tag:blogger.com,1999:blog-9174025374821038087.post8849959936998365126..comments2024-01-29T17:51:55.608+00:00Comments on Nige's Diet & Nutrition Blog: Why (LDL particle) size matters.Nigel Kinbrumhttp://www.blogger.com/profile/03368973941328529619noreply@blogger.comBlogger7125tag:blogger.com,1999:blog-9174025374821038087.post-77996842555864501552014-09-24T13:47:03.024+01:002014-09-24T13:47:03.024+01:00Sorry it took so long to approve your first commen...Sorry it took so long to approve your first comment, but I mistakenly thought that I'd already white-listed you. I have, now!Nigel Kinbrumhttp://nigeepoo.blogspot.com/noreply@blogger.comtag:blogger.com,1999:blog-9174025374821038087.post-54392307265415534412014-09-22T13:17:04.365+01:002014-09-22T13:17:04.365+01:00Q "Why does arterial tunica intima become neo...Q "Why does arterial <i>tunica intima</i> become neovascularized in the first place?"<br /><br />A Because "...the cells in the coronary <i>tunica intima</i> possess inherently high proliferative capacity...[so that] these cells respond by proliferating to any stimuli, exogenous or endogenous...Regardless of the nature and magnitude of stimuli/insults, cells that appear in the arterial intima compartment...always proliferate in response."<br /><br />Now note: those various stimuli and insults that induce the intimal proliferation—that according to his hypothesis <b>initiate</b> the whole atherosclerosis process—<b>do not include LDL's</b> because "...the outer DIT does not have direct contact with the blood, and <b>interaction with LDL-C is PREVENTED by diffusion distance and the properties of this molecule (20nm)."<br /><br />∴ It is <b>not LDL particle number</b> that <b>determines</b> the infiltration of LDL cholesterol into the media of artery walls.<br /><br />Oui? Non???<br /><br />So while I still don't buy the ubiquitous view [dietary sat fat →↑LDL-C →invasion of arterial wall/atherosclerosis], I do like your other candidate for initiating the "insult"—and which remains compatible with the "neovascularization hypothesis"—b>calcium.</b><br /><br />Takuo Fujita has written several papers which have persuaded me that the initiating culprit in atherosclerosis—and a slew of the other diseases of aging—could very well be what he called <b>"the calcium shift phenomenon"</b>: i.e., the process that leads to the deposition of calcium into the soft tissues: <br /><br />http://www.ncbi.nlm.nih.gov/pubmed/2943880<br />"Calcium deficiency is a constant menace to land-abiding animals, including mammals...Low calcium and vitamin D intake, short solar exposure, decreased intestinal absorption, and falling renal function with insufficient 1,25(OH)2 vitamin D biosynthesis all contribute to calcium deficiency, secondary hyperparathyroidism, bone loss and possibly calcium shift from the bone to soft tissue, and from the extracellular to the intracellular compartment, blunting the sharp concentration gap between these compartments. The consequences of calcium deficiency might thus include not only osteoporosis, but also <b>arteriosclerosis and hypertension due to the increase of calcium in the vascular wall</b>, amyotrophic lateral sclerosis and <b>senile dementia due to calcium deposition in the central nervous system</b>, and a decrease in cellular function, because of blunting of the difference in extracellular-intracellular calcium, leading to <b>diabetes mellitus</b>, immune deficiency and others."<br /><br />Also here:<br />http://www.ncbi.nlm.nih.gov/pubmed/1959348<br /><br />[it's a big reason why I aim to get some sun & have at least a quart of milk—or it's equivalent— a day]billy the knoreply@blogger.comtag:blogger.com,1999:blog-9174025374821038087.post-2330340130404015472014-09-21T16:40:13.583+01:002014-09-21T16:40:13.583+01:00I think that infiltration of LDL (also Ca) into th...I think that infiltration of LDL (also Ca) into the media impedes the diffusion of O2 from the adventitia to the intima, and the resulting hypoxia in the intima induces neovascularisation.Nigel Kinbrumhttp://nigeepoo.blogspot.com/noreply@blogger.comtag:blogger.com,1999:blog-9174025374821038087.post-79161406373473996032014-09-21T16:02:19.409+01:002014-09-21T16:02:19.409+01:00And—unless I'm mistaken—the LDL's themselv...And—unless I'm mistaken—the LDL's themselves do not <b>cause</b> the DIT enlargement that in turn causes the hypoxia that induces neovascularization as an adaptive response.billy the knoreply@blogger.comtag:blogger.com,1999:blog-9174025374821038087.post-2892307073123547382014-09-21T01:02:53.863+01:002014-09-21T01:02:53.863+01:00Nige, it's true that LDL-P and LDL-C are both ...Nige, it's true that LDL-P and LDL-C are both relevant to the <i>relative risk</i> for CHD, but doesn't the author of your linked article dismiss the importance of this relevance here?:<br /><br />[p.5] "High levels of LDL are an important <i>risk factor</i>... however, <b>the statement that high levels of LDL are the main cause of coronary atherosclerosis is inconsistent with established medical concepts."</b><br /><br />And here:<br />[p.6] "...the fact that lowering LDL levels does not prevent cardiac events in 60-70% of individuals <b>at risk</b> contradicts the causative role of LDL. Unfortunately, it appears that the scientific and medical communities are focusing on and emphasizing <i>biomarkers that can predict risk, without proof that these biomarkers <b>cause</b> the risk."</i><br /><br />Also his "hypothesis" statement:<br />[p.2] "Neovascularization of the normally avascular coronary DIT [diffuse intimal thickening] by permeable vasculature from the adventitial vasa vasorum is the cause of LDL deposition and CA. DIT enlargement, seen in early CA and aging, causes hypoxia of the outer DIT and induces neovascularization. According to this alternative proposal, coronary atherosclerosis is not related to inflammation and <b>can occur in individuals with normal circulating levels of LDL</b>, consistent with research findings."<br /><i><br />"...can occur in individuals with normal circulating levels of LDL..."</i><br />[i.e., "normal levels"—that is: NOT "high levels of LDL"—isn't this hypothesis saying here that the <b>LDL particle number</b> per se does not <b>determine</b> the infiltration?]<br /><br />True, it <b>is</b> the <i>lipoproteins</i> that do invade the coronary intima, but these statements from Subbotin's article do not seem to <br />point to the necessity of taking care to reduce one's <b>LDL particle number</b>in order to avoid coronary atherosclerosis—i.e., via rigorous daily monitoring of one's intake of <i>saturated fats & sugars & fast starches</i>—especially this statement on p. 17:<br /><br /> "...it logically follows that since the presence of LDL-C in plasma is a <b>fundamental metabolic requirement</b> for humans, theoretically <b>there is no “safe LDL-C level” that would be 100% certain to prevent coronary atherosclerosis if intimal neovascularization has already occurred."</b>billy the knoreply@blogger.comtag:blogger.com,1999:blog-9174025374821038087.post-46261184621151813532014-09-20T20:28:02.575+01:002014-09-20T20:28:02.575+01:00A1. It's difficult to say. Dr Dayspring said t...A1. It's difficult to say. Dr Dayspring said that if LDL-C is extremely high, LDL-P becomes irrelevant.<br /><br />A2. I subscribe to http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3492120/ LDL-P and LDL-C are both relevant to the RR for CHD.Nigel Kinbrumhttp://nigeepoo.blogspot.com/noreply@blogger.comtag:blogger.com,1999:blog-9174025374821038087.post-58423691571186863922014-09-19T16:14:05.112+01:002014-09-19T16:14:05.112+01:00Nigel, as always, I find your articles useful and ...Nigel, as always, I find your articles useful and sometimes entertaining.Babs Hogannoreply@blogger.com