Maria Thommessen

Maria Thommessen PhD was a prominent Norwegian/international nutritionist. She sadly died of bowel cancer in 2006, aged 47, having fought the disease for 6 years.

Here is a translation from the norwegian (again thanks to Jakob from the AHOA forum) which sums up, for me, the tragedy of a highly intelligent person who has dedicated their life to preventing disease though diet, but has ended up in a wrong paradigm. The one fully backed by mainstream medicine. Her certainty is what keeps me looking for the possibility that I might be horribly wrong to eat high fat, low carbohydrate.

Maria Thomessen:

"I wanted to show that you could think positive thoughts and be optimistic even with such a diagnosis. I was very convinced that I should be able to win this battle. It feels like a paradox that it was I that got cancer. I don't think many have eaten as many carrots as me"

Sigh.

Selling fiber and bacteria

I watch the Simpsons. I consider it essential viewing for the maintenance of sanity. Apparently an awful lot of people with either IBS or "normal" constipation do too, judging by the marketing wizards' placement of advertisements for probiotics and/or soluble fiber in the central ad slot. Drives me up the wall. So how effective are these interventions in improving bowel function?

Well, probiotics appear to be very strain related but can have benefits in some situations. Dr Hunter is a gastroeneterologist at Addenbrooks in Cambridge. Taking a combination of bifidobacteria and lactobacillus that looks remarkably like yogurt minimises anaerobic overgrowth when you are on an antibiotic for helicobacter. Fair enough. I ferment my cream with these bugs.

But the role of probiotics in IBS "has not been clearly defined". Probably depends on who funded the study. Certainly lactobacillus plantarum 299v is not too hot.

Lactobacillus casei strain Shirota is pretty interesting according to the company which sells it. Lovely graphics on the homepage BTW. How much did the web site cost? I guess nothing compared to their TV advertising budget.

But are they needed anyway? Two interventions which do work are compared, by Dr Hunter again, here:

Metronidazole (an antibiotic aimed at anaerobic lower bowel bacteria) is pretty good, reducing peak gas production from 671ml/min to 422ml/min. Obviously no one wants to take metronidazole long term in view of its serious interaction with alcohol and its occasional neurological toxicity. But it makes a fairly convincing case that the problem is a bacterial problem. What do bacteria eat that humans cannot digest? Fiber.

So the other intervention is a no-fiber diet. Peak gas production dropped from 564ml/min to 205ml/min. This looks to be very effective and very interesting.

Both improved symptoms. As fiber is of no use to humans and it appears to feed the bacteria that cause IBS, including good old klebsiella, you have to wonder where the medical fascination with fiber comes from...

We all know where fiber ends up, why suffer the gut problems it causes as it gets there?

Peter

How many eggs per day?

Some people like eggs. This man did. Maybe he still does!

Here's a summary as it's not available on pubmed:

Normal Plasma Cholesterol in an 88-Year-Old Man who Eats 25 Eggs a Day: Mechanisms of Adaptation (1991) Kern Jr, New England J Medicine 324(13):896-899

The effect of dietary cholesterol intake on serum cholesterol level is known to vary among individuals. The homeostatic and regulatory mechanisms which tend to keep serum cholesterol constant operate at different levels of efficiency in different individuals. An extreme case is reported here. A physician and colleagues from the University of Colorado School of Medicine have studied an 88-year-old man who, for ill-defined psychological reasons, has consumed 20 to 30 eggs daily for at least 15 years. This individual has maintained normal serum lipid levels and has no history of clinically important heart disease. He consented to participate in a variety of tests of cholesterol metabolism; the findings were compared with those obtained in an ongoing study of 11 normal volunteers who were tested while consuming normal diets and diets supplemented with five eggs per day. It was found that this individual had extremely efficient mechanisms that compensated for his phenomenally high cholesterol intake. In particular, he absorbed only 18 % of the cholesterol that he consumed; the comparison subjects absorbed 54.6% when on low-cholesterol diets and 46.4% when on high-cholesterol diets. He also showed a doubling of the usual rate of conversion of cholesterol to bile acids, moderately reduced cholesterol synthesis, and a possible increase in biliary cholesterol secretion. "These physiologic adaptations would leave little if any of the dietary cholesterol to elevate plasma cholesterol levels and be deposited in arterial walls."


That's assuming you subscribe to the cholesterol myths anyway. I have to say six egg yolks is my normal daily consumption, only occasionally does it reach nine in a day. Never 25, at least so far...

Thanks to Jakob on the AHOA discussion forum for the above text.

Peter

Arteriosclerosis and saturated fat

Observational studies are useless for proving anything, but they do provide interesting starting points for speculation. They can also give some interesting insights in to human behaviour. I particularly enjoyed the American Paradox study.

On the raw data a high intake of saturated fat didn't quite reverse the women's arteriosclerosis, but after modeling it did. Modeling appears to involve adjusting your results to estimate what the values would have been if your patients didn't smoke, didn't have diabetes, didn't eat cholesterol (gasp) etc.

Glancing through the patient characteristics in table 1 you can see why adjustment might be needed.

Look at smoking. The high saturated fat group had the highest percentage of smokers and a hugely higher pack-years value (34 pack-years) than any other group (all below 18). They boozed the most, ate most trans fats and pooped the least fibre. They may even, wait for it, have eaten an egg a day! On the plus side they obviously had the highest HDL cholesterol and lowest triglycerides, because they also ate the least carbohydrate.

If you had to describe this group in one word it would have to be "naughty". These naughty people did all the WRONG things (according to the AHA) and, after adjustments, began the reversal process of their IHD. Thumbing your nose at the AHA, even in this mild manner (by my standards), looks to be good for you.

The lowest saturated fat group had the highest carbohydrate intake, let's call them the Goody Goodies. They made excellent progress as coronary bypass fodder.

Just observational. But what an observation of disobedience!

Peter

How toxic is wheat?

Well, the first point is that Wheat Germ Agglutinin (WGA), the main lectin in wheat, is an insulin mimetic in tissue culture. A very good insulin mimetic. If you want to give someone, male or female, that "ten-months-pregnant" look you can either use masses of insulin, as produced by an insulinoma or perhaps have them take an insulin mimetic like WGA by mouth with every meal...

But does WGA, a protein, cross from the gut in to the blood stream intact to then have a biological effect? Well, that depends on who you ask and what dose you give. Pusztai, funded by the Scottish equivalent of DEFRA, says that, at high doses, WGA not only crosses in to the blood stream but also glues itself to the lining of blood vessels and lymphatics. I cannot think of a better way of producing an autoimmune vasculitis than sticking WGA to your blood vessels. Or of producing a massive insulin like effect, ie beer gut.

Another group of researchers, funded by the Italian government this time, say WGA doesn't cross their artificial model of the gut lining. They also found WGA wasn't heat stable, in contrast to Pusztai. But both groups do agree that WGA trashes the gut lining cells.

So these two research groups disagree about the penetration of wheat toxicity in to the body, but neither argues with the toxicity per se. I believe Pusztai is correct, especially for those poor people who regard wheatgerm, with its lectin load, as a health food. Apparently they take it in multigram doses. No thanks.

That's before we consider the effect of gliadin from wheat on gut permeability disrupting the tight junctions between enterocytes. Damaging the integrity of the gut allows all sorts of dietary proteins to gain access to the blood stream and, obviously, the immune system. I guess it helps WGA in to the circulation too.

It probably helps the two insulin stimulating peptides derived from the partial digestion of gluten in to the blood stream too.

It probably also helps WP5212 in to the path of the immune system of potential type one diabetics, allowing them to achieve their full disease potential.

I won't mention coeliac disease and schizophrenia. Or gluten ataxia. Or a host of other problems.

Today a drug rep provided pizza for lunch at work. I ate my chocolate and drank my fermented cream sitting alongside the 4 giant pizzas in the rest room. Several people asked if I wasn't tempted to indulge.

Too much information, too much toxicity and ZERO temptation.

There is no doubt about the toxicity of wheat.

Peter

Lipoprotein(a) and oxidised cholesterol

Lipoprotein(a) is a subgroup of LDL cholesterol which has had an extra protein added to it. This extra protein is sticky, particularly to the lysine and proline residues of collagen which get exposed in damaged arterial walls. Like LDL cholesterol, it is a method of applying a sticking plaster to damaged vascular endothelium. If you have lots of damage to your arteries you would expect your liver to make lots of lipoprotein(a). It's not stupid. Lipoprotein(a) is especially needed if you have defective LDL receptors, so in familial hypercholesterolaemia you would expect lipoprotein(a) to be high. That's what you find. Using a second choice repair system is likely to be associated with a poor repair and so with heart disease. It is. Oddly enough, if you live long enough this extra repair system becomes rather important and centenarians have rather high levels of lipoprotein(a). So it can't be all bad.

Anyway, a quick google or pubmed search on lipoprotein(a) will tell you that that it is a risk factor for heart disease (now there's a surprise) and that your blood level is genetically determined, so there's nowt you can do about an elevated level anyway. Wrong.

In the simplistic world of cardiology you lower blood lipids by lowering dietary fat. Under this intensely stupid idea it is impossible to lower lipoprotein(a) by dietary means.

Of course you could still go on and try that low fat idea. The Finns tried it. They, like most of the world, follow the low fat line in heart disease prevention. Just take 37 women who are already down at 70g fat per day (appallingly low to begin with) and reduce it to either 56g with minimal veggies or 59g with lots of healthy veggies plus nuts. Then flip the diets in a crossover study. Let's see what happens to lipoprotein(a). Both diets crank up lipoprotein(a). The 56g low veggie diet increase lipoprotein(a) by 7%. With those lovely veggies it cranked up by 9%. Note, another confirmation that fruit and veggies are BAD.

The converse has been nicely done. Just use a LC diet and lipoprotein(a) drops by 11.3%

Genetically determined hey? Duh.

Oh, and look how the low fat diet, with or without veggies, oxidised the LDL cholesterol. Low fat diets are very nice if you are in the cardiac business. As these squirming editors seem to be. What a load of twaddle. Bad is good. Really. It's good. Really, bad is good.

How many fingers, Winston?

Peter

Do you believe in MRI scanners?

I was thinking about mitochondria, but I got sidetracked when I remembered Ling and his opinion about ATP. Here's how it went:

The vast majority of the energy production in our bodies occurs in our mitochondria. These are the tiny powerhouses which generate most of the high energy adenosine tri phosphate (ATP) on which we ultimately run our metabolism.

NB an aside; Gilbert Ling does not believe in ATP as an energy source for cells (though he thinks it is a crucial molecule), any more than he believes in the lipid bi-layer cell membrane or the sodium/potassium ATP pump. He is truly out on a limb with his "Association Induction Hypothesis" of life at cell and below cell level. A fruitcake, obviously. Except his ideas on the localisation of cell water around proteins led to the invention of the MRI scanner. If MRI scanners work, that cookie Ling is right. And almost all of modern physiology is wrong.

It is, for me personally, MUCH easier to think within the "normal" physiology of my education. But, because MRI scanners work, this is the equivalent of thinking that the table in front of me is "solid" when quantum mechanics tells me that it is anything but solid...

Now there's a thought.

Peter

Dietary sins of Swedish children

Dr Haglund Garemo is a paediatric nutritionist at Göteborgs University in Sweden. She defended her PhD in December 2006. The abstract is available here. She studied the socioeconomic status, diet, weight and health markers in a group of 4 year old children.

The relevant quotes from the abstract are

"The energy intake/kg was according to Nordic nutrition recommendations"

"Most children had a higher intake of saturated fat and sucrose than recommended"

"A higher BMI was associated with lower fat and higher sucrose intake"

"A lower fat intake was associated with higher BMI and higher HOMA ß-cell function"


If you had to summarise these findings they would be, with a little license, as follows: Eating fat makes you thin. Eating sugar makes you fat. Eating sugar makes you hyperinsulinaemic.


Here are some interesting interview quotes from Dr Garemo in addition to her thesis abstract:

Food and Drink Europe quote her in an interview as commenting:

"analysis of the children's body build showed that weight increases was a result of the body storing more fat, but those who ate the most fat were not the ones who weighed most. Instead, children who ate less fat had higher BMIs"


News-medical have this quote. Odd way of phrasing it, "less heightened"!

"Insulin production was less heightened in girls who ate more fat"

"Such results would go against the common perception that fat causes increased insulin production as a result of insulin resistance"



Overall, eating fat came out rather well. Most of it was saturated. That is an understatement. Interestingly that last quote above is the explanation of the bizarre medical idea that eating fat raises your blood sugar level.

It's wrong, excepting the ideas in my post on physiological insulin resistance. I doubt any of these children were eating enough fat to be in ketosis! BTW if you ever come across a diabetic person having a severe hypoglycaemic episode, please do NOT give them butter to try and raise their blood sugar, they might well die. Try sugar.

That should tell you something. Duh.

Peter

Physiological insulin resistance

Back in mid summer 2007 there was this [unfixable link] thread on the Bernstein forum. Mark, posting as iwilsmar, asked about his gradual yet progressively rising fasting blood glucose (FBG) level over a 10 year period of paleolithic LC eating. Always eating less than 30g carbohydrate per day. Initially on LC his blood glucose was 83mg/dl but it has crept up, year by year, until now his FBG is up to 115mg/dl. Post prandial values are normal.

He wanted to know if he was developing diabetes.

I've been thinking about this for some time as my own FBG is usually five point something mmol/l whole blood. Converting my whole blood values to Mark's USA plasma values, this works out at about 100-120mg/dl. Normal to prediabetic in modern parlance. However my HbA1c is only 4.4%, well toward the lower end of normality and healthy. That's always assuming that I don't have some horrible problem resulting in very rapid red blood cell turnover. I don't think so...

I spend rather a lot of my life in mild ketosis, despite the 50g of carbs I eat per day. So I can run a moderate ketonuric urine sample with a random post-chocolate blood glucose value of 6.5mmol/l. What is happening?

Well, the first thing is that LC eating rapidly induces insulin resistance.

This is a completely and utterly normal physiological response to carbohydrate restriction. Carbohydrate restriction drops insulin levels. Low insulin levels activate hormone sensitive lipase. Fatty tissue breaks down and releases non esterified fatty acids. These are mostly taken up by muscle cells as fuel and automatically induce insulin resistance in those muscles. There are a couple of nice summaries by Brand Miller (from back in the days when she used her brain for thinking) here and here and Wolever has some grasp of the problem too.

This is patently logical as muscle runs well on lipids and so glucose can be left for tissues such as brain, which really need it. Neuronal tissue varies in its use of insulin to uptake glucose but doesn't accumulate lipid in the way muscle does, so physiological insulin resistance is not an issue for brain cells. However, while muscles are in "refusal mode" for glucose the least input, from food or gluconeogenesis, will rapidly spike blood glucose out of all proportion.

This is fine if you stick to LC in your eating. It also means that if you take an oral glucose tolerance test you will fail and be labelled diabetic.

In fact, even a single high fat meal can do this, extending insulin resistance in to the next day.

Here's a reference for this.

The general opinion in LC circles is that you need 150g of carbohydrate per day for three days before an oral glucose tolerance test. I did this carb loading thing, then performed my own OGTT. It came out very normal except for mild reactive hypoglycaemia.

So, I often walk around with a fasting blood glucose of 5.9mmol/l and in mild ketosis, yet have normal pancreatic and muscle function, provided I carb load before the test. 

BTW my FBG dropped to 4.3mmol/l after three days of carb loading. That then raises the question as to whether Mark "iwilsmar" and myself are typical of LC eating people, or an oddity or two.

This brought to mind the self selected macronutrient study performed on mice by Ortman, Prinzler and Klause. They allowed mice to select their own diet and, lo and behold, the mice chose (by calories, not weight!) 82% fat and 5.6% carbohydrate. Sensible mice. NB These German mice should each be given Professorships of Nutrition at medical schools in the most obese nations of the world. Quite what we should do with the current professors I'm not sure, but I bet the mice could think of something.

Anyway, these mice are cool. The only thing that bugged me when I first read the paper was that they had a higher fasting blood glucose than those poor mice fed the normal junk which passes for laboratory mouse "chow". This now fits in to an overall pattern. Elevated non esterified fatty acids induce physiological insulin resistance and a higher than expected FBG level.

A simple switch to higher carbohydrate eating (in myself) allows the normal underlying pancreatic and muscle function to show. It also fits in with the FBG of 3.5mmol/l found in the carbohydrate fuelled natives in the Kitava studies. So do I worry about a FBG of over 5.5mmol/l? Not while my HbA1c is 4.4%.

Peter

Familial Hypercholesterolaemia

Familial hypercholesterolaemia (FH) is a common genetic disease. That says something quite profound to me. If it is both genetic and common there cannot be too strong a disadvantage to it on an evolutionary basis. There are also lots and lots and lots of variants. All affect the LDL-C receptor. If you get one copy of any one of a large selection of defective receptor genes, you have quite high levels of cholesterol in your blood and... well, you know the story about clogged arteries and heart attacks. In fact, if LDL-C is such lethal stuff you would have thought that evolution would not have been so careless with the stability of the crucial piece of DNA coding for its receptor. But it wasn't careful and there are a myriad of FH variant genes. Oddly enough people in the 1800s with FH lived as long as, or even longer than, "normal" people, check out the Dutch pedigree and Utah pedigree studies.

Now this is interesting. In 1807 LDL-C at above normal levels was beneficial, particularly in Holland. In 2007 it is an automatic statin deficiency and don't try to get life insurance. What's going on?

If you ask a cardiologist about the function of the LDL-C receptor you will find that it is used by the liver to mop up that horribly artery clogging LDL-C before the patient secumbs. However, there are LDL-C receptors in other places than the liver. Such as on the endothelial cells lining the arteries. If FH sufferers have non functional receptors in their livers I am willing to bet they have poor receptors on their endothelial cells too. But wait a minute, this should be good! If you have reduced receptors you should have reduced stickiness and LESS clogging of the arteries.

But there again, the receptor is normally present and evolution does not go to the effort of building a complex structure just for the fun of wasting protein resources. No, that receptor is there for a reason, and that reason is to stick LDL-C to endothelial cells when they need it. Interestingly, isolated endothelial cells produce lots of LDL-C receptors, where as endothelial cells in contact with their brethren don't. The conclusion from this is that in areas of damage, the endothelial cells are isolated and express lots of receptors which cry out for cholesterol. In FH they don't get the cholesterol they need because the receptors don't work. Cell repair is difficult without a handy supply of lipids.

So, if you had to suggest what sort of problem might be caused by a defective cholesterol receptor, then vascular problems might be a good guess. Possibly heart attack.

NB What do you think might happen if you got two genes for a defective LDL-C receptor? This is homozygous FH. It's bad. You can see why.

So why wasn't heart attack common in FH carriers in 1807? How common was sugar in 1807? Not very. Perhaps there is a link here.

Just a minute. Where did all of that cholesterol come from in the arteries of modern sufferers? Well, you can stick LDL-C to vascular tissue with things other than the apoB-100 receptor. Try the LOX1 receptor for a start. This binds oxidised LDL-C rather nicely. Oxidised cholesterol is seriously nasty stuff. What oxidises cholesterol in your bloodstream? Try fruit and vegetables. Try sugar. Try a low fat diet. My guess is that these were thin on the ground in 1807 in Utah or Holland.

Peter

Niacin and beta hydroxybutyrate

There is nothing about antioxidants in general that affect lipoprotein levels. Niacin undoubtedly does have significant action on blood lipids so undoubtedly is more than an antioxidant. I find that interesting. Why should that be? Many biological processes act through receptors. The niacin effect on lipids, and the niacin flush (ever tried this? It's fun fun fun, not!), are receptor mediated. Clever people have found at least a couple of receptors. The first was HM74, now joined by HM74A. These receptors were not sitting there waiting for either psychiatrists or cardiologists to prescribe multigram doses of nicain, useful though that may be.

No, they have a natural ligand, beta hydroxybutyrate. Beta hydroxybutyrate is a substance dear to my heart, and your heart too, see here. It's a ketone body, naturally manufactured by the liver in times of starvation or carbohydrate restriction. Plus times of coconut fat consumption too, as medium chain triglycerides (MCTs) will produce ketone bodies even in the presence of carbohydrate. By the way, this is not my preferred fat, and it worries me a little that humans break down MCTs as fast as the liver can do so, plus they are shunted down the hepatic vein rather than the thoracic duct, minimising their access to the general circulation. It just reminds me of our metabolism's approach to fructose a bit. Still, coconuts have an excellent track record as a human food in the tropics, so I'm probably just being a bit paranoid here.

Low carbohydrate diets naturally produce ketone bodies. They will certainly elevate HDL cholesterol levels too. To which you may ask, "so what?". Well, elevated HDL cholesterol appears to be a marker of a high fat, low carbohydrate diet and its associated beta hydroxybutyrate. So it is a marker of good things happening in the metabolism. As such I welcome it, but not if it is an effect of some drug. Of course if your primary protection against heart disease is normal blood sugars and low insulin levels the elevated HDL-C is not essential, as seen on Kitava. On western food supply a little exercise plus LC eating seems to be the easiest way to maintain normal blood sugars, and coincidentally elevated beta hydroxybutyrate and so HDL-C. Statins and niacin may elevate HDL cholesterol but my guess is that their benefits (however small from the statins) are unrelated to their effect on HDL-C. And of course, once you are on a drug to elevate HDL-C, there is no way of telling if your metabolism is doing well or badly in terms of insulin sensitivity. If you combine a statin plus niacin plus the dreaded AHA Coco Krispies based low fat diet, you may well be on the road to a cardiovascular disaster, despite having the appearence of a "good" "good" cholesterol level...

Peter

Niacin and adrenochrome

We know that torectrapib was excellent at raising "good" HDL cholesterol, while simultaneously increasing the human death rate from heart attack to the point where it couldn't be ignored. We know that the Kitavans have low "good" HDL cholesterol and no heart disease. So we should forget good and bad cholesterol and concentrate on the things that really matter, which are probably hyperglycaemia, hyperinsulinaemia and wheat. Plus a few other things like trans fats. But the HDL as "good" cholesterol hypothesis will not lie down, although it seems to have been dead for some time. The statins raise HDL, but can be ignored due to their host of confounding pleiotropic effects, inseparable from their cholesterol effects. The current flavour of the month for raising HDL, since the demise of torcetrpib, appears to be niacin, vitamin B3, in multigram doses.

There is no doubt that niacin elevates HDL cholesterol levels and, according to those who follow these things, decreases overall mortality. Now niacin is a very interesting drug. Oh, at 2.0g a day niacin is a drug, not a vitamin. Its career began with Abraham Hoffer, who is still going strong, back in the 1950s. On the basis that "vitamin" doses of niacin had half emptied the psychiatric wards when the problem of pellagra was solved by Goldberger, Hoffer tried massive doses of B3 on schizophrenic patients. The idea was to see if they had a poor response to "normal" doses of B3 which could be overcome by high doses. It worked.

Hoffer's publication in 1954 was last-authored by Smythies, so I assume he was Hoffer's supervisor.

Smythies is also still going strong and has recently summarised the adrenochrome theory of schizophrenia in one of his many publications.

My guess is that niacin may be working by reducing adrenochrome in the brains of schizophrenics. I've no idea of how this works, but it is interesting to note that adrenochrome is an oxidation product and niacin is an effective antioxidant.

That dynamo of genuine cardiovascular research, Kummerow, has looked at adrenochrome in the blood of hypertensive patients. It's there and it mangles the vascular epithelium. Now, does niacin reduce adrenochrome in the blood stream as well as in the brain? It is, after all, a significant antioxidant and anti inflammatory agent. No one has looked at this as far as I know. I certainly don't know if this is the case, but I'm suspicious.

If it does, who cares about the HDL cholesterol effect? Like the statins, niacin appears to be a useful drug, possibly a very useful drug, chosen for the wrong reason. Unlike the statins, niacin has relatively little "badness" attached to it. The problem with torcetrapib was that it ONLY adjusted cholesterol levels. Whatever its associated "badness" or "goodness" might have turned out to be.

That's what happens when you spend millions or maybe billions of dollars developing a drug based on a wrong hypothesis.

Peter

The asterisk

The official title of the fruit and vegetable depletion study I've been discussing recently is this:

Green tea extract only affects markers of oxidative status postprandially: lasting antioxidant effect of flavonoid-free diet*

Did you notice the asterisk? It got dropped from pubmed but is there in the full text pdf.

Why is it there in the paper title? It's there because a major funder for the research wishes to distance itself from the results! That's the EU for you. Fund the research and "IN NO WAY" (direct quote) use the results, as they do not fit your pre concieved ideas, to influence policy!!!!! This is the text associated with the asterisk:

* The study has been carried out with financial support in part from a Danish Food Technology grant (FØTEK2, ‘Antioxidants from plants’) and in part from the Commission of the European Communities, Agriculture and Fisheries (FAIR) specific RTD programme, CT 95-0158 ‘Natural Antioxidants from Foods’. It does not necessarily reflect its views and in no way anticipates the Commission’s future policy in this area.

Hats off to the Danish veterinarians who published this important piece of work and who probably have had their last ever grant from the EU coffers.

I don't think I have ever seen a comment like this ever before on a technical paper.

Wow!

Peter

Fruit and vegetables, last post (almost)

I've posted twice on the links between fruit and vegetables and oxidative damage to lipids, protein and DNA. This then begs the question as to why diets high in fruit and vegetables, on an epidemiological basis, are associated with less chronic diseases than diets deficient in fruit and vegetables. There seems to be a paradox here, fruit and veggies are repeatedly associated with oxidative damage, avoiding them is repeatedly beneficial, yet overall they look good for health when studied at the population level.

So, epidemiology finds fruit and veg are associated with better health. They shouldn't be. But epidemiology shows only shows association, never causality. Only interventions studies do that. On the basis of controlled intervention studies fruit and vegetable consumption shouldn't improve health, so there must be confounding factors here.

You have to ask what the confounding factors might be. Is there anything about the sort of person who eats lots of fruit and veg, compared to those who don't, which might over ride the damage done by the vegetables?

Well, some factors come to mind.

Poverty has to be the first. Poor people do worst on a health basis on just about every measurement possible. They also don't buy much in the way of vegetables. I remember one study showing that poverty is associated with very poor outcomes in diabetes. The conclusion was that we should spend lots of money educating poor people to spend their limited resources on vegetables. You can guess what I think about that. The obvious solution is to give MONEY to those in poverty. When they are rich enough, their health might improve. They might even be able to tolerate eating vegetables with impunity. Of course the link between poverty and ill health is epidemiological. I haven't seen an intervention trial where a large group of impoverished people were give £100,000 each per year and the placebo group given a similar notional value in Enron shares. I'm waiting for that one.

The second consideration is to ask what vegetables might displace from the diet. That is, what do people eat instead of vegetables. Chances are it is sugar or high fructose corn syrup that forms a big chunk. In the fruit and vegetable wash out study a typical daily diet is given. The diet, including total calories, was very strictly controlled. The depletion diet was high in carbohydrate, but mostly from potatoes, rye bread and white bread. The only fructose in the menu was from sucrose in carrots (which are loaded) and in the cake. So this is a pretty low sucrose diet. Eating sucrose and high fructose corn syrup is like getting all the bad aspects of fruit and vegetables but none of the vitamins needed to process the sugars.

Vegetables are bad, but refined sugar is probably worse.

It is possible.

Peter

Vegetables damage your DNA, latest study headline!

Here we go again:

Less vegetables, less DNA damage, the key quote from this abstract is:

"African-Americans had ... lower self-reported intake of most antioxidants (than whites). Levels of oxidative DNA damage, measured using the alkaline comet assay, were lower in African-Americans than Whites"

I'll just repeat, plants make antioxidants to protect themselves from oxidation. They contain nasty pro oxidative substances, which drop on to your DNA whenever you eat those lovely plant based antioxidants.

The only lutein and zeaxanthin worth eating are from egg yolks!

Peter

Unpleasant lipid blockage, personal

There are some pretty nasty spin offs from eating a diet based around saturated fat. Over the last few days I've run it to a particular problem which is a direct result of my eating habits. It was very unpleasant and involved a serious lipid blockage.

A blockage of the main drain from my washing up sink, that is. Not the little U bend in the kitchen, I mean the outside drain, deep, dark, stinking and which must have been overflowing in to the gravel for quite some time. The water was disgusting. I had to hand bale it out down to a steel grid. This was stuck solid and I still haven't been able to remove it. But by slotting an aluminium blade through a gap in the grid and wiggling it back and forth I got the bulk of the water to slowly drain away.

Next move was a trip to B&Q for a large bottle of concentrated caustic soda solution. Sodium hydroxide reacts with fats to form soap, which is soluble, and so clears the drain. Unfortunately it also does the same to the lipids in your skin, so this stuff is not nice to handle. Goggles, gloves and great care are needed, and serious chemical burns result from significant skin contact. I followed it with a kettle of boiling water to speed the process up. Once the drain was clear I ran a large volume of very hot water through it. So far so good, it cleared and has stayed clear.

But it got me thinking. Why on earth have cardiologists not tried running hot caustic soda through peoples' coronary arteries? It should be pretty obvious that if the cause of clogged arteries and clogged drains is the one and the same devil, saturated fat, maybe the same solution should be applied. This is the level of thought that comes up with stupid comments about "artery clogging" saturated fats. Give me a break. Arteries are NOT NOT NOT drains. They do not clog with saturated fat. Do not accept a place in a trial of caustic soda angioplasty when offered it by your cardiologist.

Although my drains do block with saturated fat, my arteries don't. The occasional drain blockage is a price well worth paying for cardiac health.

Peter

Queen Hatshepsut

I've mentioned the health problems of the ancient Egyptians featuring ankylosing spondylitis and its associated IBS. Now add to that obesity, dental abcesses, diabetes and disseminated bone cancer. That was just one queen who ate to the USDA food pyramid.

I wonder how the tooth was snapped off. I wouldn't have wanted to have been her dentist!

Peter

PS Here's the quote as the NY Times link needs registration:

"CT scans led physicians to conclude that the woman was about 50 when she died. She was overweight and had bad teeth. She probably had diabetes and died of bone cancer, which had spread through her body"

and about the broken tooth from SAWF news:

"They said the final clue was a tooth found within a wooden box inscribed with the female Pharaoh's name, which matched exactly to the space of the missing molar and the broken root in the mummy’s jaw socket"

Ouch!

Cholesterol ratios through the looking glass

It is a foundation stone of modern cardiology that cholesterol causes heart disease. The roll of LDL-cholesterol is central. This is "bad" cholesterol. The cholesterol of the Dark Side. Then there is HDL-cholesterol, the "good" cholesterol. Feel the Force Luke.

You know the theory, people eat lots of fat and eggs, make lots of LDL-C. This sticks to the artery walls, bungs them up and a heart attack happens. You've seen all the ads on TV for cholesterol lowering by this or that health food.

But until the statin drugs arrived on the scene this theory was pretty well moribund. Every method of lowering cholesterol ever developed, from diet through cholestyramine to fibrates, had a nasty habit of leaving total mortality unchanged. In some studies it even went up, and almost always in unpleasant ways.

Not so with the statins. The big plus side for statins is that they save lives. Ok, only if you have already had a heart attack first. And not many lives, but some. Being a bloke helps them work too, rather a lot. They do this, we are told, by decreasing bad cholesterol levels, particularly LDL-C, while increasing HDL-C, the good one. Yawn.

Now just imagine a "super drug" which could be added to the weakling statins to produce such a fantastic fall in LDL-C combined with such a rise in HDL-C that it is now possible to actually have an HDL-C level HIGHER than your LDL-C level. By quite a lot! This no minor feat. How good was the outcome? In this drug induced cardiological Nirvana, heart attacks must be banned for ever. Surely they must be. Please.

Except they're not.

The drug is (oops I mean was) torcetrapib and it's been pulled from development by Pfizer because adding it to atrovastatin doubles the cardiovascular catastrophe rate.

These two studies (RADIANCE 1 and RADIANCE 2) were published side by side in NEJM, to which I don't have access. Fortunately the nice people at the HDLforum.org do.

They give the cardiovascular catastrophe rate for torcetrapib combined with atrovastatin as 5.2% vs. 2.4% for atrovastatin alone from the RADIANCE 1 study. The same values from the RADIANCE 2 study are 9.5% vs. 5.6% respectively. These values are not in the abstracts for pretty obvious reasons!

So where does this leave torcetrapib? It appears to be in the rubbish bin, where it belongs! What about the good vs bad cholesterol hypothesis? This goes on as before, despite the increased heart attack rate in the subjects with deliriously high HDL-C and almost no LDL-C . I believe the usual phrase is something like "We wus unlucky, Guv" accompanied by head scratching.

Lowering LDL-C while raising HDL-C has been the Holy Grail of cardiology for some time. Now it's been done, with a vengeance, and it sucks.

The statins are the only lipid lowering drugs to decrease overall mortality in heart attack patients. Not by much, and you have to have had a heart attack first. They only work because they're anti thrombotic, anti inflammatory, anti proliferative, anti oxidant and anti a few other things too. Isn't the toxin (lovastatin) from a mould which grows on rice clever. Especially when compared to Big Pharma's torcetrapib! The cholesterol lowering aspect of lovastatin is an unpleasant and unnecessary side effect. Like the coenzyme Q10 depletion.

Your cholesterol ratios are useless. Thank you Pfizer for torcetrapib. RIP the lipid hypothesis. Again.

Peter

PS torcetrapib was doomed from the start because it had no X Y Z or V in its name. Blame the marketing folks.

Fruit, vegetables and DNA damage

I accidentally deleted this post by some strange miss click of the mouse. I'll re post the bare bones I get the chance. Sorry

Peter


Here is the re post

More from Kitava

Lindeberg and associates (as in the Kitava studies) postulated that elevated uric acid protected the Kitavans from heart disease (it's a good antioxidant). To check this out they compared the blood uric acid levels of these non westernised islanders to a Swedish population. Uric acid levels are basically the same, maybe 10% lower on Kitava. Conclusion:

"The rather similar uric acid levels between Kitava and Sweden imply that uric acid is of minor importance to explain the apparent absence of cardiovascular disease in Kitava"

Lets go back to the low HDL-C and elevated triglycerides levels on Kitava, which also were essentially the same as those in Sweden:

"the relationship between TGs and HDL-C (in Kitava) was similar to that observed in Caucasians"

Yet the conclusion was

"Evaluation of TGs and HDL-C as cardiovascular risk factors must thus be restricted to the study population"

These two papers and statements were written by the same research group. Let's clarify. Essentially uric acid, triglycerides and HLD cholesterol were pretty much the same in Kitava or Sweden. The conclusions from this group are that uric acid is unimportant in keeping the Kitavan's healthy but "bad" lipid levels are important in Sweden yet not in Kitava. Don't forget the levels of uric acid, triglycerides and HDL-C were the same in both populations.

I hadn't read the uric acid paper when I posted on the Kitava study and metabolic syndrome... Nobody will be upset by uric acid bashing. Not so the lipid hypothesis. It just strikes me that researcher's conclusions are determined by their preconceptions

And their future funding.

Peter