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
Saturday, July 21, 2007
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.
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