- Shopping Bag ( 0 items )
Posted September 10, 2013
I am a Board Certified Internist and have passed the Lipidology Boards of the National Lipid association. I think this book is important because it gets half of it right. Kudos for promoting LDL-P, CAC and CIMT. Jimmie has not yet gotten a CIMT. He also did not publish his HDL-P of 30.7. As he writes, it is about the particles not the cholesterol. His high HDL-C is meaningless as he has a small amount of HDL particles loaded with cholesterol. This has no bearing on the functionality of his HDL-P.
" It has also been demonstrated that small, dense, spherical HDL particles are more effective in mediating the antioxidant, anti-inflammatory, antiapoptotic, and anti-infective properties of HDL."
"Importantly, the cholesterol content itself of HDL particles is not atheroprotective.
Thus, HDL-C should not be considered a surrogate marker of HDL functionality."
"Unlike LDL cholesterol, HDL-C appears not to be associated with varying levels of cardiovascular risk nor to have a causal role in the atherosclerotic disease process."
"In the current issue of Circulation, Mora et al14 present further data highlighting the potential clinical distinction between cholesterol- and particle-based measures of HDL.
In an analysis of 10886 patients from the JUPITER study (Justification for the Use of Statins in Primary Prevention: An Intervention Trial Evaluating Rosuvastatin), the authors reported that the on-treatment concentration of HDL particles, as measured by nuclear magnetic resonance spectroscopy, was inversely associated with adverse cardiovascular events both in patients given placebo and in rosuvastatin-treated patients.
This contrasts with a previous report by this group in which HDL-C was found to not be significantly associated with cardiovascular events in the statin-treated group"
My major concern with the book is that in patients with elevated LDL-P greater than 1,000 and with positive CAC (coronary arterial calcium done with CT scan) and/or a positive CIMT (carotid intimal media thickness by Ultrasound) are told to treat the plaque with (page 164) magnesium, co-enzyme Q, resveratrol, curcumin, vitamin D, vitamin C, and citrus bergamot (Dr. Bowden). Chelation therapy (Dr Fred Pescatore) p 165.
On page 163 a chapter is titled "The Risks from Statins outweighs the absolute risks of having a heart attack." However in the chapter Dr Ravnskov says "there is a minuscule increase of two percentage points in your survival."
No matter how he couches it, he says there is decrease of mortality on statins.
Thus a patient with a calcium score above zero and/or a CIMT of 75% tile has found out he has sub-clinical plaque.
A vulnerable plaque can rupture and cause sudden coronary death. There are 100,000 sudden coronary deaths a year with 50% of those people having death as the first sign of the disease.
The best way to regress the plaque and reduce the inflammation is by getting the LDL-P less than 750.
At least Jimmie could advise a wax matrix over the counter niacin at the low dose of 1,000 mg.
Then Zetia is a good non-statin alternative to add on if the LDL-P goal is not reached.
Finally this anti-statin crowd needs to consider to break the lowest dose of atorvastatin in half and take 5 mg. If they think the statin is affecting them, they can take atorvastatin 5 mg every other day.
Then follow the CiMT every two years.
Circulation Sept 10,2013 Nicholls and Puri
Circulation Sept 10, 2013 Rosenson et. al.
1 out of 2 people found this review helpful.Was this review helpful? Yes NoThank you for your feedback. Report this reviewThank you, this review has been flagged.
Posted January 12, 2014
No text was provided for this review.