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 https://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

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 https://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? T2DM is a disease of chronic excess. Chronic over-consumption was caused by Food Industry marketing, not carbohydrates.

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 https://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 https://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 https://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 (~600kcals/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 https://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!

Diogenes: High protein + low GI = Weight-loss maintenance WIN.

See Diets with High or Low Protein Content and Glycemic Index for Weight-Loss Maintenance.

LP = Low Protein. HP = High Protein. LGI = Low GI. HGI = High GI.

"In conclusion, in this large, randomized study, a diet that was moderately high in protein content and slightly reduced in glycemic index improved the rate of completion of the intervention and maintenance of weight loss and therefore appears to be ideal for the prevention of weight regain."

Note that Low GI isn't the same as Low carb. The Low GI diets had ~43% of total energy from carbohydrate. The Low GI diets were not Low carb diets. They weren't as High carb as Healthy Eating Guidelines (55% of total energy from carbohydrate).

On burning, storing and recomposing.

Burning

I couldn't resist!


On my adventures around the interwebs, I've noticed the following:- "Humans aren't Calorimeters. Therefore calories are irrelevant to humans." While I agree with the first sentence, I don't agree with the second one.

Calorimeters burn (oxidise) foods at high temperatures with a flame using oxygen, which produces carbon dioxide, water (depending on what's being burned) & heat energy.

Humans burn (oxidise) foods at 37ºC with enzymes , charge transporters etc using oxygen, which produces carbon dioxide, water (depending on what's being burned), mechanical energy & heat energy.

As both oxygen & carbon dioxide are gases, these can be measured by a respiratory gas analyser, to establish the rate of burning and what's being burned at any instant. See It's all in a day's work (as measured in Joules). When resting, burning occurs at a rate of ~1kcal/minute and, as it's measured while fasted, ~0.11g/min of fat is burned, & ~0.01g/min of carbohydrate is burned. Also note that a lot of mechanical energy can be produced, which can increase the rate of burning by a factor of seventeen.

In conclusion, humans burn (oxidise) foods, though not with a flame, and they can produce mechanical energy in addition to heat energy. The rate of burning and what's being burned at any instant can be measured.

Storing

When we eat food, it's digested and absorbed. As a digested meal is absorbed, it appears in the blood as glucose, triglycerides & amino acids. These then disappear from the blood due to burning and storage.

Fig. 1 Extended effects of evening meal carbohydrate-to-fat ratio on fasting and postprandial substrate metabolism

Fig. 1 above shows the effects of a 100g Oral Glucose load (▪▫) or a 40g Oral Fat load (●○) on blood glucose level over a period of 360 minutes. Note that subjects are resting during the 360 minutes. As the 100g Oral Glucose load produces a large insulin response (See Fig. 2 below ▪▫), fat-burning is temporarily reduced.

Fig. 2 Extended effects of evening meal carbohydrate-to-fat ratio on fasting and postprandial substrate metabolism

Therefore, ~1kcal/minute resting burning rate is derived ~100% from carbohydrate. Therefore, carbohydrate-burning rate is ~0.25g/min. At this rate, it would take ~400 minutes to burn 100g of glucose. If less than 100% of energy is derived from carbohydrate, it would take longer. However, it actually takes ~180 minutes for blood glucose level to fall from maximum to minimum. Therefore, some glucose from the Oral Glucose load is stored (mostly as glycogen in muscles and liver).

Fig. 3B Extended effects of evening meal carbohydrate-to-fat ratio on fasting and postprandial substrate metabolism

Fig. 3B above shows the effects of a 40g Oral Fat load (●○) on blood triglyceride (fat) level over a period of 360 minutes. Note that subjects are resting during the 360 minutes. As the 40g Oral Fat load produces no significant insulin response (See Fig. 2 above ●○), fat-burning is unaffected.

Therefore, fat-burning rate is ~0.11g/min. At this rate, it would take ~364 minutes to burn 40g of fat. If less than 100% of energy is derived from fat, it would take longer. Everyone is Different. shows the variation in % of energy from fat at rest. However, it actually takes 180 to 240 minutes for blood triglyceride (fat) level to fall from maximum to minimum. Therefore, some fat from the Oral Fat load is stored (as fat in adipocytes), even though there is no significant insulin response.


Therefore there are times when stuff is stored (anabolism) and there are times when stuff is withdrawn from stores (catabolism). If more stuff is stored than is withdrawn over a period of time, weight goes up, and vice-versa.

Recomposing

After doing intense exercise e.g. sprinting, resistance training with weights etc, muscles become very sensitive to insulin. Therefore, if intense exercise is done just before stuff is stored, amino acids & glucose are preferentially stored in muscles rather than adipocytes. This increases muscle mass relative to fat mass.

If non-intense exercise is done at times when stuff is withdrawn from stores, this maximises the amount of fat withdrawn from adipocytes and minimises the amount of amino acids withdrawn from muscles. This decreases fat mass relative to muscle mass.

It's therefore possible to increase muscle mass at certain times and decrease fat mass at other times, while keeping overall mass relatively constant i.e. it's possible to gain muscle and lose body-fat without being in an overall caloric deficit.


See The Energy Balance Equation, for more information.

Ghrelin, the other "in"

Having just written about Leptin, it's Ghrelin's turn now. When your stomach is empty, serum ghrelin level is high and when your stomach is full, serum ghrelin level is low. Interestingly, high serum ghrelin has a beneficial effect on the hippocampus (responsible for learning stuff) so do your studying when you're hungry!

As a full stomach reduces serum ghrelin and thus reduces appetite, anything that keeps the stomach full for longer reduces appetite for longer. This is where enterogastrones come in. The most useful one in terms of appetite control is cholecystokinin, the secretion of which is stimulated by proteins & fats. This is one reason why diets high in proteins & fats keep you full for longer. Another useful filler is fibre/fiber, of course. As shown on the BBC programme "The Truth about Food", blending a meal with water or some other low-calorie liquid like soup also slows stomach emptying.

Finally, sleep deprivation raises ghrelin so I must try harder to spend less time on my computer and get some shut-eye.

Linseed/Flaxseed & Flaxseed oil.

"Where flax is eaten...health abounds!" - Mahatma Gandhi.

These little seeds pack a quadruple-whammy of protein, omega-3 Essential Fatty Acids (EFAs), soluble fibre/fiber and vitamins, minerals & other anutrients.


What's in flaxseed and flaxseed oil?

Click https://www.nutritiondata.com/facts/nut-and-seed-products/3163/2 and set serving size: to 100g, to see what nutrients there are in flaxseeds.
Click https://www.nutritiondata.com/facts/fats-and-oils/7554/2 and set serving size: to 100g, to see what nutrients there are in flaxseed oil.


How do I eat flaxseed and flaxseed oil?

Flaxseed/Linseed have a fibrous coat which swells-up when wet and passes through our guts undigested. To get the benefit of the protein, omega-3 essential fatty acids, vitamins & minerals in flaxseeds, the seeds need to be powdered, crushed, cracked, chopped-up, sliced-up or ground-up using a coffee grinder, adjustable pepper grinder or most simply, a blender with a sharp blade.

The resulting powder can be mixed with liquids or sprinkled on foods, though extra fluid must be drunk, as the soluble fibre/fiber absorbs a lot of water.

Although whole flaxseed keeps fresh at room temperature, once powdered, it's advisable to keep the powder in a cool dark place to minimise oxidation of any exposed fat. Flaxseed oil must be kept refrigerated with the lid on the bottle at all times after opening and it must never be used for cooking.

The oil is O.K. drizzled over hot food, as long as the food is eaten shortly afterwards. Oxidised flaxseed oil tastes bitter and has lost its health benefits, so it should either be chucked, used to varnish something or soften hardened putty. Unoxidised flaxseed oil has a nutty flavour, or it may taste a bit like tea. Powdered flaxseed has virtually no flavour.

See Milled flaxseed stability information.


How much flaxseeds and flaxseed oil do I need to eat each day?

Men are much poorer converters of alpha-linolenic acid (the omega-3 fatty acid in flaxseed) into DHA than women.

See Eicosapentaenoic and docosapentaenoic acids are the principal products of α-linolenic acid metabolism in young men,

Conversion of α-linolenic acid to eicosapentaenoic, docosapentaenoic and docosahexaenoic acids in young women and

Extremely Limited Synthesis of Long Chain Polyunsaturates in Adults: Implications for Their Dietary Essentiality and Use as Supplements.

Therefore, men should eat ~50g/day of ground flaxseed and women should eat ~25g/day. The amount of flaxseed oil for men is ~20g/day and the amount for women is ~10g/day. Vegan men should also supplement with ~1000mg/day of vegan DHA.


Where can I buy flaxseeds and flaxseed oil?

Flaxseed/linseed come in different colours. The cheapest linseed are brown/bronze ones which are often sold as bird seed in pet shops, but they can also be found in small independent health food shops. There are also golden linseed, which is the type most often found in supermarkets. Linusit and Granovita are two well-known brands. Granovita organic flaxseed oil is a good brand and it comes in dark bottles to keep light out, as light causes photo-oxidation of omega-3 fats.

Proteins: Dogs' Doodads.

"Mmmm! These Korean meatballs really are the dogs' b*llocks!" said Hugh Dennis on "Mock the Week" as "Things you don't hear on TV cookery programmes".

For an overview on Protein, see https://en.wikipedia.org/wiki/Protein.
For an overview on Protein in nutrition, see https://en.wikipedia.org/wiki/Protein_in_nutrition.

I'm not going to write any more about protein, as somebody else already has. So, I am referring you to Lyle McDonald's protein articles, as what Lyle doesn't know about protein fits on a postage stamp........a very small one!

I shall now take a break. Merry Christmas everyone!