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!

A new low for denialists.

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

Originally from http://scienceblogs.com/startswithabang/2009/08/15/weekend-diversion-how-to-argue/

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 http://diettrialclaims.blogspot.com/2013/06/is-cholesterol-really-that-important.html 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!

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!

From http://www.amazon.com/Keto-Clarity-Definitive-Benefits-Low-Carb/dp/1628600071/

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.

Exactly!

Gluconeogenesis also isn't very accurate in terms of generating blood glucose.
Sometimes, it can result in high blood glucose.
http://nigeepoo.blogspot.co.uk/2012/04/how-eating-sugar-starch-can-lower-your.html

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.
http://nigeepoo.blogspot.co.uk/2014/06/ultra-high-fat-80-diets-good-bad-and.html
http://nigeepoo.blogspot.co.uk/2014/07/nutritional-ketosis-what-is-it-good-for.html
http://nigeepoo.blogspot.co.uk/2014/08/ketogenic-diets-and-sudden-cardiac-death.html

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.
http://www.ncbi.nlm.nih.gov/pubmed/19687389

I have no axe to grind against Jimmy Moore. I hate pseudoscience and sadly, Jimmy's book is full of it. Check the list.
http://nigeepoo.blogspot.co.uk/2014/06/guest-post-science-versus-pseudoscience.html
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.
http://nigeepoo.blogspot.co.uk/2014/06/guest-post-denialism-as.html
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!

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!).

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).

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.

From Page 10 of HIGH CARBOHYDRATE DIETS: MALIGNED AND MISUNDERSTOOD:-

Human erythrocytes (red blood cells) contain cholesterol and it can contribute towards atherosclerosis. See https://twitter.com/Drlipid/status/496625195738619904.

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.

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.

From https://annals.org/data/Journals/AIM/929862/6ff2_Figure_2_RRs_for_coronary_outcomes_in_prospective_cohort_studies_of_circulating_fatty_acid.jpeg

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).

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

Here's Fig. 1. from http://www.sciencedirect.com/science/article/pii/S0163782714000253

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.

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

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

From http://commons.wikimedia.org/wiki/Main_Page

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.

Negative feedback loops, Tolerance, Dependence & Withdrawal.

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

From http://www.tpub.com/neets/book9/37k.htm

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

e_R 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).

Nonequilibrium thermodynamics and energy efficiency in weight loss diets, by Richard D Feinman and Eugene J Fine.

From http://www.caloriegate.com/the-black-box/9-pictures-that-prove-beyond-a-reasonable-doubt-that-calories-dont-count

From Nonequilibrium thermodynamics and energy efficiency in weight loss diets:-

"Conclusion
Emphasis on kinetics and nonequilibrium thermodynamics provides a conceptual framework for understanding the effect of macronutrient composition on maintenance and change of body mass and possibly for analysis of adipocyte metabolism in general. The simple model presented is intended to be consistent with a general shift away from equilibrium thermodynamics and towards a more dynamic analysis of cellular processes."

Sounds plausible. There's only one thing wrong with Feinman et al's article - it's completely wrong!

Consider two rooms:-

Room "A" has an adjustable heater. The heater is adjusted until the room temperature is 20°C.

Room "B" has a radiator, controlled by a wall-stat set to 20°C. The radiator is on, and the room is at 20°C.

We have two rooms of the same size, at the same temperature.

If you plug in & turn on a 2kW fan heater in each room, what happens to the temperature in each room?

Room "A" gets warmer, because there is 2kW more heat power entering it.

Room "B" stays at 20°C, because the wall-stat reduces the heat power from the radiator by 2kW.

The human body stays at 37°C ±~2°C, because there's a Negative Feed-Back loop adjusting the heat power produced, via UCP's, futile cycles, thyroid hormones, shivering and heat conservation/wasting behaviours.

∴ Variable heat power generation due to variable Dietary Efficiency doesn't change E_out.

EDIT: By request, here's Figure 1 from the above study.

This suggests that fat mass & therefore weight can increase indefinitely - at maintenance energy intake, due to the effect of insulin on HSL. This, of course, is quite impossible!

From The Energy Balance Equation:-

Change in Body Stores = E_in (corr for digestion) - E_out (BMR/RMR + TEF + TEA + SPA/NEAT)
__BMR/RMR & TEA ∝ weight
∴ ↑ weight → ↑ E_out
__If E_in = constant, ↑ E_out → ↓ (E_in - E_out) → ↓ weight
∴ ↑ weight → ↓ weight
∴ Figure 1 is wrong.

The Ketogenic Diet: Uses in Epilepsy and Other Neurologic Illnesses.

Fools claim that I am anti-ketogenic diets. Am I ****! beta-Hydroxybutyric acid has its uses...

From http://www.fuelforthought.co/the-ketogenic-diet-uses-in-epilepsy-and-other-neurologic-illnesses-2/

From The Ketogenic Diet: Uses in Epilepsy and Other Neurologic Illnesses:-

"Inconsistencies in studies attempting to correlate seizure protection with levels of ketone bodies suggest that another mechanism may be involved in the diet’s beneficial effects on seizures. Several mechanisms have been proposed, including changes in ATP production making neurons more resilient in the face of metabolic demands during seizures; altered brain pH affecting neuronal excitability; direct inhibitory effects of ketone bodies or fatty acids on ion channels; and shifts in amino acid metabolism to favor the synthesis of the inhibitory neurotransmitter GABA."

GABA is an interesting neurotransmitter, as it's the chief inhibitory neurotransmitter in the mammalian central nervous system.

I know of two other substances that enhance GABA's effects - Alcohol and Benzodiazepines.


In conclusion:

I'm in favour of ketogenic diets under medical supervision, as therapy for neurologic conditions etc.

I'm not in favour of ketogenic diets under lay supervision, as a supposed aid for weight loss.

Dietary Carbohydrate restriction as the first approach in diabetes management. Critical review and evidence base, by Richard D Feinman et al.

Another Bookmarking post.

From https://dgeneralist.blogspot.co.uk/2013/11/the-low-carb-high-fat-diet.html

The study in question is Dietary Carbohydrate restriction as the first approach in diabetes management. Critical review and evidence base. Here are my comments on the 12 points.

Point 1 is wrong. For ~85% of people who have T2DM, hyper*emia is the salient feature, where * = glucose, TG's, cholesterol, NEFAs, uric acid etc. For ~85% of people who have T2DM, it's a disease of chronic excess.

Ad lib LCHF diet → ↓ Blood glucose & ↓ fasting TG's, but ↑ PP TG's, ↑ LDL-C, ↑ LDL-P & ↑ NEFAs. See Postprandial lipoprotein clearance in type 2 diabetes: fenofibrate effects.
↑ PP TG's is associated with ↑ RR of CHD.
↑ LDL-P is associated with ↑ RR of CHD.
↑ NEFAs are associated with ↑ RR of Sudden Cardiac Death.

Point 2: So? T2DM is a disease of chronic excess. Chronic over-consumption was caused by Food Industry marketing, not carbohydrates.

Point 3 is wrong. A caloric deficit is essential, to reverse liver & pancreas ectopic fat accumulation. See Reversing type 2 diabetes, the lecture explaining T2D progression, and how to treat it.

Point 4 is misleading. Feinman doesn't distinguish between different types of carbohydrates. Starches, especially resistant starches (e.g. Amylose) are beneficial. See Point 11.

Point 5 is moot. Prof. Roy Taylor found that motivation determines adherence. Prof. Roy Taylor's PSMF was adhered to. See Point 3.

Point 6 is correct. Prof. Roy Taylor's PSMF is ~1g Protein/kg Bodyweight, some ω-6 & ω-3 EFAs & veggies for fibre. See Point 3.

Point 7 is misleading. Siri-Tarino et al gave a null result by including low fat studies, also a dairy fat study which had a RR < 1 for increasing intake. Chowdhury et al gave a null result, as some fats have a RR > 1 for increasing intake and some have a RR < 1 for increasing intake.

Point 8 is irrelevant. ↑ Dietary fat → ↑ 2-4 hour PP TG's. See Point 1.

Point 9 is partly correct. Microvascular, yes. Macrovascular, no. See Point 8.

Point 10 is mostly irrelevant. See Point 8.

Point 11 ignores results obtained with high-starch diets, where the starch contains a high proportion of Amylose. See Walter Kempner, MD – Founder of the Rice Diet and From Table to Able: Combating Disabling Diseases with Food.

Point 12 is misleading. The low-carbohydrate part is fine. It's the high-fat part that can cause problems. See Point 8.

Some thoughts on the essentiality of dietary carbohydrates.

I didn't know that there's a watch strap called Essentiality. I do, now.

From http://svpply.com/item/3229602/Swatch_Skin_Collection_Silver_Essentiality

This is a book-marking post for thoughts I had in https://www.facebook.com/TheFatEmperor/posts/1442430506020812.

"The human body does not need carbohydrates from an external food source, because it is capable of very precisely and correctly assembling its own amounts of glucose that is needed in very small amounts for auxiliary and specialized functions." - Igor Butorski.

1) It's not precise. See How eating sugar & starch can lower your insulin needs.

2) It's not enough to fuel sustained medium-intensity exercise for everybody EDIT: if there's insufficient protein intake. See "Funny turns": What they aren't and what they might be and Everyone is Different.

From Blood Sugar is Stable:-

After liver glycogen has been depleted in starvation or on Nutritional Ketosis (Ketogenic Diets with less than 14% of total energy from Protein), total glucose production from liver & kidneys is ~100g/day.

From It's all in a day's work (as measured in Joules), the body oxidises carbohydrate at a rate exceeding ~4g/hour at exercise intensities exceeding ~25%, on a LCHF diet. This is unsustainable.

EDIT: If protein is consumed, total glucose production increases, up to a maximum of ~400g/day.

3) It's wasteful. Glucose production from protein converts ~50% of the most expensive macronutrient (protein) into the cheapest macronutrient (carbohydrate). It creates expensive urine, as the nitrogen part of amino acids is detoxified by being converted into urea by the liver and then wee'ed out by the kidneys.

4) Using the above argument, the human body does not need saturated fats & monounsaturated fats from an external food source, because it is capable of very precisely and correctly assembling its own amounts of saturated fats & monounsaturated fats (out of carbohydrate) that are needed in very small amounts for auxiliary and specialized functions.

If we consume only Essential Fatty Acids, Essential Amino Acids, Vitamins, Minerals, Fibre/Fiber, Water & Anutrients, there won't be much to eat. Also, there won't be a source of chemical energy to generate heat energy & mechanical energy. That's what dietary carbohydrates & fats are for!

Respiratory Exchange Ratio/Respiratory Quotient (RER/RQ) varies with carbohydrate & fat intake, as the body preferentially oxidises the fuel that's most readily available, when it's working properly. If it's not working properly, due to Insulin Resistance (IR), fix the IR rather than kludge the diet (by eating LCHF) to compensate for it. See Insulin Resistance: Solutions to problems for how to do this.

RER/RQ varies with Exercise Intensity.
Low-intensity exercise results in mostly fats being oxidised.
High-intensity exercise results in mostly carbohydrates being oxidised.
Medium-intensity exercise results in a mixture of fats & carbohydrates being oxidised.

A *very* special dual-fuel car analogy for the human body that I just invented.

The human body is like a very special dual-fuel car.

From http://www.aa1car.com/library/alternative_fuels.htm

In this very special dual-fuel car:-

Glucose is represented by Ethanol, 'cos Ethanol is a carbohydrate, according to Robert Lustig ;-)
Glucose is C₆H₁₂O₆. Ethanol is C₂H₆O. 3(C₂H₆O) = C₆H₁₈O₃. It's not very close, but it'll do!

Caprylic acid is represented by Octane, 'cos fatty acids are hydrocarbons, don'tcha know? ;-)
Caprylic acid is CH₃(CH₂)₆COOH and Octane is CH₃(CH₂)₆CH₃, which is actually pretty close.

Storage depots:

 

Carbohydrates:

For Ethanol, there's a large storage tank (≡ muscle glycogen) and a small storage tank (≡ liver glycogen). The contents of the large storage tank cannot be used to top-up the small storage tank, but the contents of the small storage tank can be used to top-up the large storage tank. The contents of the small storage tank are used to fuel a generator (≡ Hepatic Glucose Production) to keep the ECU (≡ brain) working at all times. The contents of the large storage tank are used to fuel the engine.

Fats:

For Octane, there's a large storage tank (≡ subcutaneous adipose tissue) and a small storage tank (≡ visceral adipose tissue). The contents of the small storage tank are used to produce hormones etc. The contents of the large storage tank are used to fuel the engine.

Substrate Utilisation:

When the car is driven at low speed, the engine burns mostly Octane (≡ RQ=0.7).
When the car is rapidly accelerating or driven at high speed, the engine burns mostly Ethanol (≡ RQ=1).
When the car is being driven intermediately, the engine burns a mixture of Octane & Ethanol.

Overeating/Undereating:

 

Carbohydrates:

If the large Ethanol storage tank becomes full, excess Ethanol overspills to the small storage tank.
If the small storage tank becomes full, a gizmo kicks-in and converts excess Ethanol into Octane (≡ De-Novo Lipogenesis).
It also shifts fuel usage of the engine towards Ethanol, to deplete Ethanol as quickly as possible.
If the small storage tank becomes full, the car malfunctions (≡ fatty liver).

Conversely, if the small storage tank becomes nearly empty, it shifts fuel usage of the engine towards Octane, to conserve Ethanol.

Fats:

If the large Octane storage tank becomes full, excess Octane overspills to the small storage tank.
If the small storage tank becomes full, the car malfunctions (≡ insulin resistance/metabolic syndrome/type 2 diabetes).

Ancel B. Keys' critique of "Diet and coronary thrombosis. Hypothesis and fact, by John Yudkin. The Lancet, 1957."

Ancel B. Keys has come in for a lot of flak recently over alleged "cherry-picking" of data for his 6/7 Countries studies. Here's Keys' critique:- "SUCROSE IN THE DIET AND CORONARY HEART DISEASE" of Dr. John Yudkin's "15 Countries" article.

Keys accuses Yudkin of bias, cherry-picking countries that fit his own hypothesis.

Here are some plots from Keys' 11 Countries article.

5-Year CHD cases/1,000 men vs Sucrose %E.

5-Year CHD cases/1,000 men vs Sat Fats %E.

Sucrose %E vs Sat Fats %E.

So there you have it.

Dr. John Yudkin's "Diet and coronary thrombosis. Hypothesis and fact", The Lancet, 1957.

Twitter did it again. From http://www.abc.net.au/catalyst/heartofthematter/download/Yudkinssugartheory.pdf

This looks like bad news for the fat-lovers.

There's good correlation between Coronary mortality and total fat intake, for countries 15 to 7. For countries 7 to 1, there's no correlation between Coronary mortality and total fat intake, suggesting that other differences (e.g. quality of health-care, social stress, antioxidant status etc) are significant factors.

This looks like bad news for the meat/fowl/fish/cheese/egg-lovers.

This looks like bad news for the sugar-lovers.

Of course, association ≠ causation.

This looks like bad news for rich people.

In conclusion, total fat intake, animal protein intake, sugar intake & annual income are all associated with increased Coronary mortality, over a certain range of values.

Why do some people have trouble doing things in moderation?

This is related to my previous post.

From http://www.kindredcommunity.com/2013/01/xtreme-eating-awards-2013-extremism-running-amok-at-americas-restaurant-chains/

Some people take low-carbing to an extreme, 'cos if reducing carbohydrate intake has benefits, reducing it to zero must be better. Oy!


We're told that eating 5 portions of fruit and vegetables a day is good for us. One patient who was admitted to St George's with malnutrition, had been eating more than 50 portions of fruit and vegetables a day, 'cos if 5 portions of fruit and vegetables a day is good for us, 50 portions of fruit and vegetables a day must be better. Oy!


People who are taking the anti-clotting medication Warfarin need to maintain an accurate balance between their warfarin dose and their Vitamin K intake to keep their INR between 2 and 3, as warfarin antagonizes vitamin K₁ recycling, depleting active vitamin K₁.
"Between 2003 and 2004, the UK Committee on Safety of Medicines received several reports of increased INR and risk of haemorrhage in people taking warfarin and cranberry juice. Data establishing a causal relationship is still lacking, and a 2006 review found no cases of this interaction reported to the FDA; nevertheless, several authors have recommended that both doctors and patients be made aware of its possibility. The mechanism behind the interaction is still unclear." Here's a clue...

From Possible interaction between warfarin and cranberry juice (emphasis, mine):-
"After a chest infection (treated with cefalexin), a man in his 70s had a poor appetite for two weeks and ate next to nothing, taking only cranberry juice as well as his regular drugs (digoxin, phenytoin, and Warfarin). Six weeks after starting cranberry juice he had been admitted to hospital with an INR (international normalised ratio) > 50. Before, his control of INR had been stable. He died of a gastrointestinal and pericardial haemorrhage. He had not taken any over the counter preparations or herbal medicines, and he had been taking his drugs correctly." Cranberry juice contains no Vitamin K. Oy!

"The Committee on Safety of Medicines has received seven other reports through the yellow card reporting scheme about a possible interaction between warfarin and cranberry juice leading to changes in INR or bleeding. In four cases, the increase in INR or bleeding after patients had drunk cranberry juice was less dramatic. In two cases, INR was generally unstable, and in another case INR decreased. Limited information is available about whether patients complied with their treatment in these cases.

Cranberry juice (Vaccinium macrocarpon) is popular and is also used to prevent cystitis. Interaction with warfarin is biologically plausible, because cranberry juice contains antioxidants, including flavonoids, which are known to inhibit cytochrome P450 enzymes, and warfarin is predominantly metabolised by P450 CYP2C9. The constituents of different brands of cranberry juice may vary, and this might affect their potential for interacting with drugs. Whether the constituents of cranberry juice inhibit CYP2C9 and therefore the metabolism of warfarin or interact in another way needs further investigation. Until then, patients taking warfarin would be prudent to limit their intake of this drink." Oy!

So, one man's inadvertent (his doctor should have warned him about eating next to nothing while taking warfarin) dietary extremism resulted in his own death and the restricted intake of cranberry juice for everybody else taking warfarin. Oy. :-(


P.S. It's about time an alternative to warfarin was found. It's difficult to maintain an accurate balance between warfarin dose and Vitamin K intake.

Jumping through hoops, and my Blog List.

I'm seeing a curious thing. The VLC "camp" seems to be "jumping through hoops" to prove a point.

From http://davidbressler.com/2013/08/26/easier-harder/

From Neuron fuel and function (emphasis & formatting, mine):-
"Ketones and lactate do not drive reverse electron flow through complex I. Glucose can. Palmitate certainly can. What you want from a metabolic fuel depends on the remit of your cell types. Neurons within the brain preserve information by their continued existence.

This is best done by burning lactate or ketones. NOT glucose and, of course, not FFAs.

Anyone who claims that glucose is the preferred metabolic fuel of the brain has not though (sic) about what a neuron has to do and what an astrocyte actually does do. Or much about the electron transport chain."

Basically, glucose is bad mmm-kay. Also, anyone who claims that glucose is the preferred metabolic fuel of the brain is a dumb-ass. Damn our livers & kidneys churning out glucose! Are they trying to kill us?

∴ Carbohydrates are bad and must be avoided at all cost! This, of course, is utter nonsense.

Glucose can drive reverse electron flow through complex I. Can means that it's possible. Is it probable?

On a hypercaloric Western diet of excessive crap-in-a-bag/box/bottle, yes.

On a Kitavan diet of ~70%E from tubers, no.

On a diet of Basmati rice & beans, no.

On a diet of whole fruits, no.

See also Another crash and burn on low carb paleo and CrossFit. Enough of the 'carbs are evil' nonsense. Carbphobia is hurting a lot of people.

I have a list of blogs that I read on a regular basis. As a result of the bad science & cherry-picking displayed in various VLC blogs, I have deleted them from my Blog List.

See also Guest post: Denialism as Pseudoscientific Thinking.

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!