On burning, storing and recomposing.

Burning

I couldn't resist!


On my adventures around the interwebs, I've noticed the following:- "Humans aren't Calorimeters. Therefore calories are irrelevant to humans." While I agree with the first sentence, I don't agree with the second one.

Calorimeters burn (oxidise) foods at high temperatures with a flame using oxygen, which produces carbon dioxide, water (depending on what's being burned) & heat energy.

Humans burn (oxidise) foods at 37ºC with enzymes , charge transporters etc using oxygen, which produces carbon dioxide, water (depending on what's being burned), mechanical energy & heat energy.

As both oxygen & carbon dioxide are gases, these can be measured by a respiratory gas analyser, to establish the rate of burning and what's being burned at any instant. See It's all in a day's work (as measured in Joules). When resting, burning occurs at a rate of ~1kcal/minute and, as it's measured while fasted, ~0.11g/min of fat is burned, & ~0.01g/min of carbohydrate is burned. Also note that a lot of mechanical energy can be produced, which can increase the rate of burning by a factor of seventeen.

In conclusion, humans burn (oxidise) foods, though not with a flame, and they can produce mechanical energy in addition to heat energy. The rate of burning and what's being burned at any instant can be measured.

Storing

When we eat food, it's digested and absorbed. As a digested meal is absorbed, it appears in the blood as glucose, triglycerides & amino acids. These then disappear from the blood due to burning and storage.

Fig. 1 Extended effects of evening meal carbohydrate-to-fat ratio on fasting and postprandial substrate metabolism

Fig. 1 above shows the effects of a 100g Oral Glucose load (▪▫) or a 40g Oral Fat load (●○) on blood glucose level over a period of 360 minutes. Note that subjects are resting during the 360 minutes. As the 100g Oral Glucose load produces a large insulin response (See Fig. 2 below ▪▫), fat-burning is temporarily reduced.

Fig. 2 Extended effects of evening meal carbohydrate-to-fat ratio on fasting and postprandial substrate metabolism

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

Fig. 3B Extended effects of evening meal carbohydrate-to-fat ratio on fasting and postprandial substrate metabolism

Fig. 3B above shows the effects of a 40g Oral Fat load (●○) on blood triglyceride (fat) level over a period of 360 minutes. Note that subjects are resting during the 360 minutes. As the 40g Oral Fat load produces no significant insulin response (See Fig. 2 above ●○), fat-burning is unaffected.

Therefore, fat-burning rate is ~0.11g/min. At this rate, it would take ~364 minutes to burn 40g of fat. If less than 100% of energy is derived from fat, it would take longer. Everyone is Different. shows the variation in % of energy from fat at rest. However, it actually takes 180 to 240 minutes for blood triglyceride (fat) level to fall from maximum to minimum. Therefore, some fat from the Oral Fat load is stored (as fat in adipocytes), even though there is no significant insulin response.


Therefore there are times when stuff is stored (anabolism) and there are times when stuff is withdrawn from stores (catabolism). If more stuff is stored than is withdrawn over a period of time, weight goes up, and vice-versa.

Recomposing

After doing intense exercise e.g. sprinting, resistance training with weights etc, muscles become very sensitive to insulin. Therefore, if intense exercise is done just before stuff is stored, amino acids & glucose are preferentially stored in muscles rather than adipocytes. This increases muscle mass relative to fat mass.

If non-intense exercise is done at times when stuff is withdrawn from stores, this maximises the amount of fat withdrawn from adipocytes and minimises the amount of amino acids withdrawn from muscles. This decreases fat mass relative to muscle mass.

It's therefore possible to increase muscle mass at certain times and decrease fat mass at other times, while keeping overall mass relatively constant i.e. it's possible to gain muscle and lose body-fat without being in an overall caloric deficit.


See The Energy Balance Equation, for more information.

Not exactly rocket science, is it?

If Paul (astrophysicist) Jaminet met Jack (neurosurgeon) Kruse ;-)

The paleo diet was recently ridiculed as a food fad in Natural’s Not In It. It also came last in a US News Best Diets survey.

Ways of eating such as very-low-carbohydrate, low-carbohydrate, low-reward, paleo, primal, ancestral, just eat real food etc discourage the consumption of manufactured food products and encourage the consumption of produce. If a large percentage of the population stop filling their shopping baskets with manufactured food products and start filling them with produce, who suffers? Not exactly...

This is why the food manufacturing industry tries to ensure that the population gets the best nutritional and dietetic advice that money can buy. See also New study: Big Food’s ties to Registered Dietitians.

While libertarians and anarchists moan about freedom from government interference, the food manufacturing industry has the freedom to crap all over the aforementioned diets and influence people to buy manufactured food products. Morbidity is also very profitable for healthcare and drug companies.

I think that I've now flogged this particular horse to death!

It’s the Calories, Stupid.

I thought I'd mark my return to blogging by taking the piss out of a certain Diet Doctor for his post It’s the Insulin, Stupid, who takes (and tweaks) Fig 7A from Hyperinsulinemia Drives Diet-Induced Obesity Independently of Brain Insulin Production.

At first glance, Fig 7A looks like a CIH believer's dream come true (apart from the words "High Fat Diet").

Hyperinsulinemia → Obesity.

Obesity is caused by too much insulin. Game, Set and Match to insulin.

Not so fast! Let's take a look at the rest of Fig 7.

Figure 7. Revisiting the Current Model of Obesity and Type 2 Diabetes(A) The most widely accepted model of the pathogenesis of obesity and type 2 diabetes posits that a high-fat diet leads to obesity and insulin resistance (there is debate about the relative order and causality of these). In this widely held view, insulin resistance then leads to hyperinsulinemia, which is followed by β cell exhaustion, and then type 2 diabetes. The accepted model is incompatible with our results that put the insulin hypersecretion genetically upstream of obesity.(B) Our data support a model whereby insulin levels must be kept low to maintain energy expenditure in white adipose tissue via the expression of Ucp1. Our data do not address the order of subsequent events after obesity (outside the yellow box), such as insulin resistance and/or type 2 diabetes, since they were not observed in our studies. In other words, the effects of insulin gene dosage on obesity are independent of sustained changes in glucose homeostasis or insulin resistance.

↑ Peripheral Hyperinsulinemia → ↓ Uncoupling Proteins (WAT) → ↓ Energy Expenditure → ↑ Obesity.

Obesity is caused by a reduction in energy expenditure in these mice. Game, Set and Match to The Energy Balance Equation. It’s the Calories, Stupid. In these mice, energy expenditure is strongly influenced by insulin levels. In humans, not a lot. In humans, insulin can act as a stimulant or a sedative.

I'm not an insulin denier as is obvious from my other blog posts. I'm still restricting my carbohydrate intake to ~125g/day from whole foods.

I'm not a food reward denier. I've been using food reward principles to lose weight.

This post will probably annoy some people. Before wasting your time writing a comment, please read my Moderation Policy.

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.

Hyperinsulinaemia and Insulin Resistance - An Engineer's Perspective.

Another techie post.

From https://en.wikipedia.org/wiki/Negative_feedback_amplifier

There's been some arguing discussion over whether Hyperinsulinaemia (HI) causes Insulin Resistance (IR). My answer is...Yes and No.

HI increases IR, long-term. See Downregulation and upregulation: The Insulin Receptor and Insulin oscillation.

HI doesn't increase IR, short-term. How can I claim this? The above diagram represents a Negative Feedback (NFB) control system, which is how Blood Glucose is regulated.

"Input" represents Glucose from digested sugars and starches. The arrow pointing at AOL represents Blood Glucose (BG). The triangle containing AOL represents pancreatic beta cells. "Output" represents Insulin Secretion (ISec). More BG = More ISec.

The box containing ß represents three things that work in parallel to reduce Blood Glucose.
1) The Liver. More ISec = Hepatic Glucose Production rate decreased.
2) Muscle mass. More ISec = Glucose intake to Muscle mass rate increased, via Glu-T4.
3) Fat mass. More ISec = Glucose intake to Fat mass rate increased, via Glu-T4.
The three things aren't of equal strength, but they provide overall negative feedback.

If overall negative feedback is halved due to doubling of overall IR in the above three paths, ISec doubles. If you don't believe me, see Idealised Negative Feedback Inverting Amplifier using an idealised op amp on WolframAlpha. Double the value of resistance 2 (the negative feedback resistor R2). and the output voltage on the inverting amplifier doubles from -10V to -20V.

The idealised Negative Feedback Inverting Amplifier using an idealised op amp on WolframAlpha is interesting in that an idealised op amp (the triangle with + and - inputs) has infinity gain and ±infinity voltage on its power supplies. As a result, there is zero volts (output voltage divided by infinity) between the idealised op amp's + terminal and its - terminal. If the idealised op amp's + terminal is connected to 0V (a.k.a. "Earth"), its - terminal is at 0V (a.k.a. "Virtual Earth") and has zero variation, whatever the input voltage. An actual op amp has a voltage gain of ~140dB (~10,000,000), so an output voltage of -10V can be achieved with a voltage of 1uV (one millionth of a Volt) on its - terminal.

If pancreatic beta cells had a zero threshold and infinity gain like an idealised op amp, BG would be zero and have zero variation with varying Glucose input. Pancreatic beta cells actually have a positive threshold and low gain, so BG is positive and varies slightly with varying Glucose input.

If ISec becomes zero (as in type 1 diabetes), there is zero negative feedback and BG increases. The same thing happens to the voltage on the idealised op amp's - terminal if its power supplies are 0V instead of ±infinity.

If ISec becomes insufficient (as in type 2 diabetes), there is insufficient negative feedback and BG increases. The same thing happens to the voltage on the idealised op amp's - terminal if its power supplies are limited to ±5V.

Having established that ISec is proportional to overall IR, what would happen if overall IR was proportional to ISec? If ISec doubled, overall IR would double, which would double ISec, which would double overall IR, ad infinitum. ISec would increase to maximum instantly. THIS DOESN'T HAPPEN. Therefore, IR doesn't increase in proportion to ISec, short term.

Long-term, increased ISec increases IR for a variety of reasons, one of them being that increased ISec increases the rate at which cells fill with glycogen. Once full of glycogen, cells must down-regulate their intake by down-regulating Glu-T4 and Glu-T2 (fat and liver cells also up-regulate their output of stuff) or burst.

Reduce your IR by addressing all of the factors in Insulin Resistance: Solutions to problems.

Chris Highcock emailed me a link to Muscular strength and markers of insulin resistance in European adolescents: the HELENA Study.

Weird Filters.

Here's a weird picture.

From http://cstrips.bitstrips.com/MVGHP_6XV9.png

Why is it that some people see the world through weird cognitive bias filters? It makes discussion with them impossible, as what I write is remixed with weird filters into something completely different. They then argue against something completely different, not what I wrote. This is the classic Straw Man argument.

Here are some examples of remixing with weird filters, taken from Insulin, the Un-dead and coffin nails.

1) ""A" is..." is remixed into "I believe that "B", "C", "D",..."Z" do not exist".

2) ""A" is caused by "B"" is remixed into "A is only caused by "B"". This is similar to 1).

3) "As cells are emptied (of glycogen)..." is remixed into "Once cells are completely emptied (of glycogen)...". The "As" at the beginning of the sentence signifies an ongoing process. Next time, I'll write "As cells are depleted (of glycogen)..." EDIT: Rewritten using c/p'ed text.

4) The statement "eating too much and moving too little" is remixed into "Gluttony and Sloth". Gluttony and Sloth are conscious actions. Eating too much due to ravenous hunger and moving too little due to lethargy/sleepiness are unconscious actions. Anybody who thinks that I mean/insinuate the former rather than the latter is an idiot/insane.

Having remixed what I wrote into something completely different, I am then accused of intellectual dishonesty. Oy!

Dirty Rotten Scoundrels.

Who, these guys?

From http://www.bbc.co.uk/programmes/b00kz6jc

No. I'm referring to Manufacturers of Crap-in-a-Bag/Box/Bottle (CIAB), or MOCIAB for short.

In Obesity is multi-factorial, spectra and other stuff, I mentioned Mayor of NYC Michael Bloomberg's ban on the use of cups larger than 16oz for the sale of sugary sodas. Note that Mayor Bloomberg is not trying to ban sugary sodas or tax anything. People are still free to buy as many cups of sugary soda as they want. However, the whining from people is deafening!

Surprise, surprise! MOCIAB have retaliated with the usual dirty tricks.

1) Lies, damned lies and MOCIAB statistics.

Cherry-picked studies, much?

2) Have a number of MOCIAB/pro-MOCIAB groups/sites drown-out good advice with bad. This is a standard marketing trick pioneered by Edward Bernays. Some examples of MOCIAB/pro-MOCIAB groups are:- Academy of Nutrition and Dietetics, http://www.ameribev.org/, http://www.consumerfreedom.com/, http://www.letsclearitup.org/ and http://www.livepositively.com/.


In Psychological manipulation, there was a link to a story about a hypnotist who used his freedom of speech to influence women into "freely" handing him cash. So, why is he not allowed to use his freedom of speech to influence people (Italian police were hunting him) whereas MOCIAB are?

EDIT: I'll repeat it here, in case you missed it in the other post. Confessions of a former Dirty Rotten Scoundrel.

A comment, a simile and insanity.

1) The comment: I'm just about to leave the following comment on Peter (Hyperlipid)'s blog post Insulin and the Rewards of overfeeding. I thought that it was so good at summing-up, I'll post it here first!
"All,

Insulin increases the amount of glucose & FFAs entering fat cells, muscle cells & the liver.

Insulin decreases the amount of glycerol & FFAs exiting fat cells & the amount of glucose exiting the liver.

Hyperinsulinaemia (which can produce sedation) results when one or more of the following tissues loses insulin sensitivity:- fat cells, muscle cells & the liver.

So, why do people keep saying that hyperinsulinaemia locks nutrients away in fat cells only, thus robbing other cells of nutrients, thus causing lethargy?

The relative insulin sensitivity of tissues determines the relative partitioning of nutrients into those tissues.

When tissues lose sensitivity to insulin, blood glucose control becomes impaired. This results in roller-coaster blood glucose levels after eating high-glycaemic carbohydrates. A rapidly-falling blood glucose level causes ravenous hunger. I have experienced this during medically-monitored tests (OGTTs & an insulin shock test).

Low-carb/ketogenic diets don't result in a roller-coaster blood glucose level and therefore don't cause ravenous hunger. Simples!

Overeating due to ravenous hunger is NOT gluttony, just as under-moving due to sedation is NOT sloth.

THIS is gluttony."

EDIT: This didn't go in my comment but should have:- "Low-carb/ketogenic diets result in the avoidance of moreish & calorific foods such as sweets, chocolate, cake, biscuits, pizza, Pringles etc. A single bite of such foods has a negligible effect on blood glucose & insulin levels, but encourages another bite and another and another ad nauseam, due to Food Reward.


2) The simile: I use similes. I used the simile "As happy as a pig in shit" in a comment somewhere on Woos blog. Now, you may (or may not) have noticed that my user-name is Nigeepoo. We Brits are obsessed by two things - The weather and our bowel movements. I find things to do with poo and farting amusing (schoolboy humour, I know!). I used the simile "As happy as a pig in shit" because it is amusing.


3) The insanity: According to Woo in the following comment:-
"Re: the comment...Sorry, not convinced.
You are basically refusing to admit your choice of words implied moral judgement. The phrase "happier than a pig in shit" is always applied to examples of people being content in immorality/bad behavior particularly gluttony and sloth... unless it is used ironically. Only an autistic or a non-english speaker would believe this crap."

Woo, you are as mad as a March hare. IMO of course, like everything I write. Duh!

"The Diet Debacle" debacle.

What's that funny smell?

According to Robert H. Lustig in The Diet Debacle,"If a calorie is a calorie, then any food can be part of a balanced diet; and, if we are what we eat, then everyone chooses what they eat."

Firstly, the first nutritional maxim isn't "A calorie is a calorie". It's actually "Where bodyweight is concerned, a calorie is a calorie". Leaving out the first four words makes a huge difference to the meaning.

Secondly, the second nutritional maxim actually means "Your body is made out of what you eat. Therefore, if you eat/drink rubbish, you get a rubbish body.

Apart from that, the rest of the article is absolutely fine*.

*The above sentence ending in "*" is pure irony. See also Review & Critique: The Skinny on Obesity ~ Intro and Part I and Review & Critique: The Skinny on Obesity ~ Part II Sickeningly Inaccurate.

The sad thing is that I actually sympathise with Robert H. Lustig's aim, which is to reduce the humongous amount of sugar that Americans shove down their throats in solid or liquid form each year.

I don't want to come across as a Socialist Asshole (it's Arsehole, Sean!), but intervention is sometimes needed to stop certain humans and groups thereof (e.g. companies/corporations) from harming other humans and groups thereof (e.g. the general population).

In City of New York Bureau of Food Discipline, Sean wrote "Never mind that the record of government diet intervention is abysmal, this time it will work." I can't speak for the US, as I don't know how things work over there. Here in the U.K, DEFRA aims to maintain standards in the way that crops are grown and in the management of farm animals. The FSA aims to maintain standards for food safety, although they do occasionally issue some dubious nutritional advice (read the comments to see some familiar names).

Just because government agencies occasionally cock things up, does that mean that we should have zero government intervention where food is concerned? I obviously think not!

See also What Is Food? and Former Coke executive slams ‘share of stomach’ marketing campaign.

Addendum: If (as I believe) corporations should be prevented from unduly influencing the general population in their food choices by banning all advertisements for foods & drinks, then governments should also be prevented from unduly influencing the general population in their food choices by banning food policies and crop subsidies. All that governments should do food-wise is enforce food safety standards.

Of mice and men, Kleiber's Law & FIRKO.

More musings from my fevered brain!

I remembered a discussion on Hyperlipid about FIRKO mice.

Note: FIRKO stands for Fat Insulin Receptor Knock Out and it results in White Adipose Tissue (WAT) having vastly reduced uptake of nutrients, thus inhibiting gain of WAT. Brown Adipose Tissue (BAT) has up-regulated uncoupling proteins i.e. BAT produces heat.

Of great interest was that, in a study where a FIRKO mouse's VMH (VentroMedial Hypothalamus) was deliberately damaged, the mouse ate more food but didn't gain weight. This appears to defy Energy Balance theory.

Mice weigh ~30g, so they can't burn much energy through physical activity. How can mice eat more food but not gain weight?

Peter Dobromylskyj gave me the answer. As a veterinary surgeon, he works on rodents, so he knows about this. Rodents under anaesthesia easily get hypothermia. Mice have a high surface area to mass ratio (see the above graph) compared to adult humans. As heat is lost through the skin, small animals like mice are at a disadvantage when it comes to heat conservation. They have behaviours for conserving heat e.g. covering themselves in bedding (which reduces heat loss) or huddling together in groups (which reduces overall surface area to mass ratio). Anaesthesia prevents heat conservation behaviours.

Any excess energy intake that cannot be stored due to FIRKOisation is disposed of by increased heat production in BAT and increased heat loss by reduced heat conservation behaviours.

Most adult humans have a tiny amount of BAT, so they can't do this. If an adult human raises their metabolic rate significantly (say, by taking 2,4-Dinitrophenol), they tend to die from hyperthermia.

You could try sitting in a bath of cold water. ;-p That would make me really cold and hungry (and wet!), so I would eat ravenously afterwards. But that's me. Your Mileage May Vary.

See also It’s the Calories, Stupid.

Obesity is multi-factorial, spectra and other stuff.

This post is a hotch-potch of thoughts that are currently whizzing around in my brain.

1) Obesity: Like just about everything in life, obesity is multi-factorial. Each factor may have only a small impact on obesity. Tackling one factor alone won't solve the problem. Every factor has to be tackled, one at a time.

So, New York City Mayor Michael Bloomberg announcing a ban on sales of sugary drinks larger than 16 ounces in restaurants, delis, sports arenas, and movie theaters won't solve the obesity problem, but it will help.

EDIT: In shops and supermarkets in the UK, tobacco products now have to be kept out of sight. I'd like to see the same thing happen to Crap-In-A-Bag/Box/Bottle (CIAB).

2) Spectra: As also mentioned in my first link, there is a spectrum of fatness in the general population which probably follows a bell distribution curve. From skinniest to fattest, there are people who are:-
Extremely skinny. Very skinny. Skinny. A bit skinny. Average. A bit fat. Fat. Very fat. Extremely fat.

If you take somebody in a category who isn't currently consuming CIAB and introduce CIAB to their diet, what happens? They move to a category to the right. Therefore, it's possible for there to be very skinny people who consume CIAB. Therefore, anybody who (or should that be Wooo?) states that the existence of very skinny people who consume CIAB is proof that Food Reward doesn't exist is wrong.

3) Other stuff: I am concerned with people overlooking postprandial (a.k.a. nonfasting) triglycerides (a.k.a. triacylglycerols a.k.a. TAGs a.k.a. TGs) after eating large amounts of fat. According to Fasting Compared With Nonfasting Triglycerides and Risk of Cardiovascular Events in Women, serum TGs 2-4 hours post-meal are very significantly associated with Cardiovascular Events (fully adjusted hazard ratio [95% confidence interval] for highest vs lowest tertiles of levels, 4.48 [1.98-10.15] [P < 0.001 for trend]).

After 4 hours post-meal, serum TGs are cleared from circulation by being burned by muscles and/or by being stored in fat cells. See Figure 3B in Extended effects of evening meal carbohydrate-to-fat ratio on fasting and postprandial substrate metabolism.

PPP - another bijou rant-ette.

Blame it on the hot weather and screaming kids! :-D

From http://www.thamesvalleytango.co.uk/images/Rant.jpg

PPP stands for Piss Poor Parenting.

Why, oh why, oh why do some feckless parents allow children to dictate what they eat? As if children know what's good for them! At an event I attended recently, "Johnny*" was given a plate of chicken drummers (mechanically-recovered chicken formed into the rough shape of chicken drumsticks and coated with breadcrumbs) and oven chips. I asked Johnny if he would like a beefburger, sausage or pork steak. He replied. "I don't like them". He only wanted manufactured crap. Seriously, WTH?

When I was a lad, I was given the same food as my parents. If I didn't eat it, I went without. I ate it!
Nowadays, "children's menus" in restaurants (I'm being quite generous in the use of the word restaurant) consist of lots of manufactured crap that children like. Unlike veggies & fruit, this crap contains very little fibre/fiber or Magnesium.

Is it any wonder that childhood constipation is a problem? Why are children being given PEG or even Lactulose, when there's a much better solution - Epsom Salts (which contains 10% Magnesium by weight). The brain needs Magnesium to remain cool, calm and collected i.e. function properly. The brain also needs EPA, DHA and Vitamin D3 to function properly. Many kids don't like oily fish, so they won't eat it. It's not rocket science to purée some sardines or wild red salmon with some Bolognese/Sweet chilli/w.h.y. sauce so that they won't notice it. Many kids play indoors or are smothered in sunblock when they do go outdoors, so they get little or no Vitamin D3. Is it any wonder that childhood ADD & ADHD is much more common? Medication and psychotherapy? Seriously, WTH?

See Effect of MAGNE-B6 on the clinical and biochemical manifestations of the syndrome of attention deficit and hyperactivity in children.

Supplementation of polyunsaturated fatty acids, magnesium and zinc in children seeking medical advice for attention-deficit/hyperactivity problems - an observational cohort study.

Moderators of treatment response in adults with ADHD treated with a vitamin-mineral supplement.


When I was a lad, there were a couple of show-offs in my class at school, but nobody behaved like "Jimmy*" (physically and mentally hyperactive with bad behaviour, screaming and shouting). Johnny was also badly behaved, but not as bad as Jimmy. The parents at the event seemed perfectly happy that, every day, their children had to be given "uppers" (e.g. Ritalin) to help them concentrate during the day and "downers" to help them sleep at night. Seriously, WTH?

I will now take a deep breath and count to twenty. There, that's better!

*Names changed.

Testing hypotheses - a rant.

My brain just exploded! On Why conventional view of obesity / FR is wrong, ItsTheWoo wrote "...there is not a doubt in my mind obesity is entirely 100% an illness, a disorder... "

According to ItsTheWoo's hypothesis, the increasing incidence of obesity all around the world since 1970 is 100% caused by the increasing incidence of illness all around the world since 1970. Seriously, WTF?

According to Nigeepoo's hypothesis, the increasing incidence of obesity all around the world since 1970 is significantly caused by the increasing influence of Crap-in-a-Bag/Box/Bottle (CIAB) manufacturers on the population by cunning marketing and on the Government by bribery lobbying since 1970.

The former results in increasing consumption of CIAB and the latter results in increasing subsidies on the raw materials used for manufacturing CIAB, making CIAB cheaper (also more profitable) than natural foods, thus increasing consumption of CIAB. See Why are Twinkies cheaper than carrots?

There are other factors causing increased obesity e.g. increasing numbers of towns/cities which discourage walking. See also Determinants of the Variability in Human Body-fat Percentage.

Highly-engineered and highly-calorific CIAB encourages subconscious over-eating via Food Reward. The hyper-secretion of insulin (compensatory hyperinsulinaemia) caused by the subconscious over-eating of CIAB causes subconscious under-moving by inducing drowsiness and lethargy, sometimes followed by the munchies if blood glucose goes too low. Insulin is just a hormone that is secreted for the storage of stuff and a reduction in the burning of stuff. Don't blame insulin for doing its job. If you have zero insulin (e.g. untreated type 1 diabetes), your body stops storing stuff and starts burning stuff uncontrollably. Before the invention of insulin injections, people with type 1 diabetes usually died within 2 years.

Subconscious over-eating is good for the profits of CIAB manufacturers. An increasing number of dyslipidaemic/hypertensive/depressed/diabetic/demented/w.h.y. people is good for the profits of health-care providers and drug manufacturers. These organisations currently make huge profits, so it's not going to be easy to change anything that will reduce them.

I deleted the last part of my rant as it was a bit too ranty, but I'm reinstating it in a toned-down form as I've mentioned it in the comments.

ItsTheWoo continually conflates subconscious over-eating and under-moving with conscious over-eating and under-moving (gluttony and sloth). The vast majority of over-fat people become over-fat due to subconsciously over-eating and under-moving. A tiny minority of over-fat people are gluttonous and slothful.

Telling people to consciously Eat Less, Move More doesn't work. This doesn't mean that Eat Less, Move More doesn't work. It means that Eat Less, Move More has to be done subconsciously. This is where low-carb/paleo/real food diets come into their own.

Rant over.

Get in! Part 4. Get out! Get this!

First, here's a rather jolly but not safe for work song from The Beautiful South.

Mum's GP has approved mum getting 500mg/day Thiamine. I'm waiting for it to arrive from Vitacost.

Mum's GP has approved the discontinuation of Aspirin 75mg/day and Omeprazole 20mg/day, as they are of little benefit and it reduces the number of pills that mum has to swallow each day.

I sang backing vocals for my friend Ray Langstone with a group of excellent musicians at the Unicorn pub on Monday evening. That's the first time I've done something like that.

Good Health: You can get it if you really want.

You'll never guess!

Some people moan about their health problems a lot. If somebody tries my advice and their health doesn't improve, they are justified in moaning about it.

If however I give them advice, they ignore it and then carry on moaning, it's time to ignore them. I don't have time for...

You're free, and a testimonial.

First, the music video.


I have to admit that I'm not exactly what you'd call "exciting". Apart from driving my yellow MX-5 very fast in the middle of the night when there's nobody around, I'm not an adrenaline junkie. My mother used to throw herself out of light aircraft with a parachute on her back. There were occasions where her main 'chute either failed to open or it became tangled and had to be "cut away" before deploying the reserve.

I'll fly through the air when I've grown a pair of wings. I'll swim when I've grown a set of gills. I'll climb up the side of a mountain when I've grown two extra legs and have the strength & balance of a goat.

In some ways, I'm lucky to have slightly defective hearing & vision. I'm happy with the sound quality of inexpensive stereos and I don't need HDTV. I get my kicks from singing and from helping people to improve their health. I believe that health is number one priority as, without it, you can't properly do or enjoy things in life.

So, you're free to do what you want to do. Also, you're free to take or leave my advice! Anyway...

Somebody who I've known for about 14 years had been suffering from fairly obvious signs of magnesium deficiency (anxiety, poor sleep, cramps, spasms etc) for quite a while, so I virtually frog-marched him to the pharmacy at Tesco on bank holiday Monday and got him to buy a pot of Epsom Salts and add some to a smoothie.

He wishes to remain anonymous, but last night he informed me that he's feeling much better and is now pooing normally for the first time in 20 years. That's probably how long he's been deficient in magnesium. I've also given him 14 Vitamin D3 5,000iu mini gelcaps to try, as he suffers from low moods and rarely gets any sun on his skin.

Our bodies work so much better when they have all the nutrients that they need.

Feel-good Friday.

Nothing to report, so crank the volume knob up to 11 for the following two music videos.





A big "thank-you" to Ann Gibbs for bringing these songs into my life at Monday night jam sessions at the Unicorn pub in Aldershot. I hadn't heard either of them until I went there!

Look after your brain, Part 5.

This is another bookmarking post.

I spotted an article by Emily Deans M.D. called Nutritional Brain Bomb - Thiamine Deficiency.

So there's yet another way to knacker the brain, resulting in Wernicke's encephalopathy and in severe cases, Korsakoff's psychosis. Both of these conditions are partially irreversible due to neuron death. Both of these conditions are partially reversible by high-dose thiamine therapy.

Thiamine 500mg/day is one last therapy to try mum on after I've got her back on Vitamin K2 (hopefully today).

Continued on Quality >> Quantity.

Use 'em or lose 'em, Part 2.

I'm talking about your brain(s). Last year, I became depressed for several months for personal reasons that I won't go into. On December 8th 2011, something happened and the depression went away in an instant.

Unfortunately, several months of lying around doing very little had turned my brain to stodge. I tentatively resumed blogging in January 2012.

I find that the more I use my brain, the better it works, the more I can remember and the more I want to use it.

On the minus side, I find that I'm more impatient than I used to be. I'm now quite intolerant of, erm, f***wits on the roads and on the internets. Don't mention Giant Pandas!

How eating sugar & starch can lower your insulin needs.

This is a bookmarking post. Jason Sandeman is a chef who had a couple of web-sites at Well Done Chef! and Jason Sandeman — Real Food For Your Life. He has Latent Autoimmune Diabetes of Adulthood (LADA), which has resulted in a total loss of his pancreatic beta cells which means that he has to inject insulin.

Now, it's generally believed in low-carb circles (and by myself) that people with Type 1 Diabetes Mellitus (T1DM) should minimise their intake of sugary & starchy carbohydrates as these promote wild fluctuations in blood glucose. See The problem with Diabetes.

Jason wrote the following comment on Richard Nikoley's blog. The relevant part is as follows:-
"Even more weird – now that I have introduced the starches into the diet – I have actually got better control now. I thought my insulin needs would go up – but they haven’t. They’ve gone down."

To which I replied:-"How about this for an explanation? You now have a well-controlled glucose input to your circulation via diet, which has suppressed the poorly-controlled glucose input to your circulation via hepatic glucose production."

Hepatic glucose production (HGP) is increased by Glucagon, Cortisol & Adrenaline/Epinephrine. These are secreted as blood glucose level falls below certain values in order to keep our brains alive. See Blood Glucose, Insulin & Diabetes.

As keeping our brains alive is rather important (!), the mechanism is fairly crude in operation and blood glucose can overshoot in a positive direction, as a bit of glycation is less harmful than brain death. See "Funny turns": What they aren't and what they might be. Hyperglycaemia requires insulin to lower blood glucose back to the normal range.

Therefore, eating some (but not too much) sugar & starch can result in lower blood glucose level and lower insulin secretion. Eating fibre/fiber (a carbohydrate) is also good for keeping blood glucose low, as only just mentioned in Fiber and Insulin Sensitivity. Ain't the human body weird?"