Sunday, August 16, 2015

When low fat wins

I think I’ve said before, I’m a calories-in, calories-out sort of person. Nothing as simple as losing a kilo of stored fat for every 9000kcal deficit in dietary consumption (or increase in exercise) of course. This is, as we all know, incorrect and of absolutely no use whatsoever in planning an attempt to generate a normal bodyweight.

I am also very aware that, outside a metabolic ward, it is very difficult to even approximately assess a given person’s level of energy output, assuming they are fully compliant with a fixed composition, fixed caloric input. Which they probably aren’t, much of the time. But calories out will be reflected in many more outputs than can achieved by the limited exercise opportunities afforded during the restrictions of an in-patient metabolic ward study.

As Hall commented, the repeated superiority of weight loss by carbohydrate restriction has always been achieved in outpatient studies, never in tightly controlled metabolic ward studies. He didn’t mention that the advantages from carbohydrate restriction were always achieved under calorically unrestricted circumstances in comparison to calorically restricted alternative diets. I’ll just mention that now.

We can also say, with some degree of certainly, that under very tightly controlled in-patient conditions, extreme dietary fat restriction (less than 8% of calories) produced more stored fat loss than a modest reduction in carbohydrate restriction, provided both groups are rigidly forced to cut calories and to limit their exercise to a specified level, for six days. My own feeling is that this is probably true under the circumstances of the study. It provides a very small piece of data of very limited application to the real world. As Hall writes:

"Translation of our results to real-world weight-loss diets for treatment of obesity is limited since the experimental design [and model simulations] relied on strict control of food intake, which is unrealistic in free-living individuals".

I am very lucky.

I don’t live in a metabolic ward. If the weather is cool outside and I feel warm enough to not need my jacket when I let the chickens out in the morning, so be it. If both the air and water temp are 4degC but there is a four foot swell with clean waves shaping up in First Bay I’m going to be thinking about the roof rack, my playboating kayak and my drysuit. I’m guessing that there are few near freezing surf opportunities in a metabolic ward.

People might also be aware that I rather like fatty acids, especially free fatty acids. These uncouple respiration. Uncoupled respiration, at the mitochondrial level, generates heat and so increases metabolic rate. For people with a heathy interest in cold water kayaking, this has its advantages. Sitting in a metabolic ward eating 140g of carbohydrate per day is not going to increase my free fatty acids to a level were uncoupling is going to feature in my metabolism.

The average person with a BMI of 35 is probably going to be running their metabolism under the Crabtree effect. Increased dependence on glycolysis at the expense of reduced utilisation of mitochondrial beta oxidation. While it is quite possible to immediately and markedly increase fatty acid oxidation, there are limits set by how many mitochondria a given cell possesses. The moderate carbohydrate group did increase their fatty acid oxidation, but not enough to compensate for the loss of carbohydrate available from the diet. This is perhaps most clearly seen in Table 3 where a significant drop in sleeping metabolic rate occurred in the moderate carb group and an actual increase was seen in the very fat restricted group. It's probably why the moderate carbohydrate group had a suggestion of increased protein degradation compared to the very low fat group.

Even thought it was nearly 15 years ago, I can still recall Atkins Flu™ as I switched to deeply ketogenic eating from a fairly reasonable modern diet. The "flu" lasted about 6 days (apologies for exactifying my recall to fit with the study duration!) with further acclimatisation over the next few months. There should be no such problem with increasing glycolysis in the very low fat group if you are already running your metabolism on starch combined with HFCS. It is no major problem to up regulate carbohydrate metabolism when it is your normal metabolic fuel source.

So for the first six days of an enforced, calorically restricted, non-ketogenic diet, cutting fat rules provided the restriction is very, very extreme. Do this long term and you will, of course, fail.


13 comments: said...

Hi Petro,
I recently wrote a review about metabolic ward studies, and my conclusion is that low-carb diets do show a metabolic advantage also when feed is completely controlled. You can read it here (spanish language, sorry).

"never in tightly controlled metabolic ward studies" is just not true.

A review of 87 weight loss studies also concluded that low-carb diets make people lose more fat mass even when diets are isocaloric (study). Do scientific studies always have a bias that favors low-carb diets? That is nonsense, IMO.

I believe this article from Michael Eades also helps to clarify who is lying here.

Charles Grashow said...

Question for thr group.

Assume one follows a ketogenic diet like Peter.

Afte a year the person goes for blood work.

Test results are as follows

Direct measured LDL-C >200
LDL-P >2,000
ApoB >200

hsCRP 0.5
A1C 5.2

Cause for worry or not?

Boundless said...

CG: Test results are as follows

CG: Direct measured LDL-C >200
Is that a contradiction in terms?
The “C” stands for “calculated”.

CG: LDL-P >2,000
Been tested for ApoE polymorphisms?

CG: hsCRP 0.5, A1C 5.2
If the TG is also that nice (say, 60mg/dl or less), my layperson inclination is to suspect some sort of familial lipidemia.

Charles Grashow said...

ApoE 3/3 - so it's not FH. Perhaps it's the diet

PhilT said...

Being a bit of a mathematical modeller & engineer myself I was concerned that the biggest flaw in this study is that it is not done in a steady state. Taking away 800 kcals of CHO resulted in an increased fat burn of only +400 kcal/d with CHO oxidation only falling 600 kcal/d which says that glycogen reserves were being pulled down at 200 kcal/d to compensate for the reduced CHO intake.

That can't last for long, and once at equilibrium we would see a different picture - perhaps another 200+ or more kcal/d of fat oxidation.

I could live with six days of study after 2-3 weeks of the diet under consideration, but this is like analysing the performance of your engine while it idles cold on the drive right after starting up in the morning.

ivor cummins said...


You are mostly referring to 'associational' variables there, so I'm not sure what you are implying? LDL-C, LDLp/ApoB only have relevance when one is exposed to the inflammatory milieu, like all the poor souls who created the association in the first place....

Also, A1c is ok at 5.2% - this is not hyperglycemic, and anyway the hyperinsulinemia is more important when in conjunction with true hyperglycemia. So again I'm not sure what your point is?

(CRP around 0.5 has little notable relevance either....)


raphi said...

talking about bad science...Did you known Karen Hardy in her recent "carbs were fundamental to human encephalization" paper used the CPT1a mutation as a PRO-starch argument? Oh, and we were lucky to learn that "an association" has been made with ketones-infertility-low IQ births.

I suggested emailing them a high-school biochemistry textbook....but maybe we should wait for the new ones given that Phinney & Volek have shown that max fat oxidation isn't 1g/min but >2g/min!

Oh my....(sigh)

Ash Simmonds said...

Wonder how many more times this stuff will be rehashed...


Passthecream said...

I'm thinking of getting in a herd of yearling dieticians so I can run them out to grass and plump them up before trucking them off to market. Those lush high calorie grasses fatten up the cows nicely.


tess said...

i can never decide if i enjoy Peter's posts more, or the comments which ensue.... :-D

Galina L. said...

How reasonable is it to make any conclusions about diets based on a such study? What is more effective(for a weight loss), a very LF diet of a diet where carbs are somewhat reduced? It is like comparing apples with oranges. So far it looks like that a so called "balanced" diet is not a winner at all.

v/vmary said...

from lyle mcdonald:

"One final comment, it’s often been claimed by folks like Gary Taubes, who are intent on holding to the insulin hypothesis that low-calorie diets still work by reducing carbohydrate and insulin. And this paper, done under the most meticulous of conditions shows that that is simply not the case. Carbohydrates were not reduced in the RF group and neither was insulin. And there was still a measurable negative fat balance. The researchers even took the time out to mention that explicitly."


PhilT said...

@v/vmary the RF diet (it's a crossover study so most subjects did both diets) saw a reduction in fasting insulin in men (-26%) whereas the RC diet dropped the fasting insulin in women by ~1/3rd. The men were insulin sensitive, the women somewhat insulin resistant. 24h insulin secretion via C-peptide was reduced in RC fig 2B but same in RF.

The fasting insulin levels in these subjects were fairly low and not at the level that would strongly inhibit release of fat in the first place. There's no data of 24h insulin profiles.

The large increase in fat oxidation ties in with the reduction in insulin secretion in RC. I suspect we need to see individual data to get a true picture.

Yes fat loss occurred by reducing fat intake at constant carbohydrate in this case, so it would be fair to say that fat loss is not wholly dependent on carb restriction, just as sugar intake doesn't prevent fat loss or other absolutes.