Thursday, November 29, 2007

Gluten ataxia

Nottingham and Sheffield are about 30 miles apart. If you have neurological problems presenting as ataxia and live in Mansfield you can either go North to Dr Hadjivassiliou's group, who will undoubtedly work you up for gluten induced problems.

Or you can go South to The Queen's Medical Centre, where you may not get worked up in the same manner. In fact, this letter to the editor of the journal Brain is about as critical as respectable doctors get of each other in public.

It is particularly notable that the main reference cited by Wills and Unsworthy for the incidence of coeliac disease only tested antibody positive patients and only accepted them as coeliac if they had intestinal signs on biopsy. Clearly depending on EMA antibodies, as used in Cook's study, missed many patients so the incidence of intestinal coeliac disease MUST be underestimated.

"The value of EMA as a screening tool is therefore limited"

Still, an incidence of 1% is massively higher than was the accepted incidence 20 years ago. This estimate will continue to increase as people realise how widespread the problems from wheat are.

Backing away from intestinal disease as a pre requisite for gluten problems:

The whole point of Hadjivassiliou's work is that there may not be ANY gut signs with neurological gluten induced disease.

We know full well that the zonulin system in the gut is disrupted by gluten. This is irrespective of the presence of intestinal coeliac disease. Once the gut is permeable to proteins you can take your pick of auto immune diseases. If you get neurological problems AND gut problems Nottingham might accept that you have gluten ataxia. If you get neurological signs without gut damage then it's time to get in your wheelchair.

Sheffield will drive you to a gluten fee diet. It might just work.

If I lived in Mansfield and had some weird neurological disease, personally I'd head North to Sheffield.

Peter (Born in Nottingham but Sheffield is good, just don't take your car)

Low fat moods

These two papers caught my eye. The first is observational and uses very limited in data points but clearly suggests the hypothesis that sugar is a cause of major depression. The biochemistry is supportive of this, a high carbohydrate meal increases blood insulin, which increases blood tryptophan, which increases brain serotonin.

So you fall asleep after a high carb meal.

I used to be a standing joke in our family before I went LC. One of the joys of avoiding rice and pasta was getting my evenings back. The aftermath of sleeping through a serotonon spike is that about three to six hours later your brain serotonin plummets and you can't sleep. Ah, those nights of looking at the clock every five minutes from 2am to 4.30 am. The switch to LC not only gave a good night's sleep every night but I woke feeling good each morning. That's better.

So I find it highly plausible that sugar causes depression. Kick your serotonin system often enough and it will go on strike. Or develop "serotonin resistance" comparable to "insulin resistance".

The second paper looks at the effect of a low fat diet on mood. The abstract is self explanatory and here are the important lines:

"ratings of anger-hostility significantly increased in the intervention group after 1 month on the low-fat diet"

and this

"The results suggest that a change in dietary fat content from 41 to 25% energy may have adverse effects on mood"

One month is VERY rapid for a mood disorder to emerge. Healthy volunteers are not usually prone to anger hostility episodes. This is an intervention study with the subjects acting as their own controls. It's good.

Next time you get carved up in a minor road rage episode, just ask yourself if the perpetrator will have had bacon and eggs fried in butter for breakfast. Alternatively perhaps a bowl of sugared cereals lubricated with skim milk followed by toast and jam lubricated with a low fat spread. Probably has a heart problem and is on a statin too. Anger hostility rating? Is this problem growing?

Dr Ancel Keys again?


Obviously what is missing from the second study is a period when the subjects ate 80% fat in their diet. I assure you it feels good.

Wednesday, November 28, 2007

Getting fat is bad when you stop

There comes a point beyond which getting fat becomes counter productive. This happens when you are too fat. What do I mean by too fat? Being fat is supposed to have survival benefits... I was thinking along the lines of type 2 diabetes, an enormously complex disease.

This problem is obviously "associated" with obesity, yet most obese people do NOT develop diabetes. Plus many thin people can and do develop type 2 diabetes.

From my perspective I think that type 2 diabetes occurs when people loose the ability to put on any more fat. This can happen at assorted body sizes, not just the seriously obese. In fact a huge person who is still gaining weight may well be safe.

We know that obesity requires just a small excess of fat per day to be locked in to adipose tissue by the insulin produced in response to dietary carbohydrate.

That's fine for a few tens of years. But there are limits on both the number of fat cells and the size to which they can be pumped. Eventually they get so full that they just say NO to any more fat. Bearing in mind that it is insulin which puts the fat in to fat cells, the easiest way to say NO is to refuse to put out any insulin receptors, the phenomenon of insulin resistance.

What happens when a fat cell refuses to listen to insulin's storage message? Well, it allows hormone-sensitive lipase freedom from insulin's restraint. This results in an outpouring of the energy set aside, over many years, for a rainy day which never came. Non esterified fatty acids (NEFA) in the plasma increase rapidly. NEFA are the high energy rival to glucose for cell power supply. The control of NEFA flow is at their release point (fat cells), not their uptake point. When the adipocytes thumb their nose at insulin, they release a flood of inappropriate energy which is taken up by just about every cell that can remotely use NEFA for fuel.

Packing NEFA in to cells beyond their wildest possible needs means that they have no logical use for glucose. Muscle tissue is the primary "sink" for glucose. Muscles love NEFA. Once they are packed with NEFA why should they accept glucose? They just say NO by becoming insulin resistant too. If there is no where for glucose to go, it builds up in the bloodstream (especially if you live on bagels and waffles) and you get the label of type 2 diabetes.

Much of this I worked out by slogging sentence by sentence through Dr Raz's article here. He gets hopelessly lost in ideas on treatment. His basic idea is that because the problem is one of excessive fat storage (it is) and the stored fat is from dietary fat (it is) then the correct approach is to reduce dietary fat (WRONG). The correct approach is to reduce the hormone which is causing the excess storage. That is insulin. The spectacular success of low carbohydrate diets for management of type 2 diabetes clearly show this is the way to go.

As soon as you drop insulin levels the fat cells, no longer over bombarded with the message to hyper-inflate themselves, start to listen to the voice of reason. Basal insulin can inhibit lipolysis to levels appropriate for energy needs of the body. Blood glucose normalises because the bagels are in the bin, not your bloodstream. Lipolysis without carbohydrate overload allows ketosis which controls appetite.

I also had some fun with this paper, which gets the prize for worst title ever on a diabetes paper.

Please Pass the Chips: Genomic Insights into Obesity and Diabetes

I guess that the chips are bits of information. I couldn't find anything in the paper about what I would call chips. It is an American paper so I guess they would have used the term French Fries if they had really meant chips... Still, an appalling suggestion for a diabetic diet.

Anyway. The paper has some interesting points. Ignore all the garbage about micro arrays and gene switching etc etc. Throwing money at a problem does not always mean that you understand it.

No, they discuss the lipodystrophies, spontaneous in humans and engineered in lab animals. The basic message is:

Total absence of fat cells equals severe type 2 diabetes, in an organism without any fat at all.

No fat cells means nothing to listen to insulin, so nowhere to store energy. The lack of adipocytes is the equivalent of being born with 100% ineffective adipocytes. If you have no storage space you have to shove your dietary fat in to whatever tissue will take it. Once the tissue, particularly muscle, has a generous supply of fat it will, as above, say no to glucose.

So, as I see it, type 2 diabetes is a condition where adipose tissue cannot accept energy, either through years of hyperinsulinaemia or because it never actually formed. The end result in both cases is muscle fatty acid build up to a level which causes glucose refusal.

You then pee the glucose down the loo. Or eat LC and fix your problem. If you have a lipodystrophy I'm not sure how effective LC eating would be, but it certainly works for standard type 2s.


Getting fat is good

After discussing the two rat experiment and applying it to Kitava, it must be pretty obvious that getting fat in the good times improves your chances of surviving the lean times.

Being fat is good for you.

Anyone going in to the next poor harvest with a BMI of 18.5 is significantly less likely to come out alive for the next good harvest than someone of BMI 29.9. Thinking Kitava here, same applies to hunter/gatherers. But is it possible to have too much fat?

Well a BMI of 18.5-25 is considered "ideal". Looking at this paper we find that:

"Overweight was not associated with excess mortality (-86,094 deaths; 95% CI, -161,223 to -10,966)"

That is BMI 25-30 has lowest all cause mortality. Lower mortality than our ideal target range. Perhaps it's time to move the goal posts. Maybe BMI <25 should be a cause for concern. I'm in trouble on that one!

My only consolation of running my own BMI at 20.5 is that being slim on a high fat diet is almost certainly not as bad for you as when you are on a carbohydrate based diet. It may be good for you. No one will ever find this out looking at USA health statistics. On their Food Pyramid everyone suffers.


PS I tried to understand this paper in depth and it is strictly for the statisticians. I'll have to take Katherine Flegal's word for the results being true.

Tuesday, November 27, 2007

Professor John Yudkin and Dr Ancel Keys

Here's a page or so (p163-4) from John Yudkin's book "Pure White and Deadly", 1972 edition. Yudkin begins the chapter with an apology for talking about such uncomfortable disagreements in public. But he liked the truth.

This quote covers opinion from Prof John Yudkin and Dr Meyer Friedman. You can hear their dislike of Keys. Keys was the architect of what has become the current world obesity epidemic and never one to let the truth get in the way of a good idea, as with his six nations "fat causes heart disease" study. Unfortunately Meyer's list of those easily misled did not include gullible politicians who set food policy. Keys was a very successful politico, with intense conviction of his own correctness. Fine if he had been right, which he wasn't.

Yudkin begins:

I have already mentioned Dr Ancel Keys and his pioneer work in relation to diet and heart disease. A year or so ago he wrote a memorandum which he sent to a large number of scientists working in this field and which with very few changes has now been published in a medical journal 'Atherosclerosis'. It consists entirely of a strong criticism - I nearly said virulent criticism - of the work I have published from time to time on the theory that sugar is the main dietary factor involved in causing heart disease.

The publication contains a number of quite incorrect and unjustified statements; for instance; that we had never tested our method for measuring sugar intake; that no one eats the amounts of sugar that we and others have used in our experiments; that it was absurd of me in 1957 to use intemational statistics of 41 countries as evidence for the relationship between sugar and heart disease (exactly tbe same statistics that Dr Keys had previously used for only 6 selected countries to show the relationship between fat and heart disease).

He ends by triumphantly pointing out that both sugar and fat intakes are related to heart disease, but that the cause must be fat, not sugar, because he had just found in 1970 that fat intake and sugar intake are themselves closely linked. You will remember my own discussion of this link in Chapter 5, based on the fact that, as far back as 1964, I had shown this relationship to exist between fat intake and sugar intake. Let me therefore quote from a recently published book Pathogenesis Of Coronary Artery Disease written by Dr Meyer Friedman, another distinguished worker in this field:

"It is sad, for example, to observe that essentially honourable investigators omit published data (including some of their own data obtained earlier) which refute or call into question their contemporary data and the interpretations they have made of them. It is even sadder to observe how these same observers eagerly and indiscriminately collect studies (no matter how poorly or incompletely performed) supporting their respective hypotheses but peruse with the most "nit-picking" and distrustfuI eye other studies which tend to subvert the interpretive verity of their own. But this is not really a very important cause of our present confusion because only a few investigators indulge in these practices and their foibles are quite well known to their scientific peers. They essentially succeed in misleading only themselves and those physicians and laymen who can not be expected to know of the self-imposed enslavement of these investigators to their respective concepts"

Hmm, Friedman on Keys sounds like Ravnskov on Keys' modern followers.

Plus ça change (plus c'est la même chose)


Monday, November 26, 2007

Two rat experiment

While I'm talking about fat I ought to just run through the two rat experiment described by Daniel Quinn.

You place a breeding pair of rats in a very large cage with, let's say, 5kg of rat food. At the end of 24 hours you remove any left over food, put in a fresh 5kg and repeat the process ad infinitum. Remove the excess, never allow more than 5kg. Clean them out occasionally.

They will breed. Their children will breed. Their children's children will breed. The population will grow. Eventually there will come a day when there is no rat food spare at the end of 24 hours. The young rats will continue to grow, maybe some of the older ones will die, those in their prime may loose a little weight. That's life for rats in the cage.

Ultimately an equilibrium will be reached between 5kg of food and a dynamic population of rats. That population will not fluctuate wildly.

You cannot make new rats out of thin air. Older rats dying will free up some food supply so more youngsters will survive. It will balance out.

This was exactly the situation for the humans on Kitava when Lindeberg did his study. On an isolated island, using limited subsistence agriculture and no external power or fertiliser input, there must be a balance struck between population and food.

Back when everyone on the Earth either subsistence farmed or hunted/gathered the same situation must have applied. Hunting on the neighbouring tribe's patch might be highly unpopular and this would set limits on food availability, even with a full continent to use. People were everywhere that would support life.

I don't think that continuous hunger was ever the norm, but obesity would be unheard of. A sustained glut of food would produce extra sprogs to take up the slack. Hard times would be hard on the vulnerable. We humans did this successfully for millions of years. We are no different to rats. We can only breed to our food supply, but we always will breed to that supply.

There never was enough spare food for obesity until the Egyptians started with storable Spelt. It all went down hill from there.


Getting fat, staying fat, follow on

One kilo of lard contains 9,020kcal of energy. A chunky 40kg of lard represents 360,800kcal.

In the simplistic world of calories-in versus calories-out, how many excess calories per day is this, spread over a reasonable weight gain period? Let's assume it was gained over 20 years, or 7,300 days, ignoring leap years.

That gives 49kcal/day of stored fat. If calories-in equals calories-out anyone carrying 40kg of excess weight could have stopped it by eating just one tiny spoonful less of butter per day. EASY. For goodness sake, these people must be such weak willed, greedy slobs that we should withdraw NHS medical care until they get their act together and stop pigging out on a spoonful of excess butter per day.

But just a minute, how many obese people WANT to be obese? If you believe the calories-in calories-out drivel, weight loss should be easy. Anyone can back off this much butter. Weight Watchers would go bankrupt.

But telling an overweight person to avoid eating fat (gasp, all those calories per gram) means that their diet must be based around carbohydrate. Which raises insulin. Which blocks fat loss. Just 49kcal of blocked fat loss each day over 20 years equals an obesity epidemic. It's not the calories from dry bread, spread with low fat goo, that does this but the insulinaemia that goes with it.

Most people do not read biochemistry texts for fun, they expect their nutritionist to have been paid to do that.


PS How DO people loose weight on low fat diets? They eat low everything, get hungry and dip their insulin low enough between meals to loose weight, especially in the early hours of the morning. This is hard, especially to sustain. Fat is your friend when you want to loose weight. No hunger in ketosis.

Getting fat, staying fat

Fat gets in to fat cells from lipoproteins in the blood stream. Dietary fat is transported in chylomicrons, big fat ladened lipoproteins made by the gut wall. Their production is as random as fat consumption is variable.

Our the bodies never just move fat molecules intact. They are always broken down in to fatty acids, moved across cell membranes in this form, and then reassembled in to triglycerides for long term storage.

The enzyme which performs this break down process is called lipoprotein lipase. Lipoprotein lipase is thus essential for fat storage. That's important.

Fat breakdown, for use as an energy supply, is performed by a completely different lipase, this time it is hormone-sensitive lipase. This enzyme acts on the stored triglycerides inside fat cells and releases free fatty acids in to the blood stream. This is a highly regulated process, finely tuned to supply the energy needed by the body. It is very different from the bulk transport of dietary fat in lipoproteins. As such, the fatty acids can be transported in free form called non esterified fatty acids (attached to albumin in plasma) and simply released as they are needed. Hormone-sensitive lipase is crucial to fat breakdown. That's important too.

It is very obvious, from its name, that hormone-sensitive lipase is under hormonal control. The only hormone which turns off this lipase is insulin.

This paper (From way back in 1964, this is not new information. Physiologists asked very basic questions in those days) shows clearly that insulin, at levels way too low to do anything related to glucose, stops the release of fatty acids from fat tissue. So anything which raises insulin levels blocks fat break down. Carbohydrate raises insulin levels. Insulin blocks fat breakdown. Carbohydrate blocks fat breakdown.

Back to that other lipase, the one that puts the fat in to fat cells in the first place. Is that under any sort of control? Of course it is, our bodies control everything. Guess which hormone controls lipoprotein lipase.

Yes, insulin again.

So insulin has two effects on body fat. It puts it on and keeps it on.

But dietary fat, the primary source of the fat we store, has absolutely no effect on blood insulin levels what so ever. You can eat a block of lard and not budge your insulin levels one iota (or a cup of cream, much more enjoyable). What causes us to store dietary fat, as a big bum or tum, is dietary carbohydrate, because it elevates blood insulin level more than any other food source.

So the take home message from this post is that insulin is the key hormone for fat storage. Dietary carbohydrate makes you store dietary fat, and eating carbohydrate stops you burning stored fat.

It makes you think of those Swedish children. Eating sugar makes them fat, eating saturated fat keeps them slim. Now you know why.

If only nutritionists understood this.


PS does eating half a kilo of lard per day make you put on weight? Possibly, as there is a basal rate of lipoprotein lipase activity irrespective of insulin levels. More importantly, have you ever tried to actually eat 500g of lard in a day? Palatability apart, if you did actually succeed, you would feel dreadful and I doubt you would be tempted to repeat the experience. The vast majority of people on mildly ketogenic high fat diets seem to stabilise their food intake somewhere between 1500 and 2500kcal/day. That is appropriate for weight loss or weight stability, depending on your baseline weight and activity level.

Wednesday, November 21, 2007

Sugar poisoning

I don't think much of the cholesterol hypothesis. OK, it's junk.

But I do find cholesterol levels interesting, in so far as they reflect the degree of carbohydrate poisoning a population is suffering. Researchers are starting to understand this, though I guess they still think the cholesterol levels really matter, rather than looking at the primary problems with glucose and insulin. Obviously low HDL and high triglycerides are appalling things to have because, in general, they represent sugar poisoning.

A chink of light occurred with this study. It's epidemiological, observational and not available in full text without being ripped off by the American Journal of Clinical Nutrition. So not much use to anyone. But the press release by the group contains one of the best lines I've ever seen and gets 110% for deep insightful perception. Here's the line I love:

"Previous research has identified ethnic differences in cholesterol and other blood fat levels that couldn't be explained by genes, obesity, lifestyle factors or diet, Merchant and his team note, but these analyses usually looked at dietary fat, not carbohydrate consumption"

Woo hoo, now there's a surprise! People are poisoning themselves with glucose and fructose and researchers were absolutely focused on dietary fat. FAT! This is not focus, this is preconceived blinkering.

I quite like this line too:

"Reducing the frequency of intake of sugar-containing soft drinks, juices and snacks may be beneficial"

Obviously elimination is highly preferable to reduction, but these people seem to know what they are talking about, though I suspect they still think of triglycerides in terms of hot fat down a cold sewer.

Actually, the other publication from this group looks very sensible too. I'll stop being grudging and just say THANKS.


Tuesday, November 20, 2007

J-LIT update

Here's a quick update on the J-LIT study using low dose simvastatin for primary prevention of heart disease.

My thanks to Stan for pointing out that I missed the six fold increase in risk of CARDIOVASCULAR mortality in the lowest cholesterol group compared to the "normal" (200-219mg/dl) cholesterol group in this study.

There it is in Table 6 on page 1092. For goodness sake, it's on the first line! I must have been asleep when I read the paper:

Cardiac mortality relative risk was 6.23 in patients who's cholesterol dropped below 160mg/dl compared to those with TC 200-219mg/dl.

That is; you are more than six times as likely to be dead of a cardiovascular problem if your TC dropped to a level to make the average cardiologist grudgingly happy.

Boy, when you need cholesterol, you need it.


Sunday, November 18, 2007

Best ever statin study?

I missed this landmark paper last year, full text here. Possibly because, as it continues the demolition of the cholesterol hypothesis, it received absolutely zero publicity. I posted about the J-Litt study here, but this one is even better.

The paper is from the Essen group (in Germany) and describes their study comparing normal dose atrovastatin (10mg/d) with high dose atrovastatin (80mg/d).

Same drug, different dose rates, different cholesterol levels. Follow your patients for a year and have the coronary artery calcification progress tracked by electron-beam computed tomography. This is a reasonably well designed study, except see the "phew" comment below.

How much difference does it make if you drop your LDL-cholesterol to 87mg/dl as compared to 109mg/dl?

I think the answer is technically known as "diddly squat". Or zero, zilch, nuthin, nowt.

The answer as to why is pretty clear from table 3 shown here.

Look at the falls in hsCRP and fibrinogen on low vs high dose atrovastatin. They're the same between groups. Ie the anti inflammatory effect and anti thrombotic effects are maxed out at 10mg, so no further benefit is seen at 80mg. From my point of view this is fortunate. Had these pleiotropic effects not maxed out the study might have suggested lowering cholesterol was beneficial. But 80mg of atrovastatin is no better an anti inflammatory agent than 10mg is. Phew.

The paper discussion is an amusing catalogue of excuses and references to studies "better" designed to show the benefits of aggressive statin use. The trick is to use different drugs and give the best anti inflammatory statin at the highest dose rate. Then the lowest cholesterol correlates with, but is not responsible for, the least CV problems. It is also sensible NOT to measure CRP or fibrinogen, otherwise you end up with a study like this one, where people can see what's going on.

This group strike me as genuine medics who believe in the lipid hypothesis and are genuinely surprised that they have trashed the cholesterol hypothesis by accident. Still, I'll leave them with the best line from their conclusions, ignoring the squirming in the discussion and the plea for more time to get an effect. Here it is:

"we did not observe a relationship between on-treatment LDL cholesterol levels and the progression of calcified coronary atherosclerosis"


Thank you to Dr Davis of Track Your Plaque for citing this unheard of paper

and to

Drs Axel Schmermund, MD; Stephan Achenbach, MD; Thomas Budde, MD; Yuri Buziashvili, MD; Andreas Förster, MD; Guy Friedrich, MD; Michael Henein, MD; Gert Kerkhoff, MD; Friedrich Knollmann, MD; Valery Kukharchuk, MD; Avijit Lahiri, MD; Roman Leischik, MD; Werner Moshage, MD; Michael Schartl, MD; Winfried Siffert, MD; Elisabeth Steinhagen-Thiessen, MD; Valentin Sinitsyn, MD; Anja Vogt, MD; Burkhard Wiedeking, MD; Raimund Erbel, MD

for this excellent study, published in a full-text-for-free journal.

Wednesday, November 07, 2007

Torcetrapib again

I posted on torcetrapib here but missed some information. You always miss some interesting facts when you don't have the full paper. Those nice people on the HDL forum never mentioned the increases seen in deaths from cancer and infection. Fortunately that made it in to the NY Times recently.

Quote from the NY Times article:

"Besides having more heart problems, patients taking torcetrapib were more likely to die of cancer and infection than those on a placebo. In all, 93 patients taking torcetrapib died, compared with 59 who took a placebo"

and from Dr. Daniel J. Rader of the University of Pennsylvania:

“It appears that HDL evolved as a component of the innate immune system and that its composition is critically important to its function.”

Dr Rader gets this week's prize for least well read cardiologist. It's the LDL that matters! But how many cardiologists would read Ravnskov? After all he is one of the most effective critics of the lipid hypothesis. Would you, as a cardiologist, read papers by someone convinced that yourself and the rest of the cholesterol industry is wrong?

Cholesterol and both arteriosclerosis and infection

Cholesterol and cancer

Note that Ravnskov explains all three of the problems seen in the Illuminate trials.

Again a quote from Dr Rader via the NY Times:

"But over all... it is premature to announce the death of CETP inhibitors on the basis of the torcetrapib experience alone"

My opinion?

He's wrong.


Tuesday, November 06, 2007

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"


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?


Monday, November 05, 2007

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.


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!


Friday, November 02, 2007

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.


Thursday, November 01, 2007

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?