Showing posts with label Protein. Show all posts
Showing posts with label Protein. Show all posts

Monday, December 16, 2013

Nutrient Fates after Absorption

Random Bump

This held the top spot in terms of readership here at the Asylum for quite some time.  Always worthy of a bump.


Original post:  7/15/10

Nutrient effects: post-absorptive interactions BY ERIC JEQUIER   (1995)
After a meal, the metabolic fuel selection at the whole-body level depends on the plasma concentrations of nutrients such as glucose, non-esterified fatty acids (NEFA) , amino acids, and on hormonal responses. Over the last 10 years, there has been great interest in studying the metabolic effects following the ingestion or the intravenous (i.v.) infusion of the three macronutrients, carbohydrate (CHO), fat, and protein (or amino acids for i.v. infusion). The aim of the present brief review  {I'm thinking it's not so brief!}  is to summarize the main mechanisms which determine the post-absorptive interactions between the nutrients.
This is an older paper, but still recent enough to provide some good info on the basics.  I'm going to do something a bit different with this one and I otherwise would be quoting huge chunks.  So I'll do bullet point summaries with select summary quotes from the paper in italics.

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Thursday, June 27, 2013

Protein Metabolism

This one I'm bumping for myself, but perhaps some folks might find it interesting.  The red bolding is new.

Original Publication:  4/17/10

Looking for some info on protein, I came across this link:
http://www.nutrition-partner.com/index.cfm?C27B8FF7FABF494CAA480EF21E0D228D

The page focuses on changes in dietary requirements and/or the impact on the body of malnutrition, disease and stress, but I found this site through the following graphic on protein metabolism:

Something in the numbers doesn't add up here, but I was surprised to see how much protein is "recycled" in our guts.  Perhaps the total protein synthesis is balanced by catabolism/turnover and that is the missing number?  Not sure.  Here is the quoted text referring to this diagram (my apologies for the messed up formatting).  
Protein in the body is not static; protein synthesis and breakdown is constantly taking place. However, the total body protein pool in a healthy adult is constant. Synthesis of protein from endogenous and exogenous amino acids is equal to degradation and external losses. Some proteins have a long lifetime, such as muscle protein and plasma albumin, while others have a high turnover rate. Muscle protein constitutes up to approximately 50% of total body protein, but contributes only approximately 30% of the protein turnover in the body, because in visceral and other organs, protein turnover rates are several times higher than in muscle tissue. 
Protein metabolism is dependent on a vast number of endogenous mediators. These mediators define the balance between anabolic and catabolic processes. Insulin is the major anabolic hormone and also has an important role in amino acid and protein homeostasis. During injury and stress two major alterations in insulin are noted: a catecholamine-mediated suppression of insulin release and an insulin resistance, leading to a release of skeletal muscle amino acid for gluconeogenesis and, at the same time, a decreased utilisation of glucose by insulin-dependent tissues. This mechanism provides glucose to the insulin-dependent tissues that are important for survival and the healing of injury, such as the central nervous system (CNS), immune system and red blood cells. Other hormones, like glucagon and the catecholamines, control or counteract the effects of insulin and are more or less proteolytic; the exact role of catecholamines is still under discussion, however.
In order to define protein requirements, an overview of protein metabolism is necessary. By determining the renewal of proteins susceptible to measurement, such as plasma, muscle and digestive secretion proteins, it has been possible to estimate the daily turnover in proteins. Considerable recycling of endogenous amino acids seems to occur, the quantity amounting to twice the daily intake.   Hence, normal protein metabolism incorporates about 100 g of dietary amino acids and over 200 g of endogenous amino acids daily. Allowance must therefore be made for increased losses of endogenous proteins when assessing patients´ protein intake. 
So fully 2/3rds of our daily protein metabolism comes from proteins in our body -- the amino acid pool in our cells and/or breakdown of tissues.  Another factoid:  Structural proteins have about a 6 month half life, while hormones/peptides/etc. can have half-lives of a matter of minutes.  However hormones etc. constitute a very small amount of protein weight wise.

Thursday, April 18, 2013

Ancestral Rabbit Starvation Medical Vacations! The next craze?

I came across this study a bit ago and it caught my eye as I was transfering some stuff between computers:  Marked Improvement in Carbohydrate and Lipid Metabolism in Diabetic Australian Aborigines After Temporary Reversion to Traditional Lifestyle
The rationale for the present study was that temporarily reversing the urbanization process in diabetic Aborigines should improve all aspects of their carbohydrate and lipid metabolism that are linked to insulin resistance. Ten full-blood, diabetic Aborigines from the Mowanjum Community (Derby, Western Australia) agreed to be tested before and after living for 7 wk as hunter-gatherers in their traditional country in northwestern Australia. They were middle aged (53.9 ±1.8 yr) and overweight (81.9 ± 3.4 kg), and all lost weight steadily over the 7-wk period (average, 8 kg). A detailed analysis of food intake over 2 wk revealed a low energy intake (1200 kcal/person/day). Despite the high contribution of animal food to the total energy intake (64%), the diet was low in total fat (13%) due to the very low fat content of wild animals.
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Thursday, February 21, 2013

The New Paleo Diet Study: Paleo-type-style-ish Diets vs. "Paleo"

There's a new Swedish paleo diet study out: A Palaeolithic-type diet causes strong tissue-specific effects on ectopic fat deposition in obese postmenopausal women.  The title sounds promising, but my first reaction to it, sadly, not so much about the potential findings, but, what exactly is this paleo-TYPE diet??  It would appear to be based loosely on Cordain's original Paleo Diet (I hear that's trademarked).  

This was a small study, 10 women, no control group, lasting only 5 weeks.  There were some benefits including around 10 lbs average weight loss and almost 50% reduction in liver fat.  This shall be for another blog post.  But what diet was tested?  Here's the diet description from the full text:
Participants were given prepared meal portions that were intended to provide an average intake of about 30 energy percentage (E%) protein, 40 E% fat (mostly unsaturated) and 30 E% carbohydrates for breakfast, lunch and dinner, together with 40 g nuts (walnuts and sweet almonds) on a daily basis for 5 weeks.

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Sunday, September 23, 2012

Childhood Nutrition ... The Egg Survey Results!

I haven't forgotten my Egg Survey!  Thanks to all who participated, and essentially confirmed my memories of this aspect of childhood were quite "average".   There were also quite a few new names amongst the responders so I'd like to extend my belated welcome to the Asylum!


 First my own answers (and for my husband as well), and then a brief summary:
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Thursday, September 6, 2012

Egg Survey

Question for you all, and I'm going to limit this to the 40+ members of the audience (or if your parents really did just ignore the egg/cholesterol scares).  

When you were a kid, say in the 4-12 year old range, did you:
  • Eat eggs regularly for breakfast?
  • If so, how many?
  • Eat eggs for protein at other meals?
  • If so, did you also eat eggs at breakfast?
  • How many eggs per week did you eat as a kid?
Feel free to add other details.  Thanks in advance for participating!

Tuesday, August 7, 2012

Super High Fat Ketogenic Diets v. Paleolithic/Ancestral Nutrition

As the trend towards even higher fat diets continues in a faction of the community, it should become ever the more clear to those not engulfed in dogma that this is not consistent with our evolution.  There is no way, repeat NO way, that our ancestors could have eaten a diet of the 80-10-10 variety -- as in 80% fat, and 10% protein, 10% carbs ... or any of the various higher fat lower carb ratios, perhaps allowing for an extra couple few percent of protein.  

One would have to believe that humans evolved in an environment of such abundance where killing was accomplished with such ease, that they would kill another animal to eat just its fatty parts before consuming the meat.  Does that sound plausible to you?  Or that humans foraged for only fatty plant stuffs like nuts and fatty fruits like avocados and left the sugary and starchy stuff they may have happened upon in the process alone.  Sounds right, eh?  We're to believe that cultivation of plants has altered their sugar and starch content vs. the days of old, but domestication of animals and even "wild life" existing on the fringes of human developments has not altered the composition of said same ... even if fed a "natural diet" (e.g. grass fed beef).  Your fatty fish are mostly around 60% fat or less.  Are all these paleo lipophiles having seal oil and whale blubber shipped in from the Arctic?  
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Thursday, May 24, 2012

Amino Acids in Human Metabolism

Just putting this up here, from this study courtesy of Julianne Taylor:  Quantitative Analysis of Amino Acid Oxidation and Related Gluconeogenesis in Humans  (this is an older, large file, I've shared the full text in Google Docs, and I'll come back and edit in the link when GD decides to behave in my browser).   Mind boggling!




Tuesday, May 22, 2012

Excess protein turned to glucose?

It seems that part of the more recent trend of defining a "proper" low carb diet as being one that is moderate in protein and high (very) in fat is this notion that excess protein will just be turned to glucose.  Quite often I've seen Dr. Richard Bernstein cautions against eating too much protein because it just gets turned to glucose.  (I did look for a link but was unsuccessful, so if I'm misstating Bernstein here, please do correct me in comments.)   I had looked into this long ago, but never really said much about it, but there are two reasons why this never made sense to me.

First, a little biochemistry.  There are exceedingly few reactions that occur in our bodies without the involvement of an enzyme.   This includes not only anabolic (synthesis, building, energy storing/requiring) reactions, but also catabolic (break down, energy releasing reactions) reactions.  Glucose and fatty acids no more "spontaneously combust" in our bodies than does propane in my grill.  Enzymes are the catalysts of reactions, and reactions that require energy (all of those "genesis" reactions for example) are coupled with energy producing reactions that "drive" them.   Enzyme action is regulated by the amount of the enzyme produced and/or some mechanism of activating/deactivating the enzyme.  While enzyme mediated reactions can be related to substrate (reactant) availability and/or influenced by product availability/build-up, this isn't always the case.  I'd even go so far as to say that unless the reaction occurs in a highly compartmentalized fashion (e.g. within mitochondria), substrate/product concentrations generally have little effect on the reaction rates directly. 
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Tuesday, March 27, 2012

The First Law of Thermo still doesn't violate The Second Law

Well, I've been meaning to weigh in on the Bray overfeeding study (Effect of Dietary Protein Content on Weight Gain, Energy Expenditure, and Body Composition During Overeating) that made a bit of a splash a little while back. George Bray is especially hated by ardent low carb advocates because he wrote a particularly unfavorable review of GCBC published in Obesity Reviews.   Bray is what Adam Kosloff refers to as a "Calorie Wizard":
Regardless of diet, it is a positive energy balance over months to years that is the sine qua non for obesity. Obese people clearly eat more than do lean ones, and food-intake records are notoriously unreliable, as documented by use of doubly labelled water.  Underreporting of food intake is greater in obese than in normal-weight people and is worse for fat than for other macronutrient groups.  Accepting the concept that obesity results from a positive energy balance does not tell us why energy balance is positive.  This depends on a variety of environmental factors interacting with the genetic susceptibility of certain individuals.  Weight loss is related to adherence to the diet, not to its macronutrient composition.
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Friday, March 16, 2012

Odds, Ends and Battery Acid

Hey everyone!  I cannot believe it is Friday already ... this week flew by but we have 2 full days more here and then back to our other hotel for the last night.  We've been here before so we know all the tricks and such.  Even though check in isn't until 3, we arrived in beachwear with a pool bag packed, they slapped a bracelet on each of us, and we were off to sun and lunch while our luggage waited for the room.  Sunday we'll check out early and then catch lunch and perhaps even a dunk in the cold plunge and hot tubs before heading out.   It's almost like getting an extra day this way but with no stress of flying out.   So this worked out really well for us in many ways, not the least of which is the stress of flying always eats into the relaxation, this way we get full relaxation mode for the all-inclusive with so much to enjoy.
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Wednesday, November 2, 2011

Glycine Power?!

One of the things I've been doing regularly for the past year or so is making carcass broths and bone broths and making stews and soups with it.  I make the distinction of carcass v. bone because I mostly make two versions:  (1) pork from pork shoulder bones my amazing pork guy provides me free by the bagful (so I don't have to save up bones in the freezer which is a huge bonus!) and (2) chicken from the whole carcass from chickens or everything from the parts -- e.g. a fair amount of skin and cartilage and "stuff".  

There was a question about pork rinds and satiety the other day on PaleoHacks that reminded me of a few things.  One was that whenever I would hear of the health bennies of gelatin protein, I always remembered reading that it was not a good major protein source because it is not a complete protein.  Well, the protein from such broths may not be complete, but it is special indeed.  I'm not one for anecdotes but my less-than-perfect-diet hubby is prone to getting bronchitis or worse at least a couple of times every winter and he's had issues with prolonged bouts that turn into one long episode.  Last winter?  One short cold!  I tend to think that's no coinky dink.  
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Monday, October 24, 2011

Commercial Milk: Full Fat vs. Non-Fat Nutrient Comparison

Just the Facts Ma'am from www.nutritiondata.com for Milk

Whole, 3.5%                             NonFat w/o Vit A

  

  
  


Yes, fat-borne vitamins and minerals are missing from the non-fortified non-fat milk.  But (1) low fat is not non-fat, (2) most low fat milk is fortified with vitamins A&D, and (3) The differences are small unless you're talking getting large percentages of daily calories in liquid milk form.   

Saturday, October 22, 2011

High Protein Diet Induces Sustained Reduction in Ad Libitum Intake Despite Diurnal Leptin Compensation

I've written several hundred posts on this blog.  There are some, especially from early on in 2010, that I would really like my readers to see, and I sure don't expect folks who are just finding this blog now to go back and read everything to find some that I feel are key.  I refer to this study quite often because I think for those finding themselves gaining a little bit each year and not wanting to hop on some "diet rollercoaster", there is merit to -- especially for us women -- upping the protein as a percentage in the diet.  So when I was compiling graphics for the 24 Hour Leptin Profiles post, this study was the first I knew to go to for a graphic.  So, I'm bumping the original, adding a little emphasis to the text but not changing it, and I'll add some commentary on leptin at the end.  



Original Publish Date:  4/30/10


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Tuesday, July 19, 2011

Dr. Eades on Starvation Diets

When the recent news broke that a Crash Diet (600 cal/day) cured diabetes, discussed HERE,  HERE,  HERE, there was the inevitable invoking of the Minnesota Starvation Experiment in the low carb circles.   A while back, I addressed the MSE in a post entitled Starvation Diets shortly after I had blogged on a study in which one part involved putting three obese women on a 1500 cal/day liquid reducing diet.

The point of that last blog post was that  in the 1970's, the average intake of American women was 1550 cals.   Now folks, keep in mind that averages mean that some women ate less and some ate more.   Dr. Michael Dansinger -- he of the famous diet comparison study and consultant on The Biggest Loser -- told Jimmy during his interview with him that they generally cut the contestants' intake in half on that show.  I don't have time to go back and listen, and the exact numbers aren't really all that important, but the women generally start out eating around 3000 cal/day, so their reducing diet is 1500 cal/day.  Lots of low carbers sneer at TBL as, of course, being the wrong way to lose weight, they could just go low carb and achieve the same results by eating more.  
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Sunday, June 5, 2011

Protein, Insulin-like Growth Factor-1 (IGF-1) and Glucose Homeostasis

I've blogged previously on the LoBAG diets for treatment of diabetes.  These diets are higher in protein that standard recommendations - 30% vs. 15% - with varying carb content (20,30 & 40% have been studied).  With both of the lower carb diets, this group has achieved good improvements in HbA1c levels in relatively short time (5-10 weeks).  In comparing their diets  they observed:
Increasing the protein content of the diet from 15 to 30% resulted in an 35% increase in IGF-I regardless of whether the carbohydrate content was 40%, 20%, or 30% as in the present study. Thus the dietary protein-induced increase in IGF-I is independent of the amount of dietary carbohydrate and fat.
I believe the near-OCD obsession with insulin in the LC community overshadows the vast body of research on other hormones and peptides that's out there and their role in metabolism.
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Monday, July 5, 2010

Recommended Reading on Insulin

A shout-out to James Krieger who seems to think a lot like me (or me like him? or we just think alike??!).  I would like to encourage anyone reading this to go and take in an excellent post by James:

Insulin…an Undeserved Bad Reputation

Here's my bottom line on all this:  If the "alternate hypothesis" were true, then all cultures eating a higher carb diet would be obese and nobody could lose weight on a high carb calorie restricted diet.  We know neither is true.

Sunday, June 13, 2010

Protein for Energy





I've held off on posting this for a while because it's a screen shot and I have no idea whom to credit. But, since the metabolic pathways are common knowledge, I've decided there's no real harm done "publishing" any depiction of them on my li'l old blog. (If anyone recognizes the graphic, please notify me so I can extend credit)

An enduring point of controversy exists in the LC community over higher protein intake vs. higher fat. My personal experience is that the former works for me, but there are plenty of folks doing well on high fat controlled protein approaches.

One of the advocates of lower protein intake is Dr. Bernstein the diabetes specialist. Most that advocate his approach agree with his central premise that excess protein is converted to sugar or metabolized as such. While theoretically possible, I've been doing some "re-educating" of myself where protein metabolism, specifically what becomes of any excess is concerned.

OK, so here it is:


This is the most concise depiction of the various amino acids and where they can feed into metabolic pathways.  The "green boxed" AA's are termed glucogenic AA's because they can be turned into glucose under certain conditions.  The "white boxed" AA's are ketogenic as they cannot be converted to glucose entering the metabolic paths at these junctures.  You will note that certain AA's are potentially ketogenic or glucogenic because they can be converted to different substrates.

The blue-arrowed cycle here is the Citric Acid Cycle, aka Kreb's Cycle.  Of note is that the central linking molecule of carb and fat metabolism, Acetyl CoA, is the primary "external substrate" feeding into this cycle (black arrow).  The primary substrate for glucose formation (gluconeogenesis) is oxaloacetate -- the last "stop" on the cycle.  Pyruvate is the product of glycolysis -- glucose metabolism -- but it's both a product and substrate for other metabolic pathways.

The pink arrows are gluconeogenesis (and we know there's also glyceroneogenesis from pyruvate).  However  my research points to these pathways being stimulated in response to the carbohydrate restriction component of fasting and not to amino acid levels although that might be possible.  This seems to be the concensus in the LC community as well -- our bodies will only turn protein to glucose to meet needs.  Some of the excess may be "burnt like sugar" because it enters the Krebs Cycle by going through the pyruvate pre-cursor, but this really just means another step to get to the ultimate central molecule of Acetyl CoA.

So, excess protein gets used for energy like ... well ... excess amino acids (as opposed to glucose or fatty acids).   Or if you want to get semantically picky, some feed into metabolic pathways involving glucose, and some into pathways for fatty acids, and some like neither of the other macronutrients.  Too much available energy from any source and Acetyl CoA gets converted to fatty acids -- de novo lipogenesis!  In this regard, protein would be the least lipogenic of the macronutrients.  For a while there I was under what I now realize to be an incorrect assumption, that protein-to-fat would go through glucose to AcCoA to fatty acid by DNL.  But this seems an unlikely path except, perhaps, in the diabetic with issues of over-active gluconeogenesis.  Still, I'm unsure if that path would be further enhanced simply by an excess of pyruvate and/or oxaloacetate made available by excess AA's.

Limiting protein for weight loss does not seem to be a very good strategy unless someone wants to lose muscle mass, particularly for someone consuming a VLC diet.  The VLCer's body will make glucose and get the necessary AA's from where it will -- better the diet than the body IMO.  Protein is almost impossible to overeat.  For diabetics, however, relying on protein as an energy source may present other issues as relates to various complications of that disease.

Previously I've characterized protein as a poor energy source.  However, I no longer believe this to be true.  It is not a preferred energy source, perhaps, but it seems to feed pretty efficiently into Krebs.

Friday, April 16, 2010

Protein in optimal health: heart disease and type 2 diabetes

Protein in optimal health: heart disease and type 2 diabetes

Aside:  The lead author (I believe), is affiliated with the Australian CSIRO research group that is well regarded in the LC community -- except when, in the end, CSIRO's highly successful weight loss plan does not advocate for high fat  VLC after all.  I would also point out that the authors and the summit from which this article originated were highly subsidized by "Big Egg", "Big Dairy", "Big Beef" and "Big Pork".  I point this out not because I question the findings that seem pretty sound, but to point out that discounting research based on the sponsor just because one doesn't like the outcome is common practice amongst "debunkers".

So, that said, on to this article.  I won't repeat the whole thing.  It is a review, and although requires slow reading to digest, it's not overly clouded with technical lingo.  Some highlights of interest in no particular order:
  • Regardless of dietary makeup, LDL seems to be ultimately related to one's weight status  both in terms of degree of excess weight and whether one is maintaining, losing or gaining weight.
  • Protein's  "power" in weight loss may and glycemic control may well be its insulin stimulating action (particularly, leucine and glycine) -- this goes counter to LC theory, but makes sense to me.  If the post prandrial insulin response is increased by protein with reduced carb intake, BG's will not rise as high, and will fall more rapidly.  Protein seems to help insulin sensitivity.  If this occurs, chronic (basal) insulin levels should go down b/c the insulin manufactured in response to food is more effective, hence the pancreas is not pumping out more and more insulin in response to chronically elevated BG's.  Eggs, BTW, are particularly high in leucine.  Carbs and fats are still the prefered energy substrates, so insulin in-and-of-itself does NOT drive net fat storage, it merely directs energy traffic to the priority of available glucose or more towards fats when carbs are restricted.
  • Infused amino acids raised BG levels and insulin, while ingested whole proteins seem to have the opposite effect.  I've seen many studies demonstrating similar effects for infused vs. ingested fats, and liquid glucose vs. whole carbs.  As the review points out, this underscores the involvement of our digestive systems and livers in the whole picture.
High protein is not defined here.  But there is some info on diets in which carbs are replaced with protein (as opposed to fats as is highly recommended in the LC world these days).  For me, this seems to be where it's at for weight loss.

Wednesday, March 17, 2010

Protein & Satiety I

A few studies and such on protein and satiety:

Weight, Protein, Fat, and Timing of Preloads Affect Food Intake
Two foods, one rich in protein (HP) and one rich in fat (HF), were employed to evaluate the effect of macronutrients on food intake and to underline the differences that occurred when the foods were served as uniform meal, as first course of a varied meal, and as a snack 2 h before a varied meal. Our results showed that HP food always exerted a higher effect on both intrameal satiation and postingestive satiety than HF food. When a uniform meal was consumed, satiation for the specific food was reached before fullness; in this condition, sensory characteristics of foods played an important role in controlling food intake and made the uniform meal more satiating than the varied one. The consumption of a snack far from a meal did not contribute to satiety; consequently, gastric filling seems to be an important factor determining the amount consumed in a varied meal.
Add this to my list of articles I have to get a hold of the full text of. 

The influence of thermic effect of food on satiety.

OBJECTIVES: To evaluate energy expenditure after three isoenergetic meals of different nutrient composition and to establish the relationship between the thermic effect of food (TEF), subsequent energy intake from a test meal and satiety sensations related to consumption.

DESIGN: The study employed a repeated measures design. Ten subjects received, in a randomized order, three meals of 2331+/-36 kJ (557+/-9 kcal). About 68% of energy from protein in the high protein meal (HP), 69% from carbohydrate in the high carbohydrate meal (HC) and 70% from fat in the high fat meal (HF).

SETTING: The experiments were performed at the University of Milan. Subjects: Ten normal body-weight healthy women.

METHODS: Energy expenditure was measured by indirect calorimetric measurements, using an open-circuit ventilated-hood system; intake was assessed 7h later by weighing the food consumed from a test meal and satiety sensations were rated by means of a satiety rating questionnaire.

RESULTS: TEF was 261+/-59, 92+/-67 and 97+/-71 kJ over 7 h after the HP, HC and HF meals, respectively. The HP meal was the most thermogenic (P < 0.001) and it determined the highest sensation of fullness (P=0.002). There were no differences in the sensations and thermic effect between fat and carbohydrate meals. A significant relationship linked TEF to fullness sensation (r=0.41, P=0.025). Energy intake from the test meal was comparable after HP, HC and HF meals.

CONCLUSIONS: Our results suggest that TEF contributes to the satiating power of foods.
Breakfasts high in protein, fat or carbohydrate: effect on within-day appetite and energy balance.

OBJECTIVE: To compare the effect of isoenergetically-dense, high-protein (HP), high-fat (HF) or high-carbohydrate (HC) breakfasts (at 08.30) on subjective hunger, fullness and appetite (measured hourly on a 100 mm visual analogue scale), macronutrient balance and ad libitum energy intake (EI), at a test meal (13.30) and throughout the rest of the day (until 23.00).

DESIGN: Six men each spent 24 h in a whole-body indirect calorimeter on three separate occasions during which they received breakfasts designed to match 75% of BMR and that comprised, on average 3.1 MJ of protein (HP), carbohydrate (HC) or fat (HF), respectively, the remainder being split between the other two macronutrients. Every item of the ad libitum diet comprised 13% protein, 40% fat and 47% carbohydrate by energy, with an energy density of 550 kJ/100 g.

RESULTS: Subjectively-rated pleasantness did not differ between the breakfasts, or any of the subsequent ad libitum meals. Subjective hunger was significantly greater during the hours between breakfast and lunch after the HF (26) treatment relative to the HP (18) or HC (18 mm) meals (P < 0.001), although the HP treatment suppressed hunger to a greater extent than the other two treatments over 24 h. However, mean ad libitum lunch intakes were similar at 5.38, 5.30 and 5.18 MJ (NS) on the HP, HC and HF treatments, respectively. After-lunch intakes were also very similar at 6.14, 6.18 and 5.83 MJ (NS). Mean 24-h energy expenditure amounted to 11.12, 11.14 and 10.93 MJ, respectively, producing energy balances of 5.71, 5.83 and 5.04 MJ (NS), respectively. The HP, HF and HC breakfasts led to enhanced P, F and C oxidation, respectively (P < 0.003).

CONCLUSIONS: Large HP, HC or HF breakfasts led to detectable changes in hunger that were not of sufficient magnitude to influence lunch-time intake 5 h later, or EI for the rest of the day. A single positive balance of each macronutrient can be buffered by oxidation and storage capacity, without leading to changes in meal-to-meal EI, when subjects feed ad libitum on unfamiliar diets of fixed composition.
Interesting indeed.  Hunger INCREASED after HF vs. HC or HP (the scores of which seem similar).  But not enough to influence intake.  Still, this flies in the face of the Low Carbventional Wisdom.