Can CRP be reduced?

The JUPITER study has sparked a lot of discussion about c-reactive protein, or CRP.

If we follow the line of reasoning that prompted this study, reducing CRP may correlate with reduction of cardiovascular events. Thus, in the JUPITER study, Crestor 20 mg per day reduced cardiovascular events by nearly half.

From a CRP perspective, starting values were 4.2 mg/dl in the Crestor group of the trial, 4.3 mg/dl in the placebo group. After 24 months, CRP in the Crestor group was 2.2 mg/dl, 3.5 mg/dl in the placebo group, representing a 37% reduction.

Now, in our Track Your Plaque program--an experience that has yielded the virtual ELIMINATION of cardiovascular events--we aim for a CRP level of 1.0 mg/dl or less, ideally 0.5 mg/dl or less. The majority of people achieve these ambitious levels. In fact, it is a rare person who does not.

How do we achieve dramatic reductions in CRP? We use:

--Weight loss through elimination of wheat and cornstarch--This yields impressive reductions.

--Vitamin D--I have no doubt whatsoever of vitamin D's capacity to exert potent anti-inflammatory effects. I am not entirely sure why this happens (enhanced sensitivity to insulin, reduced expression of tissue inflammatory proteins like matrix metalloproteinase and others, etc.), but the effect is profound.

--Elimination of junk foods--like candies, cookies, pretzels, rice cakes, potato chips, etc.

--Exercise--Amplifies the benefits of diet on CRP reduction.

--Not allowing saturated fats to dominate--Yes, yes, I know. The demonization of saturated fat conversation has been largely replaced by the Taubesian saturated fat has not been confidently linked to heart disease conversation. But controlled feeding studies, in which a single component of diet is manipulated (e.g., saturated vs. monounsaturated vs. polyunsaturated fat) have clearly shown that saturated fats do activate several factors in the inflammatory response.

--Fish oil--Though I am a firm believer in the huge benefits of omega-3 fatty acid supplementation/restoration, the anti-inflammatory effect is modest from a CRP perspective. However, there are anti-inflammatory benefits beyond that of simple CRP (via normalization of eicosanoid metabolism and other pathways).

--Weight loss--A BIG effect. Weight loss drops CRP like a stone. The CRP-reducing effect is especially large if achieved via carbohydrate reduction.

Of course, this is much more complicated than taking a pill. But it is effective to achieve health benefits outside of cardiovascular risk, is enormously useful as part of a weight loss effort, and doesn't cost $1400 per year like Crestor.

In short, if CRP reduction is the goal, it certainly does not have to involve Crestor.

Comments (17) -

  • stephen_b

    11/13/2008 7:23:00 PM |

    Here are a couple of data points:

    2007-10: Vit D 25-hydroxy: 34.7 ng/mL
    CRP: 0.33 mg/L

    2008-05: Vit D 25-hydroxy: 39.7 ng/mL
    CRP: 0.26 mg/L

    I don't know how significant it is, but increasing vitamin D levels for me resulted in a better CRP.

    StephenB

  • Anonymous

    11/13/2008 7:48:00 PM |

    Were the controlled feeding studies done on high carb diets?  Are there any studies like this on low carb diets?  I think Cassandra Forsythe studied the short term  difference between MUFA/omega 3 and saturated fat on a eucaloric low carb diet but I don't believe she has finished writing her thesis yet and I don't know if she checked CRP.  It seems to me that a high carb diet amounts to a high saturated fat diet since what the body does with the carbs is make it into saturated fat, no?  So eating a lot of saturated fat on a low carb diet may well amount to less saturated fat in the body than eating lots of carbs on a low fat/saturated fat diet.  Wait a minute, don't i remember hearing about a study like that?

  • Jenny

    11/13/2008 8:10:00 PM |

    Dr. Davis,

    Can't you extract data from cases from your files and publish in one of the journals?

    One problem I have always had with Dr. Atkins is that he made a lot of claims but never published a single study using data from the thousands of cases he claimed to have had.

    You have the credential to report your results to mainstream journals. I see plenty of doctor-published studies with tiny numbers of participants, as few as 10 (completely statistically meaningless!) If you have hundreds or thousands, why not analyze the data and publish. That way it goes from "anecdotal" to peer-reviewed.

    Yes, it is a lot of work, but that is the kind of work that helps everyone. You might be able to find a grad student in epidemiology or a related field to help you with the number crunching, too.

  • Anonymous

    11/13/2008 10:08:00 PM |

    How about getting dental/periodontal inflammation cleared up?

  • Jeff Consiglio

    11/13/2008 10:10:00 PM |

    "But controlled feeding studies, in which a single component of diet is manipulated (e.g., saturated vs. monounsaturated vs. polyunsaturated fat) have clearly shown that saturated fats do activate several factors in the inflammatory response."

    I tend to agree with you that animal based long-chain saturated fatty acids may not be quite as benign as some in the low-carb community assert. But was wondering if you had an opinion on the medium-chain saturated fatty acids in coconut oil?

  • Anonymous

    11/14/2008 12:50:00 AM |

    I absolutely agree with you, Dr. Davis. I am living proof that your wellness plan works.

  • Anne

    11/14/2008 1:00:00 AM |

    Years ago my hs-CRP was over 13. I tried taking 3 different statins and they all caused muscle pain.

    My hs-CRP has slowly fallen as I tried to optimize my health with lifestyle changes. It is now 3 - not perfect, but much better. I have lost about 25lbs. I have eliminated gluten(wheat, barley, rye) and rarely eat any grain. Junk food is out except for a small piece of dark chocolate. Trying to get my vitamin D to optimal. Through food choices I am keeping my blood glucose from spiking.  I take fish oil. I exercise....oops, I should say I still need get on an exercise program. Maybe exercise will bring down the CRP to <1.

    Yup, I agree, CRP can be decreased without statins. I wonder if decreasing CRP through lifestyle changes is more beneficial than reducing it with a pill? It would be nice to see such a study, but I don't think that will happen.

  • Anonymous

    11/14/2008 1:36:00 AM |

    I tried these measures and reduced my hs-CRP to less than 0.2. It works.

  • Anonymous

    11/14/2008 7:23:00 AM |

    Part of the confusion over saturated fats could be that UN-saturated fats have been shown to deaden our immune system, while saturated fats had no effect. [1][2]

    So any comparison of the two in patients with growing inflammation will appear to show greater inflammation with sat fats.

    Deadening our immune system can be helpful if for some reason we have chronic inflammation (like atherosclerosis) or an autoimmune disease, but deaden our immunity too much and cancer deadens us instead.

    I'd prefer to find the cause of the inflammation, address it, and keep my immune system at full strength with more sat fats.

    Saturated fats also convert our most dangerous LDL subclasses to the harmless varieties, resulting in very little of the dangerous LDL IIIa, IIIb, and IVb subclasses.  It also boosts our most helpful HDL subclass 2b.

    I'd guess the studies you referred to used hydrogenated saturated fats [they were STILL making that mistake even in 1994!] or fats from grain-fed animals which are high in omega-6. Both of those WILL raise inflammation. I like to stick to grass-fed meats and dairy whenever possible.

  • The Vitamin Tutor

    11/14/2008 7:46:00 AM |

    Let's not forget vitamin C. Cheap. Proven effective in multiple clinical studies. Safe.

    http://www.berkeley.edu/news/media/releases/2008/11/12_vitaminc.shtml

  • Olga

    11/14/2008 2:09:00 PM |

    Hi Dr. Davis:

    I was wondering if you read Michael Eades review of the Jupitor study.  It can be found on his protien power blog site at:

    http://www.proteinpower.com/drmike/cardiovascular-disease/1853/#more-1853

  • Olga

    11/14/2008 3:43:00 PM |

    Hi Dr. Davis:

    Have you come across a recent research paper which showed significant reduction of arterial calcification after administration of vitamin K to rats.  Very compeling research published in April 2007, by Dr. Cees Vermeer and his group.  Here is a link to a review of the paper with a link to the actual research paper.  Keep up the great work!

    yhttp://wholehealthsource.blogspot.com/2008/11/can-vitamin-k2-reverse-arterial.htmlou

  • Dr. Dwight Lundell

    11/16/2008 1:55:00 PM |

    Dr. Davis,
    The reduction in events was not 55% but O.O9% you continue to fall into the dishonest use of statistics by the statin makers. the number needed to treat to avoid one event is 120! The jupiter study and the
    Vytorin study should clearly show that LDL reduction has little benefit and is only a marker for a poor diet. The LDL theory is dead.
    That said your program is right on the mark, reduction of carbohydrate intake, exercise and fish  oil along with vitamin D will do more to save lives and prevent heart attack than all the statins on the world.

  • Anonymous

    11/16/2008 1:59:00 PM |

    I'm reading a new book from Ulf Ravnskov, Fat and Cholesterol is Healthy. Saturated fat seems to be harmless after Ulf's researh of all relevant studies.
    I've also read a lot on Weston A Price and it seems that saturated fat was dominating the fats in the food of the native americans (healty ones). In sweden, a doctor reviewed almost every study that said "saturated fat is bad" and came up with the conclusion that not a single study we're trusted. Also beacuse a lot of studies said the opposite.
    Wille, Sweden. Low Carb High Fat for 3 years.

  • Nancy LC

    11/24/2008 4:32:00 PM |

    This is tangentially related to your posting but I thought you might be able to comment on, or be interested in reading about, the types of fat found in "atherosclerotic plaques and xanthomas".  Here's a link to the abstract: http://www.jlr.org/cgi/content/abstract/24/10/1329

    Some interesting individual fats were palmitic (16:0) 12.7%, stearic (18:0) 1.5%, oleic (18:1) 25.5%, linoleic (18:2) 38.1%, arichidonic (20:4) 8.3%, EPA (20:5) 0.7%, and DHA (22:6) 0.6%

  • Research Papers Writing

    11/19/2009 6:40:23 AM |

    Many institutions limit access to their online information. Making this information available will be an asset to all.

  • buy jeans

    11/3/2010 2:33:17 PM |

    --Weight loss--A BIG effect. Weight loss drops CRP like a stone. The CRP-reducing effect is especially large if achieved via carbohydrate reduction.

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Making sense out of lipid changes

Making sense out of lipid changes

Maggie had been doing well on her program, enjoying favorable lipids near our 60-60-60 targets (HDL 60 mg/dl or greater, LDL 60 mg/dl or less, triglycerides 60 mg/dl or less). Last fall, her last set of values were:

Total cholesterol: 149 mg/dl
LDL cholesterol: 67 mg/dl
HDL cholesterol: 73 mg/dl
Triglycerides: 43 mg/dl

The holidays, as with most people, involved a frenzy of indulgent eating: Christmas cookies, cakes, pies, stuffing, potatoes, candies, etc.

Maggie returned to the office 6 pounds heavier with these values:

Total cholesterol: 210 mg/dl
LDL cholesterol: 124 mg/dl
HDL cholesterol: 57 mg/dl
Triglycerides: 144 mg/dl

In other words, holiday indulgences caused an increase in LDL cholesterol, a reduction in HDL, an increase in triglycerides, an increase in total cholesterol.

What happened?

At first glance, many of my colleagues would interpret this as fat indulgence and/or a "need" for statin drug therapy.

Having done thousands of lipoprotein panels, I can tell you that, beneath the surface, the following has occurred:

--Overindulgence in carbohydrates from the goodies triggered triglyceride (actually VLDL) formation in the liver, released into the blood.
--Increased triglycerides and VLDL triggered a boom in conversion of large LDL to small LDL (since triglycerides are required to form small LDL particles) via cholesteryl-ester transfer protein (CETP) activity.
--Increased triglycerides and VLDL interacted with HDL particles, causing "remodeling" of HDL particles to the less desirable, less protective small particles, which do not persist as long in the blood, resulting in a reduction of HDL.

The critical factor is carbohydrate intake. This triggered a domino effect that is often misintepreted as excessive fat intake or a genetic predisposition. It is nothing of the kind.

I discussed this phenomenon with Maggie. She now knows to not overindulge in the holiday snacks in future and will revert promptly back to her 60-60-60 values.

Comments (9) -

  • Rick

    1/27/2009 4:37:00 AM |

    Wow. I hadn't realised that a short period of over-eating could trigger such big changes.

    Is there any danger from triglycerides going much below the target of 60?

  • Diana Hsieh

    1/27/2009 5:23:00 AM |

    Dr. Davis --

    What might cause a substantial rise in LDL, while triglycerides and HDL are lower than ever?

    Here's what happened with my tests over the last year and a half:

    ** Summer 2007, eating the standard American diet **
    Total Cholesterol: 266
    Triglycerides: 109
    HDL: 79
    LDL: 165

    ** Summer 2008, just a few weeks into my new diet (no processed foods, no grains, no sugars, no vegetable oils) **
    Total Cholesterol: 225
    Triglycerides: 63
    HDL: 72
    LDL: 140

    And now, January 2009 (same diet as before):
    Total Cholesterol: 341
    Triglycerides: 55
    HDL: 99
    LDL: 231

    My triglycerides and HDL are better than ever, but my LDL has gone way up.  I didn't overindulge over the holidays, but I was losing weight (slowly) when I got that latest test.

    I know -- thanks to your blogging -- that inferred LDL values are highly unreliable.  And I also know that there's a difference between small LDL (bad, caused by eating high carb) and the bigger, fluffier (okay) LDL.  The LDL number doesn't differentiate between those values.  Or might something else be the cause?

    My doctor wants to do a cholesterol recheck next month -- and I'm thinking that I ought to ask for a measured LDL value and a particle size test.  Does that seem reasonable to you?  

    BTW, my heart scan from six months ago is totally clear.  So I don't care how much my doc pushes, I absolutely refuse to go on any kind of cholesterol-lowering medication.

    Also, thanks to you, I got a vitamin D test -- and my values were excellent.  (I do supplement.)  Yeah!

  • Jenny

    1/27/2009 2:19:00 PM |

    Dr. Davis,

    While it is true that overindulging in carbs causes all the changes you cite here, if your patient really wants to stick with the program life-long, she'll do better learning how to carb up a bit at the holidays, and then correct afterwards, rather than getting into a lifestyle of self-denial that will build up an undercurrent of feelings of deprivation that will eventually blow her completely off course.

    I've been there, done that. Three family holiday seasons without eating any of our traditional foods left me depressed and miserable. Food is a complex issue with deep emotional roots.

    Something like a family death or a cancer diagnosis can trigger binges that derive from that deprivation and really derail the diet.

    I have found it much better to build in safety valves into the diet, here and there.  The lipids will recover very fast once she goes back to eating the low carb diet.  

    I've been doing a low carb lifestyle for going on 11 years now, and I attribute its success to the safety valves. Yes, I do gain a few pounds over the holidays, but I take them off in January.  

    The psychology of successful dieting is often to accept "good enough" rather than perfect. Perfect has a nasty way of ending up in disaster.

    If you doubt this, just read the low carb diet boards where for every person who has maintained perfectly for 5+ years there are 25 people back after catastrophic regains caused by being too stringent.

  • Alan S David

    1/27/2009 3:36:00 PM |

    Is it carbs in general or should we be more consciously eliminating the wheat and corn products?  
    I eat quinoa,oatmeal,  buckwheat,beans,brown rice, etc. Not to excess but as a part of my usual diet.
    Just wondering?

  • Grandma S.

    1/27/2009 4:51:00 PM |

    Question: I understand no wheat and what it does to the LDLs, but does that include potatoes? Thank you!

  • Anonymous

    1/28/2009 5:57:00 AM |

    Dr. Davis,

    I have a similar issue as Diana Hsieh.  

    My Total Cholesterol: 258
    Triglycerides : 60
    HDL : 61
    LDL- 181

    I've been on a low carb diet avoiding wheat, rice, starches, sugar, high fructose corn syrups and fruits for the last 6 months.  I've lost 35 pounds and reduced my triglycerides from 296 to 60.  Taking fish oil and slo-niacin. I have been eating alot of saturated animal fats (rib-eye steaks, baby back pork ribs, eggs) Is eating the saturated animal fat causing my total cholesterol to be too high?  Is total cholesterol above 200 dangerous if Triglycerides and HDL are in the 60's?

  • vin

    1/28/2009 10:11:00 AM |

    I am trying for last three years to get my HDL numbers high. So far without success. I have tried exercise and cutting out wheat but without significant improvement. I have now added 4000iu vitamin D. Will do a follow up blood test after about two months to see if HDL level increases.

    Any other tips?

  • Jmuls

    1/28/2009 12:34:00 PM |

    Dr. Davis,

    Is there often a direct correlation between low triglycerides and a greater proportion of large LDL particles?  Thanks

    - John

  • Trinkwasser

    2/8/2009 2:08:00 PM |

    Here were my lipids on a Heart Healthy (sarcasm) Diet

    Trigs 380
    HDL 25
    LDL 165

    Add simvastatin

    Trigs 185
    HDL 33
    LDL 75

    Here they are on a low carb diet with my BG more or less normalised
    (70 - 90 and postprandials mostly below 110 and seldom over 120)

    Trigs 39
    HDL 47
    LDL 105

    Adding more saturated fat

    Trigs 62
    HDL 55
    LDL 94

    Spot the reversal of HDL to LDL

    IME low carbing decimates the trigs and tends to increase HDL and LDL both, tinkering with the fat content and type adjusts the balance between these BUT there's a lot of individual variation as to exactly how this works. Some people just seem to have high LDL whatever they do, maybe a long term change from years of insulin resistance and hyperinsulinemia, maybe genes which would respond to a different balance of fat types in the diet.

    My #1 weapon has been BG testing

    http://www.alt-support-diabetes.org/NewlyDiagnosed.htm

    which is deprecated in the UK. Lipid breakdowns are often unavailable and Full Lipid Panel is deprecated in favour of TChol which is pointless but cheaper. The money saving is probably to pay for the blanket prescription of statins, and it also serves to conceal the toxic nature of the diet

    http://www.nhs.uk/Change4Life/Pages/default.aspx

    here's the diabetic version

    http://www.diabetes.org.uk/Guide-to-diabetes/Food_and_recipes/Food_and_diabetes/Balancing_your_diet/

    I feel like part of a eugenics experiment

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