Wednesday, 27 August 2014

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

It looks something like this:-

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:-

Wheat, Constipation, Ischaemic Heart Disease, Type 1 Diabetes, Schizophrenia and Autism.

Did you see this coming?
Gliadorphin 7, from

The above 7-peptide chain contains 3 molecules of proline (the pentagon with a "N" at one corner), just like:-
Bovine β-casomorphin 7, from

From Further research for consideration in 'the A2 milk case'.
"Prior to discussion it must be clarified that the hypothetical link between A1 consumption with autistic spectral disorder (ASD) and schizophrenia relates not to the cause of the condition but to the aggravation of symptoms associated with these neurological conditions. More specifically, the hypothesis states that the absorption of food-derived exomorphins such as beta casomorphin 7 (BCM 7) may aggravate symptoms associated with ASD or schizophrenia.

This hypothesis is the basis of 'dietary intervention' that excludes gluten and casein (Knivsberg et al., 2002) from the diet of ASD patients. The former, gluten, has been shown to release gliadamorphin, an exomorphin comparable in opioid activity to BCM-7. A number of laboratories in the United States and Europe offer urine tests, which determine the level of peptides including BCM 7 and other beta casomorphins to serve as an indication of the potential usefulness of dietary intervention in the treatment of ASD patients. One published study reports that a casein- and gluten-free diet was accompanied by improvement in 81% of autistic children within 3 months (Cade et al., 2000)."

According to What is gliadorphin?
"What is gliadorphin? Gliadorphin (also called alpha-gliadin or gluteomorphin) is a substance that resembles morphine. Ordinarily, this is a short-lived by-product from the digestion of gluten molecules (found in wheat, barley, rye, oats, and several other grains). Gliadorphin is very similar to casomorphin. Gliadorphin has been verified by mass spectrometry techniques to be present in unusual quantities in urine samples of children with autism, and are believed by many to be a central part of the system of causes and effects that cause autistic development. The most probable reasons for the presence of these molecules are:
* One or more errors in the breakdown (digestion) process caused by enzyme deficiency and/or
* Abnormal permeability of the gut wall (that would allow these relatively large molecules to enter the bloodstream from the intestine in abnormal quantities)."

Continued on Rheumatoid Arthritis: It's the food!

Tuesday, 26 August 2014

Cow's milk, Schizophrenia and Autism.

As a result of comments to my previous blog post, I did a bit of digging. I dug up something.

Stella Barbone linked to The A2 milk case: a critical review.

This was refuted by A critique of Truswell's A2 milk review.

That referenced Autism and schizophrenia: Intestinal disorders , Can the pathophysiology of autism be explained by the nature of discovered urine peptides? , Enzymatic release of neocasomorphin and beta-casomorphin from bovine beta-casein. & Opioid activities of human b-casomorphin.

Babies have naturally-high gut permeability, so wrong milk proteins may cause damage. Human breast milk contains only A2 casein.

In older humans, gut permeability is modulated by several factors.

1. Insufficient sun exposure, causing hypovitaminosis D. See[All+Fields]+AND+%22tight%20junction%22+AND+hasabstract[text]

2. Excessive consumption of oils high in polyunsaturated fatty acids. See Dietary Fat Can Modulate Intestinal Tight Junction Integrity.

3. Excessive consumption of Wheat. See[All+Fields]+AND+%22tight+junction%22+AND+hasabstract[text]

4. Excessive exercise. See Shedding Some Light on the Leaky Gut <> Exercise Connection. Plus: 20+ Things You Should or Shouldn't Do to Protect and Restore the Integrity of Your Intestinal Wall.

5. Lack of dietary Sulphur. See Sulphation and Autism: What are the links? A good source of sulphate is Epsom Salts.

See also Physiology and Immunology of Digestion.

Continued on Wheat, Constipation, Ischaemic Heart Disease, Type 1 Diabetes, Schizophrenia and Autism.

Sunday, 24 August 2014

Cow's milk, Constipation, Ischaemic Heart Disease & Type 1 Diabetes.

Hat-tip to Jamie Scott and , which led to A1 threat to NZ dairy.

There are a few problems with feeding cow's milk to baby humans.

1. It contains bovine beta casein A1. During digestion, this is broken down into a 7-amino acid peptide chain beta-casomorphin7 (BCM7), which appears to cause issues (e.g. increased gut permeability) increasing the RR of diseases like Type 1 Diabetes and Ischaemic Heart Disease. See[All%20Fields]%20AND%20%22beta-casein%22[All%20Fields]%20AND%20%22humans%22[MeSH%20Terms]%20AND%20%28hasabstract[text]%20AND%20%22humans%22[MeSH%20Terms]%29 A solution is to use A2 milk, or goat's milk which is apparently naturally A2. See also Further research for consideration in 'the A2 milk case'.

2. It's much higher in protein (4g/100mL) than human breast milk (1.1g/100mL), as baby cows are supposed to grow very rapidly, unlike baby humans. As 80% of the protein in milk is casein, and casein is joined to calcium as calcium caseinate, this increases the calcium intake, and too much calcium relative to magnesium is constipating. A solution is to increase magnesium intake, or dilute 1 part cow's milk with ~3 parts water & add some coconut oil, to get the fat content back up to 4.4g/100mL.

Continued on Cow's milk, Schizophrenia and Autism.

Friday, 22 August 2014

"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.

I never expected THAT to happen!

Fancy some Ramen Noodles?

As I clicked on the video, I was thinking "I bet those instant Ramen Noodles disintegrate instantly, causing a big surge of glucose into the blood".

Watch and learn. Well, did you expect that to happen? If instant Ramen Noodles are a heart health risk, it's not because they digest too quickly. BPA? Something else?

Tuesday, 19 August 2014

The Facts of Life.

No, not those Facts of Life!

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 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 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!

Monday, 18 August 2014

Dry carbohydrates, wet carbohydrates & energy density.

Karen N Davids thought of it first!

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

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!

Sunday, 17 August 2014

A new low for denialists.

Here's a new Pyramid of Argument, with an extra level added below name-calling.
Originally from

What's worse than name-calling? When I defecate science all over my opponents, it makes it difficult for them to respond with refutation. If they are unable to use the top 3 levels of the pyramid, they usually use the 4 levels below that. Until the other day.

See Seth Yoder's review of "The Big Fat Surprise: Why Butter, Meat and Cheese Belong in a Healthy Diet" - by Nina Teicholz.

If you think that Seth's review is a bit verbose, check out The Big Fat Surprise: A Critical Review; Part 1 and The Big Fat Surprise: A Critical Review; Part 2. They make "War and Peace" look like a pamphlet!

Anyway, Seth got the usual logical fallacies, including the inevitable ad-hominem from Skruby of "You're a vegan, so you don't know what you're talking about/you're biased!"

As Seth is a science guy, and I don't stand by & let science guys get attacked without doing something about it, I pitched-in with some comments in support of Seth. Well...

Check Zahc's comment out. And Allen I. Branson's comment. The new low is the BLATANT LIE.

Notice how the troll Zahc uses standard baiting practices to "suck me in" to replying to him. He:-
1) Repeats the lie about me cherry-picking 2 studies. Those are the only studies that produced results reaching statistical significance, as all of the other studies had RR ~1, with 95% CI's less than 1 and greater than 1.
2) Makes an irrelevant point about mortality. Siri-Tarino et al & Chowdhury et al are about CHD.
3) Repeats the lie about dairy fat not being protective.
4) Issues a challenge to me to comment on his blog post I've already commented on Zahc's blog. His blog contains two posts riddled with cholesterol denialism and backed-up by a bunch of cherry-picked studies.
5) Gets aerated over me linking to his comment. Things are about to get worse.

I replied to Zahc's comment.
Zahc wrote another comment. He:-
1) Repeats the lie about me cherry-picking 2 studies. Persistent, isn't he?
2) Criticises Dr. Dayspring behind his back, a cowardly thing to do. Zahc has no intention of ever debating Dr. Dayspring, as he knows that Dayspring would destroy his uninformed opinions with data.
3) Issues another challenge to me to make another comment. Luckily, I have this blog, so I don't need to waste any more time debating cholesterol denialists.

Zahc has written another comment. He:-
1) Continues with pointless arguments. Typical troll behaviour.
2) Continues to get confused over basic English. "Uninformed Opinion" wasn't referring to what you wrote in your previous comment, you dumbass. It was referring to what you'd be giving Dr. Dayspring. Jeez!
3) Had my previous comment deleted by Amazon. What was I saying about cowardly behaviour?
4) Continues to insult me, in the vain hope that I might leave another comment answering his points. That ain't ever gonna happen. I'll just leave comments with links to this post, or links to other comments. I know a cholesterol denialist when I see one. I know cherry-picked studies when I see them. I know a shite blog when I see one.

Are we done now, Zahc? I can continue this, ad infinitum. This blog post is all about you (& Allen I. Branson). You're just making yourself look like a total pillock. Have you "debated" with Dr. Dayspring or Dr. Edwards, yet? Somehow, I think not.

Blatant lies are worse than Straw man fallacies, as such fallacies are usually caused by my opponent being ignorant of my argument and confabulating.

Blatant lies work on the assumption that the opponent can't or won't ever see them. This is a risky strategy, as if the opponent does see them and calls the liar out on them, the liar's credibility is destroyed. This is what happened with Fredrick Hahn, after I blocked him on Facebook for repeatedly tagging me in Here are the results after one month on my high fat, lower protein, SAME carbohydrate intake. The main differences are: , after I told him to stop tagging me.

He posted Nigel Kinbrum is a coward. He enjoys poking fun at people, but blocks them from commenting. He has blocked me. Someone give this guy what for please. , thinking that I'd never see it. I had a tip-off from a friend, who PM'ed me a screen-shot taken from a logged-out browser (as they had been blocked by Fred and couldn't see him or his content when they were logged-in to Facebook). The rest, as they say, is history!

Saturday, 16 August 2014

Keto Clarity: Your Definitive Guide to the Benefits of a Low-Carb, High-Fat Diet - My "Review".

I haven't bought the book - surprise, surprise!

If anybody thinks that I can't review this book because I haven't read it, you really haven't been paying attention! Here's what I wrote in reply to JoAnn Schreffler's comment:- N.B. Hyperlinks added.


Gluconeogenesis also isn't very accurate in terms of generating blood glucose.
Sometimes, it can result in high blood glucose.

To reduce blood glucose, reduce protein intake. Unfortunately...

1) Minimising dietary protein starves the liver & kidneys of gluconeogenic precursors.
2) Blood glucose level drops.
3) The pituitary gland secretes ACTH.
4) ACTH stimulates the adrenal cortex to secrete cortisol.
5) Cortisol cannibalises LBM* to create gluconeogenic precursors.
*LBM = Lean Body Mass = muscles & organs.
This doesn't sound like a good idea to me.

Also, ultra-high-fat diets are not healthy.

Low-carb diets with up to 50%E from fats are fine. There's no Metabolic Advantage to ketogenic diets and there are many disadvantages to long-term ketogenic diets. If you suffer from refractory epilepsy, a medically-supervised ketogenic diet is fine. Branched Chain Amino Acids can be added as adjunctive therapy, as they are ketogenic.

I have no axe to grind against Jimmy Moore. I hate pseudoscience and sadly, Jimmy's book is full of it. Check the list.
I practise science and I back up everything I say with quality peer-reviewed evidence. If you don't like it, tough.
Science doesn't care if you believe in it or not. It's still valid. I expect that my comment will be down-voted by pseudoscientific thinkers & cholesterol denialists.
I don't care if you believe in it or not. It's still valid.

I'm an omnivore. I'm NOT a vegan, just so's you know!

I've only just added the last line, as I've noticed a tendency for some (stupid) Amazon commenters to accuse an author of being a Veg*n, when they don't agree with the review!

Thursday, 14 August 2014

And now for something completely different.

This video from 1979 is still relevant to the problems of the world today. Too much. Too young.

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!).

See What I believe and what I don't.
The basic The Energy Balance Equation:- Change in body stores = Ein - Eout
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
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).

Friday, 8 August 2014

Ketogenic Diets and Sudden Cardiac Death.

Last night, thanks to comments on my previous post, I stumbled across The therapeutic implications of ketone bodies: the effects of ketone bodies in pathological conditions: ketosis, ketogenic diet, redox states, insulin resistance, and mitochondrial metabolism, then a Google search led me to Sudden Cardiac Death and Free Fatty Acids.

The following graph is Figure 1 from Lack of suppression of circulating free fatty acids and hypercholesterolemia during weight loss on a high-fat, low-carbohydrate diet.
Nice Insulin, shame about the FFAs.

From the first link above:-
"Current ketogenic diets are all characterized by elevations of free fatty acids, which may lead to metabolic inefficiency by activation of the PPAR system and its associated uncoupling mitochondrial uncoupling proteins."

From the third link above:-
"Weight loss was similar between diets, but only the high-fat diet increased LDL-cholesterol concentrations. This effect was related to the lack of suppression of both fasting and 24-h FFAs."

See also Elevated plasma free fatty acids predict sudden cardiac death: a 6.85-year follow-up of 3315 patients after coronary angiography, and Circulating Nonesterified Fatty Acid Level as a Predictive Risk Factor for Sudden Death in the Population.

I think that's quite enough bad news for a Friday afternoon.

EDIT: So much for fat being a "clean-burning" fuel for the heart. Some people believe that, because dietary fats pass from the small intestine, via the Lacteals, to circulation at the Subclavian vein, this means that the heart prefers to burn fatty acids.


Human erythrocytes (red blood cells) contain cholesterol and it can contribute towards atherosclerosis. See

See also Evidence for a cholesteryl ester donor activity of LDL particles during alimentary lipemia in normolipidemic subjects. This is more evidence that very high fat meals are atherogenic, which is relevant to Ultra-high-fat (~80%) diets: The good, the bad and the ugly.

Thursday, 7 August 2014

Chowdhury et al, More forests & more trees and more "Eureka!" moments with cheese.

Like Siri-Tarino et al, Forests & Trees and "Eureka!" moments, Chowdhury et al is a meta-analysis of many studies. See Association of dietary, circulating, and supplement fatty acids with coronary risk: a systematic review and meta-analysis. I don't have access to the full study, but Google Image Search found Figure 2.

All saturated fatty acids have a RR for CHD of 1.06 (95% CI 0.86 - 1.30).
∴ There's no association between saturated fat intake and the RR for CHD.

Before LCHF'ers do a dance of joy, consider the Forest plot for individual saturated fatty acids.
Palmitic acid has a RR for CHD of 1.15 (95% CI 0.96 - 1.37).
Stearic acid has a RR for CHD of 1.23 (95% CI 0.93 - 1.61).

Red meat & saturated fats synthesised by DNL aren't looking too good. However...
Pentadecanoic acid has a RR for CHD of 0.94 (95% CI 0.67 - 1.32).
Margaric acid has a RR for CHD of 0.77 (95% CI 0.63 - 0.93).
Pentadecanoic acid and Margaric acid combined have a RR for CHD of 0.81 (95% CI 0.62 - 1.06).

What are Pentadecanoic acid & Margaric acid found in? The clue's in the title:-
Say cheese: saturated fat in dairy may protect against diabetes.

The article in the Telegraph is actually referring to Differences in the prospective association between individual plasma phospholipid saturated fatty acids and incident type 2 diabetes: the EPIC-InterAct case-cohort study.

The above study is about T2DM not CHD, but Dietary intake of saturated fat by food source and incident cardiovascular disease: the Multi-Ethnic Study of Atherosclerosis shows that small amounts (5-10g/day) of dairy SFAs are protective against CHD, possibly due to the Vitamin K2 content.

Of the omega-3 fatty acids...
Eicosapentaenoic acid has a RR for CHD of 0.78 (95% CI 0.65 - 0.94).
Docosahexaenoic acid has a RR for CHD of 0.79 (95% CI 0.67 - 0.93).
Eicosapentaenoic acid and Docosahexaenoic acid combined have a RR for CHD of 0.75 (95% CI 0.62 - 0.89).

Of the omega-6 fatty acids...
Arachidonic acid has a RR for CHD of 0.83 (95% CI 0.74 - 0.92).

Of the trans-fatty acids...
Trans-oleic acid has a RR for CHD of 1.20 (95% CI 0.39 - 3.73).
Trans-linoleic acid has a RR for CHD of 1.36 (95% CI 0.83 - 2.22).

Monday, 4 August 2014

Historical perspectives on the impact of n-3 and n-6 nutrients on health, by Bill Lands.

Here's Fig. 1. from
Relating tissue HUFA balance with blood cholesterol and heart attacks. Results from the 25-year follow-up in the Seven Countries Study [35] were discussed in an earlier review [10] which noted that “Food energy imbalances which elevate blood cholesterol may be fatal only to the degree that omega-6 (n-6) exceeds omega-3 (n-3) in tissue HUFA. Such evidence raises questions about the hypothesis that blood cholesterol levels cause CHD.” Northern Europe and Southern Europe have abbreviations “No.” and “So.”, respectively. The Figure is reprinted with permission of the publisher.

Hat-tip to Dr. Thomas Dayspring for Tweeting this review.

Fig. 1 is interesting, as it shows a significant association between 25-year CHD mortality and Serum Total Cholesterol for every region except Japan. What's different about Japan, compared to Northern Europe, USA, Serbia, Southern Europe & Crete?

According to Measuring Blood Fatty Acids as a Surrogate Indicator for Coronary Heart Disease Risk in Population Studies , Philippines & Iceland have lower % linoleic acid than Japan. Where's the CHD vs TC data?

Could another difference be that the Japanese eat rice, a relatively intact grain, instead of foods made from wheat grain dust (i.e. flour) as their main source of dietary carbohydrates?

See also Using 3–6 differences in essential fatty acids rather than 3/6 ratios gives useful food balance scores , and Omega 3-6 Balance Score.

Sunday, 3 August 2014

Depression: The similarity between magnesium and ketamine in inducing amnesia for bad memories.

Here's a 2D-skeletal model of the ketamine molecule.

Thanks to Emily Deans for bringing Ketamine, magnesium and major depression – From pharmacology to pathophysiology and back to my attention some time ago, in a Tweet.

"The link to the pathophysiology of depression is not clear. An overlooked connection is the role of magnesium, which acts as physiological NMDA-receptor antagonist:

1. There is overlap between the actions of ketamine with that of high doses of magnesium in animal models, finally leading to synaptic sprouting.

2. Magnesium and ketamine lead to synaptic strengthening, as measured by an increase in slow wave sleep in humans.

3. Pathophysiological mechanisms, which have been identified as risk factors for depression, lead to a reduction of (intracellular) magnesium. These are neuroendocrine changes (increased cortisol and aldosterone) and diabetes mellitus as well as Mg2+ deficiency.

4. Patients with therapy refractory depression appear to have lower CNS Mg2+ levels in comparison to health controls.

5. Experimental Mg2+ depletion leads to depression and anxiety-like behavior in animal models.

6. Ketamine, directly or indirectly via non-NMDA glutamate receptor activation, acts to increase brain Mg2+ levels. Similar effects have been observed with other classes of antidepressants.

7. Depressed patients with low Mg2+ levels tend to be therapy refractory. Accordingly, administration of Mg2+ either alone or in combination with standard antidepressants acts synergistically on depression like behavior in animal models.

I'm wondering whether the amnesia for vivid dreams (if you wake up in the middle of one) is mediated by magnesium, as amnesia is a ketamine-like effect.

Therefore, a deficiency in magnesium may cause bad memories to linger, increasing the risk factor for situational depression.

4g/day of Epsom Salts provides 400mg/day of Magnesium. Dissolve the Epsom Salts in warm water and add the solution to your drinks over a 24 hour period, to maximise absorption & minimise laxation.

See also Ketamine, and Mechanisms underlying differential effectiveness of memantine and ketamine in rapid antidepressant responses.

Friday, 1 August 2014

Negative feedback loops, Tolerance, Dependence & Withdrawal.

I couldn't find the plot that I was looking for, but this electrical plot is equivalent.

eA represents the amount of a substance that perturbs one of the body's negative feedback loops. The amount oscillates between 0V & 100V.

eR represents the effect of the substance on the body. 100V represents maximum effect and -100V represents maximum anti-effect.

The very first time that the substance is taken, there is 100V of effect, initially. As the time-constant of the negative feedback loop "kicks-in", the effect decays exponentially. Just before the substance is discontinued, the effect is down to 36.8V. Just after the substance is discontinued, the anti-effect is -63.2V. If the input continues to oscillate between 0V & 100V, the effect & anti-effect eventually become equal in magnitude. This is known as "cycling".

If the substance is applied continuously, the effect decays exponentially to 0V. When the substance is discontinued, the anti-effect is -100V initially, but decays exponentially to 0V.

This is analogous to drug tolerance, dependence & withdrawal, where eventually, the user has to take the drug just to feel normal, and discontinuing the drug gives the worst withdrawal symptoms ever, initially. After the drug has been discontinued for a while, the withdrawal symptoms decay exponentially to zero.

The above also applies to supplements that perturb one of the body's Hypothalamic Pituitary NFB loops e.g. the HPA (Adrenal), the HPG (Gonadal) or the HPT (Thyroid) Axes, or any other system (as everything in the body is regulated by a negative feedback loop).

This explains why a supplement can work really well at first, then its effect decays exponentially, until there is zero effect. The loop has compensated for it.

EDIT: If a loop is broken, due to zero secretion of one of the hormones controlling it, then a prescription drug/hormone restores the loop's output level to normal. E.g.

1) Prednisone for a broken HPAA (primary, secondary or tertiary hypoadrenalism) e.g. Addison's Disease.
2) Testosterone (men) or progesterone (women) for a broken HPGA (primary, secondary or tertiary hypogonadism).
3) Levothyroxine for a broken HPTA (primary, secondary or tertiary hypothyroidism) e.g. Hashimoto's thyroiditis.

I'm on 2) & 3), due to a broken pituitary gland. Luckily, it's not completely broken, so I don't need 1).