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. Cheese is probably made from A1 milk, so should be avoided.

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

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.
I know that this is a diagram of a chylomicron, but bear with me!

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, it's advisable to keep cholesterol synthesis to a minimum by keeping fat intake to a reasonable level * (i.e. not Nutritional Ketosis level) and keeping LDL particle size to a maximum by keeping sugars & fast starches intake to a reasonable level*.

Before someone asks, what I mean by a reasonable level is a level that is burned by the body without having a chronic excess. An acute excess can be stored, provided that mean intake is less than mean burning.
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 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)."

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 the wrong milk proteins can do a lot of damage. Human breast milk is naturally A2.

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.

See also Physiology and Immunology of Digestion.

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.

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, 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!

Hat-tip to Melissa McEwen for

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!