Thursday, February 09, 2006

New Reader 'Impressed' By Low-Carb Success

With thousands of new visitors coming to my blog on a weekly basis (THANK YOU, by the way!), there are so many brand new eyeballs looking at what I have written here about my experience on the low-carb lifestyle. While I try to keep the content you read here on a daily basis fresh, entertaining and educational, I do get a lot of people asking me questions that I have already previously addressed in older posts.

I certainly don't mind answering those questions and absolutely appreciate the fact that people want to learn more about what it means to be livin' la vida low-carb. This lifestyle has totally transformed my life from a 400+ pound slob into the healthy, athletic 220-something pound man I have become in 2006!

If you are a relatively new reader or even if you have been coming here for months, let me encourage you to use that white search box up in the upper left hand corner of my blog. Go ahead, look at it now. I'll wait...(doo doo doo doo -- JEOPARDY theme music -- doop do doo doo doo...doo...doo, bong bong!). Okay, did you see it?

To see if I have blogged about a certain subject, all you have to do is type in the word or phrase into that white box and then click on the button. You will then be taken to a search results page where you can find any blog post I have written about that particular topic.

For example, if you type in the phrase "Biggest Loser" in the white box and click on "Search This Blog," then this is where it will take you. Once you are on that page, you can click on any of the headlines to read what I have written about that subject previously. See how easy that is?

Go ahead and play around with it a little bit and see what other interesting posts you can find that way. But let me give you a little bit of a warning. If you type in the phrase "low-carb" or even "low-fat," then be prepared to read my ENTIRE BLOG! LOL! Just about every post I write has one or both of those phrases in them, so don't do that to yourself.

But if you want to know what I have written about "exercise," for example, then you will find what you are looking for.

Okay, now that I've got that explained to you, let me share with you another e-mail from a BRAND NEW READER (yee haw, we like those!) who has been livin' la vida low-carb for the past five years.

Here's his encouraging e-mail I received on Thursday:

Today is the first time I visited your site, and I must say I am impressed by your low-carb experience. I too have been low-carbing since a friend loaned me his Atkins paperback one day back in 2001. That was the first time I had ever read about the truly high-risk situation I was in with my LOW HDL levels combined with HIGH triglycerides. Since my TWELVE year low-fat diet had done nothing to improve my lipids risk profile, I decided to give low-carb a try.

Six weeks later, during my annual physical, I was stunned to see a 55% increase in my HDL and my standard risk profile dropped from a 12-year average of 6.3, to 3.7! My doctor had been skeptical about my decision to abandon low-fat in favor of low-carb, so he could only concede that low-carb works for maybe "thirty or forty percent!" Too bad he didn't mention this little "factoid" earlier so that I could have experienced the many advantages of a low (now CONTROLLED-carb) carb diet years sooner.

Anyway, I didn't intend to tell you what you already know. Rather, I was curious if your VLDL level is around TEN (mg/dl)? I based this level of ten on the HDL and triglycerides you mentioned in one of your blogs (52 triglycerides and that STUNNING 72 HDL!).

Where am I going with all this? I seldom see much, if any, mention of the dramatic improvements in the triglyceride/HDL risk ratio that is so typical of anyone in the "metabolic syndrome" group. Dr. Atkins was the first source that ever alerted me to the fact that I WAS in that unfortunate group of Americans that he estimated to be in excess of FIFTY million (as I recall,
could have been SIXTY million).

Since YOU enjoyed a monumental improvement in that same ratio (from 11.2 down to .7), I wonder if you ever highlight the fact that your "Atkins risk ratio" improved by a factor of SIXTEEN!? Another way to look at it is that several medical studies suggest YOU are now sixteen times LESS likely to have a CHD event than you were before going low-carb!

If you got this far, I wish you well in your low-carb lifestyle, and keep up the good work in alerting the low-fat folk that there is a better way!

Obviously, my new reader is a very well-educated man who not only talks the talk, but walks the walk.

Here was my response to him:

THANKS so much for writing. I'm glad to see you were rescued from low-fat hell (LOL!) and are now living in the promised land of livin' la vida low-carb.

Here is a link to my latest lab results as of October 2005. According to that, my VLDL stands at 11 (you were close!). I stun people all the time when I tell them what my HDL is and that my ratio is outstanding, despite the fact that my total cholesterol is over 200 (it's 201).

My own doctor (a former low-carb dissenter turned believer after my miraculous turnaround in health) even said recently that I shouldn't worry about my total cholesterol because my ratio is so incredibly good. I don't mention this as much in my posts because it really doesn't translate to the average Joe.

Perhaps I could explain the ratio thing in an upcoming post to help continue the education. I too wish Dr. Atkins was still around to see he was RIGHT ON about the low-fat diets. Something tells me he's looking down from heaven with a big grin on his face. LOL!

THANKS for writing! Keep on livin' la vida low-carb, my friend!

Since the HDL/triglyceride ratio is one of the topics that was discussed at the recent Nutritional & Metabolic Aspects of Carbohydrate Restriction conference in Brooklyn, New York (now there's another phrase you could look up using my blog search!), I will save that explanation for another post. But it is a fascinating and unique aspect of the low-carb lifestyle that sets it apart from the other nutritional approaches.

If you are a new reader to "Livin' La Vida Low-Carb" and you just have to get something off your chest or if you have a burning question you want me to answer (I'll do my best!), then drop me a line! THANKS again for your readership and I hope you'll keep coming back to learn more about low-carb living and how it can change your life forever.

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Blogger Lowcarb_dave said...

There are some interesting debates happening out there is regards to weither cholesterol has an impact on CHD.

This is from for the science buffs out there!

LDL Cholesterol Does NOT Cause Atherosclerosis or Heart Disease.

How much longer will the medical establishment keep lying to us?

By Anthony Colpo,
May 29, 2005

LDL cholesterol does not cause heart disease.

The above statement runs counter to everything your doctor, the media, and allegedly 'respectable' and 'impartial' health organizations have ever told you.

Nonetheless, it's true.

It's no big secret that, throughout history, those in power--and the network of individuals who rely on these powerbrokers for their livelihood--have often lied and misled the general public in order to preserve the status quo.

Our time is no different.

For the last four decades, the medical establishment has been successfully operating one of the biggest health scams of all time. Through the use of extensive propaganda, they have convinced millions of people the world over that cholesterol, especially LDL cholesterol, is a direct cause of heart disease. They have further convinced millions that the key to avoiding heart disease is to reduce cholesterol levels via the use of lipid-lowering drugs and diets low in saturated fats. This racket has produced billions in profits for drug companies and the manufacturers of low-fat food products.

While cholesterol paranoia is an extremely lucrative phenomenon for the food and drug industries, it has delivered no benefit whatsoever to the rest of us. Heart disease is still the number one killer in cholesterol-phobic Western countries. Sure, the number of deaths from heart disease has decreased since the late sixties, but the overall incidence of heart disease has not declined one iota.(1-4) If cholesterol reduction were effective in preventing heart disease, then it would surely lower both fatal and non-fatal heart disease. This has not happened. Modern medicine has made breathtaking strides in extending the lives of those who have already had heart attacks, but has failed dismally in helping people avoid heart disease in the first place.

The anti-cholesterol campaign has been more than just an unproductive failure. The inordinate focus on cholesterol, a perfectly natural substance that performs many crucial functions in the body, has taken valuable resources and attention from the things that do cause heart disease. An inestimable number of lives have been lost that could have been saved had the medical community and general public been aware of the truly causative factors.

Let us now find out why the anti-cholesterol campaign is a mess of contradictory, scientifically untenable nonsense.

LDL (Lies, Damn Lies)

To allow their pet theory to accommodate the inescapable fact that cholesterol is a vitally important substance, the purveyors of the cholesterol hypothesis invented the "good cholesterol, bad cholesterol" dichotomy.

LDL cholesterol, which transports cholesterol from the liver to the tissues and organs of the body, was deigned the "bad" cholesterol. As part of its delivery function, so the story goes, LDL brings cholesterol to the arteries, where it is then deposited to form arterial plaque. These plaques then grow, rupture, and stimulate the formation of artery-blocking blood clots.

HDL cholesterol, on the other hand, is the swash-buckling knight in shining armor that counters the action of its evil twin LDL by sweeping cholesterol from the arteries and transporting it back to the liver, from whence it can be safely disposed.

This "good cholesterol, bad cholesterol" paradigm is, quite frankly, a scientific absurdity.

Fact versus Fiction

Let's get one thing perfectly clear right from the outset: atherosclerotic plaques are not simply big wads of fat and cholesterol that have stuck to the walls of arteries like mud inside a pipe. That so many supposedly intelligent people have even contemplated entertaining such a notion, let alone accepted it as gospel truth, is a sad, sad reflection of the extremely low intellectual standard dominating the health sciences, and society in general, today.

The growth of atherosclerotic plaques begins inside the artery wall, between the inner and outer layers. These plaques are actually complex entities comprised of numerous components, including smooth muscle cells, calcium, connective tissue, white blood cells, and cholesterol and fatty acids. The proliferation of these various components occurs, not because of elevations in blood cholesterol or because one has eaten too much butter and cream, but because of unfavorable physiological conditions that damage or weaken the structure of the artery. This triggers an inflammatory state in which the body recognizes the injury and sets about to repair it. Cholesterol is present in atherosclerotic plaque for the same reason all the other components are present--as part of the body's attempt to repair itself. Blaming cholesterol for atherosclerotic plaque makes about as much sense as blaming paramedics for the carnage they are faced with after arriving at the scene of an accident.

This 'response-to-injury' scenario is well accepted by the vast majority of serious cardiovascular researchers. The problem is that many of these same individuals insist on clinging to the untenable notion that LDL cholesterol is somehow involved in triggering or aggravating the inflammatory state that promotes atherosclerosis and eventually leads to heart disease or stroke.

Follow the Cholesterol Trail

If LDL cholesterol 'caused' atherosclerosis, then logic dictates that there should be a strong correlation between blood levels of LDL cholesterol and atherosclerosis. Proponents of the lipid hypothesis would have you believe this is exactly the case.

They're wrong.

Oxidized LDL

Before we continue, it's important to distinguish between 'standard' LDL cholesterol, and 'modified' LDL cholesterol. The former is the type of LDL that your body produces each and every day as a part of perfectly normal and healthy metabolic function. Modified LDL, in contrast, has undergone some sort of deleterious alteration; the most widely studied example is 'oxidized' LDL. This is LDL that has been subject to free radical damage.

During the eighties, some researchers began to wake up to the fact that LDL itself was not a reliable independent risk factor for CHD. After all, half of those who suffer CHD have LDL levels within the normal limit. Among the 28,000-plus participants of the Women's Health Study, for example, forty-six percent of first cardiovascular events occurred in women with LDL cholesterol levels under 130 mg/dL--the 'desirable' target for primary prevention set by the NCEP.(5)

Research in both animals and humans has shown that oxidized LDL is a far better predictor of atherosclerosis and cardiovascular disease than regular LDL cholesterol. This would indicate that a person's antioxidant status, rather than their LDL levels, is a more important determinant of whether or not they will develop advanced plaques.

That, of course, is not how the medical orthodoxy interpreted the findings. The discovery of oxidized LDL cholesterol, they insisted, simply gave further support to the importance of lowering LDL cholesterol. Lower LDL, they claimed, and you will also lower oxidized LDL levels.

Wrong again.

In animal studies, administration of antioxidant drugs like probucol impairs LDL oxidation and arterial plaque formation, even when there is no change in blood cholesterol levels.(6-10)

In fact, administration of the antioxidant butylated hydroxytoluene (BHT) significantly reduces the degree of atherosclerosis on the aortic surface of rabbits even though it raises LDL cholesterol levels!(9)

A similar phenomenon is observed in humans. Among elderly Belgians, higher levels of oxidized LDL were accompanied by a significantly increased risk of heart attack, regardless of overall LDL levels.(11,12)

In Japanese patients undergoing surgery to remove plaque from their carotid arteries, blood levels of oxidized LDL were significantly higher than those measured in healthy controls. Advanced carotid plaques extracted from the patients showed far higher levels of oxidized LDL than neighboring sections of artery that were disease-free. Elevated oxidized LDL was also associated with an increased susceptibility of plaque rupture. However, there was no association between oxidized LDL concentrations and overall LDL levels.(13)

The irrelevance of total LDL levels was further underscored when patients given aggressive LDL cholesterol-lowering treatment were compared with those receiving less aggressive treatment. Despite greater LDL reductions in the former group, there were no differences in calcified plaque progression as detected by electron beam tomography.(14)

It's the Antioxidants, Stupid!

In 1997, Swedish researchers published a comparison of CHD risk factors among men from Vilnius in Lithuania and Linkoping in Sweden. These two groups were selected because the former had a four-fold higher death rate from CHD than the latter. Very little difference in traditional risk factors existed between the two groups, except that the men from CHD-prone Vilnius had lower total and LDL cholesterol levels!

According to common wisdom, the lower total and LDL cholesterol of the Lithuanian men should have placed them at reduced risk of heart disease. When the researchers probed further, they discovered that the men from Vilnius had significantly higher concentrations of oxidized LDL.(15) They also displayed significantly poorer blood levels of important diet-derived antioxidants such as beta carotene, lycopene, and gamma tocopherol (a form of vitamin E).(16,17) Blood levels of these particular nutrients are largely determined by dietary intake, especially from the consumption of antioxidant-rich fruits, nuts, and vegetables. So while the Lithuanian men had lower LDL levels, they had a greater susceptibility to oxidized LDL due to what appeared to be a poorer intake of antioxidant-rich foods.

This may well have explained their greater susceptibility to cardiovascular disease; in tightly-controlled clinical trials, individuals randomized to increase their intake of fruits and vegetables have experienced significant reductions in cardiovascular and all-cause mortality.

The LDL Theory on Trial

Speaking of tightly-controlled clinical trials, none have ever conclusively demonstrated that LDL cholesterol reductions can prevent cardiovascular disease, nor increase longevity.

In the massive GISSI-Prevenzione trial in Italy, the mortality benefits of omega-3-rich fish oil appeared early on in the study--as did an increase in LDL cholesterol levels! Mean LDL levels in the subjects given fish oil rose from 136mg/dl at baseline to 150mg/dl after six months, before gradually returning to initial levels at 42 months. A similar pattern was observed in the control group. This extended period of elevated LDL levels did not in any way prevent the fish oil patients from experiencing significantly more favorable cardiovascular and mortality outcomes.(18)

In the Lyon Diet Heart Study, an experimental group advised to increase consumption of root vegetables, green vegetables, fish and fruit, and omega-3 fatty acids also experienced greatly improved cardiovascular and survival outcomes. The study was originally intended to follow the patients for 4 years, but death rates diverged so dramatically early on that researchers decided it would be unethical to continue and called an end to the trial. After an average follow-up of 27 months, the overall death rate of the control group was more than twice that of the experimental group.

One little publicized finding from this well-known trial was that the total and LDL cholesterol levels of the treatment and control groups were virtually identical throughout the entire study. Those in the treatment group, however, did show significantly higher blood levels of omega-3 fatty acids and antioxidants (19).

What about Statins?

What about statin drugs? According to medical 'opinion leaders' (those who tell the rest of the unthinking masses what to believe), recent trials with statin drugs have proven once and for all that LDL reduction is beneficial. Allegedly, these trials have also shown that the greater the LDL reductions, the better.

Again, this is completely false.

Statins Do a Whole Lot More Than Just Lower LDL

Statin drugs exert their lipid-lowering effect by blocking an enzyme in the liver that is involved in the early stages of cholesterol synthesis. Statins inhibit the synthesis of mevalonate, a precursor not only to cholesterol, but also to a substance known as geranyl-geraniol. Inhibition of geranyl-geraniol produces beneficial effects on levels of nitric oxide (NO), a substance with anti-inflammatory and artery-dilating properties.(20,21) The consequences of this dual action are widespread:

In research with mice, statins markedly reduce measures of both inflammation and atherosclerosis, even though there is little change in serum cholesterol levels.(22)

Statins reverse or impede the progression of atherosclerosis in rabbits, without any accompanying change in serum cholesterol.(23,24)

In human volunteers with slightly elevated cholesterol, researchers found that four weeks of simvastatin therapy significantly enhanced forearm blood flow, a measure of arterial function. The amount of improvement was unrelated to the degree of cholesterol reduction.(25)

In elderly diabetic patients, cerivastatin increased dilation of the brachial artery after only 3 days, before any change in cholesterol levels had occurred.(26)

Statins have been shown to reduce blood platelet production of thromboxane, an eicosanoid that encourages blood-clotting. This effect was not seen with the older drugs that lowered total or LDL cholesterol such as cholestyramine, cholestipol, and fibrates.(27)

Statins have also been observed to inhibit the migration of smooth muscle cells seen in atherosclerotic plaque formation.(28,29)

Statins may prevent advanced atherosclerotic plaques, or atheromas, from rupturing. Plaque rupture is believed to be the instigating factor in a significant portion of coronary events.(30)
Clearly, the effects of statins go far beyond merely lowering cholesterol. The multi-faceted nature of statins is no doubt why almost all of the major controlled, randomized trials with statin drugs have shown no association between the degree of total or LDL cholesterol lowering and the CHD survival rate. In most of these studies, the risk of a fatal heart attack was similarly reduced whether total or LDL cholesterol levels were lowered by a small or large amount.(31-37)

There are two exceptions--the PROSPER trial, which recorded the highest survival rates in both the treatment and control groups among those with the highest LDL levels.(38)

In the Japanese Lipid Intervention Trial (J-LIT), a six-year study of over 47,000 patients treated with simvastatin, those with a total cholesterol level of 200-219 mg/dL had a lower rate of coronary events than those whose levels were above or below this range. The lowest overall mortality rate was seen in the patients whose total and LDL cholesterol levels were between 200-259 mg/dL and 120-159 mg/dL. The highest death rate in the study, by the way, was observed among those whose cholesterol levels were below 160 mg/dL.(39)

The Establishment Method of Dealing With Contradictory Evidence

When confronted with non-supportive evidence, the medical establishment usually does what any good purveyor of profitable misinformation would do--ignores it. Additionally, it simultaneously seeks out supportive evidence, no matter how flimsy, and then embarks on an aggressive propaganda campaign to 'educate' as many people as possible to this allegedly supportive evidence. The end result is that the public receives a highly distorted version of events that, while far from the truth, is nonetheless far more palatable to the reigning orthodoxy.

A perfect example of this phenomenon occurred in April 2004, when the results of the Pravastatin or Atorvastatin Evaluation and Infection Therapy trial (PROVE-IT) were published.

The PROVE-IT researchers randomized patients who had recently been hospitalized for an acute coronary event to either 40 milligrams of pravastatin (Pravachol) or 80 milligrams of atorvastatin (Lipitor) daily. Not surprisingly, median LDL cholesterol levels were lowered to a greater extent on high dose atorvastatin.

After an average follow-up of two years, the high dose atorvastatin group enjoyed a 30 percent reduction in CHD mortality and a 28 percent decrease in overall mortality(40). Establishment spokespeople could barely hide their euphoria; after a continual stream of non-supportive major trials, they finally had a study in which LDL reduction appeared to be correlated with improved clinical outcomes! According to the barrage of publicity awarded to the trial by an ever compliant media, PROVE-IT finally 'proved' that the lower the LDL level, the better!

Actually, PROVE-IT proved no such thing.

Neither did TNT, the highly-hyped study published in March 2005 which also supposedly proved the value of aggressive LDL-lowering. In this study, 10,001 CHD patients with LDL cholesterol levels of less than 130 mg/dl were randomly assigned to either 10 or 80 milligrams of atorvastatin (Lipitor) daily. TNT was sponsored by Pfizer, the manufacturer of Lipitor (currently the world's best-selling drug).

Those receiving low-dose atorvastatin reduced their mean LDL cholesterol levels to 101 mg/dl, while those taking the high dose brought their LDL readings down to 77 mg/dl. After a median follow-up of 4.9 years, 2.5 percent of the low-dose group had died from coronary causes, compared to 2 percent in the high dose group, a twenty percent relative risk reduction.(41) Glowing media reports enthusiastically hailed these results as triumphant confirmation of the PROVE-IT findings. According to the hype, the "lower is better" era of LDL reduction had officially arrived.

Wait Just a Minute…

That statins exert a whole host of biochemical effects beyond mere lipid-lowering is beyond question. In light of this inescapable fact, how can anyone confidently conclude that it was LDL reduction--and not amplification of one or more of these other effects--that produced the favorable cardiovascular outcomes seen in PROVE-IT or TNT?

The answer, of course, is that they can't.

Cut the CRP

C-reactive protein (CRP) is a substance that serves as a marker for inflammatory activity inside the body. CRP has attracted a great deal of attention ever since a large study published in 2002 suggested that this protein was a significantly better predictor of future cardiovascular events than LDL cholesterol.

In January 2005, the New England Journal of Medicine published two studies examining the interplay between statin use, CRP levels, and subsequent coronary event rates. The first of these, using data from the aforementioned PROVE IT study, found that: "Patients who have low CRP levels after statin therapy have better clinical outcomes than those with higher CRP levels, regardless of the resultant level of LDL cholesterol."(42)

In the second study, researchers used intravascular ultrasonography to examine the association of LDL and CRP with the continued development of atherosclerosis in 502 CHD patients. They found that "Atherosclerosis regressed in patients with the greatest reduction in CRP levels, but not in those with the greatest reduction in LDL cholesterol levels."(43)

These results reinforce what is already obvious to those whose minds have not been thoroughly dulled by the massive anti-cholesterol offensive--namely, that the favorable results seen in PROVE-IT were due to the non lipid-lowering actions of statins. The strong correlation between CRP and improved clinical outcomes indicates that the anti-inflammatory effects of statins played a key role.

Of course, the CRP analysis of the PROVE-IT trial was published almost a year after the initial paper that focused on LDL. This was more than enough time to milk the LDL publicity machine for all it was worth, and to use the PROVE-IT results as primary justification for a further reduction in the official NCEP cholesterol-lowering guidelines.

The Charade Continues

With the sole exception of two selectively interpreted trials (PROVE-IT and TNT), decades of dietary and drug intervention trials have repeatedly shown a complete disconnect between total and LDL cholesterol reduction and clinical outcomes.

As such, there exists no proof that LDL cholesterol causes cardiovascular disease, nor that LDL reduction can lower the incidence of CVD events. So how much longer will the medical mainstream keep up the LDL cholesterol charade?

A long, long time, if comments by one of the leading proponents of this nonsensical paradigm are anything to go by.

Commenting on recent research that questions a causal role for C-reactive protein in cardiovascular disease, Dr Steven Nissen, a cardiologist at Ohio's Cleveland Clinic, says the debate "reminds him of the resistance experienced 20 years ago when the importance of cholesterol was first discovered."

According to Nissen, "Many nihilists fought vociferously against the concept of LDL as a causative agent in atherosclerosis. A few of them still don't accept the concept."(44)

Planet Earth to Steve Nissen…

Nissen's response to critics of the cholesterol agenda is a classic textbook example of the kind of dismissive, evasive arguments used by those who propagate scientifically untenable nonsense. Orthodoxy knows full well that it can't rationally address all of the numerous contradictions and fallacies inherent in its pet hypothesis, so it instead attempts to portray dissenting commentators as lone quacks who are out of step with scientific reality.

For those tempted to believe such rot, I would strongly suggest you first visit the home page for The International Network of Cholesterol Skeptics. This is a worldwide network of researchers, doctors, and science writers who are highly critical of the anti-cholesterol campaign. It includes such highly esteemed researchers as Dr. Uffe Ravnskov, MD, PhD, (who has published dozens of papers on kidney disease and the cholesterol hypothesis), Kilmer McCully, MD, (the pioneer researcher who uncovered the link between homocysteine and cardiovascular disease), Peter Langsjoen, MD, (foremost authority on the interaction between statin drugs and coenzyme Q10), and Mary Enig, PhD, (the renowned biochemist who first raised the alarm on trans fatty acids).

While Nissen would have his colleagues and the public believe that opposition to the cholesterol hypothesis is limited to a handful of disgruntled "nihilist" crackpots, the truth is that a growing number of highly esteemed and accomplished individuals are joining the campaign to alert the public to the fact that this hypothesis is a total sham.

Always was, and always will be.

Share the facts--recommend this article to a friend!


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2/09/2006 9:20 PM  
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2/10/2006 7:45 AM  

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