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 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 the 1st phase insulin response is lost*.
∴ 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/T2D 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 carbohydrate restriction causes loss of the 1st phase insulin response. See https://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 https://academic.oup.com/bja/article/85/1/69/263650

PROLONGED MEAT DIETS WITH A STUDY OF KIDNEY FUNCTION AND KETOSIS.

BY WALTER S. MCCLELLAN AND EUGENE F. Du BOIS.
It's the 1 year study on Vilhjalmur Stefansson and K. Andersen at Bellevue Hospital.

Vilhjalmur Stefansson

See http://www.jbc.org/content/87/3/651.full.pdf The reason why I'm posting this is because of what Stefansson and Andersen drank. I was under the impression that the men drank water only. That was not the case. They drank coffee, black tea, meat broths and water. Black tea is high in tannins, which bind somewhat to haem iron and very strongly to non-haem iron.

Therefore, if you like to eat lots of red meat but you don't like your greens (not even a tablespoonful of spinach), drink strong black tea or eat foods rich in phytates and/or calcium. Vitamin E supplements also help. See Red meat and colon cancer: should we become vegetarians, or can we make meat safer?

Everybody knows.........Part 2

.........that ketogenic diets like the Atkins diet destroy your kidneys and rot your bones, right? Wrong!
.........that the Atkins diet causes ketoacidosis which is a very dangerous condition requiring urgent hospital treatment, right? Wrong!

There's a lot of nonsense spoken about ketogenic diets by people who really should know better. I suspect that they have been taught wrongly at uni or med school as per the quote in Everybody knows.........Part 1.

Benign Dietary Ketosis is NOT Ketoacidosis.

Consider the following four cases:- Note: Figures are from "Introduction to Nutrition and Metabolism" By David A Bender (Senior Lecturer in Biochemistry, UCL)

1) Healthy human, fed state: Glycogen stores are replete. Serum glucose = ~5.5mmol/L. Serum fatty acids = ~0.3mmol/L. Serum ketones = 0mmol/L. No gluconeogenesis is taking place. Amino acid pool is replete. Cortisol level is normal so there is no loss of muscle mass.

2) Healthy human, fasting for 7 days: Glycogen stores are depleted. Serum glucose falls to ~3.5mmol/L. Serum fatty acids rise to ~1.2mmol/L. Serum ketones (mainly D-3-hydroxybutyrate) rise to ~4.5mmol/L (not high enough to cause acidosis). Gluconeogenesis is occurring. Amino acid pool is depleted. Cortisol level is high, causing slow loss of muscle mass. This is bad ketosis.

3) Healthy human, low-carbohydrate diet: Glycogen stores are depleted. Serum glucose falls to ~5mmol/L.
Serum fatty acids rise to ~1.2mmol/L. Serum ketones (mainly D-3-hydroxybutyrate) rise to ~4.5mmol/L (not high enough to cause acidosis). Gluconeogenesis is occurring. Amino acid pool is replete (due to protein intake). Cortisol level is normal so there is no loss of muscle mass. This is good ketosis.

4) Human with untreated type 1 diabetes: Glycogen stores are depleted. Due to lack of insulin, the Glu-T4 transporters in cells cannot move to the surface so glucose cannot enter cells. Serum glucose = >20mmol/L. This causes major damage to kidneys, arteries, eyes, nerves etc by cross-linking with proteins (glycation) resulting in major disability and eventual death. As the body is forced to run on fatty acids & ketones, metabolic processes are out of control and ketones rise to much higher levels than in 2) or 3) (I don't know how high exactly) resulting in acidosis and eventual death. This is ketoacidosis.

Conclusion: Low-carbohydrate, very-low-carbohydrate & ketogenic dieting is similar to fasting in that serum glucose levels are lower than normal and glycogen stores are depleted. The body is encouraged to burn less glucose and more fatty acids & ketones, but the metabolic processes are all under control. The big difference between low-carbohydrate dieting and fasting is in the amino acid pool and cortisol levels.