There's a diagram of the structure of human Lp(a) here. The apolipoprotein(a) molecule is the curvy bit partly wrapped around the lipid particle. The section which varies on a genetic basis is the number of repeats of the kringle IV type 2 (shown in black). There can be as few as 10 repeats or more than 50. The rule of thumb, within a given population, is that the lower the number of repeats there are, the higher your total plasma Lp(a) is likely to be. NB comparisons between populations are notoriously difficult. Better control your variables and stick to one population.
It almost looks as if the liver wants a certain number kringle IV repeats in the circulation. If there aren't many kringle IVs in the gene, the liver puts more whole protein molecules out to get the number up. Each protein is attached to a single LDL cholesterol particle. Short repeats mean more individual apo(a) proteins are needed to get the number up, which means a higher Lp(a) concentration. It's not a complete equalisation of kringle IV repeats, but that's the general organisation.
The vegetarian Bantu have two things which are special about their Lp(a).
The first is that, despite considerable intermarriage with fishing Bantu, they are genetically short on the kringle IV repeat front so, naturally, they produce more apo(a), attach each to an LDL, so have higher Lp(a) levels across the board compared to their more carnivorous cousins.
The second is that, if you control for this effect by selecting and comparing two genetically apo(a) matched groups, one veggie and the other fish eating, the difference decreases but is still significant.
What can you make of this? The first thing must be that there is a selection pressure to maintain the differences in apo(a) genetics. Either the fishermen don't need much Lp(a) or the vegetarians need lots. I think the vegetarian environment is such that people with high Lp(a) are more likely to survive.
Second follow on is that the extra Lp(a) from the genetics of the vegetarians is not enough. There is some scope for "pushing" Lp(a) levels up or down from the level you might expect from the genetics of apo(a). The vegetarian environment requires higher Lp(a) than the fishing environment.
We know from intervention studies such as DELTA that a simple change of 7% of calories in the SAD from saturated fat to carbohydrate will increase Lp(a) levels by 20%. What does this mean?
If you subscribe to the "Lp(a) is a suicide lipoprotein" theory, you have to conclude that replacing saturated fat with carbohydrate makes your liver want you dead, by 20% more than it did when you ate butter.
Using monounsaturates instead of saturated fats is not quite as bad, the hepatic homicide lipoprotein only goes up by 11%.
The other way of looking at the changes is to suggest that your liver either monitors your macronutrient intake (you think it doesn't?) or some marker of vascular damage. If you do something which is either is outright damaging, or which is sensed as potentially damaging, your liver acts to save your life. If it "perceives" that you need more Lp(a), you get it.
What each of us gets in terms of the genetic number of kringle IV repeats is probably determined by where our personal ancestors lived. Not much we can do about that. What ever we do to tweak this background level of Lp(a) production is up to us.
From the DELTA study it's pretty clear that no one is going to drop their Lp(a) by eating "healthy" monounsaturates or carbohydrate. From the fish oil study we can see that you won't get any joy from adding omega 3 fatty acids either. I've not seen the effect of omega 6s on Lp(a), but I'd guess they're probably as bad as carbohydrate.
As I see it Lp(a) is a very interesting lipid. I think it's hard to get much information from a single measurement in isolation, but changes in Lp(a) probably give you marks out of 10 for your changes in food choices. "Healthy" oils and carbohydrate score you zero. These are likely to damage your vascular system as judged by your liver's increased output of Lp(a). A surrogate for vascular damage would be the increasing blood pressure with age seen in the vegetarian Bantu, probably related to their 82% carbohydrate diet, and so they will need more Lp(a). They get it.
Down at 70% carbs the fish eating Bantu cope well and don't have degenerating arteries to raise their blood pressure, so they don't need so much Lp(a). They don't make it.
I'd predict that substituting beef dripping for both carbohydrate and olive oil would give you the lowest Lp(a) concentration within your genetic window.
Peter
Saturday, April 26, 2008
Wednesday, April 23, 2008
PCOS and LC; is pregnancy a side effect?
This review dropped out of Pubcrawler today. How to get pregnant if you have PCOS.
"Fat should be restricted to < or =30% of total calories with a low proportion of saturated fat"
Of course it must, what else would you expect? Now here's the real giggle:
"High intake of low GI carbohydrate contributes to dyslipidaemia and weight gain and also stimulates hunger and carbohydrate craving"
I'm sure it does, but who would have expected the low fat brigade to realise this? I can't get the full text to see if this is a typo (it MUST be!), but if not, you can't eat fat and you can't eat low GI carbs. Sounds like sugar on your veggie burger is all that's left! The abstract gives no indication of how likely you are to conceive if you follow this advice. I don't think I'd trust it as a form of contraception but...
Of course you could always try living within the limits of your insulin resistance, but (gasp) you might have to eat >30% of calories from fat. This was a pilot study. Only five of the eleven women completed the 24 weeks on the diet. Which diet?
"They were instructed to limit their carbohydrate intake to 20 grams or less per day for 24 weeks"
Result?
"Two women [out of five] became pregnant despite previous infertility problems"
For anyone who might not want to get pregnant, you do have to do something more than eat LC for pregnancy to happen... and be female!
Peter
"Fat should be restricted to < or =30% of total calories with a low proportion of saturated fat"
Of course it must, what else would you expect? Now here's the real giggle:
"High intake of low GI carbohydrate contributes to dyslipidaemia and weight gain and also stimulates hunger and carbohydrate craving"
I'm sure it does, but who would have expected the low fat brigade to realise this? I can't get the full text to see if this is a typo (it MUST be!), but if not, you can't eat fat and you can't eat low GI carbs. Sounds like sugar on your veggie burger is all that's left! The abstract gives no indication of how likely you are to conceive if you follow this advice. I don't think I'd trust it as a form of contraception but...
Of course you could always try living within the limits of your insulin resistance, but (gasp) you might have to eat >30% of calories from fat. This was a pilot study. Only five of the eleven women completed the 24 weeks on the diet. Which diet?
"They were instructed to limit their carbohydrate intake to 20 grams or less per day for 24 weeks"
Result?
"Two women [out of five] became pregnant despite previous infertility problems"
For anyone who might not want to get pregnant, you do have to do something more than eat LC for pregnancy to happen... and be female!
Peter
Lipoprotein(a), a prickly subject
Convergent evolution is a fascinating subject. Lipoprotein(a) has been independently evolved at least twice, not only to produce a remarkably similar (but not identical) molecule each time, but on both occasions it has been by a modification of the same gene, that for plasminogen. The two groups with well characterised Lp(a) are of course old world primates (including man) and the hedgehog. You thought the non primate was the guinea pig? Well, I've not been able to find any replication of Pauling and Rath's work with lipoprotein(a) in guinea pigs and the people who did the work with hedgehogs have looked for the apoprotein(a) gene in guinea pigs, pretty thoroughly... and without success.
What is lipoprotein(a)? It's perhaps best described as a super LDL. Just imagine taking a lethal LDL particle and wrapping it up in a second protein, apo(a), which is not only specifically designed to bind the whole lipid particle to the fibrin present in a blood clot, but which also inhibits clot dissolution. On top of that (could it get worse?) apo(a) is heavily and specifically glycosylated with a sticky sugar coating which will bind to the arterial wall. Hmmmm, if you wanted to clog an artery with lipid, this has got to be your glue!
A quick trip to St Tiggywinkles Hedgehog Hospital would be expected to reveal cages of recuperating hedgehogs, victims of strokes, aortic aneurisms, heart attacks, peripheral vascular disease, all of the problems associated with elevated Lp(a) in humans. In truth my guess is that most of them (the hedgepigs) will actually be victims of road traffic accidents, lung worm infection (a killer in hedgehogs) and late summer birthed toddlers who won't overwinter successfully in the wild.
Perhaps Lp(a) in hedgehogs is different to Lp(a) in humans. It has certain structural differences, but it still acts in as an inhibitor of clot dissolution in models based on human tissue. The fact that it doesn't seem to cause vascular problems in hedgehogs is all the more surprising when you realise that it is THE bulk lipid transport particle in hedgehogs!
The other very strange thing about Lp(a) is that it tends to be rather good for you if you (as a human) make old bones:
"lipoprotein(a) elevation in centenarians, in the absence of other coronary artery disease risk factors, appears as a positive survival factor"
It's worth noting that many of the risk factors for heart disease are turned on their head anyway in the elderly, once you look at all cause mortality. If you are over 65 years old, white or African-American then better think twice about popping that statin! You might end up in that lowest quartile of LDL cholesterol, maybe down at 60mg/dl:
"hispanics had the best overall survival, followed by African-Americans and Whites. Whites and African-Americans in the lowest quartiles of total cholesterol, non-HDL cholesterol and low-density lipoprotein cholesterol (LDL cholesterol) were approximately twice as likely to die as those in the highest quartile"
Just to simplify, low LDL cholesterol=death. That got missed out of the conclusion line! For hispanics, all lipids were irrelevant once you cracked 65 years of age, ie high LDL is not protective in elderly hispanics, nor is it a problem. Of course this is only New York, things may be different in other places. Maybe.
Well, that got me side tracked. Back track with Lp(a) next post.
Peter
What is lipoprotein(a)? It's perhaps best described as a super LDL. Just imagine taking a lethal LDL particle and wrapping it up in a second protein, apo(a), which is not only specifically designed to bind the whole lipid particle to the fibrin present in a blood clot, but which also inhibits clot dissolution. On top of that (could it get worse?) apo(a) is heavily and specifically glycosylated with a sticky sugar coating which will bind to the arterial wall. Hmmmm, if you wanted to clog an artery with lipid, this has got to be your glue!
A quick trip to St Tiggywinkles Hedgehog Hospital would be expected to reveal cages of recuperating hedgehogs, victims of strokes, aortic aneurisms, heart attacks, peripheral vascular disease, all of the problems associated with elevated Lp(a) in humans. In truth my guess is that most of them (the hedgepigs) will actually be victims of road traffic accidents, lung worm infection (a killer in hedgehogs) and late summer birthed toddlers who won't overwinter successfully in the wild.
Perhaps Lp(a) in hedgehogs is different to Lp(a) in humans. It has certain structural differences, but it still acts in as an inhibitor of clot dissolution in models based on human tissue. The fact that it doesn't seem to cause vascular problems in hedgehogs is all the more surprising when you realise that it is THE bulk lipid transport particle in hedgehogs!
The other very strange thing about Lp(a) is that it tends to be rather good for you if you (as a human) make old bones:
"lipoprotein(a) elevation in centenarians, in the absence of other coronary artery disease risk factors, appears as a positive survival factor"
It's worth noting that many of the risk factors for heart disease are turned on their head anyway in the elderly, once you look at all cause mortality. If you are over 65 years old, white or African-American then better think twice about popping that statin! You might end up in that lowest quartile of LDL cholesterol, maybe down at 60mg/dl:
"hispanics had the best overall survival, followed by African-Americans and Whites. Whites and African-Americans in the lowest quartiles of total cholesterol, non-HDL cholesterol and low-density lipoprotein cholesterol (LDL cholesterol) were approximately twice as likely to die as those in the highest quartile"
Just to simplify, low LDL cholesterol=death. That got missed out of the conclusion line! For hispanics, all lipids were irrelevant once you cracked 65 years of age, ie high LDL is not protective in elderly hispanics, nor is it a problem. Of course this is only New York, things may be different in other places. Maybe.
Well, that got me side tracked. Back track with Lp(a) next post.
Peter
Tuesday, April 15, 2008
Kwasniewski and cancer
Some problems are more difficult to influence than others. I have this mental image of nutrition as comparable to having your car serviced. Treat your car with respect and you will have to be unlucky for it to break down. If you ignore servicing, say you never top up the brake fluid, eventually the brakes will fail. If you end up writing the car off, say by being unable to stop at a roundabout, there is no point going back to the wreck, pouring some brake fluid in to the master cylinder and expecting the car to become functional again. It won't.
Some people get broken, I suppose all of us do eventually. But it seems improbable that diet could reverse the degree of "broken-ness" represented by cancer, one of the most serious of metabolic train wrecks. But there are reports of remission. Spontaneous remission is one thing. Engineering that spontaneity is quite another.
Can it be done?
Kasha Mikoda has left a comment on the Praise the Lard post. It's a personal account of the management of her father's non-small cell carcinoma of the lung, with mets. By Kwasniewski. It's there for the reading. Non-small cell cancer includes squamous cell, large cell and adenocarcinoma, prognosis guarded.
Her comment brought to mind an old article I read some time ago about the nutritional management of lung cancer, here.
And of course there are always the two children described by Nebeling.
In terms of an evidence base, case reports in peer reviewed publications carry little weight and non published case reports are just off the radar. But then getting a prospective trial set up to provide an evidence base, even a pilot study, is fraught with difficulties. For a flavour of the current state of difficulty anyone can browse the article which started Kasha off on her journey to Kwasniewski. Attempts at collaboration with mainstream medicine by Kwasniewski never got off the ground.
After that there is patient compliance! Look at this quote from Dr Schmidt in the article cited by Kasha:
Four of the patients were so ill, they died within the first week of the study. Others, says Schmidt, dropped out because they found it hard to stick to the no-sweets diet: "We didn't expect this to be such a big problem, but a considerable number of patients left the study because they were unable or unwilling to renounce soft drinks, chocolate and so on."
Of course these people were end stage and probably considered themselves beyond hope, so why not enjoy whatever food they could manage... But for the life of me I can't see why one has to be absolutely at the end stage of cancer before it is considered ethical to advise that you should stop eating sweets, especially when a PET scan confirms that the cancer lights up like a... Well, like a cancer feasting on glucose in a PET scanner.
Peter
Some people get broken, I suppose all of us do eventually. But it seems improbable that diet could reverse the degree of "broken-ness" represented by cancer, one of the most serious of metabolic train wrecks. But there are reports of remission. Spontaneous remission is one thing. Engineering that spontaneity is quite another.
Can it be done?
Kasha Mikoda has left a comment on the Praise the Lard post. It's a personal account of the management of her father's non-small cell carcinoma of the lung, with mets. By Kwasniewski. It's there for the reading. Non-small cell cancer includes squamous cell, large cell and adenocarcinoma, prognosis guarded.
Her comment brought to mind an old article I read some time ago about the nutritional management of lung cancer, here.
And of course there are always the two children described by Nebeling.
In terms of an evidence base, case reports in peer reviewed publications carry little weight and non published case reports are just off the radar. But then getting a prospective trial set up to provide an evidence base, even a pilot study, is fraught with difficulties. For a flavour of the current state of difficulty anyone can browse the article which started Kasha off on her journey to Kwasniewski. Attempts at collaboration with mainstream medicine by Kwasniewski never got off the ground.
After that there is patient compliance! Look at this quote from Dr Schmidt in the article cited by Kasha:
Four of the patients were so ill, they died within the first week of the study. Others, says Schmidt, dropped out because they found it hard to stick to the no-sweets diet: "We didn't expect this to be such a big problem, but a considerable number of patients left the study because they were unable or unwilling to renounce soft drinks, chocolate and so on."
Of course these people were end stage and probably considered themselves beyond hope, so why not enjoy whatever food they could manage... But for the life of me I can't see why one has to be absolutely at the end stage of cancer before it is considered ethical to advise that you should stop eating sweets, especially when a PET scan confirms that the cancer lights up like a... Well, like a cancer feasting on glucose in a PET scanner.
Peter
Monday, April 14, 2008
Metabolism; mitochondria and uncoupling
Just a final couple of aspects of Nick Lane's ideas about mitochondria, diet and aging before I finally leave them alone. There are some factors which he suggests might be associated with longevity.
The first is high numbers of mitochondria per unit basal metabolism. This is the approach taken by birds and bats (which live far longer than similar sized non flight mammals). The metabolic rate needed for flight is such that resting metabolic rate can be met by the copious mitochondria running at tickover. This is effective at supplying energy without free radical leakage, especially with factor two taken on board. I don't think we'll ever get near to bird numbers of mitochondria, but upping the numbers doesn't seem like a bad idea. How about a few ketones to help?
The second is uncoupling proteins. These allow the hydrogen ion gradient in the mitochondria to be dissipated as heat. This in turn allows through flow of electrons down the electron transport chain, even if there are buckets of unused ATP hanging around. Through flow without obstruction means minimal sewer leakage, less free radicals, less apoptosis...
From this abstract, note that:
"Fatty acids are known to enhance mitochondrial uncoupling protein (UCP) activity"
No mention of glucose doing this! The point of the paper is that ketones do exactly the same thing. I don't see the need for frank ketonuria, but I do like to have ketones on tap for whenever they might be needed!
Peter
The first is high numbers of mitochondria per unit basal metabolism. This is the approach taken by birds and bats (which live far longer than similar sized non flight mammals). The metabolic rate needed for flight is such that resting metabolic rate can be met by the copious mitochondria running at tickover. This is effective at supplying energy without free radical leakage, especially with factor two taken on board. I don't think we'll ever get near to bird numbers of mitochondria, but upping the numbers doesn't seem like a bad idea. How about a few ketones to help?
The second is uncoupling proteins. These allow the hydrogen ion gradient in the mitochondria to be dissipated as heat. This in turn allows through flow of electrons down the electron transport chain, even if there are buckets of unused ATP hanging around. Through flow without obstruction means minimal sewer leakage, less free radicals, less apoptosis...
From this abstract, note that:
"Fatty acids are known to enhance mitochondrial uncoupling protein (UCP) activity"
No mention of glucose doing this! The point of the paper is that ketones do exactly the same thing. I don't see the need for frank ketonuria, but I do like to have ketones on tap for whenever they might be needed!
Peter
Sunday, April 13, 2008
Cynthia Kenyon link
Here is a link to an interview with Cynthia Kenyon, published in New Scientitst back in 2003. It's subscription only now and though I've got a copy on my hard drive it might be better if I just direct you to a site where someone called James Hughes will provide the text!
She is heavily committed to finding a life extending drug. To me, personally, this will run smack bang in to the Law of Unintended Consequences head on. Lowering insulin by diet choices, as she currently practices, seems to be the best plan for a reduction in the diseases old age. (Peter crosses fingers).
Peter
She is heavily committed to finding a life extending drug. To me, personally, this will run smack bang in to the Law of Unintended Consequences head on. Lowering insulin by diet choices, as she currently practices, seems to be the best plan for a reduction in the diseases old age. (Peter crosses fingers).
Peter
Tuesday, April 08, 2008
Cholesterol, MESA and EBCT
Thanks to Dave Lull for a copy of the latest MESA paper. I guess you could just say EBCT looks like a good predictor of heart attack risk, irrespective of age or ethnicity and leave it at that. It looks to be true.
I was just browsing through table one of the results and a few strange things came out. First is that it doesn't include LDL cholesterol at baseline! Most people with any shred of intelligence will realise that calculated LDL cholesterol is garbage, but it's not typical of the average cardiologist to get that far.... These guys must be good!
The second gem was that HDL was lower in the coronary event group, as happens in Framingham. But the difference between the means was 51.0 minus 47.3, I make that 3.7mg/dl. The standard deviation was 15 ish in both groups. If they had a Normal Distribution, which they should have, the range to include most participants is about three standard deviations around the mean. The overlap is phenomenal between heart attack and non heart attack groups. On a personal basis having an HDL of 20 could easily put you in either group, as could an HDL of 60. I guess cardiologists just get used to this.
Taking lipid lowering medication appears to be as bad as being a current of former smoker. Must be a message there but I can't work it out...
Anyone tempted to crash diet might be disappointed by the BMI in the coronary event group being .2 units lower than the spared group. Good job this has neither biological or statistical significance, or participants might have to be encouraged to gain a few pounds. Or get shorter!
I know all of these things need to be factored in to correct for know interactions as it's likely that all of the diabetics were on statins while being encouraged to eat healthy starches and shoot up with insulin, but the raw data still give me a chuckle.
So Detrano et al provide more evidence that coronary calcium, the physical evidence of on going disease, is a better marker of a physical on going disease process than a surrogate of any sort. They also seem less wedded to conventional risk factors. But I guess that's why they're doing the study...
Peter
I was just browsing through table one of the results and a few strange things came out. First is that it doesn't include LDL cholesterol at baseline! Most people with any shred of intelligence will realise that calculated LDL cholesterol is garbage, but it's not typical of the average cardiologist to get that far.... These guys must be good!
The second gem was that HDL was lower in the coronary event group, as happens in Framingham. But the difference between the means was 51.0 minus 47.3, I make that 3.7mg/dl. The standard deviation was 15 ish in both groups. If they had a Normal Distribution, which they should have, the range to include most participants is about three standard deviations around the mean. The overlap is phenomenal between heart attack and non heart attack groups. On a personal basis having an HDL of 20 could easily put you in either group, as could an HDL of 60. I guess cardiologists just get used to this.
Taking lipid lowering medication appears to be as bad as being a current of former smoker. Must be a message there but I can't work it out...
Anyone tempted to crash diet might be disappointed by the BMI in the coronary event group being .2 units lower than the spared group. Good job this has neither biological or statistical significance, or participants might have to be encouraged to gain a few pounds. Or get shorter!
I know all of these things need to be factored in to correct for know interactions as it's likely that all of the diabetics were on statins while being encouraged to eat healthy starches and shoot up with insulin, but the raw data still give me a chuckle.
So Detrano et al provide more evidence that coronary calcium, the physical evidence of on going disease, is a better marker of a physical on going disease process than a surrogate of any sort. They also seem less wedded to conventional risk factors. But I guess that's why they're doing the study...
Peter
Gluten and cardiomyopathy
Again, just a brief note. You want cardiomyopathy? Eat your healthy whole grains and start saving for that heart transplant! Or crossing your fingers if you're in the NHS.
Bear in mind that antibody production is far from necessary for gluten damage, so there is no reason why the two antibody negative patients might not have gluten related damage. Also many "non" coeliac people could equally have gluten damage without gut signs.
Peter
Bear in mind that antibody production is far from necessary for gluten damage, so there is no reason why the two antibody negative patients might not have gluten related damage. Also many "non" coeliac people could equally have gluten damage without gut signs.
Peter
Metabolism nuts and bolts
Nick Lane has produced an interesting book in Power, Sex, Suicide. When it gets down to basics, the electron transport chain of the mitochondria is a bit like a cracked sewage pipe. If that supplies all the information you wanted to know about aging, stop reading now.
What he means is that it leaks unpleasant stuff but usually only in small amounts unless there is a blockage, which fills the pipe and increases leakage pressure. Otherwise just a little of the nasty stuff escapes.
Just to leave sewer analogies aside for a while, what is the electron transport chain? It's a set of very complex molecular structures embedded in the innermost membrane of the mitochondria. It takes an electron (from where, later) and passes it through a series of "mills" and "conduits" until eventually it off loads it on to an oxygen molecule (this is why we breathe, oxygen isn't needed for much else). As it goes through the "mills" its energy is used to pump hydrogen ions from the innermost recesses of the mitochondria in to the outer zones. The more electrons through the mill, the more pumping. The hydrogen ions want to get back in. The only route back in is through a turnstyle. As the turnstyle turns, rotated by a returning hydrogen ion, a mechanism pushes an extra phosphate group on to an ADP molecule to form an ATP molecule. ATP is exported and used as the energy currency of the cell. Most, but not all, ATP is made this way. There are other routes back for hydrogen ions too, but that's another story.
Back to the sewer metaphor. The electron transfer chain leaks. It leaks raw electrons. Electrons react with anything and everything. Many things affect the rate of leakage and the consequences of leakage, but ultimately the knock on effect of this is damage to the mitochondrial DNA, which codes for certain essential components of the electron transport chain... As the DNA degrades over the years the electron chain components become more leaky and more damage is done and we age.
So much comes from PSS. There are very detailed and mostly convincing arguments for this view of aging and a number of other aspects of Life the Universe and Everything. The answer does not appear to be 42.
That got me thinking. Back to Moseby's Crash Course in Metabolism and Nutrition. A quick comparison of the break down of glucose and palmitic acid comes out with this: Glucose goes through glycolysis to pyruvate. Pyruvate enters the mitochondria, gets converted to acetyl CoA and drops in to the ubiquitous tricarboxylic acid cycle (unless your metabolism is VERY strange, like H. pylori). Palmitic acid, my favourite calorie source, gets an executive ticket straight in to the mitochondria where it undergoes beta oxidation to acetyl CoA and after that it could have been sugar (ie acetyl CoA from any source goes down the same cyclical plug hole).
So the difference in metabolism is between glycolysis and beta oxidation. These provide electrons for the electron sewer in different forms. You can't shift electrons around "neat" unless you are using some copper wire or the like. Neat electrons are what do all of the damage. No, electrons are shifted about as chemical electron equivalents. One is NADH, the other is FADH2. Doesn't matter what these stand for. Converting glucose to Acetyl CoA provides a little NADH and that's it. Converting palmitic acid to acetyl CoA provides a whole load of "electrons", in the form of an equal amount of NADH and FADH2. After that it's all acetyl CoA and the same as glucose. But for every calorie of glucose you burn, you generate a higher proportion of NADH to FADH2 than by burning palmitic acid. So what?
NADH puts its electron in to the start of the electron transport chain at complex I. Complex I is leaky. FADH2 puts its pair of electrons in to complex II, which isn't. There is some leakage at complexes III and IV, but complex I one is the worst and fatty acids partially bypass it. I'd like to keep my mitochondria as happy as possible, as they decide when my cells are going to age and die. The later the better. Minimising leakage seems like a good idea (although some is necessary for health, read PSS).
The biochemistry suggests that running your metabolism on fat may release less free radicals than running it on glucose. As I am hopelessly biased in favour of fat metabolism and I enjoy the nuts and bolts of biochemistry, this makes me happy.
It also puts some logic and a mechanism on to Cynthia Kenyon's comment (in reply to being asked why she restricts her carbohydrate intake, ie is it to extend her life expectancy):
"That's not necessarily why I do it. I do it because it makes me feel great and keeps me slender. And I don't feel really tired after a meal. But I think if I wanted to eat in a way that extended lifespan this is how I would do it. In fact, I stopped eating carbohydrates the day we found that putting sugar on the worms' food shortened their lifespans."
I know what she means about feeling good and staying awake after a meal.
Personally I think old age is a not the problem, it's getting there without those diseases normally associated with it that would be nice. If you can become aged and stay disease free, the longer it goes on for the better.
Peter
What he means is that it leaks unpleasant stuff but usually only in small amounts unless there is a blockage, which fills the pipe and increases leakage pressure. Otherwise just a little of the nasty stuff escapes.
Just to leave sewer analogies aside for a while, what is the electron transport chain? It's a set of very complex molecular structures embedded in the innermost membrane of the mitochondria. It takes an electron (from where, later) and passes it through a series of "mills" and "conduits" until eventually it off loads it on to an oxygen molecule (this is why we breathe, oxygen isn't needed for much else). As it goes through the "mills" its energy is used to pump hydrogen ions from the innermost recesses of the mitochondria in to the outer zones. The more electrons through the mill, the more pumping. The hydrogen ions want to get back in. The only route back in is through a turnstyle. As the turnstyle turns, rotated by a returning hydrogen ion, a mechanism pushes an extra phosphate group on to an ADP molecule to form an ATP molecule. ATP is exported and used as the energy currency of the cell. Most, but not all, ATP is made this way. There are other routes back for hydrogen ions too, but that's another story.
Back to the sewer metaphor. The electron transfer chain leaks. It leaks raw electrons. Electrons react with anything and everything. Many things affect the rate of leakage and the consequences of leakage, but ultimately the knock on effect of this is damage to the mitochondrial DNA, which codes for certain essential components of the electron transport chain... As the DNA degrades over the years the electron chain components become more leaky and more damage is done and we age.
So much comes from PSS. There are very detailed and mostly convincing arguments for this view of aging and a number of other aspects of Life the Universe and Everything. The answer does not appear to be 42.
That got me thinking. Back to Moseby's Crash Course in Metabolism and Nutrition. A quick comparison of the break down of glucose and palmitic acid comes out with this: Glucose goes through glycolysis to pyruvate. Pyruvate enters the mitochondria, gets converted to acetyl CoA and drops in to the ubiquitous tricarboxylic acid cycle (unless your metabolism is VERY strange, like H. pylori). Palmitic acid, my favourite calorie source, gets an executive ticket straight in to the mitochondria where it undergoes beta oxidation to acetyl CoA and after that it could have been sugar (ie acetyl CoA from any source goes down the same cyclical plug hole).
So the difference in metabolism is between glycolysis and beta oxidation. These provide electrons for the electron sewer in different forms. You can't shift electrons around "neat" unless you are using some copper wire or the like. Neat electrons are what do all of the damage. No, electrons are shifted about as chemical electron equivalents. One is NADH, the other is FADH2. Doesn't matter what these stand for. Converting glucose to Acetyl CoA provides a little NADH and that's it. Converting palmitic acid to acetyl CoA provides a whole load of "electrons", in the form of an equal amount of NADH and FADH2. After that it's all acetyl CoA and the same as glucose. But for every calorie of glucose you burn, you generate a higher proportion of NADH to FADH2 than by burning palmitic acid. So what?
NADH puts its electron in to the start of the electron transport chain at complex I. Complex I is leaky. FADH2 puts its pair of electrons in to complex II, which isn't. There is some leakage at complexes III and IV, but complex I one is the worst and fatty acids partially bypass it. I'd like to keep my mitochondria as happy as possible, as they decide when my cells are going to age and die. The later the better. Minimising leakage seems like a good idea (although some is necessary for health, read PSS).
The biochemistry suggests that running your metabolism on fat may release less free radicals than running it on glucose. As I am hopelessly biased in favour of fat metabolism and I enjoy the nuts and bolts of biochemistry, this makes me happy.
It also puts some logic and a mechanism on to Cynthia Kenyon's comment (in reply to being asked why she restricts her carbohydrate intake, ie is it to extend her life expectancy):
"That's not necessarily why I do it. I do it because it makes me feel great and keeps me slender. And I don't feel really tired after a meal. But I think if I wanted to eat in a way that extended lifespan this is how I would do it. In fact, I stopped eating carbohydrates the day we found that putting sugar on the worms' food shortened their lifespans."
I know what she means about feeling good and staying awake after a meal.
Personally I think old age is a not the problem, it's getting there without those diseases normally associated with it that would be nice. If you can become aged and stay disease free, the longer it goes on for the better.
Peter
Tuesday, April 01, 2008
Athletic acid reflux
If you work on the basis that gastroesophageal reflux is carbohydrate poisoning, you would expect a LC diet to provide remission of symptoms. Just reading through the abstract of this paper from g, that would appear to be the case. Six days is a pretty short period to sort our GERD and no doubt there would be further improvement with time. The other tweak would be gluten elimination, not that much would be coming through at 20g of carbs per day.
This goes nicely back-to-back with another paper which has been lying around on my hard drive for some time. There is a fairly large literature as to why exercise results in an omprazole deficiency in athletes, with lots of ideas floated around about pressure changes, hormones etc. I think it's reasonable to describe many endurance athletes, the ones worst affected, as indulging in "carb loading". Apart from furring up their coronary arteries with sugar, GERD would seem be (yet) another price that must be paid by athletes for this practice. I'm glad so say that I have no personal experience of GERD, though my wife could write a book bout it.
Peter
BTW Nice to see Grete Waitz doing well.
This goes nicely back-to-back with another paper which has been lying around on my hard drive for some time. There is a fairly large literature as to why exercise results in an omprazole deficiency in athletes, with lots of ideas floated around about pressure changes, hormones etc. I think it's reasonable to describe many endurance athletes, the ones worst affected, as indulging in "carb loading". Apart from furring up their coronary arteries with sugar, GERD would seem be (yet) another price that must be paid by athletes for this practice. I'm glad so say that I have no personal experience of GERD, though my wife could write a book bout it.
Peter
BTW Nice to see Grete Waitz doing well.
Fiber, sucrose and ulcers
Thanks to g for this paper. It's a little observational study looking sucrose vs fiber and their possible association with peptic ulcer. Cleave suggested refined carbohydrate caused duodenal ulcers. The carbophillic nature of post-Keys medicine suggested that fiber could redeem carbohydrate as a source of nutrition. This group from Nottingham (my place of origin) appear to be dubious about this. This phrase comes from the discussion:
"Despite the current healthy diet lobby there were no claims of increased (or decreased) fibre intake by patients or control subjects"
The clear association of ulcers with sucrose was interesting. The total lack of protection from cereal fiber was too (sorry, lack of negative association). But the best bit was vegetable fiber. This was slightly "protective". Until you corrected for social class (and a few other things), at which point the association was lost. Looks a bit suggestive that vegetable fiber intake might just be a surrogate for being more well off.
Another throw away comment from Nottingham in the late 1980s was that Crohn's disease is consistently associated with high refined sugar intake. I think I've seen quite a number of studies coming to that conclusion. But surely sucrose (or HFCS for that matter) can form part of a healthy balanced diet...
Peter
"Despite the current healthy diet lobby there were no claims of increased (or decreased) fibre intake by patients or control subjects"
The clear association of ulcers with sucrose was interesting. The total lack of protection from cereal fiber was too (sorry, lack of negative association). But the best bit was vegetable fiber. This was slightly "protective". Until you corrected for social class (and a few other things), at which point the association was lost. Looks a bit suggestive that vegetable fiber intake might just be a surrogate for being more well off.
Another throw away comment from Nottingham in the late 1980s was that Crohn's disease is consistently associated with high refined sugar intake. I think I've seen quite a number of studies coming to that conclusion. But surely sucrose (or HFCS for that matter) can form part of a healthy balanced diet...
Peter
Monday, March 31, 2008
Cholesterol; statins kill?
Just a quickie.
Go read Dr Eades' blog here. For anyone who has read the J-litt study, or more especially line one of table 6 on page 1092, none of this will come as a surprise. There is a level of LDL below which repair cells just won't get enough cholesterol and lipid to patch the hole in the intima left by the apoptosis of an endothelial cell. The repair will then be botched with a next best like Lp(a).
Interesting development.
Peter
Go read Dr Eades' blog here. For anyone who has read the J-litt study, or more especially line one of table 6 on page 1092, none of this will come as a surprise. There is a level of LDL below which repair cells just won't get enough cholesterol and lipid to patch the hole in the intima left by the apoptosis of an endothelial cell. The repair will then be botched with a next best like Lp(a).
Interesting development.
Peter
Sunday, March 30, 2008
Helicobacter and glucose
Helicobacter is a bad bug. Really bad. So bad that in the recent consensus conferences, like this one, the plan is clear. Hunt, find, kill. Sounds like the cholesterol consensus to me. The only good cholesterol molecule is a dead cholesterol molecule. Oops, getting a bit random there. Back to reality:
"The consensus conference boldly recommended population-based screening and treatment for H. pylori in particularly high-risk population settings"
Anyway, some time around 60,000 years ago humans walked out of Africa in to what is now the Middle East and kept going. Taking their Helicobacter pylori with them. Yes, H pylori has been around the human gut for a long time. There is a nice neat diagram and discussion of human/helicobacter co-expansion on this person's blog. The basic idea is that you can get some idea of the spread of humans by looking at the genes of their H pylori. Presumably the hunter-gatherers were dying like flies from gastric carcinoma along the way.
So, the consensus plan is to eliminate a bug which has been with us on a timescale of up to 100,000 years, and this will stop gastric cancer. Truly a bold recommendation.
If you go back to the early accounts of the missionary hospitals tending to native populations before the introduction of Western lifestyles, cancer was very very very rare. Stefansson summarises it rather well in his 1960 book Cancer: Disease of Civilisation. It's hard to get hold of a copy and rather expensive too, but it makes an interesting read. Cancer searches came back negative. I'm willing to accept that H. pylori wasn't causing cancer in human hunter gatherers, although they were all "infected", if that's the right word for a gastric commensal.
So why does helicobacter cause cancer in humans nowadays? Some light was shed on the problem by the Japanese who noticed that elevated fasting plasma glucose levels are associated with gastric cancer, but only in those patients who carry helicobacter.
Helicobacter is quite a specialised bug. This paper has some interesting snippets. H pylori appears to love glucose. It will do both aerobic and anaerobic metabolism with it, but look at this:
"Under aerobic conditions acetate was the major oxidation product from pyruvate; no evidence was obtained for tricarboxylic acid cycle activity"
H. pylori doesn't appear to use the tricaboxylic acid cycle! Certainly not in this set up. Pyruvate is converted to acetate without acetyl CoA entering the TCA. This looks to me as if fermentation might be producing the bulk of its ATP. In fact if you look further you find that helicobacter does actually run a TCA cycle of sorts, but it runs it in reverse, and it's non cyclical and it runs as a reducing system, non oxidative... I'm not sure how much this set up could do with a fatty acid! I get the impression that glucose might just be the preferred fuel...
Back in the big world there is a mass of anecdotal evidence that LC eating "sorts out" many cases of dyspepsia. I can't find any specific studies since Yudkin's open cross over diet trial detailed in chapter 12 of Pure, White and Deadly, where LC eating worked for many, but not all, dyspepsia patients.
I think it's a reasonable speculation that anything which increases blood glucose might just encourage helicobacter to have a field day and do some cancer generating. Dropping blood glucose might just do the opposite. Actually, maybe just eating the glucose non-stop is a bad idea! Certainly a LC diet might have a better long term outcome for those people currently dependent on ranitidine or omeprazole for control of the extremely unpleasant effects of dyspepsia.
Or of course we could just kill all the Helicobacter pylori in people at risk of gastric cancer, and stop them ever getting infected again. That's the consensus.
Ha ha ha.
Peter
"The consensus conference boldly recommended population-based screening and treatment for H. pylori in particularly high-risk population settings"
Anyway, some time around 60,000 years ago humans walked out of Africa in to what is now the Middle East and kept going. Taking their Helicobacter pylori with them. Yes, H pylori has been around the human gut for a long time. There is a nice neat diagram and discussion of human/helicobacter co-expansion on this person's blog. The basic idea is that you can get some idea of the spread of humans by looking at the genes of their H pylori. Presumably the hunter-gatherers were dying like flies from gastric carcinoma along the way.
So, the consensus plan is to eliminate a bug which has been with us on a timescale of up to 100,000 years, and this will stop gastric cancer. Truly a bold recommendation.
If you go back to the early accounts of the missionary hospitals tending to native populations before the introduction of Western lifestyles, cancer was very very very rare. Stefansson summarises it rather well in his 1960 book Cancer: Disease of Civilisation. It's hard to get hold of a copy and rather expensive too, but it makes an interesting read. Cancer searches came back negative. I'm willing to accept that H. pylori wasn't causing cancer in human hunter gatherers, although they were all "infected", if that's the right word for a gastric commensal.
So why does helicobacter cause cancer in humans nowadays? Some light was shed on the problem by the Japanese who noticed that elevated fasting plasma glucose levels are associated with gastric cancer, but only in those patients who carry helicobacter.
Helicobacter is quite a specialised bug. This paper has some interesting snippets. H pylori appears to love glucose. It will do both aerobic and anaerobic metabolism with it, but look at this:
"Under aerobic conditions acetate was the major oxidation product from pyruvate; no evidence was obtained for tricarboxylic acid cycle activity"
H. pylori doesn't appear to use the tricaboxylic acid cycle! Certainly not in this set up. Pyruvate is converted to acetate without acetyl CoA entering the TCA. This looks to me as if fermentation might be producing the bulk of its ATP. In fact if you look further you find that helicobacter does actually run a TCA cycle of sorts, but it runs it in reverse, and it's non cyclical and it runs as a reducing system, non oxidative... I'm not sure how much this set up could do with a fatty acid! I get the impression that glucose might just be the preferred fuel...
Back in the big world there is a mass of anecdotal evidence that LC eating "sorts out" many cases of dyspepsia. I can't find any specific studies since Yudkin's open cross over diet trial detailed in chapter 12 of Pure, White and Deadly, where LC eating worked for many, but not all, dyspepsia patients.
I think it's a reasonable speculation that anything which increases blood glucose might just encourage helicobacter to have a field day and do some cancer generating. Dropping blood glucose might just do the opposite. Actually, maybe just eating the glucose non-stop is a bad idea! Certainly a LC diet might have a better long term outcome for those people currently dependent on ranitidine or omeprazole for control of the extremely unpleasant effects of dyspepsia.
Or of course we could just kill all the Helicobacter pylori in people at risk of gastric cancer, and stop them ever getting infected again. That's the consensus.
Ha ha ha.
Peter
Friday, March 28, 2008
Food; sausages
Tonight was sausages. First buy some Norfolk pork sausages from these people.
I asked them what filler they used in their wide range of gluten free sausages. The answer was that if you buy a sausage making machine which costs as much as a small Mercedes car you don't need any filler. No filler.
If you're not in the UK just hunt down some all meat sausages if you can get them.
We had about half a pound each. Fry them gently until lightly browned but not cooked through using butter/oilve oil as prefered. Stick them in a bowl to one side and fry a small onion and two red peppers (all chopped) in the fat. Put the sausages back in, add a tin of tomatoes, some pepper, crushed garlic and generous red wine plus lots of oregano. Simmer for as long as you can wait. About half an hour is needed, longer blends the flavours better. Tastes best with olive oil but I suspect lard would be healthier....
Peter
I asked them what filler they used in their wide range of gluten free sausages. The answer was that if you buy a sausage making machine which costs as much as a small Mercedes car you don't need any filler. No filler.
If you're not in the UK just hunt down some all meat sausages if you can get them.
We had about half a pound each. Fry them gently until lightly browned but not cooked through using butter/oilve oil as prefered. Stick them in a bowl to one side and fry a small onion and two red peppers (all chopped) in the fat. Put the sausages back in, add a tin of tomatoes, some pepper, crushed garlic and generous red wine plus lots of oregano. Simmer for as long as you can wait. About half an hour is needed, longer blends the flavours better. Tastes best with olive oil but I suspect lard would be healthier....
Peter
Thursday, March 27, 2008
Kwasniewski; praise the lard
This article was originally published in 2004 in the Chicago Tribune. It's still knocking around on the web in various places but the original seems to have disappeared. You can't have too much of a good thing. Obviously Stephan's recent posts on lard prompted me to put this one up. The imported nutritionist doesn't seem quite as dismissive as you might expect! But notice in the last paragraph that the big bogeyman is protein overload damaging the kidneys! On 60g/d of protein??? Sobor clearly knows nothing about high fat diets, certainly not the one he is commenting so authoritatively about in this case!
Peter
Praise the LARD
By Monica Eng
Chicago Tribune
CHICAGO -- Vinka Peschak starts each day by knocking back a full cup of heavy whipping cream.
That's at 8 a.m.
"At around 11 o'clock I take three or four egg yolks and make some kind of omelet with lard for breakfast," the Portage Park resident explains. Peschak, a native of Poland, eats her omelet with a cup of buttery boiled vegetables and a slender piece of almond toast slathered in more butter or lard.
Dinner is usually a fatty piece of pork or some kind of organ meat with lard-cooked french fries and more butter-soaked vegetables.
In the middle of the day she might have a cup of coffee, "but only with a lot of heavy whipping cream in it."
Peschak has been eating like this for more than five years. She is slim, energetic, and says, "I feel wonderful, never tired and never hungry."
She is not on Atkins. She is not on South Beach.
Peschak, along with an estimated 2 million folks worldwide is on the Optimal Diet, a Polish eating plan that requires the consumption of prodigious amounts of animal fat -- preferably lard.
The diet was hatched in Poland some 40 years ago by Dr. Jan Kwasniewski, who started developing it while working as a dietician for a military sanitarium in Ciechocinek, Poland. There he observed that many of his patients were sick, "not because of any pathogenic factors ... but the result of one underlying cause -- bad nutrition," according to his English language "Optimal Nutrition" book. After experimenting on his family and himself, Kwasniewski concluded that the ideal nutritional combo came from eating three grams of fat for every one gram of protein and half a gram of carbohydrates.
After a couple of decades of refining this theory, Kwasniewski published his first book in Poland in 1990. But it wasn't until converts came forward with their stories of weight loss and recovery from disease in the mid-'90s that the diet really took off it its native land and Kwasniewski's books went into wide circulation. Today there are at least two magazines devoted to the Optimal lifestyle and Kwasniewski writes a twice weekly column for the regional Polish newspaper Dziennik Zachodni.
It wasn't until 2001, though, that Chicago would become the North American capital for this eating plan. That's when Tomasz Zielinski bought a little storefront on Milwaukee Avenue and opened Calma Optimal Foods. The first and only one of its kind in the nation, it operates as a deli, meeting center and, as of this spring, a restaurant for those on the lard-laden plan. Peschak serves as its manager.
Sometimes called the Polish Atkins, the Optimal Diet severely restricts the intake of carbohydrates and sugars, but differs from Atkins by de-emphasizing protein and beefing up, or more accurately porking up, the fat to a level that would have even made the late Robert Atkins reach for his heart.
On average, the diet recommends a whopping 250 grams of fat per day, about four times what the FDA recommended for the average person to maintain his/her weight and about 10 times the amount of saturated fat allowed.
So despite its popularity in Poland -- Lech Walesa is reported to have lost 44 pounds and cured his diabetes on it recently -- the mainstream medical establishment there and here is skeptical.
"I am very against diets like this," says Jadwiga Roguska, a practicing internist at the Feinberg School of Medicine at Northwestern University. "All high-fat diets are unhealthy in the long term and there is absolutely no benefit to weight reduction of this sort because it is threatening to health. ... Of course, high-fat diets will give you the benefits of energy and weight loss, but they are just not good for you."
Roguska based her comments on a brief overview of its principles, but Chicago physician Mark Sobor has seen it up close and has watched an increasing number of his patients in the Polish community embrace it.
"Kwasniewski is pure fat," says Sobor who practices in Jefferson Park and is also a licensed acupuncturist. "Eat fat non-stop. Everything is pure fat. The more fat you can take in the better and these people are fanatics about it. But the thing is they're all skinny."
On a recent Sunday morning at the Optimal deli/center in Portage Park, Ill., about 30 mature, fairly slim followers of the Kwasniewski plan gathered for a weekly meeting and shared their stories.
There was the ginger-haired firecracker Irena Kozlowicz, 78, who went on the diet five years ago after Kwasniewski came to speak at the Copernicus Center in 1999. At the time she was suffering from chronic eye problems, asthma and pain in her knees.
"Now I can walk better than a young person," she chirps. "I can run up six floors of stairs and my grandson can't catch me. He's 17 years old. I meet young ladies and they are always tired and sweating, but I never am. I didn't need to lose weight, but I lost 8 pounds. I am 78, but I feel like I am 50. I thank God for the diet."
Then there is Jozef Michael Ostrowski, 71, who says he has been on a variation of the diet his whole life.
"Since the occupation of Poland my parents could only afford pork meat and liver and blood sausage and lard," Ostrowski says through an interpreter. "It is not like I was following this diet precisely but generally. At that time I didn't know this kind of natural food was good for me. I just knew that I could eat scrambled eggs with a thin piece of bread and lard and I would be full all day. I started eating regular food like McDonald's and I could not handle the pain and so I went back to the diet and have felt better and better every day."
Zofia Pawlik, 56, started the diet last year when she went on an Optimal vacation, a retreat to the Wisconsin Dells to learn about the program and eat its foods. Over the course of a year, she says she has lost 10 pounds while improving her energy and overall health.
IMPRESSIVE RESULTS
Chicago physician Christopher Kubik wasn't at the meeting, but in a phone interview he said that four and a half years ago he was overweight and suffering from fatigue and stones in the bladder. But within a couple of months of embarking on this high-fat journey he saw results.
"I was losing weigh gradually (he lost about 25 pounds in six weeks) but I felt fine. Since then, I didn't have any more problems with stones, my skin complexion improved and I am still feeling a lot of energy," says Kubik, 57, who reports that he breakfasts on fried eggs, bacon and string cheese seven days a week. "So I experienced myself significant detectable improvement even though I generally had good health to begin with. While I was losing the weight I could feel the ketones as a metallic tasted on the mouth, but after I reached my optimal weight, (the ketosis) stopped. Now my weight has remained steady at about 185, which is in the upper limit of normal for my height."
Kubik, who also has degrees in public health and health law, says he does not actively promote the diet, "because it is not considered a standard of care and the medical community still recommends low-fat diets and it is not something I could support if I were sued." But if patients ask, "I tell them that I am on it and have seen positive results."
Dr. Sobor has also seen a growing number of Kwasniewski converts who claim weight loss is only one of the benefits they've reaped.
Chester Matuszewski, 46, for instance says that four years ago he was diagnosed with rheumatoid arthritis and was told that there was no way he could be totally cured.
"Every single joint imaginable in my hips, elbows, knees and hands hurt," Matuszewski recalled. Remembering something he had read in a Polish newspaper about the Optimal diet, he decided to check it out even though it seemed unappetizing.
"For years I thought that pork is not good for you and I didn't like the smell, but I forced myself. ... After two months I started to feel better and I didn't want to attribute it to the diet. But my friends also saw a difference in me and I had so much energy. Today after four years, I have no pain and no swelling and I am totally cured."
Sobor hears these stories all the time, but still has his reservations.
"I'm sure you've heard their claims that their joint pain is gone and diabetes is gone," he says. "And they say it because it's true. You can apparently get a lot of benefits if you decrease your carbohydrate intake, and stop taking in all the white flour and stop taking in all the refined foods because you are not stressing your body out all the time with all of the insulin spikes and becoming hyperglycemic and hypoglycemic."
"But do I recommend the diet? I don't know," he says. "I don't think Kwasniewski is as good as Atkins or that it is something you should go on for a long time. Now the South Beach Diet that is a nice diet with more flexibility. But this Optimal diet is the most radical of the low-carb diets."
Despite the popularity of the diet in its country of origin, it remains controversial there among traditional Polish nutritionists who oppose its high cholesterol and fat recommendations.
"They don't like it because they see it endangers their own positions as nutritional authorities," says Peschak.
NO POSITION FROM THE AMA
In the U.S. the Optimal Diet hasn't yet caught the attention of the medical establishment. The American Medical Association doesn't have a position on Atkins, much less Optimal. And Lisa Dorfman, spokeswoman for the American Dietetic Association, had not heard of it either.
Still, based on a quick description of the diet, she didn't condemn it outright.
"I can see how this would be a very attractive program, certainly in the senior citizen community because these are nutrient dense foods and seniors don't need to eat a lot of food," says Dorfman, a licensed nutritionist.
"And some of the foods are very nutritious albeit very high in fat and cholesterol. Liver is very high in iron and B vitamins, which would be lovely for senior citizens because they need those vitamins and are usually on a budget in that time of life.
"But for the general public I see where there could be potential problems. We just know that long-term high-fat diets leave one with a heightened risk of heart disease, stroke and hypertension. This is certainly not for children, teenagers or pregnant women.
Most Americans are getting too much fat as it is and they are not getting enough activity and they have incredible risk for heart disease because of a whole multiple list of factors including genetics and stress. And so I can't imagine that adding fat and lard and cholesterol into the mix would be beneficial to that."
"But for this group of Polish seniors I think it's adorable, especially if it was developed by someone from the old country. As a psychotherapist, I can see where they must feel like you've got to be healthy eating this because there is a psychological connection to eating these foods. It's old country eating."
Going back to the basics. It is different from the commercial processing chemical laden foods. I certainly believe these people are benefiting in some way, but it may be more than one way and it may be for certain groups and not for others is my gut hunch. It might not be appropriate for three-quarters of the population but maybe they've hit the nail on the head and this is perfect for them."
WHAT WILL IT DO LONGTERM
Although there is general agreement in the health community that lots of refined flours and sugars and their accompanying insulin spikes are not healthful, most conventional nutritionists are still not ready to embrace low-carb, high-protein and high-fat diets because of their perceived effects on the organs.
But could wear and tear on the liver, kidneys and heart be worth it for an older person to be free of the health risks of obesity?
"That I don't know," Sobor says. "No one on Atkins has died of kidney failure yet, but you can probably find a nephrologist (kidney specialist) who says it's good, one who says its bad and one who is in between. Because the truth is no one really knows yet."
"The final question is who dies faster, the people who are obese or the people who go on these diets. You would have to take 2,000 people on the diet and then 2,000 controls to see what is going to kill them first, the extra pounds or the extra protein load on the kidneys or whatever this diet will do to you. The pounds are going to do it in the short and medium term. There's no question about that. But the jury is out on the long term. The final arbiter is death. If they live longer than you do, then they won."
Peter
Praise the LARD
By Monica Eng
Chicago Tribune
CHICAGO -- Vinka Peschak starts each day by knocking back a full cup of heavy whipping cream.
That's at 8 a.m.
"At around 11 o'clock I take three or four egg yolks and make some kind of omelet with lard for breakfast," the Portage Park resident explains. Peschak, a native of Poland, eats her omelet with a cup of buttery boiled vegetables and a slender piece of almond toast slathered in more butter or lard.
Dinner is usually a fatty piece of pork or some kind of organ meat with lard-cooked french fries and more butter-soaked vegetables.
In the middle of the day she might have a cup of coffee, "but only with a lot of heavy whipping cream in it."
Peschak has been eating like this for more than five years. She is slim, energetic, and says, "I feel wonderful, never tired and never hungry."
She is not on Atkins. She is not on South Beach.
Peschak, along with an estimated 2 million folks worldwide is on the Optimal Diet, a Polish eating plan that requires the consumption of prodigious amounts of animal fat -- preferably lard.
The diet was hatched in Poland some 40 years ago by Dr. Jan Kwasniewski, who started developing it while working as a dietician for a military sanitarium in Ciechocinek, Poland. There he observed that many of his patients were sick, "not because of any pathogenic factors ... but the result of one underlying cause -- bad nutrition," according to his English language "Optimal Nutrition" book. After experimenting on his family and himself, Kwasniewski concluded that the ideal nutritional combo came from eating three grams of fat for every one gram of protein and half a gram of carbohydrates.
After a couple of decades of refining this theory, Kwasniewski published his first book in Poland in 1990. But it wasn't until converts came forward with their stories of weight loss and recovery from disease in the mid-'90s that the diet really took off it its native land and Kwasniewski's books went into wide circulation. Today there are at least two magazines devoted to the Optimal lifestyle and Kwasniewski writes a twice weekly column for the regional Polish newspaper Dziennik Zachodni.
It wasn't until 2001, though, that Chicago would become the North American capital for this eating plan. That's when Tomasz Zielinski bought a little storefront on Milwaukee Avenue and opened Calma Optimal Foods. The first and only one of its kind in the nation, it operates as a deli, meeting center and, as of this spring, a restaurant for those on the lard-laden plan. Peschak serves as its manager.
Sometimes called the Polish Atkins, the Optimal Diet severely restricts the intake of carbohydrates and sugars, but differs from Atkins by de-emphasizing protein and beefing up, or more accurately porking up, the fat to a level that would have even made the late Robert Atkins reach for his heart.
On average, the diet recommends a whopping 250 grams of fat per day, about four times what the FDA recommended for the average person to maintain his/her weight and about 10 times the amount of saturated fat allowed.
So despite its popularity in Poland -- Lech Walesa is reported to have lost 44 pounds and cured his diabetes on it recently -- the mainstream medical establishment there and here is skeptical.
"I am very against diets like this," says Jadwiga Roguska, a practicing internist at the Feinberg School of Medicine at Northwestern University. "All high-fat diets are unhealthy in the long term and there is absolutely no benefit to weight reduction of this sort because it is threatening to health. ... Of course, high-fat diets will give you the benefits of energy and weight loss, but they are just not good for you."
Roguska based her comments on a brief overview of its principles, but Chicago physician Mark Sobor has seen it up close and has watched an increasing number of his patients in the Polish community embrace it.
"Kwasniewski is pure fat," says Sobor who practices in Jefferson Park and is also a licensed acupuncturist. "Eat fat non-stop. Everything is pure fat. The more fat you can take in the better and these people are fanatics about it. But the thing is they're all skinny."
On a recent Sunday morning at the Optimal deli/center in Portage Park, Ill., about 30 mature, fairly slim followers of the Kwasniewski plan gathered for a weekly meeting and shared their stories.
There was the ginger-haired firecracker Irena Kozlowicz, 78, who went on the diet five years ago after Kwasniewski came to speak at the Copernicus Center in 1999. At the time she was suffering from chronic eye problems, asthma and pain in her knees.
"Now I can walk better than a young person," she chirps. "I can run up six floors of stairs and my grandson can't catch me. He's 17 years old. I meet young ladies and they are always tired and sweating, but I never am. I didn't need to lose weight, but I lost 8 pounds. I am 78, but I feel like I am 50. I thank God for the diet."
Then there is Jozef Michael Ostrowski, 71, who says he has been on a variation of the diet his whole life.
"Since the occupation of Poland my parents could only afford pork meat and liver and blood sausage and lard," Ostrowski says through an interpreter. "It is not like I was following this diet precisely but generally. At that time I didn't know this kind of natural food was good for me. I just knew that I could eat scrambled eggs with a thin piece of bread and lard and I would be full all day. I started eating regular food like McDonald's and I could not handle the pain and so I went back to the diet and have felt better and better every day."
Zofia Pawlik, 56, started the diet last year when she went on an Optimal vacation, a retreat to the Wisconsin Dells to learn about the program and eat its foods. Over the course of a year, she says she has lost 10 pounds while improving her energy and overall health.
IMPRESSIVE RESULTS
Chicago physician Christopher Kubik wasn't at the meeting, but in a phone interview he said that four and a half years ago he was overweight and suffering from fatigue and stones in the bladder. But within a couple of months of embarking on this high-fat journey he saw results.
"I was losing weigh gradually (he lost about 25 pounds in six weeks) but I felt fine. Since then, I didn't have any more problems with stones, my skin complexion improved and I am still feeling a lot of energy," says Kubik, 57, who reports that he breakfasts on fried eggs, bacon and string cheese seven days a week. "So I experienced myself significant detectable improvement even though I generally had good health to begin with. While I was losing the weight I could feel the ketones as a metallic tasted on the mouth, but after I reached my optimal weight, (the ketosis) stopped. Now my weight has remained steady at about 185, which is in the upper limit of normal for my height."
Kubik, who also has degrees in public health and health law, says he does not actively promote the diet, "because it is not considered a standard of care and the medical community still recommends low-fat diets and it is not something I could support if I were sued." But if patients ask, "I tell them that I am on it and have seen positive results."
Dr. Sobor has also seen a growing number of Kwasniewski converts who claim weight loss is only one of the benefits they've reaped.
Chester Matuszewski, 46, for instance says that four years ago he was diagnosed with rheumatoid arthritis and was told that there was no way he could be totally cured.
"Every single joint imaginable in my hips, elbows, knees and hands hurt," Matuszewski recalled. Remembering something he had read in a Polish newspaper about the Optimal diet, he decided to check it out even though it seemed unappetizing.
"For years I thought that pork is not good for you and I didn't like the smell, but I forced myself. ... After two months I started to feel better and I didn't want to attribute it to the diet. But my friends also saw a difference in me and I had so much energy. Today after four years, I have no pain and no swelling and I am totally cured."
Sobor hears these stories all the time, but still has his reservations.
"I'm sure you've heard their claims that their joint pain is gone and diabetes is gone," he says. "And they say it because it's true. You can apparently get a lot of benefits if you decrease your carbohydrate intake, and stop taking in all the white flour and stop taking in all the refined foods because you are not stressing your body out all the time with all of the insulin spikes and becoming hyperglycemic and hypoglycemic."
"But do I recommend the diet? I don't know," he says. "I don't think Kwasniewski is as good as Atkins or that it is something you should go on for a long time. Now the South Beach Diet that is a nice diet with more flexibility. But this Optimal diet is the most radical of the low-carb diets."
Despite the popularity of the diet in its country of origin, it remains controversial there among traditional Polish nutritionists who oppose its high cholesterol and fat recommendations.
"They don't like it because they see it endangers their own positions as nutritional authorities," says Peschak.
NO POSITION FROM THE AMA
In the U.S. the Optimal Diet hasn't yet caught the attention of the medical establishment. The American Medical Association doesn't have a position on Atkins, much less Optimal. And Lisa Dorfman, spokeswoman for the American Dietetic Association, had not heard of it either.
Still, based on a quick description of the diet, she didn't condemn it outright.
"I can see how this would be a very attractive program, certainly in the senior citizen community because these are nutrient dense foods and seniors don't need to eat a lot of food," says Dorfman, a licensed nutritionist.
"And some of the foods are very nutritious albeit very high in fat and cholesterol. Liver is very high in iron and B vitamins, which would be lovely for senior citizens because they need those vitamins and are usually on a budget in that time of life.
"But for the general public I see where there could be potential problems. We just know that long-term high-fat diets leave one with a heightened risk of heart disease, stroke and hypertension. This is certainly not for children, teenagers or pregnant women.
Most Americans are getting too much fat as it is and they are not getting enough activity and they have incredible risk for heart disease because of a whole multiple list of factors including genetics and stress. And so I can't imagine that adding fat and lard and cholesterol into the mix would be beneficial to that."
"But for this group of Polish seniors I think it's adorable, especially if it was developed by someone from the old country. As a psychotherapist, I can see where they must feel like you've got to be healthy eating this because there is a psychological connection to eating these foods. It's old country eating."
Going back to the basics. It is different from the commercial processing chemical laden foods. I certainly believe these people are benefiting in some way, but it may be more than one way and it may be for certain groups and not for others is my gut hunch. It might not be appropriate for three-quarters of the population but maybe they've hit the nail on the head and this is perfect for them."
WHAT WILL IT DO LONGTERM
Although there is general agreement in the health community that lots of refined flours and sugars and their accompanying insulin spikes are not healthful, most conventional nutritionists are still not ready to embrace low-carb, high-protein and high-fat diets because of their perceived effects on the organs.
But could wear and tear on the liver, kidneys and heart be worth it for an older person to be free of the health risks of obesity?
"That I don't know," Sobor says. "No one on Atkins has died of kidney failure yet, but you can probably find a nephrologist (kidney specialist) who says it's good, one who says its bad and one who is in between. Because the truth is no one really knows yet."
"The final question is who dies faster, the people who are obese or the people who go on these diets. You would have to take 2,000 people on the diet and then 2,000 controls to see what is going to kill them first, the extra pounds or the extra protein load on the kidneys or whatever this diet will do to you. The pounds are going to do it in the short and medium term. There's no question about that. But the jury is out on the long term. The final arbiter is death. If they live longer than you do, then they won."
Wednesday, March 26, 2008
Back home
Got to paddle on Easter Sunday as soon as the wind dropped, four foot and clean. I kept most of the wet snow out of my dry suit, and the sun even came out when the snow stopped.
About the only Hyperlipidy aspect was that there doesn't appear to be a fall off in endurance ability with lack of practice. Paddled for about two and a half hours and could have carried on but the surf was dropping with the rising tide. The reflexes and muscles still work after what must be two years off of the surf...
What do you do with five days off line? Well, Nick Lane's "Power, Sex, Suicide" has been a very interesting read. Well over half way through it and it makes a great deal of sense.
Lots of catching up to do!
Peter
About the only Hyperlipidy aspect was that there doesn't appear to be a fall off in endurance ability with lack of practice. Paddled for about two and a half hours and could have carried on but the surf was dropping with the rising tide. The reflexes and muscles still work after what must be two years off of the surf...
What do you do with five days off line? Well, Nick Lane's "Power, Sex, Suicide" has been a very interesting read. Well over half way through it and it makes a great deal of sense.
Lots of catching up to do!
Peter
Thursday, March 20, 2008
Monday, March 17, 2008
Food; carnitas
Tonight was carnitas.
Buy some strips of belly pork. Be sure to pick over the selection for the fattiest if you're in a supermarket. Any time from lunch time onwards stick them in a large sauce pan and just cover with water. Add salt and pepper, a chopped onion and a whole root of garlic, cut in half horizontally. Two bay leaves are essential. Buy a bay tree if necessary. Dried might be okay, dunno, I've got the tree.
Cover tightly, bring to boil, turn heat very low and forget about for at least 3 hours. Five hours is fine. You can do this the night before, but the smell is so good I prefer to eat them on the day.
Pick out the strips (gently, they tend to break up) and cut up in to chunks about 2 inches long. I don't use the stock for anything. Transfer the meat pieces to a non stick heavy frying pan and cook them slowly in their own fat. Sprinkle with salt, pepper, chili powder, some cumin and some more chili powder. Flip the pieces once. You're aiming to have a crispy outside and the fat within fully softened. If you over-fry them all the fat runs out and you end up with hard meat in lard. Avoid!
That's it. We had them with sweet potatoes. They should absolutely melt in the mouth. They did.
Peter
Buy some strips of belly pork. Be sure to pick over the selection for the fattiest if you're in a supermarket. Any time from lunch time onwards stick them in a large sauce pan and just cover with water. Add salt and pepper, a chopped onion and a whole root of garlic, cut in half horizontally. Two bay leaves are essential. Buy a bay tree if necessary. Dried might be okay, dunno, I've got the tree.
Cover tightly, bring to boil, turn heat very low and forget about for at least 3 hours. Five hours is fine. You can do this the night before, but the smell is so good I prefer to eat them on the day.
Pick out the strips (gently, they tend to break up) and cut up in to chunks about 2 inches long. I don't use the stock for anything. Transfer the meat pieces to a non stick heavy frying pan and cook them slowly in their own fat. Sprinkle with salt, pepper, chili powder, some cumin and some more chili powder. Flip the pieces once. You're aiming to have a crispy outside and the fat within fully softened. If you over-fry them all the fat runs out and you end up with hard meat in lard. Avoid!
That's it. We had them with sweet potatoes. They should absolutely melt in the mouth. They did.
Peter
Sunday, March 16, 2008
Diabetes and hunger
I can vaguely remember being hungry, way back before LC eating. The sort of day when you would get home at 5.30 and you HAD to have to have two doorsteps of wholemeal bread, spread with peanut butter (to avoid the saturated fats) and filled with a sliced banana, because there was NO WAY you could wait the hour it was going to take you to get supper ready. In the door, slice the bread. I remember hopping on the scales at work once and thinking that skipping a meal here and there might drop that pound or two around my tummy. Then trying it!
At the time my need to eat didn't seem like greed.
We all know that if you are a type 2 diabetic you must have been greedy for years before getting your just comuppance (thinks your GP). It's self evident that fat people get fat by eating too much food and obviously it's the dietary fat which is the main factor. Obesity is clearly the cause of type 2 diabetes (except in skinny type 2s and those naughty extremely skinny people with lipodystrophy, duhh). It's also self evident that once you have a serious blood sugar regulation problem you should eat as much sugar as possible and avoid fat like the plague because otherwise you might get even fatter, which gives you more blood sugar problems (ADA advice).
So a type 2 diabetic should eat a diet which is as carbohydrate based as practical and make sure they loose weight, lots of it. I think it's reasonable to say that that's current diabetes advice.
One day I found this paper on diabetic rats. I'm not really sure how similar streptozotocin induced diabetes in lab rats is to type 2 diabetes in humans. Insulin production is blunted but not eliminated, so perhaps it is the equivalent to fairly late type 2, when the pancreas has finally started to give up under the strain of the ADA carbohydrate based diet. The paper was quite interesting from the point of view of hunger.
Lab rats don't generally get described as being lazy glutttons. Sitting in a cage all day limits your trips to the gym. You eat what the investigator gives you. It seems quite reasonable that rats eat to satiety and no more. Beyond that would be gluttony. But if you make a rat diabetic, then feed it a carbohydrate based diet, it exhibits "hyperphagia". It eats a LOT. And it becomes fat. Perhaps a little bit of streptozotocin and some lab chow equals gluttony.
Obviously no self respecting rat wants to be either diabetic or hyperphagic. Luckily rats are not stupid and, given a choice of macronutrients after its streptozotocin, a lab rat will automatically dump the carbs, eat the fat and keep both its waistline slim and its blood glucose within acceptable limits. Given the ADA diet they don't, or rather they can't. Why can't they?
Because they're hungry. Very, very hungry.
This looks to be what is happening, from the abstract:
"When maintained on a HC [high carbohydrate] diet, diabetic rats also exhibit increased gene expression of the orexigenic peptide neuropeptide Y (NPY) in the hypothalamic arcuate nucleus, and reduced expression of the anorectic peptide corticotropin-releasing hormone (CRH) in the paraventricular nucleus, and these changes are hypothesized to contribute to diabetic hyperphagia"
Orexigenic means hunger generating. Anorectic is the opposite.
Diabetic rats on the ADA diet are RAVENOUS. Oops, sorry, gluttenous. Diabetic rats on a genuine high fat diet are not. They're not very diabetic either.
Now take that to humans. I don't think humans are particularly different to rats. Telling a human diabetic to eat a carbohydrate based diet will bump up their neuropeptide Y levels and will drop their corticotropic releasing hormone levels. They'll be ravenous. Bit of a cruel trick really.
But here's the really funny bit.
You then tell them they MUST lose weight. When they fail to lose weight, you underline the bit in their case notes where it says glutton/failed to comply.
Don't laugh too much, it's not funny really.
Peter
At the time my need to eat didn't seem like greed.
We all know that if you are a type 2 diabetic you must have been greedy for years before getting your just comuppance (thinks your GP). It's self evident that fat people get fat by eating too much food and obviously it's the dietary fat which is the main factor. Obesity is clearly the cause of type 2 diabetes (except in skinny type 2s and those naughty extremely skinny people with lipodystrophy, duhh). It's also self evident that once you have a serious blood sugar regulation problem you should eat as much sugar as possible and avoid fat like the plague because otherwise you might get even fatter, which gives you more blood sugar problems (ADA advice).
So a type 2 diabetic should eat a diet which is as carbohydrate based as practical and make sure they loose weight, lots of it. I think it's reasonable to say that that's current diabetes advice.
One day I found this paper on diabetic rats. I'm not really sure how similar streptozotocin induced diabetes in lab rats is to type 2 diabetes in humans. Insulin production is blunted but not eliminated, so perhaps it is the equivalent to fairly late type 2, when the pancreas has finally started to give up under the strain of the ADA carbohydrate based diet. The paper was quite interesting from the point of view of hunger.
Lab rats don't generally get described as being lazy glutttons. Sitting in a cage all day limits your trips to the gym. You eat what the investigator gives you. It seems quite reasonable that rats eat to satiety and no more. Beyond that would be gluttony. But if you make a rat diabetic, then feed it a carbohydrate based diet, it exhibits "hyperphagia". It eats a LOT. And it becomes fat. Perhaps a little bit of streptozotocin and some lab chow equals gluttony.
Obviously no self respecting rat wants to be either diabetic or hyperphagic. Luckily rats are not stupid and, given a choice of macronutrients after its streptozotocin, a lab rat will automatically dump the carbs, eat the fat and keep both its waistline slim and its blood glucose within acceptable limits. Given the ADA diet they don't, or rather they can't. Why can't they?
Because they're hungry. Very, very hungry.
This looks to be what is happening, from the abstract:
"When maintained on a HC [high carbohydrate] diet, diabetic rats also exhibit increased gene expression of the orexigenic peptide neuropeptide Y (NPY) in the hypothalamic arcuate nucleus, and reduced expression of the anorectic peptide corticotropin-releasing hormone (CRH) in the paraventricular nucleus, and these changes are hypothesized to contribute to diabetic hyperphagia"
Orexigenic means hunger generating. Anorectic is the opposite.
Diabetic rats on the ADA diet are RAVENOUS. Oops, sorry, gluttenous. Diabetic rats on a genuine high fat diet are not. They're not very diabetic either.
Now take that to humans. I don't think humans are particularly different to rats. Telling a human diabetic to eat a carbohydrate based diet will bump up their neuropeptide Y levels and will drop their corticotropic releasing hormone levels. They'll be ravenous. Bit of a cruel trick really.
But here's the really funny bit.
You then tell them they MUST lose weight. When they fail to lose weight, you underline the bit in their case notes where it says glutton/failed to comply.
Don't laugh too much, it's not funny really.
Peter
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