The Paleo approach to meal frequency

Furthering our discussion of postprandial (after-eating) phenomenona, including chylomicron and triglyceride "stacking" (Grazing is for cattle and Triglyceride and chylomicron stacking), here's a comment from the recent Palet Diet Newsletter on the closely related issue, meal timing and frequency:


We are currently in the process of compiling meal times and patterns in the worlds historically studied hunter-gatherers. If any single picture is beginning to emerge, it clearly is not three meals per day plus snacking ala the typical U.S. grazing pattern. Here are a few examples:

--The Ingalik Hunter Gatherers of Interior Alaska: 'As has been made clear, the principal meal and sometimes the only one of the day is eaten in the evening.'
--The Guayaki (Ache) Hunter Gatherers of Paraguay: 'It seems, however, that the evening meal is the most consistent of the day. This is understandable, since the day is generally spent hunting for food that will be eaten in the evening."
--The Kung Hunter Gatherers of Botswana. "Members move out of camp each day individually or in small groups to work through the surrounding range and return in the evening to pool the collected resources for the evening meal."
--Hawaiians, Tahitians, Fijians and other Oceanic peoples (pre-westernization). 'Typically, meals, as defined by Westerners, were consumed once or twice a day. . . Oliver (1989) described the main meal, usually freshly cooked, as generally eaten in the late afternoon after the day’s work was over."

The most consistent daily eating pattern that is beginning to emerge from the ethnographic literature in hunter-gatherers is that of a large single meal which was consumed in the late afternoon or evening. A midday meal or lunch was rarely or never consumed and a small breakfast (consisting of the remainders of the previous evening meal) was sometimes eaten. Some snacking may have occurred during daily gathering, however the bulk of the daily calories were taken in the late afternoon or evening. This pattern of eating could be described as intermittent fasting relative to the typical Western pattern, particularly when daily gathering or hunting were unsuccessful or marginal. There is wisdom in the ways of our hunter gatherer ancestors, and perhaps it is time to re-think three squares a day.



In other words, the notion of "grazing," or eating small meals or snacks throughout the day, is an unnatural situation. It is directly contrary to the evolutionarily more appropriate large meal followed by periods of no eating or small occasional meals.

I stress this point because I see that the notion of grazing has seized hold of many people's thinking. In my view, grazing is a destructive practice that is self-indulgent, unnecessary, and simply fulfills the perverse non-stop hunger impulse fueled by modern carbohydrate foods.

Eliminate wheat, cornstarch, and sugars and you will find that grazing is a repulsive impulse that equates with gorging.


The full-text of the Paleo Diet Newsletter can be obtained through www.ThePaleoDiet.com. You can also read and/or subscribe to the new Paleo Diet Blog, just launched in November, 2009.

Even mummies do it


Lady Rai, nursemaid to Queen Nefertari of Egypt, died in 1530 BC, somewhere between the age of 30 and 40 years. Her mummy is preserved in the Egyptian National museum of Antiquities in Cairo.

A CT scan of her thoracic aorta revealed calcium, representing aortic atherosclerosis, reported by Allam et al (including my friend from The Wisconsin Heart Hospital, Dr. Sam Wann, who provided me a blow-by-blow tale of this really fascinating project). Ladi Rai and 14 other Egyptian mummies were found to have vascular calcification of a total of 22 mummies scanned. (The hearts of the mummies were too degenerated to make out any coronary calcium.)

But why would people of that age have developed atherosclerosis?

The authors of the study comment that "Our findings that atherosclerosis was not infrequent among middle-aged and older ancient Egyptians of high social status challenges the view that it is a disease of modern humans. . . Although ancient Egyptians did not smoke tobacco or eat processed food or presumably lead sedentary lives, they were not hunter-gatherers. [Emphasis mine.] Agriculture was well established in ancient Egypt and meat consumption appers to have been common among those of high social status."

Fascinating. But I don't think that I'd blame meat consumption. Egyptians were also known to have cultivated grains, including wheat, and frequently consumed such sweet delicacies as dates and figs. Egyptians were also apparently beer drinkers. Unfortunately, no beer steins were seen in any of the scans.

Life Extension article on iodine

Here's a link to my recent article in Life Extension Magazine on iodine:

Halt on Salt Sparks Iodine Deficiency

Iodized salt, a concept introduced into the U.S. by the FDA in 1924, slowly eliminated goiter (enlarged thyroid glands), along with an enormous amount of thyroid disease, heart attack, mental impairment, and death. The simple addition of iodine to salt ensured that salt-using Americans obtained enough iodine sufficient to not have a goiter.

Now that the FDA, goiters long forgotten from their memories, urges Americans to reduce salt, what has happened to our iodine?

I talk at length about this issue in the Life Extension article.

The healthiest people are the most iodine deficient

Here's an informal observation.

The healthiest people are the most iodine deficient.

The healthier you are, the more likely you are to:

--Avoid junk foods--30% of which have some iodine from salt
--Avoid overuse of iodized salt
--Exercise--Sweating causes large losses of iodine.

So the healthy-eating, exercising person is the one most likely to show iodine deficiency: gradually enlarged thyroid gland (in the neck), declining thyroid function. Over time, if iodine deficiency persists, excessive sensitivity to iodine develops, as well as abnormal thyroid conditions like overactive nodules.

Even subtle levels of thyroid dysfunction act as a potent coronary risk factor.

It's the score, stupid

Sal has had 3 heart scans. (He was not on the Track Your Plaque program.) His scores:

March, 2006: 439

April, 2007: 573

October, 2009: 799

Presented with the 39% increase from April, 2007 to October, 2009, Sal's doctor responded, "I don't understand. Your LDL cholesterol is fine."

This is the sort of drug-driven, cholesterol-minded thinking that characterizes 90% of primary care and cardiologists' practices: "Cholesterol is fine; therefore, you must be fine, too."

No. Absolutely not.

The data are clear: Heart scan scores that continue to increase at this rate predict high risk for cardiovascular events. Unfortunately, when my colleagues hear this, they respond by scheduling a heart catheterization to prevent heart attack--a practice that has never been shown to be effective and, in my view, constitutes malpractice (i.e., performing heart procedures in people with no symptoms and with either no stress test or a normal stress test).

It's the score, stupid! It's not the LDL cholesterol. Pay attention to the increasing heart scan score and you will know that the disease is progressing at an alarming rate. Accepting this fact will set you and your doctor on the track to ask "Why?"

That's when you start to uncover all the dozens of other reasons that plaque can grow that have nothing to do with LDL cholesterol or statin drugs.

Heart Scan Blog Redux: Cheers to flavonoids

Because in Track Your Plaque we've been thinking a lot about anthocyanins, here's a rerun of a previous Heart Scan Blog post about red wine. (Anthocyanins are among the interesting flavonoids in red wine, along with resveratrol and quercetin.)


The case in favor of healthful flavonoids seems to grow bit by bit.

Flavonoids such as procyanadins in wine and chocolate, catechins in tea, and those in walnuts, pomegranates, and pycnogenol (pine bark extract) are suspected to block oxidation of LDL (preventing its entry into plaque), normalize abnormal endothelial constriction, and yield platelet-blocking effects (preventing blood clots).

Dr. Roger Corder is a prolific author of many scientific papers detailing his research into the flavonoids of foods, but wine in particular. He summarizes his findings in a recent book, The Red Wine Diet. Contrary to the obvious vying-for-prime-time title, Dr. Corder's compilation is probably the best mainstream discussion of flavonoids in foods and wines that I've come across. Although it would have been more entertaining if peppered with more wit and humans interest, given the topic, its straightfoward, semi-academic telling of the story makes his points effectively.

Among the important observations Corder makes is that regions of the world with the greatest longevity also correspond to regions with the highest procyanidin flavonoids in their wines.




Regarding the variable flavonoid content of wines, he states:

Although differences in the amount of procyanidins in red wine clearly occur because of the grape variety and the vineyard environment, the winemaker holds the key to what ends up in the bottle. The most important aspect of the winemaking process for ensuring high procyanidins in red wines is the contact time between the liquid and the grape seeds during fermentation when the alcohol concentration reaches about 6 percent. Depending on the fermentation temperature, it may be two to three days or more before this extraction process starts. Grape skins float and seeds sink, so the number of times they are pushed down and stirred into the fermenting wine also increases extraction of procyanidins. Even so, extraction is a slow process and, after fermentation is complete, many red wines are left to macerate with their seeds and skins for days or even weeks in order to extract all the color, flavor, and tannins. Wines that have a contact time of less than seven days will have a relatively low level of procyanidins. Wines with a contact time of ten to fourteen days have decent levels, and those with contact times of three weeks or more have the highest.

He points out that deeply-colored reds are more likely to be richer in procyanidins; mass-produced wines that are usually "house-grade" served at bars and restaurants tend to be low. Some are close to zero.

Wines rich in procyanidins provide several-fold more, such that a single glass can provide the same purported health benefit as several glasses of a procyanidin-poor wine.

So how do various wines stack up in procyanidin content? Here's an abbreviated list from his book:

Australian--tend to be low, except for Australian Cabernet Sauvignon which is moderate.

Chile--only Cabernet Sauvignon stands out, then only moderate in content.

France--Where to start? The French, of course, are the perennial masters of wine, and prolonged contact with skins and seeds is usually taken for granted in many varieties of wine. Each wine region (French wines are generally designated by region, not by variety of grape) can also vary widely in flavonoid content. Nonetheless, Bordeaux rate moderately; Burgundy low to moderate (except the village of Pommard); Languedoc-Roussillon moderate to high (and many great bargains in my experience, since these producers live in the shadow of its northern Bordeaux neighbors); Rhone (Cote du Rhone) moderate to high, though beware of their powerful "barnyard" character upon opening; decanting is wise.

Italy--Much red Italian wine is made from the Sangiovese grape and called variously Chianti, Valpolicella, and "super-Tuscan" when blended with other varietals. Corder rates the southern Italian wines from Sicily, Sardinia, and the mainland as high in procyanidins; most northern varieties are moderate.

Spain--Moderate in general.

United States--Though his comments are disappointingly scanty on the U.S., he points out that Cabernet Sauvignon is the standout for procyanidin content. He mentions only the Napa/Sonoma regions, unfortunately. (I'd like to know how the San Diego-Temecula and Virginian wines fare, for instance.)

The winner in procyanidin content is a variety grown in the Gers region of southwest France, a region with superior longevity of its residents. The wines here are made with the tannat grape within the Madiran appellation; wines labeled "Madiran" must contain 40% or more tannat to be so labeled (such is a quirk of French wine regulation). Among the producers Dr. Corder lists are Chateau de Sabazan, Chateau Saint-Go, Chateau du Bascou, Domaine Labranche Laffont, and Chateau d'Aydie. (A more complete list can be found in his book.)

How does this all figure into the Track Your Plaque program? Can you succeed without red wine? Of course you can. I doubt you could do it, however, without some attention to flavonoid-rich food sources, whether they come from spinach, tea, chocolate, beets, pomegranates, or red wine.

Though my wife and I love wine, I confess that I've never personally drank or even seen a French Madiran wine. Any wine afficionados with some advice?

Can wheat elimination cure ulcerative colitis?

Tammy is a 36-year old mother of three young children. Since age 20, she has suffered with the debilitating symptoms of ulcerative colitis: constant, gnawing abdominal pain; frequent diarrhea, often bloody.



Tammy has had to take several medications, some with significant side-effects, all of which provided only partial relief from the pain and diarrhea. Her gastroenterologist and surgeon were planning a colectomy (removal of the colon) with creation of an ileostomy (rerouting of the small intestine to the abdominal surface, which would require Tammy to wear an ileostomy bag under her clothes for the rest of her life).



Although Tammy had previously tested negative for celiac disease (an allergic sensitivity to the gluten in wheat products), I urged her to attempt a trial of a wheat-free diet. Having witnessed many people experience relief from irritable bowel syndrome, acid reflux, and other common gastrointestinal complaints, all while trying to reduce blood sugar and small LDL, I'd hoped that Tammy would obtain at least some small improvement in her terrible symptoms.



I therefore urged Tammy to try it. After all, what was there to lose? Tammy grudgingly agreed.



She returned 6 months later. Her report: She had lost 38 lbs, virtually all of it within the first 6-8 weeks. Her diarrhea and cramping were not better, but gone. She was down to a single medicine from her former list of drugs.



I am unsure what proportion of people with ulcerative colitis or other inflammatory bowel diseases like Crohn's will experience a result like Tammy's. Perhaps it's only a minority. But I take this another piece of evidence that this enormously destructive thing called wheat has no place in the human diet.



We have no facts or figures on the prevalence of various forms of wheat intolerance in the U.S. When I contacted the Celiac Disease Foundation, they had no figures on the number of fatalities per year in the U.S. from celiac disease. But if there are 2-3 million Americans with celiac disease, there are probably 100 times that many people with various forms of wheat intolerance.



Postprandial pile-up with fructose

Heart disease is likely caused in the after-eating, postprandial period. That's why the practice of grazing, eating many small meals throughout the day, can potentially increase heart disease risk. Eating often can lead to the phenomenon I call triglyceride and chylomicron "stacking," or the piling up of postprandial breakdown products in the blood stream.

Different fatty acid fractions generate different postprandial patterns. But so do different sugars. Fructose, in particular, is an especially potent agent that magnifies the postprandial patterns. (See Goodbye, fructose.)

Take a look at the graphs from the exhaustive University of California study by Stanhope et al, 2009:



From Stanhope KL et al, J Clin Invest 2009. Click on image to make larger.

The left graphs show the triglyceride effects of adding glucose-sweetened drinks (not sucrose) to the study participants' diets. The right graphs show the triglyceride effects of adding fructose-sweetened drinks.

Note that fructose causes enormous "stacking" of triglycerides, meaning that postprandial chylomicrons and VLDL particles are accumulating. (This study also showed a 4-fold greater increase in abdominal fat and 45% increase in small LDL particles with fructose.)

It means that low-fat salad dressings, sodas, ketchup, spaghetti sauce, and all the other foods made with high-fructose corn syrup not only make you fat, but also magnifies the severity of postprandial lipoprotein stacking, a phenomenon that leads to more atherosclerotic plaque.

Track Your Plaque: Safer at any score

Imagine two people.

Tom is a 50-year old man. Tom's initial heart scan score was 500--a concerning score that carries a 5% risk for heart attack per year.

Harry is also 50 years old. His heart scan score is 100--also a concerning score, but not to the same degree as Tom's much higher score.

Tom follows the Track Your Plaque program. He achieves the 60:60:60 lipid targets; chooses healthy foods, including elimination of wheat; takes fish oil at a therapeutic dose; increase his blood vitamin D level to 60-70 ng/ml, etc. One year later, Tom's heart scan score is 400, representing a 20% reduction from his starting score.

Harry, on the other hand, doesn't understand the implications of his score. Neither does his doctor. He's casually provided a prescription for a cholesterol drug by his doctor, a brief admonition to follow a low-fat diet, and little else. One year later, Harry's heart scan score is 200, a doubling (100% increase) of the original score.

At this point, we're left with Tom having a score of 400, Harry with a score of 200. That is, Tom has twice Harry's score, 200 points higher. Who's better off?

Tom with the score of 400 is better off. Even though he has a significantly higher score, Tom's plaque is regressing. Tom's plaque is therefore quiescent with active components being extracted, inflammation subsiding, the artery in a more relaxed state, etc.

Harry's plaque, in contrast, is active and growing: inflammatory cells are abundant and producing enzymes that degrade supportive tissue, constrictive factors are released that cause the artery to pinch partially closed, fatty materials accumulate and trigger a cascade of abnormal responses.

So it's not just the score--the quantity of atherosclerotic plaque present--but the state of activity of the plaque: Is it growing, is it being reduced? Is there escalating or subsiding inflammation? Is plaque filled with degradative enzymes or quiescent?

Following the Track Your Plaque program therefore leads us to the notion that it's not the score that's most important; the most important thing is what you're doing about it. We sometimes say that Track Your Plaque makes you safer at any score.
Thank you, Crestor

Thank you, Crestor

I'm sure everyone by now has seen the Crestor ads run by drugmaker, AstraZeneca. TV ads, magazine ads, and the Crestor website all echoing the same message:

"While I was busy building my life, something else was busy building in my arteries: dangerous plaque."

While previous drug trials with Mevacor, Pravachol, Zocor, and Lipitor have focused mostly on examining whether the drugs reduced incidence of cardiovascular events, Crestor studies have also focused on effects on atherosclerotic plaque volume. The best example is the ASTEROID trial that demonstrated approximately 7% reduction in plaque volume by intracoronary ultrasound.

So the AstraZeneca decision makers took the leap from cholesterol reduction to plaque reduction.

I'm sure this switch wasn't taken lightly, but was the topic of discussion at many meetings before the decision to make plaque reduction the focus of hundreds of millions of dollars of advertising. After all, billions of dollars are at stake in this bloated statin market.

Ordinarily, I couldn't care less about how the drug manufacturers conduct their advertising campaigns. But this one I paid attention to because the Crestor ads are helping fuel a new way of thinking about coronary heart disease: It's not about the cholesterol; it's about the atherosclerotic plaque that accumulates in arteries.

It's not cholesterol that grows, limits coronary blood flow, and causes angina. It's not cholesterol that "ruptures" its internal contents to the surface within the interior of the blood vessel and causes blood clot and heart attack. It's not cholesterol that fragments from the carotid arteries and showers debris to the brain, causing stroke. It's all plaque.

I took the same leap years ago, though not backed by hundreds of millions of dollars of marketing money. When I first called my book Track Your Plaque, some of the feedback I got from editors included comments like "I thought this was a book about teeth!" Even now, the word "plaque" in the book title and website is responsible for confusion.

But AstraZeneca is helping me clear up the confusion. As the word plaque gains hold in public consciousness, it will become increasingly clear that cholesterol reduction is not what we're after. We are looking for reduction of plaque.

If you are trying to develop an effective means to reduce or reverse coronary heart disease, then there are two simple equations to keep in mind:


Plaque = coronary heart disease

Cholesterol ? coronary heart disease


Plaque is the disease, cholesterol is not. Cholesterol is simply a crude risk for plaque.

While I'm no friend to the drug industry nor to AstraZeneca, some good will come of their efforts.

Comments (9) -

  • Greg

    3/20/2009 6:12:00 PM |

    This is all so true. What makes me even more mad is my Dad is on some cholesterol lowering drug and no matter how much evidence I show against it he does not believe that his doctor would not do what is best for him. Makes me sick when I think about it.

  • Judy Graves

    3/21/2009 3:43:00 AM |

    I am currently in a battle with my "preventative" cardiologist.  she just handed me a bunch of Crestor due to a very high Lp(a) and family history of heart disease.  I have gone round and round with her about statins and she was willing to go the Niacin route first.  I was convinced that would work but something very strange occurred.  I don't mind the Niacin flush at all and I did take with food, aspirin, the whole 9 yards.  After being on the Niaspan for 12 days, I suddenly broke out into horrible hives all over my body and now 3 weeks later I still have some lingering rash/hives on my arms.  My diet and exercise program couldn't be better - I walk 6 miles a day, yoga 3 times a week, eat whole foods only, drink lots of water and I am just not sure what to do next.  My Lp(a) number is 135 and my total cholesterol is 267 with a not so good "ratio".  If anybody has any suggestions or comments I would love to hear them!

  • David

    3/21/2009 7:18:00 PM |

    Judy, make sure you take a close look at the hormones (estrogen, DHEA, thyroid, etc.), as these can influence Lp(a) to a pretty large degree.

    High dose EPA/DHA from fish oil is also really important. Consider up to ~6,000 mg EPA + DHA daily.

    Consume raw nuts and seeds. Almonds and ground flaxseed are great, and can help in dropping Lp(a).

    L-carnitine can help in lowering Lp(a), at least by a little bit.

    Not sure what you're including when you say your diet is made up of "whole foods." If this refers to things like "whole wheat," then that's problematic. Based on the research I've seen, those of us with Lp(a) (and yes, I am one of them too) are quite a bit more sensitive to the carbs. Eat carbs, and your Lp(a) goes up. Eat lower carbs, higher fat (particularly saturated), and your Lp(a) goes down. I would be loving on the coconut oil if I were you (and that's exactly what I do).

    As for exercise, I would start changing it up. That's an awful lot of walking, and it's not going to create the hormonal response that you need. The real benefit is in the high intensity stuff. Short, vigorous sprints, squats, that sort of thing. Check out www.crossfit.com for some idea of what I'm talking about.

  • Adam Wilk

    3/22/2009 3:30:00 PM |

    Judy,
    I second what David says above--it sounds like good, solid advice.
    I would add 3 things to the supplement category--Vitamin C (min 6000mgs/day) L-Lysine (min 6000mgs/day) and NAC, (min 1200mgs/day)
    The Vitamin C and L-Lysine combination is I'm sure you know, the Pauling-Rath formula--it's been around a long time, many swear by it, but it's never been clinically double-blind tested.  The NAC, I recently learned, is possibly the most powerful natural Lp(a) inhibitor out there, for now, anyway.  I was so swayed by what I read about it, I purchased a couple of bottles of it to add to Pauling-Rath, since I, too, am sometimes irked by the Niacin flushes I begin experiencing as I get closer to the 500mg dose--and this is after weeks of slowly titrating the dose so that I may avoid that uncomfortable event.
    Judy, also keep in mind, I've always read that 1)It's better for women to have higher cholesterol levels and 2) up until a few years ago, a cholesterol level of over 300 was considered high.  Now that '200' is the new '300', there seems to be quite a market for new prescriptions, nu?
    Adam

  • David

    3/22/2009 7:49:00 PM |

    The Pauling/Rath therapy is indeed intriguing. Before I discovered Dr. Davis and the TYP program, I thought that the Pauling therapy was the answer to heart disease.

    I now believe and am convinced that there's more to it than that, and I think Dr. Davis has one of the best, most comprehensive programs for heart disease out there.

    However, this is not really a criticism, and I remain convinced that there is value to the Pauling/Rath therapy. It makes so much sense, at least theoretically in terms of reducing Lp(a), and it has quite a bit of anecdotal evidence behind it (not to mention the research carried out by Rath, complete with CT scans). It seems like the experience of doctors using this therapy with their patients varies quite a bit, though. Some doctors swear by it, while others say it just doesn't work. It's only for this reason that I usually don't bring it up until I've brought other ideas to the front that I know are very effective.

    I've got my dad on the Pauling therapy, along with these other things (basic TYP stuff), and we'll be getting his Lp(a) rechecked soon. Should be interesting to see how much it has come down, though I won't know which factor (niacin, diet, carnitine, fish oil, etc.) is creating the most change. I just decided to hit it with everything we've got.

    Oh, and it's the same with the NAC. There are pockets of stunning success, but there's also worry about long term safety and the development of pulmonary hypertension. Is that a real danger? I don't know. I would guess not, personally, but at the same time I'd rather mention the "tried and true" methods first that have the most overall benefit.

    I'm glad the Pauling therapy was brought up, here. I think it definitely should be looked into more, and people need to be aware of it as an option that many are having success with.

    David

  • xenolith_pm

    3/31/2009 4:00:00 PM |

    This may be of interest to those who may want to reduce the risk of venous thromboembolism (VTE) with a statin (Crestor):

    http://www.usatoday.com/news/health/2009-03-29-statin-clots_N.htm

    Statin Crestor lowers risk of deep-vein clots

    "ORLANDO — (3/30/09) Researchers have shown for the first time that a potent cholesterol-lowering drug, Crestor, reduces the risk of deep vein thrombosis, or "economy-class syndrome," caused by potentially lethal blood clots that start in the veins and migrate to the lungs, sometimes after long flights.

    The evidence, out today, is the latest to emerge from the landmark JUPITER trial, which showed that statin treatments can cut in half the risk of heart attacks and strokes even in people with normal cholesterol levels."

    No other medicine has been shown to safely prevent these blood clots, which occur in at least 350,000 people a year and kill as many as 100,000 of them. The standard remedy once thrombosis has occurred is the drug warfarin, which, unlike statins, can promote bleeding.

    Statins are "a remarkably benign therapy," says senior investigator Paul Ridker of Brigham and Women's Hospital in Boston. "The thing that's really exciting is that there is no bleeding risk."

    Other studies have hinted that statins also reduce clot formation, but their power to prevent deep vein thrombosis was unknown. Ridker and his co-workers decided to use JUPITER to test the theory. A total of 17,802 people were randomly assigned to treatment and placebo groups. They were followed for nearly two years, on average.

    Deep vein thrombosis occurred in 34 patients taking Crestor and 60 people who were taking placebos, indicating that treatment reduced the risk of clots by 43%. Ridker says he believes that other statins would also reduce the risk.


    What I take from this;

    The dose of Crestor in JUPITER was 20mg.  Paul Ridker said that this is a remarkably benign therapy?  I think not, given Dr. Davis' descriptions of intolerable side effects that will inevitably occur to the majority of people at this dosage.  I've never used Crestor, but I have used 10mg Zocor and developed mild myopathy in my legs after only three weeks, so I'll take his word that I would be a poor candidate.

    I think the most interesting part of the press release is that JUPITER (like the other statin trials) in no way confirms what mechanism may be behind the reduced risk of VTE.  Could it be due to a lowering of vascular inflammation as indicated by a lower CRP?  That certainly makes sense.  It would be really great to get a definitive answer, since CRP can be effectively managed by other means than taking such a strong statin like Crestor.

    AstraZeneca's press release of CRESTOR® REDUCED RISK OF BLOOD CLOTS IN THE VEINS (3/29/09):

    http://www.prnewswire.com/mnr/astrazeneca/37394/

  • crestor

    5/9/2009 10:48:00 AM |

    AstraZeneca’s (AZN.L)(AZN.N) powerful cholesterol drug Crestor cut the risk of dangerous blood clots in the vein by 43 percent in a large study, researchers said on Sunday.

  • buy jeans

    11/2/2010 8:36:56 PM |

    After being on the Niaspan for 12 days, I suddenly broke out into horrible hives all over my body and now 3 weeks later I still have some lingering rash/hives on my arms.

  • Crestor

    11/16/2010 11:53:59 AM |

    Took it for a year or so, but now I need it again and my insurance wont pay for it and my other medicines are over $400.00 a month and they want $160.00 more for Crestor. We just can't do it.

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