Friday, 19 December 2014

Variations in weight change for a given Calorie change - An Engineer's Perspective.

Another techie post, inspired by Insulin Doesn't Regulate Fat Mass. Consider the inverting amplifier using an Op-Amp, below:-

As the amplifier is inverting (i.e. a ↑ input on Vin results in a ↓ output on Vout), the feedback from Vout via R2 opposes Vin via R1 at the - terminal of the Op-Amp.

If R1 = R2 and Vin changes from 0V to 1V, the change in V- (the voltage on the - terminal of the Op-Amp) varies with A (the magnitude of the Op-Amp gain) as follows*:-

A_____________Change in V-(V)

As the body operates on biochemical principles, slopes of input/output transfer functions aren't steep at their steepest points. E.g.

Therefore, the gains in the various parts of the Leptin "adipostat" NFB loop are not very high. Therefore, there will be a significant variation in weight change vs Calorie change, and there will be significant variations in the variation due to loop gain variations from person to person.

Insulin Resistance makes the slopes of  the above input/output transfer functions shallower, reducing the gain in the system. This increases the variation in weight change vs Calorie change. For ways to reduce Insulin Resistance, see Insulin Resistance: Solutions to problems.

*In case anyone thinks that I've made the numbers up, here's the maths:-
Current in/out of the - terminal of the Op-Amp = 0.
∴ IR1 = IR2
I set R1 = R2 to keep the maths simple. By Ohm's Law, V = I * R.
∴ VR1 = VR2
With a 0V input:-
All currents & voltages = 0.

With a 1V input:-
VR1 = 1 - V-
VR2 = V- - Vout.  As Vout is negative, - Vout is positive.
- Vout = A * V-
∴ VR2 = V- + (A * V-)
∴ 1 - V- = V- + (A * V-)
1 = (2 * V-) + (A * V-)
Dividing both sides by V-:-
(1/V-) = 2 + A
∴ V- = 1/(2 + A)

Monday, 10 November 2014

Is the world getting better, or worse?

A few days ago, on Facebook, the following graphic caught my eye.

Average life expectancy in England in 1843 was only 40 years. According to How the Mid-Victorians Worked, Ate and Died., those who survived being born, accidents & infections in the first five years of life lived to a ripe old age, despite no modern drugs or other medical technology.

This suggests that mortality between the ages of zero to five was ~50% back then. Yikes.

Click the link in the caption to see other ways in which the world has got better.

Wednesday, 5 November 2014

Fibromyalgia: It's the food, again! (probably).


Serendipity strikes again! On Facebook, I saw . That linked to Fibromyalgia and non‑celiac gluten sensitivity: a description with remission of fibromyalgia.

For people unfamiliar with scientific terms, here are some definitions:-
Non-celiac gluten sensitivity: A reaction to gluten, not due to Celiac (Coeliac in the U.K.) Disease.
Remission: (medicine) An abatement or lessening of the manifestations of a disease.

So, is Gliadorphin-7 (formed during the digestion of gluten) to blame?

Could Beta CasoMorphin-7 (formed during the digestion of A1 cow's milk) also be a problem?

Is Increased/Excessive Intestinal Permeability allowing the above large molecules to pass through insufficiently tight junctions?
Definitely, maybe.

Is there really no cure for Fibromyalgia? It's possible to tighten-up insufficiently tight junctions. Insufficiently tight junctions can be caused by:-

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%20Fields]%20AND%20%22tight%20junction%22[All%20Fields]%20AND%20hasabstract[text]%20AND%20%22humans%22[MeSH%20Terms]

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.

And finally...
If a science person ever tells you "Increased/Excessive Intestinal Permeability a.k.a. "Leaky gut" just doesn't exist because, you know, I'm a scientist.", point out that it's an Appeal from authority fallacy, and demand that they provide high quality evidence to support their statement.

Because, you know, I'm a retired Electronic Engineer! :-)

Monday, 20 October 2014

A bijou rant-ette: Robbing bastards and Misapplication of laws.

The title of this post is based on The dirty, robbing bastards!

1. Robbing bastards.

Once upon a time, I used to enjoy driving. Maybe getting older has made me less tolerant, but I now hate driving, for several reasons.

1. Increased road congestion, increasing journey times and frustration.

2. Slow-coaches driving well below the speed limit, increasing journey times and frustration.

3. P.I.G.S (People Incapable of Giving Signals). I'm not a %^&*ing mind-reader!

4. P.P.P.R.P. (People with Piss-Poor Road Positioning), obstructing the road when they're manoeuvring, causing delays and frustration.

5. P.P.P.L.D. (People with Piss-Poor Lane Discipline), causing me stress, especially on roundabouts.

6. "Chelsea Tractors" and other large vehicles, obstructing the road when they're manoeuvring, causing delays and frustration.

7. Cyclists wobbling from side to side, or riding two abreast, obstructing the road, causing delays and frustration.

8. P.P.P.H.A. (People with Piss-Poor Headlight Alignment). High headlight aim fails the MOT test. Therefore, vehicles with high headlight aim are technically unroadworthy. Why are so many unroadworthy vehicles on the road and why do the traffic police do nothing about it? Also, H.I.D. (High-Intensity Discharge) headlights. When sitting in a Mazda MX-5, my eyes are only 3'6" (I measured it) above the ground, making me very susceptible to being dazzled by oncoming headlights that are aimed too high. I find H.I.D. (High Intensity Discharge) headlights particularly dazzling. Being dazzled causes me stress, as I can't see properly.

I've been emphasising the words frustration and stress, as these raise levels of the stress hormone cortisol. Chronic frustration and stress while driving chronically elevate cortisol, which is bad for health for several reasons. See Cushing's syndrome.

Here's a video I shot, using the camera on my Samsung Galaxy SII phone, mounted on the driver's door window with the lens 3'6" above the ground. The video is shaky, due to a combination of uneven roads and very firm suspension. When the headlights flare-out on the video, it means that the sensor in the camera is being overloaded. Ditto my eyes. I speeded it up to shorten the duration, and added an appropriate soundtrack, using Windows Live Movie Maker. Enjoy!

When I can't take being dazzled any longer, I lower the visor to the point where it blocks light from oncoming headlights. This makes seeing high-up objects (e.g. road signs and traffic lights) difficult.

9. Reading Borough Council. Here's a video I'd rather not have been in (published with permission).

Salient points from the above video:-

1. Reading Borough Council are enforcing Bus Lanes at all hours. Where I live, Bus Lanes are only enforced during peak hours, which is reasonable, as Bus Lanes allow Public Transport to travel freely on roads that become congested during peak hours. Sarcasm Alert! Note the heavy traffic congestion in the non-Bus Lane at 01:32 in the middle of the night.

2. The road surface is shiny, due to surface water. There's quite a high reflection coefficient, when viewed from the high angle of incidence of the Bus Lane enforcement camera. As the angle of incidence decreases, the reflection coefficient increases. At low angles of incidence, such as my view of the road from 3'6" above the ground, the reflection coefficient is nearly 100%.

3. There's an oncoming vehicle with bright headlights. I would have had the visor down, so I wouldn't have seen the red traffic light, until I was so close that it was visible around the side of the visor.

See also:-
Bus lane fine in Reading - PistonHeads.
Vastern Road Reading bus lane - FightBack Forums
Is Reading Anti Motorist?

Reading and I have history!

My first encounter was with Reading Borough Council and was on 7.11.2009. It involved the Parking Permit below (Reg. No. deleted):-

Reading Borough Council tried to prosecute me for non-display of the above permit. I appealed on the grounds that Reading Borough Council didn't provide a self-adhesive strip to stick the flimsy bit of paper to the windscreen (as is the case with virtually all car park tickets), and that their flimsy bit of paper had blown off the dashboard of my Mazda MX-5. My appeal was accepted. That's the only time I've come out on top with Reading Borough Council.

My second encounter was with Thames Valley Police and was on 4.10.2010 at 23:56. It involved the (Sarcasm Alert!) Vastern Road revenue generation scheme.
See also:-
Positioning of "Safety" speed cameras - WhatDoTheyKnow

The two lanes each way dual-carriageway was virtually deserted at 23:56, so virtually every driver that drove down that road at that time (about one a minute) was prosecuted for exceeding 30mph.

"It wouldn't be very profitable if everyone stuck to the speed limit" Kate Smith, Thames Valley Police.
No shit, Sherlock! The main indication that the road has a 30mph speed limit are lamp-posts. The West end of the road is part residential. The East end of the road has offices on the North side and a trading estate on the South side, both closed at night. When a motorist comes across a virtually deserted two lanes each way dual-carriageway in the middle of the night, there are two possible responses:-

1. Oh, look! A two lanes each way dual-carriageway with lamp-posts. I'd better drive at ≤30mph.
2. Oh, look! A two lanes each way dual-carriageway. National speed limit (70mph) applies.

I'm guessing that 2. is the usual (though incorrect) response. Why is the 30mph speed limit enforced in the middle of the night down the East end, when the offices and trading estate are closed and the road is virtually deserted?

Thought Experiment in Logic: If Reading Borough Council was concerned about the 25 injuries (1 serious) that occurred in the previous 3 years, they could have done more than just having one of THESE (seen on a recent stroll up Vastern Road using Google Street View) e.g. by adding THESE (as per the A325 in Farnborough) and THESE (as per the A325 in Farnborough). However, that would result in fewer drivers speeding and a drop in revenue from speeding fines.

There have been other encounters (e.g. the GATSO on a downhill road, where speed creeps up unless the speedometer is regularly checked, also police enforcement of a 40mph speed limit on the three lanes each way dual-carriageway section of the A33 at 00:23), but I won't bore you with the details.

2. Misapplication of laws.

Laws are intended to deter people from causing harm, or punish people who cause harm. I've noticed a tendency for organisations to use laws to extract money from people, and cover their own backs. I received a 61 page evidence pack from Reading Borough Council for a case before the Traffic Penalty Tribunal, to which I am taking them, as they refused to accept my mitigating circumstances for driving in the Bus Lane (poor visibility and excessive reflection from a wet road when viewed from 3'6" feet above the ground). Most of the evidence pack was to show that Reading Borough Council met all laws with their street and road signs. They also informed me that Mazda met all laws in the design and manufacture of my car, therefore the offence must be entirely my fault. Their evidence pack also contained a straw man fallacy, plus the implication that I nearly went through the red traffic light due to driving at "such a speed".

Some readers will think that I'm a careless driver who's trying to justify my carelessness. When I drive, I have priorities. They are as follows, followed by results achieved since passing my driving test in August 1979:-

2. DON'T HIT OTHER CARS. Result: Number hit at ≥5mph = 0. Number hit at ≤5mph = 3. Number hit requiring exchange of details = 1.
3. DON'T HIT HARD OBJECTS. Result: Number hit at ≥5mph = 0. Number hit at ≤5mph = ~3.

Sunday, 12 October 2014

A tale of the unexpected & an analogy.

The tale.

A friend had a faulty lap-top mains adaptor. It was one of these:-

I offered to fault-find it. I measured the output voltage with my multimeter.

The output voltage was 0V.

I felt the lead where it exited the connector. It didn't feel right, so I cut the connector off & stripped-off some insulation. Lo and behold, the inner conductor (it was co-axial cable) was broken. I prepared the conductors, tinned them, soldered them and powered the adaptor, with a sense of impending triumph.

The output voltage was 0V.

I tested the continuity from conductors to connector. That's when I discovered that there was a short-circuit between the inner and outer conductors. I snipped-off the connector and confirmed that it was the connector that was short-circuited, not the adaptor or cable. I fitted a replacement connector and powered the adaptor, with a sense of impending triumph.

The output voltage was 0V.

At this point, I decided that the adapter was Beyond Economic Repair and advised the friend to buy a new one, which subsequently worked perfectly.

So, how did the adapter get to have not one, not two but THREE faults on it? It turned out that the lead had been yanked sideways, which bent the connector. The friend had straightened the connector with pliers (!). This short-circuited the connector, resulting in an internal fuse blowing in the adapter. The friend then "jiggled" the connector in the socket, in a vain attempt to make it work. This broke the inner conductor of the co-axial cable.

The analogy.


Some health problems are multi-factorial. Fixing only one, but not all of the problems, results in not fixing the problem. So, if you try "A" and there's no improvement, either "A" isn't one of the problems, or "B", "C"......"Z" need fixing, too.

This post was inspired by Effects of 12 weeks high dose vitamin D3 treatment on insulin sensitivity, beta cell function, and metabolic markers in patients with type 2 diabetes and vitamin D insufficiency - a double-blind, randomized, placebo-controlled trial.

Taking an effective dose of Vitamin D3 for a reasonable length of time didn't make a significant difference to insulin sensitivity or beta cell function. It did for me, as my main problem was Vitamin D insufficiency. I got lucky.

You are *never* going to guess what happened on Saturday night - Part 2.

In You are *never* going to guess what happened on Saturday night, I got to sing with a band called Mirrorball at The Falkners Arms in Fleet. I think that you can probably now guess what happened last night!
"When you're gone", by Bryan Adams & Melanie Chisholm
"Summer of '69" by Bryan Adams.
More "Summer of '69".

If I'd known that a friend was going to be there with her camera, I would have worn smarter clothes!

Thursday, 25 September 2014

Calcium shift: An interesting hypothesis.

More serendipity! Billy the k left a comment that piqued my curiosity.
From The atheroma 'junk' in the media is cholesterol + calcium in older people.

From Aging and calcium as an environmental factor. (emphasis mine)
"The consequences of calcium deficiency might thus include not only osteoporosis, but also arteriosclerosis and hypertension due to the increase of calcium in the vascular wall, amyotrophic lateral sclerosis and senile dementia due to calcium deposition in the central nervous system, and a decrease in cellular function, because of blunting of the difference in extracellular-intracellular calcium, leading to diabetes mellitus, immune deficiency and others.

I highlighted amyotrophic lateral sclerosis in red, as many Facebook friends have been having buckets of water & ice cubes tipped over themselves to raise money for research into this horrible & ultimately fatal condition.

So, what prevents & reverses migration of calcium from hard tissues to soft tissues?
Clue: It carboxylates osteocalcin in bone matrix Gla proteins. Yes, it's Vitamin K2.

See also Calcium, parathyroids and aging. N.B. 50iu/kg bodyweight/day of Vitamin D3 significantly lowers parathyroid hormone.

ItsTheWoo, Me, and Sheeple.

This post is about

EDIT 28th Feb 2019: Having just taken a look at the above post, she's edited it a lot, possibly as a result of reading this.

I don't mince my words, but I didn't stalk her and I didn't create a dummy account called Janey Planey. Itsthewoo isn't averse to making defamatory statements about me, which makes it obvious as to who actually has severe mental problems.
From I am "That man", where diet & nutrition is concerned.

My cunning plan worked! I needed an excuse to never have to visit that cluster-f*ck of a blog ever again, so I gradually increased the level of (well-deserved, may I add) snark & insults, in response to ItsTheWoo's insults to me, and misrepresentations about me, until she did what I wanted - i.e. banned me forever. Thank you!

In, I rebutted & debunked ItsTheWoo's strawman fallacies about me. I thought that she was merely ignorant of me, so I sent her a Friend Request on Facebook, which she accepted. I thought that if she knew more about me, she wouldn't use so many strawman fallacies.

Well, that was a complete waste of time! I took the opportunity to get to know her better, and what did I learn? She appears to be completely self-obsessed, and is mainly concerned with being as popular as possible, with as many followers as possible. To achieve this requires her to be constantly zany & "off the wall", with regular melt-downs to keep the troops entertained. She also likes nail varnish!

I don't actually have anything against her, other than her constant misrepresentations of me, which she's taken to an entirely new level in her latest melt-down.

After asking her pertinent questions in a friendly way, I ascertained that she was probably urinating excessive amounts of magnesium. See Magnesium and the Brain: The Original Chill Pill.
"Finally, magnesium is sequestered and wasted via the urine in times of stress."
This can create a vicious circle, whereby magnesium deficiency increases anxiety, which further increases stress. ItsTheWoo was complaining that dietary protein was making her too "wired", so I suggested that she increase her magnesium intake, and collect 24 hours of urine for analysis. I didn't even ask her to stick a needle in her arm for a blood test (as serum magnesium means nothing).

You'd think that I'd asked her to sell her mother from the way she carried on, making excuse after excuse to not wee into a 5 Litre container. I'm done with her, now. She obviously isn't interested in finding out the underlying reason why she has to eat a ketogenic diet all the time. She admitted that she's spent 12 years on a ketogenic diet, going from one supplement to the next, when tolerance develops. She's even tried Lithium. She's currently faffing about with a supplement called Kratom.

I'm sticking to Epsom Salts. It's cheap, it works and if you do overdose on it, you get a good run for your money! :-D As magnesium is a substance found naturally in the body, tolerance never develops.

The "Sheeple" part of the title is referring to ItsTheWoo's followers, who are no doubt slagging me off. Number of f*cks given = 0. It's interesting how she's built up a large following of mostly feeble-minded people who can't think for themselves, and who praise her for every post she writes, no matter how incorrect it might be.

I don't blog to be popular. I blog to help people, with accurate & up-to-date information about ways to treat nasty medical conditions that impair people's lives.

Hopefully, my next post will be back to business as usual. There's something big coming, and this time it's got nothing to do with Gluten or A1 Casein!

EDIT: As a result of the 191(!) comments to this post, here are some thought experiments in logic:-

Q1. If Woo's followers don't give a f*ck about me, why post about banning me?
A1. Because Woo is an attention-whore.

Q2. Woo could have shut me up by saying that she'd already had a 24-hour urine test for excessive Mg excretion. She didn't. Why?
A2. Because in 12 years of suffering mental issues, she's never had a had a 24-hour urine test for excessive Mg excretion.

Q3. Woo could have shut me up and shown that she's right and I'm wrong, by taking a 24-hour urine test for excessive Mg excretion. She didn't. Why?
A3. Because she knows that she's wrong and I'm right, because a 24-hour urine test for excessive Mg excretion would show excessive Mg excretion.

Q4. Why does Woo insist that a 24-hour urine test for excessive Mg excretion is worthless (it isn't)?
A4. Because EITHER she's worried that she'll lose her "shtick" of nuttiness and will lose followers (she's playing you for fools in which case she should be avoided), OR she's scared of change (she's mentally ill in which case she should be avoided).

Please discuss the above statements without deflecting onto irrelevancies e.g. my Aspergic tendencies. Yes, I admit that I have Aspergic tendencies. I've also admitted to being a nerd (click Nerds). So shoot me ;-)

Blindly following someone & believing everything that they say without ever verifying facts is dangerous, and can lead to the situation depicted in the picture at the top of this post (Godwin's Law alert). The opposite (total cynicism) is also unhealthy.

People need to do research of their own, or just read my blog, as I've already done loads of research. If your health problem isn't mentioned anywhere in my blog (check the labels first), please email me (there's a disguised email link in my "About me" section) and ask. I love doing research, as I never know what I'm going to discover, and I occasionally stumble across something really important by accident, as my recent posts on Constipation/IHD/Type 1 Diabetes/Schizophrenia/Autism, Hyperinsulinaemia, Age-related Macular Degeneration, Rheumatoid Arthritis & Calcium Shift have shown.

If I've been of help to you, please tell any family members or friends who are suffering from any conditions that are impairing their life. My suggestions must always be checked by someone's GP first, in case of contraindications with other medical conditions or medications that I don't know about. My suggestions must always be used as adjuncts to, NOT replacements for, someone's existing medication(s).

If symptoms improve, people should negotiate with their GP for a reduction in the dose of their medication(s), if their medication(s) has/have undesirable effects (e.g. bad side-effects, or a need for further medications such as PPI's like Omeprazole to reduce stomach acidity when taking NSAID's like Aspirin or Naproxen).

Sunday, 21 September 2014

A "discussion" with Dr. Garth Davis M.D.

I put "discussion" in quotes, for reasons which will become obvious.
The Pyramid of Disagreement. You should be using the top 3 levels at all times.

I've written this because Dr. Davis has blocked me from leaving comments on his Facebook page, and I really need to reply to his last reply to me.

I was acutely aware as an omnivore, of "walking into the lion's den", by posting a dissenting comment on a vegan's thread, but it was necessary as I had evidence of harm of vegan diets. The evidence on Denise Minger's teeth is supported by her own blog. The evidence on Jay Dinshah's fatal heart attack at the age of 66 is supported by a YouTube video by Dr Michael Greger, the vegan M.D. Dr Greger's video showed evidence of other harms caused by vegan diets that were lacking in vegan DHA & Vitamin B12.

EDIT: Dr. Davis has deleted all of my comments. However, he hasn't deleted his replies to them.

It's impossible to prove a hypothesis, even with n=1,000,000, as the 1,000,001th subject could be the "Black Swan" that disproves it. On the other hand, it only takes 1 "Black Swan" to disprove it. Therefore, n=1 evidence of harm is sufficient to disprove a hypothesis that something is harmless. See Falsifiability.

I provided n=2 evidence of harm.

Dr Davis's final comment to me:-
" Nigel Kinbrum really? You are giving me a n of 2. There is no data that vegans teeth fall out. If she was vitamin K deficient then she was eating a crappy diet lacking greens. It so stupid it's just silly. I also laugh at the idea that authority is some how bad. I have written a book with thousands of references. I give lectures on the topic and have treated thousands of patients yet Denise knows more than me. Silly."

My reply:-
1. As stated above, an n of 2 is double the n needed to disprove your hypothesis that there is no evidence of harm for vegan diets. I'd already pointed that out to you in a previous comment that you've since deleted.

2. I said that Denise's teeth were disintegrating. I didn't say that they fell out. That's a strawman fallacy.

3. Greens contain phylloquinone (Vitamin K1), not menatetrenone (Vitamin K2). Only Vitamin K2 carboxylates osteocalcin in MGP's. The only vegan source of Vitamin K2 is Nattō, a.k.a. pungent beans in a snot sauce.

4. See 3. Denise Minger was not eating a "crappy diet". That's an extremely insulting & uninformed comment for a medical professional to make about someone.

5. I never claimed that authority is bad. When you say "I am an expert in "X", therefore I am never wrong about "X".", that's an "Appeal to authority" fallacy. Jeez!

6. See 5. I never claimed that Denise Minger knows more than you. That's another strawman fallacy.

So, there you have it. Comments will only be approved if they meet my Moderation Policy. As long as I am blocked from commenting on Dr. Davis' Facebook page, Dr. Davis is blocked from commenting on my blog.

Saturday, 20 September 2014

Rheumatoid Arthritis: It's the food!

I had an email query about Rheumatoid Arthritis, so off to PubMed I went.

I found Controlled trial of fasting and one-year vegetarian diet in rheumatoid arthritis.

"Fasting is an effective treatment for rheumatoid arthritis, but most patients relapse on reintroduction of food."
This suggests that rheumatoid arthritis (RA) is an ongoing process, triggered by something that's consumed.

"After an initial 7-10 day subtotal fast, they were put on an individually adjusted gluten-free vegan diet for 3.5 months. The food was then gradually changed to a lactovegetarian diet for the remainder of the study."
Are you thinking what I'm thinking? I'm thinking Gliadorphin-7, as per Wheat, Constipation, Ischaemic Heart Disease, Type 1 Diabetes, Schizophrenia and Autism.

This suggests that RA is caused by peptide chains passing through loose "tight junctions" in the gut, triggering an (inappropriate) autoimmune response. For ways to improve gut integrity, see Cow's milk, Schizophrenia and Autism.

BCM-7 can be avoided by drinking A2 milk. Most cheeses are made from A1 milk, so should be avoided. Swiss cheeses like Gruyère and Emmental are probably made from A2 milk, so suck 'em and see.

To reduce inflammation in joints, consuming oily fish may help, as an adjunct to prescribed anti-inflammatory medications.

Continued on Fibromyalgia: It's the food, again! (probably).

Friday, 19 September 2014

Why (LDL particle) size matters.

Having gone through the math(s) with several people, I thought I'd stick it in a blog post for posterity.
This is a diagram of a chylomicron or VLDL-c (high TG/C ratio) 'cos I couldn't find one for LDL-c!

Cholesterol synthesised in the liver is exported in LDL particles. The more cholesterol that's synthesised, the more particles there need to be to carry it.

∴ LDL-P (particle number) ∝ LDL-C (total amount of cholesterol)

The particles are roughly spherical with a very thin wall (consisting of a phospholipid mono-layer, the yellow wiggly lines with a green end bit in the above diagram).

Volume of a sphere = 4/3 * π * r3, where r = half the diameter.

If there's a 10% reduction in LDL particle size, the volume reduces to 0.729, relative to the original size. Therefore, to carry the same amount of cholesterol requires 1/0.729 = 1.37 times more particles, which is a 37% increase in the number of LDL particles, relative to the original size.

∴ LDL-P (particle number) ∝ 1/LDLsize3

As it's LDL particle number that determines the infiltration of LDL cholesterol into the media of artery walls (see image below), it's advisable to keep cholesterol synthesis to a reasonable level by keeping fat intake to a reasonable level (i.e. not Nutritional Ketosis!) and keeping LDL particle size to a reasonable level by keeping added sugar (e.g. sucrose & fructose) intake and rapidly hydrolysed/overcooked starches (e.g. amylopectin & maltodextrin) intake to a reasonable level (i.e. a level that's oxidised by the body without having a chronic excess). An acute excess of carbohydrate can be stored as liver/muscle glycogen, provided that mean carbohydrate intake is less than mean carbohydrate oxidation.

How COULD I write a post about LDL-P and forget to include THIS?

Friday, 12 September 2014

Neovascularization/Neovascularisation: It doesn't ONLY cause CHD.

Another serendipitous moment.
After talking to someone with Age-related Macular Degeneration (AMD), I Googled the condition and spotted the word neovascularisation. This reminded me of Neovascularization of coronary tunica intima (DIT) is the cause of coronary atherosclerosis. Lipoproteins invade coronary intima via neovascularization from adventitial vasa vasorum, but not from the arterial lumen: a hypothesis.

So I did a search on PubMed for Neovascularization/Neovascularisation. This is what I got:-,%20pathologic%22[MeSH%20Terms]%20OR%20%28%22neovascularization%22[All%20Fields]%20AND%20%22pathologic%22[All%20Fields]%29%20OR%20%22pathologic%20neovascularization%22[All%20Fields]%20OR%20%22neovascularization%22[All%20Fields]%29%20OR%20%28%22neovascularization,%20pathologic%22[MeSH%20Terms]%20OR%20%28%22neovascularization%22[All%20Fields]%20AND%20%22pathologic%22[All%20Fields]%29%20OR%20%22pathologic%20neovascularization%22[All%20Fields]%20OR%20%22neovascularisation%22[All%20Fields]%29%29%20AND%20%28%28hasabstract[text]%20AND%20%22loattrfree%20full%20text%22[sb]%29%20AND%20%222009/09/14%22[PDAT]%20:%20%222014/09/12%22[PDAT]%20AND%20%22humans%22[MeSH%20Terms]%29%20AND%20%28hasabstract[text]%20AND%20%22loattrfree%20full%20text%22[sb]%29%20AND%20%222009/09/14%22[PDAT]%20:%20%222014/09/12%22[PDAT]%20AND%20%22humans%22[MeSH%20Terms]%20AND%20%28%28hasabstract[text]%20AND%20%22loattrfree%20full%20text%22[sb]%29%20AND%20%222009/09/14%22[PDAT]%20:%20%222014/09/12%22[PDAT]%20AND%20%22humans%22[MeSH%20Terms]%29%20AND%20%28%28hasabstract[text]%20AND%20%22loattrfree%20full%20text%22[sb]%29%20AND%20%222009/09/14%22[PDAT]%20:%20%222014/09/12%22[PDAT]%20AND%20%22humans%22[MeSH%20Terms]%29%20AND%20%28%28hasabstract[text]%20AND%20%22loattrfree%20full%20text%22[sb]%29%20AND%20%222009/09/14%22[PDat]%20:%20%222014/09/12%22[PDat]%20AND%20%22humans%22[MeSH%20Terms]%29

Even after restricting results, there were 5253 results. Wow!

It would appear that AMD has a lot in common with CHD. Ischaemia/Ischemia (lack of oxygen) to tissues causes the body to produce an adaptive response by growing new blood vessels (neovascularization/neovascularisation). Unfortunately, the new blood vessels are a bit crap, and cause other problems to develop e.g. CHD & AMD.

Therefore, prevention is better than cure. The things that lower the RR for CHD may also lower the RR for AMD. See Cholesterol And Coronary Heart Disease.

Saturday, 6 September 2014

Another penny drops: Why severe hyperinsulinamia can occur with a small increase in exogenous carbohydrate intake.

This blog post is a result of Vim's comments in the previous blog post. A penny suddenly dropped!

Insulin has a Chalonic (inhibitory) action on blood glucose level (via the liver, muscle mass & fat mass), blood FFA level (via fat mass) and blood ketone body level (via the liver).

As mentioned in the comments, GHB has a stimulant effect - up to a certain level of blood GHB. Beyond that level, there's a powerful sedative effect. This is because at low levels of exogenous ketone body input, insulin secretion increases slightly to reduce hepatic ketogenesis.

At a certain level of exogenous ketone body input, hepatic ketogenesis falls to zero and cannot be reduced any further. Any slight increase beyond this point in exogenous ketone body input, results in a large increase in insulin secretion, as the pancreas increases Ketone body-Stimulated Insulin Secretion to maximum in a (failed) attempt to reduce blood ketone body level.

Exactly the same thing happens with exogenous carbohydrate or BHB input.

At a certain level of exogenous carbohydrate input, hepatic glucogenesis falls to zero and cannot be reduced any further. Any slight increase beyond this point in exogenous carbohydrate input, results in a large increase in insulin secretion, as the pancreas increases Glucose-Stimulated Insulin Secretion to maximum in a (failed) attempt to reduce blood glucose level.

Fun with maths: How many grams of "X" does it take to achieve "Y" mmol/L of "X" in the blood?

There are ≤3 fuels in blood - Glucose, Palmitic acid (FFA) & Beta-HydroxyButyric acid (Ketone body).

Taking blood volume as 5L (a petite woman has less):-

5mmol/L of Glucose ≡ 4.5g of Glucose.

1mmol/L of Palmitic acid ≡ 1.28g of Palmitic acid.

6mmol/L of Beta-HydroxyButyric acid ≡ 3.12g of Beta-HydroxyButyric acid.

Instead of going on a ketogenic diet (with all of the health hazards associated with it), why not just add Beta-HydroxyButyric acid to your drinks?

There's a problem. All metabolic fuels produce an insulin response (from functioning pancreatic beta cells) - this is one of the ways the level of each fuel is regulated in a NFB loop. Therefore, drinking more than 3.12g of BHB (more than 2.76mL) produces a large insulin response, which results in sleepiness. Ditto for GHB.

Friday, 5 September 2014

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

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

Hat-tip to James Beckerman, MD for, which refers to Comparison of Named Diet Programs Finds Little Difference in Weight Loss Outcomes.

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

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

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

Tuesday, 2 September 2014

When good science goes bad, part n+1.

In When good science goes bad , I looked at the effect of funding bias on research.

Effects of Low-Carbohydrate and Low-Fat Diets: A Randomized Trial has just been published. As expected, low-carbers are positively creaming themselves over it. I instantly smelled a rat, as the full study was behind a pay-wall.

Remembering Krauss' shenanigans with "carbohydrate", consisting of 50% sugars + 50% "complex" carbs (maltodextrin & amylopectin are complex carbs that hydrolyse into glucose so rapidly that they have a GI of 100 on the "Glucose=100" scale.), I suspected dodgy carbs in the "Low-fat" group.

Luckily, David L. Katz, MD, MPH, FACPM, FACP had read the full study, and wrote about it in Diet Research, Stuck in the Stone Age.

As I suspected, it was another "fix-up" job, rigged to make low-carb diets look good, and low-fat diets look bad.

See also:-
Low-carbohydrate vs. Low-fat diets for Weight Loss: New Evidence,
What I Learned By Actually Reading That Low-Carb Is Best Study,
Is low-carb really the best weight loss diet? and
A Question about the latest diet study ...

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!