Nutritional Ketosis: What is it good for?

I have a video in mind...


Having previously shown you what I look like on a diet of ~125g/day low-GL carbohydrates, here are a couple of recent pictures of Jimmy Moore, who's on a very-low-carb, very-high-fat diet (~85%E from fats), a.k.a. Nutritional Ketosis. It involves adding Kerrygold butter to just about everything, even eating sticks of it from a block. I'm not kidding.

I told you I wasn't kidding.

From Google Image Search on "Jimmy Moore" OR "Livin la Vida low carb", images in the last 7 days:-

On 6.7.14.

On 8.7.14.

The only recent footage of Fredrick Hahn, is the following video from the Low Carb Cruise...


To my eyes, Nutritional Ketosis is good for absolutely nothing. Dietary fat can be stored as body fat, in the absence of dietary carbohydrates. Gary Taubes' claim "You can basically exercise as much gluttony as you want, as long as you're eating (only) fat and protein." is pure fantasy, not supported by evidence.

The low protein intake in Nutritional Ketosis, combined with the high serum cortisol that's almost inevitable on this way of eating, results in a loss of muscle mass. I give Nutritional Ketosis a thumbs-down.
 

Summary:-

1) No Energy Deficit → No Weight Loss. There is no Metabolic Advantage to Nutritional Ketosis. See http://www.jbc.org/content/92/3/679.full.pdf

2) Insufficient carbohydrate intake and insufficient protein intake starves the liver & kidneys of gluconeogenic pre-cursors, which raises cortisol, which converts muscle mass into gluconeogenic pre-cursors e.g. Glutamine, Alanine etc. This is standard Biochemistry. No links required.

3) While excess carbohydrates are converted into triglycerides by the liver, excess fats are converted into cholesterol by the liver, which is exported to tissues as LDL-C.

LDL-P ∝ LDL-C. High LDL-P is strongly associated with increased risk factor for CHD. See http://www.lecturepad.org/dayspring/lipidaholics/pdf/LipidaholicsCase291.pdf

CHD is not an inflammation-mediated phenomenon. It's an LDL-P and neovascularisation-mediated phenomenon. See http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3492120/

Postprandial lipaemia is atherogenic. See Ultra-high-fat (~80%) diets: The good, the bad and the ugly.

4) Read Page 10 of https://www.drmcdougall.com/misc/2013nl/feb/pritikinpdf3.pdf, starting from "Could such a cream meal precipitate an angina attack because the oxygen-carrying capacity of the blood is lowered?" It's an actual trial on humans with clogged coronary arteries. It's not a hypothesis.

5) Chronically-raised cortisol causes aggressive behaviour (cortisol is a stress hormone) and adversely affects short-term memory storage in the Hippocampus. See http://evolutionarypsychiatry.blogspot.co.uk/search?q=cortisol

6) Eskimos, Sami, Masai, Samburu, Tokelauans etc, get ~50% of their total energy from fats. There are zero populations that get ≥80%E from fats.


Update 25th July 2014: I appear to have rustled Fredrick Hahn's Jimmies. See https://www.facebook.com/FredrickHahn/posts/10152227780827864

I can safely state that Fredrick Hahn is a liar (I am not poking fun at anybody and I have only blocked him (not his followers) from posting here, for a flagrant breach of my Moderation Policy on his first attempt at commenting), and intellectually-dishonest (for repeatedly mis-quoting me, and using other logical fallacies). He posted the above post knowing that, as I had blocked him on Facebook, I wouldn't see it. I only learned of its existence after a friend PM'ed me on Facebook Messenger. He instructed his "followers" to leave comments here and then accuse me of lying about white-listing, back on his page, because their comments didn't appear immediately. He's a real piece of work! From ABOUT ME:-

Moderation Policy: Comments from first-time & untrusted commenters are moderated ← (click for details). Please be patient. Now that I have a Smart Phone, I can publish your comments during the day when I'm away from my lap-top, but I prefer to type replies on my lap-top. Comments from anonymous commenters, containing links in any form, are deleted.

This is a function of Disqus, as it's impossible to retrospectively white-list a commenter who's never commented here before. There appears to be a severe lack of cognitive function in these people. I really can't think why that is ;-)

Why am I being so hard on Jimmy Moore and Fredrick Hahn? I don't know these people personally.

1) These people are making money out of peddling pseudoscience.

2) These people meet all the criteria in Guest post: Science versus Pseudoscience and have created an alternative science, where sky-high LDL cholesterol, sky-high LDL-P and sky-high postprandial TG's are not risk factors for CHD, but are either harmless or beneficial.

Bray et al shows that a calorie *is* a calorie (where weight change is concerned).

Continued from Everyone is Different, Part 3.

EDIT: I made an error in stating that all of the extra calories came from fat, in the fat overfeeding phase. Thanks to commenter CynicalEng for pointing that out. It doesn't change the conclusion at all.

At 01:17 on 6th June, during a Facebook discussion, Fred Hahn told me:-
"Nigel Kinbrum - read this please.
Bray, et al. Shows that a Calorie is Not a Calorie and that Dietary Carbohydrate Controls Fat Storage.
Perhaps you'll learn something from a real expert who teaches metabolism to medical students at the largest medical school in the country."

So I did.

At 02:22, I replied:-
"Thanks for that. I read Feinman's blog post about Bray et al http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3777747/ some time ago.
There's a fundamental error in Feinman's analysis. As LeonRover pointed out in his comment http://feinmantheother.com/.../bray-et-al-shows-that.../...
In Diets:- "Absolute carbohydrate intake was kept constant throughout the study."
Also, in COMMENT:- "The extra calories in our study were fed as fat, as in several other studies, and were stored as fat..."
Oh, whoops! That may be why it was rejected by the editor."

Here's Figure 6 from Bray's study.

From http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3777747/

Some Definitions:-

LBM = Lean Body Mass
FM = Fat Mass = Body Fat

Weight change = (LBM change + FM change)

Weight change varies from ~+3.5kg (@ +2,500kJ/d) to ~+9.1kg (@ +5,900kJ/d).

(Maximum weight increase)/(minimum weight increase) = 2.6
(Maximum kJ/day increase)/(minimum kJ/day increase) = 2.36

∴ A calorie *is* a calorie (where weight change is concerned) ± some inter-personal variation.
∴ Insufficient protein can result in LBM loss (this is bad).
As LBM has a lower Energy Density (~400kcals/lb) than FM (~3,500kcals/lb),  LBM loss can increase weight loss, when in a Caloric Deficit.
See The Energy Balance Equation, for a simple explanation, and The Dynamics of Human Body Weight Change, for an incredibly complicated one!


I was rather chuffed when Alan Aragon left the following comment at 04:34:-
"Nigel is correct. From Bray et al's text:
"The extra calories in our study were fed as fat, as in several other studies [33,34], and stored as fat with the lower percentage of excess calories appearing as fat in the high (25%) protein diet group. The higher fat intake in the low protein group probably reduced nutrient absorption (metabolizable energy) relative to the other groups and this would have brought the intake and expenditure closer together in this group.""

Feinman has deleted his blog post. However, his post I Told George Bray How to do it Right is still there. I believe that Dr. George A. Bray M.D. sort-of did it right.

Dr. George A. Bray used a "weight maintenance formula" in all three groups for the weight maintenance phase. He then changed the formula in all three groups to low-P, med-P and high-P formulas, for the fat overfeeding phase. Carbohydrate grams remained constant in all three groups for all phases, but additional fat grams were fewer in the high-P group than in the low-P group, for the fat overfeeding phase.

I would have used the low-P, med-P and high-P formulas for the weight maintenance phase and for the fat overfeeding phase, to equalise the additional fat grams in all three groups.

Continued on Everyone is different Part 4, Fallacies and another rant!

Completing the trine: vive la différence!

First, the obligatory picture of Hannah Spearritt :-)

Women have a harder time losing weight than men. Women retain water more than men for hormonal reasons, but a factor that's overlooked is that, on average, healthy women have higher body-fat percentages than healthy men. This is because women have babies and men don't. Who knew? On the plus side, women produce more DHA than men.

Why should having higher body-fat percentages make a difference to weight loss? See What is the required energy deficit per unit weight loss? The energy deficit required to lose 1lb of body-weight increases with increasing body-fat percentage. It's rarely 3,500kcals per lb.

If you really love mathematics, see The Dynamics of Human Body Weight Change by Carson C. Chow and Kevin D. Hall.

From the above paper:- ΔU = ΔQ - ΔW

where ΔU is the change in stored energy in the body, ΔQ is a change in energy input or intake, and ΔW is a change in energy output or expenditure. This is the Energy Balance Equation. As I said back in Back to black, CIAB, pharmaceutical drug deficiencies & nerds.

Where body weight is concerned, calories count (but don't bother trying to count them).
Where body composition is concerned, partitioning counts.
Where health is concerned, macronutrient ratios, EFAs, minerals, vitamins & lifestyles count.

N.B. Poor health can adversely affect body weight and/or body composition, by increasing appetite and/or by adversely affecting partitioning.

Bursting from the seams: "Obese adipocytes" literally "explode" and leave a nasty inflammatory mess.

I just read a Public post on Facebook from someone I follow and whose blog is in my list.

https://www.facebook.com/profdrandro/posts/533941643320863

It contained a word that I've never seen before, but would like to see more often - Pyroptosis. 
See Obese adipocytes show ultrastructural features of stressed cells and die of pyroptosis.

Adipocytes dying, huh? You know what that means? Loss of body-fat. Unfortunately, there is an issue with the nasty inflammatory mess left, after adipocytes "explode". This limits the rate at which adipocytes can be "exploded".

See also SuppVersity Cellulite Special: The Etiology of Cellulite, Genetical and Behavioural Risk Factors? Physical and Supplemental Treatment Strategies & Their Efficacy. Warning! Not Safe For Work, due to pictures of naked botties.

Fructose: this may blow your mind.

Hat-tip to Beth@WeightMaven for posting a link to this.

 Nicked from sodahead.com

Watch the following video.