Rheumatoid Arthritis: It's the food!

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

From http://www.webmd.com/rheumatoid-arthritis/ss/slideshow-ra-overview

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).

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?

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

Another serendipitous moment.

From http://www.aao.org/theeyeshaveit/optic-fundus/retinal-neovascularization.cfm

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:-
http://www.ncbi.nlm.nih.gov/pubmed/?term=%28%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%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.

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!

From http://bja.oxfordjournals.org/content/85/1/69.full

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).

From http://www.medbio.info/horn/time%203-4/homeostasis1.htm#Sources%20of%20blood%20glucose:

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.

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

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

From http://covermyfb.com/covers/27316/say%2Csee+and+hear+no+evil

Hat-tip to James Beckerman, MD for https://twitter.com/jamesbeckerman/status/507544419847786496, 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!
 

When good science goes bad, part n+1.

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

From https://www.youtube.com/watch?v=sJ5jbxMjexo

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 ...