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Tuesday, 24 November 2015

My rant about David Katz's double identity and the meaning of consensus.

(I posted the first part of this rant on this RetractionWatch post but the moderator seems to have decided that it doesn't meet their policy. Fair enough as I find it hard to be restrained about such nonsense.)

I don’t care that David Katz wrote the fake review. Fiction about fiction, all very meta.
What I do care about is the Big Lie he repeats in his defenses – that those criticizing the dietary guidelines and the DGAC process “are the very group employing every means at their disposal to scuttle dietary guidance dedicated to public (and planetary) health to serve their own pecuniary interests”.
This is the paranoid underside to the grandiose self-image that Katz displayed in the reviews. Those critiquing the guidelines have few pecuniary interests and I would be surprised if any of them are as wealthy as Dr Katz. That Dr Katz sees fit to call them for “want of qualifications” begs a question – why is it that PHD students, engineers, psychologists, cell biologists, hard-working journalists, and auto-didacts can see and point-out glaring omissions and bias in the way the DGAC selects and interprets evidence, yet someone like Dr Katz, with enough letters after his name to write another novel, refuses to see them? (Indeed, why, with all these qualifications, did Dr Katz get involved with pseudocience in his practice?).
Katz, the CSPI, and the DGAC committee themselves have brought great guns to bear to find a few minor inaccuracies in Nina Teicholz’ long analysis, none of which seem to affect the conclusions. Yet nowhere do we see them addressing the countless accuracies, which surely need to be addressed if the DGAC is to recover its credibility.
Whatever the DGAC may end up recommending in the near future, it will be different from what they currently recommend, meaning that the current recommendations are not supported by current science. If the science is this labile, why were such far-reaching recommendations being made at all? Why not stick to the basics of nutrition – eat foods rich in vitamins and minerals, not refined foods – get enough protein and essential fats, preferably from natural protein-and-fat foods rather than refined foods or grains – and be aware that diabetes and obesity usually indicate an intolerance to carbohydrates, especially refined ones. These are choices that will improve or maintain health in the present. Theories about what will reduce this or that disease at the end of our lives, based on interventions that do not reduce mortality, should never have been allowed to distort nutritional advice.
Nor should unproven theories about what is best for the planet. Someone who wants what is best for the planet won’t tell us to remove the fat from meat and not cook with animal fat – this advice wastes most of the energy produced by raising animals, which then needs to be replaced with energy derived from growing additional plants. In the case of the unsaturated fat energy these experts are so keen on, these nutritionally unnecessary plants need to be processed in an environmentally damaging and industrially hazardous way.
This inane suggestion comes from people who claim to be dedicated to planetary health (another grandiose Sci Fi claim when you think about it). Surely it would be better to leave the effect of diet on planetary health aside until it can be addressed by someone with more information, better sense, and no other axe to grind.

This is why I do not accept the notion of consensus peddled by Katz, Hu, Willett and others after their recent Oldways celebration. It fails to address any of the inconsistencies in the advice given by most of the attendees. In the case of Paleo expert Boyd Eaton's presentation, it is plainly compromise rather than consensus that is being offered. No doubt this is the price Paleo needs to pay to enter the elite plant-based bullshit club, but the idea of "fat-free" dairy replacing whole meat in a future-paleo menu suggests the price is too high, and not even consonant with mainstream nutritional research in the present day.

Perhaps what sticks in the craw most is the call for the media to avoid reporting research with fear-mongering headlines that contradict each other. This is priceless when one of the signatories is Walter Willett, who feeds this stuff to media outlets verbatim.
But not always.

It is really the question of context that bedevils compromise consensus. However you interpret the evidence for phytochemicals, there are people who don't tolerate plants all that well but have no problem with meat. You may think that it's the saturated fat in pizza that makes it artery-clogging, but saturated fat seems to make no difference to metabolic profiles when carbs are restricted (if anything, it makes them non-significantly better). And when you're supplying advice to a population with a high rate of carbohydrate intolerance, you need to take the relative metabolic superiority of fat into account, yet there was no-one at Oldways speaking for LCHF. Saturated fat and whole-grains are the shibboleths, and you still can't enter the hallowed precincts if you can't pronounce their "artery-clogging" and "healthy" prefixes. 

I'm sure there is plenty of room for agreement between all of us - absolutely no-one here thinks that commercially processed food, frequent deep-frying, and a high content of added sugars are a good idea. But people need to eat, and used to cook meals based on meat, eggs, animal fats, and dairy which were easy to prepare using knowledge handed down in families. A media campaign that painted those foods as killers for decades is one factor behind a tragic and damaging decline in basic cooking abillity and increased reliance on a well-and-truly depraved food industry. Industry can place products with added fibre or low in saturated fat as "healthy" with the backing of epidemiological nutritionists, and sell the alternatives as "treats" which are fine in moderation as part of a balanced diet according to the dietitians. With what results we see.

And, seriously, you want to fix this by feeding Americans (and by extension, the English-speaking world) a watered-down but still costly Mediterranean diet, when there are other foods their grandparents ate which will do the job equally as well?

Everyone in nutrition is influenced, more-or-less unscientifically, by their own dietary choices or those of their culture. On the one hand we have a clique of mandarins who were "born on second base and think that they've hit a home run" with regard to diet and metabolic health. On the other hand we have people such as Tim Noakes, on trial for his opinions as I write, who have overcome metabolic disadvantages with the help of diets that have included the prohibited elements. By any objective test, the second narrative should be the more convincing, but perhaps not in a society that worships unearned success. It is obvious enough that the selection and appreciation of evidence in the DGAC process is distorted by unthinking acceptance of the first narrative. We owe a real debt to Nina Teicholz for bringing this out to be debated in the public domain.

What is the right thing to do when this happens? To blame it on "t
he very group employing every means at their disposal to scuttle dietary guidance dedicated to public (and planetary) health to serve their own pecuniary interests”? To call in the sponsors, circle the wagons, and manufacture consensus for the media? 

Or to hold a full and frank investigation into the reasons for the debacle, one which includes the evidence gathered by those who don't think your conduct of operations has met a satisfactory standard?

Tuesday, 3 November 2015

Medium Chain Fatty Acids and Brain Metabolism

This post relates in some way to each of the three previous posts.

The definition of MCFA is a little unclear. Wikipedia lists lauric acid as a MCFA, making the range C:6-12, whereas commercial MCTs are almost completely made from C:8 and C:10, as C:6 is not available in any significant amount from coconut oil, and about 32% of lauric acid is not deposited into to the hepatic portal vein, whereas the totality of shorter chain MCFAs is. It is likely that both lauric and myristic (C:14) acids exist in a grey zone where they have partial MCFA properties. It is also relevant that triglycerides that contain longer chain fatty acids are hydrolysed more slowly and a rapid rate of hydrolysis in the gut is one of the properties desired of MCTs.

In a previous post I wrote about a case study where a ketogenic diet prevented symptomatic hypoglycaemia in a child with hyperinsulinism. I wrote at the time that this was as close as we would get to a proof that slightly elevated ketone levels due to carbohydrate restriction are protective against symptomatic hypoglycaemia in people with type 1 diabetes treated with insulin.
I was wrong - there has been a human trial of the concept, using MCT oil.[1]

In this study "A total of 11 intensively treated type 1 diabetic subjects participated in stepped hyperinsulinemic- (2 mU · kg−1 · min−1) euglycemic- (glucose ∼5.5 mmol/l) hypoglycemic (glucose ∼2.8 mmol/l) clamp studies. During two separate sessions, they randomly received either medium-chain triglycerides or placebo drinks and performed a battery of cognitive tests."

"During the medium-chain triglycerides session, a total of 40 g of medium-chain triglycerides (derived from coconut oil containing 67% octanoate, 27% decanaote, and 6% other fatty acids; Novartis) was ingested at 25-min intervals with front loading of 20 g then 10 g twice. During the control session, cherry-flavored water sweetened with sucralose was ingested at identical time intervals."
The beta-hydroxybutyrate level attained 40 minutes after the MCT drinks was about 3.4 mmol/l.

"We conclude that ingestion of medium-chain triglycerides improves cognitive function without affecting the adrenergic hormonal or symptomatic responses to acute hypoglycemia in intensively controlled type 1 diabetic patients. These findings suggest that medium-chain triglycerides could be used as prophylactic therapy for such patients with the goal of preserving brain function during hypoglycemic episodes, such as when driving or sleeping, without producing hyperglycemia."

BOHB levels for MCT vs Placebo in insulin-induced hypoglycaemia after overnight fast, down arrows = 20g, 10g, 10g MCT or placebo drinks. 100 umol/l = 0.96 mmol/l.

There was another interesting aspect of this experiment.

"In vitro rat hippocampal slice preparations were used to assess the ability of β-hydroxybutyrate and octanoate to support neuronal activity when glucose levels are reduced."

The reason for this is, that the authors wanted to be sure whether the protective effects of MCT oil were due to the brain using ketone bodies or due to the brain's use of MCFAs. It turns out that the MCFAs used in MCTs can cross the blood-brain barrier and be used in brain metabolism. In another rat paper, "We found that oxidation of 13C-octanoate [C:8] in brain is avid and contributes approximately 20% to total brain oxidative energy production."[2]

The C:8 is mainly being oxidised by astrocytes. If this happens in a hypoglycaemic brain, it's possible that due to lack of oxaloacetate ketone bodies will be produced, which can be used by the neurons.

What I really want to know is how coconut oil compares to MCT oil as a means to elevate serum ketone bodies. I suspect that ketone elevation from coconut oil has a slower onset and is more protracted due to the slower rate of hydrolysis of MCFAs from triglycerides with some longer-chain fatty acids, and if so this "time release" effect could be beneficial during sleep.

There is only one study I can find online which shows ketone levels after feeding coconut oil, and this is Mary Newport's n=1 experiment.[powerpoint here]

I don't know what to make of this, beyond the expected drop in glucose (due to insulin response to lauric acid - this wouldn't apply in type 1 diabetes); the levels, though elevated by both interventions, are still within the reference range (and very different from those in the diabetes paper), unless I'm reading the measurements wrong, and the time scale with coconut oil stops short. I'd like to see many more comparisons like this, with higher doses, in healthy volunteers. The coconut oil industry and coconut oil aficionados have been accused of extrapolating from MCT studies in the absence of evidence about coconut oil, for example by the Heart Foundation of New Zealand here. While I don't think it's justifiable to ignore animal studies of coconut oil, which tell us that coconut oil protects the liver and pancreas from chemical injury, totally consistent with the MCT research, I don't see why the coconut oil industry can't fund proper comparative studies of ketogenesis in humans, which would not be at all expensive.

A 1982 review of medium chain triglycerides stated that "MCTs are ketogenic in the normal subject

and even more in the patient with hyperosmolar diabetic syndrome (117). Hence, MCTs should not be given to patients with diabetes. They should also not be given to patients with ketosis or acidosis."[3]
Whilst no-one would treat diabetic ketoacidosis with MCTs, the statement "MCTs should not be given to patients with diabetes" is unfounded. People with type 2 diabetes, due to hyperinsulinaemia, are not at an increased risk of diabetic ketoacidosis*, and the experiment I posted above shows that those with intensively controlled type 1 diabetes may benefit from their use. The reference (117) which is the only reference in this section is a rat experiment; the hyperosmolar diabetic syndrome described is high glucose with normal ketones, not DKA.
A 2010 review cites several reports that "suggest that MCFAs/MCTs offer the therapeutic advantage of preserving insulin sensitivity in animal models and patients with type 2 diabetes".[4]

This is consistent with the Malmö Diet and Cancer study epidemiology I posted here. Which implies that even the small amounts of MCFAs in foods such as coconut and dairy are beneficial for maintaining metabolic homeostasis at a population level.

*Edit: thanks to Carol Loffelman for reminding me of this - type 2 diabetes is a risk factor for ketoacidosis if it's being treated with a SLGT2 inhibitor. See this link, but there are many cases of ketoacidosis on SLGT2 inhibitors where a low carb diet is not involved. I have looked for case studies of ketoacidosis in diabetic patients that were triggered by carbohydrate restriction or MCTs without SLGT2 administration and have not yet found one.
This is a case study of DKA in a woman with decompensated T2D [link] where there is not enough insulin to prevent it. There's no low carb diet or SGLT2i involvement, and my expectation is that a normal calorie very low carbohydrate diet would most likely have prevented the syndrome in this patient as it did in the patients of Newburgh and Marsh back in the day.

[1] Page KA, Williamson A, Yu N et al. Medium-Chain Fatty Acids Improve Cognitive Function in Intensively Treated Type 1 Diabetic Patients and Support In Vitro Synaptic Transmission During Acute Hypoglycemia. Diabetes. 2009 May; 58(5): 1237–1244

[2] Ebert D, Haller RG, Walton ME. Energy contribution of octanoate to intact rat brain metabolism measured by 13C nuclear magnetic resonance spectroscopy. J Neurosci. 2003 Jul 2;23(13):5928-35.

[3] Bach AC, Babayan VK. Medium-chain triglycerides: an update. Am J Clin Nutr. 1982 Nov;36(5):950-62.

[4] Nagao K, Yanagita T. Medium-chain fatty acids: functional lipids for the prevention and treatment of the metabolic syndrome.  Pharmacol Res. 2010 Mar;61(3):208-12. doi: 10.1016/j.phrs.2009.11.007. Epub 2009 Nov 30.