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
Sunday, September 23, 2007
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
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
Thursday, August 30, 2007
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
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
Saturday, July 21, 2007
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
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
Tuesday, July 03, 2007
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!
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.
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.
Thursday, June 28, 2007
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
Peter
Here is the re post
Thursday, June 07, 2007
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
"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
Heroin and IBS
Kurt Cobain, the late singer/guitarist from Nirvana, had a lot of problems. Both mental and physical. He self medicated with heroin, leading to serious addiction. On an archive BBC interview earlier this year he described the dramatic relief he got from his gut pain by using heroin. He freely admitted that he had multiple other problems leading to his addiction, but the relief from abdominal pain was a significant factor. No one believed him, this was just another junkie excuse. After all, none of the doctors he had consulted for years had an explanation or any therapy for the pain so it was all in his head, wasn't it...
I mention this because I read another account of a person with abdominal pain, this time there was a diagnosis, the label being IBS. This condition varies from modestly inconvenient through to unspeakably painful, with pulsing waves of cramping visceral pain going on for hours. This guy was posting on a discussion board specialising in poppy tea. Poppy tea is a morphine like opioid mixture reported to be more addictive than heroin as judged by withdrawl severity. It is 100% absolutely illegal just about everywhere in the world and DO NOT USE THIS. I only mention it because this poor guy posted to report the dramatic relief he had obtained from his severe IBS by drinking a cup of this poppy tea. The poppy tea board is a very easy going and very supportive place on the net for opioid addicts to hang out, but they all jumped on this guy like a ton of bricks. No one would remotely accept the reality of the relief he had obtained and the universal condemnation was centered around his using IBS as an excuse to consume the opioid tea, rather than coming clean and admitting he was a straightforward addict. I was shocked at the severity of the responses. Kurt Cobain must have gone through the same thing.
Why on earth am I posting all of this?
Well, my disillusionment with the bulk of the medical profession and my journey in to nutrition began with a close friend who was suffering from severe gut problems without a specific label. Over a year or so the problem had been getting progressively worse. On medical advice she had been increasing her fibre intake. Food consisted of whole meal pasta, brown rice, lentils, chickpeas, whole meal bread and vegetables. Some meat and as little fat as possible completed it. During the final consult her doctor suggested increasing the fibre still further, without explaining quite how this might be achieved. My friend mentioned that she had found, quite by accident, that codeine produced dramatic symptomatic relief. After the doctor had been scraped off of the ceiling there followed a lecture on the constipating effects of codeine and the advice to use ibuprofen to control the pain. This was to a patient in whom a duodenal ulcer was high on the list of possibilities. Please don't do this at home either. Even if your doctor tells you to.
At this point I started reading the medical litterature for myself and we had my friend off of omeprazole and pain free within a month. She never went back to the medic, who is probably still recommending fibre and ibuprofen to her IBS patients and steadfastly refusing to think about why they don't get better.
What really struck me with all three stories was the absolute disbelief in all quarters that opioids could produce symptomatic relief in severe IBS. The impression is that people with severe gut problems are considered to use their "functional" problem as an excuse for recreational opioid abuse. Where is the "That's interesting" reaction from doctors? Nowhere.
The cure, by the way, is the elimination of almost all fibre, absolutely all grains and a marked reduction of carbohydrate consumption. She initially ate 20g/d of carbohydrate but currently anything under 70g/d seems fine for maintenance. Some people have to go a little further and eliminate starches and unfermented dairy too, but that wasn't needed in my friend's case. Grain ingestion, especially wheat, causes an immediate flare. No wonder the high fibre diet was a disaster.
So what is the link between IBS, opioids and especially grains?
Our bodies manufacture many short polypeptides for use as neurotransmitters. One specific group of them are the endorphins. These are naturally produced to control many biological processes. Gut motility and the limitation of both physical and emotional pain are two major functions under endorphin control. Morphine-like drugs, including its diacetylated derivative heroin, drop on to endorphin receptors and produce constipation and happiness. Withdrawl does the opposite. Badly.
Endorphins are produced by ourselves. Exorphins are similar peptides produced from our diet. Partially digested gluten from wheat is a major source. Eating a high gluten diet produces lots of exorphins. Constipation, often after an initial spasm reaction, is the result, just as it is from heroin. And pain too, because although exorphins do reach the brain, they never get there in the quantity needed to produce pain relief or happiness. In fact depression is common in IBS patients, but then chronic severe pain coupled with totally wrong advice tends to lead to depression!
When an IBS patient eventually has a bowel movement there is an immediate removal of the exorphins in contact with the gut wall. Acute opioid withdrawl produces diarrhoea. Remember the opening scenes of Trainspotting, with the methadone suppository and the worst public lavatory in Scotland?
So IBS is a functional problem of constipation with gut spasm alternating with diarrhoea. Eating grains is the commonest trigger. Wholegrains are the worst! Try telling that to your doctor.
BTW there are also exorphins in casein, haemoglobin and spinach but these do not seem to be as indestructible as the gluten derived peptides, although casmorphins do come a close second for many people.
Grains and heroin have a lot in common. Avoid both!
Peter
I mention this because I read another account of a person with abdominal pain, this time there was a diagnosis, the label being IBS. This condition varies from modestly inconvenient through to unspeakably painful, with pulsing waves of cramping visceral pain going on for hours. This guy was posting on a discussion board specialising in poppy tea. Poppy tea is a morphine like opioid mixture reported to be more addictive than heroin as judged by withdrawl severity. It is 100% absolutely illegal just about everywhere in the world and DO NOT USE THIS. I only mention it because this poor guy posted to report the dramatic relief he had obtained from his severe IBS by drinking a cup of this poppy tea. The poppy tea board is a very easy going and very supportive place on the net for opioid addicts to hang out, but they all jumped on this guy like a ton of bricks. No one would remotely accept the reality of the relief he had obtained and the universal condemnation was centered around his using IBS as an excuse to consume the opioid tea, rather than coming clean and admitting he was a straightforward addict. I was shocked at the severity of the responses. Kurt Cobain must have gone through the same thing.
Why on earth am I posting all of this?
Well, my disillusionment with the bulk of the medical profession and my journey in to nutrition began with a close friend who was suffering from severe gut problems without a specific label. Over a year or so the problem had been getting progressively worse. On medical advice she had been increasing her fibre intake. Food consisted of whole meal pasta, brown rice, lentils, chickpeas, whole meal bread and vegetables. Some meat and as little fat as possible completed it. During the final consult her doctor suggested increasing the fibre still further, without explaining quite how this might be achieved. My friend mentioned that she had found, quite by accident, that codeine produced dramatic symptomatic relief. After the doctor had been scraped off of the ceiling there followed a lecture on the constipating effects of codeine and the advice to use ibuprofen to control the pain. This was to a patient in whom a duodenal ulcer was high on the list of possibilities. Please don't do this at home either. Even if your doctor tells you to.
At this point I started reading the medical litterature for myself and we had my friend off of omeprazole and pain free within a month. She never went back to the medic, who is probably still recommending fibre and ibuprofen to her IBS patients and steadfastly refusing to think about why they don't get better.
What really struck me with all three stories was the absolute disbelief in all quarters that opioids could produce symptomatic relief in severe IBS. The impression is that people with severe gut problems are considered to use their "functional" problem as an excuse for recreational opioid abuse. Where is the "That's interesting" reaction from doctors? Nowhere.
The cure, by the way, is the elimination of almost all fibre, absolutely all grains and a marked reduction of carbohydrate consumption. She initially ate 20g/d of carbohydrate but currently anything under 70g/d seems fine for maintenance. Some people have to go a little further and eliminate starches and unfermented dairy too, but that wasn't needed in my friend's case. Grain ingestion, especially wheat, causes an immediate flare. No wonder the high fibre diet was a disaster.
So what is the link between IBS, opioids and especially grains?
Our bodies manufacture many short polypeptides for use as neurotransmitters. One specific group of them are the endorphins. These are naturally produced to control many biological processes. Gut motility and the limitation of both physical and emotional pain are two major functions under endorphin control. Morphine-like drugs, including its diacetylated derivative heroin, drop on to endorphin receptors and produce constipation and happiness. Withdrawl does the opposite. Badly.
Endorphins are produced by ourselves. Exorphins are similar peptides produced from our diet. Partially digested gluten from wheat is a major source. Eating a high gluten diet produces lots of exorphins. Constipation, often after an initial spasm reaction, is the result, just as it is from heroin. And pain too, because although exorphins do reach the brain, they never get there in the quantity needed to produce pain relief or happiness. In fact depression is common in IBS patients, but then chronic severe pain coupled with totally wrong advice tends to lead to depression!
When an IBS patient eventually has a bowel movement there is an immediate removal of the exorphins in contact with the gut wall. Acute opioid withdrawl produces diarrhoea. Remember the opening scenes of Trainspotting, with the methadone suppository and the worst public lavatory in Scotland?
So IBS is a functional problem of constipation with gut spasm alternating with diarrhoea. Eating grains is the commonest trigger. Wholegrains are the worst! Try telling that to your doctor.
BTW there are also exorphins in casein, haemoglobin and spinach but these do not seem to be as indestructible as the gluten derived peptides, although casmorphins do come a close second for many people.
Grains and heroin have a lot in common. Avoid both!
Peter
Tuesday, June 05, 2007
Living on the isolated island of Kitava
On the island of Kitava there are coconuts, sweet potatoes, yams, a few other starches and fish to eat. This leads to an interesting diet. The estimated percentages of energy from protein, fat and carbohydrates are 10%, 21% and 69% in Kitava. Most of the fat is saturated. Three quarters of the population smoke.
Obviously high carb eating should mean catastrophic blood lipids. You would expect low HDL cholesterol and high triglycerides. And this is exactly what you find. HDL-C down at 1.1mmol/l (some as low as 0.5mmol/l) and triglycerides up at 1.7mmol/l (some up at 3.0mmol/l). Not a good ratio. They smoke too. Must be a hotbed of cardiovascular disease. Especially as some of the total cholesterol readings were up around the (gasp) 7.0mmol/l mark. Pravastatin in the local well water is the obvious answer.
Except they have no heart disease. On a diet of 70% carbohydrate. Life expectancy, ignoring neonatal mortality which appears to be high, is around seventy years. That's without any medical facilities. How do they do it?
BTW there were two amusing comments in the discussion of this paper. The best was:
"Evaluation of TGs and HDL-C as cardiovascular risk factors must thus be restricted to the study population"
I'll rephrase that. In Sweden "bad" lipds (and smoking!) are BAD. Not so in Kitava, here "bad" lipids are not bad. They're a product of diet composition. As there is no heart disease they must be good!
So what's happening? Do horrible triglycerides block to your arteries like hot beef fat blocks a cold sewer in Sweden, but then by magic they become non sticky in Kitava? Go figure. Hint, maybe it's not the lipids that trigger the blocked arteries.
Second comment was
"our findings lend no support to the concept that a very high intake of carbohydrates (>60% of energy) increases the risk of cardiovascular disease"
ie living on low fat doughnuts is safe for everyone. Everyone. No suggestion that you have to live in Kitava for this to be the case. So if you eat a junk diet in Sweden and get Kitava lipids in Sweden plus smoke Kitava cigarettes, will you be OK? Somehow I doubt it!
So why are the Kitavans free of heart disease?
Their average fasting glucose is 3.7mmol/l and their fasting insulin 4.0 microU/ml. They do not have any features of metabolic syndrome! Except the lipids of course. Despite eating appalling quantities of carbohydrate. If we define metabolic syndrome as carbohydrate intolerance how do the Kitavans manage this?
I think that this goes back to the main limit on population growth, which is food. Daniel Quinn is the best source of information on this subject. As the Kitavans live with minimal Western food it seems they must be living within the food production capacity of their island. The basic principle is that populations grow to the limit set by their food supply. On Kitava you cannot make babies out of thin air. No extra yams means no extra people. The fluctuations in food and population must mean there are fluctuations in hunger and plenty, but if populations really do expand to the limits of food supply, the island location must ultimately apply calorie restriction. On average.
Ad lib food on a global basis has resulted in a population explosion. On an individual basis it results in a waistline explosion. As carbohydrate is cheap, addictive and hunger generating it is what usually fuels the metabolic syndrome, hence "bad" lipids are associated with metabolic syndrome as carbohydrates are the usual tool of excess calorie intake.
Calorie restriction, intermittent fasting and once daily eating all limit the development of insulin resistance and hyperglycaemia, pretty well independent of macro nutrient ratio. On Kitava there must be accidental calorie restriction as the population is in equilibrium with with a fixed food supply, hence no metabolic syndrome. Despite the "bad" lipids, which merely reflect the composition of their restricted diet.
Can we all do the same? Probably yes, but having read about life on the calorie restricted optimal nutrition (CRON) diet this is definitely not for me. Licking the plate clean because the sauce is delicious is one thing. Doing it because you are starving is quite another! No, there does appear to be a better way.
Eating a ketogenic diet appears to mimic calorie restriction. Ketosis limits appetite so allows modest calorie restriction without any hunger. Forget any drug which may be developed to mimic eating a high fat diet. Better pile on the lard, dump the "healthy" carbohydrate and generate a few ketone bodies. Enough to keep your energy intake reasonable without that desperate dreaming of food which is reputed to go with CRON.
Or you can starve on a balanced diet.
Peter
Obviously high carb eating should mean catastrophic blood lipids. You would expect low HDL cholesterol and high triglycerides. And this is exactly what you find. HDL-C down at 1.1mmol/l (some as low as 0.5mmol/l) and triglycerides up at 1.7mmol/l (some up at 3.0mmol/l). Not a good ratio. They smoke too. Must be a hotbed of cardiovascular disease. Especially as some of the total cholesterol readings were up around the (gasp) 7.0mmol/l mark. Pravastatin in the local well water is the obvious answer.
Except they have no heart disease. On a diet of 70% carbohydrate. Life expectancy, ignoring neonatal mortality which appears to be high, is around seventy years. That's without any medical facilities. How do they do it?
BTW there were two amusing comments in the discussion of this paper. The best was:
"Evaluation of TGs and HDL-C as cardiovascular risk factors must thus be restricted to the study population"
I'll rephrase that. In Sweden "bad" lipds (and smoking!) are BAD. Not so in Kitava, here "bad" lipids are not bad. They're a product of diet composition. As there is no heart disease they must be good!
So what's happening? Do horrible triglycerides block to your arteries like hot beef fat blocks a cold sewer in Sweden, but then by magic they become non sticky in Kitava? Go figure. Hint, maybe it's not the lipids that trigger the blocked arteries.
Second comment was
"our findings lend no support to the concept that a very high intake of carbohydrates (>60% of energy) increases the risk of cardiovascular disease"
ie living on low fat doughnuts is safe for everyone. Everyone. No suggestion that you have to live in Kitava for this to be the case. So if you eat a junk diet in Sweden and get Kitava lipids in Sweden plus smoke Kitava cigarettes, will you be OK? Somehow I doubt it!
So why are the Kitavans free of heart disease?
Their average fasting glucose is 3.7mmol/l and their fasting insulin 4.0 microU/ml. They do not have any features of metabolic syndrome! Except the lipids of course. Despite eating appalling quantities of carbohydrate. If we define metabolic syndrome as carbohydrate intolerance how do the Kitavans manage this?
I think that this goes back to the main limit on population growth, which is food. Daniel Quinn is the best source of information on this subject. As the Kitavans live with minimal Western food it seems they must be living within the food production capacity of their island. The basic principle is that populations grow to the limit set by their food supply. On Kitava you cannot make babies out of thin air. No extra yams means no extra people. The fluctuations in food and population must mean there are fluctuations in hunger and plenty, but if populations really do expand to the limits of food supply, the island location must ultimately apply calorie restriction. On average.
Ad lib food on a global basis has resulted in a population explosion. On an individual basis it results in a waistline explosion. As carbohydrate is cheap, addictive and hunger generating it is what usually fuels the metabolic syndrome, hence "bad" lipids are associated with metabolic syndrome as carbohydrates are the usual tool of excess calorie intake.
Calorie restriction, intermittent fasting and once daily eating all limit the development of insulin resistance and hyperglycaemia, pretty well independent of macro nutrient ratio. On Kitava there must be accidental calorie restriction as the population is in equilibrium with with a fixed food supply, hence no metabolic syndrome. Despite the "bad" lipids, which merely reflect the composition of their restricted diet.
Can we all do the same? Probably yes, but having read about life on the calorie restricted optimal nutrition (CRON) diet this is definitely not for me. Licking the plate clean because the sauce is delicious is one thing. Doing it because you are starving is quite another! No, there does appear to be a better way.
Eating a ketogenic diet appears to mimic calorie restriction. Ketosis limits appetite so allows modest calorie restriction without any hunger. Forget any drug which may be developed to mimic eating a high fat diet. Better pile on the lard, dump the "healthy" carbohydrate and generate a few ketone bodies. Enough to keep your energy intake reasonable without that desperate dreaming of food which is reputed to go with CRON.
Or you can starve on a balanced diet.
Peter
Sunday, January 07, 2007
Paradoxes
Most of us have heard about the French Paradox, which basically says that the French eat masses of saturated fat and have a particularly low rate of heart disease. The usual explanation is that they are protected by all that red wine or their relaxed lifestyle or.... Unfortunately these do not protect the pasta based cuisine consumers of Italy. Quote "in contrast to the French Paradox, which examined how the indulgent French diet could produce favorable health outcomes, the studies of the Mediterranean diet has had the reverse effect in Italy". So do we now have a paradox within a paradox?
But then what about the
Spanish paradox Those naughty Spaniards are eating more fat and less carbs and getting LESS heart disease, now there's a suprise. Good job their medical system is so marvelous.
Sri Lanka paradox In Srilanka they eat <25% calories from fat and still get lots of heart disease. Tut tut.
Israeli paradox The Israelis eat buckets of polyunsaturated fat yet have a much higher heart attack rate than Europe.
Japanese paradox Not only are the naughty Japanese eating more fat, but it is RAISING THEIR SERUM CHOLESTEROL. GASP. So why is their heart attack rate dropping? Easy.
There is even an American paradox!
Particularly note the phrase in that last abstract
"a greater saturated fat intake is associated with less progression of coronary atherosclerosis, whereas carbohydrate intake is associated with a greater progression"
The basic puzzlement in all of these is that the more fat, particularly saturated fat, a nation consumes the LOWER its incidence of heart disease. Low fat consumption, or increased polyunsaturate consumption, INCREASES heart disease.
Of course all paradoxes resolve when you realise saturated fat is not the cause of heart disease....
Peter
But then what about the
Spanish paradox Those naughty Spaniards are eating more fat and less carbs and getting LESS heart disease, now there's a suprise. Good job their medical system is so marvelous.
Sri Lanka paradox In Srilanka they eat <25% calories from fat and still get lots of heart disease. Tut tut.
Israeli paradox The Israelis eat buckets of polyunsaturated fat yet have a much higher heart attack rate than Europe.
Japanese paradox Not only are the naughty Japanese eating more fat, but it is RAISING THEIR SERUM CHOLESTEROL. GASP. So why is their heart attack rate dropping? Easy.
There is even an American paradox!
Particularly note the phrase in that last abstract
"a greater saturated fat intake is associated with less progression of coronary atherosclerosis, whereas carbohydrate intake is associated with a greater progression"
The basic puzzlement in all of these is that the more fat, particularly saturated fat, a nation consumes the LOWER its incidence of heart disease. Low fat consumption, or increased polyunsaturate consumption, INCREASES heart disease.
Of course all paradoxes resolve when you realise saturated fat is not the cause of heart disease....
Peter
Saturday, January 06, 2007
How to increase heart attack risk
The Women's Health Initiative was a massive study of the benefits of reducing the percentage of dietary calories from fat. It involved 48,835 women, so not a small study. Remember that small effects require large studies to detect them. Big effects will show in small groups, so I don't like this study. However it involved a massive input of money to produce a snippet of interest. It also kept 47 authors in gainful employment for over eight years. The women in the intervention group achieved intakes of saturated fat and cholesterol that were less than 10% of energy intake and less than 300 mg/d, respectively. The question is, does reducing your fat intake by 8.2% provide any benefit on cardiovascular disease risk?
The answer is "No", not if you were free of heart disease to begin with. Summary:
There is no benefit. I mean
*******THERE IS NO BENEFIT********
NONE.
What if you are already suffering from heart disease? There was a small subgroup (1,656 women) who had cardiovascular disease at the start of the study. This is what happened to them, and I quote
"The intervention was associated with increased risk in the 3.4% of women with baseline CVD; this may be a chance observation, or rates in this small subset may be confounded by concurrent therapy or comorbid conditions"
The hazard ratio was 1.26 for this group. That is, there was a 26% increase in risk of a cardiovascular incident. You notice from the quote that this "may be a chance observation". I'll translate this for you. What the authors mean is:
They found that reducing the amount of fat in your diet INCREASES your risk of cardiovascular disease. They've tried every possible way of explaining this away and have COMPLETELY failed. If you have already got heart disease you must not reduce your fat intake, unless you really want increase your risk of another heart attack.
You could call this a paradox. I mean yet another paradox.
Or just accept that fat is not the cause of heart disease.
By the way, none of this made it in to the abstract, you must access the full text of the JAMA paper, where you have to trawl through the results to get the Hazard Ratio number.
Funny that!
Peter
The answer is "No", not if you were free of heart disease to begin with. Summary:
There is no benefit. I mean
*******THERE IS NO BENEFIT********
NONE.
What if you are already suffering from heart disease? There was a small subgroup (1,656 women) who had cardiovascular disease at the start of the study. This is what happened to them, and I quote
"The intervention was associated with increased risk in the 3.4% of women with baseline CVD; this may be a chance observation, or rates in this small subset may be confounded by concurrent therapy or comorbid conditions"
The hazard ratio was 1.26 for this group. That is, there was a 26% increase in risk of a cardiovascular incident. You notice from the quote that this "may be a chance observation". I'll translate this for you. What the authors mean is:
They found that reducing the amount of fat in your diet INCREASES your risk of cardiovascular disease. They've tried every possible way of explaining this away and have COMPLETELY failed. If you have already got heart disease you must not reduce your fat intake, unless you really want increase your risk of another heart attack.
You could call this a paradox. I mean yet another paradox.
Or just accept that fat is not the cause of heart disease.
By the way, none of this made it in to the abstract, you must access the full text of the JAMA paper, where you have to trawl through the results to get the Hazard Ratio number.
Funny that!
Peter
Wednesday, December 06, 2006
Which drink causes gout?
Uric acid is a breakdown product of the purines, adenine and guanine. These compounds are found in relatively high amounts in meat, especially organ meats. Obviously, anyone with gout should avoid dietary sources of purines. Ah, if only life were so simple! It reminds me of the truism that eating fat makes you fat... If that were true your average dietician would have cured the current obesity epidemic easily by now.
No, gout is much more interesting.
Gout is triggered by the presence of crystals of uric acid in your joints. It extremely painful. Many people with gout have high levels of uric acid in their blood stream. Oddly enough some people with gout do not have high levels of uric acid in their blood. Dig deeper.
Fructose is an unusual sugar for humans to eat. We have no system to break down fructose polymers. The only sources of fructose we can use are the simple sugar in fruit or honey and as the molecule combined with glucose as sucrose, ie table sugar. Drenching your metabolism with fructose is a recent innovation for humans. The current preferred sweetener for soft drinks is "high fructose corn syrup", a product of our dearly beloved food industry in the last thirty years or less.
What happens when you drench you metabolism with fructose? It enters the metabolic pathway of carbohydrate below its main control step and is immediately converted to fructose-1-phosphate. Quite why evolution has arranged things this way is a mystery, but my suspicion is that evolution does not like free fructose in human metabolism. So drinking a small bucket of cola will put 100gm of fructose in to your liver. This will require a large input of phosphate to for the fructose-1-phosphate, leaving very little for the generation of adenosine tri phosphate (ATP), the primary energy currency of our cells. A lack of ATP triggers activity of the degradation system for adenine and the production of, guess what, uric acid! Gout, and not a serving of kidneys in sight. Until 100 years ago only the rich could afford enough sugar to get gout, now it is a feature of metabolic syndrome and available to all.
Incidentally the fructose has to be "put" somewhere, and that is in to fat for storage, via elevated triglyceride levels in the blood. It causes insulin resistance too. Even the full metabolic syndrome!
In fact, probably the truth is that fructose causes insulin resistance, which causes gout. The hyper uricaemia and the fact that the joints produce uric acid crystals do not have to be causally related. I'd say they're not.
Incidentally, these bright researchers are looking for ways to minimise the self poisoning caused by fructose. They are actually suggesting looking for a drug to allow you to drink high fructose corn syrup without the rise in uric acid.
A drug for life to enjoy your cola. But of course that won't stop the insulin resistance from fructose, so......
Peter
No, gout is much more interesting.
Gout is triggered by the presence of crystals of uric acid in your joints. It extremely painful. Many people with gout have high levels of uric acid in their blood stream. Oddly enough some people with gout do not have high levels of uric acid in their blood. Dig deeper.
Fructose is an unusual sugar for humans to eat. We have no system to break down fructose polymers. The only sources of fructose we can use are the simple sugar in fruit or honey and as the molecule combined with glucose as sucrose, ie table sugar. Drenching your metabolism with fructose is a recent innovation for humans. The current preferred sweetener for soft drinks is "high fructose corn syrup", a product of our dearly beloved food industry in the last thirty years or less.
What happens when you drench you metabolism with fructose? It enters the metabolic pathway of carbohydrate below its main control step and is immediately converted to fructose-1-phosphate. Quite why evolution has arranged things this way is a mystery, but my suspicion is that evolution does not like free fructose in human metabolism. So drinking a small bucket of cola will put 100gm of fructose in to your liver. This will require a large input of phosphate to for the fructose-1-phosphate, leaving very little for the generation of adenosine tri phosphate (ATP), the primary energy currency of our cells. A lack of ATP triggers activity of the degradation system for adenine and the production of, guess what, uric acid! Gout, and not a serving of kidneys in sight. Until 100 years ago only the rich could afford enough sugar to get gout, now it is a feature of metabolic syndrome and available to all.
Incidentally the fructose has to be "put" somewhere, and that is in to fat for storage, via elevated triglyceride levels in the blood. It causes insulin resistance too. Even the full metabolic syndrome!
In fact, probably the truth is that fructose causes insulin resistance, which causes gout. The hyper uricaemia and the fact that the joints produce uric acid crystals do not have to be causally related. I'd say they're not.
Incidentally, these bright researchers are looking for ways to minimise the self poisoning caused by fructose. They are actually suggesting looking for a drug to allow you to drink high fructose corn syrup without the rise in uric acid.
A drug for life to enjoy your cola. But of course that won't stop the insulin resistance from fructose, so......
Peter
Saturday, November 18, 2006
Cholesterol Bogeyman
I was going to suggest it is currently accepted wisdom that an elevated blood cholesterol level is a "risk factor" for heart disease. That is not strictly true as there is a small group of medical practitioners who object to the idea that elevated cholesterol is a cause of heart disease. This even applies to those doctors who are so enthusiastic about cholesterol lowering drugs (statins) that they preach that everyone should take a statin IRRESPECTIVE of their cholesterol level. I find it hard to find a more convincing argument that cholesterol is irrelevant.
Anyway, let's look at one of the few reasonable cholesterol lowering trials ever completed. It was done in Japan. It simply involved taking 47,294 men, all of whom had a total cholesterol level above 240mg/dl (that's 6.15mmol/l in new money, but the paper is written in Noddy units). Everyone got either 5mg or 10mg of simvastatin per day (I presume based on body weight, the authors forgot to say how they decided!). They followed them for six years, then looked at death rates.
Now one strange thing about humans is that we are all different. If you give a big group of people the same dose of a drug most people will respond to it. Some by a lot, some by a little, a few not at all. That's exactly what happened. So now we can split those 47,294 men up in to those who lived with high, low or medium cholesterol levels for six years, all of whom had the same dose of simvastatin kicking around in their blood stream.
What do you get? I like death rates as a measure of outcome. There is no arguing with an outcome of being dead or a live. It's pretty clear cut. Even to a cardiologist. So what happened to death rates?
Those men who's cholesterol level ended up between 200 and 219mg/dl had the lowest risk of dying. In fact if the value ended up anywhere between 180mg/dl and 259mg/dl the risk of dying was pretty much the same as in the lowest risk group. Anything above 260mg/dl was associated with increased mortality. Above 280mg/dl the effect was most marked. Mostly heart disease. I'll write about inherited familial hypercholesterolaemia another day.
Wow, cholesterol must be really bad for you! Except there were a number of men who developed cholesterol levels below 160mg/dl on this dose of drug. Now this is a cholesterol level which would might once have made a cardiologist very happy. I believe they are harder to satisfy nowadays. How good for your overall health is a cholesterol level below 160mg/dl? Well, in this study, by six years later you are considerably more likely to be dead than if your level had only dropped to 210mg/dl. In fact you are 2.76 times more likely to be dead. This is actually a marginally higher death rate than if you had failed to respond to the drug at all. But your cardiologist would still be happy because the excess death rate is not due to heart disease.
The men who dropped their cholesterol below 160mg/dl tended to died of cancer.
Imagine going to your doctor and being offered a pill which would switch your future life from one ending in heart disease to one ending in cancer. Well, we've all got to die some time. Which disease would you prefer? Go on, really. A quickie heart attack or the big C?
By the way the Japanese appear somewhat more clued up about heart disease that the West. A nice commentary here. Pity the free full text is in Japanese!
Anyway, let's look at one of the few reasonable cholesterol lowering trials ever completed. It was done in Japan. It simply involved taking 47,294 men, all of whom had a total cholesterol level above 240mg/dl (that's 6.15mmol/l in new money, but the paper is written in Noddy units). Everyone got either 5mg or 10mg of simvastatin per day (I presume based on body weight, the authors forgot to say how they decided!). They followed them for six years, then looked at death rates.
Now one strange thing about humans is that we are all different. If you give a big group of people the same dose of a drug most people will respond to it. Some by a lot, some by a little, a few not at all. That's exactly what happened. So now we can split those 47,294 men up in to those who lived with high, low or medium cholesterol levels for six years, all of whom had the same dose of simvastatin kicking around in their blood stream.
What do you get? I like death rates as a measure of outcome. There is no arguing with an outcome of being dead or a live. It's pretty clear cut. Even to a cardiologist. So what happened to death rates?
Those men who's cholesterol level ended up between 200 and 219mg/dl had the lowest risk of dying. In fact if the value ended up anywhere between 180mg/dl and 259mg/dl the risk of dying was pretty much the same as in the lowest risk group. Anything above 260mg/dl was associated with increased mortality. Above 280mg/dl the effect was most marked. Mostly heart disease. I'll write about inherited familial hypercholesterolaemia another day.
Wow, cholesterol must be really bad for you! Except there were a number of men who developed cholesterol levels below 160mg/dl on this dose of drug. Now this is a cholesterol level which would might once have made a cardiologist very happy. I believe they are harder to satisfy nowadays. How good for your overall health is a cholesterol level below 160mg/dl? Well, in this study, by six years later you are considerably more likely to be dead than if your level had only dropped to 210mg/dl. In fact you are 2.76 times more likely to be dead. This is actually a marginally higher death rate than if you had failed to respond to the drug at all. But your cardiologist would still be happy because the excess death rate is not due to heart disease.
The men who dropped their cholesterol below 160mg/dl tended to died of cancer.
Imagine going to your doctor and being offered a pill which would switch your future life from one ending in heart disease to one ending in cancer. Well, we've all got to die some time. Which disease would you prefer? Go on, really. A quickie heart attack or the big C?
By the way the Japanese appear somewhat more clued up about heart disease that the West. A nice commentary here. Pity the free full text is in Japanese!
Saturday, November 04, 2006
Sweet Heart Disease
Sugar is sticky. Not just on your fingers, it's sticky in your bloodstream too. The higher your blood glucose concentration rises, the more glucose sticks to the haemoglobin in your red blood cells. It's easy to measure how much this has happened and it gives a pretty good idea of how sugary your bloodstream has been over the last few months. It's called the HbA1c value. Wouldn't it be fun to get together a few thousand people and measure how sugary their blood is, then wait and see how many die in the next six years? Well, even if you don't think so, the EPIC researchers thought it might be, so they did just that.
If you filled a room with 100 people, all with a HbA1c below 5% in 1997, and then invited the same 100 people back for a chat in 2003, how many empty places would there be at the second meeting? The answer is that about 4 people would be absent through having died. If you had a separate meeting arranged for people who's HbA1c was over 7%, how many empty seats might there be after that same six years? The answer is about 19. Having high sugar in your blood is very bad news. Those are the figures for men, the approximate numbers for women are 2 deaths in the low HbA1c group and 25 deathsin the high group. It's a simple relationship, the higher the HbA1c, the worse the outcome.
What did these people die of, associated with their high sugar levels?
Heart disease appeared to be quite important.
Did the researchers check cholesterol levels? You bet they did! Nil, zero, zilch association with heart disease.
So I'll stick with my six eggs for breakfast and pass on the toast and marmalade.
If you filled a room with 100 people, all with a HbA1c below 5% in 1997, and then invited the same 100 people back for a chat in 2003, how many empty places would there be at the second meeting? The answer is that about 4 people would be absent through having died. If you had a separate meeting arranged for people who's HbA1c was over 7%, how many empty seats might there be after that same six years? The answer is about 19. Having high sugar in your blood is very bad news. Those are the figures for men, the approximate numbers for women are 2 deaths in the low HbA1c group and 25 deathsin the high group. It's a simple relationship, the higher the HbA1c, the worse the outcome.
What did these people die of, associated with their high sugar levels?
Heart disease appeared to be quite important.
Did the researchers check cholesterol levels? You bet they did! Nil, zero, zilch association with heart disease.
So I'll stick with my six eggs for breakfast and pass on the toast and marmalade.
Thursday, November 02, 2006
Food Pyramids, food and pyramids
The people who built the Egyptian pyramids developed arthritis. That's what you might expect from pushing around 20 tonne blocks of stone with a few levers. There is an very interesting article on the excavation of the graves of pyramid builders in National Geographic. They are not talking about the pharaoh and the like, but about the people doing the donkey work.
To an archeologist this arthritis does not come as a surprise. Hard labour should produce lots of wear and tear. What is a little more strange is the fact that the Egyptian women were also severely affected. There are no depictions of women moving stone blocks. What is even stranger is that much of the arthritis is found in the women's necks. How heavy a water jug do you have to put on your head, and for how long, to develop severe degenerative arthritis of your cervical spine?
The answer is you don't have to do it at all. Spinal arthritis is rife in the modern, sedentary, middle classes of London or any other city. How many people do you know who are free of back problems? You do not need to be moving pyramid blocks to develop ankylosing spondylitis. But you do need to eat grain.
There is a fairly innocent little bug called klebsiella pneumoniae which lives not only in the soil but in the intestine of many of us, probably most of us. It is a niche bacterium which exploits a particular food source. It eats starch, but not just any starch. Starch is made of long chains of glucose. The chains are branched. At the branch points there are triplets of glucose which will not fit in to the normal digestive machinery possessed by human beings, so they get left undigested. Klebsiella eats these triplets of glucose. It has a special enzyme, pullulanase, to break them down. Happy bacterium.
Unfortumately there is a large subgroup of the population who's immune system "sees" pullulanase as something to attack. These people have a special marker on their white blood cells called HLA B27. They attack pullulanase as if it were an invading nasty. It is unfortunate that the structure of pullulanase and the structure of the collagen which forms our joints is similar. An attack on pullulanase results in collateral damage to the collagen of our ligaments and joints, most particularly those of our spine.
You don't need to carry 20 tonne "lego bricks" around on your head to get cervical spinal arthritis. You just have to eat grains and be unlucky with your HLA type. The Egyptians were amongst the first people on Earth to eat spelt, a precursor of wheat, and they suffered. So here's the £20,000 question; is the USDA Food Pyramid currently causing more arthritis than did the building of the Egyptian Pyramids?
How's your backache and would you like another slice of bread?
Peter
To an archeologist this arthritis does not come as a surprise. Hard labour should produce lots of wear and tear. What is a little more strange is the fact that the Egyptian women were also severely affected. There are no depictions of women moving stone blocks. What is even stranger is that much of the arthritis is found in the women's necks. How heavy a water jug do you have to put on your head, and for how long, to develop severe degenerative arthritis of your cervical spine?
The answer is you don't have to do it at all. Spinal arthritis is rife in the modern, sedentary, middle classes of London or any other city. How many people do you know who are free of back problems? You do not need to be moving pyramid blocks to develop ankylosing spondylitis. But you do need to eat grain.
There is a fairly innocent little bug called klebsiella pneumoniae which lives not only in the soil but in the intestine of many of us, probably most of us. It is a niche bacterium which exploits a particular food source. It eats starch, but not just any starch. Starch is made of long chains of glucose. The chains are branched. At the branch points there are triplets of glucose which will not fit in to the normal digestive machinery possessed by human beings, so they get left undigested. Klebsiella eats these triplets of glucose. It has a special enzyme, pullulanase, to break them down. Happy bacterium.
Unfortumately there is a large subgroup of the population who's immune system "sees" pullulanase as something to attack. These people have a special marker on their white blood cells called HLA B27. They attack pullulanase as if it were an invading nasty. It is unfortunate that the structure of pullulanase and the structure of the collagen which forms our joints is similar. An attack on pullulanase results in collateral damage to the collagen of our ligaments and joints, most particularly those of our spine.
You don't need to carry 20 tonne "lego bricks" around on your head to get cervical spinal arthritis. You just have to eat grains and be unlucky with your HLA type. The Egyptians were amongst the first people on Earth to eat spelt, a precursor of wheat, and they suffered. So here's the £20,000 question; is the USDA Food Pyramid currently causing more arthritis than did the building of the Egyptian Pyramids?
How's your backache and would you like another slice of bread?
Peter
Tuesday, October 31, 2006
Now Alzheimer's Disease
There is a laboratory mouse strain which has been genetically engineered to develop Alzheimer's Disease. Not nice for the mouse, but very useful for research purposes. If you have a look at this abstract, it suggests that limiting calorie intake completely protects against Alzheimer's in this strain of mouse. So why does Alzheimer's still progress in humans, even when weight maintenance becomes very difficult due to the effects of the disease?
Well, the abstract is somewhat disingenuous. It is spectacularly silent about the type of calorie restriction used. Luckily the full paper is available as a pdf at the click of a link. Be warned though, this paper is about as readable as a telephone directory, in the dark, but not as well written. You have to read the abstract, the introduction, the materials and methods until finally you get to the results section. Then you find the best kept secret so far. It's on line three of the results.
Carbohydrate restriction.
OK, yes these animals were calorie restricted, but the ONLY calories removed were carbohydrate.
The discussion actually uses the C word quite a lot. That is, it mentions carbohydrate restriction rather than calorie restriction. But the final paragraph, the sum it all up paragraph, the "this is what we found" paragraph, drops right back to calorie restriction.
Can you imagine the outcry if this group had come up with the headline "Atkins type diet provides 100% protection against Alzheimer's disease in highly susceptible mouse model"? You would actually have heard the "pop" as their funding evaporated. Anyway, it was only mice.
What about humans? No one has done the study yet, though one is planned by the group that did the Parkinson's work I mentioned yesterday. What has already been done is the flip side. That is, increasing the carbohydrate intake of nursing home patients with Alzheimer's disease. This was done to try to limit their weight loss. Adding extra carbohydrate resulted in "increased carbohydrate preference, poorer memory and increased aberrant motor behavior".
And it made them fatter too.
Peter
Well, the abstract is somewhat disingenuous. It is spectacularly silent about the type of calorie restriction used. Luckily the full paper is available as a pdf at the click of a link. Be warned though, this paper is about as readable as a telephone directory, in the dark, but not as well written. You have to read the abstract, the introduction, the materials and methods until finally you get to the results section. Then you find the best kept secret so far. It's on line three of the results.
Carbohydrate restriction.
OK, yes these animals were calorie restricted, but the ONLY calories removed were carbohydrate.
The discussion actually uses the C word quite a lot. That is, it mentions carbohydrate restriction rather than calorie restriction. But the final paragraph, the sum it all up paragraph, the "this is what we found" paragraph, drops right back to calorie restriction.
Can you imagine the outcry if this group had come up with the headline "Atkins type diet provides 100% protection against Alzheimer's disease in highly susceptible mouse model"? You would actually have heard the "pop" as their funding evaporated. Anyway, it was only mice.
What about humans? No one has done the study yet, though one is planned by the group that did the Parkinson's work I mentioned yesterday. What has already been done is the flip side. That is, increasing the carbohydrate intake of nursing home patients with Alzheimer's disease. This was done to try to limit their weight loss. Adding extra carbohydrate resulted in "increased carbohydrate preference, poorer memory and increased aberrant motor behavior".
And it made them fatter too.
Peter
Monday, October 30, 2006
Parkinson's Disease
There is a good summary of what to expect from Parkinson's Disease available at the USA based National Parkinson's Foundation website. Briefly, the problem is incurable, progressive and not particularly pleasant. This is the story of a Parkinson's sufferer who was given the possibility of modifying the usual outcome and the pressures which influenced her choice.
Last year, 2005, there was a report in the medical journal Neurology. It described a pilot study of a special diet for the management of Parkinson's Disease. The whole trial only lasted 28 days and only involved seven people, of whom only five completed the full month. In these five there was an improvement in their Parkinson's disease. Keep in mind Parkinson's is supposed to be irreversible... By the way, a small trial like this is VERY significant. If you have a therapy which makes a big difference it will show in a small trial. If your trial needs 100,000 people to show a minor benefit, the benefit for an isolated individual will clearly be pretty well undetectable.
That's interesting in its own right. But much more interesting was the interview with one of the participants published in USA Today. The article tells us what she ate and mentions that she lost 26lb. The study lasted 28 days. That is an impressive weight loss. So what sort of a diet combines modest reversal of an irreversible disease with dramatic weight loss? The diet is what is known as a ketogenic diet. Just a little meat or eggs each day, plus lots and lots of fat. No carbohydrate. Under these conditions the liver manufactures large quantities of ketone bodies, which are an excellent fuel for the brain and easily able to replace at least half of the daily glucose which is usually considered "essential".
It appears that if you feed dopaminergic brain cells on ketone bodies they stop dying, and maybe the sick-but-not-yet-dead ones recover. The brain likes ketone bodies. Why did the weight loss happen? It is self evident that eating fat makes you fat. Just ask any dietician. It's obvious. Very obvious. But not true. Ketogenic diets are excellent for weight loss. The physiology is logical and unimportant here, but minimal carbohydrate intake is essential for it to work.
The USA Today interview finished with the plan for the next phase of the investigation, using a less extreme ketogenic diet. Ketogenic diets are not easy to adhere to. The interviewee had been invited to take part in this next phase but she had refused. That would be fair enough for a minor problem. Having flicked through the description of advanced Parkinson's disease, I personally would want a serious reason to discontinue a diet which might protect me from the ravages described.
What is so wrong with a ketogenic diet that this lady couldn't stand it?
No carrots were allowed.
There is at least one person out there who would rather allow progression of their Parkinson's Disease than give up nice crispy raw carrots.
Carrots. Raw. And pass me the l-dopa please.
Peter
Last year, 2005, there was a report in the medical journal Neurology. It described a pilot study of a special diet for the management of Parkinson's Disease. The whole trial only lasted 28 days and only involved seven people, of whom only five completed the full month. In these five there was an improvement in their Parkinson's disease. Keep in mind Parkinson's is supposed to be irreversible... By the way, a small trial like this is VERY significant. If you have a therapy which makes a big difference it will show in a small trial. If your trial needs 100,000 people to show a minor benefit, the benefit for an isolated individual will clearly be pretty well undetectable.
That's interesting in its own right. But much more interesting was the interview with one of the participants published in USA Today. The article tells us what she ate and mentions that she lost 26lb. The study lasted 28 days. That is an impressive weight loss. So what sort of a diet combines modest reversal of an irreversible disease with dramatic weight loss? The diet is what is known as a ketogenic diet. Just a little meat or eggs each day, plus lots and lots of fat. No carbohydrate. Under these conditions the liver manufactures large quantities of ketone bodies, which are an excellent fuel for the brain and easily able to replace at least half of the daily glucose which is usually considered "essential".
It appears that if you feed dopaminergic brain cells on ketone bodies they stop dying, and maybe the sick-but-not-yet-dead ones recover. The brain likes ketone bodies. Why did the weight loss happen? It is self evident that eating fat makes you fat. Just ask any dietician. It's obvious. Very obvious. But not true. Ketogenic diets are excellent for weight loss. The physiology is logical and unimportant here, but minimal carbohydrate intake is essential for it to work.
The USA Today interview finished with the plan for the next phase of the investigation, using a less extreme ketogenic diet. Ketogenic diets are not easy to adhere to. The interviewee had been invited to take part in this next phase but she had refused. That would be fair enough for a minor problem. Having flicked through the description of advanced Parkinson's disease, I personally would want a serious reason to discontinue a diet which might protect me from the ravages described.
What is so wrong with a ketogenic diet that this lady couldn't stand it?
No carrots were allowed.
There is at least one person out there who would rather allow progression of their Parkinson's Disease than give up nice crispy raw carrots.
Carrots. Raw. And pass me the l-dopa please.
Peter
Subscribe to:
Posts (Atom)
