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

Dietary Carbohydrate restriction as the first approach in diabetes management. Critical review and evidence base, by Richard D Feinman et al.

Another Bookmarking post.

From http://dgeneralist.blogspot.co.uk/2013/11/the-low-carb-high-fat-diet.html

The study in question is Dietary Carbohydrate restriction as the first approach in diabetes management. Critical review and evidence base. Here are my comments on the 12 points.

Point 1 is wrong. For ~85% of people who have T2DM, hyper*emia is the salient feature, where * = glucose, TG's, cholesterol, NEFAs, uric acid etc. For ~85% of people who have T2DM, it's a disease of chronic excess.

Ad lib LCHF diet → ↓ Blood glucose & ↓ fasting TG's, but ↑ PP TG's, ↑ LDL-C, ↑ LDL-P & ↑ NEFAs. See Postprandial lipoprotein clearance in type 2 diabetes: fenofibrate effects.
↑ PP TG's is associated with ↑ RR of CHD.
↑ LDL-P is associated with ↑ RR of CHD.
↑ NEFAs are associated with ↑ RR of Sudden Cardiac Death.

Point 2: So?

Point 3 is wrong. A caloric deficit is essential, to reverse liver & pancreas ectopic fat accumulation. See Reversing type 2 diabetes, the lecture explaining T2D progression, and how to treat it.

Point 4 is misleading. Feinman doesn't distinguish between different types of carbohydrates. Starches, especially resistant starches (e.g. Amylose) are beneficial. See Point 11.

Point 5 is moot. Prof. Roy Taylor found that motivation determines adherence. Prof. Roy Taylor's PSMF was adhered to. See Point 3.

Point 6 is correct. Prof. Roy Taylor's PSMF is ~1g Protein/kg Bodyweight, some ω-6 & ω-3 EFAs & veggies for fibre. See Point 3.

Point 7 is misleading. Siri-Tarino et al gave a null result by including low fat studies, also a dairy fat study which had a RR < 1 for increasing intake. Chowdhury et al gave a null result, as some fats have a RR > 1 for increasing intake and some have a RR < 1 for increasing intake.

Point 8 is irrelevant. ↑ Dietary fat → ↑ 2-4 hour PP TG's. See Point 1.

Point 9 is partly correct. Microvascular, yes. Macrovascular, no. See Point 8.

Point 10 is mostly irrelevant. See Point 8.

Point 11 ignores results obtained with high-starch diets, where the starch contains a high proportion of Amylose. See Walter Kempner, MD – Founder of the Rice Diet and From Table to Able: Combating Disabling Diseases with Food.

Point 12 is misleading. The low-carbohydrate part is fine. It's the high-fat part that can cause problems. See Point 8.

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!

Protein reduces endurance (in mice), food processing vs food refining & Schrödinger.

I saw the following study via Twitter. Dietary protein decreases exercise endurance through rapamycin-sensitive suppression of muscle mitochondria.

Mmm, protein!

Hmmm! In mice, a high protein diet significantly decreased the amount of muscle mitochondria, the mitochondrial activity and the running distance at 50 weeks, although it increased muscle mass and grip power.

A mouse's natural diet is fruit or grain from plants, though mice will eat virtually anything, including Kevlar insulation on wiring. Fruit & grains aren't particularly high in protein, so it's quite possible that eating a sub-optimal diet results in sub-optimal health.

If the results do translate to humans, we have a choice between endurance, and muscle mass & strength in our old-age. I know which I would choose. You'll have to prise the proteins from my cold, dead fingers!

More from Twitter:  A Major Communication Challenge of Our Times: What on Earth Do We Say About Processed Foods? The word "refine/refined" doesn't appear in the above article. I don't have a problem with food processing. What I do have a problem with is food refining. Just after the Mid-Victorian period, it became fashionable to eat foods that had been stripped of "impurities". Goodbye essential co-factors. Hello, degenerative diseases.

Finally, today is the 126th anniversary of Erwin Schrödinger's birthday. I have only one comment:-

Blatantly stolen from http://memegenerator.co/instance/31138345

:-)

Defending the indefensible: Gary Taubes and *that* statement about gluttony.

Here's another "video" (it has sound and static images only). As I haven't learned how to embed a YouTube video that starts at a specific time, here's a link to it and a picture of it:- Gary Taubes' "Why We Get Fat" IMS Lecture On August 12, 2010 (Part 8 of 8), starting at 8 minutes and 13 seconds in.

To quote: "You can basically exercise as much gluttony as you want, as long as you're eating fat and protein."

Itsthewoo told me that Taubes was being ironic i.e. he was joking. I call bull-shit on that, for the following reasons.

1) You don't joke about something as important as diet, in a video that's likely to be heard by many people.

2) If you are foolish enough to joke about something as important as diet, you make 100% certain that listeners know that you're joking, by stating in the very next sentence that the preceding sentence was a joke. Taubes didn't do that.

3) I didn't hear chortling or any other audible clue that Taubes was joking. Did you?

I therefore conclude that itsthewoo is hearing (and seeing) the world through "cognitive bias" Weird Filters , resulting in her hearing what she wants to hear. Sorry!