I'd hate to return this thread back to the original topic, cholesterol, but I was reading a discussion forum on Medscape about the "cause" of atherosclerosis, and the role of cholesterol and statins. This was docs spouting off mostly about how great statins are, but a significant minority brought Malcolm Kendrick and other skeptics into the discussion.

One funny guy posted some info I wasn't aware of:


I kinda like this theory. Gotta look into C-reactive protein a little. I didn't kow it was an antibody.

Then someone answered with an explanation about the deposition of choesterol and calcium in damaged vessel walls, with a link to some nice electron micrographs:



This makes some sense, I think.

There is a lot of disagreement what causes the initial damage leading to atherosclerosis and a lot of agreement on the process after. A problem with the glycolization theory is that it doesn't adaquately explain why the atheromas only seem to form at certain locations. One theory, also incomplete, is that they form in areas of high shear stress. Anyway, it's a mess

Kind regards

The data on okinawans was still unpublished when phelan went along with okinawa gained very little. The study above by wilcox shows this is not true.

Heres the quote again:

Phelan:


Here is what the more RECENT published paper says

"Okinawan septuagenarian population appeared to be in a relative "energy
deficit" consistent with CR until the late 1960s" "but only for half their adult lives." - Refering to their CR (they werent CR'd in their entire life as phelan says)

Americans were eating 2100k/cal in the 1960's, compared with okinawans eating 1600k/cal. Thats 23% less than americans at that time period. Okinawans then in 1993 okinawa calorie consumption to 1927k/cal per day, (probably too much for their small frames) compared to 2176 for americans! ( They were eating ONLY ABOUT 10% FEWER CALORIES!)

But still Okinawans only contribute a small 0.0002% to the worlds population, yet they can boast 15% of the worlds documented SUPER-CENTENARIANS. Impressive eh?


THE BOTTOM LNE

The Okinawans are only a mild example of what CR can do, and the CR effect is underestimated because they HAVE been De-CRing since the 1950's actually. When calorie intake was only 1539k/cal per day! The Japanese and Okinawans now consume aroudn the same number of calories. Okinawans used to have half the mortality of the japanese, now the stats are very similar since calorie intake increased.

1) There is no arguing with a fanatic.
2) From dina1957 "I am not going to continue, " Thank you.

Dragging the thread back to its original intent, I thought that posters here might be interested to read the following rebuttal about Malcolm Kendrick's book from the resident doctor at The Times (London):




I have to say that I've never really been one to take much notice of Dr S's advice, and I think I'm even less inclined to do so now.

Interesting to note that Dr S doesn't provide many FACTS to support his contention that if people stop statins and eat a high fat diet, there will be a 'disaster'. He simply repeats (without backup) the same myth over again.

He also notes that statins, according to him show benefit 'immediately'. Which Kendrick, and many others, suggest is proof that statins don't work by lowering cholesterol. Because (a) the cholesterol doesn't always drop 'immediately', and (b) no one has ever observed statins shrinking plaques 'immediately'. Or even slowly.

Intensive Statin Therapy Can Partially Reverse Plaque Build-up In Arteries
http://www.medicalnewstoday.com/med...hp?newsid=39470

for the first time, that very intensive cholesterol lowering with a statin drug can regress (partially reverse) the buildup of plaque in the coronary arteries. This finding has never before been observed in a study using statin drugs, the most commonly used cholesterol lowering treatment

I take the quote from Phelan to mean his took his data set not from the most recent population but rather from the time of most restriction. Are you purposefully being obtuse? The current paper seems to be another analysis of current trends in the population, it does not invalidate the earlier research with respect to CR and supposed life extension.

I noticed again you harp upon a non-issue with Phelan but ignore the bulk of the post. Again, it is being suggested that the bulk of Okinawan greater lifeSPANS is due to other factors that CR, and that CR contributes only a small part to life-EXTENSION. You blather incessantly about all of the centarians, but their lifespans of the Okinawans are not remarkably greater than other long-lived populations - ones that enjoy eating as part of life. With all the centarians there must be a lot of early death to keep the average lifespans lower.

The folowing essay by Dr. Kendrick addresses that exact topic. If “high” cholesterol is the cause, why would stopping a medication after the cause was corrected matter? Other than to the manufacturer’s bottom line?
Oh, as to the origional question posed by this thread, to me at least, the answer is a resounding yes.

That was an absolutely wonderful essay. Not only is Dr. Kendrick spot on, he delivers his message with brilliant humor.
"Read that paragraph you naughty people you. Exercise all you like, lose all the weight you can, but it will make no difference. YOU MUST TAKE YOUR STATINS. Now, go to bed and no pudding for you."

There's a good reason that the good doctor is often parodied as 'Dr. Utterfraud'.

Wrong again Matt. Statins are well known to exert an antinflammatory effect. Less infammation is bound to reverse ( I loved the 'partial' caveat on the so called plaque reducing effect of statins ) plaque build up in arteries. This is yet another example of confusing correlation and causation.

Hope this helps .

Hmmm...if this is so, do we see other anti-inflammatory agents reducing atheromas? Seems to me that news would be all over town. The only other plaque-reducing treatment that I recall hearing about is HDL treatment.

Close, but no cigar Whoa. "Atherosclerosis progression was assessed at baseline and after at 24 months of treatment."

That's not 'immediate'.

If statins' effects happen quickly -- as the 'experts' say -- in a matter of weeks, it has nothing to do with reducing plaque by an average of 8% (tiny) after 24 months.

It's not about cholesterol lowering or plaque reduction.

That's the whole point. Anti inflammatories do reduce atheromas. That the news is not 'all over town' is full testament to how conned the medical profession (and by extension the credulous and intimidated public) has been about the 'cholesterol connection'. But even statins, which are quite powerful anti inflammatory agents, still take years (2 in this study) to exert even a tiny atheroma reducing effect. Eight percent is hardly anything to get excited about, particularly when the side effects of statin use are so catastrophic. One of the most potent anti inflammatory approaches is a low carb diet, yet it will probably be years before much research money is thrown at its atheroma preventative power, let alone any slow acting plaque reducing effects. Big pharma is hardly likely to direct much money at dietary strategies to prevent degenerative disease, because there's no return. And they probably are only too aware that most people just love their starch and sugar anyway. And even the wrong ( anti cholesterol) dietary message is not getting through. Sure people spend megabucks on the 'low fat' chimera. But that just adds to the problem, because most low fat food replaces the fat with carbohydrate.

Unfortunately human beings are slaves to their tastebuds. They're always going to prefer a drug bullet to a lifestyle change. They'll whinge and sue when the inevitable side effects show up, but they'll eagerly await the next 'quick fix' announcement by Pfizer et al. This forum alone is a 'straying' confessional. Not that the intention is less worthy because of it, but it's tragic that the 'insula' factor has us all by the short and curlies. And I would say that unless the aesthetic bodyfat loss incentive existed, there would be very few people eating a low carb diet just because it was the way humans were designed to eat.