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

Low-carbohydrate High-fat diets: Green flags and Red flags.

Fun with flags. But first, a poem!

Atkins Antidote


Eating low carbohydrate what threat that poses

Do my friends think I’m suffering from halitosis?

I’ve got these sticks for measuring ketoacidosis

I’m taking supplements but I don’t know what the dose is

I’m trying hard to keep in a state of ketosis

I’m not sure what the right amount of weight to lose is

I’m sure I’ve put on a pound just through osmosis

Is eating this way risking osteoporosis

Are my kidneys wrestling with metabolic acidosis

My store of liver glycogen I don’t know how low is

Who knows what the glycemic load of oats is

Does anyone know if I can eat samosas?


Ian Turnbull

I do. The answer's "No!" :-D

From https://forum.nationstates.net/viewtopic.php?f=23&t=13567&start=8925

The Green flags...

1. For a person with Insulin Resistance, an ad-libitum low-carb diet results in more weight loss than an ad-libitum high-carb diet.

See How low-carbohydrate diets result in more weight loss than high-carbohydrate diets for people with Insulin Resistance or Type 2 Diabetes , for an explanation.

2. For a person with Type 1 Diabetes Mellitus (T1DM), a lowish-carb (~100g/day), highish fat diet results in minimal disturbances to blood glucose levels and minimal bolus insulin doses.

See Diabetes: which are the safest carbohydrates? , to see which foods should comprise the ~100g/day. N.B. As ~50% of dietary proteins can be converted into glucose by gluconeogenesis, ~100g/day of slow-digesting proteins such as meats, eggs & cheeses can contribute ~50g/day of glucose towards the ~100g/day total.

3. For a person with LADA or MODY, see 2.

4. For a person with Type 2 Diabetes Mellitus (T2DM), a LCLF 600kcal/day Protein Sparing Modified Fast can normalise BG in 1 week and reverse T2DM in 8 weeks (provided there are sufficient surviving pancreatic beta-cells).

See http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3168743/
"After 1 week of restricted energy intake, fasting plasma glucose normalised in the diabetic group (from 9.2 ± 0.4 to 5.9 ± 0.4 mmol/l; p = 0.003)."

"Maximal insulin response became supranormal at 8 weeks (1.37 ± 0.27 vs controls 1.15 ± 0.18 nmol min−1 m−2)."

After 8 weeks, transition to a diet based on whole, minimally-refined animal & vegetable produce.

See also http://www.fend-lectures.org/index.php?menu=view&id=94

As Insulin Resistance is multi-factorial, ALL of the potential causes need to be addressed. Once this has been done, IR should be reversed, allowing restrictions on dietary carbohydrate intake to be lifted. See also Can supplements & exercise cure Type 2 diabetes?

The Red flags...

The low-carb diet is a temporary patch to ameliorate IR/IGT/Met Syn/T2DM, a bit like replacing a failed circuit-breaker by sticking a nail in its place, to allow the house to function while you fix the problem by buying a new circuit-breaker. Although the house functions fine with a nail in place of a circuit-breaker, you wouldn't want to spend the rest of your life without a working circuit-breaker protecting the house.

So, why do low-carbers seem to want to spend the rest of their lives using a temporary patch to ameliorate their IR/IGT/Met Syn/T2DM?

Long-term use of very-low-carb, very-high-fat diets is not recommended.

1. Cortisol level can gradually increase, resulting in increasing fasting BG level. See How eating sugar & starch can lower your insulin needs.

2. If you do too much high-intensity exercise, you may momentarily black-out, fall and hurt yourself. See "Funny turns": What they aren't and what they might be.

3. Some people seem to gradually go bat-shit crazy. See Can very-low-carb diets impair your mental faculties? Read the comments in https://www.facebook.com/TheFatEmperor/posts/1633434020253792. Do the behaviours of Ivor Cummins & Gearóid Ó Laoi seem normal to you?

4. Insulin Resistance is bad, mmm-kay? See Lifestyle-induced metabolic inflexibility and accelerated ageing syndrome: insulin resistance, friend or foe?

5. Dyseverything elseaemia isn't addressed. See Type 2 diabetes: between a rock and a hard place , Type 2 diabetes: your good signalling's gonna go bad and When the only tool in the box is a hammer.

6. Dietary deficiencies may develop. See Rigid diets & taking loadsa supplements to compensate for them.

7. High-fat diets with no energy deficit result in high postprandial TG's. Postprandial lipaemia is atherogenic. See Ultra-high-fat (~80%) diets: The good, the bad and the ugly.

There may be more but I'm knackered, so I'm Publishing!

Another penny drops: Why severe hyperinsulinamia can occur with a small increase in exogenous carbohydrate intake.

This blog post is a result of Vim's comments in the previous blog post. A penny suddenly dropped!

From http://bja.oxfordjournals.org/content/85/1/69.full

Insulin has a Chalonic (inhibitory) action on blood glucose level (via the liver, muscle mass & fat mass), blood FFA level (via fat mass) and blood ketone body level (via the liver).

As mentioned in the comments, GHB has a stimulant effect - up to a certain level of blood GHB. Beyond that level, there's a powerful sedative effect. This is because at low levels of exogenous ketone body input, insulin secretion increases slightly to reduce hepatic ketogenesis.

At a certain level of exogenous ketone body input, hepatic ketogenesis falls to zero and cannot be reduced any further. Any slight increase beyond this point in exogenous ketone body input, results in a large increase in insulin secretion, as the pancreas increases Ketone body-Stimulated Insulin Secretion to maximum in a (failed) attempt to reduce blood ketone body level.

Exactly the same thing happens with exogenous carbohydrate or BHB input.

At a certain level of exogenous carbohydrate input, hepatic glucogenesis falls to zero and cannot be reduced any further. Any slight increase beyond this point in exogenous carbohydrate input, results in a large increase in insulin secretion, as the pancreas increases Glucose-Stimulated Insulin Secretion to maximum in a (failed) attempt to reduce blood glucose level.

Why you really can't outrun your fork.

Hat-tip to Yoni Freedhoff.

From http://www.blacksheepfitness.co.uk/you-cant-outrun-your-fork.html

See Effect of school-based physical activity interventions on body mass index in children: a meta-analysis.
"Meta-analysis showed that BMI did not improve with physical activity interventions (weighted mean difference -0.05 kg/m², 95% confidence interval -0.19 to 0.10). We found no consistent changes in other measures of body composition."

Some people believe that if going to the gym isn't making them lose weight, they're not exercising hard enough. Chronically over-exercising can chronically raise serum cortisol, which makes the kidneys retain water, causing a stall in weight-loss, as well as causing raised fasting blood glucose, irritability, poor memory and a slower metabolic rate, due to the reduced conversion of thyroxine into tri-iodothyronine.

Don't over-exercise!

A healthy body weight is made in the kitchen, not the gym. Buy produce, cook it and eat it!

Although I totally support the use of low-carbohydrate/calorie diets for people with insulin resistance or Type 2 diabetes, now that I'm no longer insulin resistant, I can eat natural carbohydrates, without any problems.

A medium-sized (orange-fleshed) Sweet Potato takes only 4 minutes to bake in its jacket in a 700W microwave oven. The flesh is moist & sweet, unlike that of a Yam or potato.

I eat the whole thing, including the jacket. It's very filling and I'm still able to lose weight. For active and insulin sensitive people, a Kitavan-style diet is absolutely fine.

How a B.Sc.(Hons) in Electronic Engineering is relevant to Diet & Nutrition.

The human body regulates various processes using negative feedback loops. Here's blood glucose regulation.

From http://www.studyblue.com/notes/note/n/ch-47-chemical-signals-in-animals/deck/3085387

Here's a generic Hypothalamus-Pituitary-X Axis loop, where X may be thyroid, adrenal, gonadal etc.

From http://www.studyblue.com/notes/note/n/ch-47-chemical-signals-in-animals/deck/3085387

Electronic Engineers understand how negative feedback systems work, such as phase-locked loops & amplifiers.

Negative feedback control systems can overshoot, especially if there's a delay in the feedback path that's longer than the rise time of the input step.

An example of this is the first-phase insulin response. Loss of the first-phase insulin response occurs in over-fat people who are hyperinsulinaemic. Without the first-phase insulin response, there's a delay between an increase in blood glucose and an increase in insulin secretion. A rapid upwards step in blood glucose (say, from eating a high-GL meal) causes a massive overshoot in insulin secretion, resulting in postprandial sleepiness, also down-regulation of insulin receptor activity in the appetite centres of the brain, causing ravenous hunger when the insulin level falls to normal.

See also Blood Glucose, Insulin & Diabetes.

People shouldn't be too quick to write-off the knowledge of an Electronic Engineer who's delving into the mysteries of the human body.

Another tasty analogy.

Here's a tasty analogy.

From http://grannychoe.com/recipe3_Soup.php

In Ultra-high-fat (~80%) diets: Fat storage, and a delicious analogy, I analogised the effect of carbohydrate consumption on mean serum glucose level with the effect of fat consumption on mean serum triglyceride level. Here's another one.

Chronic excessive consumption of carbohydrates relative to what are being burned results in excessive fat synthesis in the liver, resulting in excessively-high fasting serum triglyceride level, which is harmful.

Chronic excessive consumption of fats relative to what are being burned results in excessive cholesterol synthesis in the liver, resulting in excessively-high fasting VLDL, LDL & IDL level, which is harmful.

Seems legit.

Gizmag: Injectable nanoparticles maintain normal blood-sugar levels for up to 10 days.

Fascinating technology featured in Gizmag & posted by someone HERE.

The nano-network that releases insulin in response to changes in blood sugar

"The injectable nano-network is made up of a mixture that contains nanoparticles with a solid core or insulin, modified dextran (which is commonly used to reduce blood viscosity), and glucose oxidase enzymes. When exposed to high levels of glucose, the enzymes convert glucose into gluconic acid, which breaks down the modified dextran to release the insulin. The gluconic acid and dextran, which are biocompatible, dissolve in the body, while the insulin brings the glucose levels under control.

The nanoparticles are given a positively or negatively charged biocompatible coating so that when they are mixed together, they are attracted to each other to form a “nano-network.” The positively charged coatings are made of chitosan, a material found in shrimp shells that has also found applications in self-healing car paint, while the negatively charged coatings are made of alginate, a material normally found in seaweed."

Wow! Cool bananas!

When the only tool in the box is a hammer...

Everything that needs fixing looks like a nail.

What are the action and reaction forces when a hammer hits a nail?

People with diabetes mellitus are issued with blood glucose meters - and nothing else.

For people with type 1 diabetes, that's fine. They lack insulin, so they have to inject insulin in the right amounts & types to keep their blood glucose levels within reasonable limits. Applying Bernstein's Law of small numbers by reducing glycaemic load to a minimum keeps blood glucose levels within reasonable limits (between 3 & 7mmol/L) most of the time. See also The problem with Diabetes.

For people with type 2 diabetes and a fat belly (~85% of type 2 diabetics), that's not fine. Their disease is a disease of chronic excess fuel intake relative to fuel oxidation, causing dyseverythingaemia (hyperglycaemia, hypercholesterolaemia, hypoHDL-cholesterolaemia, hyperNEFAaemia, hypertriglyceridaemia, hyperuricaemia, etc). People who have type 2 diabetes don't have only postprandial hyperglycaemia - they also have postprandial hypertriglyceridaemia. See Postprandial lipoprotein clearance in type 2 diabetes: fenofibrate effects.

However, because the only tool in their box is a blood glucose meter, their disease looks like a disease of hyperglycaemia only. Applying Bernstein's Law of small numbers by reducing carbohydrate intake to a minimum keeps blood glucose levels within reasonable limits, but makes everything else worse if energy from carbohydrates is replaced by energy from fats.

Only if energy from carbohydrates is reduced AND energy from fats isn't increased to compensate (i.e. eat a LCLF PSMF or Modified PSMF), does carbohydrate restriction help people with type 2 diabetes.