But what would it mean if actual inflamed atherosclerotic plaque was examined and inflammatory cells were found to be “colocalized” with the presence of Lp(a).  Might that not suggest that this Lp(a) “recruitment mechanism” (i.e., it’s stickiness) was a critical determinant of the increased morbidity of high Lp(a)?

The authors of this study did just that.  Here’s what they have to say about it.

Lp(a)/apo(a) promotes the transendothelial migration of monocytes in a Mac-1-dependent manner, suggesting that Lp(a) and apo(a) in the atherosclerotic vessel wall may not only mediate the attachment of leukocytes, but may alsoattract these inflammatory cells to the atherosclerotic vessel wall. 5) In atherosclerotic plaques that were positive for Lp(a) expression, Lp(a) was found in close proximity to infiltrating mononuclear cells, and a high degree of colocalization was observed between Lp(a) and Mac-1,  indicating that these interactions may occur in vivo. Thus, in addition to up-regulating endothelial adhesion molecules and thereby indirectly affecting leukocyte recruitment (47),Lp(a) may directly promote inflammatory cell recruitment to the atherosclerotic plaque through its interaction with Mac-1.

So, what’s the practical implication of this colocalization of inflammatory cells with Lp(a)/apo(a) in plaque for those with high Lp(a)?

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I received an email this morning noting that St John’s Wort has been found to be effective for major depressive symptoms.  Here’s the link…

A review published online by Cochrane Systematic Reviews on October 8, 2008 concluded that extracts of the herb St John’s wort are as effective for treating major depression as standard drugs.

Notice in the article on the bottom left of that page, LEF writes as follows:

The mechanism of action of St. John’s wort in depression is not entirely clear. One idea is that St. John’s wort affects presynaptic serotonin uptake and inhibits norepinephrine reuptake (Nangia M et al 2000).

Where do we find ourselves with this kind of understanding?  Well, we find ourselves in a state where we have a seemingly random list of herb and other supplements that treat depression without any deeper understanding of why these substances work.

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But are there other ways that Lp(a), and perhaps even low Lp(a), does harm?   Before we think about that question, some background is in order. 

• Apo(a) and LDL attach to each other to form Lp(a).  (See the graphic in the first post of this thread.)
• Lp(a) attaches itself to artery walls

One interesting question is this…  Do these two attachments take place through the same mechanism?  I believe the answer is no but I’m not 100% certain about this.

Notice, however, that there is nothing about these two attachment types that imply anything other than that Lp(a) volume and particle number need to be measured.

But suppose there was a 3rd type of attachment related to Lp(a) that was significant.

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The TYP program is relatively unique in that Dr. Davis emphasizes the importance of measuring Lp(a) particle number (via a Liposcience NMR test).

This is fantastic!

It seems to me, however, that there are some additional questions we need to ask ourselves.

• What is the CONCEPT underlying the view that it is only Lp(a) volume and particle number that we need to worry about?

• Is it really true that those of us with high Lp(a) only need to worry about Lp(a) volume and particle number?

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The loan broker could get them ARM financing (an ACTUAL Rate Mortgage) for 2 points under the current standard rate and that rate would be the Actual Rate rate for the life of the Mortgage. It’s ARM financing. Your kids are really excited about this. After all, if they don’t get the ARM mortgage, they’ll have to get a FIXED Rate Mortgage and face changing and rising interest rates all the time because the interest rate on this sort of loan would change by a FIXED amount higher than the current standard interest rate.

What would you tell them?

(image courtest of TonyWatson.net)

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In a study published in the New England Journal of Medicine, Low Carbohydrate and Mediterranean Diets were found to be more helpful for controlling obesity and the blood lipids related to Coronary Artery Disease than a Low Fat Diet.

One of the most devastating ways that Medical Professionals have contributed to the increase in obesity and heart disease has been their insistence on a “one size fits all” approach to nutrition for these problems. One only needs to stroll down grocery store aisles to understand that the dominance of the “Low Fat Diets are best” ideology is coincidently timed with great increases in obesity.

Thankfully, more scientific studies are showing these recommendations to be flawed at best.

HeartWire at TheHeart.org has a great rundown on this new study.

At a minimum, what this study does is confirm that my personal experience is not an anomaly.

Here’s the link to the journal article and the abstract appears after the jump.

(image courtesy of the New England Journal of Medicine)

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And there’s even more of a need to highlight the statement when that cardiologist’s professional colleagues fail to do so.

Such is the case in a recently begun thread at the “ClubwebMD” forum at TheHeart.org.

A cardiologist in that thread (who I won’t name but can be found by the diligent using Google) uttered something that boils down to the title of this post.

“My patients are too poor or too stupid to get the best cardiac care.”

At the outset, let’s grant that this cardiologist deserves at least some credit for being honest. Or maybe you think I’m exaggerating. No doctor, not even a FACCer, would make this point so baldly, right? (I use the designation “FACCer” as shorthand for describing a Fellow of the American College of Cardiology with whom I am particularly taken.)

Well, how about we do this? I’ll provide the verifiable online quotations and commentary and then you decide whether my interpretation of his remarks in this post’s title is a fair one.

Deal? Ok then, follow me after the jump for more…

(image courtesy of thechaly.wordpress.com)

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He was buried on Sunday at the summit of the mountain at 20,320 feet above sea level because of the difficulty and danger involved in bringing his body back down the mountain.

According to the Chicago Tribune…

James Nasti was an avid runner, cyclist and mountaineer who had been on an 11-year quest to climb the highest points in all 50 states.

But upon reaching his 49th high point on the 4th of July, the Naperville father of three collapsed and died on the summit of Mt. McKinley in Alaska, apparently of a heart attack…

James Nasti belonged to the Highpointers Club, whose members try to visit the highest points in 50 states. He had only White Butte, N.D., left to scale, his son said.

Nasti was a runner and cyclist who had trained for the climb up Mt. McKinley and had no known history of heart trouble, his family said.

“He had done a stress test two years ago and there was no indication of heart trouble, no family history of the disease,” his son said.

Nasti did not appear to be sick or in distress and was climbing strongly before the collapse, McLaughlin said.

“It sounds like from the guides that this was a particularly strong team as a whole and he was a strong climber. It was unexpected,” she said.

Meanwhile, in the first of a series of reports on Cardiovascular Disease Risk Assessment, (the MESA study), a measure of coronary calcium was shown to be better than carotid IMT for predicting CVD risk.

As the “baby boomer” generation ages and the cardiology and medical communities continue to ignore the results of dozens, if not hundreds, of studies of the predictive power of Coronary Artery Calcium scanning, we will continue to read stories about people taken down by heart attack at the pinnacle of their life and achievements.

But I’m well and I’m back and more determined than ever to address my coronary artery disease in as serious a way as the science will allow and I am capable.

A special thanks to my local Jedi Master and especially to Dr. Davis of Track Your Plaque for their descriptions and explanations of that path and for their encouragement.

In the near future, I’ll post about what I’ve been up to related to my heart disease for the last few months.

But for now, and to celebrate my return in this brief post, I quote a Life Extension Foundation news release on a study published in the Journal of the American College of Cardiology just today.

The text of the LEF news release entitled Large study links obesity and inflammation to heart failure follows after the jump.

(image courtesy of  http://krystalmae.blogspot.com)

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For now, I wanted to point you to an online webinar that Dr. Davis will be conducting on Vitamin D3 this week.

Here’s the link to register for the webinar…

See ya’ there.

And just for fun, how about that “Vitamin D3 Song” by John Denver?