No Iron for a month before cycle

Obviously increased muscle mass don't do a damn thing if you don't work those muscles. But as muscle mass increases and resistance training continues, RMR will noticeably improve. Actually, rats metabolize and transport glucose very similar to humans, this is why they are used in studies related to humans. Where did you learn that glucose being stored as fat is a myth? This has been proven in peer-reviewed research articles using both human clinical trials as well as rat models.

Here is Lyle McDonald on RMR as it relates to muscle mass, a whopping 6cal/lb of muscle roughly is burned. So if one gains 20lbs of muscle that's only about 120cals a day burned. Assuming a 3000cal maintenance and that's only 4% of TDEE. Once again, that's hardly a large impact.


Title and Abstract

McClave SA, Snider HL. Dissecting the energy needs of the body. Curr Opin Clin Nutr Metab Care. (2001) 4(2):143-7.

The majority of the resting energy expenditure can be explained by the energy needs of a few highly metabolic organs, making up a small percentage of the body by weight. The relationship of the specific size, individual metabolism, and proportional contribution to the actual body weight and total energy expenditure for each of these organs is a dynamic process throughout growth and development, the onset of disease, and changes in nutritional status. Defining the energy needs of the individual tissues and organ systems immeasurably enhances our understanding of the body’s response to these clinical processes, which otherwise could not easily be evaluated by focusing solely on total energy expenditure, fat-free mass, nitrogen imbalance, or actual body weight. Recently reported studies have served mainly to reinforce concepts described previously, and clarify some areas of controversy.

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Background

Last month, I answered a Q&A on http://www.bodyrecomposition.com/fat-loss/reducing-body-fat-percentage-by-gaining-muscle-qa.html and in that article I mentioned that the actual caloric burn of skeletal muscle is actually quite low compared to what is often claimed. In the comments section someone mentioned a recent seminar where the value of 50 cal/lb for muscle was thrown out and asked for clarification on my claim.

Unlike previous research reviews, today’s paper isn’t an actual study but rather a review paper so my discussion will be a little bit different in terms of what I want to look at. The paper itself is actually fairly technical and I don’t want to focus so much on the technical aspects as on the concepts and implications that the paper deals with as they pertain to issues of body composition.


More specifically I want to look at some of the common claims that are often thrown around in the world of body composition such as “Adding muscle mass significantly raises metabolic rate.” and “Fat cells burn no calories, they are metabolically inert.” While this paper was examining the issue from a different perspective, it actually provides good data on both questions.

Specifically today’s paper examines in some detail how different tissues of the body (e.g. muscle vs. fat vs. organs) contribute to the body’s resting energy expenditure. As well, factor such as disease, growth/development and under-nutrition are examined in terms of how they impact on different tissues in the body and their energy expenditure.

As I discuss in detail in http://www.bodyrecomposition.com/fat-loss/metabolic-rate-overview.html, there are four primary components to total daily energy expenditure: Resting Energy Expenditure (REE), Thermic Effect of Activity (TEA), Thermic Effect of Food (TEF) and Non-Exercise Activity Thermogenesis/Spontaneous Physical Activity (NEAT/SPA).

Of those four, resting energy expenditure plays the major role in total daily energy expenditure, generally comprising 65-70% of the total. So looking at the differential impact of each tissue on REE tends to give pretty decent picture of what’s going on.

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The Paper

The paper begins with an introduction to the overall concepts, pointing out estimating REE in individuals of different body sizes has been classically difficult. While body weight per se is a decent indicator, REE actually tends to scale better with body surface area. However, this gives no indication of which tissues (and in what proportion) are contributing to overall REE.

Readers may have seen the statement that ‘The largest predictor of REE is lean body mass” and there is certainly some truth to that. However, lean body mass (aka fat free mass) only predicts 53-88% of the variability in energy expenditure. There are a number of reasons for this not the least of which being that lean body mass/fat free mass is not a single homogeneous tissue.

Rather, as discussed in http://www.bodyrecomposition.com/fat-loss/what-does-body-composition-mean.html, lean body mass represents organs, skeletal muscle, bone, skin and basically everything in the body that isn’t fat mass. And as you’ll see shortly, each of those tissues burns very different numbers of calories on a day to day basis. Which means that variability in the amounts and proportions of those tissues will impact on overall resting energy expenditure.

Next the paper discusses the different methodologies used to estimate the resting energy expenditure of different tissues. I don’t want to get into huge detail on this. Suffice to say that newer technology has allowed for more and more accurate methods of estimating the caloric expenditure of different tissues in the body.

While they are still not error-free (nothing in science ever is), some of the newer methods of measurement may explain why some of the oft-held beliefs about caloric expenditure and values that are often thrown out are turning out to be wrong. Of course that also means that future developments may render current values incorrect.

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The Normal Human

The next topic addressed in the paper is an examination of the different tissues and how they contribute to resting energy expenditure in a fairly ‘average’ human being. I’ve reproduced Table 1 from the paper below, honestly this was the main reason I wanted to examine this paper, to get this chart up on the site.

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Organ or Tissue
Metabolic Rate (kcal/kg/day)

Metabolic Rate (kcal/lb/day) % Overall REE Weight in Kg Weight in Lb %Body Weight
Adipose 4.5 2.0 4 15 33 21.4%
Muscle 13 5.9 22 28.2 61.6 40
Other 12 5.4 16 23.2 51 33.1
Liver 200 90.9 21 1.8 3.96 2.6
Brain 240 109 22 1.4 3.08 2.0
Heart 400 181 9 0.3 0.66 0.5
Kidneys 400 181 8 0.3 0.66 0.5
Other refers to bone, skin, intestines and glands.
Note: the lungs have not been measured for methodological reasons but have been estimated at 200 kcal/kg similar to the liver.

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As you can see above, and quite contrary to what is commonly stated, skeletal muscle actually has a fairly low resting energy expenditure, roughly 6 calories per pound. This is contrast to very old values of 100 calories/pound or even more recent claims that a pound of muscle will raise metabolic rate by 40-50 calories per pound.

Additionally, an in contrast to what is commonly claimed, fat cells do burn calories. Admittedly the value is not massive (roughly 2 calories per pound) but the idea that fat cells are completely inert is also incorrect. We now know that fat cells produce a variety of hormones, etc. (e.g. leptin, adiponectin) and that expends calories. Again, not much per unit mass of fat, but for someone carrying a lot of fat mass, this does add up.

Perhaps of more relevance, and getting back to the paper per se, the primary contributor to resting energy expenditure comes from the organs with the liver, heart, kidneys and brains contributing roughly 70-80% of total resting energy expenditure. This is despite the fact that they only make up approximately 7% of total body weight. That is, despite their relatively small weight, they are simply massively metabolically active on a day to day basis.

In contrast, while skeletal muscle may contribute roughly 40% of total weight (a little bit less in women), it only contributes 28% of total resting energy expenditure. Essentially, the relatively small caloric burn of a single pound of muscle mass is made up for by the sheer quantity of it. Which doesn’t change the fact that adding muscle mass still won’t have a massive impact on resting energy expenditure.

To put that into mathematical perspective, gaining 20 pounds of muscle would be expected to increase resting energy expenditure by approximately 120 calories per day. Certainly that does have an impact overall (equivalent to perhaps 10 minutes per day of moderate intensity cardio) but also keep in mind the time frames involved to gain that much muscle mass. Expecting that adding a bit of muscle to have massive impacts on metabolic rate in the short-term is simply unrealistic; a few pounds gained simply won’t have any major impact.

Rather, I would expect that any real impact of building muscle mass on http://www.bodyrecomposition.com/research-review/fat-loss/the-energy-balance-equation.html is going to come through the training done to stimulate/maintain muscle mass increases along with the caloric cost of building the muscle in the first place. But once it’s there, the caloric expenditure at rest of skeletal muscle is simply very low.

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Factors Affecting Energy Expenditure

Having examined the average contribution of different tissues to the body, the researchers then look at a host of other topics, only a few of which I’m going to really look at in any detail.

Growth and development is covered first, examining how the ratios of energy expenditure to body weight changes over the lifespan. Since most reading this are full grown adults, the changes that occur from childhood to maturity don’t seem that relevant.

One issue of some importance is covered next and that’s the effect of differences in body size between individuals. In general, if you look at two people of different body sizes, larger folks tend to have lower resting energy expenditures relative to their body mass. This is most likely related to differences in the proportion of organ weight (recall from above that the organs contribute the most to overall resting energy expenditure) to total body weight.

Meaning this: on average, organ weight won’t vary much between individuals. So if one person is larger than another, that difference in size is likely to occur through changes in either muscle mass or fat tissue, neither of which makes massive contributions to resting energy expenditure (and differences in body composition won’t have nearly the impact that most think given the relatively small difference in caloric expenditure between muscle mass and fat mass).

Practically, this means that equations that estimate resting energy expenditure based solely on body weight will tend to overestimate larger individuals to some degree. Of course, as I recently discussed in http://www.bodyrecomposition.com/fat-loss/adjusting-the-diet.html, since all estimates of energy expenditure and/or caloric intake have to be adjusted based on real-world changes anyhow, I’m not sure how important this is practically.

I should probably address a question that I imagine will come up in the comments, given the enormous variability in energy expenditure per pound of tissue, where does the quick estimate of 10-11 calories/pound (22-24 cal/kg) come from? And the answer is that it’s basically a weighted average of the above values. That is, if you took the values for caloric expenditure/unit weight times their contribution to overall weight and worked it out, you’d get a value that was pretty close to the quick estimate value. Again, this will tend to vary based on actual body size due to differences in the relative contribution of each tissue to the body’s total weight.

Next the researchers looked at the impact of both undernutrition and refeeding on energy expenditure at rest. During underfeeding, they point out that skeletal muscle and fat are generally the major tissue lost while organs are spared. This tends to have the impact of raising the relative proportion of energy expenditure to body weight (because the low energy expenditure tissues are being lost). Of course, with extended dieting, there is also an adaptive component of metabolic rate reduction as all tissues in the body tend to slow their overall energy expenditure.

In contrast, during refeeding, there is often a hypermetabolic state that occurs, possibly due to increases in protein synthesis, core temperature and the thermic effect of food. As well, there are a number of hormonal effects that occur when calories are raised, a topic I discuss in more detail in http://www.bodyrecomposition.com/fat-loss/the-full-diet-break.html, all of which may have potentially beneficial impacts on overall energy expenditure and metabolic rate.

Finally the researchers examine the impact of disease and injury on energy expenditure but I don’t find that terribly relevant to this article.

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Summing Up

The main point that I wanted to make with today’s research review was to clear up some of the oft-held (and unfortunately incorrect) ideas regarding the impact of things like skeletal muscle mass and fat mass on resting energy expenditure. Based on current data, the idea that skeletal muscle burns massive numbers of calories would appear to be 100% incorrect.

Rather, skeletal muscle actually burns fairly few calories on a per pound basis; it primarily has a major impact on resting energy expenditure because there is a good bit of it. But adding even moderate amounts of muscle are unlikely to massively impact on energy expenditure. As noted above, I expect the major effect to be from the effort of stimulating muscle mass gains along with the energy needed to synthesize that muscle tissue. But once it’s there it doesn’t burn many calories.

Rather, the majority of resting energy expenditure is generated by the organs which, despite their small size, burn a massive number of calories per unit weight. Someone on the http://forums.lylemcdonald.com/ jokingly asked “So how do I hypertrophy my liver?”

Finally, fat cells, while not having much of a calorie burn do burn calories. In fact, they are only about 1/3rds of the burn of skeletal muscle (2 cal/lb vs. 6 cal/lb respectively). While low, someone carrying a lot of fat will have this add up and it will contribute to overall resting energy expenditure.
 
Rats do process carbs differently than humans. They make great models for protein research but not carbohydrate research

Once again, Lyle:


In that piece I answered a very specific question with a very specific answer. I made no implications of anything beyond the exact answer I gave to that specific question. And somehow people managed to read all kinds of asinine stuff into it, things that I never said or even began to imply. It’d amaze me if I hadn’t seen people do this consistently over the past 15 years.

The basic confusion in that article was that folks interpreted my saying that carbs and protein can’t be converted to fat as ‘Lyle says you can’t get fat overeating carbs and protein’. Which I absolutely didn’t say. But people inferred, incorrectly. Basically, what I said and what they heard were not the same thing.

I’d note before continuing that if folks had taken 30 seconds to click on and read the article I linked http://www.bodyrecomposition.com/nutrition/nutrient-intake-nutrient-storage-and-nutrient-oxidation.html, they would have realized the mistake they were making as I specifically said that overeating carbs can still make you fat, just not through direct conversion (rather through indirect mechanisms). But in addition to a lack of basic literacy, laziness seems to be endemic on the net as well. And for not taking a couple of minutes to read the piece that I specifically linked to, a bunch of people got confused and then aggro.

I’d also note that if folks reading the protein piece had taken time to read the, I dunno, 200+ other articles on the site, they’d realize that I am making no such claim that you can eat all the carbs you want (or that lowcarb diets are superior, or whatever nonsensical conclusions they reached). Or that one specific dietary approach (e.g. lowcarbs) is automatically superior to another.


But rather than do that, they took a single article, addressing a single specific question, and ran with it. That’s not a good thing to do, you can’t take a single answer to a single specific question out of context and take that to represent what I believe. Well you can but it’s stupid to do so. That’s what a lot of people did.

But since they couldn’t do any of that, couldn’t take the time to even read the single linked article much less the rest of what’s on the site, rather than writing about something more interesting today, I’m going to clear it up once and for all. And I still expect someone to read this completely wrong and go around the Internet mis-representing what I’m saying. I’m used to it at this point.

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How We Get Fat Part 1: Energy Intake Exceeds Energy Output

At a fundamental level, fat storage occurs when caloric intake exceeds caloric output, a topic I discussed in some detail inhttp://www.bodyrecomposition.com/fat-loss/the-energy-balance-equation.html. Now, I know that a lot of people claim that basic thermodynamics don’t hold for humans. Simply, they are wrong. Invariably, the studies used to support this position are based on a faulty data set: to whit, they are drawing poor conclusions about what people SAY that they are eating.

For example, one popular book bases one of its many incorrect theses on a 1980 report suggesting that the obese ate the same number of calories as the lean. Ergo, obesity was caused by something else. The problem is this, the data set is wrong. A fact we’ve known for nearly 30 years but that the author was somehow unable to become aware of in his ‘5 years of dedicated research’.

Study after study after study over the past 30 years shows that the obese systematically under-report their food intake (by up to 30-50%) and over-report their activity (by about the same). So when they say they are only eating 1800 calories per day, they may be eating calories per day. And their activity isn’t nearly what they think.

And when you put those same folks in controlled metabolic ward conditions and control their food intake and/or activity output…voila, the energy balance equation holds. It’s only when you believe the (incorrect) self-reported data that it doesn’t.

And make no mistake I am NOT saying that the obese are lying about their intake, not consciously anyhow. Most people simply suck at knowing how much they are actually eating. Leave them to self-report it and they almost always screw it up. If you’re mistaken enough to believe the self-reported values, you reach even more screwed up conclusions about things.

In that vein, I have found that the chronically underweight “I can’t gain weight no matter what I do” are invariably vastly over-estimating what they are eating. That is, they are eating far less than they think. Other studies show that ‘health conscious people’ tend to under-report their true ‘junk food’ and dietary fat intake; to appear more healthy they conveniently forget or leave out that trip to the burger joint.

Put differently, this isn’t something that only occurs in the obese (so spare me accusations of ‘hating the obese’ or some nonsense). Am I clear or are people going to misinterpret me some more in the comments and claim I said that fat people lie about their food intake? Because I’m not saying anything of the sort. Make no mistake, I’m sure some do lie about it; most are just clueless about how much they are actually eating.

Now let me make it clear that there is obviously a lot more going on here, hormones and all manners of other stuff impact on the energy balance equation. For example, chronically elevated cortisol does a lot of nasty things in terms of reducing metabolic rate (reducing the energy out side of the equation) as well as negatively impacting on calorie partitioning (where calories go when you eat them as discussed in http://www.bodyrecomposition.com/muscle-gain/calorie-partitioning-part-1.html and http://www.bodyrecomposition.com/uncategorized/calorie-partitioning-part-2.html). But for the most part, a lot of that is outside of our control. It’s relevant but you can’t do much with most of it. So I’ll focus on calories.

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How We Get Fat Part 2: Nutrient Intake, Oxidation and Storage Part Deux

The primary storage of fat in the body is in fat cells, duh. Most of that is found in what is called subcutaneous fat, which is found under the skin. There is also fat stored around the gut area called visceral fat (this surrounds the organs). Fat can also be stored in ‘bad’ places like the liver and pancreas under certain conditions; this is called ectopic fat storage.

I’m going to focus here on subcutaneous fat. There, whether or not fat is stored or removed comes down to a concept called fat balance, which I discuss in some detail in http://www.bodyrecomposition.com/ultimate-diet-20. You can think of fat balance as the fat specific equivalent of energy balance. That is

Net Change in Fat Stores = Fat Stored – Fat Burned

I’d note that the same nutrient balance holds for protein, carbohydrates and alcohol (which I’m not going to talk about today). That is, the net effect on bodily stores, whether protein or carbohydrate stores in the body increases, decreases or stays the same comes down to the balance of protein/carb stored vs. protein or carbs/burned.

So at a fundamental level, fat gain occurs when fat storage exceeds fat burning (technically oxidation). And fat loss occurs when fat oxidation exceeds fat storage. I’d note that both processes take place in some amounts throughout the day, controlled by a host of processes I’m not going to talk about. Just recognize that what happens over time in terms of your fat stores comes down to the relationship between those two processes: fat storage – fat oxidation.

So what determines fat oxidation and fat storage rates?

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How We Get Fat Part 3: Back to Nutrient Intake, Oxidation and Storage

Now, here’s where people got confused by http://www.bodyrecomposition.com/nutrition/excess-protein-and-fat-storage-qa.html, and where they would have been unconfused by clicking the linked article on http://www.bodyrecomposition.com/fat-loss/nutrition/nutrient-intake-nutrient-storage-and-nutrient-oxidation.html. In fact, I’d suggest you go read it right now, it’s not that long and since I’m not going to retype all of it here (that’s why I wrote it the first time), it’d be a good idea. I’ll wait.

However, since I know most of you will have just ignored my suggestion to actually read that piece, I’m going to summarize a few points from it (as well as from the Q&A):

  1. Carbs are rarely converted to fat and stored as such
  2. When you eat more carbs you burn more carbs and less fat; eat less carbs and you burn less carbs and more fat
  3. Protein is basically never going to be converted to fat and stored as such
  4. When you eat more protein, you burn more protein (and by extension, less carbs and less fat); eat less protein and you burn less protein (and by extension, more carbs and more fat)
  5. Ingested dietary fat is primarily stored, eating more of it doesn’t impact on fat oxidation to a significant degree
Let’s work through this backwards. When you eat dietary fat, it’s primary fate is storage as its intake has very little impact on fat oxidation (and don’t ask me a bunch of questions about “But people say you have to eat fat to burn fat?” in the comments. That idea is fundamentally wrong but would take an entire article to address). It also doesn’t impact greatly on the oxidation of the protein or carbohydrates.

Carbohydrates are rarely converted to fat (a process called de novo lipogenesis) under normal dietary conditions. There are exceptions when this occurs. One is with massive chronic overfeeding of carbs. I’m talking 700-900 grams of carbs per day for multiple days. Under those conditions, carbs max out glycogen stores, are in excess of total daily energy requirements and you see the conversion of carbohydrate to fat for storage. But this is not a normal dietary situation for most people.

A few very stupid studies have shown that glucose INFUSION at levels of 1.5 total daily energy expenditure can cause DNL to occur but this is equally non-physiological. There is also some evidence that DNL may be increased in individuals with hyperinsulinemia (often secondary to obesity). There’s one final exception that I’ll use to finish this piece.

But when you eat more carbs, you burn more carbs and burn less fat. And that’s why even if carbs aren’t directly converted to fat and stored as such, excess carbs can STILL MAKE YOU FAT. Basically, by inhibiting fat oxidation, excess carbs cause you to store all the fat you’re eating without burning any of it off. Did you get that? Let me repeat it again.

Carbs don’t make you fat via direct conversion and storage to fat; but excess carbs can still make you fat by blunting out the normal daily fat oxidation so that all of the fat you’re eating is stored. Which is why a 500 cal surplus of fat and a 500 cal surplus of carbs can both make you fat; they just do it for different reasons through different mechanisms. The 500 calories of excess fat is simply stored; the excess 500 calories of carbs ensure that all the fat you’re eating is stored because carb oxidation goes up and fat oxidation goes down. Got it? If not, re-read this paragraph until it sinks in.

Oh yeah, the same holds for protein. Protein isn’t going to be converted to and stored as fat. But eat excess protein and the body will burn more protein for energy (and less carbs and fat). Which means that the other nutrients have to get stored. Which means that excess protein can still make you fat, just not by direct conversion. Rather, it does it by ensuring that the fat you’re eating gets stored.

Of course protein also has the highest thermic effect, more of the incoming calories are burned off. So excess protein tends to have the least odds of making you fat under any conditions; but excess protein can make you fat. Just not by direct conversion to fat; rather it’s indirectly by decreasing the oxidation of other nutrients.

Ok, is the above clear enough? Because I can’t really explain it any simpler but will try one last time using bullet points and an example. Let’s assume someone is eating at exactly maintenance calories. Neither gaining nor losing fat. Here’s what happens with excess calories. Assume that all three conditions represent identical increases in caloric intake, just from each of the different macros. Here’s what happens mechanistically and why all three still make you fat:

  1. Excess dietary fat is directly stored as fat
  2. Excess dietary carbs increases carb oxidation, impairing fat oxidation; more of your daily fat intake is stored as fat
  3. Excess dietary protein increases protein oxidation, impairing fat oxidation; more of your daily fat intake is stored as fat
Got it? All three situations make you fat, just through different mechanisms. Fat is directly stored and carbs and protein cause you to store the fat you’re eating by decreasing fat oxidation.

And I’d note again, since someone will invariably misread this that that doesn’t mean that a low-carb and/or low-protein diet is therefore superior for fat loss. I’m not saying that and don’t think that I am. Because in such a situation, while you may be burning more fat, you’re also eating more dietary fat. So net fat balance can be unchanged despite the dicking around with macronutrient content. It still comes down to the deficit.

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The Obvious Question: Why Not Just Eat Zero Dietary Fat?

And now I’ll answer the question that I know every person who has read (and hopefully understood) the above is asking: so if carbs and protein are rarely converted to and stored as fat, and make you fat by decreasing fat oxidation and causing all ingested dietary fat to get stored as fat, can’t I eat as much as I want of protein and carbs so long as my dietary fat intake is zero?

And the asnswer is still no. Remember how I teased you above with one other exception, when carbs are converted to fat for storage? That exception is when dietary fat is below about 10% of total daily calories. Under that condition, the body ramps up de novo lipogenesis. So you still get fat.

Because the body is usually smarter than we are. Under conditions where dietary fat intake is ‘adequate’ (meaning 10% of total calories or more), the primary fate of that fat is storage and protein and carbs are used for other things. And when dietary fat is too low, the body will start converting ingested carbs (and probably protein, though it would still be rare) to fat for storage.

Oh yeah, the other question you’re going to ask in the comments “What about alcohol?” That’s going to require a full article so be patient. I know that’s another thing lacking on the Internet but so be it.

And I really hope that clears things up. If it doesn’t, read this piece and the linked articles until it is.


 
Eur J Clin Nutr. 1999 Apr;53 Suppl 1:S53-65.
De novo lipogenesis in humans: metabolic and regulatory aspects.
Hellerstein MK1.
Author information

Abstract
The enzymatic pathway for converting dietary carbohydrate (CHO) into fat, or de novo lipogenesis (DNL), is present in humans, whereas the capacity to convert fats into CHO does not exist. Here, the quantitative importance of DNL in humans is reviewed, focusing on the response to increased intake of dietary CHO. Eucaloric replacement of dietary fat by CHO does not induce hepatic DNL to any substantial degree. Similarly, addition of CHO to a mixed diet does not increase hepatic DNL to quantitatively important levels, as long as CHO energy intake remains less than total energy expenditure (TEE). Instead, dietary CHO replaces fat in the whole-body fuel mixture, even in the post-absorptive state. Body fat is thereby accrued, but the pathway of DNL is not traversed; instead, a coordinated set of metabolic adaptations, including resistance of hepatic glucose production to suppression by insulin, occurs that allows CHO oxidation to increase and match CHO intake. Only when CHO energy intake exceeds TEE does DNL in liver or adipose tissue contribute significantly to the whole-body energy economy. It is concluded that DNL is not the pathway of first resort for added dietary CHO, in humans. Under most dietary conditions, the two major macronutrient energy sources (CHO and fat) are therefore not interconvertible currencies; CHO and fat have independent, though interacting, economies and independent regulation. The metabolic mechanisms and physiologic implications of the functional block between CHO and fat in humans are discussed, but require further investigation.
 
Am J Clin Nutr. 1987 Jan;45(1):78-85. Links
Carbohydrate metabolism and de novo lipogenesis in human obesity.

Acheson KJ, Schutz Y, Bessard T, Flatt JP, Jéquier E.
Respiratory exchange was measured during 14 consecutive hours in six lean and six obese individuals after ingestion of 500 g of dextrin maltose to investigate and compare their capacity for net de novo lipogenesis. After ingestion of the carbohydrate load, metabolic rates rose similarly in both groups but fell earlier and more rapidly in the obese. RQs also rose rapidly and remained in the range of 0.95 to 1.00 for approximately 8 h in both groups. During this time, RQ exceeded 1.00 for only short periods of time with the result that 4 +/- 1 g and 5 +/- 3 g (NS) of fat were synthesized via de novo lipogenesis in excess of concomitant fat oxidation in the lean and obese subjects, respectively. Results demonstrate that net de novo lipid synthesis from an unusually large carbohydrate load is not greater in obese than in lean individuals.
 
Not only was that tl;dr but it is current at all.
Once again, I'm not talking about RMR when you haven't been exercising, I am talking about BMR that is raised after resistance training and thus effect is compounded as muscle mass increases. Excess glucose is stored as fat in humans when it is not needed to replace glycogen storages, etc. There is no arguing this.
 
Did you run out of free gear so you have to stop for a month? Or do you need a month to scam someone else out of some more free gear?
 
A alan aragon:

  • Humans are not rats, especially when it comes to carbohydrate metabolism. The metabolic pathway where carbohydrate is converted to fat within the liver (called de novo lipogenesis, or DNL), is far more efficient in rats than in humans. I discuss this and other physiological differences in my research review.
http://www.alanaragonblog.com/2010/10/01/chris-shugart-drops-the-hammer/
 
Not only was that tl;dr but it is current at all.
Once again, I'm not talking about RMR when you haven't been exercising, I am talking about BMR that is raised after resistance training and thus effect is compounded as muscle mass increases. Excess glucose is stored as fat in humans when it is not needed to replace glycogen storages, etc. There is no arguing this.

I just have argued that using the research and those very knowledgeable in the field. So please provide some research of your own or quit using outdated myths please.
 
I just have argued that using the research and those very knowledgeable in the field. So please provide some research of your own or quit using outdated myths please.

Well, since we aren't using current literature...
http://www.ncbi.nlm.nih.gov/pubmed/8675642
"Fractional de novo hepatic lipogenesis (DNL) increased more than 10-fold on surplus CHO and was unmeasurable on deficient CHO diets; thus, the preceding 5-d CHO intake could be inferred from DNL."

The research on this is overwhelming. Perhaps we are arguing two different points?

QUOTE="Docd187123, post: 1251258, member: 62972"]I can use the big bold letters if that's easier for you to read....[/QUOTE]

Not sure why you felt the need for disrespect here.

It was written within the last 4 - 5 years. You really should read it because it contains a lot of valuable info. Lyle McDonald is highly respected.

I'm not saying it doesn't. I'm referring to his references being outdated.
 
Well, since we aren't using current literature...
http://www.ncbi.nlm.nih.gov/pubmed/8675642
"Fractional de novo hepatic lipogenesis (DNL) increased more than 10-fold on surplus CHO and was unmeasurable on deficient CHO diets; thus, the preceding 5-d CHO intake could be inferred from DNL."

The research on this is overwhelming. Perhaps we are arguing two different points?

QUOTE="Docd187123, post: 1251258, member: 62972"]I can use the big bold letters if that's easier for you to read....

Not sure why you felt the need for disrespect here.



I'm not saying it doesn't. I'm referring to his references being outdated.[/QUOTE]

Your tl;dr comment was disrespecting me was it not? Nevertheless I apologize for my comment to you.

From YOUR citation:

Nevertheless, absolute hepatic DNL accounted for < 5g fatty acids synthesized per day even on +50% CHO. Whole-body CHO oxidation increased sixfold and fat oxidation decreased > 90% on surplus CHO diets.

Even through hepatic DNL ramped up 10fold the resulting fatty acid synthesis was still less than 5g/day. Not clinically significant even though it showed statistical significance.

Also from your citation:

and that surplus CHO is not substantially converted by the liver to fat as it spares fat oxidation, but that fractional DNL may nevertheless be a qualitative marker of recent CHO intake.

Hepatic DNL is still minimal^^^
 
It does to a statistically significant degree yes but CLINICAL significance is still zero. There's a difference between clinical and statistical significance.

I realize that. Nonetheless, the points you've made here have sparked my interest. I'll probably take some time to read into this more in the future. I wasn't arguing for the sake of arguing; I simply was trying to see if your info was credible. I'm actually working on my biology seminar and it deals with the mechanism in which obesity causes insulin resistance because of the effects of the cytokines released from the fat cells. My thesis is that tumor necrosis factor released from adipocytes causes a decreased glucose transporter expression in adipocytes which impacts the release of certain adipokines. These adipokines (adiponectin, leptin, RBP4, etc.) cause a decreased translocation of glucose transporter in muscle cells. I'm focusing on RBP4. This is irrelevant but I thought you might find it interesting. Thanks for the info though.
 
I realize that. Nonetheless, the points you've made here have sparked my interest. I'll probably take some time to read into this more in the future. I wasn't arguing for the sake of arguing; I simply was trying to see if your info was credible. I'm actually working on my biology seminar and it deals with the mechanism in which obesity causes insulin resistance because of the effects of the cytokines released from the fat cells. My thesis is that tumor necrosis factor released from adipocytes causes a decreased glucose transporter expression in adipocytes which impacts the release of certain adipokines. These adipokines (adiponectin, leptin, RBP4, etc.) cause a decreased translocation of glucose transporter in muscle cells. I'm focusing on RBP4. This is irrelevant but I thought you might find it interesting. Thanks for the info though.

I'm glad something positive came out of this and sorry I was rash to judge.
 
I am too. If you don't mind me asking, what is your educational background? Specifics aren't necessary, I'm just curious if you did any grad school work or if your knowledge is all from independent research and discovery.
 
I'd still personally jump on the treadmill for 15 minutes, jump on the weights with short rest periods, then hop on the treadmill again for 30 minutes. I think that will get the long term results in the long run.
 
I am too. If you don't mind me asking, what is your educational background? Specifics aren't necessary, I'm just curious if you did any grad school work or if your knowledge is all from independent research and discovery.

My current studies are unrelated to this....finance. I've taken chemistry and biology courses in the past when I wanted to major in something else although I don't have and grad work in those fields. What I know comes from my own research and following those I deem top in the field (Alan Aragon, Lyle McDonald, Will Brink, Layne Norton, Jaime Hale, Ian McCarthy, etc).
 
My current studies are unrelated to this....finance. I've taken chemistry and biology courses in the past when I wanted to major in something else although I don't have and grad work in those fields. What I know comes from my own research and following those I deem top in the field (Alan Aragon, Lyle McDonald, Will Brink, Layne Norton, Jaime Hale, Ian McCarthy, etc).

Haha I had a strange feeling something along those lines was gonna be the answer. That's great though. I'll have to some more reading on this Lyle McDonald. Norton is the only one of those you mentioned that I've ever heard and that's probably a bad thing - for my sake, at least.
 
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