In starvation or ketosis, protein should have NO EFFECT on blood glucose level, not RAISE it.

From Blood Sugar is Stable:-

In a healthy person, BG (blood glucose) is held at a fairly constant value with slowly-varying glucose inputs (except after high-GL meals, which produce rapidly-varying glucose inputs) by a NFB (negative feed-back) loop. See Blood Glucose, Insulin & Diabetes.

When protein is eaten, this produces a glucagon response from pancreatic alpha cells, which tries to raise blood glucose level by stimulating the liver to convert liver glycogen plus water to glucose. Protein also produces an insulin response from pancreatic beta cells, which tries to lower blood glucose level by a) increasing glucose uptake from the blood and b) inhibiting HPG (hepatic glucose production). The net result is no change in BG level.

In extended fasting or on VLC (very low carbohydrate)/ketogenic diets, there's no liver glycogen left after ~1 day.
∴ The glucagon response has no effect on HGP.

The insulin response still has an effect, until physiological IR* develops.
∴ Blood glucose tries to decrease, but the HPAA keeps it steady by raising cortisol level.

RE How eating sugar & starch can lower your insulin needs: Blood glucose level on a VLC/ketogenic diet can be RAISED, due to the BG NFB HPAA (hypothalamic pituitary adrenal axis) loop not having a precise set point with the cortisol/adrenaline response (hyperglycaemia is not fatal, whereas hypoglycaemia can be fatal, as the brain always needs some glucose to function (~50%E from glucose)).

So, how come people on LCHF (low carbohydrate, high fat) diets can have normal or slightly low BG levels?

1. Luck. The BG NFB HPAA loop isn't very precise.

2. Excessive intake of Booze. Ethanol inhibits HGP (dunno about RGP (renal glucose production)).

3. Insufficient intake of Protein. This deprives the liver & kidneys of glucogenic amino acids (Alanine & Glutamine are the 2 main ones), forcing BG down and making the HPAA run open-loop and raise cortisol level. There's another source of Alanine & Glutamine available - Lean Body Mass. Uh-oh!


Consuming more protein on extended fasting or a VLC/ketogenic diet can result in higher BG level for three reasons.

1. It allows the HPAA to run closed-loop, as it's supposed to.

2. The lack of a 1st phase insulin response in people with IR/IGT/Met Syn/T2DM* results in a temporary BG level spike with the intake of rapidly-absorbed proteins e.g. whey. There's an unopposed glucagon response, until the 2nd phase insulin response begins.

See http://care.diabetesjournals.org/content/early/2015/11/29/dc15-0750.abstract

*Long-term drastic carbohydrate restriction kills the 1st phase insulin response! See http://carbsanity.blogspot.co.uk/2013/10/insulin-secretion-in-progression-of.html

P.S. This only applies to people who have sufficient liver glycogen, due to them eating some (50 to 100g/day, say) carbohydrate.

3. Hepatic Insulin Resistance results in the insulin response inadequately suppressing Hepatic Glucose Production. As 50g of protein (an 8oz steak, say) yields ~25g of glucose from glucogenic amino acids, there's an increase in the amount of glucose entering circulation, which raises BG level.

See http://bja.oxfordjournals.org/content/85/1/69.long

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.

I'm NOT a lipophobe, I'm a very naughty boy!

First, postprandial triglycerides again. From Fasting Compared With Nonfasting Triglycerides and Risk of Cardiovascular Events in Women, here's a plot of HR for future CHD vs TG's at various times after eating.

Hazard ratio (HR) and 95% confidence interval (CI) for highest vs lowest tertiles of triglyceride level (see Table 3 for values), adjusted for age, blood pressure, smoking, hormone use, levels of total and high-density lipoprotein cholesterol, diabetes mellitus, body mass index, and high-sensitivity C-reactive protein level.

Notice how the HR falls with increasing time from last meal. As TG's ≥12 hours after eating are a surrogate for Insulin Resistance (IR) and the HR is only 1.04 (95% CI 0.79 - 1.38), this strongly suggests that IR is not a significant factor.

It's been suggested that IR might increase PP TG's in the 2 - 4 hour period due to impaired clearance. According to Fig. 3B in Extended effects of evening meal carbohydrate-to-fat ratio on fasting and postprandial substrate metabolism, TG clearance in healthy men doesn't significantly start until after 4 hours has elapsed. Therefore, an impairment in TG clearance isn't going to make a significant difference to TG level in the 2 - 4 hour period.

Second, the reason why I'm having to repeat myself is due to Cholesterol: Do chylomicrons clog your arteries? (2), where I've been called "my resident lipophobe". As I drink Gold Top milk (5.2g of fat/100mL) and eat pork including belly slices (you know, those strips of pork with a lot of fat on them), I'm being attacked for something that I'm not.

What I'm criticising is dietary extremism. Eating fats in foods is fine by me, but eating sticks of Kerrygold butter and/or dumping loads of butter and/or MCT oil into coffee to achieve "Nutritional Ketosis" is not a good idea. Anyway, here's an amusing spoof on Bulletproof coffee.