In my last couple of blood tests, along with my elevated cholesterols, I discovered that despite having a normal CRP of less than 1.0, my Lp-PLA2 levels were high (March 2015 and May 2015). This was extremely puzzling to me. CRP is a very sensitive marker for inflammation, so if there is any underlying inflammation in my body, it should be elevated. Lp-PLA2 on the other hand is marketed as a marker that is specific for vascular inflammation.
Here’s a brief review about Lp-PLA2:
The Lp-PLA2 test is used for assessing cardiovascular risk. It’s an inflammatory marker that is thought to be specific to inflammation within the blood vessels. According to labtestsonline.org:
An Lp-PLA2 test may sometimes be used along with an hs-CRP test to evaluate a person’s level of underlying inflammation associated with CVD risk. However, unlike hs-CRP, the Lp-PLA2 test is not affected by conditions other than CVD that can cause general inflammation, so it may be used when someone has an inflammatory condition, such as arthritis.
According to the company that offers the test, which they call the Plactest:
High PLAC activity is found in plaque deposits that are unstable. Because they are unstable, they are more prone to rupturing. Studies show that a PLAC Test for Lp-PLA2 Activity result ≥225 nmol/min/mL points to an increased risk of CHD events. These coronary heart disease, or CHD, events can include heart attack, revascularization (such as stent placement or coronary artery bypass grafting), or death from a cardiac event, even in patients with normal cholesterol levels.
If you want to learn more about the mechanism of this test there’s a nice video here and a good handout here.
It didn’t make sense to me that the results between the CRP and Lp-PLA2 would be so discordant.
Cholesterol, Lp-PLA2, and Periodontal Disease
After some digging around, one explanation I came across for this divergence in results is the presence of gum disease.
I first came across a small pilot study in 6 patients published in Cardiovascular System in 2014 (full pdf here) in which they found:
This pilot study reports on unique findings where six patients with periodontal disease were treated with the Perio Protect Method and their Lp-PLA2 levels improved as their periodontal conditions improved. The results of this study appear to support the hypothesis that a relationship exists between periodontal disease and patient’s systemic inflammatory Lp-PLA2 levels and that treating the periodontal disease may correlate with improved patients Lp-PLA2 levels
In a study out of Columbia University, published in the American Journal of Cardiology in 2008 (full pdf here) they found that:
In a diverse population of individuals eligible for the primary prevention of CVD, a history of periodontal disease was associated with significantly higher levels of Lp-PLA2 compared with those without periodontal disease. When adjusted for potential confounders and lifestyle factors, this association remained statistically significant. To our knowledge this is the first report of an association between oral health and Lp-PLA2. These data support a possible independent association between oral health and inflammation, suggesting that inflammation may be a factor in the relationship between oral health and CVD. We also showed that diagnosed periodontal disease is present in patients without traditional CVD risk factors and that many of these individuals have increased inflammatory markers (hsCRP or Lp-PLA2).
In contrast to some studies, we did not find an association between oral health and hsCRP after adjustment.
A study published in 2002 in the Journal of Periodontology found:
…the presence of periodontal pockets as measured by CPITN was positively associated with total cholesterol and LDL-cholesterol. The findings of the study support the reports linking increased prevalence of cardiovascular mortality among patients with periodontal disease.
In the Journal of the Indian Society of Periodontology in 2013, they found:
The levels of TGL, TC, and LDL cholesterol were significantly higher for periodontitis group (P<0.05) as compared to gingivitis and periodontally healthy groups. HDL cholesterol levels were significantly lower in periodontitis group (P<0.05) as compared to periodontally healthy and gingivitis groups.
Hmmmmmm. My periodontal health definitely seemed like a good place to investigate! In the hustle and bustle of changing jobs this past year, I had neglected to go to the dentist and was overdue for a visit anyways.
Dr. Rocky Patel also introduced me to the MyPerioPath Test as a method of determining my oral biome to see if there are any bad pathogens hanging around that can be participating in the elevation of my Lp-PLA2.
After searching for a dentist in my area that provided the MyPerioPath Test, I found that there were only two…. and both of them were high end boutique practices that didn’t accept insurance. My pocketbook will have to take another hit for the sake of self-experimentation… and my health of course.
I chose the dentist closest to me and scheduled an appointment.
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Seeing the Dentist
My biggest fear when seeing the dentist is cavities. Well, not so much the cavities themselves, but the drilling that comes after. The thought of a high powered drill in my mouth just makes me shudder. I’m not entirely sure if this is a rational or irrational sure… but I’m damn sure I don’t like it.
I had a lot of cavities as a kid and teenager because I hated flossing… and every time I went to the dentist they would find a cavity which would need to be drilled and filled. For some reason the local anesthetic they used was never enough and I would always start feeling things in the middle of the procedure. And the smell… the smell of burning tooth and the whir of the drill mixed together always made me nauseous.
The last cavity I had was in my early 20s, when I finally resolved to draw a line in the sand, and vowed to never have another cavity again. I floss and brush religiously now and am proud to say that I haven’t had a cavity since! But each time I go to the dentist, my heart flutters a bit because I’m scared they’ll find one.
Before they even evaluated me, they had me swish around some saline solution and spit it out into a vial for the MyPerioPath test.
Then they took some x-rays and began poking and prodding my teeth.
Fortunately they didn’t find any cavities! Whew. No drilling.
What they did find however were some pockets in my gums measuring 4 mm near my molars on both sides which contained some areas of biofilm and bleeding… gingivitis!
This pamphlet actually does a great job of explaining what biofilm is, how it forms, and how it affects gum health. The hygienist actually gave me this exact one on my way out.
Here’s a graphic taken directly from the paper:
What happens is that bacteria stick to your teeth and then start secreting a special goop around them which protects them from the surrounding environment, helps them grow, and helps them to recruit more bacteria. As the colony grows they secrete more and more toxins that erode the enamel of the teeth and cause inflammation of the surrounding tissue.
When these biofilm colonies form below the gum-line brushing, rinsing, and flossing can’t get to them. The only way to remove them is by direct mechanical debridement.
This is what I had around my molars and I actually watched the hygienist remove these biofilms. I asked for a mirror to see what was going on, and I could see she was using one of those metallic dental instruments to scrape under my gum-line around my molars.
When some bloody gel like material oozed out, she informed me that that’s what biofilm looks like. She kept digging away until there was no more bloody oozing. Then she moved on to the next tooth.
It’s strange…while I hate dental drilling, I actually enjoy dental scraping. I find it gratifying some how. Identify a problem, scrape the crap out of it, and there you go, it’s gone.
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My Dental Homework
I was instructed to continue my regimen of flossing and brushing. The hygienist seemed pleased that I was using an Oral B Electric Toothbrush but wanted me to focus my brushing on the gum line.
The technique she wanted me to use for each molar was to brush 20 seconds along the front gum line, then 20 seconds along the back gum line, and then 10 seconds around the rest of the tooth.
She also gave me a goody bag filled with a bunch of paraphernalia to clean between my teeth including:
- Soft Picks
- Hard Brush Picks
- Interdental Cleaners
- Go Between Brushes of varying sizes
I was instructed to try each of them and choose the one that I liked best.
They also handed me a full bottle of Oxyfresh Mouthwash to use daily. This one was a little strange for me because you’re not supposed to rinse with water afterwards. You swish it in your mouth for a minute, then spit it out, and that’s it. No rinsing. It’s the first mouthwash I’ve used that doesn’t require rinsing and took me a couple days to get used to.
For the first few days I’m also supposed to use one of those Go Between Brushes and dip them in a cap full of the Oxyfresh Mouthwash and then brush between my molars until there’s no more bleeding. This part is important because biofilm pockets can regrow protective caps within a few hours, so they need to be mechanically disrupted to break them down.
I’ve been dutifully doing my homework, so it will be interesting to see if the removal of those biofilm pockets and my new oral hygiene regimen will have any effect on my cholesterol and Lp-PLA2.
Incidentally, I’ve found that these angled go between brushes work the best for me to reach my molars.
Next up, MyPerioPath results.
*Image found here
Interesting to know! I struggled with getting cavities when I had Lyme Disease. I was told then that tooth/gum health was often the sign if an underlying health issue. Seems that this is the reverse. I never had cavities as a kid, and got my first at 21. I’ve “lister-brushed” for about 12 years now, and it seems to keep my teeth and gums pretty healthy, too. I learned about that from my ex who was advised to do that for gum health. That sounds much like what you’re doing with the Oxyfresh. Looking forward to knowing the outcome of your next bloodwork and visit!
Its good to know that lister brushing keeps your gum healthy now for the past decade. Have you noticed any improvement in blood markers?
So I started treating my gum disease aggressively when nothing else was working
I have been working on it for almost a year and it is almost gone. I use the sonic toothbrush and Panasonic portable water-pic. I use the water-pic twice a day one with peroxide and once with water. I used peroxide twice a day but it caused my lips to crack. I got a prescription for Arestin which my Dr sactioned. I didn’t see an effect on my LDL but then nothing else seemed to affect it.
Interesting. Did you notice any correlations between your gum health and inflammatory markers?
I wish I could do a correlation, but at the time it was a case of throwing everything at the wall to see if anything would stick. My inflammation seemed to be correlated to saturated fat and or coffee. Those were the two constants between when my CRP went up and when it went down. My fibrinogen levels were high and after trying several things to reduce I did find links to high LDL being a cause. My fibrinogen levels have come down a little, which could be mean it is genetic or I haven’t found the cause. My inflammation seemed to randomly spike up and has only stayed low since I reduced my saturated fat and started eating breakfast. I had a full panel of inflammation markers and the only one that was IL7 (I think that was the name) which was correlated to obesity, which confused both me and my doctor since my bf is 15%. My gut was probably the source of my random inflammation if I was to guess.
I have just recently found your blog, and I already read most of it, because your case seems to be VERY similar to mine.
That includes hsCRP, lppla2, cholesterol, nmr-lipoprofile, thyroid symptoms (didn’t check markers yet), etc… though I’m a couple of years behind you…
I wonder whether you thought about the following possible explanations:
A:
Food sensitivity: I randomaly found someone who discovred that he has inflamation-response to eggs!
http://www.bengreenfieldfitness.com/2012/08/how-to-self-test-your-body/
Combine this with: 1) many keto-dieters rely a lot on consuming eggs. 2) eggs known as food that, relativley, a lot of pepole sensitive\ellergic to.
B:
What if, after all, it’s the cholesterol, and not the saturated fat. I’m saying that, because you cut the SF, not the cholesterol – you still eat a lot of eggs. Actually, I had an official meetting with a lipidologist(!) Who insisted that it’s the cholesterol intake, rather then the SF, that elevated my serum choleterol. Though, I don’t know if he meant it’s true in the general case, or it’s just me.
This thought has actually crossed my mind too… but my understanding lead me to believe that this would cause an elevation in CRP also. Right now… there aren’t too many things that cause an elevation in Lp-PLA2 but a normal CRP… gum disease is the only thing I’ve come across so far.