What do Salmonella, E coli, and bread have in common?

Say you happen to eat some chicken fingers contaminated with bacteria because the 19-year old kid behind the counter failed to wash his hands after using the toilet, or because the kitchen is poorly managed with unwashed counters and cutting boards, or because the food is undercooked. You get a bout of diarrhea and cramps, along with a desire to banish chicken from your life.

Here's yet another odd wheat phenomenon: About 30% of people who eliminate wheat from their lives experience an acute food poisoning-like effect on re-exposure. You've been wheat-free for, say, 6 months. You've lost 25 lbs from your wheat belly, you've regained energy, joints feel better. You go to an office party where they're serving some really yummy looking bruschetta. Surely a couple won't hurt! Within a hour, you're getting that awful rumbling and unease that precede the explosion.

The majority of people who experience a wheat re-exposure syndrome will have diarrhea and cramps that can last from hours to days, similar to food poisoning. (Why? Why would a common food trigger a food poisoning-like effect? It happens too fast to attribute to inflammation.) Others experience asthma attacks, joint pains that last 48 hours to a week, mental fogginess, emotional distress, even rage (in males).

Wheat re-exposure in the susceptible provides a tidy demonstration of the effects of this peculiar product of genetic research. So if you are wheat-free but entertain an occasional indulgence, don't be surprised if you have to make a beeline to the toilet.

Comments (22) -

  • Steve

    1/28/2011 3:55:24 PM |

    I'm finishing a jar of "dry" (not oil suspended) Vitamin D3 capsules and taking them with enteric coated fish oil. Might the enteric coating prevent the fish oil from helping the "dry" D3 absorption?

  • kathyj333

    1/28/2011 4:03:56 PM |

    Really interesting post. I think I'm sensitive to wheat, but can't seem to stop eating it right now. Once I gave it up for about two months and lost 20 pounds. I should probably try to eliminate it again. Thanks for the insight.

  • Geoffrey Levens

    1/28/2011 5:05:26 PM |

    Interesting.  I have just the opposite experience though.  My very rare (maybe once every 6 months or so) consumption of wheat causes no obvious symptoms whatsoever though I have in the past had severe sinus allergy response to wheat/gluten

  • Laurie D.

    1/28/2011 5:09:28 PM |

    When I first went gluten-free, I was not as careful as I am now and had several incidences of acute joint pain (with incredible heat) upon exposure to minute amounts of gluten.  The last time I knowingly ate gluten (crumbs from a crouton on a salad) I woke up the next day with the most intense back pain I have ever had.  My usual response to gluten is in the form of migraines. This pain was definitely not muscle pain but neurological with squeezing pains from my spine to the front.  That was the last time I had any gluten - I am extremely careful now and I have been GF 3 years and feel so much better.   I think gluten is a poison, plain and simple, and everyone would be better off not consuming it in any way.

  • Haggus

    1/28/2011 5:18:55 PM |

    I'm one of the lucky ones.  I caved during the silly season and stole a couple of my sisters' delicious homemade double chocolate cookies.  Alas, no mad dashes to the procelean apparatus.

  • Might-o'chondri-AL

    1/28/2011 5:53:36 PM |

    Wheat breeding sounds to be at fault for the way it's protein folds into an antigen trigger for a lot of people. Granny gave me jam with bread, pie and sugar cookies which didn't provoke malaise, but that was older breed of wheat.  

    Now-a-days professional diet advice is to avoid sugar, substitue sweetener. So, many don't get that sugar binding to  the gluten protein fragments. For people with metabolic syndrome adding back in sugar doesn't make sense; they can't use it to "goop-up" the gluten. Cutting out the wheat for them solves the dilema.

  • Tony

    1/28/2011 6:13:19 PM |

    Gluten are metabolized into opioids. Both the digestive system and the immune system have lots of neurons AFAIK. Is a nice system to protect the brain, I would guess. Evolution and natures way to say: Don't eat that, it'll mess you up.

  • Anonymous

    1/28/2011 6:21:51 PM |

    Why diarrhea with wheat rechallenge etc.?
    Perhaps because your bacterial intestinal flora has changed since wheat/grain elimination.

  • Paul Rise

    1/29/2011 1:11:19 AM |

    I have suffered from gastroparesis for 20+ years. Some medication has helped, but nothing has worked better than a carb/wheat free diet. If I avoid them my digestion seems fine. One cookie and within a few hours the rumbling and belching begins . . .

  • Anonymous

    1/29/2011 1:24:45 AM |

    There's this Ethiopian restaurant here in LA. They serve a flat bread called Injera.

    I must have it once or twice a year, I tell you, I must! Even though it causes sores in my mouth by the next morning. It never did that when I was eating wheat regularly. Now that I've given up wheat, BAM! Sores!

    Otherwise, I'm a sore-free, wheat-free good boy the rest of the year. Smile

  • Sean Preuss

    1/29/2011 1:37:21 AM |

    Dr. Davis,

    Great post.  I believe I have experienced exactly what you described.  I gave up drinking beer (my only grain) last summer and recent grain encounters led to stomach pain and quick trips to the bathroom.  One time I felt really sick for hours.

    There are never a shortage of reasons to avoid grains.

  • Might-o'chondri-AL

    1/29/2011 2:27:08 AM |

    @ Anonymous,
    I did some work in Ethiopia in 1970 & ate a lot of Injera;
    fermented Teff grain with a soaking phase. This increases the % of Arginine amino acids in Injera. People with cold sores are often agravated by arginine foods. Your sensitive mouth tissue is probably reacting to the high level of arginine. (Your individual sensitivity would likely extend to Indian Idli, soaked/fermented rice with dhall bean puff; it's bio-converted a lot of arginine too.)

  • Patricia D.

    1/29/2011 5:24:16 AM |

    For those of us that are cutting way back on wheat in our diets, but not eliminating it - what are our best options?  I'm finding heirloom wheat flour available on the internet.  And here's an interesting article I found on Heirloom wheats:
    'Are Heirloom Wheat Varieties the Next Big Baking Trend?"
    http://www.seriouseats.com/2010/01/is-heirloom-wheat-the-next-big-baking-trend-jim-lahey.html

    And what about Kamut?  Any comments?  Here's a write-up on it - it has some very nice features.
    http://www.suite101.com/content/kamut-ancient-grain-in-modern-times-a89648

  • majkinetor

    1/29/2011 12:39:23 PM |

    I try to avoid wheat all the time.

    However, I found one bread here, that is made without Flour but uses wheat sprouts instead. The recipe is made by Russian academic scientist.
    You have some English language info at

    http://www.zernohleb.ru/health_eng.html

    What do you think about it ?

    Thx

  • caphuff

    1/29/2011 1:02:17 PM |

    My digestion was always lousy (but I didn't know it) until I cut out wheat.

    Now if I reintroduce the reaction varies depending on the form of poison. Pasta is worst, sending the gi tract into the red zone for a week, plus migraines and sinus.

    other forms (cookies, pizza) the reaction is less volcanic, but still noticeable. The baseline reaction is the sensation that the lining of my stomach has been scrubbed with a brillo pad, and sometimes joint and back pain, with a touch of sinus fun.

    All this I used to think of as"normal".

    Anyone have any success with enzyme products (like "Gluten Ease“) to help deal with occasional exposure?

  • brec

    1/29/2011 2:03:44 PM |

    "The majority of people who experience a wheat re-exposure syndrome will have diarrhea and cramps..."

    This seems to say that of those who DO have symptoms ("experience a ... syndrome"), a majority will have diarrhea and cramps and a minority will have other symptoms.  But what proportion experience any symptoms?  Like Geoffrey above, I don't.

  • Mark__S

    1/29/2011 4:31:33 PM |

    Wow... that just happened to me.  But only after being wheat free for like a week.  I was experimenting with a gluten free paleo diet but went out with some friends to the mall to see a movie.  I drank one beer ate 4 slices of pizza and a big cookie.  I ended up screaming at a friend over a stupid comment, nothing serious, but I felt SO angry .  Something that is not usual for me.  Then that night I woke up in the middle of the night with stomach pain and diarrhea.  
    This was after just 1 week with no wheat.

  • Mark__S

    1/29/2011 4:32:57 PM |

    I forgot to add that I had bad headaches just 30 minutes or so after eating the pizza slices too..

  • Anonymous

    1/29/2011 11:46:04 PM |

    Don't you think this could also have something to do with the 1 in 133 statistic for celiac disease? Alot more are gluten intolerant and on down the spectrum to gluten sensitive.  

    That adds up to a whole lot of people out there who are on the continuum of mere sensitivity --->celiac

  • Robin

    2/2/2011 9:16:41 AM |

    That's me in a nutshell. Re-exposed to wheat and it was two days of unspeakable nastiness... I lapsed into this silliness as an experiment with the 4HB which necessitates a weekly wild day. It was wild alright...

  • jimbo

    2/13/2011 1:19:46 PM |

    Great post. I would love it if someone could explain the mechanism by which this re-exposure horror happens.

    Since cutting out gluten, even tiny exposures have sent my stomach into paroxysms of pain. This is accompanied by nausea and an all over sick feeling, like I have been poisoned.

    My bloods tested negative for coeliac though so I don't understand why I have such a bad reaction.

  • Jane Kaylor

    2/15/2011 4:18:18 AM |

    I am one of those people prone to headaches, migraine and colds. Usually, my first recourse is White Flower Embrocation (embrocation.50webs.com), also called White Flower Oil

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Vytorin study explodes--But what's the real story?

Vytorin study explodes--But what's the real story?

The makers of Vytorin, Merck/Schering-Plough Pharmaceuticals, issued a press release about the the Enhance Study yesterday. The news has triggered a media frenzy.

The NY Times reporting of the story:

Drug Has No Benefit in Trial, Makers Say

The 700 participants in the trial all had a condition called "heterozygous hypercholesterolemia," a genetic disorder that permits very high LDL cholesterols. The average LDL at the start was 318 mg/dl.

The Times reported that, while Vytorin cut "LDL levels by 58 percent, compared to a 41 percent reduction with simvastatin alone," but "the average thickness of the carotid artery plaque increased by 0.0111 of a millimeter in patients taking Vytorin, compared to an increase of 0.0058 of a millimeter in those taking only simvastatin." There was no difference in heart attacks or other "events" between the two groups.

(Vytorin is the combination of simvastatin and Zetia.)

In other words, the participants taking Vytorin had 53 ten-thousands of a millimeter more plaque growth than the group taking just simvastatin.

I am always uncomfortable when put in the position of defending a drug or drug company. However, it is patently absurd that this study has generated such attention. I suspect the public and media are waiting for another Vioxx-like debacle, with memories of concealed or suppressed data that suggested heightened heart attack risk that was dismisssed by the drug manufacturer. (That's not to say that the company hasn't been trying to delay or modify the outcome of the study, which they apparently have, much to the objections of the FDA.)

However, at this point, there is no reason to believe that this question possesses any parallels to the Vioxx fiasco.

If we accept the data as reported, however, we might say it calls the entire "Lipid Hypothesis" into question: If LDL cholesterol is significantly reduced but is not correlated with reduction in plaque, is LDL the means by which atherosclerotic plaque progresses? This trial does not answer that question, but does serve to raise some doubt.

Another issue: Heterozygous hypercholesterolemia, and thereby LDL cholesterol, may not be the overwhelming driver of plaque growth in this population. It is probably the number of small LDL particles, a factor which is not revealed by LDL cholesterol. For this reason, heterozygous hypercholesterolemia by itself is insufficient to cause heart disease. Some other factor(s) needs to be present. I would propose that it is the size of the LDL particle: When small, heart disease develops; when large, heart disease is less likely to develop. This issue was not addressed by this study. Readers of The Heart Scan Blog know that conventional LDL cholesterol, the number used in this study, is a virtually worthless number for truly gauging plaque behavior because of its flagrant inaccuracy.

So, there are substantial uncertainties, contrary to the absolute certainty expressed by people like Dr. Steve Nissen (who, by the way, has no expertise in lipoprotein disorders). It is premature to reach any firm conclusions from this study. The only conclusions that I personally come to are 1) Is this yet another reason to question the entire Lipid Hypothesis as it stands? and 2) What would the results have been had LDL particle number and LDL particle size been examined, not just LDL?

I would not automatically conclude that Zetia causes carotid plaque. This is absurd. And I am definitely not one to come to the rescue of a drug or drug manufacturer. I am simply after understanding and truth.

As an interesting aside, Dr. Howard Hodis of the University of Southern California and an expert in carotid scanning for heart disease prevention research, made a comment relevant to us in the Track Your Plaque program:

"Clearly, progression of atherosclerosis is the only way you get events,” Dr. Hodis said. “If you don’t treat progression, then you get events."

Comments (28) -

  • Anonymous

    1/16/2008 1:01:00 AM |

    What am I missing here? Has it not been proven that Statin + Niacin combo is like 90% affective in stopping plaque progression in its tracks? Why does that not say that LDL reduction AND particle size reduction,(Niacin for LP(a),works best? Its not just LDL, I developed heart disease with a 90-100 LDL before my Dr discovered  high LP (a). Treated with 10mg statin,1500 Niacin, diet,I am at a30/30 count. OVER&OUT

  • Peter

    1/16/2008 11:20:00 AM |

    Let's just summarise. First there was Keys with his total cholesterol. This turned out to be garbage. Then there was LDL vs HDL. But LDL is calculated and, as we know from this site, tells us nothing about anything. Then we have LDL particle size. Small dense is bad, big fluffy is good, noting that big fluffy contains lots of cholesterol per particle and can increase your calculated, or even absolute, LDL. Two factors, most studies use calculated LDL. The bin is there, file promptly.

    The second is that something controls your LDL particle size. How, on a practical basis, does Dr Davis control LDL size and density? No wheat and no sugar. Does wheat and sugar elimination alter anything in the body? Wheat contains both an insulin mimetic and two insulin potentiators, plus starches and sugars both increase blood insulin levels per se. Perhaps there is a message here. It's been known for decades that insulin drives the proliferation of the arterial media we call arteriosclerosis.

    If insulin also controls LDL particle size (I have no information on this, but I'm willing to bet it does) then Yudkin and Stout are correct, Keys is wrong and the cholesterol hypothesis, what remains of it, describes the effects of insulin on blood lipids. While insulin and glucose do the damage to the arteries.

    Just a cholesterol skeptic view.

    Peter

    Statins are anti-inflammatory, antioxidant, anti-proliferative and probably anti other things too. Unfortunately they drop cholesterol levels (in humans anyway). Zetia, like torcetrapib and clofibrate, does the cholesterol dropping thing without the anti everything else that statins bring along. No wonder they killed so many people in the clinical trials. Clofibrate. Torcetrapib.

    If a drug company develops a drug which converts small dense LDL to light fluffy LDL without affecting insulin sensitivity or glucose, I predict it will go the way of clofibrate and torcetrapib. There's the bin.

  • Dr. Davis

    1/16/2008 1:06:00 PM |

    I especially find it interesting that, among the so-called pleiotropic, or non-lipid, effects of statin drugs is a modest rise in 25-OH-vitamin D3 levels.

  • Anonymous

    1/16/2008 3:25:00 PM |

    I think this just once again shows that statins DO reduce heart disease but NOT because of the reduction in LDL. I'm always amazed at the Dr. who say you don't need to be on a statin your LDL is fine. Statins have been proven to reduce death rates in cardiovascular disease by 30 to 40% and yes with niacin by 90%!!!!!!!! Anybody worried about heart disease should be taking them. And save me the "side effects" alarm of statins that is so over blown. The fact is we invented a drug to reduce LDL, it does that but thats not why it reduces heart attacks and we're still not sure why they do. We accidently created a great class of drugs.

  • kdhartt

    1/16/2008 3:31:00 PM |

    I remember in Taubes reading that small LDL are the result of particles being formed in a high-triglyceride environment--if so there is a more direct link to diet than through insulin.

    About the merits of statins, can't we at least say that through reducing the number of all LDL particles and hence the number of small particles arteries are protected?

    Keith

  • Jenny

    1/16/2008 4:29:00 PM |

    The drug company slanted this study so that they'd get a wonderful result, that they didn't and the lengths that they went to hide or misrepresent the data that came out of the study has to make you suspicious of what ELSE they have learned.

    Did you catch that they also suppressed other study results showing liver damage from Zetia?

    Also, did you catch the BMJ story today about the calcium supplementation trial that lowered LDL raised HDL and increased cardiac and stroke events in older women?

    While that too isn't a death blow to the LDL hypothesis, it certainly doesn't bolster it.

  • Bad_CRC

    1/16/2008 6:03:00 PM |

    Peter,

    Good post; you have an impressive grasp of the literature on this!  I have a question for you, though:  Besides the epidemiology (which I know you don't buy), aren't there still tons of animal studies linking atherosclerosis to dietary saturated fat?  In fact, to promote atherogenesis in lab animals so they can study it, don't they feed them a diet rich in palmitic, stearic, myristic and lauric acids from animal and tropical plant fats, which works predictably?

  • Dr. Davis

    1/16/2008 6:24:00 PM |

    Drug companies are actually scrutinized fairly closely, though plenty of shenanigans still go on.

    What scares me even more is what may have been going on BEFORE the intensified scrutiny began a few years ago.

    Nowadays, the return on investment for treatment of chronic diseases like cholesterol, osteoporosis, and hypertension are so substantial that it is causing them to see a blur between right and wrong.

  • Dr. Davis

    1/16/2008 6:41:00 PM |

    Yes. I believe that the evidence for that effect of statin drugs is quite confident.

    When I question the Lipid Hypothesis, what I really mean is that I question the wisdom of the simple "high cholesterol means more atherosclerosis" philosophy, a belief that is clearly oversimplified, though it contains a germ of truth.

  • Peter

    1/16/2008 8:12:00 PM |

    For anonymous,

    Of course statins reduce cardiac mortality and obviously it's nothing to do with LDL cholesterol lowering. But before you pop one on the off chance (they are available OTC in the UK) go very carefully through this paper.

    You need the full text, the abstract tells you nothing, so here's a summary:

    There were 2913 patients in the placebo group. A total of 306 died during their 3 years of not taking a statin. That is 10.5% died. In the treatment group there were 2891 patients and 298 died, that's 10.3%. Bear in mind that these were high risk cardiovascular patients, the sort for whom statin therapy is supposed to be effective in saving lives.

    There was undoubtedly a significant improvement in cardiac mortality WITHOUT improvement in overall mortality. To sum up the PROSPER trial, you can have the cause of death changed from heart attack to cancer, but not the date on the death certificate. You choose. Perhaps you're too young to be in the PROSPER trial, but live long enough and you won't be!

    PS if you EVER see a statin trial without the overall mortality figures, just assume there was no benefit or worse. If there is even a miniscule benefit it will be broadcast far and wide.

    Keith,

    Thanks for the pointer. Obviously high triglycerides are a classic marker of hyperinsulinaemia and insulin resistance. I'll follow that one when I get that far in to Taubes' book. Seems it's looking good for Yudkin.

    bad_crc,

    Yes, there are thousands of papers like that. They usually use D12451 or something like it. High fat alright, 45% calories from lard. As the rest is? A bit of corn starch, a mass of maltodextrin and an even bigger mass of sucrose!!!!! But of course it's the lard that kills....

    Whereas using a real high fat diet you get this paper. I would suggest the 60% of calories from fat us a little low for a rodent. Choosing for themselves they can go to around 80%, get plump but don't develop insulin resistance.

    Peter

  • Jenny

    1/16/2008 10:11:00 PM |

    My understanding is that studies show that statins are effective in reducing heart attacks ONLY in people who have already HAD heart attacks. Not in the general population.

    This would confirm the growing suspicion that statins work by limiting the inflammation associated with heart disease. Not through their effect on lipids.

    To get back to Zetia/Vytorin, what Dr. Nissen pointed to, which IS in my mind worth noting, was that while the variation in individual endpoints did not rise to statistical significance every single endpoint measured went in the wrong direction. That argues against random effects in my mind.

    Beyond that, we know that in most people heart disease develops over a longer period than that spanned by this study, which only lasted 2 years. If all these parameters measured were trending negatively at 2 years, what happens at 5? Or 10? This is one of those drugs that once they put on on it, you take them forever. So the 5 or 10 year result could be devastating if this turns out to be a significant finding.

    My suggestion would be continue testing this drug in small studies involving people who are very well informed of the risks, but end the writing of the current 1 million prescriptions a month. That's a LOT of guinea pigs, and if there turned out to be an accelerating pace of problems with it, a lot of people could die unnecessarily.

  • Dr. Davis

    1/16/2008 10:20:00 PM |

    Statins reduce the number of LDL particles, which is very poorly represented by the conventional (Friedwald)calculated LDL cholesterol.

    More importantly, when someone with heterozygous hypercholesterolemia (as in this Vytorin study) has a high number of SMALL LDL particles, then statin drugs, in my view, do provide benefit. But a superior effect would be to specifically reduce the number of small LDL particles, best accomplished with such strategies as elimination of wheat, weight loss via low carbohydrate diet, fish oil, vitamin D, and niacin.

    This raises the question of how well the two groups in this study were matched for the number of small LDL particles. To my knowledge, this was not measured.

    Let me also remind everybody that the measure obtained and used for comparison was carotid IMT, not carotid plaque.

  • wccaguy

    1/16/2008 10:39:00 PM |

    I'm certain I'm not alone in feeling bewildered that such a dominant theory of the disease could turn out to have been so wrong for so long at such great cost in lives and treasure.

    Just as a question of historical interest, how far back in the history of science do we have to look to find this kind of reversal of understanding of what the facts are with such broad and great consequence?

  • Dr. Davis

    1/16/2008 11:45:00 PM |

    Hi, WC--

    I'm not sure, but it's not the first time.  

    Is the earth still flat?

  • wccaguy

    1/17/2008 12:49:00 AM |

    Hi Dr. D.

    I was thinking of Galileo also and his remarkable discovery that the earth orbits the sun.

    But then I thought "surely we don't have to go that far back do we to get to such a broad and consequential paradigm shift?"

    Maybe we do.

  • Richard A.

    1/17/2008 3:52:00 AM |

    Could zetia be interfering with the absorption  of simvastatin?

  • Peter

    1/17/2008 5:52:00 AM |

    Hi wccaguy,

    You may enjoy this discussion article from PLoS. The authors intend it to be provocative, put it does pose the question "on which day did medicine stop making mistakes?"

    Peter

  • Anonymous

    1/17/2008 11:23:00 AM |

    In response to Jenny, not all studies on reducing heart attack death havwe been done on people who already had a heart attack. The reduction of 30 to 40% is whether you've had one or not.

  • kdhartt

    1/17/2008 1:18:00 PM |

    Our saturated fat question keeps coming up, but the current common wisdom is that saturated fats are "neutral" in the sense that they raise both LDL and HDL. But do we know what they do to the number of small particles? Of course, if LDL is raised by making particles fluffy then saturated fats are clearly protective.

    Keith

  • Dr. Davis

    1/17/2008 1:34:00 PM |

    Hi, Richard-
    No, there was indeed a substantial further drop in LDL with Vytorin over simvastatin.

  • Dr. Davis

    1/17/2008 1:41:00 PM |

    There is a very modest shift from small to large LDL.

  • Jenny

    1/17/2008 1:47:00 PM |

    Zetia dropped my very high, inherited LDL to normal, BUT I afer a couple months on Zetia my post-menopausal body stopped making estrogen--my gynecologist remarked on it.  

    I also started having a problem with persistent visual afterimages which the ophthalmologist said might also be from having too little cholesterol.

    Both problems went away when I stopped the Zetia. I have very high LDL but I also have the "longevity" cholesterol gene which makes for big fluffy LDL as well as very low Apo(b). My doctors--including the cardiologist I saw--are ignorant about the implications of both findings and just obsess about the high LDL.

    Since naturally produced estrogen seems to be protective for heart disease, I wonder if some people with inherited high LDL are like me have the large fluffy LDL molecules which give a deceptively high LDL value on tests. For them lowering it with Zetia drops LDL TOO low, so that the body doesn't have the cholesterol it needs for important functions, like making the naturally produced female hormones that may be protective against heart disease.

  • Dr. Davis

    1/17/2008 1:52:00 PM |

    Hi, Jenny-
    Keep in mind that conventional LDL is a flagrantly inaccurate number. In my experience, LDL of 150 when accurately measured (we use the NMR LDL particle number as the "gold standard"), the true number is between 80 and 270 mg/dl.

    In my view, conventional LDL is a silly number. It is also the basis of a $23 billion (annual revenue) industry.

  • Anonymous

    1/24/2008 4:06:00 AM |

    In Dec 05 I had a heart scan score of 145.  I went from 10 mg of Lipitor to 80mg of Vytorin and 1000 Niacin, 1 fish oil.  At that time my particle number was 1325 and small particle # 977.  A year later it went to 1503/1277.

    In Nov 07 my heart scan went to 291. I then went to 2000 mg of Niacin and 150 COQ10,4 fish oil, 500 mg C, Vitamin D.

    My new liposcience profile taken Dec 27 07 shows small particle down to 249 and particle number down to 279.

    I dont know why my plaque increased so much but the new lipo profile is impressive in reduction.

    Is there anything here that seems weird or is it just the plaque grew fast and is likely now under control with the much improved scores?  All other factors on the profile were great and my Vitamin D is very good and CRP excellent too.  My homosistine was 15.7 is the only thing a bit high.

    Thanks!!

  • Dr. Davis

    1/24/2008 12:53:00 PM |

    Sorry, but I do not assess entire programs on this blog.

    I would invite you to participate in the conversations in the Track Your Plaque Forum for detailed discussions like this. There is also a free report on "10 steps to take if your heart scan score increases" on the www.trackyourplaque.com website.

  • buy jeans

    11/2/2010 7:37:41 PM |

    I would not automatically conclude that Zetia causes carotid plaque. This is absurd. And I am definitely not one to come to the rescue of a drug or drug manufacturer. I am simply after understanding and truth.

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