How carbs and insulin make you fat and/or ill!

[ATZ]

Fine, I'm willing to accept that's probably not the best piece of research I've posted on reflection.

However, all this side track arguing is distracting from the main crux of this thread: that carbs make you fat. If this was the case, in any of the studies you or myself posted dietary interventions involving diets with a high proportion of CHO wouldn't yeild weight loss. Yet they do. So how is insulin and cho's effects on it the only determinor in fat gain as a result?

[NU_nutrition_TS]

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Fine, I'm willing to accept that's probably not the best piece of research I've posted on reflection.

However, all this side track arguing is distracting from the main crux of this thread: that carbs make you fat. If this was the case, in any of the studies you or myself posted dietary interventions involving diets with a high proportion of CHO wouldn't yeild weight loss. Yet they do. So how is insulin and cho's effects on it the only determinor in fat gain as a result?

You've really just answered you own question (note the parts in bold - how they differ) though I had already posted an answer for you (today) a couple of pages back: http://forum.myprotein.co.uk/357554-post317.html and countless times before that. If you read that post again pay careful attention to where the term weight loss/gain overlap or diverge from the term fat loss/gain. When you lose or gain weight you are also usually altering body composition - lean to fat mass ratio.

And there are examples (already posted) where both a calorie reduction and a high carb ratio have resulted in no weight loss or even gain.

[ATZ]

Of course you have Nu.

Insulin is not the only factor in fat/loss or gain. Insulin is primarily concerned with the regulation of blood glucose, not fat metabolism. Focusing solely on insulin neglects the role of overall energy balance on fat gain and metabolism. And why as per your other posts contention is it easier to overeat on carbs? Fat contains over twice as many calories per gram and this is without taking into account individual responses to these macro's - some people feel fuller on one over the other.

And this so call "other evidence" you supplied has already been refuted or it's validity questioned.

[NU_nutrition_TS]

I'm afraid I have to disagree with you again - insulin has many functions. It's primary function is (or, at least, currently appears to be due to our predominantly high carb diets) glucose control but it has many functions including fat metabolism. In fact, insulin has been around since life on earth began and all life forms have insulin. It is probable that many of the functions of insulin have been relegated to subordinate levels of priority by our adoption of higher and higher carb diets since the neolithic period and may explain the onset of many of the diseases of civilisation. All of this can be checked and confirmed in any standard biology and endocrinology text.

I think I laid all this out in my OP but since that was 30-odd pages back and memories appear to be short (and maybe I did not explain myself very clearly) I will give you another way to think about the mechanism.

In any body weight gain or loss ask yourself this question: Is there a change in body composition?

Now think very carefully before reaching a conclusion. Body composition is essentially a ratio between lean mass and fat mass. The ratio can change: a gain of lean and no change in fat. A gain in fat with no change in lean. A change in both lean and fat - both up, both down or one up while the other comes down. In any case there is a change in internal body composition that registers on the scales as a change in weight (MASS).

Now ask yourself this question: How are those changes in body composition achieved? Again, think very carefully.

Lean mass as exemplified by muscle tissue is increased when we place an overload stress on it and cause a degree of damage to the tissue. This initiates a response that causes the body to release certain hormones and biochemicals that, in turn, signal the stimulation of various physiological processes that result in repair and augmentation of the damaged tissue. Those processes require both energy, in the form of ATP, and raw materials, such as amino acids, to rebuild muscle tissue. This creates a need to supply both the energy and raw materials, so the physiological factors precede (or should) the increased intake of raw materials and energy as food.

What about fat mass? You can't really physiologically overload the fat tissue with exercise so there is no reason there to initiate an adaptive response that would create more.

Adipose cells are pretty much set from childhood and adolescence and then we carry them forward through adulthood. They can be empty or they can be full, or at any stage in between, with triglycerides - the form in which fatty acids are stored longer term. In order to make triglycerides you need both fatty acids and glycerol. Glycerol is synthesised from glucose via alpha glycerol phosphate and the action of insulin. So you need fatty acids, glucose and insulin to be present in large enough amounts for fat to be stored in a form that is resistant to be being released from the adipocytes without the action of other hormones and enzymes.

So what hormones do you need to release triglycerides from fat cells? Before answering that it is as well to say what you don't need - insulin.

You need lipolytic hormones; those that serve the complimentary function of insulin. One of the major ones - and the yang to insulin's yin - is glucagon. Glucagon triggers 7TM receptors (G protein-coupled receptors), which activate adenylate cyclase. This results in increased production of cAMP, which activates protein kinase A, which subsequently activate lipases found in adipose tissue. The lipases hydrolyse the triglycerides breaking them back down into fatty acids and glycerol. The fatty acids bind with albumin (a protein) in blood and get transported to cells to be used as a source of energy.

Since insulin release blocks the release of glucagon and most other lipolytic hormones, we can see that a absence of high levels of insulin release is required as well as glucagon release to reduce fat storage.

So what can we see as the primary initiating factors in either fat storage or fat release? Hormones. For fat storage we need - beside the fatty acids - glucose and insulin release. Eating carbs that raise blood glucose and insulin provide these. For fat release we need glucagon and little or no insulin so, if we do not eat carbs that raise blood glucose and release insulin, we have the perfect hormonal environment for fat breakdown.

Ordinarily the body relies on fatty acids for energy for most of its cellular functions most of the time with glucose only coming into play when physical activity is very intense and cells need to respire anaerobically. So we need a hormonal environment, through diet, that allows the free flow of fatty acids to those cells that need it throughout the day. The hormones decide how the various forms of energy we consume are partitioned, both for oxidation when fuelling the energy needs of cells and when being stored as either glycogen or triglycerides (Note: glycogen is stored glucose as triglycerides are stored fatty acids).

Now if we eat a sub-maintenance level of calories as mainly carbs with very little fat (a typical low fat, calorie reduced diet) what do you think happens, bearing in mind the preceding information? Think carefully.

The CHO increases blood glucose levels and that releases insulin. If you have eaten lunch and are spending the next few hours behind your desk at the office, you do not really need to burn a lot of glucose as, in this state the body prefers to use fatty acids. But your diet has minimal fats and lots of carbs.

You have already raised your blood glucose and released insulin. Insulin release from the pancreas due to excess blood glucose blocks the release of glucagon so existing fat stores cannot be accessed or released. Blood glucose needs to be returned to normal quickly so it either has to be oxidised as an energy source or stored as glycogen. Since you are not physically active enough for the cells to want to use a great deal of glucose - because you are sitting at your desk - it has to store it. However, if your glycogen stores are already full, it will have to convert it to fatty acids as that is what your body requires at this level of activity to function best.

It is likely, however, that if this is the habitual diet over a long period, you will have adapted to burning glucose instead of the scarce fatty acids, so the fatty acids may float around unused, and with the presence of glucose and insulin they can be stored as triglycerides in the adipose cells - certainly the insulin will block any extra fatty acids being released from them.

Now if you are eating sub-optimal levels of total calories it is likely you will quickly burn through the excess glucose you have introduced into your blood stream and the cells will once again be starving for fatty acids. Unfortunately any free fatty acids you had may have been stored as triglycerides and since insulin is slower to return to baseline than is the glucose that induces it's secretion, your blood glucose drops even lower. At this point, as you begin to enter hypoglycaemia, the insulin will be dropping back to baseline and that will allow the low blood sugar to activate the release of glucagon. The presence of glucagon will enable the aforementioned hormonal cascade that releases fat from the adipocytes. But at this point you feel hungry, weak and craving a chocolate bar or a biscuit. So you go to the vending machine and get a Snickers bar or something and eat that at your desk - and the whole cycle begins again - blood sugar shoots up, as does insulin, lipolysis is abruptly shut down and you wait for the next hypoglycaemic crash to start the cycle again.

Assuming you can't have (or deny yourself the sugary snack) will the drop in blood sugar and insulin, and rise in glucagon, release sufficient fatty acids to fuel those starving cells? Well, again, if you are habituated to a high carb low fat diet - the biochemical machinery within cells that allow the passage of fatty acids and their oxidation as fuel are not as well expressed as those for glucose. Although you will survive you will still feel grotty with cravings (hence why dieters so often fall of the wagon and raid the biscuit tin). Because your body is better adapted to oxidise glucose than fatty acids, a lot of the fatty acids won't get used and glucagon will start to break down liver glycogen to keep blood glucose levels elevated and then proteins in the body (maybe some muscle tissue) to release glucogenic amino acids so that it can start making more glucose endogenously.

Once that glucose is released and cells can start oxidising it the fatty acids again float around unused. When you next have a carb-rich meal there is the likelihood they will end up back in the fat cells as triglycerides thanks to the lipogenic effects of glucose and insulin.

With this scenario it is easy to see how this person could lose WEIGHT as LEAN tissue and keep, if not increase, their FAT stores. There body composition has changed due to the partitioning effects of hormones that released as a consequence of the macronutrients that are eaten, Calories then become of secondary importance. In other words - macros eaten induce the hormonal environment needed to partition energy in such a way that body composition is altered which, as a consequence may result in a change in scale weight.

[ATZ]

Ok Nu, you win the internets. You're ignoring thermodynamics and my contention that none of the above applies with adequte protein. That and the fact that insulin can't produce mass from nothing.

This post sums you up: Utilitarianism and Exercise: Analyzing “It Works For Me” | AmpedTraining.com | Matthew Perryman, CSCS

[NU_nutrition_TS]

No, it is in line with the second law of thermodynamics. The first law doesn't apply so easily because the calories in=calories out are not dependant variables. In that particular scenario I wasn't showing the appearance of MASS from nothing as the MASS decreased with a change in composition to more fat and less lean. I was hoping you would be able to work out the process the other way - without me having to do it for you - it was a lot of typing!

EDIT: Actually I did briefly mention the opposite scenario:

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Lean mass as exemplified by muscle tissue is increased when we place an overload stress on it and cause a degree of damage to the tissue. This initiates a response that causes the body to release certain hormones and biochemicals that, in turn, signal the stimulation of various physiological processes that result in repair and augmentation of the damaged tissue. Those processes require both energy, in the form of ATP, and raw materials, such as amino acids, to rebuild muscle tissue. This creates a need to supply both the energy and raw materials, so the physiological factors precede (or should) the increased intake of raw materials and energy as food.

I'll have to draw you a picture!

[ATZ]

The scenario you propose simple does not hold true. If you are in a caloric defdcit the body will metabolise fat preferentially as muscle mass and other tissues are important. If sedentary your protein requirements are far lower than a trained individual, but protein being sufficient in both cases this will support muscle tissue. It makes no sense for the body to do what you alledge above, and the scenario would be far different in trained individuals.

All the studies I've posted show similar fat losses in isocalorific studies, of low carb verses low fat and they've certainly been more credible than the efforts you have posted. Yet your contention is that somehow, even in a caloric defecit, when carbs are present the body will somehow change it's composition to support more fat and less muscle tissue? The literature and real life experience just does not support your "theory" above.

People get fat due to excess calories not carbs.

[NU_nutrition_TS]

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The scenario you propose simple does not hold true. If you are in a caloric defdcit the body will metabolise fat preferentially...

That would depend on how high the carb content of the diet/meal is, how high it sends up blood glucose and how quickly insulin drops back once blood glucose has normalised. There is a much greater propensity for blood glucose and thus insulin to be spiked by a high carb meal than by a low carb/high fat meal - whatever the calorie content. And if you eat more meals more frequently, that makes it worse (which most dieters are told to do).

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The Journal of Clinical Endocrinology & Metabolism Vol. 88, No. 4 1617-1623
Copyright © 2003 by The Endocrine Society

A Randomized Trial Comparing a Very Low Carbohydrate Diet and a Calorie-Restricted Low Fat Diet on Body Weight and Cardiovascular Risk Factors in Healthy Women

Untested alternative weight loss diets, such as very low carbohydrate diets, have unsubstantiated efficacy and the potential to adversely affect cardiovascular risk factors. Therefore, we designed a randomized, controlled trial to determine the effects of a very low carbohydrate diet on body composition and cardiovascular risk factors. Subjects were randomized to 6 months of either an ad libitum very low carbohydrate diet or a calorie-restricted diet with 30% of the calories as fat. Anthropometric and metabolic measures were assessed at baseline, 3 months, and 6 months. Fifty-three healthy, obese female volunteers (mean body mass index, 33.6 ± 0.3 kg/m2) were randomized; 42 (79%) completed the trial. Women on both diets reduced calorie consumption by comparable amounts at 3 and 6 months. The very low carbohydrate diet group lost more weight (8.5 ± 1.0 vs. 3.9 ± 1.0 kg; P < 0.001) and more body fat (4.8 ± 0.67 vs. 2.0 ± 0.75 kg; P < 0.01) than the low fat diet group. Mean levels of blood pressure, lipids, fasting glucose, and insulin were within normal ranges in both groups at baseline. Although all of these parameters improved over the course of the study, there were no differences observed between the two diet groups at 3 or 6 months. ß- Hydroxybutyrate increased significantly in the very low carbohydrate group at 3 months (P = 0.001). Based on these data, a very low carbohydrate diet is more effective than a low fat diet for short-term weight loss and, over 6 months, is not associated with deleterious effects on important cardiovascular risk factors in healthy women.

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"A calorie is a calorie" violates the second law of thermodynamics

The principle of "a calorie is a calorie," that weight change in hypocaloric diets is independent of macronutrient composition, is widely held in the popular and technical literature, and is frequently justified by appeal to the laws of thermodynamics. We review here some aspects of thermodynamics that bear on weight loss and the effect of macronutrient composition. The focus is the so-called metabolic advantage in low-carbohydrate diets – greater weight loss compared to isocaloric diets of different composition. Two laws of thermodynamics are relevant to the systems considered in nutrition and, whereas the first law is a conservation (of energy) law, the second is a dissipation law: something (negative entropy) is lost and therefore balance is not to be expected in diet interventions. Here, we propose that a misunderstanding of the second law accounts for the controversy about the role of macronutrient effect on weight loss and we review some aspects of elementary thermodynamics. We use data in the literature to show that thermogenesis is sufficient to predict metabolic advantage. Whereas homeostasis ensures balance under many conditions, as a general principle, "a calorie is a calorie" violates the second law of thermodynamics.

A review of simple thermodynamic principles shows that weight change on isocaloric diets is not expected to be independent of path (metabolism of macronutrients) and indeed such a general principle would be a violation of the second law. Homeostatic mechanisms are able to insure that, a good deal of the time, weight does not fluctuate much with changes in diet – this might be said to be the true "miraculous metabolic effect" – but it is subject to many exceptions. The idea that this is theoretically required in all cases is mistakenly based on equilibrium, reversible conditions that do not hold for living organisms and an insufficient appreciation of the second law. The second law of thermodynamics says that variation of efficiency for different metabolic pathways is to be expected. Thus, ironically the dictum that a "calorie is a calorie" violates the second law of thermodynamics, as a matter of principle.

The analysis above might be said to be over-kill although it is important, intellectually, not to invoke the laws of thermodynamics inappropriately. There are also, however, practical consequences. The seriousness of the obesity epidemic suggests that we attack it with all the means at our disposal. Metabolic advantage with low carbohydrate diets is well established in the literature. It does not always occur but the important point is that it can occur. To ignore its possibilities and to not investigate the precise conditions under which it appears would be cutting ourselves off from potential benefit. The extent to which metabolic advantage will have significant impact in treating obesity is unknown and it is widely said in studies of low carbohydrate diets that "more work needs to be done." However, if the misconception is perpetuated that there is a violation of physical laws, that work will not be done, and if done, will go unpublished due to editorial resistance. Attacking the obesity epidemic will involve giving up many old ideas that have not been productive. "A calorie is a calorie" might be a good place to start.

[NU_nutrition_TS]

Continued...
Isocaloric diets: effects of dietary changes


See also: http://forum.myprotein.co.uk/diet-nu...tml#post358045

[ATZ]

Ok, lets have a proper look at what you've posted above Nu. The first study by Brehm et al looked at differing diets, but ultimatley not isocalorific diets. If you look at the paper the researchers clearly state this:

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Untested alternative weight loss diets, such as very low carbohydrate diets, have unsubstantiated efficacy and the potential to adversely affect cardiovascular risk factors. Therefore, we designed a randomized, controlled trial to determine the effects of a very low carbohydrate diet on body composition and cardiovascular risk factors. Subjects were randomized to 6 months of either an ad libitum very low carbohydrate diet or a calorie-restricted diet with 30% of the calories as fat.

Check the bit in bold.

So they designed a study where one set of subjects were calorie restricted, the other were restricted on carbs but could eat unlimited amounts of fat and protein. Now an ad-libitum low carb diets (LCD) produce spontanious caloric reduction, as noted by numerous other studies. The subjects lost more weight as they ingested fewer cals on the LCD. It was alos probably higher protein as a result. Simple really.

And I find it highly ironic and damn right amusing that you posted that study by Brehm, when she has in fact done further follow up research showing that the LCD was not any better, just her previous work was undermined by the self reporting aspect.

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Brehm BJ, Spang SE, Lattin BL, Seeley RJ, Daniels SR, D'Alessio DA.

R.D., University of Cincinnati, P.O. Box 210038, Cincinnati, Ohio 45221-0038, USA. bonnie.brehm@uc.edu

We have recently reported that obese women randomized to a low-carbohydrate diet lost more than twice as much weight as those following a low-fat diet over 6 months. The difference in weight loss was not explained by differences in energy intake because women on the two diets reported similar daily energy consumption. We hypothesized that chronic ingestion of a low-carbohydrate diet increases energy expenditure relative to a low-fat diet and that this accounts for the differential weight loss. To study this question, 50 healthy, moderately obese (body mass index, 33.2 +/- 0.28 kg/m(2)) women were randomized to 4 months of an ad libitum low-carbohydrate diet or an energy-restricted, low-fat diet. Resting energy expenditure (REE) was measured by indirect calorimetry at baseline, 2 months, and 4 months. Physical activity was estimated by pedometers. The thermic effect of food (TEF) in response to low-fat and low-carbohydrate breakfasts was assessed over 5 h in a subset of subjects. Forty women completed the trial. The low-carbohydrate group lost more weight (9.79 +/- 0.71 vs. 6.14 +/- 0.91 kg; P < 0.05) and more body fat (6.20 +/- 0.67 vs. 3.23 +/- 0.67 kg; P < 0.05) than the low-fat group. There were no differences in energy intake between the diet groups as reported on 3-d food records at the conclusion of the study (1422 +/- 73 vs. 1530 +/- 102 kcal; 5954 +/- 306 vs. 6406 +/- 427 kJ). Mean REE in the two groups was comparable at baseline, decreased with weight loss, and did not differ at 2 or 4 months. The low-fat meal caused a greater 5-h increase in TEF than did the low-carbohydrate meal (53 +/- 9 vs. 31 +/- 5 kcal; 222 +/- 38 vs. 130 +/- 21 kJ; P = 0.017). Estimates of physical activity were stable in the dieters during the study and did not differ between groups. These results confirm that short-term weight loss is greater in obese women on a low-carbohydrate diet than in those on a low-fat diet even when reported food intake is similar. The differential weight loss is not explained by differences in REE, TEF, or physical activity and likely reflects underreporting of food consumption by the low-fat dieters.

Note the bit in bold again.

Then you go on to cite the famous (well within the low carb world) Feinman and Fine work, which as far as I can is as much a bunch of theoretical masturbation as anything else.

If LCD have a metabolic advantage (in terms of caloric expenditure), it should be measurable by current technology (e.g. indirect calorimetry). And if current technology (which we know can show a 3-5% difference in things like carb vs. fat intake) can't measure it, then it's not worrying about. Because if it only amounts to 1%, then that is not worth staking a whole lot of effort on it.

Plus, these "researchers" as many in the LCD field fail to make the ditinction between:

low carb vs high protein.

Of course a diet higher in protein will have a higher TEF, hence comparing an ad-lib low fat diet to a controlled LCD or vice versa the LCD will always contain more protein, so much for a "metabolic advantage".

In terms of whther calovies in - calories out is a valid presumption you might want to read this


So Nu, over the last 34 pages of this thread you've failed to show me its carbs that are specifically to blame for gaining fat verses excess calories. You've posted info and studies that are either:

1. Anecdotal
2. Poorly performed
3. Outdated
4. Have since been refued
5. Involve small sample sizes

Yet with the studies I posted you're best effort was to say that the statistically insignificant differences observed between the diets were "significant" in your opinion. Even though those differences could have been due to random chance. You best go tell the paper authors that.

You've failed spectacualry to show carbs and not excess calories make you fat so far, and the burden of proof remains with you (being the thread author and all) before you go off trying to discredit what I've posted.