In defense of CHO

El_Dangeroso

I eat rice!

See I agree with your fundamental point, blanket demonisation of carbs is dumb and reductionist.

But what I take issue with is that carbs somehow magically don't make you as fat as fat does. We've had a good 30 years of advising people to lower fat and it hasn't helped, it may have even exacerbated the situation.

That study was very small and over a short period of time.

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 [Energy Intake] for the rest of the day.

So what's the point in have lower 'perceived' fullness if it doesn't make you consume less calories later in the day?

So as I mentioned before, carbs do cause higher short-term satiety, but fat slows gastric emptying and prompts the release of the satiety hormone CCK. That doesn't really make one better than the other, but in the context of a wholefoods diet, you can go with whatever your preference is.

rocky

Hey, I know you know, but this thread is for the others

That doesn't really make one better than the other, but in the context of a wholefoods diet, you can go with whatever your preference is.

See? We agree.

But what I take issue with is that carbs somehow magically don't make you as fat as fat does. We've had a good 30 years of advising people to lower fat and it hasn't helped, it may have even exacerbated the situation.

When I started being interested in nutrition, I was explaining to people that it's not dietary fat that makes you fat, it's total calories. In the last few months, I kept reading studies and articles that point out some small advantages of overeating carbs, rather than fats (yeah I know, this is not relevant to the real world, majority of people are not concerned with calories, only with satiety - that's grand, but I'm a CICO kind of guy and find it very easy to manipulate my hunger or lack thereof with other strategies such as Intermittent Fasting). My preliminary conclusion is that having a higher proportion of fat in the diet will lead to a higher weight set point (not a lot higher, maybe 1%), a lower muscle definition, a faster reaching of dietary intake 'target', and a worse outcome when exceeding maintenance calories. Whether it's worth it or not, it's up to the individual to decide.

Also it turns out the fat we store comes mostly from dietary fat (a net gain in fat stores only happens in the presence of sufficient calories, for sure - but there is still that mental block of eating less fat to have less to store...). And carbohydrates are rarely stored as fat through DNL, even rarer in physically active people that use up glycogen regularly.

I'm arguing a bit from a point of view I don't really follow, I probably have at least a 40% fat diet (every day 4 scrambled eggs in butter, 4-5/7 days fried liver in coconut oil and so on...), but I also am not afraid to eat carbs (even sugar).

El_Dangeroso

Ah I love a good game of devil's advocate!:)

I couldn't stick to VLC either, impossible to get enough calories for maintenance for me. Though I do notice I tend to put up weight if I go very heavy on the carbs (even if I'm not really adding any fat).

I do wonder why you get such high levels of satiety on a low carb diet though, you don't even have to go that low carb, there was a study a while ago that dropped carbs from 230g to 100g:

http://www.sciencedaily.com/releases/2011/06/110606092532.htm

Ok, 11% difference in belly fat isn't gonna set the world on fire, but it makes me wonder. I know there's been an undue focus on insulin as the root of the obesity epidemic, but that doesn't mean it still doesn't play a part.

Peter from hyperlipid had an excellent post recently:

http://high-fat-nutrition.blogspot.com/2011/05/energy-expenditure-in-obese-vs-slim-non.html

If obese people have a higher metabolism (and they do, as in they burn more calories daily) then why don't they lose as much as lean people do on a fast? Peter's idea is that high fasting insulin will inhibit lipolysis. That makes a good case as low carbohydrate approaches for 'the default' approach for obesity, as fasting insulin can be reduced more on a LC diet via improving insulin sensitivity.

I'm not saying everyone will get on well with this approach, I know some people who run so much better on carbs. But it would be worth trying as an option, and that's what isn't happening now. Don't forget those that are interested in nutrition are already sorted and more educated about food than 99% of people out there.

I fear getting people to care about their quality of food will be more of a challenge than demonising a macronutritient, which is why everyone seems to have gone down the latter route.

rocky

I thought here would be a good place for this article

Insulin: understanding its action in health and disease

pdf
html

Some interesting snippets:

The effects of this ‘black age’ are still with us because these incorrect hypotheses have, with the passage of time, been turned into dogma and become cast into ‘tablets of stone’ in undergraduate textbooks. They are also carried forward into postgraduate teaching. For example, even in well respected texts it is still common to find statements such as ‘The basic action of insulin is to facilitate glucose entry into cells, primarily skeletal muscle and hepatocytes.’

It is now well established that what Schafer called insulin’s ‘chalonic’ (or inhibitory) actions are the physiologically more important. Indeed, its autacoid (excitatory) action has recently been shown to be, on the whole, physiologically unimportant.

in states of relative insulin lack such as prolonged fasting, insulin concentrations fall low enough to allow release of sufficient gluconeogenic amino acids to maintain blood glucose in the normal range. The price for this is a gradual but progressive loss of structural protein.

The magnitude of the hyperglycaemia is determined by the absolute rate of hepatic glucose production (Fig. 3) and this in turn is determined by the extent of, on one hand, the insulin deficiency and, on the other hand, the magnitude of the glucagon rise in response to insulin deficiency.

Glucose uptake into cells is usually normal and often high in untreated diabetes

insulin deficiency itself leads to over‐secretion of the ‘anti‐insulin’ hormones glucagon, cortisol, growth hormone and catecholamines. This in turn aggravates the metabolic effects of insulin lack.

Once insulin deficiency develops this control is lost, and energy substrates are over‐produced and flood the system. The metabolic consequences result from the excess of substrates not (as is often misconceived) by a lack of energy substrate getting to the tissues.

I think I'm going to increase my carbs

boomtown84

Very good series of articles here too which i posted before: http://weightology.net/weightologyweekly/?page_id=319

rocky

Stephan Guyenet has an article on sugar:

http://wholehealthsource.blogspot.com/2012/02/is-sugar-fattening.html

It is difficult to escape the conclusion that our ancestors have been consuming sugar, in the form of whole fruit, continuously for the last 60 million years.

Overall, the observational evidence suggests that sugar in the form of SSBs is associated with elevated body fatness, but total sugar intake is not. This is our first clue that this story may be more complicated than "sugar makes you fat".

There are several studies showing that high-sugar diets do not impair weight loss in the context of a low-calorie diet (32, 33), once again confirming the primacy of calorie intake in weight loss.

This result is consistent with a number of other fructose feeding studies in humans, reviewed in a brand new paper in the Annals of Internal Medicine (35). The investigators reviewed 41 human fructose feeding trials. They concluded that fructose is not fattening when substituted for other carbohydrate in the diet, but it can be fattening if consumed in addition to the typical diet. This fattening effect is equivalent to what one would expect based on the increase in calorie consumption in these trials.

Robert LOLstig

Conclusions

Here are the take-home points from this post:

Sugar, including fructose, is not inherently fattening relative to other calorie sources, and unrefined sugar is compatible with fat loss in the context of simple whole food diets.

Sugar can be fattening in certain contexts, specifically if it is added to foods and beverages to increase their palatability, reward value and energy density.

Sugar-sweetened beverages are probably one of the most fattening elements of the modern diet.

Fruit is not fattening, and it may actually be slimming.

In excess, refined sugar can cause body fat to redistribute from the subcutaneous depot (under the skin, where you want it) to the visceral depots and the liver (where you don't want it). It can also cause insulin resistance in the liver and increase blood pressure, all components of the 'metabolic syndrome'. This is caused specifically by the fructose portion of the sugar.

rocky

Richard Nikoley's carb experiment
http://freetheanimal.com/2012/02/the-moderate-starchy-carbohydrate-experiment.html

Richard Nikoley wrote:

In looking around about glucose spikes, it seems that a spike up to 180 by the 1 hour mark is perfectly physiologically normal, causing to wonder if a lot of LCers who are not diabetic are unnecessarily freaking themselves out by expecting their BG to never rise above 110 or so.

Interesting input by Kurt G. Harris in the comments...

Harris wrote:

It’s never been about insulin or macro ratios, rather about avoiding non-foods and limiting reward.

As far as Jimmy goes, he simply can’t reassess low carb, even though he has already had countless guests explain to him that the CIH [Carbohydrate-Insulin Hypothesis of obesity] is wrong and why. Jimmy [Moore] is basically boxed in at this point.

Harris wrote:

And few want to admit that everyone is fat primarily because they are trying to entertain themselves with food, and it has bollocks to do with insulin or “damaged mitochondria” or micronutrient deficiencies. These are all revisionist fantasies promoted by those who don’t want to give up the Taubesian conceit that you can eat as much as you like as long as you minimize X or supplement with Y, or whatever.

:pac:

El_Dangeroso

I'd disagree with the micronutrient deficiency bit. It's not the whole story by any stretch of the imagination but I do think malnutrition can contribute to weight gain, we have too many trials of isolated nutrients (mct's, selenium, chromium) aiding weight loss to exclude it entirely from the equation. Sure you don't get people in third world countries who are malnourished becoming obese, but they don't have enough food to even try.

I think the Pima indians are a good example, the food they became obese on was not high reward by any stretch of the imagination.

Plus to chuck in a bit of anecdata, my morning vitamins keep my sleep on track and when I sleep well I'm not as hungry all day.

I definitely think reward is a huge piece of the puzzle but it's so individual it's almost circular reasoning. Gaining weight? Too much food reward. Losing weight eating the exact same food? Low food reward. My analytical side is just annoyed at the lack of an objective 'reward' measure I suppose!

El_Dangeroso

Oh look Stephan heard me

http://wholehealthsource.blogspot.com/2012/02/palatability-satiety-and-calorie-intake.html

I've seen this paper before.. meh, I don't place much emphasis at all on short term satiety effects, I think the extreme ends of the scale (v high and low satiety) then yeah that might have a long term effect, but otherwise it's context context and context again.

Weird fact, I find haagen dazs vanilla ice-cream quite low reward. As in I eat about 250 calories of it and I really don't want any more. Fat and sugar combo? Check. Delicious flavour? Check. Low fiber? Check. Why is it not high reward for me? Rice crackers on the other hand I can eat until the end of time (Like about 700 cals worth) and they are the blandest thing in existence.

mloc

Some of this makes for painful reading.

The issue is really oversimplification. It's not as simple as fat v. carb, good v. bad.

The kind of fat or carb is a factor, and what we measure as good or bad is a factor.

We can talk about weight loss, fat loss, CVD risk, diabetes risk etc. all with different measures of good/bad, all in themselves different, although usually related goals.

We can talk about SFA, MUFA, different kinds of PUFA, simple carbs, complex carbs and so on. Even within each of these, we know there are huge differences (fructose v glucose, for example). We also know that these are rarely consumed alone and the interactions between them have important biological effects.

On top of this, we also have the individual factor; both genetic (and epigenetic) and phenotypic (i.e. non-genetic factors such as current metabolic status etc.)

The idea that we can say absolutely that one nutrient is good or bad is nonsense.

rocky

mloc wrote: »

The idea that we can say absolutely that one nutrient is good or bad is nonsense.

I agree, hence this thread

rocky

Chris Masterjohn interviewed by Chris Kresser http://chriskresser.com/chris-masterjohn-on-cholesterol-and-heart-disease-part-3

Direct link to audio: http://www.podtrac.com/pts/redirect.mp3/media.blubrry.com/thehealthyskeptic/p/traffic.libsyn.com/thehealthyskeptic/RHR_Chris_Masterjohn_on_Cholesterol_and_Heart_Disease_Part_3.mp3

Carb restriction and thyroid

when we look at these studies in the context of some of the biochemistry that has been studied regarding insulin’s interaction with thyroid hormone, then I think what we are seeing is a definite effect of the level of carbohydrate in the diet. [...] But if we look at what insulin does, we find that there is evidence from humans, from cells, and from rats that insulin cooperates with thyroid-stimulating hormone, or TSH, to increase the production of the enzymes and proteins involved in making thyroid hormone, and we find that it contributes to the enzymes that activate thyroid hormone from T4 into T3, the active form.

I think that if you find that T3 or reverse T3 are out of whack, probably the best way to address that is to try increasing the carbohydrate intake — not necessarily meaning you have to go on a high-carbohydrate diet, but, you know, like, Paul Jaminet had sort of concluded at the end of that series that he still advocates a low-carbohydrate diet, but it’s possible to go too low for some people, and that’s when you might get deficiency in thyroid signaling.