Free will? It's just an illusion! How the Food Product Industry gets people to dance to their tune, part 3.

Cont'd from Free will? It's just an illusion! How the Food Product Industry gets people to dance to their tune, part 2.
 
Derren Brown shows how easy it is to manipulate your thoughts, by the use of subliminal images.


I may have mentioned it somewhere on this blog, but everyone is different. The reactions of the kids in the "I ate all your Halloween candy" video in the previous blog post varied from total melt-downs, through feigned deaths, through tears, to "That's all right!". Candy/sweets have different importance to different people and people's suggestibility varies from "Very easy to manipulate" to "Very hard to manipulate".

There's engineering of foods to be as moreish as possible. "The trouble is, they taste too good!" (Crunchy Nut Cornflakes), "Bet you can't eat just one!" (some savoury snack made from refined starch, salt & flavourings) and "Once you pop, you can't stop!" (Pringles). As Harry Hill once said "The problem with heroin is, it's rather moreish!" Although addiction to pure table sugar isn't a thing, addiction to hyperpalatable foods is a thing (which can be reduced by Naltrexone). See Food cravings engineered by industry and Sugar addiction: pushing the drug-sugar analogy to the limit.

Then there's the incessant marketing, including direct adverts, sponsorships, product placements, celebrity endorsements, tie-ins etc. See The Money Spent Selling Sugar to Americans Is Staggering and It’s Not Your Imagination: Celebrities Hawk Pretty Much Only Junk Food.

Then there's the bribery lobbying of government to:-
1. Water-down Dietary Guidelines so that crap-in-a-bag/box/bottle (CIAB) meets them. As people get fatter and sicker, the Guidelines and the government get the blame.
2. Subsidise the ingredients of CIAB so that it's cheaper than produce.

Then there's corruption of science e.g. getting doctors to advertise cigarettes years ago. Organisations with vested interests are created, to promulgate conflicting dietary information. Is it any wonder that the public distrust science and scientists?

Edward Bernays' manipulation techniques have worked exceedingly well. If you're too fat and someone says to you "Nobody made you over-consume that crap", point out the above.

What can you do? You can't sue Food Product manufacturers, as their products don't immediately harm you. See How Ultra-Processed Foods Are Killing Us. Hit them where it hurts i.e. in their bank accounts, by eschewing CIAB and basing your diet on whole, minimally-refined animal and vegetable produce. CIAB should be treat foods, not staple foods.

Finally, here's a video on how to form good habits for life.


Cont'd on Free will? It's just an illusion! How the Food Product Industry gets people to dance to their tune, part 4.

Free will? It's just an illusion! How the Food Product Industry gets people to dance to their tune, part 2.

Cont'd from Free will? It's just an illusion! How the Food Product Industry gets people to dance to their tune, part 1.

Remember the video "YouTube Challenge - I Told My Kids I Ate All Their Halloween Candy 2015"?


Some of those kids reacted as if their life had just come to an end!

Disclaimer: I don't know anything about psychotherapy, so I don't know how accurate the information is in Hypoglycemia and Neurosis.

Please don't pacify crying babies/toddlers/children with sugary crap.

Cont'd on Free will? It's just an illusion! How the Food Product Industry gets people to dance to their tune, part 3.

Free will? It's just an illusion! How the Food Product Industry gets people to dance to their tune, part 1.

Cont'd from Public Service Announcement: Calling all Low-carb, Low-fat and Veg*n advocates.

I feel a music video coming on.


Start of clarification.
I've noticed some confusion over the term "Crap-in-a-bag/box/bottle" (CIAB). My previous post received the following comment, which I'll annotate.
"Is highly processed the problem? Yes.
Tinned tomatoes are processed, what's wrong with including those in your diet. Nothing, other than the fact that they're too salty for me if they're tinned in brine.
What about low sugar baked beans? Nothing, other than the fact that they're too salty for me.
What's wrong with a burger if all it is, is minced beef? Nothing.
Other processed food:
Smoked mackerel Fine.
Frozen peas Fine.
Milled porridge oats Fine.
Parma ham Fine.
Cheese Fine.
Nitrate free bacon Fine.
Prunes Fine.
Almond butter Too calorie-dense & moreish for me.
Filtered milk Fine.
Low sugar jam Fine.
Roasted chestnuts Fine.
Haggis Fine. I think."

CIAB is stuff like French fries/chips, chips/crisps, "fast food", take-aways, pizzas, biscuits/cookies, chocolate, sweets/candy, sugar-sweetened beverages, sugary cereals etc.
End of clarification.

In How to lose weight and get slim by eating "fast food" for 180 days. I showed that it's possible to be healthy on a diet of fast food, if you have a plan and you stick to it. The vast majority of people who eat fast food don't have a plan!

Between the ages of 5 & 8, I spent my 12d/week (that's 5p/week, for those of you who are too young to remember £,s,d.) on sweets. Aniseed balls were 4 for 1d. I also ate French Fancies (small sponge cakes covered in fondant icing) and drank Corona Lemonade (~15% sugar content) at home.

How did I get such a ferocious sweet tooth? Here's the probable answer:- Farley's Rusks.

Look at the health-washing.
"Farley’s Rusks have been loved by mums and babies for generations. Each rusk is lovingly baked using baby grade ingredients."

Let's take a look at the baby grade ingredients:-
"Wheat Flour, Sugar, Palm Oil, Raising Agents (Ammonium Carbonates), Calcium Carbonate, Emulsifier (Monoglycerides), Niacin, Iron, Thiamin, Riboflavin, Vitamin A, Vitamin D."

The first three ingredients are refined starch, refined sugar and refined fat. The refined sugar content is 29% by weight. Perfect food for a baby! The previous sentence may contain traces of sarcasm.

Cont'd on Free will? It's just an illusion! How the Food Product Industry gets people to dance to their tune, part 2.

Why using macronutrient percentages is so wrong.

From https://sciencelearn.org.nz/Contexts/Food-Function-and-Structure/Sci-Media/Images/Macronutrient-percentages

1. Deception

Consider Lies, damned lies and statistics, part n+1. Riera-Crichton et al.  

Relative fat intake in %E decreased and obesity increased.

The conclusion:- "Carbohydrates are fattening and fat is slimming." Yeah, right!

Absolute fat intake in grams/kcals has always increased, according to More Thoughts on Macronutrient Trends. Absolute protein intake in grams/kcals has also always increased.

Gary Taubes & Nina Teicholz use this deliberate misrepresentation of data to create the false narrative that low-fat healthy eating guidelines caused the obesity epidemic in the US. It's a pack of lies.

2. The terms "Low Fat" and "High Fat" are meaningless

Take 55g of fat (500kcals), 125g of protein (500kcals) and 375g of carbohydrate (1,500kcals). It adds up to 2,500kcals, with a percentage C/F/P split of 60/20/20. It's a High Carb, Low Fat diet.

Now remove 125g of carbohydrate to leave 250g of carbohydrate (1000kcals). It now adds up to 2,000kcals, with a percentage C/F/P split of 50/25/25. It's still a High Carb, Low Fat diet.

Now remove another 125g of carbohydrate to leave 125g of carbohydrate (500kcals). It now adds up to 1,500kcals, with a percentage C/F/P split of 33/33/33. It's now a Medium Carb, Medium Fat Zone diet.

Now remove another 62.5g of carbohydrate to leave 62.5g of carbohydrate (250kcals). It now adds up to 1,250kcals, with a percentage C/F/P split of 20/40/40. It's now a Low Carb, Highish Fat diet.

Now remove another 62.5g of carbohydrate to leave 0g of carbohydrate (0kcals). It now adds up to 1,000kcals, with a percentage C/F/P split of 0/50/50. It's now a Very Low Carb, High Fat diet.

So, 55g/day of fat can be Low Fat, Medium Fat, Highish Fat or High Fat. Which leads to...

3. Confusion

When someone sees the term LCHF (Low Carb, High Fat), they think it means "Eat less carbohydrate and eat more fat". As changes in body stores are determined by Energy Balance, eating more fat leads to a slower rate of weight-loss (or even weight-gain), not a faster rate of weight-loss.

By all means cut the consumption of "bad" carbs, like burgers in buns, chips/fries, crisps/chips, pizzas, cakes, biscuits/cookies, chocolate (which are also high in fats) & sugar-sweetened beverages.

However, if you believe that "good" carbs like vegetable produce, legumes, whole grains and whole fruits make you fat and sick, you need to have your head examined, unless you're in the tiny percentage of the population who have genetic carbohydrate intolerance.

See also Insulin Resistance: Solutions to problems.

Why (LDL particle) size matters.

Having gone through the math(s) with several people, I thought I'd stick it in a blog post for posterity.

This is a diagram of a chylomicron or VLDL-c (high TG/C ratio) 'cos I couldn't find one for LDL-c!

Cholesterol synthesised in the liver is exported in LDL particles. The more cholesterol that's synthesised, the more particles there need to be to carry it.

∴ LDL-P (particle number) ∝ LDL-C (total amount of cholesterol)

The particles are roughly spherical with a very thin wall (consisting of a phospholipid mono-layer, the yellow wiggly lines with a green end bit in the above diagram).

Volume of a sphere = 4/3 * π * r³, where r = half the diameter.

If there's a 10% reduction in LDL particle size, the volume reduces to 0.729, relative to the original size. Therefore, to carry the same amount of cholesterol requires 1/0.729 = 1.37 times more particles, which is a 37% increase in the number of LDL particles, relative to the original size.

∴ LDL-P (particle number) ∝ 1/LDLsize³

As it's LDL particle number that determines the infiltration of LDL cholesterol into the media of artery walls (see image below), it's advisable to keep cholesterol synthesis to a reasonable level by keeping fat intake to a reasonable level (i.e. not Nutritional Ketosis!) and keeping LDL particle size to a reasonable level by keeping added sugar (e.g. sucrose & fructose) intake and rapidly hydrolysed/overcooked starches (e.g. amylopectin & maltodextrin) intake to a reasonable level (i.e. a level that's oxidised by the body without having a chronic excess). An acute excess of carbohydrate can be stored as liver/muscle glycogen, provided that mean carbohydrate intake is less than mean carbohydrate oxidation.

How COULD I write a post about LDL-P and forget to include THIS?

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!

Lipoproteins & apolipoproteins: E, by 'eck.

In December 2008, I wrote about Cholesterol And Coronary Heart Disease , where I used a limousine metaphor to describe how cholesterol & fat are transported around the body. Here's a diagram of a chylomicron lipoprotein "limousine". Chylomicrons transport dietary fat (triglycerides) & cholesterol from the gut to the liver & other tissues. As there's much more dietary fat than dietary cholesterol, the contents are mostly fat.

A chylomicron. T=Triglyceride C=Cholesterol. From http://en.wikipedia.org/wiki/Lipoprotein

The lipoprotein "limousines" vary a lot in size.

(a) VLDL (b) chylomicrons (c) LDL (d) HDL. 
From http://healthcorrelator.blogspot.co.uk/2011/11/triglycerides-vldl-and-industrial.html

Apolipoproteins are the "chauffeurs" which determine to where lipoproteins transport stuff.
Apo A is found mainly on HDL, which transports fat & cholesterol from tissues to the liver.
Apo B is found mainly on LDL, which transports cholesterol from the liver to tissues.
Apo C is found on HDL when fasted, but moves to chylomicrons & VLDL when fat is eaten.
Apo D is found mainly on HDL and is is associated with an enzyme involved in lipoprotein metabolism.
Apo E is found mainly on chylomicrons & IDL and transports lipoproteins, fat-soluble vitamins, and cholesterol into the lymph system and into the blood. In the CNS, Apo E transports cholesterol to neurons. Defects in Apo E result in hyperlipidaemia , cardiovascular & neurological diseases, and is the E referred to in the title.

There's also Apo H, which is a β-glycoprotein involved in the binding of cardiolipin. It has nothing to do with the above lipoproteins.

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!

Metabolic Inflexibility: What it really means.

Here's a picture from Metabolic Flexibility and Insulin Resistance.

The Metabolically-Inflexible (MI) & Insulin Resistance

Here's another picture.

Fig 2. ● = Metabolically-Flexible (MF). ○ = Metabolically-Inflexible (MI).

Salient points:
1) Excessively high serum FFA a.k.a. NEFA is bad.
2) Respiratory Quotient (RQ) a.k.a. Respiratory Exchange Ratio (RER) changes due to dietary changes are more sluggish in the MI than in the MF.
3) Under Insulin Clamp conditions, RQ/RER is lower in the MI than in the MF, due to impairment of glucose oxidation and non-oxidative glucose disposal.

I have posted this because of Danny Roddy's post Is Supplemental Magnesium A Surrogate For Thyroid Hormone? , which leads onto A Bioenergetic View of High-Fat Diets.

In the first article, Danny Roddy writes:-
"Additionally, taking magnesium while actively engaging in a diet or lifestyle that reduces the respiratory quotient (e.g., high-fat diet, light deficiency, excessive exercise) seems pretty silly. For example, as a rule, diabetics have a reduced respiratory quotient (Simonson DC, et al. 1988), tend to have higher levels of free fatty acids or NEFA (Kahn SE, 2006), and are often deficient in magnesium (De Valk HW, 1999)."

The second sentence (diabetics have a reduced respiratory quotient...and are often deficient in magnesium) seems to contradict the first sentence (...taking magnesium while actively engaging in a diet or lifestyle that reduces the respiratory quotient seems pretty silly).

Simonson DC, et al. 1988 is Oxidative and non-oxidative glucose metabolism in non-obese type 2 (non-insulin-dependent) diabetic patients.
"In conclusion, during the postabsorptive state and under conditions of euglycaemic hyperinsulinaemia, impairment of glucose oxidation and non-oxidative glucose disposal both contribute to the insulin resistance observed in normal weight Type 2 diabetic patients. Since lipid oxidation was normal in this group of diabetic patients, excessive non-esterified fatty acid oxidation cannot explain the defects in glucose disposal."

Impaired glucose oxidation with normal lipid oxidation lowers RQ/RER. Therefore, lower RQ/RER must be bad, right? Wrong. From the above study:-
"...euglycaemic insulin clamp studies were performed..."
Remember Salient point 3)? Simonson DC, et al. 1988 is an insulin clamp study, the results of which don't apply to free-living people (who aren't insulin clamped).

See also Determinants of the variability in respiratory exchange ratio at rest and during exercise in trained athletes. RER/RQ increases & decreases with increases & decreases in exercise intensity. This is Metabolic Flexibility (MF). Sorry, Danny.

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.

It's all in a day's work (as measured in Joules) Part 2.

Are you as aerobically-fit as this bloke?

Emmanuel Mutai made it a Kenyan double after winning the Virgin London Marathon in a new course record. Mutai's time of 2:04.38, beats the previous best of 2:05.10 set by Samuel Wanjiru in 2009 and also the fifth-fastest time ever.

I'll take it that's a "no", then.

Elite marathon runners have optimised their metabolisms to use the minimum possible amount of muscle glycogen as fuel. Muscle glycogen storage is limited to ~1,680kcals-worth (~420g of carb)*.
Supercompensation (depletion followed by 3 days of carb-loading) can increase this figure to ~720g*.
Fat storage can amount to ~35,000kcals-worth (~10lb of fat), even in a skinny Kenyan like Mutai.

A blogger called Thor Falk took the data from It's all in a day's work (as measured in Joules) and plotted it as a graph in Fat vs carb burning – a N=1 chart. Here's the graph:-

Even a super-fit Kenyan like Mutai burns some carbs when running at ~12.5 miles per hour. The less fit that somebody is, the more the first corner in the blue plot moves down and to the left. This results in more carbs being burned at energy consumption levels more than the first corner. This depletes muscle glycogen stores faster, resulting in "hitting the wall" (running out of muscle glycogen) sooner.

Muscles that are depleted of glycogen are more insulin-sensitive than muscles that have more glycogen, therefore the less aerobically-fit somebody is, the sooner their muscles become insulin-sensitive when they exercise.

*Assuming 20kg of muscle (Lore of Running P104)

It's all in a day's work (as measured in Joules)

Firstly, a relevant video by Flanders and Swann.


The title of this blog post is from the "Physics Man" sketch on The Now Show. Work (also heat) is another word for energy and there are two different units for it.

The calorie (cal) is the amount of energy required to heat 1g of water by 1°C. This is a tiny amount of energy. The dietary Calorie (Cal) = 1,000cal = 1kcal.

The Joule (J) is the SI unit of energy. 1J = 1kg*m^2/s^2.
1Joule/sec = 1Watt (W).

1kcal = 4.186kJ.

At rest, an average human body uses ~1kcal/min = ~4,186J/min = ~69.8J/sec = ~69.8W.

The brain uses ~5g of glucose/hour = 18.75kcal/hour (1g of carb = 3.75kcals, usually rounded-up to 4) = 78487.5J/hour = ~21.8W.

The heart uses ~10W. The liver, kidneys, gut and lungs run continuously so they use energy all of the time.

Skeletal muscle uses a variable amount of energy using a variable proportion of fuels, depending on what you're doing with it. A chap called Steve sent me a spreadsheet of results in 2004 when he underwent a metabolic test on a stationary bike while breathing through a respiratory gas analyser, which calculated kcals oxidised and fuel utilisation by measuring Respiratory Exchange Ratio (RER).

At 1kcal/min (resting), he oxidised ~95% from fat (~0.11g/min), ~5% from carb (~0.01g/min).
At 2kcal/min (12% max), he oxidised 100% from fat (0.22g/min), 0% from carb (0.00g/min).
At 3kcal/min (18% max), he oxidised 100% from fat (0.33g/min), 0% from carb (0.00g/min).
At 4kcal/min (24% max), he oxidised 99% from fat (0.44g/min), 1% from carb (0.01g/min).
At 5kcal/min (29% max), he oxidised 48% from fat (0.27g/min), 52% from carb (0.69g/min).
At 6kcal/min (35% max), he oxidised 62% from fat (0.41g/min), 38% from carb (0.61g/min).
At 7kcal/min (41% max), he oxidised 58% from fat (0.45g/min), 42% from carb (0.78g/min).
At 8kcal/min (47% max), he oxidised 46% from fat (0.41g/min), 54% from carb (1.15g/min).
At 9kcal/min (53% max), he oxidised 42% from fat (0.53g/min), 58% from carb (1.39g/min).
At 10kcal/min (59% max), he oxidised 44% from fat (0.49g/min), 56% from carb (1.49g/min).
At 11kcal/min (65% max), he oxidised 38% from fat (0.46g/min), 62% from carb (1.82g/min).
At 12kcal/min (71% max), he oxidised 41% from fat (0.55g/min), 59% from carb (1.89g/min).
At 13kcal/min (76% max), he oxidised 37% from fat (0.53g/min), 63% from carb (2.18g/min).
At 14kcal/min (82% max), he oxidised 30% from fat (0.47g/min), 70% from carb (2.61g/min).
At 15kcal/min (88% max), he oxidised 14% from fat (0.23g/min), 86% from carb (3.44g/min).
At 16kcal/min (94% max), he oxidised 0% from fat (0.00g/min), 100% from carb (4.27g/min).
At 17kcal/min (100% max), he oxidised 0% from fat (0.00g/min), 100% from carb (4.53g/min).

There are some interesting points about Steve's data:

1. Over a wide range of exercise intensities, the number of grams of fat Steve oxidised/min was fairly constant.

2. Up to 24% of maximum exercise intensity, Steve derived almost 100% of his energy from the oxidation of fat. Steve was on a LC diet, which shifts fuel usage away from carb and towards fat. This is known as "fat-adaptation".

3. Despite fat-adaptation, above about 45% of maximum exercise intensity, Steve derived more energy from the oxidation of carb than the oxidation of fat.

4. Despite fat-adaptation, above about 80% of maximum exercise intensity, Steve derived almost all of his energy from the oxidation of carb rather than the oxidation of fat.


Note that 17kcals/min = 1186.6W, or 1.19kW! Steve was aerobically fit. A less aerobically fit person derives a higher % of energy from the oxidation of carb than an aerobically fit person. This level of exercise intensity can be maintained for a few seconds only, as carb is oxidised both aerobically and anaerobically, which exhausts PhosphoCreatine stores in muscles and also causes an accumulation of lactate in muscles.

Muscle mass is very metabolically-active compared to fat mass, as one pound of fat mass oxidises only about 2kcal a day. See also Dissecting the Energy Needs of the Body – Research Review

See also It's all in a day's work (as measured in Joules) Part 2.


Here's another Physics Man.

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.

I have a hypothesis.

I was keeping quiet about this, as it contradicts Gary Taubes, Michael R Eades & Richard D Feinman and Eugene J Fine.

Please note: This post is not criticising low-carb, high-fat diets. I'm pointing out that if someone on a low-carb, high-fat diet exercises as much gluttony as they want on roast lamb/pork/duck etc, they may not lose as much weight/body fat as they expected & they may even gain.

I don't want to start a shit-storm, but as I am in the "a calorie is a calorie" (when it comes to weight gain/loss) camp and a lot of the people whose blogs I link to aren't, I need to go public. So, here it is, copied and pasted from the comments section of Diet, Carbs, Fat and Weight Loss, corrected for spelling.

"I would like to propose a theory which explains how fat cells can acquire glucose (& thus correct a deficiency in glycerol-3-phosphate) even when serum insulin level is basal.

Consider muscle cells undergoing anaerobic activity:-

Anaerobic activity is very inefficient and uses pyruvate at a very rapid rate. A deficiency in pyruvate up-regulates all of the up-stream processes, including Glu-T4 transporters so as to maximise pyruvate production.

This explains why resistance training with weights greatly increases muscular insulin sensitivity and why resistance training with weights when depleted of muscle glycogen can cause precipitous drops in blood glucose level.

Ditto for glycerol-3-phosphate in fat cells. In this case, blood glucose level is maintained by the liver & kidneys, which convert the glycerol backbone of triacylglycerols (fats) and other substrates such as lactate, pyruvate & glucogenic amino acids into glucose."

In plain terms what this means is that, like muscle cells, fat cells can acquire as much glucose as they need, independently of carbohydrate intake.

Therefore, if an excess (beyond what the body is burning) of dietary fat is eaten, this can be stored in fat cells even if serum insulin level does not increase.

There. I've said it. I expect comments. Moderation is enabled. All comments that are free from ad-hominem, straw men & other logical fallacies will be published.

EDIT: Here's evidence that dietary fat can be stored in the absence of dietary carbohydrate. It involves doing maths on an Oral Fat Tolerance Test:- On burning, storing and recomposing.

EDIT: Here's evidence that a calorie is a calorie (where weight change is concerned):- Bray et al shows that a calorie *is* a calorie (where weight change is concerned).
 
As a lot of people report that they can eat dietary fat without getting fat (& actually getting lighter & slimmer), there appears to be something "magical" going on. It's generally accepted that fat is the least thermogenic of all the macronutrients & protein is the most thermogenic. I wonder if this is the case for all types of fat and all types of people.

See Butyric Acid: an Ancient Controller of Metabolism, Inflammation and Stress Resistance.

From Battle of the Weight Loss Diets: Who's Winning (at losing):-
Insulin Resistant people lose more weight on low-carb, high-fat (LCHF) diets than high-carb, low-fat (HCLF) diets.  
Insulin Sensitive people lose more weight on high-carb, low-fat (HCLF) diets than low-carb, high-fat (LCHF) diets.

According to Gary Taubes's Carbohydrate Insulin Hypothesis, everyone should lose more weight on low-carb, high-fat (LCHF) diets than on high-carb, low-fat (HCLF) diets. Therefore, Gary Taubes's Carbohydrate Insulin Hypothesis is false.

It's possible that in people who do well on LCHF diets, kcals out on the right hand side of the Energy Balance Equation increase significantly. So keep on keeping on.

EDIT: With the benefit of four more years of knowledge, here's why LCHF & ketogenic diets have an advantage for people who have Insulin Resistance. How low-carbohydrate diets result in more weight loss than high-carbohydrate diets for people with Insulin Resistance or Type 2 Diabetes.

See also:-
Metabolic Advantage of Ketogenic Diets Debunked? An Intriguing Study You Will Want to Read
Is the Fable of Unfettered Fat Burning Derailing Your Low Carb Diet?

See also How stuff works & Enzymes.