about the importance of blood pressure. Focusing the debate on specific targets misses the larger conclusion with which all are in agreement and may hinder implementation of important public health policy. Rather than focusing on disagreements about specific targets that currently affect less than 10% of the US population (ie, sodium intake of <2300 mg/d vs <1500 mg/d), the IOM, AHA, WHO, and DGA are congruent in suggesting that excess sodium intake should be reduced, and this is likely to have significant public health effects. Accomplishing such a reduction will require efforts to decrease sodium in the food environment10 and provide individual consumers more choice in their dietary consumption of sodium.

REFERENCES

1

Institute of Medicine.  Sodium Intake in Populations: Assessment of Evidence. Washington, DC: National Academies Press.http://www.iom.edu/Reports/2013/Sodium-Intake-in-Populations-Assessment-of-Evidence.aspx. May 2013. Accessed June 4, 2013

2

US Department of Agriculture and US Department of Health and Human Services.  Dietary Guidelines for Americans, 2010. 7th ed. Washington, DC: US Government Printing Office; 2010

3

Institute of Medicine.  Dietary Reference Intakes for Water, Potassium, Sodium, Chloride, and Sulfate. Washington, DC: National Academies Press; 2005

4

Appel LJ, Frohlich ED, Hall JE,  et al.  The importance of population-wide sodium reduction as a means to prevent cardiovascular disease and stroke: a call to action from the American Heart Association.  Circulation. 2011;123(10):1138-1143
PubMed   |  Link to Article

5

World Health Organization.  Guideline: Sodium Intake for Adults and Children. Geneva, Switzerland: World Health Organization; 2012

6

Cogswell ME, Zhang Z, Carriquiry AL,  et al.  Sodium and potassium intakes among US adults: NHANES 2003-2008.  Am J Clin Nutr. 2012;96(3):647-657
PubMed   |  Link to Article

7

US Department of Agriculture and US Department of Health and Human Services.  Report of the Dietary Guidelines Advisory Committee on the Dietary Guidelines for Americans, 2010, to the Secretary of Agriculture and the Secretary of Health and Human Services. Washington, DC: USDA/ARS; 2010

8

Low sodium versus normal sodium diets in systolic heart failure: systematic review and meta-analysis [retraction]. heart.bmj.com/content/early/2013/03/12/heartjnl-2012-302337.extract. Accessed May 23, 2013

9

Aliti GB, Rabelo ER, Clausell N, Rohde LE, Biolo A, Beck-da-Silva L. Aggressive fluid and sodium restriction in acute decompensated heart failure: a randomized clinical trial.  JAMA Intern Med
PubMed  |  Link to Article

10

Institute of Medicine.  Strategies to Reduce Sodium Intake in the United States. Washington, DC: National Academies Press; 2010

Source: JAMA

What Does It Mean to Be Fat Adapted?

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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?

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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