Using studies that were debunked years ago just shows that you are trolling and nothing more.
you won't find any good trials for either. there are infinitely too many variables in the horrible shape the human body is in now, and there is a lack of funding and backing for such trials. you have to rely on biology for this.
i have found several on rats where thermogenesis was impaired in some way and they gained significant weight on a high fat chow diet, but it's not the same thing.
He who dares not offend cannot be honest.
Using studies that were debunked years ago just shows that you are trolling and nothing more.
The "metabolic advantage" was coined by Robert Atkins to sell a fad diet, he claimed you peed out up to 600 calories a day through ketones. It had and still does have hundreds of thousands of people around the world fruitlessly peeing on ketostix hoping for a purple color thinking it means they pissed out half the calories from the low carb chocolate cheesecake they just devoured.
If you really were peeing away half of your last meals calories I certainly wouldn't call it an "advantage".
There probably is an advantage to carb refeeds for a dieter, as directly after the meal it's going to be less efficient at converting it to fat and it will help increase the metabolism slightly and signal to the body that it's not starving.
I don't suppose enjoining you to deploy your Wikipedia skills towards researching metabolism and or biochemistry would serve much of a purpose?
Ok, well, no matter, let me try to give you the Cliff's notes of Cliff's notes version about how energy metabolism works:
- The fundamental driver of metabolism is the concentration gradient, you metabolise that which is most prevalent or common, meaning that if you are eating predimantly carbohydrates, that's your energy substrate. Fats, then FFAs it is, and much the same with protein. If you've ever used a blood glucose meter, then you've directly measured the concentration of glucose in your blood, which is why the units of such measurements are mmol/l in Europe. This is the scientific unit for concentration (molarity). North Americans are saddled with a non-standard unit of mg/dL.
- Unlike what you seem to believe, the body is in a constant state of gluconeogenesis. As in every second of every day of your life. Several tissues like red blood cells and the kidney medula are obligate glycolytic tissues. Lacking mitochondria, they are incapable of oxidative respiration and so can only derive energy from glycolysis. The interesting thing about this is that the end product of glycolysis in the absence of mitochondria ( or sufficient oxygen in those cells possessing mitochondria ) is lactic acid. So, of course, all of us are keeling over from extreme lactic acidosis as the lactic acid builds up in our systems catastrophically altering the pH of our bodies, right? Well, no, because lactic acid is a very nice 3 carbon chain that when combined with another such molecule in hepatocytes is used as a gluconeogenesis substrate to regenerate glucose. So, if you possess red blood cells or kidneys, guess what, you are in a constant state of gluconeogenesis.
- If you are eating large quantities of protein, then we can expect that your plasma will contain large quantities of amino acids. This is, after all, the point of digestion. According to you, then, in an environment replete with amino acids, metabolism would respond by secreting increased cortisol to produce yet more amino acids?? Even if you know absolutely nothing about metabolism, this makes absolutely no sense. I suspect that you threw cortisol bogeyman in there in an attempt to motivate readers to your point of view with fear and uncertainty. In any event, due to the increased concentration gradient of amino acids, this alone results in increased gluconeogenesis ( tada, back to #1 )
- Below is the generic structure of an amino acid. The interesting bit there is the nitrogen, or amine, group ( the purple atom in the diagram ). What do you suppose we are left with, chemically speaking, if we were to remove the amine group ( deamination )? Give yourself three gold stars if you said a fatty acid. So, metabolically speaking, a deaminated amino acid pretty much goes through the same metabolic pathways as would a free fatty acid. The complication is the amine group. Amine groups are removed via the process of hydrolysis, which means that a water molecule is basically striped down to one hydrogen, and a hydroxy ( OH ) group. The one hydrogen atom goes to the amine group which results in ammonia being produced. Ammonia is a neurotoxin similar to arsenic in its effects which must be eliminated. The elimination of toxic amine groups is the whole purpose of the urea cycle. It is this process of metabolising free amine groups that is largely responsible for the lower energy yield of protein.
Protein poisoning is a real possibility, but has nothing to do with cortisol, per se. Rather, it comes from forcing the liver to excessively deaminate proteins and the kidneys to process excess amounts of urea. The conclusion from all of this is that protein should primarily be a structural, not energetic substrate. That is, use your protein to build your tissues, and either carbohydrates or fats for energy. Note that either fat or carbohydrate will ameliorate protein poisoning, something that doesn't seem to sit well with carbohydrate apologists, particularly when you couple that with the observation that there are essential fatty acids that must be provided by the diet, unlike the case for carbohydrates.
I will give you this much, Choco: I will agree with you that overeating protein is a bad thing. The tricky bit, of course, comes from that seemingly innocuous "overating" part.
A hypocaloric diet implies an energy deficit.
An energy deficit requires metabolism to become conservative with respect to energy expenditure. This necessarily implies lower thermogenesis.
Thermogenesis is regulated via thyroid hormones. Lowering thermogenesis therefore implies a shift from T3 to rT3 production.
Therefore, _any_ hypocaloric diet, independent of macronutrient composistion, will result in a shift from T3 to rT3 production.
An organism that does not respond in this manner is an evolutionary dead end.
It wasn't a 1000 calorie diet. Not sure how much of this I'm allowed to share...Originally Posted by Neckhammer
During the 28 day treatment period, both groups consumed a daily liquid diet consisting of 530 kcal. The base diet for both groups consisted of 330 kcal as a liquid formula preparation (Cambridge Diet). This diet contained 33 gm protein, 44 gm carbohydrate, and 3 gm fat. Each diet was increased with a daily addition of 200 kcal as either carbohydrate (Polycose, Ross Laboratories, Columbus Ohio) or fat (Microlipid, Biosearch, Sommerville, NJ). Thus, the final composition of the diets were 33% and 71% carbohydrate for the LC and HC groups, respectively. Both treatment groups participated in the same exercise program consisting of jogging or brisk walking, depending on initial fitness level, to achieve a heart rate corresponding to 60% VG, max for 30 to 45 minutes. The exercise sessions took place three times per week at noon and were supervised by the experimenters. At the end of the treatment period, the participants were instructed to follow a 1,000 kcal diet of solid foods using the diabetic exchange system (20% protein, 45% carbohydrate, 35% fat) for one week post-VLCD. The exercise sessions were continued during this post-VLCD period.
If you look at the right side of the table, RMR (kcal/d/kg), the LC advantage is lost. Why? From the discussion:
Edit: The HC group weighed less on average. (My mistake, got mixed up) A 530 calorie diet doesn't seem to be the best context in which to discuss thermogenesis.A decrease in RMR may be secondary to a decrease in lean body mass since it has been shown that RMR is highly correlated with the fat free mass.4*2’ The fact that RMR, when expressed per body weight, was no longer significantly altered over time by the VLCDs supports the concept that the drop in RMR during caloric restriction coincides with a decrease in body weight.
Haven't read the second study yet.
Last edited by Timthetaco; 10-06-2013 at 08:07 AM.
@Timthetaco..... Those were a couple of examples of the type of studies I would like to see, not necessarily proof of a position in and of themselves. I understand (as zach pointed out) that these studies have issues.
Just to make it clear, I am not arguing FOR the existence of a metabolic advantage in low carb or ketogenic dieting. I am asking for the evidence to the exact contrary. A popular meme as of late is that carbohydrates increase our metabolism. I was asking if there was human trials that support that claim. If in fact a higher proportion of carbs in isocaloric diets increase our metabolic rate then it should be measurable right?
Here is a newer study that most round here are now familiar with and its a bit better in terms of methodology:
JAMA Network | JAMA | Effects of Dietary Composition on Energy Expenditure During Weight-Loss Maintenance
Conclusion Among overweight and obese young adults compared with pre–weight-loss energy expenditure, isocaloric feeding following 10% to 15% weight loss resulted in decreases in REE and TEE that were greatest with the low-fat diet, intermediate with the low–glycemic index diet, and least with the very low-carbohydrate diet.
Of course this is the study that Peter breaks down in this post
You probably recognize that I'm simply putting the onus of the "metabolic advantage" back on the high carb diet, since this..... "well its the thermogenic effect of food.... you can't argue"..... sort of mentality is beginning to take hold. I thought it was worth exploring the human trials to see how it held up to scrutiny.
I'm not trying to be a prick about it. There are surely plenty of reasons to change your macronutrient profile. I'm just not convinced that.... "because carbs have a greater thermogenic effect" is a good one. You know its kind of funny cause its the exact same thing that forgotmylastusername talks about in reverse. Some people in ketosis think you cant gain fat as long as you are peeing it out, and it seems some people eating high carb low fat think they cant gain fat cause they will just burn it all up as heat energy. I don't actually believe in either of those myself
Last edited by Neckhammer; 10-06-2013 at 09:48 AM.
Last edited by pklopp; 10-07-2013 at 08:42 AM.
A NEW DEFICIENCY DISEASE PRODUCED BY THE RIGID EXCLUSION OF FAT FROM THE DIET.*" which fed experimental rats a diet completely devoid of fat. How did the animals fare under this regime?
The pathology here is really interesting, particularly with respect to Choco's claim that fatty acid deficiencies do not manifest in any way as skin conditions, which, at least for rats, is completely wrong, and we've known about it for almost a century now.Originally Posted by A NEW DEFICIENCY DISEASE PRODUCED BY THE RIGID EXCLUSION OF FAT FROM THE DIET.
So what happens when we feed rats fat, but not the essential fatty acids that Choco doesn't believe in?Originally Posted by The essentiality of arachidonic acid and docosahexaenoic acid
Well, we certainly observe a difference, and the rats that are not fed essential fatty acids do worse with respect to growth and cold tolerance.Originally Posted by Effect of dietary linoleic acid and essential fatty acid deficiency on resting metabolism, nonshivering thermogenesis and brown adipose tissue in the rat.
Back to humans, note the bit in bold again, yeah, it's going to address skin changes among other things:
And one more for good measure:Originally Posted by The possible role of essential fatty acids in the pathophysiology of malnutrition: a review
I don't know about Choco, but imparied growth, dermatitis ( there's that pesky skin pathology again ), steatosis (fatty liver disease), renal toxicity and pulmonary abnormalities sure do sound like symptoms of a deficiency to me. And the funny thing is, all of it can be avoided by taking, GASP, toxic Cod liver oil ( you know, the equivalent of swilling WD40 in Chocos world ).Originally Posted by FISH OIL PREVENTS ESSENTIAL FATTY ACID DEFICIENCY AND ENHANCES GROWTH: CLINICAL AND BIOCHEMICAL IMPLICATIONS
So, Choco, I'm taking you up on your offer to debunk these studies. Looking forward to sparring with you! And, by the way, I do sometimes find your advice helpful insofar as I do not put my faith in the things you say and I also do my own research!