Why excessively-rapid weight loss due to starvation diets is bad.

Nearly 10 years ago, I wrote Everyone is Different. Back then, I warned about excessively-rapid weight loss, as catabolising muscle results in 5.8 times faster weight loss than losing bodyfat alone.

Recently, I was directed towards the following two studies with very similar titles:-
Change in Body Composition during a Weight Loss Trial in Obese Adolescents
&
Changes in Body Composition During Weight Reduction in Obesity: Balance Studies Comparing Effects of Fasting and a Ketogenic Diet

In the first study, the following string of text stood out:- "Although absolute LM increased in boys and decreased in girls.." Boys gained absolute lean mass and girls lost absolute lean mass. Teenage boys have much higher testosterone levels than teenage girls. Ditto for men & women.

In the second study, the full version is behind a pay-wall. There are ways to bypass pay-walls, but they're illegal, so I'm not going to include a link to the full version. I took a couple of screen-shots instead.

Here's Table 2.

Note: The Patient was a 104kg (228.8lb) man and each diet lasted for 10 days.

1. 1000kcal/day mixed diet (60%C, 20%P, 20%F) resulted in a total weight loss of 3.8kg (0.38kg/day or 0.836lb/day). Mean potassium balance was positive, so there was some net gain of LBM, even though there was weight loss. LBM gain, also glycogen+water gain explains the low total weight loss.

2. 1000kcal/day ketogenic diet (4%C, 14%P, 82%F ≡ "Nutritional Ketosis") resulted in a total weight loss of 8.2kg (0.82kg/day or 1.804lb/day), of which 6.4kg was bodyfat and 0.2kg was LBM. The rest was glycogen+water loss. Mean potassium balance was negative, so there was some net loss of LBM.

3. 0kcal/day total fast resulted in a total weight loss of 12.8kg (1.28kg/day or 2.816lb/day), of which 3.4kg was bodyfat and 6.2kg was LBM. The rest was glycogen+water loss. Mean potassium balance was very negative, so there was a large net loss of LBM.

Here's Figure 1.

Can you spot what's going on with the Nutritional Ketosis diet? The 14%P made me suspicious, as it seemed unnecessarily precise. There's a reason for that!

At the end of day 4, weight loss due to glycogen+water depletion is starting to slow down as glycogen becomes exhausted, then it speeds up again because falling blood glucose level (to ~3.3mmol/L) stimulates the pituitary gland to secrete ACTH, which stimulates the adrenal cortex to secrete cortisol, which catabolises muscle into amino acids for the liver & kidneys to use for gluconeogenesis. This speeds up the rate of weight loss for 3 days.

The Energy Balance Equation explains why losing LBM results in 5.8 times faster weight loss.

From Circulating Nutrients in Starvation, here's the Figure.

"Ketone bodies" level rises linearly from near zero to 5mmol/L by day 10 in fasting. It may rise faster on Nutritional Ketosis. As ketone level rises, glucose consumption by the various tissues falls. This is why muscle catabolism stops after 3 days - there's now sufficient dietary protein to supply the amount of glucose needed, by gluconeogenesis.

This is why protein % was set to precisely 14%. If it had been lower, weight loss would have been greater, but muscle loss would have become significant, which would have made Nutritional Ketosis look bad. If it had been higher, weight loss would have been less, which would have made Nutritional Ketosis look bad.

In conclusion, don't obsess over scale weight. It's just a rough guide. The irony is that the group of people who can't easily regain lost muscle is the same group of people who often try every fad extreme weight loss diet going - females.

In females, muscle mass is like a bargain at Tesco - When it's gone, it's gone. So please don't do excessively-rapid weight loss diets and/or not eat for more than 48 hours.

There's only one safe rapid fat loss diet and it's The Protein-Sparing Modified Fast (PSMF).

How we lose weight: Oxidation of carbohydrate & fat in the body.

1. Oxidation of Carbohydrate in the body.

Glucose is C6H12O6, or 6(CH2O)

6(CH2O)+ 6(O2) → 6(CO2) + 6(H2O) + energy

Oxygen is inhaled. Carbon Dioxide is exhaled. Water is lost in breath, wee, poo, sweat & other bodily fluids.

As 6 molecules of Oxygen produce 6 molecules of Carbon Dioxide, the Respiratory Exchange Ratio (RER) is 6/6 = 1

Converting molecular weights into their gram equivalents, 180g of Glucose combines with 192g of Oxygen to produce 264g of Carbon Dioxide plus 108g of water plus ~3,012kJ of energy. I'm using kJ rather than kcal, as the human body expends energy as mechanical energy (force x distance) and heat energy.

2. Oxidation of Fat in the body.

Fat is three fatty acids (Stearic Acid, say) attached to a Glycerol backbone. As ~95% of the energy released from a fat is from the three fatty acids, I'm ignoring the Glycerol backbone, to keep the maths as easy as possible.  Stearic Acid is CH3(CH2)16COOH. I'm approximating it to 18(CH2), to keep the maths as easy as possible.

54(CH2) + 81(O2) → 54(CO2) + 54(H2O) + energy

Oxygen is inhaled. Carbon Dioxide is exhaled. Water is lost in breath, wee, poo, sweat & other bodily fluids.

As 81 molecules of Oxygen produce 54 molecules of Carbon Dioxide, the RER is 54/81 = 0.67

Note: The RER for fats is actually 0.7, as the Glycerol backbone is converted into Glucose by the liver. As the RER for Glucose is 1, this raises the RER of my approximated fat by ~5%.

Converting molecular weights into their gram equivalents, 756g of approximated fat combines with 2,592g of Oxygen to produce 2,376g of Carbon Dioxide plus 972g of water plus ~28,468kJ of energy.

We lose weight by breathing, weeing, pooing, sweating etc. See also Majority of weight loss occurs 'via breathing'.

This doesn't invalidate Energy Balance, as the kcal/kJ values for foods merely represents the amount of chemical energy that can be released by oxidation of the various fuels in the foods. See Why Calories count (where weight change is concerned).

We gain weight by consuming fuels & water.

When bad science goes...pretty much the same!

After the previous post, you may have got the impression that things are getting worse. Hmmm!

From http://covermyfb.com/covers/27316/say%2Csee+and+hear+no+evil

Hat-tip to James Beckerman, MD for https://twitter.com/jamesbeckerman/status/507544419847786496, which refers to Comparison of Named Diet Programs Finds Little Difference in Weight Loss Outcomes.

This study comes to the opposite conclusion of the study in my previous blog post. As that study was a pile of poo, that must mean that this study is 100% correct, right? Hmmm!

Your enemy's enemy is not necessarily your friend. See What about the Other Weight Loss Diet Study??
"Previous meta-analyses, such as Hession et al, had balanced inclusion criteria that allow us to directly compare low-fat to low-carb diets.  They reported exactly what anyone would expect who is familiar with the weight loss diet literature:

1. At 6 months, low-carb diets consistently lead to greater weight loss than low-fat diets. 
2. At one year, the difference has all but disappeared. 
3. Neither diet produces particularly impressive weight loss at one year or more.
4. The weight loss effectiveness of typical low-fat diets tends to be modest at all time points.

Oh, well. It could have been a lot worse!
 

The Minimally-Processed Whole-Food Plant-Based Diet.

It looks something like this:-

From http://littlesttumor.blogspot.co.uk/2012/02/whole-food-plant-based-diet-challenge.html

The commenter Melanie McSmiley reduced her weight by 45% using something very much like the above diet, and didn't suffer from any horrible side-effects such as Metabolic Shut-down. Well done, Melanie!

Here's an interesting talk by Denise Minger, which contains some big surprises:-

"Myths, Presumptions, and Facts about Obesity" is partly a myth.

Yoni Freedhoff has already blogged about this in The New England Journal's Obesity Mythbusting

It's a mythtery.

I don't have anything to say about Yoni Freedhoff's blog post on Myths, Presumptions, and Facts about Obesity (PDF), except for Myth 1.
"Small sustained changes in energy intake or expenditure will produce large, long-term weight changes."

This is misleading. One small sustained change (say, -100kcals/day) in energy balance results in one sustained change in weight of -10lbs. If no further changes are made, there are no further changes in weight. However...

If, after the result of the small sustained change has stabilised, another small sustained change (say, -100kcals/day) in energy balance is made, there's another sustained change in weight of -10lbs. And so on...

A series of small sustained changes in energy balance will produce large, long-term weight changes.

Little changes, big results.

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!

Dry carbohydrates, wet carbohydrates & energy density.

Karen N Davids thought of it first!

From https://www.amazon.co.uk/Carbs-Weight-Manage-Nutritional-Carbohydrates-ebook/dp/B00DJF2GKU

Here's a list of commonly-eaten carbohydrates and their Energy Density, in kcals/100g. From https://nutritiondata.self.com/

Dry Carbohydrates:-
Bread, White_________________________________________________266
Bread, Multi-grain___________________________________________265
Bread, Rye___________________________________________________258
Bread, Pumpernickel__________________________________________250
Bread, Whole-wheat___________________________________________247
Bread, reduced-calorie, white________________________________207
Bread, reduced-calorie, wheat________________________________198

Wet Carbohydrates:-
Pasta, fresh-refrigerated, plain, cooked_____________________131
Rice, white, long-grain, regular, cooked_____________________130
Rice, brown, long-grain, cooked______________________________111
Peas, green, frozen, cooked, boiled, drained, with salt_______78
Beans, kidney, red, mature seeds, cooked, boiled, with salt__127
Lentils, mature seeds, cooked, boiled, with salt_____________114
Vegetables, mixed, frozen, cooked, boiled, drained, with salt_60
Broccoli, frozen, spears, cooked, boiled, drained, with salt__28
Sweet potato, cooked, baked in skin, with salt________________92
Potatoes, boiled, cooked in skin, flesh, with salt____________87
Grapes, red or green (European type), raw_____________________69
Cherries, sweet, raw__________________________________________63
Pears, raw [Includes USDA commodity food A435]________________58
Apples, raw, with skin________________________________________52


If a diet is high in carbohydrates:-
Which of the above foods are most likely to result in weight gain?
Which of the above foods are most likely to result in weight loss?
Answers on a postcard, please!

Dear ItsTheWoo, how do you do?

This post is attacking what I consider to be faulty reasoning. It's not a personal attack on ItsTheWoo, who I like (even though she drives me up the wall, sometimes!).

From http://hypetrak.com/2011/10/mayer-hawthorne-how-do-you-do-full-album-stream/

See What I believe and what I don't.
The basic The Energy Balance Equation:- Change in body stores = E_in - E_out
For a detailed mathematical analysis of weight change, see Completing the trine: vive la différence!

From Back to black, CIAB, pharmaceutical drug deficiencies & nerds:-
Where body weight is concerned, calories count (but don't bother trying to count them).
Where body composition is concerned, partitioning counts.
Where health is concerned, macronutrient ratios, EFAs, minerals, vitamins & lifestyles count.


The faulty reasoning is in Dear Nigel and other CICO zealots: you are ignorant. Charming!

I'll quote passages from it and refute them, one by one.

• "With a zero caloric deficit, there is zero weight change"

"FACT: Calories neither determine weight OR body composition with certainty. Nigel / some CICO zealots may agree body composition changes are privy to nutrition, but wt is 100% controlled by calories. This is something they pretty much made up and biological science does not at all support this idea. Calories neither control body composition OR body weight/mass with any certainty. The bulk consumed with fork and spoon does not need to stick on your body in the form of a mass laden tissue, ever."
Calories determine weight change. See Bray et al shows that a calorie *is* a calorie (where weight change is concerned). It would have been nice if Fig. 6 had contained a plot of "Effect of energy intake on change in body weight", but it didn't.
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).
∴ Insufficient protein can result in loss of LBM (bad).

The main thrust of ItsTheWoo's argument is that inter-personal variations in weight gain from subject to subject, invalidates Bray's conclusion. It doesn't.
Some subjects become more energetic on a 40% caloric surplus, which increases their NEAT & TEA, which increases their Eout, which reduces their weight gain.
Some subjects don't change their energy on a 40% caloric surplus, which doesn't change their NEAT & TEA, which results in intermediate weight gain.
Some subjects become less energetic on a 40% caloric surplus, which decreases their NEAT & TEA, which decreases their Eout, which increases their weight gain.

I believe that the Insulin Sensitivity (IS) of the subject determines which category they fall into and by how much. The higher the IS, the higher the energy, as high IS results in low serum insulin, which minimises sedation. Energy Balance always applies.

I've never stated that Calories exactly determine weight change. That's a strawman.
I've never stated that Calories determine body composition. That's a strawman.

•  " Every subject [in bray's overfeeding study] gained weight (mostly fat mass) during the 40% energy excess overfeeding period. "

"Again, making crap up. There is NO RULE IN BIOLOGY which states all consumed energy must be retained as body mass. Indeed most typical people gain fat during overfeeding (with great resistance/inefficiency of fat gain), but it is indeed possible to hardly gain any or none at all as in constitutional thinness. What happens during calorie consumption among different people (and perhaps, different DIETS and different TIMES and different ENDOCRINE situations...) is a wild card determined by the biology i.e. neuroendocrine functions of the animal in question. There is NOTHING about physics which reflects / informs physiology other than the basic fact the latter exists within the former (which, again, tells us NOTHING ultimately). How organisms process consumed nutrition is not a physics question. There is no freakin' law of physics or physiology for that matter which states nom nom time = thigh chub. You don't have to wear that pizza as a popeye's muscle or as a shelf butt."
Somewhere within all of the irrelevant waffle about rules & laws, ItsTheWoo raises an interesting point. Although a caloric surplus is always required for weight gain, eating more Calories can sometimes result in zero weight gain. How so? From ItsTheWoo's link:-
"Conclusion: This data is the first to demonstrate a resistance to weight gain in constitutional thinness (CT) population in response to 4-week fat overfeeding, associated with an increase in resting energy expenditure and an emphasised anorexigenic hormonal profile.
In CT people, their energy expenditure increases in line with their energy intake. Therefore, even though they're eating more Calories, there's no caloric surplus, therefore there's no weight gain. Energy Balance always applies.

• "Yes, kcals do get wasted. You don't understand things quantitatively i.e. how many kcals get wasted."

"I know anxious/obsessional people like the safe feeling of balancing calories. The fact reality is more complex and you can't just enter things in a phone app and be ASSURED of what is going on in your body, doesn't invalidate the truth of the fact metabolic reactions are more complex THAN CALORIES.

Just because it is *impossible* for a reasonable free living human to quantify all of the metabolic, endocrine, nervous system factors influencing adipocyte growth changes does not mean they don't fucking exist."
ItsTheWoo left out my calculations. Here they are:-"if I eat 2000 calories of a ketogenic diet in 3 hrs, most of it is wasted as heat, physical energy (I know, because I am EXTREMELY warm/energetic) and then the rest of time i am using a relatively greater percent of stored fat."
Do you know at what rate you're burning-off extra energy intake as heat energy output when you're "EXTREMELY warm/energetic"? Here's an estimate:-
If the mean TEF for your meal is 11% (assuming your meal is 50%E protein & 50%E fat), that's 220kcals (921kJ) "wasted" as heat energy. That'll make you feel EXTREMELY warm, as 220kcal raises the temperature of 57kg of water (your body) by 3.84°C.

A 2,000kcal meal (a whole day's worth of food) takes a lot longer than 3 hours to digest & absorb. I'll guesstimate it as 24 hours. 921kJ of extra heat power over the course of 24 hours = 10.7W, which is an increase of 17.7% over your normal Metabolic Rate of ~60W heat power (~1kcal/minute).
It's easy to "prove" something by being vague. That's PSEUDOSCIENCE. I do science. If you do the maths, you can see that, of the 2,000kcal ketogenic meal, most of it isn't wasted as heat, because if most of it is wasted as heat, ItsTheWoo would spontaneously combust!

• "Dr. Robert C. Atkins made the same fundamental cock-up when he said that humans pissed-out loads of kcals of ketones each day, giving a Metabolic Advantage to ketogenic diets."

"1) The advantage of a ketogenic diet (non-fasting) does exist, so it's not a 'cock up", even if his mechanism was wrong.
2) If atkins was wrong (you pee out all LCHF food) who cares? That was 30+ years ago. He was a cardiologist who observed a VLC diet made him slim. He used his medical education to hypothesize a reason why. His hypothesis was wrong, but his observations were right. This happens all the time in science or basic human reasoning; make observations, form hypothesis. The hypothesis may be wrong, the findings are STILL RIGHT (i.e. low carb diets DO make slim, just not via peeing away ketones)."
1) There is no Metabolic Advantage to ketogenic diets. See https://www.jbc.org/content/92/3/679.full.pdf
2) Atkins' observations were wrong. See The Battle of the Diets: Is Anyone Winning (At Losing?)
a) Low-Carb diets work better than High-Carb diets for people who are Insulin Resistant.
b) Low-Carb diets work worse than High-Carb diets for people who are Insulin Sensitive.
c) Low-Carb diets work the same as High-Carb diets for everybody in Metabolic Ward Studies.
If there's a Metabolic Advantage to ketogenic diets, they would work better than high-carb diets all the time. They don't. See How low-carbohydrate diets result in more weight loss than high-carbohydrate diets for people with Insulin Resistance or Type 2 Diabetes for my hypothesis, which explains a), b) and c).

The "I'm a Celebrity... Get Me Out of Here! (losing team)" diet.

This post may be a little "tongue-in-cheek", in places.


I nearly used a certain scene from Blazing Saddles. It would have been much more entertaining.

As I said in Why you really can't outrun your fork:-
"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."

In the TV series "I'm a Celebrity... Get Me Out of Here!", there are two teams at the beginning. Members of each team compete against each other, to win food for their respective teams. The winning team gets to eat all sorts of exciting animal produce from "down-under". The losing team gets to eat rice & beans.

By the end of the series, team members (especially the over-fat celebrities) had lost a lot of body-fat. Coincidence? I think not. Combining Long-grain Rice with Beans (set Serving size: to 100g) provides all the Essential Amino Acids and is very filling. How do I know this? Guess!

I never used to like rice (it was always cooked "a l'anglaise"), but adding a squirt of Sweet Chilli Sauce to Basmati rice before cooking, makes it taste great!

Nutritional Ketosis: What is it good for?

I have a video in mind...


Having previously shown you what I look like on a diet of ~125g/day low-GL carbohydrates, here are a couple of recent pictures of Jimmy Moore, who's on a very-low-carb, very-high-fat diet (~85%E from fats), a.k.a. Nutritional Ketosis. It involves adding Kerrygold butter to just about everything, even eating sticks of it from a block. I'm not kidding.

I told you I wasn't kidding.

From Google Image Search on "Jimmy Moore" OR "Livin la Vida low carb", images in the last 7 days:-

On 6.7.14.

On 8.7.14.

The only recent footage of Fredrick Hahn, is the following video from the Low Carb Cruise...


To my eyes, Nutritional Ketosis is good for absolutely nothing. Dietary fat can be stored as body fat, in the absence of dietary carbohydrates. Gary Taubes' claim "You can basically exercise as much gluttony as you want, as long as you're eating (only) fat and protein." is pure fantasy, not supported by evidence.

The low protein intake in Nutritional Ketosis, combined with the high serum cortisol that's almost inevitable on this way of eating, results in a loss of muscle mass. I give Nutritional Ketosis a thumbs-down.
 

Summary:-

1) No Energy Deficit → No Weight Loss. There is no Metabolic Advantage to Nutritional Ketosis. See http://www.jbc.org/content/92/3/679.full.pdf

2) Insufficient carbohydrate intake and insufficient protein intake starves the liver & kidneys of gluconeogenic pre-cursors, which raises cortisol, which converts muscle mass into gluconeogenic pre-cursors e.g. Glutamine, Alanine etc. This is standard Biochemistry. No links required.

3) While excess carbohydrates are converted into triglycerides by the liver, excess fats are converted into cholesterol by the liver, which is exported to tissues as LDL-C.

LDL-P ∝ LDL-C. High LDL-P is strongly associated with increased risk factor for CHD. See http://www.lecturepad.org/dayspring/lipidaholics/pdf/LipidaholicsCase291.pdf

CHD is not an inflammation-mediated phenomenon. It's an LDL-P and neovascularisation-mediated phenomenon. See http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3492120/

Postprandial lipaemia is atherogenic. See Ultra-high-fat (~80%) diets: The good, the bad and the ugly.

4) Read Page 10 of https://www.drmcdougall.com/misc/2013nl/feb/pritikinpdf3.pdf, starting from "Could such a cream meal precipitate an angina attack because the oxygen-carrying capacity of the blood is lowered?" It's an actual trial on humans with clogged coronary arteries. It's not a hypothesis.

5) Chronically-raised cortisol causes aggressive behaviour (cortisol is a stress hormone) and adversely affects short-term memory storage in the Hippocampus. See http://evolutionarypsychiatry.blogspot.co.uk/search?q=cortisol

6) Eskimos, Sami, Masai, Samburu, Tokelauans etc, get ~50% of their total energy from fats. There are zero populations that get ≥80%E from fats.


Update 25th July 2014: I appear to have rustled Fredrick Hahn's Jimmies. See https://www.facebook.com/FredrickHahn/posts/10152227780827864

I can safely state that Fredrick Hahn is a liar (I am not poking fun at anybody and I have only blocked him (not his followers) from posting here, for a flagrant breach of my Moderation Policy on his first attempt at commenting), and intellectually-dishonest (for repeatedly mis-quoting me, and using other logical fallacies). He posted the above post knowing that, as I had blocked him on Facebook, I wouldn't see it. I only learned of its existence after a friend PM'ed me on Facebook Messenger. He instructed his "followers" to leave comments here and then accuse me of lying about white-listing, back on his page, because their comments didn't appear immediately. He's a real piece of work! From ABOUT ME:-

Moderation Policy: Comments from first-time & untrusted commenters are moderated ← (click for details). Please be patient. Now that I have a Smart Phone, I can publish your comments during the day when I'm away from my lap-top, but I prefer to type replies on my lap-top. Comments from anonymous commenters, containing links in any form, are deleted.

This is a function of Disqus, as it's impossible to retrospectively white-list a commenter who's never commented here before. There appears to be a severe lack of cognitive function in these people. I really can't think why that is ;-)

Why am I being so hard on Jimmy Moore and Fredrick Hahn? I don't know these people personally.

1) These people are making money out of peddling pseudoscience.

2) These people meet all the criteria in Guest post: Science versus Pseudoscience and have created an alternative science, where sky-high LDL cholesterol, sky-high LDL-P and sky-high postprandial TG's are not risk factors for CHD, but are either harmless or beneficial.

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 low & very low-carbohydrate diets don't work.

Having explained how low & very low-carbohydrate diets work, here are a few ways in which they don't work.

Uh, nope!

1. Hormonal clogs: This is a term used by Jonathan Bailor. I don't think he's referring to wooden shoes! The "clog", I'm guessing, is supposedly caused by that dastardly hormone insulin. Uh, nope!

See the following plots of RER vs exercise intensity after being on high-fat diet or low-fat diet.

RER = 0.7 ≡ 100%E from fat. RER ≥ 1.0 ≡ 100%E from carb.

The low-fat diet results in higher RER, so the body is burning a higher %E from carb and a lower %E from fat.

However, this doesn't make any difference to weight loss, as it's merely a substrate utilisation issue. In addition, when the body is burning a higher %E from carb, this depletes muscle glycogen stores faster, which lowers RER during the course of the exercise. So, it's not a problem.


2. Insulin: This is Gary Taubes' hypothesis. Insulin makes your body store carbohydrates as body fat. Uh, nope!

The only time that there's significant hepatic DNL is when there's chronic carbohydrate over-feeding. If you eat sensibly, there's no significant hepatic DNL.


3. A Calorie isn't a Calorie, where weight change is concerned: This is Richard D Feinman's hypothesis. "A calorie is a calorie" violates the second law of thermodynamics, therefore there's a metabolic advantage with low-carbohydrate diets. Uh, nope!

Where to start? Evelyn Kocur knows her Physics, so I'll start there. See The first law of thermodynamics (Part 1) and The first law of thermodynamics (Part 2).

From Second Law of Thermodynamics:-
"Living organisms are often mistakenly believed to defy the Second Law because they are able to increase their level of organization. To correct this misinterpretation, one must refer simply to the definition of systems and boundaries. A living organism is an open system, able to exchange both matter and energy with its environment."

People on ketogenic diets excrete very few kcals as ketone bodies. See STUDIES IN KETONE BODY EXCRETION (PDF). There is no significant Metabolic Advantage with low-carbohydrate diets.

How low & very low-carbohydrate diets result in more weight loss than high-carbohydrate diets for people with Insulin Resistance or Type 2 Diabetes.

See The Battle of the Diets: Is Anyone Winning (At Losing?) for trials where insulin resistant people lose more weight on low-carbohydrate diets than on high-carbohydrate diets and insulin sensitive people lose more weight on high-carbohydrate diets than on low-carbohydrate diets.

If Gary Taubes's carbohydrate/insulin hypothesis of obesity is correct, everyone would lose more weight on low-carbohydrate diets than on high-carbohydrate diets. This isn't the case, therefore Gary Taubes's hypothesis is not correct.

Although insulin is involved, it has nothing to do with "Hormonal clogs" or "Insulin fairies".

The Aragon Insulin Fairy

The Energy Balance Equation

Change in Body Stores = Energy in - Energy out, where... 

Energy in = Energy entering mouth - Energy exiting anus, and... 

Energy out = BMR/RMR + TEF + TEA + SPA/NEAT

See The Energy Balance Equation to find out what the above terms mean.

People with Insulin Resistance (IR), Impaired Glucose Tolerance (IGT) & Type 2 Diabetes (T2DM) have excessive insulin secretion in response to meals (postprandial hyperinsulinaemia). See Hyperinsulinaemia and Insulin Resistance - An Engineer's Perspective.

People with Insulin Resistance (IR), Impaired Glucose Tolerance (IGT) & Type 2 Diabetes (T2DM) also have impaired/no 1st phase insulin response to a sudden rise in blood glucose level. This introduces a time-lag into the negative feed-back (NFB) loop that regulates blood glucose level. If the input rise-time is less than the time-lag in a NFB loop, the output of the NFB loop overshoots. This is standard NFB loop behaviour. See Control of overshoot for more information.

1. On a high-refined-carbohydrate or high-GL diet, blood glucose level rises rapidly, with a rise-time that's less than the time-lag in the blood glucose regulation NFB loop. Insulin secretion from the pancreas overshoots in a positive direction. The resulting postprandial hyperinsulinaemia results in down-regulation of insulin receptors in the brain, which reduces insulin action in the brain. When the insulin level eventually falls to normal a few hours later, the brain interprets a normal insulin level as hypoinsulinaemia. Hypoinsulinaemia results in ravenous hunger, as insulin is a short-term satiety/satiation hormone in the brain (leptin is a long-term satiety/satiation hormone in the brain). Ravenous hunger results in over-eating. Energy in increases. Postprandial hyperinsulinaemia also results in postprandial sleepiness. Energy out decreases. ∴ Body stores increase. There are also accusations of gluttony & sloth!

2. On a low-carbohydrate or low-GL diet, there are small fluctuations in blood glucose & insulin levels. There is no ravenous hunger. There is much less/no over-eating. Energy in decreases. There is no massive postprandial hyperinsulinaemia. There is much less/no postprandial sleepiness. Energy out increases. ∴ Body stores decrease.

In addition, there is a loss of water weight due to a loss of liver & muscle glycogen. This can be ~2kg in one day (it varies from person to person). Kidneys can increase their output of urine for hormonal reasons. This can increase water weight loss to ~5kg. See Why counting Calories and weighing yourself regularly can be a waste of time.

There are also other hormones involved. For a Facebook discussion with James Krieger that led to the updating of this post, see https://www.facebook.com/james.krieger1/posts/10153228943648587

In Metabolic Ward studies, food intake is tightly controlled, so postprandial hunger doesn't result in over-eating. Energy expenditure is also controlled, so postprandial sleepiness doesn't significantly affect energy expenditure. This is why varying Fat:Carb ratios (with Protein held constant) makes no significant difference to weight in a Metabolic Ward. See Energy intake required to maintain body weight is not affected by wide variation in diet composition.

Inter-personal variations in postprandial hyperinsulinaemia, postprandial sleepiness & energy out explain the inter-personal variations in weight gain seen under hypercaloric conditions. See Bray et al shows that a calorie *is* a calorie (where weight change is concerned).

Insulin Resistance can be fixed. See Insulin Resistance: Solutions to problems.

Type 2 Diabetes can also be fixed. See Reversing type 2 diabetes, the lecture explaining T2D progression, and how to treat it.

Aim to fix the problem. If it's impossible to fix the problem, a low-carbohydrate diet as an adjunct to medication is fine.

Completing the trine: vive la différence!

First, the obligatory picture of Hannah Spearritt :-)

Women have a harder time losing weight than men. Women retain water more than men for hormonal reasons, but a factor that's overlooked is that, on average, healthy women have higher body-fat percentages than healthy men. This is because women have babies and men don't. Who knew? On the plus side, women produce more DHA than men.

Why should having higher body-fat percentages make a difference to weight loss? See What is the required energy deficit per unit weight loss? The energy deficit required to lose 1lb of body-weight increases with increasing body-fat percentage. It's rarely 3,500kcals per lb.

If you really love mathematics, see The Dynamics of Human Body Weight Change by Carson C. Chow and Kevin D. Hall.

From the above paper:- ΔU = ΔQ - ΔW

where ΔU is the change in stored energy in the body, ΔQ is a change in energy input or intake, and ΔW is a change in energy output or expenditure. This is the Energy Balance Equation. As I said back in Back to black, CIAB, pharmaceutical drug deficiencies & nerds.

Where body weight is concerned, calories count (but don't bother trying to count them).
Where body composition is concerned, partitioning counts.
Where health is concerned, macronutrient ratios, EFAs, minerals, vitamins & lifestyles count.

N.B. Poor health can adversely affect body weight and/or body composition, by increasing appetite and/or by adversely affecting partitioning.

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).

The most simple tip to lose weight EVER is “Eat less and move more”.

Said Gaz at Cycle Of Life - Fix You.
He went from this...

Not a happy bunny.

To this...

A happy bunny.

Now tell me that ELMM doesn't work!

Adipocyte Hyperplasia - Good or Bad?

The answer is "It depends!".

The above plot is from Fig. 4 of Cytokine-mediated modulation of leptin and adiponectin secretion during in vitro adipogenesis: Evidence that tumor necrosis factor-α- and interleukin-1β-treated human preadipocytes are potent leptin producers and shows that leptin secretion from adipocytes increases non-linearly with increasing culture period.

As adipocytes fill, there's insignificant leptin secretion up to a certain level of fullness. Above that level of fullness, leptin secretion increases non-linearly. What this means is that reducing adipocyte fullness by x% reduces leptin secretion by more than x%.

If adipocytes become full due to a chronic caloric excess, there are two possibilities.

1a: If there is continued caloric excess, no preadipocytes are converted into adipocytes. There is no additional storage capacity available for excess nutrients, so they remain in circulation. T2DM has developed = bad.

1b: If there is subsequent caloric deficit, adipocytes start to deplete, storage capacity becomes available and T2DM goes away (if beta cells haven't been destroyed). The low number of fairly full adipocytes secrete sufficient leptin, so metabolic rate is high and hunger is low = good.
EDIT: This is the principle behind the DiRECT protocol.

2a: If there is continued caloric excess, pre-adipocytes are converted into adipocytes. This is adipocyte hyperplasia. There is additional storage capacity available for excess nutrients, so T2DM doesn't develop = good.

2b: If there is subsequent caloric deficit, adipocytes start to deplete. However, there are more adipocytes than in 1b, so for a given fat mass, adipocytes are less full than in 1b. The higher number of less full adipocytes secrete less leptin than in 1b, so metabolic rate is lower and hunger is higher than in 1b = bad.

Adipocyte hyperplasia is good for preventing T2DM as fat mass increases, but bad for metabolic rate and hunger after subsequent fat mass loss. Children are growing, so have adipocyte hyperplasia. Adults aren't growing, so have less/no adipocyte hyperplasia. Therefore, adipocyte hyperplasia during childhood will result in some protection from developing T2DM, but life-long misery due to increased hunger and reduced metabolic rate after subsequent fat mass loss. This is why I believe that children need to be protected from the persuasive marketing of manufacturers of CIAB (Crap-in-a-Bag/Box/Bottle).

See Beradinelli-Seip Syndrome – stick that in your pipe and smoke it and read the comments to see why adults with insufficient adipocytes are highly likely to develop T2DM. This is why Asians who remain skinny in childhood (so have no adipocyte hyperplasia) have a high risk of developing T2DM. Sumo wrestlers are Asians who become fat in childhood (so they have a lot of adipocyte hyperplasia) so they have a lower risk of developing T2DM.

According to Adipocyte Turnover: Relevance to Human Adipose Tissue Morphology:-
"Occurrence of hyperplasia (negative morphology value) or hypertrophy (positive morphology value) was independent of sex and body weight but correlated with fasting plasma insulin levels and insulin sensitivity, independent of adipocyte volume (β-coefficient = 0.3, P < 0.0001). Total adipocyte number and morphology were negatively related (r = −0.66); i.e., the total adipocyte number was greatest in pronounced hyperplasia and smallest in pronounced hypertrophy. The absolute number of new adipocytes generated each year was 70% lower (P < 0.001) in hypertrophy than in hyperplasia, and individual values for adipocyte generation and morphology were strongly related (r = 0.7, P < 0.001). The relative death rate (∼10% per year) or mean age of adipocytes (∼10 years) was not correlated with morphology."

If you want to remain slim, high fasting serum insulin due to hepatic and/or muscular insulin resistance and/or chronic overconsumption is bad.

Negativity is NOT an option!

Oh, wait.

I received a comment on another blog post mentioning Jeffrey M Friedman's commentary Modern science versus the stigma of obesity. I took offence to the following passage:-

"This simplistic notion is at odds with substantial scientific evidence illuminating a precise and powerful biologic system that maintains body weight within a relatively narrow range."

To say that I disagree with the above passage is an understatement of epic proportions. If this is the case, how can Extreme weight loss without surgery happen? This woman went from 265kg (583lb) to 97kg (213lb).

With the right diet, huge amounts of weight & body-fat can be lost and kept off. Lyle McDonald's Rapid Fat Loss solution is a PSMF (Protein-Sparing Modified Fast) that can produce huge weight & body-fat loss. See The Protein-Sparing Modified Fast (PSMF).

Up with this negativity I will not put!