The Maned Wolf - a lesson in deductive dentition

This is a South American canid, the Maned Wolf.



This "dog" is a true omnivore, not unlike homo sapiens. It supplements a diet of meat (frogs, fish, lizards and other small game) with fruit, tubers, and sugarcane. These supply up to 51% of its diet. It does not do well in captivity without vegetable foods, In the wild it is susceptible to infestation by the Giant Kidney Worm (Dioctophyme renale), a potentially lethal roundworm it is exposed to by eating fish. It prefers the fruit of the Wolf Apple (Solanum lycocarpum) or lobeira, a tomato like fruit (also related to the Goji or Wolfberry) which is believed to protect it against this parasite (1).
Cindy Engel writes in Wild Health (a 2002 book which is recommended reading for anyone interested in Ancestral Health):
"Although this fruit is more plentiful in certain seasons, the wolf works hard to eat a certain amount throughout the year... researchers at the Brasilia zoo found that when packs of captive wolves were fed lobeira daily, they survived. If lobeira was withheld, all the wolves died. Postmortem examinations revealed giant kidney worm infestations, and it was suspected that lobeira might be controlling these worms in the surviving wolves".
The Maned Wolf also seems unusually susceptible to cancers in captivity (2)

Whether or not the maned wolf is self-medicating, we can learn a lot by looking at its teeth:
Teeth adapted, as the Maned Wolf is, to a diet that can be 51% plant based.

Let us compare that with the dentition of Homo Sapiens, a creature adapted to eating a diet similar to that of the Maned Wolf, with, on average, a broadly similar split between animal and plant foods:



We can clearly see that the dentition of a species need not be specific for its adapted diet. The Maned Wolf finds animals hard to catch and kill; it is not going to lose its carnivorous dentition because it eats fruit (although too much indulgence in the sugar cane could conceivably have that effect in individuals). The ancestral savannah-dwelling hominid, perhaps a former insectivore and fruitarian, finding itself "tuskless in Eden" in Robert Ardrey's evocative words from African Genesis, survived by developing tools that do the work the Maned Wolf's incisors do. Humans have not needed to trade away teeth that are useful for gripping the ends of the cords used to tie spearheads onto shafts, as well as for crushing seeds and roots. We can chop and stab and saw where the Maned Wolf can only tug and gnaw. The leg joints of quadraped mammalian carnivores are well designed for maximum force in tugging as well as speed in leaping and running.

Man is neither of these things (below), but it's fair to say that for quite a few aeons now he has had more in common with the dog than with the sheep. Especially if that dog is the Maned Wolf.


For comparison, the dentition of a Kangaroo, a marsupial herbivore which has evolved separately from the sheep:


This is the Maned Wolf's closest living relative, the Bush Dog, in flagrante delicto. This tough and gregarious 5-8 Kg canid can hunt the 40 Kg peccary, and a pack has been seen hunting a 250 Kg tapir.
It seems to be a wholly carnivorous creature. 



The legs of the Bush Dog are adapted for strength in tugging at its larger prey, whereas those of the Maned Wolf are more suited for leaping on the small, swift creatures that make up its animal diet.

(1) Conservation of the Maned Wolf: fruitful relationships in a changing environment
Orin Courtenay, Canid News 1994
(2) High Incidence of Ovarian Tumours in Maned Wolves (Chrysocyon  Brachyurus) at the National Zoological Park, Munson 1991

What is a Maori Ancestral Diet?

Grant Schofield, Professor of Public Health at AUT, has done brilliant work bringing LCHF science to the mainstream media in New Zealand. To someone like myself, who enjoys science best when the most cautious and rigorous approach delivers the most revolutionary findings, Prof Schofield's approach to publicity has been exemplary. I missed the interview where he said the LCHF approach would be best for Maori, but caught the response of Maori health provider Toi Tangata:

A public health specialist says Maori should go back to a pre-European diet to stop chronic diseases such as diabetes and cancer - advice disputed by a Maori health organisation.

Auckland University of Technology Professor of Public Health Grant Schofield believes Maori should revert to a diet that debunks a founding pillar of modern nutrition: that a healthy diet is low in fat.

"What Maori ate before Pakeha turned up was most likely a diet that was highish in fat, moderate in protein and relatively low in carbohydrate, and that's true across the whole Pacific region. And you can go and study people who are still eating that way, who are more or less disease free."

His diet plan has been met with a warning from Toi Tangata, a national Maori health provider, which says there's insufficient research to support it and goes on to call the suggestion "faddish and strange".

The health provider's nutritionist, Mason Ngawhika, says Maori could get dangerous mixed messages and think it's okay to eat large quantities of fatty foods without the required balance of fruit and vegetables.

He says the diet plan is too expensive for low-income Maori and such a large diet overhaul would result in too much willpower being required, ending with what nutritionists call the "what-the-hell-effect".

Despite its concerns, Toi Tangata says the diet could have benefits for people who have, or could develop, diabetes.

This response is not the ringing put-down it might seem at first. The last paragraph makes it obvious that Mason Ngawhika knows enough about LCHF diets for diabetes to accept the evidence for their effectiveness, and diabetic and pre-diabetic are descriptions that include a larger proportion of Maori than of Pakeha. For example, here Maori have many times the rate of diabetes complications compared to non-Maori.

Population rates of renal failure with concurrent diabetes (aged 15+) were over eight-and-a-half times higher in Māori compared with non-Māori (RR 8.78, CI 7.88–9.79). Because the self-reported prevalence of diabetes is similar for Māori and non-Māori, the significantly higher rate of renal failure with concurrent diabetes would suggest that, among people with diabetes, Māori may be up to 8.8 times more likely than non-Māori to go on to develop renal failure (one of the complications of diabetes).

Similarly, population rates of lower limb amputation with concurrent diabetes were over four-and-a-half times higher for Māori compared with non-Māori (RR 4.70, CI 4.01–5.52). Therefore, among people with diabetes, lower limb amputations for Māori can be estimated as being up to 4.7 times more likely than for non-Māori.

Research into, and evidence for LCHF is accruing all the time; more importantly, its acceptance is no longer automatically blocked or ignored, the public increasingly expects it to be addressed properly, like the results of any valid science about the important subject of health.

The objections made by Mason Ngawika to Ancestral-type LCHF diets for Maori can also be seen as reasoned, and deserving of response.

The cost of any new diet is an issue for low-income earners, and adherence to dietary changes - especially those made by people acting for themselves - as well as perceptions of "strangeness" may be significant barriers in the context of Maori family life, where the generous sharing of kai (food) is tikanga (custom).

The concern about mixed messages around what are perceived fatty foods is also valid; we don't want to be giving deep-fried food the OK, and some people will always hear what they would like to hear from any message. Then, you just try changing their minds - you'll be accused of changing yours.

So there are significant obstacles against getting the right message across.

Here is a presentation which NZ Paleo nutritionist Julianne Taylor made to a Maori organisation last year on the benefits of ancestral diets.

We can run into a problem prescribing LCHF to Maori as ancestral; New Zealand had no native land mammals, so Maori, as Maori, cannot have eaten relatives of pig, sheep, cows, goats or deer. Coconuts, olives, avocadoes and other fatty fruits did not grow here.
Seal are protected and Moa are extinct; so should a modern equivalent of an ancestral Maori diet be based on chicken, fish and shellfish?

Well, no. The most current reliable evidence strongly indicates that initial settlement of New Zealand occurred around 1280CE at the end of the medieval warm period.

(That's a long way to go to some place that hasn't been discovered yet and be successful in it. Vikings and Conquistadors could learn a thing or two.)

The ancestors of New Zealand Maori probably left coastal Asia around 4,000 years ago, well within the Neolithic period. Therefore, in terms of evolutionary adaptation the foods of coastal Asia and the Asian and Melanesian archipelagos are fully ancestral for Maori, and this includes pigs, deer, and buffalo (i.e. land mammals, including ruminant species). Coconut too.

When Europeans arrived in New Zealand, six introduced cultigens (cultivated plants that have no known wild ancestor) were being grown by Māori. They were:

• kūmara (sweet potato, Ipomoea batatas)
• hue (bottle gourd, Lagenaria siceraria)
• aute (paper mulberry, Broussonetia papyrifera)
• taro (Colocasia esulenta)
• uwhi (yam, Dioscorea species)
• tī pore (Pacific cabbage tree, Cordyline fruticosa).

The history book I read a while ago stated that Kumara, the main starch staple of Maori, was brought by later waka (large outrigger canoes used in oceanic migrations), giving the new arrivals ascendancy over the earlier settlers (Archaic or Moa Hunter), whose main food sources were becoming rare or extinct. I imagine all such claims are up for rebuttal, but it seems to me that only a people desperately short of food would consume bracken roots (aruhe - PDF). Most of the cultigens only grew well in Northland and the Bay of Plenty, yet Maori inhabited, or explored and exploited for its resources of food and craft materials, the whole length of New Zealand, including some offshore island groups. The use of bracken root, by both early Maori and my own Hibernean ancestors, illustrates to me that the need for starchy or sweet food is innate to most peoples, and that sources of carbohydrate in prehistory were often so poor that their caloric contribution to the diet cannot have been great, yet they were still prepared and eaten at considerable effort and some risk. Eating a high-fat diet from giant Moa would have been an easier proposition than eating a high-carb diet from bracken root. ("The British Royal Horticultural Society recommends against consumption of bracken either by humans or livestock, since it contains carcinogens linked with oesophageal and stomach cancer": probably not "safe starches" then.)

I'm not an expert in Maoritanga or in the foods of South-East Asia, but it seems to me that expanding our concept of Maori ancestral diet in this way will make it a lot easier to construct an affordable ancestral diet for modern urban Maori. I mean, that's something that's already being done, no need for my input there, but this expanded ancestral concept may make it easier to explain what's being done and is working already to uninformed skeptics of the Paleo method.

Starches in the form of kumara, and some sugars from berries and cabbage tree (a slightly nauseating, earthy-tasting, but satisfyingly sweet concoction) were definitely important to Maori, and one would restrict them, not because they are not ancestral, they plainly are, but because carbohydrate restriction is a medical solution for problems that ail Maori. Where these problems do not exist, or have been successfully resolved by carbohydrate restriction, traditional types of starches should not be a problem.
What ancestral Maori couldn't have eaten - grains. Interestingly in The Native Diet TV series on Maori TV, which experimented with Paleo diet and Crossfit training for urban Maori families (Julianne Taylor was a consultant for this enjoyable show), paraora (bread) was the food that participants found the hardest to go without - not alcohol, not sugar. This should give food for thought to dietary reformers of all stripes. 

Usually I write these blog posts, even the long ones, in one session. So far this post has occupied three days, and I could spend longer at it, but really it's just a bookmark for some ideas. 
Here is a traditional Maori recipe I often make myself, made with a minimum of ingredients, but a satisfying and nutritious meal nonetheless:

Boil-Up.

Take enough meat, bone in (a pork hock is good, beware of bacon hock which is too salty; pork chops work, a bit of lamb or beef would work but I haven't tried these). Cover with water, salt and boil it till tender (i.e. the meat begins to come away easily). Then add kumara (peeled, whole or big chucks), add whole small potatoes if you have kids to feed (you can separate these easily when serving), and half a cabbage in big pieces. Boil till the kumara is done and add chopped watercress. Serve when the potato and watercress is cooked.

(alternately, use this proper recipe!)

Metformin's unusual mechanisms - Lower Carb and Pro-Prebiotic

Metformin is generally considered to be a drug with few vices, so I was intrigued to read some tweets a while back that mentioned GI upsets in patients. Wikipedia lists these:

"The most common adverse effect of metformin is gastrointestinal irritation, including diarrhea, cramps, nausea, vomiting and increased flatulence; metformin is more commonly associated with gastrointestinal side effects than most other antidiabetic drugs. Gastrointestinal upset is most common when metformin is first administered, or when the dose is increased. The discomfort can often be avoided by beginning at a low dose (1 to 1.7 grams per day) and increasing the dose gradually. Gastrointestinal upset after prolonged, steady use is less common."

These are side effects one associates with fibre, especially of the FODMAPs type. It occurred to me that if metformin was inhibiting the uptake of dietary carbohydrate this could account for the effect, as sugars would then became more available to gut bacteria, the population of which would tend to regain balance over time (as potato experimenters have recently reported on the resistant starch kick).
The science is conflicting on this, but most papers seem to find some reduction in glucose absorption, e.g.  "The results suggest that metformin decreases intestinal glucose absorption in a dose-dependent manner by effects on mucosal and serosal glucose transfer."This raises the possibility that some of Metformin's effects are produced through carbohydrate restriction, and others through increased butyrate production, as well as any localised effects on cells. Both Metformin and butyrate activate AMPK and protein-kinase A.

This is a simple explanation; I ran it past Silvia Price, who unlike me has extensive clinical experience with Metformin, and she turned up a stunning twist on the theory.
Metformin isn't feeding glucose to the microbiotia directly; it is stimulating the intestinal goblet cells to increase and to produce more mucus. Microbiota, specifically Akkermansia Muciniphila, then harvest sugars from the mucus.

An increase in the Akkermansia spp. population induced by metformin treatment improves glucose homeostasis in diet-induced obese mice

Abstract

Background Recent evidence indicates that the composition of the gut microbiota contributes to the development of metabolic disorders by affecting the physiology and metabolism of the host. Metformin is one of the most widely prescribed type 2 diabetes (T2D) therapeutic agents.

Objective To determine whether the antidiabetic effect of metformin is related to alterations of intestinal microbial composition.

Design C57BL/6 mice, fed either a normal-chow diet or a high-fat diet (HFD), were treated with metformin for 6 weeks. The effect of metformin on the composition of the gut microbiota was assessed by analysing 16S rRNA gene sequences with 454 pyrosequencing. Adipose tissue inflammation was examined by flow cytometric analysis of the immune cells present in visceral adipose tissue (VAT).

Results Metformin treatment significantly improved the glycaemic profile of HFD-fed mice. HFD-fed mice treated with metformin showed a higher abundance of the mucin-degrading bacterium Akkermansia than HFD-fed control mice. In addition, the number of mucin-producing goblet cells was significantly increased by metformin treatment (p 0.0001). Oral administration of Akkermansia muciniphila to HFD-fed mice without metformin significantly enhanced glucose tolerance and attenuated adipose tissue inflammation by inducing Foxp3 regulatory T cells (Tregs) in the VAT.

Conclusions Modulation of the gut microbiota (by an increase in the Akkermansia spp. population) may contribute to the antidiabetic effects of metformin, thereby providing a new mechanism for the therapeutic effect of metformin in patients with T2D. This suggests that pharmacological manipulation of the gut microbiota in favour of Akkermansia may be a potential treatment for T2D.

Comment on another "high-fat diet-induced obese mouse" study:

i. Obesity is associated with a decrease in the abundance of Akkermansia muciniphila in gut microbiota.

ii. Akkermansia muciniphila is able to cross-talk with the intestinal epithelium to control gut barrier functions in the pathophysiology of obesity. We show for the first time that obesity is associated with a decrease in the mucus layer thickness recovering epithelial cells. Interestingly, Akkermansia muciniphila is the dominant human bacterium that abundantly colonizes this nutrient-rich environment. We found that living Akkermansia muciniphila was able to control mucus layer production by the host and restore mucus layer thickness in high-fat diet-induced obese mice thereby reducing gut permeability.

iii. Akkermansia muciniphila decreases lipid storage and increases lipid oxidation in high-fat diet obese mice.

iv. Akkermansia muciniphila counteracts inflammation associated to obesity.
v. Akkermansia muciniphila controls high-fat diet-induced obesity and type-2 diabetes. 

Goblet cells. Not at all clear what's going on here, chosen for the nice colours.

    

I wonder if the missing glucose, when and if it does go missing, is being used as the substrate for mucopolysaccharide synthesis by the enhanced goblet cells. I also wonder if it is wise to give Metformin with antibiotics, and whether this increases the risk of Clostridium or Salmonella infection - or indeed, decreases it.

[Goblet] cells that line the gut extrude long chains consisting of exotic and familiar sugars linked together and known by a catch-all term: mucus. This homely product serves two valuable functions. First, by coating the inside intestinal wall, mucus forms a reasonably impervious protective barrier to keep the resident microbes, which serve useful purposes inside the gastrointestinal tract, from getting out of the gut and into the bloodstream, where they could be lethal. But the mucus has a second function as well: It gives our resident microbes a guaranteed source of various sugars, like sialic acid and fucose, that they can snap off and use in a number of ways. They can, for example, break these sugar molecules down and derive energy from them."We believe that bacterial pathogens in the gut cause disease in two steps," he continued. "Others have shown that once these pathogens attain sufficient numbers, they use inflammation-triggering tricks to wipe out our resident friendly microbes ― at no cost to the pathogens themselves, because they've evolved ways to deal with it. But first, they have to surmount a critical hurdle: In the absence of the inflammation they're trying to induce, they have to somehow reach that critical mass. Our work shows how they go about it after a dose of antibiotics. They take advantage of a temporary spike in available sugars liberated from intestinal mucus left behind by slain commensal microbes." (From Scicasts).

Note that pretreatment with Metformin lowered HCV viral load by 0.52 log in insulin-resistant patients in this small study.

On a personal note, I have started an 8-week trial of Sofosbuvir and GS-5816 (Vulcan). It is day 11 and it seems tolerable so far.
A pre-trial blood test on 22nd October was normal except for these counts:
AST 74
ALT 174
and viral load was 600,419 (log 5.78), counts consistent with the tests I've had done this last year.

But the day the trial started, 18th November, before my first dose, things were different:
AST 21
ALT 32
Viral load 27,167 (log 4.43)

The low viral load is easy to explain; I get a consistent 1 log drop (to 14,000-60,000) when I try to eat very low carb (50g/day or lower) and an elevation to 400-600,000 when my carbohydrate intake is over 50g/day. When I ate very high carb (but took antioxidant supps) it was as high as it was on 22nd October. So for me the tipping point seems to be where ketosis begins, and other variations don't have much effect; it's an on/off switch, not a dial (and the name of that switch is PPAR-alpha).
(I do however, according to CAPSCAN elastography, have zero excess fat in my liver, which is an effect of low carb in general, as well as avoiding vegetable seed oils).

The perfect AST and ALT are harder to explain. They have never been so good, not since 1991 when they were first measured. Is it the 30mg/day zinc (as gluconate) I started over a month ago? That would be cool. It's already fixed any lingering fatigue and helped me sleep better.

Dr Richard Mackarness meets low-carb and Paleo pioneers in 1958

Dr Richard Mackarness


In Chapter 7 of his influential 1970's book on food allergies "Not All In The Mind" U.K. physician Dr Richard Mackarness describes his encounters with the pioneers of low-carb medicine when he visited the States in 1958. That same year Dr Mackarness wrote "Eat Fat and Grow Slim".
"His first book, Eat Fat and Grow Slim (1958), exposed the "calorie fallacy" and proposed a non-carbohydrate "Stone Age" diet of protein and fat with no restriction as to the amount eaten. The book was immensely popular and went through six editions."




In the US Dr Mackarness interviewed, or studied the works of, the following "anti-cereal" doctors. Those that are covered in "Good Calories/ Bad Calories" or well-referenced on the internet I will treat briefly, I am mainly interested in drawing attention to some unsung heroes and their tales.

Dr Ray Lawson was a surgeon at one of the biggest hospitals in Montreal and surgical consultant to the Canadian Arctic Medical Service. Some of his Eskimo patients in the far north were still eating their old high-fat, high-protein, non-cereal diet, which seemed to him to keep them remarkably fit and give them great powers of endurance. He decided to try to lose some unnecessary weight by following an Eskimo diet himself, an enterprise in which he was completely succesful. just before I visited him, he had confounded his personal physician by curing himself of an attack of jaundice. His doctor had been treating him with orthodox methods, including a low-fat diet, without much success.Dr Lawson switched to large doses of double cream, and promptly got well. An article about him and his high-fat eating was published in the popular Canadian magazine Maclean's, and caused quite a stir.

After seeing Dr Lawson I visited the late Dr Alfred Pennington of New Jersey who was consultant physician to Du Pont, the vast chemical company...he was asked to develop a reducing plan for the company's overweight executives... most of them had high blood pressure and were potential stroke- and heart-attack victims.
The diet he prescribed completely eliminated foods of cereal origin, i.e. everything containing starches or sugars; it was virtually an all-meat diet with the fat left in. When I lunched with him at his house I found he practised what he preached; we had an all-meat meal. He told me that he gave the duPont executives about 3000 calories per day in the formof fat meat and on this regime they lost at the rate of two to three pounds per week. They liked the diet, nd by the time their weight had returned to normal, their blood pressure had returned to normal too.
The relationship between obesity and high blood pressure is recognised by doctors all over the world, and the type of high blood pressure known as 'idiopathic' (of unknown cause) is one of the commonest stress disorders of twentieth-century civilised countries, crippling millions every year. It is a forerunner of strokes and coronary thrombosis. I believe that it and its associated obesity are both diseases of maladaptation to certain foods and chemicals we have been eating in increasing quantities over the past sixty to seventy years.

From Pennington I went on to Minneapolis to talk to Dr. George L. Thorpe, a general practitioner from Wichita in Kansas, who was attending the 1958 annual meeting of the American Medical Association. At the previous annual general meeting in New York in 1957, Thorpe had been chairman of the section of General Practice and had made the cereal-elimination approach to overweight the subject of his address .
Thorpe told me that he hated to call his method a diet. "Proper eating is the normal and complete answer to the problem of excess weight," he said. "The words diet and dieting should be avoided.

"Several years ago," Thorpe went on, "while I was considering a personal problem of excess weight, it became evident that huge numbers of calories in my daily total came from three to four large glasses of milk, two to three bottles of soft drinks, numerous slices of bread, and an educated taste for cookies, candy and sweets in general, all of which are concentrated carbohydrates. Cereal grains, historically, were cultivated in order that limited agricultural areas might supply food to support population densities not otherwise possible. They are concentrated forms of food, readily assimilated in the body, containing small residue of bulk, and so may be eaten in quantities far in excess.of the calorie needs, without sensation of fullness. All carbohydrate foods and most drinks fall into this category, either by virtue of their origin or the reaction of the body to them. Milk is actually a liquid infantile food, the use of which man has carried over into his adult life and which, in general, satisfies the definition of concentrated carbohydrate.
  "The simplest to prepare and most easily obtainable high-protein, high-fat, low-carbohydrate diet and the one that will produce the most rapid loss of weight without hunger, weakness, lethargy or constipation is made up of meat, fat, and water. The total quantity eaten is not important, but the ratio of three parts lean to one part fat must be maintained, as any decrease in the fat portion will reduce the weight loss..
   "Black coffee, clear tea and water are used without restriction. reduction of salt, while not required, will increase the speed of weight loss"

The last doctor I met was the late Blake Donaldson (he died in 1963). When I saw him at his clinic in New York I found that not only was he slimming his fat patients on a cereal-elimination diet, but he was using this diet and a graduated system of simple exercises to clear up a whole variety of chronic disorders in a most remarkable manner. I saw elderly rheumatic patients made supple and pain-free, martyrs to migraine relieved of their headaches and asthmatics helped to breathe freely again. In an interview in 1962, when he came to London to visit a patient Donaldson told me how he did it.

Dr MACKARNESS: When and how did you first come on the ideas which caused you to write Strong Medicine?

Dr DONALDSON: About 1919. I was faced with the problem of people with heart disease, fat people who were short of breath, had swollen feet (oedema) and could not lose weight. I tried them for a year on a low-calorie diet with a very bad result. At the end of the year practically none had lost weight, they were still breathless and had not lost their oedema.

[I wish I could copy all of this interview but it is far too long for my single-fingered typing skills. Dr Donaldson followed an investigative route similar to that of Weston A Price, except he looked at teeth in museum specimens. I think those heads have since had to be returned. The story is told in Strong Medicine beginning on page 32. Dr Donaldson talks of an "allergy" to flour, which is a terminology and concept Dr Mackarness later adopted. Its use means that the response to these foods is maladaptive and stressful, without always implying an immunological basis for this, which the scientists of the day were in no position to determine with certainty.]

Dr DONALDSON: We found out the patients could live on just fresh meat and a cup of coffee three times a day, and lose weight at the rate of three pounds a month. (You don't want to lose weight much faster than that, otherwise the skin becomes wrinkled.)
...
When you reduce their weight to normal you have to prove their weight can stay normal; that's very important...They have to be able to eat fat meat with salt, potato with butter, raw fruit and a full cup of coffee three times a day and show no gain in weight...there is no restriction on the amount.

Dr MACKARNESS: How many patients over the last forty years have you treated on this basis?

Dr DONALDSON: About seventeen thousand. I now have a group of about fifteen hundred patients over the age of seventy, who have avoided flour for between five and forty years,.and have kept primitive food as their basic way of maintaining health.

Dr MACKARNESS: This is what I call a Stone-Age diet. Would you agree with that description? It is a pre-cereal diet.

Dr DONALDSON: Well, I should say that it is perhaps six thousand years old and twenty years ahead of its time. I think this will be a popular idea in twenty years, that flour is a bad thing for about eighty percent of the population.

Dr MACKARNESS: And do you also ban all carbohydrate derivatives - sugar, chocolate, etc?

Dr DONALDSON: Once you have an allergic fat person under control you reduce that person's weight to normal. I find that I am unable to feed them sugar in any form, and unable to feed them flour, without bringing back their obesity and their allergic symptoms.

Dr Mackarness goes on to discuss F. Curtis Dohan and his 1969 work on schizophrenia and coeliac disease. He then describes the work of Andresen (1942) that ulcerative colitis is a result of food allergy "in 66% of cases" and that of Professor S. C. Truelove of Oxford who wrote in 1961 about improvement of ulcerative colitis upon removal of milk from the diet. These are both early descriptions of a disease due to lactose (or FODMAP) intolerance.

Mackarness returned to the UK and wrote the highly successful diet book Eat Fat To Grow Slim. Dr John Yudkin, a far more conservative academic nutritionist, also wrote a low-carb book, This Slimming Business, with similar recommendations to those of Mackarness, as can be seen in this 1970 paper. I wish I knew something about the relationship between these two great men. It cannot have been an easy one, as Yudkin was a cautious sceptic and Mackarness a speculative innovator. Mackarness bears responsibility for the popularising of elimination diets; these were harmless when meat was the default food, as it was in Not All In The Mind, but are more problematic now that the idea has been adopted by Naturopaths with eating disorders and strange ideas about animal foods.

The biggest difference between the British and American low carb doctors is, that Yudkin and Mackarness were respected members of the British medical establishment, and their ideas were given common currency by a country with a then-progressive approach to preventive medicine. You can see it in this 1967 video, where an overweight child is told to eat meat and green vegetables, and avoid sweet and starchy foods. Stodge, not grease, was the enemy and the cause of Overweight and Shortness of Breath.



Regardless of whether the consumption of starch and sugar has changed during the obesity epidemic, we can be quite sure that the advice given to the most vulnerable people - the newly overweight or pre-diabetic - has. In my opinion this is what we should be looking at - whether alterations in the primary diet and exercise advice given to individuals in at-risk groups by the most authoritative agencies has been associated with any particular outcome.
But really, I think we all know the answer to that.

[EDIT: The major difference between Yudkin and Mackarness's approach to weightloss was that Yudkin as serious nutritionist emphasised the need to cut calories (carbohydrate calories being easiest and most profitable to cut), whereas Mackarness was more of the ad libitum "calories don't count" persuasion.
But in practice Yudkin believed that calories should be automatically reduced on a low-carbohydrate diet and that there was no need to count them, as you can read here (PDF) in the introduction to his recipe book Eat Well, Slim Well (1982) which summarises the argument of This Slimming Business (1958, the same year as Eat Fat and Grow Slim).Here is a list of “unrestricted” foods: those, that is, which you don’t have to limit but which limit themselves. They are meat, poultry, fish, eggs, butter, margarine, cream, leafy vegetables. In addition, you should take between half and one pint of milk a day, up to half a pound of fruit, and up to two ounces of cheese.
John Yudkin's obituary from 1995]

A Brief History of the Food Groups concept

"FOOD GROUP TO SPLIT - IRRECONCILABLE DIFFERENCES CITED" is a headline I expect to see any day now. The notion of the Food Group seems to have become the most abused concept in Nutrition. Two recent examples are the criticism of Paleo - "Excluding grains means leaving out an entire food group, that can't be healthy"; and the following mention in an otherwise laudable piece by Lucy Cavendish in support of Dr Aseem Malhotra's BMJ article in defense of saturated fat (I'm sure I don't need to link to that).
"With wheat and gluten vilified in recent years, I have, in the past, cut both food groups from our household diet – and it has cost me a small fortune."

Let's charitably assume that "gluten" in that sentence refers to the other gluten grains, or to non-grain products with a "contains gluten" warning on the box, and not to the protein itself. It's still wrong, if the Food Group concept is to mean anything. And if grains can be a food group, why not eggs? Wheat grains, barley grains, rye grains, rice grains; hen eggs, duck eggs, quail eggs, goose eggs. If we did this, how many food groups would there be?
Why do we have a concept of Food Groups in the first place? And what would be the most rational and useful system to use today, if any?

According to the NZ Nutrition Foundation website, Using food groups is a way of classifying foods according to the nutrients they provide.  Here in New Zealand, the four food groups are:

• Fruit and Vegetables
• Breads and cereals (bread, rice, pasta, breakfast cereals)
• Milk and milk products (milk, cheese, yoghurt, ice cream)
• Lean meat and alternatives (lean meat, poultry, seafood, eggs, nuts & seeds, beans and lentils)

Or, indeed, according to the nutrients they don't provide - lean meat isn't a food group, but the indication of an eating disordered way of thinking here. This is taken to a further extreme in the latest Health2000 newsletter, where there are "5 main food groups" (ignoring how many subsidiaries?)

• Fruit and vegetables
• Whole grain breads and cereals (bread, rice, pasta, oats)
• Lean protein foods or vegetarian alternatives (egg, fish, lean meat, poultry, legumes, nuts)
• Dairy products (milk, yoghurt, cheese - preferably low fat)
• Small amounts of healthy fats (olive oil, nuts, seeds, avocado)

Which fiendishly refines the 4-group scheme by removing a nutrient from two of the four groups, then introducing an additional group to supply it.
It is a relief to leave such complexities behind to return to a simpler time, when the goal of nutritional teaching was to ensure that people knew enough to be adequately fed and raise healthy children (a need that persists today, but you wouldn't know it). In 1936 there were three food groups -

• Body Building Foods (those foods that are high in protein, but not necessarily lean) 
• Protective Foods (those foods that are good sources of vitamins, especially vitamins A, D, C, and folate)
• Energy Foods (Fat, sugar, and starch; the more-or-less empty "discretionary calories")
  
  These 3 food groups are introduced at 4:00 in this short film
  
  

Now you may laugh at the idea of treating carbohydrate and fat as interchangeable, but compared to the byzantine dietary adjustments we've been discussing, and considering that the Body-building and Protective groups here already supply a generous fat intake by modern standards, it seems eminently sane to me.

This Disney educational cartoon from 1955 (made for a South and Central American audience under the Good Neighbour policy of the Cold War years it seems) takes a similar approach, except that the Energy Foods are now Grains and Roots, and the other 2 groups are Animal Foods, and Vegetables and Fruits (the latter group "builds strong bones and teeth").



Our third example is from 1967 and is interesting as a treatment of obesity at a time when this problem was rare, and because macronutrients and micronutrients are introduced (3:25). Food supplies Protein, Carbohydrate (for energy), Fat (for warmth and energy), and "those vitamins we hear so much about today".



(In part 3 of this film the doctor will tell the kid to cut down on starchy and sweet food, and to eat meat and veges. No mention of lean meat or low-fat dairy. No doubt one reason obesity was still rare in 1967)

I don't know about you but I prefer these simpler approaches. I like the idea of having four groups (remember, this is really for teaching children, and people who've never thought about nutrition much, not something adults will need to remember).

• Body building foods, i.e. protein sources. Animal foods, and maybe nuts and seeds, but unless you're avoiding meat for some reason, legumes are probably better in the next section. If you don't tolerate dairy, don't eat it. 
• Starchy foods; roots, bananas, grains, legumes and so on. If you don't thrive on gluten grains, don't eat them. Also honey, molasses and treacle. Cooked fruits.
• Fatty foods; butter, dripping, oils, cod liver oil, cream, coconut, avocado, etc. Nuts and seeds here too? In the tradition of the 1936 and 1967 films, a great deal of overlap is simply realistic and consistent with the facts (Myplate as a Venn diagram?).
• Vegetables and fruits, i.e. foods that don't supply much in the way of energy or protein but do supply vitamins, antioxidants, fibre, electrolytes and other protective factors. Herbs and spices can go here too.

This list isn't satisfying. It's judgmental, for one thing; what does one do with sugar? Fruit juice? "Treats" (odious word) and "snacks" are not food groups but social problems. As for honey, that's an animal food, isn't it? And what about alcohol, the rogue macronutrient? Where does chocolate go? What about this crazy new trend of calling water a food group?
How much propagandizing is permissible? I'd be tempted to say "as much as is necessary", but only if you can sell it in the face of questions. It would be better to include sugar in the list than to lack a good explanation for leaving it off. And so on. The virtue of a list like this is that it introduces the macronutrients and protective factors using real examples.

The rest is cookery.



Question:
I'd like to read your own suggestions for a reformed Food Group system, or, failing that, see your favourite egregious examples of depraved Food Group systems from the current culture.

How do you fix a leaky gut? New twists on old ideas.

Leaky gut, AKA intestinal permeability, is one of the determining factors in diseases of the liver, which should be tolerant of the normal adaptive quantities of lipopolysaccharides (LPS, fragments of Gram-negative bacterial cell walls) that reach it (other parts of the immune system need to be more sensitive to LPS). If too much LPS reaches the liver because the gut barrier is weakened, or if the liver is made over-sensitive to LPS by factors such as steatosis and cholesterol accumulation, LPS activation of TLR4 can set in motion the immune cascades that lead to fibrosis and necrosis.


TLRs are sensors that amongst other things help orchestrate responses to both potential pathogens and symbiotic organisms. Having just had to replace one of the many sensors in my car that keeps the engine in tune and alerts me to problems, I'm thinking that might be an acceptable analogy for now. A defective sensor crippling the engine to alert me to a problem that doesn't exist is a bit like an allergic reaction, maybe.
Gut integrity is modulated by TLR2

Our findings suggest that dietary saturated fat plays a protective role against MCDD-induced steatohepatitis, whereas TLR-2 deficiency exacerbated NASH. The mechanism underlying the response to dietary fat and TLR-2 likely involves altered signalling via the TLR-4 pathway.

TLR2 is activated by saturated fat, inhibited by polyunsaturated fat.
Dietary saturated fat protects against LPS (endotoxin) activation of TLR4 in hepatic immune cells, but different SFAs achieve this in different ways.

Am J Physiol Gastrointest Liver Physiol. 2013 Oct 10. [Epub ahead of print]

Dietary fat sources differentially modulate intestinal barrier and hepatic inflammation in alcohol-induced liver injury in rats.

Zhong W, Li Q, Xie G, Sun X, Tan X, Sun X, Jia W, Zhou Z.

Source

1University of North Carolina at Greensboro.

Abstract

Endotoxemia is a causal factor in the development of alcoholic liver injury. The present study aimed at determining the interactions of ethanol with different fat sources at the gut-liver axis. Male Sprague Dawley rats were pair-fed control or ethanol liquid diets for 8 weeks. The liquid diets were based on the Lieber-DeCarli formula, with 30% total calories derived from corn oil (rich in polyunsaturated fatty acids). To test the effects of saturated fats, corn oil in the ethanol diet was replaced by either cocoa butter (CB, rich in long chain saturated fatty acids) or medium chain triglycerides (MCT, exclusively medium chain saturated fatty acids). Ethanol feeding increased hepatic lipid accumulation and inflammatory cell infiltration, and perturbed hepatic and serum metabolite profiles. Ethanol feeding with CB or MCT alleviated ethanol-induced liver injury and attenuated ethanol-induced metabolic perturbation. Both CB and MCT also normalized ethanol-induced hepatic macrophage activation, cytokine expression and neutrophil infiltration. Ethanol feeding elevated serum endotoxin level, which was normalized by MCT but not CB. In accordance, ethanol-induced downregulations of intestinal occludin and ZO-1 were normalized by MCT but not CB. However, CB normalized ethanol-increased hepatic endotoxin level in association with upregulation of the endotoxin detoxifying enzymes argininosuccinate synthase 1 (ASS1). Knockdown ASS1 in H4IIEC3 cells resulted in impaired endotoxin clearance and upregulated cytokine expression. These data demonstrate that the protection of saturated fats against alcohol-induced liver injury occur via different actions at the gut-liver axis and are chain length dependent.


Meaning: Coconut oil MCTs (also found in butter/ghee and palm oil) normalised serum LPS level by repairing gut integrity, whereas cocoa butter protected the liver by enhancing the clearance or detoxification of LPS.

Spirulina is a TLR2 agonist and protects against inflammation in chronic hepatitis C. Probiotic (Gram-positive) bacteria also protect the intestinal epithelium via TLR2;

All the Gram(+) strains increased the number of TLR-2+ cells and the Gram(−) strains [increased the number] of the TLR-4+ cells. 

VSL#3 is a popular probiotic mix approved for medical use in Europe ("VSL#3 is a probiotic  mixture which has been frequently referred to in the literature, and contains live lyophilized  Bifidobacterium breve, Bifidobacterium longum, Bifidobacterium infantis, Lactobacillus  acidophilus, Lactobacillus plantarum, Lactobacillus paracasei, Lactobacillus bulgaricus and  Streptococcus thermophilus.").

Here is a very interesting new paper which compares, in a alcohol model of liver/gut disease, combinations of live VSL#3, heat-killed VSL#3, and l-glutamine (amino acid fuel preferred by enterocytes and protective thereof).

Results

First, compared with control group, endotoxin and TNFalpha in alcohol group was obviously high. At the same time, in VSL#3 group, the expression of endotoxin and TNFalpha obviously lower than the alcohol group. And the trends of the expression of tight junction proteins in these groups were reversed with the change of endotoxin and TNFalpha. Second, compared the groups of VSL#3 with glutamine, VSL#3+glutamine and heat-killed VSL#3, we found that both VSL#3 and heat-killed VSL#3+glutamine were as effective as VSL#3+glutamine in the treatment of acute alcohol liver disease, the expression of endotoxin and TNFalpha were lower than the alcohol group, and tight junction proteins were higher than the alcohol group whereas the expression of tight junction proteins were higher in VSL#3 + glutamine group than either agent alone, but have no significant difference.

Did you get that? The full text is a little different:

We found that both VSL#3 and heat-killed VSL#3 were as effective as 

glutamine in the treatment of acute alcohol liver disease, whereas the combination of VSL#3 

and glutamine therapy efficacy was more effective than either agent alone

So maybe - and this is backed up by other research - for some purposes the viability or resistance or age or condition of a probiotic supplement can be less important than the strains and number of organisms it contains. And yoghurt cooked into meals, which appears to be a common thing in countries where yogurt is a traditional food, with only Western faddists consistently fetishizing rawness, might have its medicinal uses too.

Lamb baked in yogurt

Certainly, a probiotic need not make it alive all the way through the digestive tract to influence host immunity, and some of the objections commonly made in "evidence based" criticisms of probiotics are simply not relevant to some important probiotic modes of action.

"The probiotic paradox is that both live and dead cells in probiotic products can generate beneficial biological responses. The action of probiotics could be a dual one. Live probiotic cells influence both the gastrointestinal microflora and the immune response whilst the components of dead cells exert an anti-inflammatory response in the gastrointestinal tract."

So here we have a mixture of strategies to combine to repair a leaky gut and reduce consequent hepatic inflammation;
1) dietary saturated fats of both MCT and long-chain classes
2) l-glutamine
3) spirulina
4) viable live probiotic cultures (and prebiotic fibres)
5) killed probiotics, as well as live commensal species that do not easily colonise the gut

PCSK9, Alirocumab, and why high linoleic acid intakes increase vulnerability to Hepatitis C

In ancient times, those suffering from ye surfeit of choleric humours were prescribed a purgative compounded of tincture of statin. Modern science, from its evidence-based wisdom, has compounded a new elixir by the name of Alirocumab (the drug being named after its father, one of the Legions of Satan listed in the Enochian Book of Revelation).

Music: Rasputina, "The Signs of the Zodiac"
Do you believe in the Signs of the Zodiac?
Haven't you found that the systems for
Planning always fail?

Can you avoid what gave Daddy his heart attack?
Have you tried everything, anything
All to no avail?

I know what you need.
This will really work.
In ancient times, if you were sick
They make you bleed.
Oh, honey I know it hurts.

Alirocumab has the remarkable property of reducing cholesterol by 47.2%. At this rate cholesterol will soon be as rare as smallpox. Alirocumab is a fortnightly-injectible antibody that inhibits a protein called PCSK9, which regulates hepatic lipoprotein uptake by degrading LDL receptors and preventing them from being re-used. Less PCSK9, more LDL receptors, more cholesterol, lipids etc. going into hepatocytes. What could possibly go wrong?

Human PCSK9 is known to enhance the degradation of membrane-bound receptors such as the hepatocyte low-density lipoprotein receptor (LDLR), ApoER2, and very low-density lipoprotein receptor. Because the LDLR is suspected to be involved in hepatitis C virus (HCV) entry, we also tested whether PCSK9 can affect the levels of CD81, a major HCV receptor. Interestingly, stable expression of PCSK9 or a more active membrane-bound form of the protein (PCSK9-ACE2) resulted in a marked reduction in CD81 and LDLR expression. Therefore, we analyzed the antiviral effect of PCSK9 in vitro using the HCV genotype 2a (JFH1) virus. The results clearly demonstrated that cells expressing PCSK9 or PCSK9-ACE2, but not the ACE2 control protein, were resistant to HCV infection. Furthermore, addition of purified soluble PCSK9 to cell culture supernatant impeded HCV infection in a dose-dependent manner. As expected, HuH7 cells expressing PCSK9-ACE2 were also resistant to infection by HCV pseudoparticles. In addition, we showed that CD81 cell surface expression is modulated by PCSK9 in an LDLR-independent manner. Finally, in the liver of single Pcsk9 and double (Pcsk9 + Ldlr) knockout mice, both LDLR and/or CD81 protein expression levels were significantly reduced, but not those of transferrin and scavenger receptor class B type 1. Conclusion: Our results demonstrate an antiviral effect of the circulating liver PCSK9 on HCV in cells and show that PCSK9 down-regulates the level of mouse liver CD81 expression in vivo. Therefore, we propose that the plasma level and/or activity of PCSK9 may modulate HCV infectivity in humans. (Hepatology 2009.)

So lowering cholesterol with Alirocumab looks set to increase the spread of hepatitis C. But what else decreases PCSK9? If PCSK9 increases LDL (the "bad" cholesterol), does saturated fat increase PCSK9?
The answers may surprise you.


Plasma PCSK9 concentrations vary minimally in response to a short term high-fat diet and they are not accompanied with changes in cholesterolemia upon high-fructose diet. Short-term high-fructose intake increased plasma PCSK9 levels, independent on cholesterol synthesis, suggesting a regulation independent of SREBP-2. Upon this diet, PCSK9 is associated with insulin resistance, hepatic steatosis and plasma triglycerides.
We previously showed that hepatic PCSK9 expression is subjected to nutritional regulation, being decreased upon fasting and increased following re-feeding with a high carbohydrate diet in rodents[14]. Insulin increases hepatic PCSK9 expression both in vitro in hepatocytes and in vivo in mice[14]. Conversely, PCSK9 is repressed by glucagon in rat liver [16]. Accordingly, fasting, but not a ketogenic diet, reduces plasma PCSK9 concentrations in healthy volunteers, with a ≈ 20–35% decrease after 18 h [17,18]. However, so far there are only two reports that describe a dietary modulation of PCSK9 in human. The Mediterranean diet [19] and n-6 PUFAs [20] have been shown to decrease plasma PCSK9 concentrations by ≈ 12% and 13%, respectively.

And again:

PCSK9 (P = 0.001), TNF receptor-2 (P < 0.01), and IL-1 receptor antagonist (P = 0.02) concentrations were lower during the PUFA diet, whereas insulin (P = 0.06) tended to be higher during the SFA diet. In compliant subjects (defined as change in serum linoleic acid), insulin, total/HDL-cholesterol ratio, LDL cholesterol, and triglycerides were lower during the PUFA diet than during the SFA diet (P < 0.05).
(Note that this was not a high-fat diet "The participants were instructed (unblinded) to change the quality of their dietary fat without altering their intakes of total fat and the type and amount of carbohydrates and protein. The participants were encouraged not to change their physical activity or their fish and alcohol intakes during the study. Some key food items were provided: the PUFA group received foods rich in n−6 linoleic acid, ie, scones (baked-on sunflower oil), margarine, sunflower oil, and sunflower seeds, and the SFA group received scones (baked-on butter) and butter.") 

Taking this all together - rather messy and unsatisfactory though it may be - it appears that saturated fat does not significantly increase PCSK9 levels, nor does protein (insulin and glucagon in balance), but that high fructose/carbohydrate and insulin do. High linoleic acid decreases PCSK9.

Now, however desirable elevated PCSK9 may be to people with HCV, we don't want to achieve it with elevated carbohydrate and insulin because this will switch off PPAR-alpha, the other antiviral protein. 

The PPAR-alpha transcriptome in a human hepatocyte

Your classic LCHF Paleo diet is designed to maximise PPAR-alpha while leaving PCSK9 intact.
And that surfeit of choleric humours? It looks very much like the fructose, carbohydrate and insulin axis was responsible for any PCSK9 contribution to that.
Will people henceforth be dosing with Aloricumab so that they can enjoy sweet and starchy treats without alarming the doctors who audit their lipid returns?
This is the world we live in.

Anyway here is The Strangest Book in the World, accompanied by some rather wonderful music

And Part 2: