The Facts of Life.

No, not those Facts of Life!

From http://www.clipartbest.com/stork-carrying-baby

It's becoming painfully obvious that there's a lot of ignorance about certain dietary "Facts of Life". This post will dispel the myths - backed up by evidence, where necessary.

1. Everyone is Different: This has been a recurring theme on my blog, starting in 2009 with the aptly-named Everyone is Different. What this means in practice, is that:-
a) You can't calculate your Energy Expenditure exactly, using one of those fancy equations (e.g. Harris-Benedict).
b) Weight change is proportional to caloric excess/deficit ± inter-personal variation.

2. CALORIES COUNT: If there's zero caloric surplus, there's zero weight gain. There can be water balance shifts due to glycogen shifts, hormonal shifts, electrolyte shifts etc. Somebody fitted a lovely straight line to the weight gain data in Bray et al shows that a calorie *is* a calorie (where weight is concerned), but their line didn't pass through 0,0. Duh!

3. Glycaemic Index (GI) has NOTHING to do with calories: A low-GI carbohydrate still has 4kcals/g. GI is a useful hint as to whether a carbohydrate may disturb blood glucose levels, but it isn't as useful as Glycaemic Load (GL = GI x grams of carbohydrate in the serving). Watermelon has a very high GI, but 100g of watermelon contains only ~5g of carbohydrates, so the GL is less than 5 i.e. watermelon is as safe as houses.

4. Exercise DOESN'T burn as many calories as you think: Exercise is for fitness, not weight loss (unless you're a professional sports-person, who can expend 1,000's of kcals a day in training).

5. Weight loss doesn't ALWAYS result in reduced Basal Metabolic Rate: Whether or not Basal Metabolic Rate reduces with weight loss depends on the degree of Adipocyte Hyperplasia that occurred during weight gain. Humongous weight gain, also weight gain in childhood, increases adipocyte hyperplasia, which is protective against developing T2DM, but makes the subsequent loss of significant amounts of FM more difficult.

6. For Muscle Hypertrophy, a STIMULUS is required: Eating too much food and/or swallowing loads of protein without hypertrophy training doesn't make muscles grow significantly bigger. See http://hillfit.com/. Chris Highcock knows what he's talking about.

7. Yo-yo dieting isn't ALWAYS a bad thing: Bodybuilders (BB'ers) do cycles of "cutting" and "bulking". Cutting is Fat Mass (FM) loss with minimal Lean Body Mass (LBM) loss. Bulking is LBM gain with minimal FM gain.

Non-BB'ers tend to get it the wrong way round. They go on crash diets with insufficient protein intake and lose loads of LBM (which increases weight loss, due to the lower Energy Density of LBM relative to FM). They then eat way too much, gaining weight way too rapidly for much (if any) of it to be LBM, even if they are doing hypertrophy training.

8. FM loss CAN be rapid: See The Rapid Fat Loss Handbook. A Scientific Approach to Crash Dieting.

9. LBM gain CANNOT be rapid: See What’s My Genetic Muscular Potential? to find out how much LBM you can gain and how quickly you can gain it.


Finally, see http://www.bodyrecomposition.com/. What Lyle McDonald doesn't know about fat loss, general nutrition, muscle mass gain and training fits on a postage stamp. He also explains things in language that the sort of person who reads my blog can understand. Just don't leave a comment asking him a question, that's already been answered elsewhere on his site!

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

:-)

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

Figure 1 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 Figure 2), fat-burning temporarily stops. Therefore, the ~1kcal/minute resting burning rate is derived 100% from carbohydrate. Therefore, the carbohydrate-burning rate is ~0.25g/min. At this rate, it would take ~400 minutes to burn 100g of glucose. However, it actually takes ~180 minutes for blood glucose level to fall from maximum to minimum. Therefore, some of the glucose from the Oral Glucose load is stored (mostly as glycogen in muscles and liver).

Figure 3B shows the effects of a 100g Oral Glucose load or 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 Figure 2), fat-burning is unaffected. Therefore, the fat-burning rate is ~0.11g/min. At this rate, it would take ~364 minutes to burn 40g of fat. However, it actually takes 180 to 240 minutes for blood triglyceride (fat) level to fall from maximum to minimum. Therefore, some of the 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 Body Recomposition.

Reasons to get moving...

First, a music video. What else but...?


Part 1. Get slimmer.
Insulin increases the amount of nutrients entering adipocytes, which makes us fat and hungry.

Er, just a minute!

If increasing the amount of nutrients entering cells makes us hungry, exercise (which increases the amount of nutrients entering muscle cells) would make us hungry. It doesn't. See Fig. 1. in Influence of resistance and aerobic exercise on hunger, circulating levels of acylated ghrelin, and peptide YY in healthy males.

If going for a walk outdoors makes you hungry, you're doing it wrong. Wrap up warm, as feeling cold increases hunger. Low blood glucose level also increases hunger, so don't over-exercise while on a long-term ketogenic diet.

By the way, insulin also increases the amount of nutrients entering muscle cells.
Q. What determines the relative amounts of nutrients entering adipocytes vs muscle cells?
A. The relative insulin sensitivities of adipocytes vs muscle cells.

Adipocytes are sensitive to insulin until they become full. To reduce the amount of nutrients entering adipocytes, divert more nutrients to muscle cells by increasing their insulin sensitivity. Emptying muscle cells by doing low-intensity exercise increases their insulin sensitivity. High-intensity exercise increases their insulin sensitivity.


Part 2. Prevent/reverse age-related sarcopenia (muscle loss).
See Use 'em or lose 'em. As diverting more nutrients to muscle cells increases muscle mass, increasing their insulin sensitivity results in increased muscle mass, unless you're eating way below maintenance calories. High-intensity exercise results in more muscle mass gain than low-intensity exercise.


Part 3. Make your brain work properly.
Thanks to Chris Highcock, who gave me a complimentary copy of Hillfit, I found IL-6 and IL-10 Anti-Inflammatory Activity Links Exercise to Hypothalamic Insulin and Leptin Sensitivity through IKKβ and ER Stress Inhibition.

In plain English, this means that exercise increases both insulin and leptin sensitivity in the hypothalamus. As the hypothalamus controls appetite and both insulin & leptin are appetite-suppressing, the net result is less appetite.

Use 'em or lose 'em

Hello world. I'm back. The title is referring to our muscles. The following image is from Figure 1 of Chronic Exercise Preserves Lean Muscle Mass in Masters Athletes.




I'm not going to start doing chronic exercise, but the above is a great incentive to continue with the walking.

I have a theory.

I was keeping this theory a bit quiet 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 in any way, shape or form. I'm just trying to point out that if someone on a low-carb, high-fat diet pigs-out on roast lamb/pork/duck etc, they may not lose as much body fat as they expected & they may even gain some.

I don't particularly 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 & 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.

As a lot of people report that they appear to be able to eat lots of dietary fat without getting fat (& actually getting slim), there's obviously something magical going on. Now, it's generally accepted that fat is the least thermogenic of all the macronutrients (protein being the most thermogenic). I'm wondering whether this is the case for all types of fat and all types of people.

Stephan Guyenet blogged on Butyric Acid: an Ancient Controller of Metabolism, Inflammation and Stress Resistance and Coconut Oil (high in medium chain fats) is also reported as being less fattening/more slimming than long-chain fats.

As Christopher Gardner said in Battle of the Weight Loss Diets: Who's Winning (at losing), insulin resistant people do better on low-carb high-fat (LCHF) diets than high-carb low-fat (HCLF) diets. Insulin sensitive people get the opposite results.

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

See also:-
More evidence comes to light that fat is not fattening
Is there such as thing as a ‘metabolic advantage’?
They're all MAD!
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 and Enzymes.